Auerbach's Wilderness Medicine PDF
Auerbach's Wilderness Medicine PDF
Auerbach's Wilderness Medicine PDF
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
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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.
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
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
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
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
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
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
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
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 Armando Márquez Jr, MD
CONTRI BUTORS
Clinical Associate Professor Assistant Clinical Professor
Department of Emergency Medicine Department of Emergency Medicine
Stanford University School of Medicine University of Illinois College of Medicine at Chicago
Stanford, California Chicago, Illinois
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
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
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- War.2 When Menelaus was wounded by a Trojan bowman, the
dren lived in austerity in the wilderness. So, the human race is fleet surgeon, Machaon (son of Aesculapius, god of medicine),
not encountering wilderness medicine for the very first time. was called to treat the wound:
Before the advent of such wonders as antisepsis, randomized Without delay he drew
clinical trials, and emphasis on evidence, and therefore through- the arrow from the fairly fitted belt.
out most of the history of human existence and eventually, civi- The barbs were bent in drawing.
lization, the practice of medicine was largely improvised and Then he loosed the plate—the armorer’s work—and
based on anecdotes and dogma, rather than evolving science. carefully
Given that humans had to make do with little or nothing before O’er looked the wound where fell the bitter shaft.
they had access to tests, drugs, and devices, the history of wilder- Cleansed it from blood, and sprinkled over it
ness medicine might be considered to largely be the history of with skill the soothing balsam of yore which
medicine itself. Advances in medicine have in general paralleled the friendly Chiron to his father gave.
other sciences, with periodic insights into its essences, but there
remain geographies and circumstances where wilderness medi- Thomas Woodall (1569-1643) perhaps deserves the title “Father
cine is uniquely essential. of Marine Medicine” because he was ahead of his time with
We are in the midst of a scientific revolution, but recognize observations of scurvy and views on the treatment of wounds,
that optimal urban science is not necessarily applicable in austere fractures, and amputations.1 His extensive practical experience,
environments. So, as we intentionally place ourselves in wild astute observations, and cautious judgment persuaded him that
places isolated from cities and machines, wilderness medicine the theories of oracles, such as Galen, often offered little in the
comes full circle and needs to remain different in certain ways way of useful medical knowledge. As stated in his 1655 book
from big city medicine. From this perspective, one might identify The Surgeon’s Mate, Woodall divided wounds into three catego-
many potential starting points for our 21st century iteration of ries: (1) puncture wounds and lacerations, (2) gunshot wounds,
wilderness medicine. However, thoughtful reflection identifies and (3) bone fractures.3 His treatment recommendations have a
two prominent threads. First, today’s wilderness medicine “began” modern ring: “…remove unnatural things forced into the wound…
when urban, high-resource medicine became too sophisticated which should be done with the least pain to the patient and
to practice in austere environments—when improvisation was avoiding arteries, nerves, and veins.” The “unnatural things” to
required to replace more sophisticated methodology that was not which he referred might include wood splinters from spars and
available. Second, and very significant from a definition stand- masts, fragments from cannon fire, and other foreign objects
point, wilderness medicine gained true identity when men and embedded into people during commerce and conflict. Anesthesia
women began in earnest to explore environments that stressed was nonexistent in this era. In the case of removal being too
normal human physiology to the point that unique pathophysiol- difficult or painful, Woodall recommended “tarry if you may,
ogy was discovered. This phenomenon notably occurred with while nature helps.” His suggestions to ligate specific vessels that
human endeavors at high altitude (mountaineering and aviation), contributed to excessive bleeding and to place dressings soaked
under the ocean surface (diving), at extremes of temperature in wine over wounds were significant departures from the usual
(cold and heat), and at the limits of endurance posed by natural treatment of the day, which was wound cauterization with hot
disasters or forays into the ultimate frontier of space travel. oil or a red-hot searing iron.
The history of wilderness medicine could be a textbook unto When limb wounds were severe, Woodall was not in a rush
itself. The following paragraphs attempt to provide key examples to amputate. This approach ran counter to the prevailing custom
of how the evolution of modern medicine simultaneously drew and for several hundred years afterward. Woodall reasoned that
from and shaped the specialty. the need for amputation should be dictated by specific criteria:
Military medicine provides many examples of this interaction. one-half or more of the limb should have been dismembered or
For much of history, the greatest threats to soldiers were not irreparably damaged; a chronic suppurating wound be present;
battlefield combatants, but weather and infectious diseases. the patient’s life be imminently in danger; or the remaining
During the American Revolutionary War, 6,200 American soldiers portion of the limb be unserviceable. His concepts were far more
were killed in action, while 10,000 died of disease. Typhus, conservative and reasonable than those of military surgeons who
smallpox, dysentery, diarrhea, and pneumonia were prevalent. practiced for the next two centuries, such as during the American
The War of 1812 generated 2,200 American combat deaths and Civil War, where immediate amputation of any limb with a
nearly 13,000 deaths from noncombat causes. Napoleon invaded gunshot wound was the customary practice. Woodall’s conserva-
Russia in 1812 with 680,000 soldiers, and retreated back to France tive principles from three centuries past seem reasonable for
five months later with 27,000. Most of the remainder had suc- modern physicians providing care for trauma patients in harsh
cumbed to hypothermia, frostbite, and typhus. It wasn’t until or remote environments.
World War II that the number of soldiers killed in combat out- It was Admiral Horatio Nelson, a senior nonmedical officer in
numbered those who died from other causes, many of them the British Royal Navy, who near the turn of the nineteenth
environmental. century brought about a revolution in medicine, particularly in
“Medicine Under Sail,” Zachary Friedenberg’s history on the disease control, practiced on the high seas. Nelson’s well-
subject,1 chronicles an oft-overlooked perspective of the early documented personal medical history provides a window into
history of medicine. In the same vein, Homer made reference in certain typical maladies and injuries for the ocean-going warrior
book 4 of the Iliad to a medical naval incident in the Trojan or explorer of his era. As a midshipman, he sustained partial
xix
paralysis from an illness contracted at age 17, was stricken with become the treatment of choice for syphilis. It was typically taken
FOREWORD
malaria in the West Indies, contracted yellow fever in Nicaragua, orally or used as a topical ointment in very liberal doses. Cures
suffered a laceration of his back and lost sight in his left eye were few and far between, and the patient often succumbed to
during battles near Corsica, endured an abdominal wound during mercury poisoning before the syphilis entered its secondary or
a military encounter at Cape St. Vincent, and had his right arm tertiary phase. During this era, cinchona for malaria was one of
amputated below the shoulder after a severe injury from grape- only a handful of medications that had the ability to produce an
shot during battle in the Canary Islands. His luck ran out in 1805 intended result. Thus, early physicians “were like hunters going
at Trafalgar, where a French sharpshooter’s bullet delivered a into the field and shooting blanks.”8
fatal blow. As exploration of the last great terrestrial and oceanic “blanks
Largely as a result of Admiral Nelson’s impressive understand- on the map” evolved into ever more sophisticated ventures in the
ing of the challenges of providing effective shipboard medical 19th and early 20th centuries, wilderness medical care further
care, medical reforms in his and other navies became a reality. evolved. “Physician/naturalists,” trained physicians who could
Much emphasis was directed at proper diet as it relates to disease multitask as field biologists, began to accompany long, arduous
prevention, a unique perspective at that time that is increasingly explorations to the ends of the earth. While their medical training
popular today. The success of this strategy is obvious from the was certainly superior to that of William Clark and they could be
historical record; the proportion of men sent sick to hospital from considered more competent healers, these physicians still needed
ships between the last decade of the 18th century and the first to be extremely skilled outdoorsmen to participate in these
decade of the 19th century fell from a high of 38.4% (in 1793) demanding adventures. To appreciate the extent of the sacrifices
to a low of 6.4% (in 1806).4 sometimes made by these physician-explorers, one need only
After the end of the American Civil War, the U.S. Army fought recall the Englishman Edward Wilson—physician, polar explorer,
with many Native American tribes in the western states and ter- natural historian, painter, and ornithologist. Wilson accompanied
ritories. Military medical personnel and civilian practitioners two of Robert Scott’s exploratory Antarctic voyages in the early
became adept at extracting arrows and other primitive penetrat- years of the 20th century, tragically perishing with his companions
ing weapons. Instruments devised as early as 500 BC (such as in March 1912 on the Antarctic plateau during the British team’s
the belulcum) for removing arrows became invaluable during the return sledge journey from the South Pole. Edward Atkinson,
1870s. These tools could dilate the point of entrance and widen research parasitologist and senior expedition surgeon for Scott’s
the channel containing the arrow, to allow the head of the arrow final, ill-fated 1910-1913 Terra Nova expedition, was part of the
to be grasped. North American Indian arrows were typically fired shore party that did not accompany Scott, Wilson, and their three
with great speed and force, and if not stopped by bone, could companions during the final push to the Pole. By March 1912,
easily pass through a horse or bison. Not surprisingly, mortality Scott’s party was clearly overdue and fear mounted that they had
from arrow wounds was high, with one 1871 report suggesting perished. That month, Atkinson, as senior officer in command of
a fatality rate of approximately 30%. 13 men facing 4 months of darkness and intense cold, led a futile
The ensuing maturation of military medicine marked a turning effort to locate Scott. In October of 1912, with the sun at last
point back to appreciation of wilderness medicine, or perhaps shedding some light and heat on the bleak Antarctic landscape,
more appropriately, austere medicine. This occurred when the Atkinson once again set out with a search party. On November
military began to move medicine to the front lines. Re-emergence 12, they discovered the dead explorers within Scott’s tent, which
of tourniquets applied in the field to extremities to control bleed- was partially buried in snow. Atkinson was first to enter the tent,
ing are illustrative. In the past two decades, bringing medicine where he read the diary entries of the polar party’s final days of
to the point of action led to creation of tactical combat casualty privation and suffering.9
care (TCCC)5 and formation of the Special Operations Medical During the 20th century, exploration of the limits of the
Association (SOMA), including collaboration with the Wilderness human body and those of the earth’s physical domain altered
Medical Society (WMS). Soldiers with life-threatening injuries that the manner in which people viewed the world and their place
previously would have been fatal are now stabilized on or near in it. While the pursuits of physical exploration and medicine
the battlefield before being evacuated to definitive trauma centers may seem unlikely siblings, they deeply informed each other.
in their home countries. Dr. Charles Houston, who served as an inspiration to many
Parallel to the contributions of military medicine were those current wilderness medicine researchers and clinicians, embod-
of intrepid explorers. Many of the early “practitioners” of wilder- ied the modern adventurer-physician.10 An accomplished moun-
ness medicine were adventurers who accepted additional respon- taineer and Harvard-trained physician, Houston led two attempts
sibilities. Although not a physician, Captain William Clark had to summit K2, included the ill-fated attempt in 1953 that claimed
sufficient medical knowledge to serve as the expedition doctor the life of one team member and nearly wiped out the entire
on the heralded Lewis and Clark expedition.6 In the early days team. While a naval flight surgeon during World War II, Houston
of exploration, expedition doctors were integral members of a conceived, and ultimately was one of the physician/scientists in
dedicated team with expertise related to the logistics of the charge of, Operation Everest in 1946. This study, sponsored by
mission. The current expeditionary practice of retaining expert the U.S. Navy, was intended to benefit the aviation community
medical guests is a relatively recent phenomenon. by shedding light on human adaptation to and tolerance of
Infection from nonsterile surgical procedures and penetrating extreme altitudes. Such research efforts were particularly timely
missiles was but one major challenge of this bygone era. Early because they occurred at a time when airplanes became capable
explorers also had to contend with infectious diseases that could of flying higher than humans could tolerate without support,
easily be passed between persons and that had the potential to such as from pressurized suits or cabins. Houston’s high-altitude
bring any journey to a sudden halt. Throughout much of the chamber research led to the first successful simulated “ascent” to
course of its explorations, the Lewis and Clark expedition the barometric pressure equivalent of the summit of Mt Everest,
encountered indigenous tribes. These tribes had not been proving it could perhaps be reached in real life without supple-
exposed to European-based diseases for many centuries, so were mental oxygen. His research team’s findings led to great advances
neither educationally nor immunologically capable of effective in understanding the challenges of altitude and etiology of high-
self-defense. The Americans learned of many settlements (espe- altitude illnesses. Houston later became a founding member of
cially along the Missouri River) that had been decimated by the WMS, and in doing so, drew attention to its mission and
devastating epidemics of smallpox following contact with persons potential.
of European background. The concept of vaccination was gather- Houston’s achievements were part of a blossoming of science
ing proponents at this time, and President Thomas Jefferson sent exemplified by the discoveries of other legendary figures in alti-
a sample of cowpox on the expedition with Lewis in hope that tude research and mountain medicine, including Drs. Herb Hult-
he could attempt to vaccinate the “natives.”7 Other infectious gren, John West, Robert Schoene, and Peter Hackett. While
maladies of regular concern to Lewis and Clark included omni- serving as a member of the American Medical Research Expedi-
present venereal diseases, such as syphilis. Prior to 1800, mercury, tion to Everest in 1981, Hackett accomplished a successful summit
already used as therapy for many infections and diseases, had of Mt Everest, climbing alone to the top from high camp, falling
xx
while traversing the Hillary step, and thereby fortunately uncov- moment’s notice to assist in humanitarian relief and disaster
FOREWORD
ering a fixed rope that enabled him to self-rescue and live to tell response. After many lessons learned from earlier treat-and-leave
the tale. He too became one of the founding members approaches, providers and organizations have embarked upon
of the WMS. During this modern era, brave and high-spirited much more sustainable approaches to health care delivery,
physician high-altitude adventurers Drs. Oswald Oelz, Charles including vital education and training.
Clarke, and Bruno Dürrer were pioneering by exploring, discov- The modern history of wilderness medicine spawned the
ering, and innovating. There were and will be so many brilliant founding and maturation of important scientific societies dedi-
men and women who combine adventure with medicine. cated to the discipline or one of its subspecialties. The WMS was
One could write equally about the oceans that cover most of formed in 1982; the International Society of Mountain Medicine
our planet, and about forests, rivers, canyonlands, or polar caps. in 1985; and the International Society of Travel Medicine in 1991.
There will hopefully always be mountains to climb, woods to Phenomenal individuals who contributed to modern wilderness
wander, deserts to cross, and lagoons to explore. Each has its medicine have become too numerous to count. Modern wilder-
wilderness medicine history, from antiquity to modern times. ness medicine was conceptualized and organized by a dedicated
There are lost people to find, victims of mishaps to rescue, and and ambitious group of prime movers, and has become an enor-
ever the need to make do with very little at the worst possible mous, growing community, reflected in part by the contributors
moments. We know more now about how to direct doctors, and to this textbook, some of whom have been involved in wilder-
how to facilitate location, stabilization, and transport of victims ness medicine for many decades. We admire the pioneers of the
from remote and geographically challenging locales. Wilderness past, and have every confidence in the ability of today’s leaders
first responders are equipped with knowledge and training that and innovators to carry us with great enthusiasm into the future.
allow for more advanced intervention that occurs with shorter
transport times.11 Search and rescue team training has become Robert H. Quinn, MD
sophisticated and intense, in large measure because the wilder- George W. Rodway, PhD
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). REFERENCES
A cooperative idea initially developed in Europe in the late 1990s 1. Friedenberg ZB. Medicine Under Sail. Annapolis, MD: Naval Institute
by the International Commission for Alpine Rescue, International Press; 2002.
Climbing and Mountaineering Federation, and International 2. Homer. The Iliad and the Odyssey. London: John Ogilby; 1660.
Society of Mountain Medicine, the extensive and comprehensive 3. Woodall T. The Surgeon’s Mate. London: John League; 1655.
DiMM curriculum blends rigorous didactic and practical educa- 4. Allison RS. Sea Diseases: The Story of a Great Natural Experiment
in Preventive Medicine in the Royal Navy. London: John Bale Medical
tion in wilderness medicine with technical mountain rescue and Publications; 1943.
self-sufficiency in the backcountry. Many mountain medicine 5. Butler FK, Hagmann J, Butler G. Tactical combat casualty care in
organizations worldwide now offer the standard (or specialty special operations. Mil Med 1996;161(Suppl. 1):1–16.
module) DiMM curriculum, in the process bridging many nations 6. Larsell O. Excerpts from: Medical aspects of the Lewis and Clark
and cultures. expedition (1804-1806). Wilderness Environ Med 2003;14:265–71.
The final linchpin in the modern enactment of wilderness 7. Chuinard EP. Only One Man Died: The Medical Aspects of the Lewis
medicine as a distinct entity is the selfless act of delivering and Clark Expedition. Fairfield, WA: Ye Galleon Press; 1999.
medical care to the farthest reaches of the globe. Less fortunate 8. Paton BC. Adventuring with Boldness: The Triumph of the Explorers.
people benefit from the emotionally taxing and sometimes coura- Golden, CO: Fulcrum Publishing; 2006.
9. Campbell WC. Edward Leicester Atkinson: Physician, parasitologist,
geous efforts of many wilderness medicine–trained volunteers and adventurer. J Hist Med Allied Sci 1991;46:219–40.
who deliver medical support that ranges from immunizations 10. McDonald B. Brotherhood of the Rope: the Biography of Charles
during peaceful times to surgeries in the aftermath of natural Houston. Seattle, WA: The Mountaineers; 2007.
disasters. Wilderness medicine breeds an ethos of service. Medical 11. Backer HD. Editorial: what is wilderness medicine? Wilderness
teams populated by wilderness medicine providers depart at a Environ Med 1995;6:3–10.
xxi
Preface
As the specialty of wilderness medicine matures, obligations edition is that anywhere the ability to practice medicine in an
grow. Education is the objective of this textbook and certainly austere setting is the task at hand, wilderness medicine knowl-
essential, but to advance the field in all aspects, leadership and edge and experience are essential.
inspiration are required. In this seventh edition of Wilderness In medical schools across the United States, and now in many
Medicine, the contributors are many of these leaders, and their other countries, wilderness medicine courses are taught and
writing and creativity are outstanding. Authors who are practitio- usually among the most popular electives. Wilderness experi-
ners and researchers with an inestimable amount of experience ences are used by undergraduate universities and medical schools
share their knowledge and wisdom, and seek not only to teach, to introduce students to one another early in their careers and
but to inspire those who will follow them. They have superbly facilitate collaborations. Competitive wilderness adventures in the
pointed out not only what we already know, but also what we cloaks of competitions and races are the backbone of reality
need to discover and learn, thereby directing a path toward entertainment. They all require medical planning and support.
observation, service, and experimentation, each of which is inte- Wilderness recreation outpaces all other forms of time away from
gral to the unique influence of wilderness medicine. the urban work existence. Respite and renewal are inextricably
The breadth and depth of content of wilderness medicine linked to the wilderness. And when we seek to reach beyond
have grown to the extent that two volumes of Wilderness Medi- ourselves, where do we go first to explore? The wilderness, of
cine are now required. The authors, assistant editors, and I are course.
grateful to the publisher for using innovative techniques to create At a time when humans are generally considered more of a
a comprehensive book with outstanding visual appeal, so that burden to than saviors of the environment, we will more often
the blend of academia and art is at once logical and stimulating. be in the wilderness, learning its ways and hopefully not
In this edition, I am enormously grateful to the remarkable team encroaching upon it. To impress upon others the need to pre-
at Elsevier, including Kate Dimock, Lucia Gunzel, Lauren Boyle, serve it, we will understand its offerings and document its beauty.
and Linda Belfus. My publishing family always sets the bar high To eliminate health care disparities, we will find a way to interact
and patiently helps me leap. My global academic family embraces with indigenous people in a way that can preserve their sur-
this exciting specialty, and my biological family graciously allows roundings and bring healing in the midst of horrific infectious
me the time to pursue this endeavor. diseases, violent conflicts, and post-disaster social and economic
Acquisition of new knowledge is exciting and challenging for chaos. To fuel our existence, we will go beyond clear-cutting
academicians, practitioners, and students. Wilderness medicine forests, pillaging oceans, and extracting fossil fuels that might
draws not only from the timeless medical specialties of surgery, never be replaced. If wilderness medicine helps make us aware
internal medicine, obstetrics and gynecology, pediatrics, and that there is a wilderness and that without a concerted effort it
psychiatry, but from anywhere that medical science reaches out will disappear, then that is a precious accomplishment by a noble
to improve the health and safety of patients. New chapters and specialty.
deeper discussions within revised chapters introduce the reader Judging by the quality of research, number of important pub-
to the trends that are most likely to become influential as we lications, and attendance at educational gatherings, such as the
approach the next five years. Evidence-based medicine, genom- combined sessions of the Wilderness Medical Society and Inter-
ics and personalization, and the imperative to translate all of this national Society for Mountain Medicine, wilderness medicine is
into how we live our lives and practice our craft in the field and here to stay. For that, we are in great debt to those who came
hospital are new features of this edition. Other notable changes before us, who preached and practiced wilderness medicine long
from the previous edition are a chapter on medical wilderness before anyone contemplated coalescing a specialty. One such
adventure races and expanded discussion of high-altitude medi- visionary is Dr. Bruce Paton, whose artwork graces this Preface.
cine, improvisation, technical rescue, and wilderness medicine We all have mentors and partners, and I have certainly had mine.
education, to name a few. We are proud to continue emphasis Notable among them are Herb Hultgren and Charlie Houston in
on how we approach the health of planet Earth. Wilderness high-altitude medicine, Jeff Davis and Bruce Halstead in dive
conservation and preservation will remain in part the purview of medicine, Warren Bowman in prehospital care, Bob Mutch in
wilderness medicine as we await a more concerted effort by the wildland fire management, Donald Trunkey in trauma care,
entire house of medicine to fulfill its obligation to play a leader- Bruce Dixon in clinical diagnosis, Murray Fowler in veterinary
ship role in efforts to maintain the desired environment to support medicine, Sherman Minton in envenomation, Bruno Dürrer in
life on our planet. rescue, Steve French in bear behavior and attack, Cam Bangs
The efforts of people and organizations engaged in all aspects and Alan Steinman in hypothermia, Joe Serra and Ed Geehr in
of wilderness medicine are growing and increasingly collabora- humanism, Wongchu Sherpa in spirituality, and Ken Kizer in
tive. Wilderness medicine is firmly embedded in the activities of determination.
the military, and vice versa. As a responder to the 2015 earth- The spark has become a flame. I regularly see young people
quake disaster in Nepal, I witnessed once again that my remark- beam when they realize that medicine can be so enjoyable. There
able colleagues in the wilderness medicine community are are hardcore science and service in wilderness medicine, but we
regularly at the front lines when calamity strikes. Whether it is are still “out there,” away from electronic medical records, cost
an Ebola outbreak in West Africa, a typhoon in the Philippines, containment, and endless political debates about universal health
or a wildfire in Washington State, this book’s contributors enthu- care. We are in the field, responding because we are responsive,
siastically volunteer to serve. What I have learned since the last sticking our necks out to accept the adventure and risk, and then
xxiii
put something back. There is heroism in medicine, and wilder- posed on the side of a mountain, in a cave during a lightning
PREFACE
ness medicine has its fair share, delightfully unsung. It is brave storm, or on the beach of a faraway atoll. Wilderness medicine
to document the wisdom of an indigenous healer, courageous takes everything we have learned and then adds to it the spice
to teach mountain safety to sherpas, and selfless to assist layper- of life. How much fun is that? Seven editions now, and I can’t
sons to fill the gaps in health care that cannot be provided during wait for the eighth.
a humanitarian crisis. The settings in which we practice may
sometimes be uncontrolled, but it is the domain of wilderness Paul S. Auerbach
medicine experts to bring best practices to the unique bedsides
Aiming High
Bruce Paton
xxiv
Video Contents
Video 2-1 Periodic Breathing Video 40-5 African Child with Severe Malaria
Video 8-1 Ocean Ranger Disaster Video 40-6 CDC: Blood Specimen Processing
Video 8-2 Marine Electric Disaster Video 40-7 BinaxNOW Malaria, the First Rapid
Diagnostic Test Approved by the FDA
Video 8-3 The Cold, Hard Facts of Winter for Use in the United States
Road Safety
Video 44-1 Neuromuscular Hyperactivity in Children
Video 8-4A Cold Water Immersion and Drowning, Part 1 with Scorpion Envenomation
Video 8-4B Cold Water Immersion and Drowning, Part 2 Video 49-1A Tooth Splinting Instruments
Video 8-4C Cold Water Immersion and Drowning, Part 3 Video 49-1B Tooth Splinting Procedure
Video 8-5A Hypothermia Video 49-2A Recementing a Crown: Armamentarium
Video 8-5B Hypothermia: Shivering Video 49-2B Recementing a Crown: Procedure
Video 8-5C Hypothermia and Alcohol Video 49-3A Replacing a Lost Filling: Armamentarium
Video 8-5D Hypothermia: Mild vs. Severe Video 49-3B Replacing a Lost Filling: Procedure
Video 8-5E Hypothermia and CPR Video 83-1 Ushahidi Haiti
Video 8-5F Hypothermia Treatment Video 126-1 Flight Deck Camera View of the
Video 8-5G Hypothermia: Rewarming STS-135 Crew
Video 8-6A Cold Water Boot Camp: Life Jackets Video 126-2 Astronaut Karen Nyberg Demonstrates Use
of U.S. Treadmill
Video 8-6B Cold Water Boot Camp: 1-10-1 Principle
Video 126-3 Astronaut Mike Hopkins Demonstrates
Video 8-6C Cold Water Boot Camp: Surviving Two Exercises Astronauts Can
Cold Water Perform Using the Advanced Resistive
Exercise Device
Video 8-6D Cold Water Boot Camp: The First
60 Seconds Video 126-4 Montage of Experienced Astronauts
Moving About Aboard the International
Video 8-7 Cold Water Boating
Space Station
Video 8-8 Transport Canada: Boating Safety
Video 126-5 Astronaut Trains for a Spacewalk in the
Video 40-1 WHO: Malaria Key Facts Neutral Buoyancy Laboratory
Video 40-2 Malaria Life Cycle, Part 1: Human Host Video 126-6 Use of Water as an Acoustic Medium
for Ultrasound Imaging in Space
Video 40-3 Malaria Life Cycle, Part 2: Mosquito Host
Video 40-4 Malaria Life Cycle, Animation
xxix
PHOTO CREDITS
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 THE ENVIRONMENT OF
meters (m), or 7874 feet, in the American West each year. Hun-
dreds of thousands visit central and south Asia, Africa, and South
HIGH ALTITUDE
America, many traveling to altitudes above 4000 m (13,123 feet). Barometric pressure (PB) falls with increasing altitude in a loga-
In addition, millions of persons live in large cities above 3000 m rithmic manner (Table 1-2). Therefore, the partial pressure of
(9843 feet) in South America and Asia. The population in the oxygen (PO2, 21% of PB) also decreases, resulting in the primary
Rocky Mountains of North America has doubled in the past insult of high-altitude: hypoxia. At approximately 5800 m (19,029
decade; 700,000 persons live above 2500 m (8202 feet) in Colo- feet), PB is one-half that at sea level, and on the summit of Mt
rado alone. Increasingly, physicians and other health care provid- Everest (8848 m [29,029 feet]), PIO2 is approximately 28% that at
ers are confronted with questions of prevention and treatment sea level (see Figure 1-1 and Table 1-1).
of high-altitude medical problems, as well as the effects of alti- The relationship of PB to altitude changes with distance from
tude on pre existing medical conditions. Despite advances in the equator. Thus, in addition to extreme cold, polar regions
high-altitude medicine, significant morbidity and mortality persist. afford greater hypoxia at any given altitude. West90 calculated
Clearly, better education of the population at risk and those that PB on the summit of Mt Everest (27 degrees north latitude
advising them is essential. [N]) would be about 222 mm Hg instead of 253 mm Hg if Mt
High-altitude medicine and physiology are discussed in the Everest were located at the latitude of Denali (62 degrees N).
first three chapters of this textbook. In this chapter the reader is Such a difference, he claims, would be sufficient to render impos-
introduced to the basic physiology of high-altitude exposure. sible an ascent without supplemental oxygen.
Chapter 2 describes the pathophysiology, recognition, manage- In addition to the role of latitude, fluctuations related to
ment, and prevention of altitude illnesses and other clinical issues season, weather, and temperature affect the pressure-altitude
likely to be encountered in both “lowlanders” and high-altitude relationship. Pressure is lower in winter than in summer. A low-
residents. Chapter 3 focuses on patients with preexisting medical pressure trough can reduce pressure 10 mm Hg in one night on
problems who travel to high altitudes (Box 1-1). 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
DEFINITIONS Temperature decreases with altitude (average of 6.5° C [11.7° F]
HIGH ALTITUDE per 1000 m [3281 feet]), and the effects of cold and hypoxia are
generally additive in provoking both cold injuries and HAPE.59,93
(1500 to 3500 meters [4921 to 11,483 feet]) Ultraviolet (UV) light penetration increases approximately 4% per
The onset of physiologic effects of diminished partial pressure 300-m (984-foot) gain in altitude, increasing the risks for sunburn,
of inspired oxygen (PIO2) includes decreased exercise perfor- skin cancer, and snowblindness. Reflection of sunlight in glacial
mance and increased ventilation (lower arterial carbon dioxide cirques and on flat glaciers can cause intense radiation of heat
partial pressure [PaCO2]). Minor impairment exists in arterial in the absence of wind. We have observed temperatures of 40°
oxygen transport (arterial oxygen saturation [SaO2] at least 90%), to 42° C (104° to 107.6° F) in tents on both Mt Everest and Denali.
but arterial oxygen partial pressure (PaO2) is significantly dimin- Heat problems, primarily heat exhaustion, are often unrecog-
ished. Because of the large number of people who ascend rapidly nized in this usually cold environment. Physiologists have not
to 2500 to 3500 m (8202 to 11,483 feet), high-altitude illness is yet examined the consequences of heat stress or rapid, extreme
common in this range of altitudes (see Chapter 2). changes in environmental temperature combined with the hy-
poxia of high altitude.
VERY 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-
(3500 to 5500 meters [11,483 to 18,045 feet]) bined with increased water loss through the lungs from increased
Maximal SaO2 falls below 90% as PaO2 falls below 50 mm Hg respiration and through the skin, typically results in dehydration
(Figure 1-1 and Table 1-1). Extreme hypoxemia may occur during that may be debilitating. Thus, the high-altitude environment
exercise, sleep, and high-altitude pulmonary edema (HAPE) or imposes multiple stresses, some of which may contribute to, or
other acute lung conditions. Severe altitude illness occurs most may be confused with, the effects of hypoxia.
frequently in this range of altitudes.
ACCLIMATIZATION TO HIGH ALTITUDE
EXTREME ALTITUDE
Although rapid exposure from sea level to the altitude at the
(higher than 5500 meters [18,045 feet]) summit of Mt Everest (8848 m [29,029 feet]) causes loss of con-
Marked hypoxemia, hypocapnia, and alkalosis characterize sciousness in a few minutes and death shortly thereafter, climbers
extreme altitude. Progressive deterioration of physiologic func- can ascend Mt Everest over a period of weeks without supple-
tion eventually outstrips acclimatization. As a result, no perma- mental oxygen because of a process termed acclimatization. A
nent human habitation is above 5500 m (18,045 feet). A period complex series of physiologic adjustments increases oxygen
of acclimatization is necessary when ascending to extreme alti- delivery to cells and also improves their hypoxic tolerance. The
tude; abrupt ascent without supplemental oxygen for other than severity of hypoxic stress, rate of onset, and individual physiol-
brief exposures invites severe altitude illness. ogy determine whether the body successfully acclimatizes or is
2
CHAPTER 1 High-Altitude Physiology
BOX 1-1 Glossary of Physiologic Terms* SaO2
160 100
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 FIGURE 1-1 Increasing altitude results in decreasing inspired oxygen
means to improve physical and cognitive performance at high partial pressure (PIO2), arterial PO2 (PaO2), and arterial oxygen satura-
altitude. tion (SaO2). Note that the difference between PIO2 and PaO2 narrows
The recent revolution in our understanding of the molecular at high altitude because of increased ventilation, and that SaO2 is well
mechanisms of human responses to hypoxia has focused on maintained while awake until over 3000 m (9843 feet). (Data from
hypoxia-inducible factor (HIF). This transcription factor modu- Morris A: Clinical pulmonary function tests: A manual of uniform lab
lates the expression of hundreds of genes, including those in- procedures, Salt Lake City, 1984, Intermountain Thoracic Society; and
Sutton JR, Reeves JT, Wagner PD, et al: Operation Everest II: Oxygen
volved in apoptosis, angiogenesis, metabolism, cell proliferation,
transport during exercise at extreme simulated altitude, J Appl Physiol
and permeability processes.20,27,67,69,88 In chronic hypoxia, HIF 64:1309, 1988.)
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 repeated exposure if rate of ascent and altitude gained are
regulator of the hypoxia response in humans, HIF has beneficial similar, supporting the role of important genetic factors and an
and harmful effects at different stages during human exposure individual’s predisposition. Successful initial acclimatization pro-
to hypoxia and in different cells in the body.36,47 Figure 1-2 pro- tects against altitude illness and improves sleep. Longer-term
vides an overview of some of the hundreds of processes by acclimatization (weeks) primarily improves aerobic exercise
which the response to hypoxia is modulated by HIF. ability. These adjustments disappear at a similar rate on descent
Individuals vary in their ability to acclimatize, reflecting certain to low altitude. A few days at low altitude may be sufficient to
genetic polymorphisms, including HIF. Some adjust quickly, render a person susceptible to altitude illness, especially HAPE,
without discomfort, whereas acute mountain sickness (AMS) on reascent. The improved ability to do physical work at high
develops in others, who go on to recover. A small percentage altitude, however, persists for up to 3 weeks.43,77 Persons who
fail to acclimatize even with gradual exposure over weeks. The live at high altitude during growth and development appear to
tendency to acclimatize well or to become ill is consistent on realize the maximum benefit of acclimatization changes; for
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
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)
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 (%)
6
hypoxemia, and thus on clinical status, while SaO2 may appear
TISSUE CHANGES 40
The next link in the oxygen transport chain is tissue oxygen 0 2 4 6 8 10 12
transfer, which depends on capillary perfusion, diffusion dis- Days at altitude
tance, and driving pressure of oxygen from the capillary to the
cell. Banchero5 has shown that capillary density in dog skeletal FIGURE 1-6 On ascent to altitude, maximal oxygen consumption
muscle doubles in 3 weeks at PB of 435 mm Hg. A recent study 2max ) decreases and remains suppressed. In contrast, endurance
( VO
in humans noted no change in capillary density or in gene time (minutes to exhaustion at 75% of altitude-specific VO 2max)
expression thought to enhance muscle vascularity.42 Ou and increases with acclimatization. (Modified from Maher JT, Jones LG,
Tenney53 revealed a 40% increase in mitochondrial number but Hartley LH: Effects of high-altitude exposure on submaximal endur-
no change in mitochondrial size, whereas Oelz and colleagues52 ance capacity of men, J Appl Physiol 37:895-898, 1974.)
showed that high-altitude climbers had normal mitochondrial
density. A significant decrease in muscle size is often noted after 2 max.11 However, mechanisms to explain impaired gas
loss in VO
high-altitude expeditions because of net energy deficit, resulting exchange and lower blood flow remain elusive. Wagner87 pro-
in increased capillary density and ratio of mitochondrial volume poses that the pressure gradient for diffusion of oxygen from
to contractile protein fraction as a result of the atrophy. Although capillaries to the working muscle cells may be inadequate. Others
there is no de novo synthesis of capillaries or mitochondria, the propose that increased cerebral hypoxia from exercise-induced
net result is a shortening of diffusion distance for oxygen.42,44 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
EXERCISE
Maximal oxygen consumption drops dramatically on ascent to
high altitude.21,62 Maximal oxygen uptake ( VO 2 max) falls from 40
sea level value by approximately 10% for each 1000 m (3281
feet) of altitude gained above 1500 m (4921 feet). Persons with Alveolar
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 Arterial
fact, many of the world’s elite mountaineers, in contrast to other 30
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-
PO2 (torr)
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 concentration.4 The “live high–train low” approach pioneered by
Optimal training for increased performance at high altitude Levine and Stray-Gundersen40,74 has been adopted by many
depends on the altitude of residence and the athletic event. For endurance athletes. The optimal dose for specific sports is still
aerobic activities (events lasting >3 minutes) at altitudes above being determined,12,13,94 but overall, endurance athletes believe
2000 m (6562 feet), acclimatization for 10 to 20 days is necessary and science supports a small but significant improvement in sea
to maximize performance.18 For events occurring above 4000 m level performance after participating in a live high–train low
(13,123 feet), acclimatization at an intermediate altitude is recom- training camp.75 The benefit appears to result from enhanced
mended. Highly anaerobic events at intermediate altitudes require erythropoietin production and increased RBC mass, which
only arrival at the time of the event, although AMS may become requires adequate iron stores and thus usually iron supplementa-
a problem. tion.46,63,73 Some individuals do not respond to the live high–train
The benefits of training at high altitude for subsequent per- low approach, perhaps related to genetic polymorphisms and
formance at or near sea level depend on choosing the training inability to increase erythropoietin levels sufficiently to increase
altitude that maximizes the benefits and minimizes the inevitable RBC mass and thus increase oxygen-carrying capacity.12,14,32
“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 REFERENCES
performance. Also, intermittent exposures to hypoxia seem to
have no benefit.33,83 Runners returning to sea level after 10 days’ Complete references used in this text are available
training at 2000 m (6562 feet) had faster running times and an online at expertconsult.inkling.com.
increase in aerobic power, plasma volume, and hemoglobin
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60. Richalet JP, Keromes A, Dersch B, et al. Physiological characteristics 78. Subudhi AW, Dimmen AC, Roach RC. Effects of acute hypoxia on
of high-altitude climbers. Sci Sport 1988;3:89–108. cerebral and muscle oxygenation during incremental exercise. J Appl
61. Roach RC. The role of the hypoxic ventilatory response in perfor- Physiol 2007;103:177–83.
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62. Roach RC. Cardiovascular regulation during hypoxia. In: Ohno H, altitude and its relation with acute mountain sickness. J Appl Physiol
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tain medicine and high altitude physiology. Matsumoto: Japanese 80. Subudhi AW, Miramon BR, Granger ME, Roach RC. Frontal and motor
Society of Mountain Medicine; 1998. p. 264–70. cortex oxygenation during maximal exercise in normoxia and hypoxia.
63. Roberts D, Smith DJ. Erythropoietin: Induction of synthesis to signal J Appl Physiol 2009;106:1153–8.
transduction. J Mol Endocrinol 1994;12:131–48. 81. Subudhi AW, Panerai RB, Roach RC. Acute hypoxia impairs dynamic
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oxygen transport at altitude. Respir Physiol 1986;64:191–202. J Appl Physiol 2009;107:1165–71.
65. Sarnquist FH. Physicians on Mount Everest: A clinical account of the 82. Subudhi AW, Panerai RB, Roach RC. Effects of hypobaric hypoxia on
1981 American medical research expedition to Everest. West J Med cerebral autoregulation. Stroke 2010;41:641–6.
1983;139:480–5. 83. Truijens MJ, Toussaint HM, Dow J, Levine BD. Effect of high-intensity
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into molecular mechanisms of oxygen homeostasis. Hematol Oncol 2003;94:733–43.
Clin North Am 1994;8:863. 84. Van Osta A, Moraine JJ, Melot C, et al. Effects of high-altitude expo-
67. Semenza GL. Targeting HIF-1 for cancer therapy. Nat Rev Cancer sure on cerebral hemodynamics in normal subjects. Stroke 2005;36:
2003;3:721–32. 557–60.
68. Severinghaus JW, Chiodi H, Eger EI, et al. Cerebral blood flow in man 85. Viault F. On the large increase in the number of red cells in the blood
at high altitude: Role of cerebrospinal fluid pH in normalization of of the inhabitants of the high plateaus of South America. In: West JB,
flow in chronic hypoxia. Circ Res 1966;19:274–82. editor. High altitude physiology. Stroudsberg, Pa: Hutchinson Ross;
69. Shweiki D, Itin A, Soffer D, Keshet E. Vascular endothelial growth 1981. p. 333–4.
factor induced by hypoxia may mediate hypoxia-initiated angiogen- 86. Villafuerte FC, Macarlupu JL, Anza-Ramirez C, et al. Decreased plasma
esis. Nature 1992;359:843–5. soluble erythropoietin receptor in high-altitude excessive erythrocy-
70. Slingo ME, Turner PJ, Christian HC, et al. The von Hippel-Lindau tosis and chronic mountain sickness. J Appl Physiol 2014;117:1356–62.
Chuvash mutation in mice causes carotid-body hyperplasia and 87. Wagner PD. Gas exchange and peripheral diffusion limitation. Med
MOUNTAIN MEDICINE
enhanced ventilatory sensitivity to hypoxia. J Appl Physiol 2014;116: Sci Sports Exerc 1992;24:54.
885–92. 88. Wang GL, Jiang BH, Rue EA, Semenza GL. Hypoxia-inducible factor-1
71. Stenmark KR, Davie NJ, Reeves JT, Frid MG. Hypoxia, leukocytes, is a basic-helix-loop-helix-pas heterodimer regulated by cellular O2
and the pulmonary circulation. J Appl Physiol 2005;98:715–21. tension. PNAS 1995;92:5510–14.
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pulmonary hypertension. J Appl Physiol 2015;jap.00283.2015. 90. West JB. “Oxygenless” climbs and barometric pressure. Am Alpine J
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volume to increase to altitude exposure in iron deficient runners 91. West JB, Boyer SJ, Graber DJ, et al. Maximal exercise at extreme
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74. Stray-Gundersen J, Levine BD. “Living high and training low” can 92. West JB. Climbing Mt. Everest without oxygen: An analysis of maximal
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Scand J Med Sci Sports 2008;18(Suppl. 1):21–8. 94. Wilbur RL. Live high + train low: Thinking in terms of an optimal
76. Suarez J, Alexander JK, Houston CS. Enhanced left ventricular systolic hypoxic dose. Int J Sports Physiol Perform 2007;2:223–38.
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8.e2
CHAPTER 2
High-Altitude Medicine and
Pathophysiology
PETER H. HACKETT, ANDREW M. LUKS, JUSTIN S. LAWLEY, AND ROBERT C. ROACH
8
in oxygen. Both will die after having presented the same
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 Moderate to Severe AMS HACE
Symptoms Headache only Headache plus one more Headache plus one or more ±Headache
symptom (nausea/vomiting, symptoms (nausea/vomiting, Worsening of symptoms seen
fatigue/lassitude, dizziness, fatigue/lassitude, dizziness, in moderate to severe AMS
or difficulty sleeping) or difficulty sleeping)
Symptoms of mild severity Symptoms of moderate to
severe intensity
LL-AMS score* 1-3, headache only 2-4 5-15 —
Physical signs None None None Ataxia
Altered mental status
Papilledema; concurrent HAPE
common
Findings None None 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)
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 coughing, or bending.443 This may not be useful for diagnosis,
distress or alteration in the normal rate of breathing so however, because headaches from a variety of causes fulfill
long as the patient is at rest. The patient may feel slightly these criteria.
giddy on rising from bed, and any attempt at exertion
increases the headache, which is nearly always confined Pathophysiology
to the frontal region.344 Sanchez del Rio and Moskowitz381 have provided a useful mul-
tifactorial concept of the pathogenesis of HAH, based on current
Drawing a distinction between HAH and AMS is rather understanding of headaches in general. They suggest that the
PART 1
artificial because they overlap. Headache is generally the first trigeminovascular system is activated at altitude by both mechani-
unpleasant—and sometimes the only—symptom resulting from cal and chemical stimuli (vasodilation, nitric oxide, and other
high-altitude exposure.178 Headache without other symptoms is noxious agents), and that the threshold for pain is likely altered
called HAH, and if associated with other typical symptoms, it is at high altitude (Figure 2-1). If AMS and especially HACE ensue,
called AMS. Therefore, investigations on HAH are also to some altered intracranial dynamics may also play a role, through
extent studies of AMS. Headache lends itself to investigation compression or distention of pain-sensitive structures (see AMS
better than some other symptoms because headache scores have Pathophysiology, below). Oxygen is often immediately (within
been well validated.199 One could argue that the headache itself 10 minutes) effective for HAH in persons with and without
causes other symptoms, such as anorexia, nausea, lassitude, and AMS, which indicates a rapidly reversible mechanism of the
insomnia, as often seen in migraine or tension headaches, and headache, most likely related to cerebral vasodilation with in-
that mild AMS is essentially caused by headache. creased cerebral blood flow and cerebral blood volume.21,159 More
Researchers have attempted to characterize the clinical fea- investigation should lead to a better understanding of the patho-
tures and incidence of headache at altitude. In one study, 50 of physiology of these often debilitating headaches, as well as new
60 trekkers (83%) in Nepal up to 5100 m (16,732 feet) devel- treatments.
oped at least one headache when over 3000 m (9843 feet).406
Older persons were less susceptible; women and those with Prevention and Treatment
headaches in daily life had more severe headaches, but no more In general, HAH can be prevented by nonsteroidal antiinflamma-
headaches than did others. Of those with headache, 52% did not tory drugs (NSAIDs),325 acetaminophen,170 and the drugs typically
have AMS by the Lake Louise criteria. Although the clinical fea- used for prophylaxis of AMS, acetazolamide and dexamethasone
tures were widely variable, in general the headaches were mild (Table 2-3). Some agents appear more effective than others, with
to severe in intensity, frontal (41%) or frontal-temporal (23%), ibuprofen and aspirin apparently superior to naproxen.57,60,63
bilateral (81%), dull (53%) or pulsatile (32%), exacerbated by Sumatriptan, a serotonin type 1 (5-HT1) receptor agonist, was
exertion or movement (81%), often occurred at night, had onset reported to be effective for HAH prevention and treatment in
in the first 24 hours at a new altitude, and resolved within the some studies61,198 but not in others.23 Flunarizine, a specific
next 24 hours. The headaches were considered to have some calcium antagonist used for treatment of migraine, was not effec-
features of increased intracranial pressure. Persons with history tive for HAH in one study.38 The response to different agents
of migraine did not have a higher incidence of headache. In might reflect multiple components of HAH pathophysiology or
contrast, another investigator found a history of migraine associ- merely the nonspecific nature of many analgesics.
ated with a higher incidence of headache at altitude.62 Various
medications alleviated the headaches, especially mild ones, in ACUTE MOUNTAIN SICKNESS
70% of cases. Based on these investigations, the International
Headache Society has defined HAH as headache developing Epidemiology and Risk Factors
after ascent to altitude above 2500 m (8202 feet) and resolving Although the syndrome of AMS has been recognized for centu-
within 24 hours of descent and having at least two of the ries, modern rapid transportation and proliferation of participants
following characteristics: (1) bilateral, (2) mild or moderate in mountain sports have increased the number of persons affected
intensity, and (3) aggravated by exertion, movement, straining, and therefore public awareness (see Table 2-1). Incidence and
10
CHAPTER 2 High-Altitude Medicine and Pathophysiology
Hypothalamus Autonomic
Brainstem response
Lower threshold
for pain
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 retained for several weeks.53,54,122,226,227 Epidemiologic studies
(especially sleeping altitude), duration of altitude exposure, level suggest that protection from AMS may persist for months after
of exertion, recent altitude exposure, and inherent physiologic acclimatization for 2 or more weeks.390,486 Retention of aug-
(genetic) susceptibility.49,156,364,390 For example, AMS is more mented hypoxic ventilatory response (HVR) might explain these
common on Mt Rainier because of rapid ascents, whereas high- results;255,359 however, studies showed that HVR returned to pre-
altitude pulmonary or cerebral edema is uncommon because of ascent values 7 days after descent.311 Recently, the AltitudeOmics
short duration (<36 hours) of exposure on the mountain. Persons project confirmed many of these findings, with retention of
with demonstrated susceptibility to AMS had twice the incidence acclimatization for protection from AMS and improvement in
of AMS compared with nonsusceptible persons, independent of exercise performance lasting for up to 3 weeks after 16 days
rate of ascent.390 The basis for inherent susceptibility is still of acclimatization.112,120,141,360,377,426-428 It was proposed that altered
unknown. gene expression was maintained after acclimatization through
Acclimatization induced by recent altitude exposure can be DNA methylation and hypoxia-sensitive microRNAs (so-called
protective; 4 nights or more in the previous 2 months above hypoxamirs),234,257 and that these processes may account for at
3000 m (9843 feet) reduced susceptibility to AMS on ascent to least part of the memory of acclimatization.109
4559 m (14,957 feet) by one-half and was as effective as slow Compared with persons living at a lower altitude, residents at
ascent390 (Figure 2-2). Repeated overnight normobaric hypoxia 900 m (2953 feet) or above had less AMS (8% vs. 27%) when
exposures before ascent may also have a preventive effect.90,130 ascending to between 2000 and 3000 m (6562 and 9843 feet) in
Depending on the duration of stay at high altitude, the pro- Colorado.178 Age may have an influence on incidence,156 with
tective effects of acclimatization persist after descent to low persons older than 50 years somewhat less vulnerable.363,406 In a
altitude. AMS did not develop in persons who acclimatized to large study in Colorado, persons older than 60 years had one-half
4300 m (14,108 feet) for 16 days, returned to low altitude for 8 the incidence of AMS as those under 60, whereas a study of 827
days, and then were reexposed to high altitude in a hypobaric mountaineers in Europe showed no influence of age on suscep-
chamber.265 In addition, ventilation, SaO2, and exercise perfor- tibility.390 Different populations and physical activity may explain
mance at altitude were maintained for at least 7 days after accli- differing results. No study has ever shown older people to be
matization,41,265,311 with some enhanced physical performance 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
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%
similarly large cohort, seems to perform well. However, the
requirement for conducting an exercise test in hypoxic conditions
Nonsusceptible limits its wide applicability, particularly in travel clinics and
60% Susceptible primary care clinics, where many high-altitude travelers obtain
consultation before their trip.
50% Diagnosis
Prevalence of AMS
confidence intervals in nonsusceptible (blue bars) and susceptible (red AMS, these symptoms may be exaggerated during AMS. Affected
bars) mountaineers in relation to the state of acclimatization defined persons usually complain of a deep inner chill, unlike mere
as slow ascent (>3 days), fast ascent (≤3 days), preexposed (≥5 days exposure to cold temperature, accompanied by facial pallor.
above 3000 m [9843 feet] in preceding 2 months), and not preexposed Other symptoms may include vomiting, especially in children,
(≤4 days above 3000 m in preceding 2 months). (Modified from and irritability. Lassitude can be disabling, with the patient too
Schneider M, Bernasch D, Weymann J, et al: Acute mountain sickness: apathetic to contribute to basic needs. Although pulmonary symp-
Influence of susceptibility, preexposure, and ascent rate, Med Sci toms such as cough and dyspnea on exertion are quite common
Sports Exerc 34:1886-1891, 2002.) 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
is mixed. Children from 3 months to puberty studied in Colorado heart rate has been noted in persons with AMS,29,322 but Singh
PART 1
had the same incidence as did young adults,444,494 whereas a small and associates410 noted bradycardia (heart rate <66 beats/min) in
study of tourists in Chile found lower oxygen saturation (SpO2) two-thirds of 1975 soldiers with AMS. Blood pressure is normal,
and higher AMS in those age 6 to 48 months at 4440 m (14,567 but postural hypotension may be present. Occasionally, localized
feet).304 The largest study of children to date, of Han Chinese rales may be present,270 but this has also been observed in
after ascent to Tibet, showed essentially the same incidence of persons without AMS.153 Slightly increased body temperature with
AMS in 464 children as in 5335 adults, 34% and 38%, respec- AMS may be present but is not diagnostic.267 Peripheral oxygen
tively.480 Kriemler and colleagues229 found a lower prevalence of saturation measured by pulse oximetry (SpO2) correlated poorly
AMS in children than in adolescents and adults on the first day with presence of AMS during rapid ascent322,363,369 but was related
at 3500 m (11,483 feet). The subjective nature of symptom report- to AMS during trekking.34,225 Although these studies suggest that
ing is problematic, especially in children, and must be taken into pulse oximetry is of limited utility in diagnosing AMS, others
account when interpreting these studies.416 suggest it may be useful for predicting who will develop AMS
Women apparently have the same incidence390 or slightly with further ascent.206,361 It seems clear that higher-than-average
greater incidence156,178,455 of AMS but may be less susceptible SpO2 is associated with wellness and lack of AMS.
to pulmonary edema.85,415 Most studies show no relationship Funduscopy reveals venous tortuosity and dilation; retinal
between physical fitness and susceptibility to AMS. However, hemorrhages may or may not be present and are neither diag-
obesity seems to increase the risk of developing AMS.178,355 The nostic nor specific for AMS. Although more common in AMS than
relationship of tobacco smoking to AMS is unclear. A recent study in non-AMS individuals at 4243 m (13,921 feet),153 a study exam-
demonstrated that smoking was a risk factor for AMS in workers ining retinal hemorrhages in climbers on Muztagh Ata suggests
at a mine at 4000 m (13,123 feet), with an odds ratio of 1.9 for these are not a harbinger of impending severe altitude illness.18
every 10 cigarettes smoked per day.456 Although one study Absence of the normal altitude diuresis, evidenced by lack of
reported smoking as a risk factor for AMS in trekkers,283 most increased urine output accompanied by retention of fluid, is an
studies in trekkers and tourists have found no such relation- early finding in AMS, although not always present.30,155,253,410,433
ship,178,210,355 and some have reported apparent reduction in AMS Neurologic signs, including altered mental status and ataxia, are
in persons who smoked.414,484,495 There is no good evidence that not a feature of AMS and, when present, should raise concern
the use of oral contraceptives increases risk for AMS.210,322 for HACE (see later).
In summary, the most important variables related to AMS Because there are no characteristic physical examination find-
susceptibly are genetic predisposition, altitude of residence, alti- ings, the severity of AMS is classified solely on the basis of
tude reached, rate of ascent, and prior recent altitude exposure. symptoms (see Table 2-2).
It remains difficult to move beyond these established risk
factors and accurately predict which individuals are susceptible Differential Diagnosis
to severe AMS, HACE, and high-altitude pulmonary edema Given the nonspecific nature of the symptoms, AMS is frequently
(HAPE). Canoui-Poitrine66 and Richalet353 and colleagues have confused with other conditions (Box 2-2). AMS is most often
proposed a prediction tool that takes into account a variety of misdiagnosed as a viral flulike illness, hangover, exhaustion,
clinical and physiologic factors, including ventilatory and gas dehydration, or medication or drug effect. Unlike infectious
exchange responses during hypoxic exercise. This model, based illness, uncomplicated AMS is not associated with fever and
on a large derivation cohort and subsequently validated in a myalgia. Hangover is excluded by history, whereas dehydration
12
and magnitude of volume expansion are mostly determined by
13
Blood pressure Hypoxia
Vessel deformation
Trigeminal vascular activation Arterial and venous dilatation
Transverse sinus
ICP stenosis
Acclimatization
Transient increases in ICP Overexpression of
• Reduced cerebral blood flow and volume
(exercise, Valsalva, sleep apnea, hypertension and corticotropin releasing factor
MOUNTAIN MEDICINE
(1)
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
15
TABLE 2-4 Risk Categories for Acute Mountain Sickness
Acetazolamide impacts brain aquaporin channels, possibly pre-
venting water transport into the brain.400,441 Which of these effects
Risk is most important in preventing AMS is unclear, but most experts
Category* Description† attribute acetazolamide’s benefit to respiratory stimulation and
increased alveolar and arterial oxygenation. Numerous studies
Low Individuals with no prior history of altitude illness together indicate that acetazolamide is approximately 75% effec-
and ascending to <2800 m (9186 ft) tive in preventing AMS in persons rapidly transported to altitudes
Individuals taking >2 days to arrive at 2500-3000 m of 3000 to 4500 m (9843 to 14,764 feet).113
(8202-9843 ft) with subsequent increases in Acetazolamide prophylaxis should be considered for persons
sleeping elevation <500 m (1640 ft)/day and an
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-
extra day for acclimatization every 1000 m (3281 ft)
vention is debated. Many studies have shown that 250 mg two
Moderate Individuals with prior history of AMS and ascending
or three times a day was effective, as well as a 500-mg sustained-
to 2500-2800 m (8202-9186 ft) in 1 day action capsule every 24 hours.74,134,143,156,238,348,477 To reduce the side
No history of AMS and ascending to >2800 m effects, especially paresthesia, clinicians have more recently been
(9186 ft) in 1 day using smaller doses (125 mg twice daily),290 and a number of
All individuals ascending >500 m (1640 ft)/day studies now support this.32,67,453,258 Renal carbonic anhydrase is
(increase in sleeping elevation) at altitudes above blocked with 5 mg/kg/day, and this may be the maximum dose
3000 m (9843 ft) but with an extra day for required, both in children and adults. Duration of medication use
acclimatization every 1000 m (3281 ft) varies; the standard advice is to begin 24 hours before ascent.
High History of AMS and ascending to >2800 m (3281 ft) For individuals ascending to and remaining at the same elevation
in 1 day for a period of time, the medication can be stopped after 2 days
All individuals with a prior history of HAPE or HACE at that elevation, although the duration might be extended if the
All individuals ascending to >3500 m (11,483 ft) in individual ascended to that elevation at a very fast rate. For
1 day individuals climbing to a peak elevation and then descending
All individuals ascending >500 m (1640 ft)/day quickly (e.g., climbing Mt Kilimanjaro), the medication is contin-
MOUNTAIN MEDICINE
(increase in sleeping elevation) above >3000 m ued until descent is initiated. Acetazolamide can also be taken
(9843 ft) without extra days for acclimatization episodically, to speed acclimatization at any point while gaining
Very rapid ascents (e.g., <7-day ascents of Mt altitude or to treat mild AMS. There is no rebound when discon-
Kilimanjaro)
tinued. Although the danger of altitude illness passes after a few
days of acclimatization, a single dose of acetazolamide at night
Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical may still be useful to promote more effective sleep.
Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Acetazolamide has side effects, most notably peripheral par-
Illness: 2014 update, Wilderness Environ Med 25:S4-S14, 2014. esthesia and polyuria, and less often nausea, drowsiness, impo-
AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, tence, and myopia. Because it inhibits the instant hydration of
high-altitude pulmonary edema.
*The risk categories described above pertain to unacclimatized individuals. CO2 on the tongue, acetazolamide allows CO2 to be tasted and
†Altitudes listed in the table refer to the altitude at which the person sleeps. can ruin the flavor of carbonated beverages, including beer. The
Ascent is assumed to start from elevations below 1200 m (3937 feet). issue of sulfonamide allergy and acetazolamide was recently
PART 1
16
dexamethasone for altitude illness prevention for 29 days sup- lassitude, and altered consciousness, including confusion,
17
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
FIGURE 2-5 Magnetic resonance image of a patient with high-altitude
making cerebral edema difficult to differentiate from primary
cerebral edema. Increased T2 signal in splenium of corpus callosum cerebrovascular events. The most common clinical presentation
(arrow) indicates edema. (Reprinted from Hackett PH, Yarnell PR, Hill of HACE is a change in consciousness associated with ataxia,
MOUNTAIN MEDICINE
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 Other neurologic complications at high altitude include globus
19
pathway has a high requirement for oxygen (Michaelis constant Case Study 2-3 HIGH-ALTITUDE PULMONARY
[Km] = 37 mm Hg).81,137 Tyrosine hydroxylase in the dopamine EDEMA: CLINICAL PRESENTATION
pathway is also oxygen sensitive. It has been suggested that
decrease in acetylcholine activity during hypoxia might explain D.L., a 34-year-old man, was in excellent physical condition and
lassitude.137 One study showed that increased dietary tyrosine had been on numerous high-altitude backpacking trips, occa-
reduced mood changes and symptoms of environmental stress sionally suffering mild symptoms of AMS. He drove from sea
in persons at simulated altitude.17 Further work with neurotrans- level to the trailhead and hiked to a sleeping altitude of 3050 m
mitter agonists and antagonists will help shed light on their role (10,007 feet) the first night of his trip in the Sierra Nevada. He
in cognitive dysfunction at altitude and could lead to new phar- proceeded to 3700 m (12,139 feet) the next day, noticing more
macologic approaches to improve neurologic function. dyspnea on exertion when walking uphill, a longer time than
usual to recover when he rested, and dry cough. He com-
HIGH-ALTITUDE PULMONARY EDEMA plained of headache, shivering, dyspnea, and insomnia the
second night. The third day, the group descended to 3500 m
The most common cause of death related to high altitude, HAPE (11,483 feet) and rested, primarily for D.L.’s benefit. That
is completely and easily reversed if recognized early and treated night, D.L. was unable to eat, noted severe dyspnea, and suf-
properly. Undoubtedly, HAPE was misdiagnosed for centuries, fered coughing spasms and headache. On the fourth morning,
as evidenced by frequent reports of young, vigorous men sud- D.L. was too exhausted and weak to exit his sleeping bag. His
denly dying of “pneumonia” within days of arriving at high companions noted that he was breathless, cyanotic, and ataxic
altitude. The death of Dr. Jacottet, “a robust, broad-shouldered but had clear mental status. A few hours later he was trans-
young man,” on Mt Blanc in 1891 (he refused descent so that he ported by helicopter to a hospital at 1200 m (3937 feet). On
could “observe the acclimatization process” in himself) may have admission he was cyanotic, oral temperature was 37.8° C
provided the first autopsy of HAPE. Angelo Mosso wrote: (100° F), blood pressure 130/76 mm Hg, heart rate 96 beats/
From Dr. Wizard’s post-mortem examination … the more min, and respiratory rate 20 breaths/min. Bilateral basilar rales
immediate cause of death was therefore probably a suf- to the scapulae were noted. Findings of cardiac examination
focative catarrh accompanied by acute edema of the were reported as normal. Romberg and finger-to-nose tests
lungs. … I have gone into the particulars of this sorrowful revealed 1+ ataxia. ABG determinations on room air revealed
MOUNTAIN MEDICINE
incident because a case of inflammation of the lungs also PO2 24 mm Hg, PCO2 28 mm Hg, and pH 7.45. Chest radio-
occurred during our expedition, on the summit of Monte graph showed extensive bilateral patchy infiltrates (see Figure
Rosa, from which, however, the sufferer fortunately 2-7C). D.L. was treated with bed rest and supplemental oxygen.
recovered.308 On discharge to his sea level home 3 days later, the pulmonary
infiltrates and rales had cleared, although ABG values were still
On an expedition to K2 (Karakorum Range, Pakistan) in 1902, abnormal: PO2 76 mm Hg, PCO2 30 mm Hg, and pH 7.45. He
Alistair Crowley86 described a climber “suffering from edema of had an uneventful, complete recovery at home. D.L. was
both lungs and his mind was gone.” In the Andes, physicians advised to ascend more slowly in the future, staging his ascent
were familiar with pulmonary edema peculiar to high alti- with nights spent at 1500 m (4921 feet) and 2500 m (8202
tude,196,252 but it was not until Hultgren and Spickard193 and feet). He was taught the early signs and symptoms of HAPE and
Houston182 offered their observations that the English-speaking advised on pharmacologic prophylaxis.
world became aware of HAPE (see Rennie349 for a review). Hult-
PART 1
20
findings. Elevated temperature up to 38.5° C (101.3° F) is common. fluffy and patchy, with areas of aeration between infiltrates and
21
A B
MOUNTAIN MEDICINE
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 pulmonary hypertension. All persons ascending to high altitude
response to the alveolar damage, rather than an initiating event.438 or otherwise enduring hypoxia, however, have some elevation
of PAP. The hypoxic pulmonary vasoconstrictor response (HPVR)
Mechanisms of High-Altitude Pulmonary Edema is thought to be useful in humans at sea level because it helps
An acceptable explanation for HAPE must take into account three match perfusion with ventilation and preserve gas exchange. For
well-established facts: excessive pulmonary hypertension, high- example, when local areas of the lungs are poorly ventilated
protein permeability leak, and normal function of the left side of because of infection or atelectasis, the HPVR directs blood away
the heart. A mechanism consistent with these facts is failure of from those areas to well-ventilated regions. In the setting of
capillaries secondary to overperfusion and capillary hypertension global hypoxia, as occurs with ascent to high altitude, HPVR is
caused by uneven hypoxic vasoconstriction (Figure 2-8). presumably diffuse and pulmonary arterioles in all areas of the
Role of Pulmonary Hypertension. Excessive PAP is the lung constrict, causing a restricted vascular bed and increase in
sine qua non of HAPE; HAPE has not been reported without PAP, which is of little if any value for ventilation-perfusion
22
flows into one lung. Other causes of overperfusion of the pul-
23
Nitric oxide—overview and in patients during HAPE and on recovery, will lead to a
much clearer understanding of the genomic contributions to
Hypoxia eNOS NO c-GMP HAPE.293-295,402,464,490
PDE-5 inhibitor
Treatment
Treatment choices for HAPE depend on severity of illness and
L-arginine logistics. As with all high-altitude illnesses, early recognition
Vascular Degradation
muscle by PDE-5 vastly improves the likelihood of successful outcome (see Box
relaxation 2-3). In the wilderness setting away from medical resources,
persons with HAPE need to be urgently evacuated to lower
FIGURE 2-9 Nitric oxide pathway and action of phosphodiesterase-5 altitude. However, because of augmented pulmonary hyperten-
(PDE-5) inhibitors. In the presence of an inhibitor, cyclic guanosine sion and greater hypoxemia with exercise, exertion must be
monophosphate (c-GMP), the second messenger of nitric oxide (NO), minimized. Because cold stress elevates PAP, the patient should
is not degraded, and vasodilation is therefore enhanced. eNOS, Endo-
be kept warm.70 Early HAPE responds rapidly to descent of only
thelial nitric oxide synthase.
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
a phosphodiesterase-5 (PDE-5) inhibitor was given to HAPE inflatable pressure bag.362 If mobilized in these circumstances,
patients9,136,269,389 (Figure 2-9). As mentioned previously, HAPE-s rescue groups should make delivery of oxygen to the patient, by
patients are also characterized by impairment of respiratory airdrop if necessary, the highest priority. In high-altitude loca-
transepithelial sodium and water transport, making it more dif- tions with oxygen supplies, such as ski resorts, bed rest with
ficult to reabsorb alveolar fluid.273,383,385 supplemental oxygen may suffice, but severe HAPE may require
Patent foramen ovale (PFO) is more common among HAPE- high-flow oxygen (4 L/min) for more than 24 hours.
susceptible than among HAPE-resistant adult mountaineers.6 Oxygen immediately increases arterial oxygenation and
Since the initial report of Levine and co-workers,247 the associa- reduces PAP, heart rate, respiratory rate, and symptoms. The use
MOUNTAIN MEDICINE
tion of PFO and HAPE has been confirmed, but cause and effect of a mask providing resistance on expiration (expiratory positive
have not been established. Allemann and associates6 performed airway pressure [EPAP]) was shown to improve gas exchange in
a case-control study of 16 HAPE-susceptible participants and 19 HAPE, and this or continuous positive airway pressure (CPAP)
mountaineers resistant to HAPE. Presence of PFO was deter- may be useful as a temporizing measure.394 The same airway
mined by transesophageal echocardiography (TEE) and esti- pressure changes can be accomplished with pursed-lip breathing,
mated PAP by Doppler echocardiography at low altitude (550 m but this intervention is difficult for an individual to sustain for
[1804 feet]) and high altitude (4559 m [14,957 feet]).6 The fre- long periods, particularly when ill. An unusual case report sug-
quency of PFO was more than four times higher in HAPE- gested that a climber may have saved his partner’s life by using
susceptible than in HAPE-resistant participants, both at low postural drainage to expel airway fluid.50
altitude (56% vs. 11%) and high altitude (69% vs. 16%). At high Drugs are of limited necessity in HAPE because oxygen and
altitude, SaO2 before the onset of pulmonary edema was signifi- descent are so effective.261 Medications that reduce pulmonary
cantly lower in HAPE-susceptible participants than in the control blood volume, PAP, and PVR are physiologically rational to use
PART 1
group (73% vs. 83%). Also, in the HAPE-susceptible group, par- when oxygen is not available or descent delayed. Singh and
ticipants with a large PFO had more severe arterial hypoxemia associates410 reported good results with furosemide (80 mg
(SaO2 65% vs. 77%) than did those with smaller or no PFO. The every 12 hours), and greater diuresis and clinical improvement
authors speculated that at high altitude, a large PFO may con- occurred when 15 mg of parenteral morphine was given with
tribute to exaggerated arterial hypoxemia and facilitate HAPE.6 the first dose of furosemide. Their use, however, has been
Others pointed out, however, that the greater hypoxemia may eclipsed by recent results with vasodilators. Caution is also war-
have been caused by subclinical pulmonary edema,119 or that ranted with diuretic use because HAPE is a capillary-leak phe-
PFO was a marker of a reactive pulmonary vascular bed.88 nomenon, and many affected individuals have intravascular
HAPE-s patients are known to have exaggerated PAP response volume depletion at presentation. The calcium channel blocker
to exercise at sea level, which could maintain an open shunt. nifedipine (30-mg sustained-release tablet every 12 to 24 hours)
Because occurrence of PFO is so common in the general popula- was effective in reducing PVR and PAP during HAPE and slightly
tion, more compelling evidence is required before suggesting that improved arterial oxygenation.25 Clinical improvement, however,
PFO is a predisposing factor to HAPE. We do not recommend was not dramatic. Nifedipine is well tolerated and unlikely to
that those with PFO should consider closure of the defect before cause significant hypotension in healthy persons and avoids the
significant altitude exposure, or as a result of an episode of danger of CNS depression from morphine and possible hypovo-
HAPE.71 lemia from diuretics. Clinical improvement is much better,
however, with oxygen and descent than with any medication.
Genetics of High-Altitude Pulmonary Edema Inhaled NO, a potent pulmonary vasodilator, improves hemody-
Although many characteristics of HAPE-susceptible persons are namics in HAPE but is rarely available, and in any event, NO is
apparently genetically determined, actual genetic studies are usually given with oxygen. The PDE-5 inhibitors, which increase
conflicting and difficult to interpret.* The genes associated with cyclic guanosine monophosphate (c-GMP) to produce pulmo-
HAPE include those in the renin-angiotensin-aldosterone system nary vasodilation during hypoxia (Figure 2-9),136,350,351 have
pathway,94,340,420 NO pathway,1,2,101 and hypoxia-inducible factor shown value for prevention of HAPE268 but have not yet been
(HIF) pathway.39,59 Some studies showed that polymorphisms of studied for treatment. Whether these agents will prove to be
nitric oxide synthase (NOS3),1,2,101 angiotensin-converting enzyme more effective than nifedipine for treatment is unknown. A
(ACE),94,420,341 heat shock protein (HSP) 70,339 pulmonary surfac- theoretical advantage is that the PDE-5 inhibitors produce less
tant proteins A1 and A2,387 and aquaporin-5403 were associated systemic vasodilation. Nifedipine, and perhaps other vasodila-
with HAPE incidence and susceptibility, but much work remains tors, might be useful adjunctive therapy but is not a substitute
to find specific genetic factors causing HAPE.264 Further investiga- for definitive treatment (see Box 2-3 and Table 2-3). β-adrenergic
tions using whole-genome scanning and studies of gene expres- agonists154,262 may also have an adjunctive role but should not be
sion, gene methylation, and microRNA expression in HAPE-s, 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
*References 1, 2, 94, 100, 101, 168, 181, 235, 256, 300, 307, 340, 339, 376, oxygen sufficient to maintain SaO2 greater than 90%; medications
412, 421, 446, 463, 466, 499. are rarely necessary after descent, and rapid recovery is the
24
slow-release tablet every 8 hours) prevented HAPE in persons
25
greater than 21 g/dL for males and 19 g/dL for females as essen- adults to develop AMS,229 no data indicate that children are more
tial for the diagnosis of CMS, as well as residence above 2500 m susceptible to altitude illness. Studying this issue is difficult,
(8202 feet) and absence of lung disease.246 The reader is referred however, because diagnosis can be more difficult in preverbal
to reviews for in-depth information.298,345,347,483 In addition, an children.493 Despite this somewhat reassuring fact, very conserva-
international consensus group has defined and scored CMS.245 tive recommendations are made regarding taking children to high
Therapy of CMS is routinely successful. Descent to a lower altitude; it should be clarified that these opinions are not based
altitude is the definitive treatment. The syndrome reappears after on science.35,335 Durmowicz and colleagues107 showed that chil-
return to high altitude. Supplemental oxygen during sleep dren with HAPE had a high frequency of concomitant respiratory
is valuable. Phlebotomy is a common practice and provides infections. Children with Down syndrome, past repair of con-
subjective improvement, although without significant objective genital shunts, following chemotherapy, and with other problems
changes.476 The respiratory stimulants medroxyprogesterone are more susceptible to HAPE.107 Acetazolamide can be used for
acetate (20 to 60 mg/day)232 and acetazolamide (250 or 500 mg/ prevention and treatment of AMS/HACE in children (5 mg/kg/
day)354 have also been shown to reduce hematocrit value by day in divided doses) (see Table 2-3),108 while dexamethasone
improving oxygenation. Acetazolamide (250 mg) increased noc- should be reserved for treatment only and not used for preven-
turnal SaO2 by 5%, decreased mean nocturnal heart rate by 11%, tion. Pollard and associates336 provide an excellent consensus
the number of apnea/hypopnea episodes during sleep by 74%, document on children at altitude,336 and excellent reviews are
and hematocrit by 7%.354 The fact that these responses likely available.108,321,493 Healthy term newborns of lowland mothers
occur as a result of increased ventilation after acetazolamide should probably avoid sleeping altitudes greater than 2500 m
administration358 emphasizes the contribution of hypoventilation (8202 feet) for the first 4 to 6 weeks of life because of concern
and nocturnal desaturation to CMS.329 Another approach was regarding cardiopulmonary transition rather than for altitude
based on the knowledge that ACE inhibitors blunt hypoxia- illness.320 Infants with viral infections, neonatal intensive care unit
mediated erythropoietin release. Plata and associates334 showed stay, transient oxygen treatment, Down syndrome, or any pul-
that 5 mg/day of enalapril for 2 years reduced hemoglobin con- monary condition or cardiac defect should be carefully evaluated
centration, packed cell volume, proteinuria, and need for phle- by a physician regarding altitude exposure (see Figure 2-10). For
botomy.334 Pulmonary hypertension and right-sided heart failure all infants going to altitude, pulse oximetry monitoring should
may also occur in persons with CMS. be considered. Parents need to be aware of potential problems
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
OTHER MEDICAL CONCERNS
dilection in populations not genetically adapted to altitude. AT HIGH ALTITUDE
Former names for SHAPH have included “pediatric high-altitude
heart disease” and “subacute infantile mountain sickness.” The
CARBON MONOXIDE POISONING
underlying pathophysiology is pulmonary hypertension result- Carbon monoxide poisoning is a danger at high altitude, where
ing in hypertrophy and dilation of the right ventricle, with even- field shelters are designed to be small and windproof. Cooking
tual right-sided heart failure. Clinically, these children have poor inside poorly ventilated tents and snow shelters during storms is
growth, fatigue, irritability, dyspnea, and cyanosis or pallor. On a particular hazard.126,216,244,373,445,449 The effects of CO and high-
PART 1
physical examination, as the illness advances, hepatomegaly altitude hypoxia are additive. A reduction in oxyhemoglobin
and leg edema signal right-sided heart failure. ABGs and pulse caused by CO increases hypoxic stress, rendering a person at a
oximetry reveal exaggerated hypoxemia. Chest radiography “physiologically higher” altitude, which may precipitate AMS.
shows cardiomegaly and enlarged main pulmonary artery and Because of preexisting hypoxemia, smaller amounts of carboxy-
sometimes infiltrates. Echocardiography usually confirms the hemoglobin produce symptoms of CO poisoning. These two
diagnosis, although ECG and cardiac catheterization can also problems may coexist. Immediate removal of the victim from the
be useful. Right ventricular hypertrophy, right atrial dilation, CO source and provision of supplemental oxygen, if available,
and persistence of PFO and patent ductus arteriosus may also constitute the treatment of choice. Portable hyperbaric therapy
be noted. might also be useful.
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
HIGH-ALTITUDE DETERIORATION
blockers, PDE-5 inhibitors, and NO and prostaglandin inhibi- The world’s highest human habitation is at approximately 5500 m
tors.246 A similar phenomenon has been also been described in (18,045 feet). Above this altitude, deterioration outstrips the
adults after weeks to years of high-altitude residence5,8 and may ability to acclimatize.217 The deterioration is more rapid the higher
respond to treatment with PDE-5 inhibitors.4 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
CHILDREN AT HIGH ALTITUDE tasks such as melting snow for water may become too difficult,
Children born at high altitude in North America appear to have and death may result from dehydration, starvation, hypothermia,
a higher incidence of complications in the neonatal period than and especially neurologic and psychiatric dysfunction.123
do their lower-altitude counterparts.319 In populations better Loss of body weight is a prominent feature during expeditions
adapted to high altitude over many generations, neonatal transi- to extreme high altitude. Pugh338 reported 14 to 20 kg (30.9 to
tion has not been as well scrutinized, but there does appear to 44 lb) of body weight loss in climbers on the 1953 British Mt
be some morbidity. High-altitude residence does not clearly Everest Expedition. Almost 30 years later, with improvement in
impact eventual stature, but growth and development are food and cooking techniques, climbers on the American Medical
slowed.321,470 In low-income countries, confounding factors, such Research Expedition to Mt Everest (AMREE) still lost an average
as nutrition and socioeconomic status, make these issues difficult of 6 kg (13.2 lb).55 This was caused in part by 49% decrease in
to assess. Children residing at high altitude are more likely to fat absorption and 24% decrease in carbohydrate absorption.
develop pulmonary edema on return to their homes from a low- During Operation Everest II (OEII), in which the “climbers” were
altitude sojourn than are lowland children on induction to high allowed to eat foods of their choosing ad libitum, they still had
altitude. Some of these children may have preexisting pulmonary large weight losses: 8 kg (17.6 lb) overall, including 3 kg (6.6 lb)
hypertension of various etiologies.87 of fat and 5 kg (11 lb) of lean body weight (muscle).374,185 At
Although several studies have shown that lowland children 4300 m (14,108 feet), weight loss was attenuated by adjusting
traveling to high altitude are just as likely336 or less likely than caloric intake to match caloric expenditure.65 In fact, recent work
26
supports hypoxic exposure as a treatment for obesity.249,315,342,404 older persons were more affected. When more demanding tasks
27
high altitude. See Chapter 3 for more detailed discussion regard- linked to periodic breathing in some studies but not in others.
ing these patients and those with previous venous thromboem- Other factors might include change in circadian rhythm and
bolism problems. 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
PERIPHERAL EDEMA simulated-altitude devices used for training have also revealed
Edema of the face, hands, and ankles at high altitude is common, deranged sleep quality in these groups.221,222,327 Although a fre-
especially in females. Incidence of edema in at least one area of quent complaint in high-altitude visitors, deranged sleep seems
the body in trekkers at 4200 m (13,780 feet) was 18% overall, to have little relation to susceptibility to altitude illness or other
28% in females, 14% in males, 7% in asymptomatic trekkers, and serious problems. Symptomatic treatment that avoids respiratory
27% in those with AMS.153 Although not a serious clinical depression is safe (see Treatment under Acute Mountain Sick-
problem, edema can be bothersome. When seen in conjunction ness, earlier).
with dyspnea or neurologic symptoms and signs, presence of
peripheral edema should prompt evaluation for pulmonary and Periodic Breathing
cerebral edema. In the absence of AMS, peripheral edema is Periodic breathing is most common in early and light sleep, may
effectively treated with a diuretic. Treatment of accompanying occur during wakefulness when drowsy, and does not occur in
AMS by descent or medical therapy results in diuresis and resolu- REM sleep. The pattern is characterized by hyperpnea followed
tion of peripheral edema. The mechanism is presumably similar by apnea (Video 2-1). Unlike in obstructive sleep apnea, where
to fluid retention in AMS but may also merely be caused by respiratory efforts are made but airflow does not occur because
exercise.291 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.
IMMUNOSUPPRESSION The phenomenon is caused by abnormal feedback control in
Mountaineers have observed that infections are common at high CNS respiratory centers.73,219 Hypoxemia leads to increased
altitude, slow to resolve, and often resistant to antibiotics.310 On peripheral chemoreceptor output and a subsequent increase in
the AMREE in 1981, serious skin and soft tissue infections devel- minute ventilation. If the ventilatory response is large enough,
MOUNTAIN MEDICINE
oped. “Nearly every accidental wound, no matter how small, PaCO2 falls below the apnea threshold in the central chemorecep-
suppurated for a period of time and subsequently healed tors, and apnea ensues. The decrease in SaO2 and increase in
slowly.”382 A suppurative hand wound and septic olecranon bur- PaCO2 that occur during the apneic period eventually trigger an
sitis did not respond to antibiotics but did respond to descent to increase in ventilation and termination of apnea. If this corrective
4300 m (14,108 feet) from the 5300 m (17,388 feet) base camp. response is excessive, the PaCO2 again falls below the apnea
Nine of 21 persons had significant infections not related to the threshold in the central chemoreceptor, leading to another
respiratory tract. Most high-altitude expeditions report similar episode of apnea. A key feature of this process is that the
problems. response to the disturbance, in this case the increase in ventila-
Data from OEII indicated that healthy individuals are more tion with hypoxemia and increasing PaCO2, is excessive. This fits
susceptible to infections at high altitude because of impaired T with the observation that persons with high hypoxic ventilatory
lymphocyte function; this is consistent with previous Russian response have more periodic breathing,48 with mild oscillations
studies in humans and animals.288 In contrast, B cells and active in SaO2,236 whereas persons with low hypoxic ventilatory response
PART 1
immunity are not impaired. Therefore, resistance to viruses may have more regular breathing overall but may have periods of
not be impaired, whereas susceptibility to bacterial infection is apnea with extreme hypoxemia distinct from periodic breath-
increased. The degree of immunosuppression is similar to that ing.160 As acclimatization progresses, periodic breathing lessens
seen with trauma, burns, emotional depression, and space flight. but does not disappear, especially above 5000 m (16,404 feet),
The mechanism may be related, at least in part, to release of and sleep SaO2 increases.11,48,430
adrenocorticotropic hormone, cortisone, and β-endorphins, all of Periodic breathing has not been implicated in the etiology
which modulate the immune response.292,115 Intense ultraviolet of high-altitude illness, but nocturnal oxygen desaturation has
exposure has also been shown to impair immunity. Persons with been implicated.48,129,114 Eichenberger and colleagues110 have also
serious infections at high altitude may need oxygen or descent reported greater periodic breathing in persons with HAPE, sec-
for effective treatment. Impaired immunity because of high alti- ondary to lower SaO2. As with fragmented sleep, intensity
tude should be anticipated in situations where infection could of periodic breathing is quite variable. Total sleep time with
be a complication, such as trauma, burns, and surgical and inva- periodic breathing has been shown to vary between 1% and
sive procedures. 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
SLEEP AT HIGH ALTITUDE tend to have higher HVR and greater average ventilation and
Disturbed sleep is common at high altitude for a variety of oxygenation.465
reasons, which have been described in detail.3,58,260,457,465,469 Almost
all sojourners complain of disturbed sleep at high altitude, with Pharmaceutical Aids for Sleep
severity increasing with the altitude. At moderate altitude, sleep Acetazolamide (125 mg at bedtime) diminishes periodic breath-
architecture is changed, with a reduction in stages 3 and 4 ing and awakenings, improves oxygenation and sleep quality,
sleep, stage 1 time increased, and little change in stage 2. and is a safe agent to use as a sleeping aid with the added benefit
Overall, there is a shift from deeper sleep to lighter sleep. In of diminishing symptoms of AMS (Figure 2-11). Other agents
addition, more time is spent awake, with significantly increased include diphenhydramine (Benadryl), 50 to 75 mg, or the short-
arousals. Clinicians have reported either slightly less rapid eye acting benzodiazepines such as triazolam (Halcion), 0.125 to
movement (REM) time or no change in REM, compared with 0.25 mg and temazepam (Restoril), 15 mg.260 Although caution is
what occurs at low altitude. REM sleep may improve over time warranted for any agent that might reduce ventilation at high
at altitude.220 The subjective complaints of poor sleep are dispro- altitude, some studies have suggested that benzodiazepines in
portionate to the small reduction (if any) in total sleep time and low doses are generally safe in this situation.102,139,318 Another
appear to result from sleep fragmentation. With more extreme option is to use both acetazolamide and a benzodiazepine. Acet-
hypoxia, sleep time was dramatically shortened and arousals azolamide (500 mg slow release PO) given with temazepam
increased, without a change in ratio of sleep stages but with a (10 mg PO) improved sleep and maintained SaO2, counteracting
reduction in REM sleep.11 The mechanisms of this change in a 20% decrease in SaO2 when temazepam was given alone.318 The
sleep architecture and fragmentation are poorly understood. nonbenzodiazepine hypnotic zolpidem (Ambien), 10 mg, was
Periodic breathing appears to play only a minor role in altering shown to improve sleep at 4000 m (13,123 feet) without adversely
sleep architecture at high altitude.380 The arousals have been affecting ventilation.40
28
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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416. Southard A, Niermeyer S, Yaron M. Language used in Lake Louise 445. Thomassen O, Brattebo G, Rostrup M. Carbon monoxide poisoning
Scoring System underestimates symptoms of acute mountain sickness while using a small cooking stove in a tent. Am J Emerg Med 2004;22:
MOUNTAIN MEDICINE
29.e8
465. Weil JV. Sleep at high altitude. High Alt Med Biol 2004;5:180–9. 486. Wu TY, Ding SQ, Liu JL, et al. Reduced incidence and severity of
29.e9
CHAPTER 3 High Altitude and Preexisting Medical Conditions
CHAPTER 3
High Altitude and Preexisting
Medical Conditions
ANDREW M. LUKS AND PETER H. HACKETT
Given the prevalence of diseases such as asthma, hypertension, 1. Will the underlying disease worsen at high altitude?
and diabetes mellitus in the general population, it is likely that 2. Will the underlying disease affect acclimatization to hypobaric
many high-altitude travelers have one or several underlying hypoxia and predispose the individual to an increased risk of
medical conditions. Although the majority of these individuals acute altitude illness?
have mild, well-controlled conditions that should not create In addition, clinicians working in high-altitude locations are
issues during planned travel, ongoing improvements in medical often faced with consequences of the interaction between alti-
care and the growing ease of travel have increased the likelihood tude hypoxia and common preexisting medical conditions of
that some high-altitude travelers have more moderate to severe travelers. This chapter provides information that can be used to
forms of underlying disease that may pose challenges in this address these questions. After presenting a general framework
environment. Regardless of the severity of their underlying prob- for evaluating the high-altitude traveler with underlying medical
lems, patients may present to their primary care provider or a conditions, we describe the available evidence regarding a wide
travel medicine clinic prior to travel seeking advice about the variety of diseases likely to be encountered in such clinical situ-
safety of their planned trip and how best to manage their disease ations. Additional information is available in extensive reviews
during the sojourn. When faced with these situations, providers on this topic,67,93 and further disease-specific studies are cited in
must ask the following two questions: the appropriate sections below.
29
A GENERAL FRAMEWORK tions should prompt evaluation to clarify the risk further and to
assess and develop risk mitigation strategies for the sojourn,
FOR EVALUATING TRAVELERS including evacuation to lower altitude. Depending on the under-
WITH UNDERLYING lying disease process, tests that may be considered as part of
such an evaluation would include pulmonary function testing,
MEDICAL CONDITIONS hypoxia altitude simulation testing,44 echocardiography, and car-
One of the challenges of evaluating individuals with underlying diopulmonary exercise testing. Canceling the planned travel is a
medical conditions who are planning high-altitude travel is that consideration if risk is deemed to be too high or if adequate risk
for many diseases, such as chronic obstructive pulmonary disease mitigation strategies are not feasible. Details of this evaluation
(COPD) or hypertension, research on how these patients fare at are provided in the discussions of specific diseases and lead to
high altitude is limited, whereas for other diseases, there is practi- another question:
cally no evidence to guide the pretravel assessment. In light of 5. At what altitude does risk increase for patients with underlying
this situation, providers can apply the following general approach medical problems? In general, important physiologic responses
to determining whether the planned sojourn is safe, whether to hypobaric hypoxia, such as the ventilatory response to
further evaluation is necessary before the trip, and whether risk hypoxia and hypoxic pulmonary vasoconstriction, occur at
mitigation strategies are indicated. about 2000 m (6560 feet) when PaO2 falls below 70 mm Hg,9
The initial assessment should be framed around four general whereas the risk of altitude illness is thought to increase when
questions, as follows: individuals ascend above 2500 m (8200 feet). These are useful
1. Is my patient at risk for severe hypoxemia or impaired tissue thresholds for trip planning, but one should not assume that
oxygen delivery at high altitude? Certain categories of patients, all patients with underlying medical conditions are safe below
such as those with chronic lung diseases, heart failure, cya- these altitudes. Patients with unilateral absence of pulmonary
notic congenital heart disease, or sleep-disordered breathing, arteries have developed HAPE at as low as 1500 m (4920
can be expected to develop increased hypoxemia beyond that feet),130 which shows that certain patients may fare poorly at
experienced by normal individuals at a given altitude. This elevations lower than these thresholds. In other cases, the
exaggerated hypoxemia will have the same effect as being at underlying medical condition may not be an issue until ascent
a higher altitude. Further information about the extent to to elevations far above these levels. In the end, the altitude
MOUNTAIN MEDICINE
which this will happen is provided in the discussion of each at which risk for problems increases will be a function of the
specific disease. More severe hypoxemia is a concern because particular disease and its severity.
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,
MITIGATING RISK WITH PLANNED ASCENT
it may impact comorbid conditions. Patients with severe Although the appropriate risk mitigation strategy will vary among
anemia will not experience a change in arterial oxygen partial travelers based on the underlying medical condition, all travelers
pressure (PaO2) at rest compared with normal individuals, but with underlying medical problems should adhere to several
anemia patients will have problems with decreased oxygen- general principles. First, the traveler must ensure that the underly-
carrying capacity, which can lead to worsening dyspnea and ing medical problem is under good control at the time of the
poor exertional tolerance. planned trip. Patients with worsening control of heart failure or
2. Can my patient mount the expected ventilatory responses to asthma, for example, should not travel to high altitude, particu-
PART 1
hypobaric hypoxia at high altitude? Arterial hypoxemia at high larly into remote areas. Second, the traveler should continue
altitude stimulates the peripheral chemoreceptors, leading to regular medications and therapies during the trip and, in some
an increase in minute ventilation, the primary role of which cases, such as diabetes or poorly controlled hypertension, should
is to defend alveolar oxygen tension (PAO2) against the effects consider more frequent monitoring of the disease, with adjust-
of decreased ambient PO2. Although the magnitude of this ment of medications according to a prespecified plan. Third,
response varies between individuals, most are able to mount patients at risk for disease exacerbations, such as those with
this response. Patients with disorders affecting respiratory asthma, COPD, or cardiac arrhythmia, should travel with an
mechanics, such as very severe COPD, morbid obesity, or adequate supply of rescue medications and a plan for using these
various neuromuscular disorders, and individuals at risk for therapies. Lastly, travelers should identify medical resources at
impaired chemoreceptor responses may not be able to mount their planned destination and travel with a plan to access these
the expected ventilatory response and thus may be at risk for resources or descend in the event of severe problems. Arranging
increased levels of hypoxemia. suitable travel insurance, particularly with international travel,
3. Is my patient at risk because of the expected pulmonary will greatly facilitate any necessary evacuation. Further details
vascular responses to hypobaric hypoxia at high altitude? about risk mitigation in specific conditions are provided in the
Decreased PAO2 triggers hypoxic pulmonary vasoconstriction, following discussions.
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- SPECIFIC MEDICAL CONDITIONS AT
viduals and is well tolerated by most travelers but could
represent a problem for patients with underlying pulmonary
HIGH ALTITUDE
hypertension. This is because the further increase in PAP Having considered this general framework, we now discuss a
may worsen right-sided heart function, leading to increased variety of medical conditions that might pose problems for
dyspnea, impaired hemodynamics, and as described later, individuals traveling to high altitude. Table 3-1 lists specific
development of high-altitude pulmonary edema (HAPE). patient groups and potential conditions that warrant consider-
4. Will hypobaric hypoxia at high altitude worsen control of the ation as well as the relative safety or risk associated with high
underlying medical condition(s)? Although data are lacking altitude.
with regard to many chronic diseases, more information has
become available in recent years regarding the effects of RESPIRATORY DISEASES
hypobaric hypoxia on common medical problems such as
asthma, hypertension, and obstructive sleep apnea, which are Chronic Obstructive Pulmonary Disease
reviewed in detail later. Patients should be assessed in light Minimal data are available regarding outcomes for patients with
of the available information to evaluate the likelihood of COPD who travel to high altitude, and most of the available
worsening disease control after ascent (see Chapter 2). information pertains to changes in oxygenation rather than
If reassuring answers are obtained with regard to all these changes in airway function.95 Aside from a single study of COPD
questions, the individual is likely safe to travel to high altitude patients at terrestrial high altitude,65 most information about the
without further evaluation. Nonreassuring answers to these ques- effects of hypobaric hypoxia on these patients comes from the
30
CHAPTER 3 High Altitude and Preexisting Medical Conditions
TABLE 3-1 High-Altitude Travel Risk Associated with Various Underlying Medical Conditions
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 porting data and are somewhat arbitrary, it is reasonable to ask
with a forced expiratory volume in 1 second (FEV1) of 1.0 to 1.5 whether COPD patients need supplemental oxygen with travel
liters (L) manifest hypoxemia when exposed to the equivalent of to similar altitudes in the mountains. How to apply such guide-
2340 m (8000 feet), with average PaO2 values approximately lines at higher elevations is unclear, however, because even
50 mm Hg (Table 3-2). Mild degrees of exertion, such as walking normal individuals will have PaO2 of approximately 50 mm Hg
on flat ground or cycling on an ergometer at a low work rate, with acute exposure to elevations greater than 4200 to 4500 m
lead to further decreases below these levels. These values are (13,770 to 14,760 feet) and clearly do not require supplemental
significant; guidelines from the British Thoracic Society, American oxygen in these circumstances.
Thoracic Society, and Aerospace Medical Association all suggest Predicting which patients will develop clinically significant
supplemental oxygen should be employed in patients whose PO2 hypoxemia at high altitude is challenging. A variety of prediction
is expected to be in this range at elevations of approximately rules are available that take into account sea level blood gases,
2340 m (8000 feet). Recognizing that these thresholds lack sup- pulmonary function test results, and other variables,30,42,61,62 but
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 Asthma
short exposures to 2340 m (8000 feet), the maximum allowed Doan and Luks45 recently reviewed the issue of asthma manage-
altitude in cabin aircraft. These rules have not been validated for ment in the wilderness, particularly at high altitude. From a theo-
the wide range of elevations that patients may visit or the dura- retical standpoint, multiple factors at high altitude could affect
tion of exposure they are likely to experience during their airway function in asthmatic patients. On the one hand, lower
travels. An alternative approach is the hypoxia altitude simula- air density and decreased number of dust mites155 would be
tion test, in which oxygenation and other parameters are moni- expected to lead to better control. On the other hand, many
tored while a patient breathes a hypoxic gas mixture at rest.44 asthmatic patients experience worsening control when exercis-
This test should more accurately reflect the degree of expected ing, particularly in the cold, dry air typical of the high-altitude
hypoxemia than do the prediction rules, but it is limited by environment. A high incidence of asthma and asthma-like symp-
its short duration relative to the duration of exposure to high toms has been documented in epidemiologic studies of cross-
altitude, the inability to account for changes in ventilation that country skiers; this activity is associated with high minute
will occur over long stays at high altitude, and difficulties admin- ventilation in a cold environment.81 Other studies have docu-
istering hypoxic gas mixtures simulating the altitude the patient mented a 50% incidence of exercise-induced bronchoconstriction
will visit. (EIB) in highly trained ski mountaineers in the Alps, even though
An important question that arises from the available literature almost three-quarters of these individuals had never been diag-
is whether supplemental oxygen is necessary to counteract the nosed with EIB.47
expected hypoxemia, as the guidelines recommend. It is note- Current evidence suggests that despite these concerns, the
worthy that in the majority of studies previously cited, most majority of well-controlled asthmatic patients do well with expo-
patients had mild symptoms and experienced few, if any, adverse sures to altitudes as high as 6000 m (19,685 feet). Several studies
events despite having hypoxemia disproportionate to that have documented decreased bronchial hyperresponsiveness to
expected for normal individuals at the same elevation. Given this hypoosmolar aerosols and methacholine after travel to altitudes
issue, as well as the logistical difficulties of traveling with supple- of 4559 and 5050 m (14,950 and 16,560 feet)5,32 and no increase
mental oxygen, a more practical alternative would be to travel in symptoms, need for medications, exacerbations, or risk of
with plans to monitor symptoms and oxygen saturation (SpO2) acute mountain sickness (AMS) with ascent to elevations of 5895
on arrival using a portable pulse oximeter and a prescription for to 6400 m (19,335 to 20,990 feet).74,147 Other studies have noted
MOUNTAIN MEDICINE
supplemental oxygen to use if difficulties arise.91 In North small decreases in FEV1 or peak expiratory flow at high altitude,
America, for example, home oxygen companies accept prescrip- but these were not associated with any changes in patient symp-
tions from physicians in any state, and oxygen is easily obtained. toms and likely were not clinically significant.89,105, In a survey
Patients already receiving supplemental oxygen should continue study of asthmatic patients seen in a travel clinic, almost 75% of
therapy during their travels but need to increase the gas flow to whom traveled to high altitude, 43% reported worsening asthma
account for the drop in barometric pressure. A useful rule of control during their trip, and 37% experienced the “worst asthma
thumb is to increase the inspiratory flow rate by the ratio of attack of my life.”60 This study, however, did not account for the
higher to lower barometric pressure. Portable oxygen concentra- altitudes attained by these patients or the fact that many high-
tors provide a convenient alternative to oxygen gas cylinders, altitude trips require transit through large cities such as Kath-
provided patients can recharge the batteries. However, these mandu or Bangkok or environments with very poor air quality.
devices may not deliver the same inspired oxygen concentration Aside from concerns about asthma control, the available literature
at altitude as at sea level. has not reported an increased incidence of acute altitude illness
PART 1
Except for the hypoxemia issue, no information in the litera- in asthmatic patients.74,147 Acetazolamide use also appears to be
ture addresses the risk of acute altitude illness in COPD patients. safe in this patient population.107
Use of acetazolamide for altitude illness prophylaxis in COPD In summary, patients with mild, well-controlled asthma can
patients has not been studied. Caution is necessary when con- travel to altitudes over 6000 m (19,685 feet). Individuals with
sidering acetazolamide in patients with FEV1 of less than 25% worsening control at the time of their planned trip or with per-
predicted, because it may lead to impaired carbon dioxide elimi- sistent, moderate to severe disease should avoid high-altitude
nation and worsening hypercarbia.95,97 In patients whose COPD travel, particularly travel into remote areas with inadequate
is complicated by pulmonary hypertension, further increases in access to medical care. All patients should continue their baseline
PAP after ascent could theoretically increase the risk of HAPE or medication regimen and carry an adequate supply of rescue
right-sided heart dysfunction. As discussed later, this issue has inhalers and prednisone in the event control worsens before they
not been formally studied in this patient population. No evidence can access care. Patients with known EIB or cold-induced bron-
suggests that patients with bullous emphysema are at increased choconstriction can consider adding or increasing the intensity
risk for pneumothorax or other forms of pulmonary barotrauma of their controller therapy or taking preexercise short-acting
after ascent, or that ascent to high altitude leads to deterioration β-agonists or leukotriene receptor blockers. Further details on
in markers of pulmonary function.95 Patients should continue asthma control in the wilderness are provided in Chapters 53 and
taking their baseline medications at high altitude and travel with 94, and several reviews on this topic are available.33,45
an adequate supply of rescue inhalers and prednisone in the
event of an exacerbation during their trip, particularly if visiting Cystic Fibrosis
an area remote from medical care. Although data on the effect of high altitude on pulmonary func-
tion in cystic fibrosis (CF) patients are inconsistent,52,133,149, CF
Interstitial Lung Disease patients experience more severe hypoxemia than normal indi-
Compared with COPD patients, fewer studies are available viduals when exposed to altitudes of 2000 to 3000 m (6560 to
regarding the risks of hypobaric hypoxia in patients with inter- 9840 feet), with the largest decrements seen in patients with
stitial lung disease (ILD), such as idiopathic pulmonary fibrosis greater degrees of impaired pulmonary function52,133 (Table 3-2).
or sarcoidosis. Limited evidence from the literature on hypoxemia As with the studies in COPD patients previously noted, these
during commercial flight demonstrates that patients with a variety exaggerated levels of hypoxemia were not associated with
of ILDs and FEV1 of about 50% to 55% predicted develop signifi- increased symptoms or an increased risk of AMS,52,133 although
cant hypoxemia with exposure to 2430 m (8000 feet), which the duration of exposure was short. There are reports of patients
worsens with exertion (Table 3-2).31,140 Prediction rules to assess with severe CF (FEV1 ~1 L) developing pulmonary hypertension
the risk of hypoxemia in ILD patients are available as for COPD and cor pulmonale during ski trips to this environment.145 Predic-
patients, but utility is limited by the same considerations noted tion rules are available to assess the likelihood of severe hypox-
earlier, and the hypoxia altitude simulation test likely remains emia at high altitude but are poor predictors of PaO2 at altitude
the best tool for assessing risk. Similar principles on traveling in CF patients and are limited by the same issues noted with
with a prescription for supplemental oxygen and monitoring COPD.52,77,118, Given significant improvements in the quality of CF
symptoms and pulse oximetry after arrival should likely be care in the past decade, it is also unclear whether older data
applied in ILD patients as well. and prediction rules still apply to the current population of CF
32
patients. There is no evidence that exposure to high altitude leads
33
some persons experiencing marked rises in BP compared to
others,132 but a priori identification of persons at risk for such 80
responses remains challenging. Several studies suggest that the
initial BP rise is followed by a decline over days to weeks.132,159 70
provide the further benefit of prophylaxis against HAPE. A recent workloads (<80 W or 5 METs), or recent myocardial infarction
field study suggested that angiotensin receptor blockade lowered should delay high-altitude travel until they have undergone
BP at 3400 m (11,150 feet), but this study was performed in revascularization. Patients with prior ventricular tachycardia or
normotensive individuals. Whether the same response would be fibrillation should also avoid travel unless stable on a recent
seen in a hypertensive patient at high altitude, particularly one exercise test. Travel should be delayed for 4 months or longer
with difficult-to-control disease, is unclear.122 after revascularization procedures, because studies have exam-
ined and demonstrated the safety of exertion in hypobaric
Coronary Artery Disease hypoxia only at 4 to 18 months after such interventions. Symptom-
The primary concern in patients with underlying coronary artery limited exercise tests can be used in these patients, as well as
disease (CAD) is that myocardial oxygen demand may outstrip those thought to be at risk for CAD, to gauge the safety of a
oxygen supply in the setting of hypobaric hypoxia, particularly planned ascent. Patients should continue their medication
with exertion, thereby leading to myocardial ischemia. This regimen throughout their planned trip. Further information on
PART 1
problem may be exacerbated because coronary vasodilation is these issues is available in several reviews.11,39
impaired in these patients, and paradoxical vasoconstriction may
even occur during exercise.64 Despite these theoretical concerns, Heart Failure
patients with stable CAD appear to tolerate exposure to moderate Heart failure patients face several physiologic challenges at high
altitudes without significant complications. Levine and associ- altitude, including increased PAP that may lead to right-sided
ates,85 for example, demonstrated a decrease in the ischemia heart strain, increased sympathetic nervous system activity, and
threshold, denoted by the double product and treadmill work- increased systemic BP. Together with the decreased ventilatory
load necessary to produce 1 mm of ST-segment depression on reserve and pulmonary compliance seen in some patients, these
the electrocardiogram (ECG), on acute exposure to high altitude, issues theoretically increase the risk of decompensated disease
which resolved after several days at the same elevation. Despite with high-altitude travel.12,129 Only a limited number of studies
these changes in the ischemia threshold, no new wall motion have evaluated this risk in detail. Erdmann et al49 examined
abnormalities were detected by echocardiography, and individu- patients with CAD and stable heart failure (ejection fraction
als did not manifest evidence of high-grade ectopy or arrhythmia. <45%) and noted no greater decrement in exercise performance
Similarly, Erdmann and colleagues49 performed cardiopulmonary compared to controls. In contrast, Agostoni and associates2 per-
exercise test (CPET) at 1000 m (3280 feet) and 2 days after ascent formed CPET at simulated altitudes up to 3000 m (9840 ft) in
to 2500 m (8200 feet) on 23 patients with myocardial infarction heart failure patients with varying degrees of functional limitation
or revascularization within the preceding 4 months and with low and noted larger decrements in maximum work rate compared
ejection fraction (<45%), and noted the same double product and to healthy controls, with the greatest decrease seen in those who
systolic BP at peak exercise between testing sites, with no evi- were most limited at baseline. No tests had to be interrupted for
dence of ischemia or arrhythmia. DeVries and associates38 per- ischemia in either study. Schmid and colleagues137 performed
formed CPET at 4200 m (13,776 feet) on eight patients with CPET with echocardiography in New York Heart Association
single-vessel disease and preserved ejection fraction; they found (NYHA) Class I and II patients (mean ejection fraction, 28.8%
no changes in wall motion score indices of left ventricular func- ±5.4%), and found that although peak oxygen consumption
tion and no evidence of arrhythmia or other adverse events. declined at high altitude by 22%, no patient developed ischemia,
These data suggest that patients with stable, well-controlled pulmonary edema, or echocardiographic evidence of left or right
CAD tolerate exposure to and exertion at altitudes as high as ventricular dysfunction. One patient developed self-limited ven-
4000 m (13,120 feet). Given the changes in the ischemia thresh- tricular tachycardia during maximal exercise.
old noted by Levine and associates,85 it may be prudent to These studies may seem reassuring, but the duration of expo-
decrease the level of physical activity in the first few days at sure to high altitude before performance of exercise testing was
altitude, although the study by Erdmann and colleagues49 sug- short relative to the duration of time patients may spend at high
gests heavy exertion may be possible as soon as 2 days after altitude. This concern is supported by anecdotal evidence from
arrival at high elevation. Patients should not engage in de novo physicians in resort areas who have noted a tendency toward
exercise at high altitude if they are not already engaged in an acute decompensation in heart failure patients within 24 hours
exercise program at lower elevation. Sleeping at moderate alti- of arrival. The etiology for this is not clear but may relate to
tude before any exercise at high altitude may also reduce the alterations in sodium and fluid balance that can develop after
risk of complications, including the risk of sudden cardiac death ascent.148 Development of AMS may pose a similar risk to heart
34
failure patients, because AMS is often associated with fluid reten- limitations of these tests as discussed earlier. High-altitude travel
35
Hemoglobinopathy an aura and focal neurologic deficits—features typically lacking
Sickle cell anemia patients should avoid travel to high altitude in AMS-associated headaches—and the character of the headache
because hypoxia can trigger red blood cell sickling and vasooc- compared to the typical migraine at lower elevations. Headaches
clusive crises.53 Even travel to modest elevations may be associ- that are different in character than typical migraines or that do
ated with risk. Previous work has demonstrated a 20% incidence not respond to standard migraine headache treatment, such as
of vasoocclusive and splenic crises in patients with sickle cell sumatriptan, should be treated as AMS. Response to oxygen
anemia or hemoglobin S/C traveling above 2000 m (6560 feet) breathing can also be helpful, because altitude headaches typi-
or flying in pressurized aircraft.102 Beyond the risk of vasooc- cally improve in 10 to 15 minutes, whereas migraine headaches
clusive crises, sickle cell anemia patients can develop pulmonary do not.
hypertension as a consequence of long-standing disease,84 which
could predispose to HAPE or worsening right-sided heart func- Seizures
tion in hypobaric hypoxia. If high-altitude travel cannot be High altitude may rarely induce seizure in healthy persons and
avoided, patients should travel with supplemental oxygen. Unlike sometimes unmask preexisting seizure disorders.98 Individuals
patients with COPD or other lung diseases, who might travel with known seizure disorders well controlled with medication
with a prescription for supplemental oxygen and use it only if are not thought to be at increased risk for increased frequency
they have problems at high altitude, sickle cell anemia patients or severity of seizures after ascent. They can trek or do other
should plan on having oxygen available immediately on arrival. activities at high altitude but should avoid technical climbing or
The risk of problems in patients with sickle cell trait has not roped travel on glaciated terrain because of the risks to the indi-
been specified, but several reports document the occurrence of vidual or travel partners if a seizure occurs in either setting.
splenic crises in patients traveling between 1600 and 3660 m Individuals who use topiramate as part of their seizure regimen
(5250 and 12,005 feet).80,54,63,150 Such reports should probably not should use dexamethasone rather than acetazolamide for AMS
preclude high-altitude travel in all sickle cell trait patients, but prophylaxis at high altitude; topiramate has carbonic anhydrase
development of left upper quadrant pain following ascent to high activity similar to that of acetazolamide, and concurrent use of
altitude should prompt urgent medical evaluation and descent to the medications for more than a few days can lead to severe
lower elevation. metabolic acidosis and nephrolithiasis.97 Persons with a past
Thalassemia has not been reported to cause problems at high history of more than one seizure who are not taking antiseizure
MOUNTAIN MEDICINE
iron supplementation. and bleeding can have significant consequences if the individual
cannot access care in a timely manner. Patients with known,
Polycythemia Vera unsecured intracranial aneurysm or arteriovenous malformation
As with anemia, evidence is scant regarding polycythemia vera should probably avoid high-altitude travel because of a theoreti-
(PV) patients at high altitude. From a theoretical standpoint, cal risk of rupture from cerebral vasodilation and increased flow,
higher hemoglobin concentrations would be expected to improve or if systemic BP increases significantly after ascent. If high-
oxygen delivery in the setting of hypoxemia. On the other hand, altitude travel cannot be avoided, efforts should be made to limit
individuals traveling at high altitude are at increased risk for exertion during the sojourn.
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
DIABETES MELLITUS
output and oxygen delivery, and increasing risk of thrombosis.146 There are multiple issues for diabetic patients traveling to high
The effect of hypobaric hypoxia on risk of gastroduodenal ero- altitude. It is important to note that the literature on short-term
sions in PV patients is unknown.152 Given these uncertainties, PV exposure to high altitude is based largely on studies done in
patients can travel to high altitude but should maintain adequate well-controlled type 1 diabetic patients engaged in climbing
hydration and mobility and should consider using low-dose expeditions.1,76,110,124 Significantly less information is available
aspirin to reduce the risk of thrombotic events. Patients with a about patients with poorly controlled type 1 or with type 2 dia-
history of gastroduodenal erosions should avoid aspirin, as well betes of any severity, so care must be used in extrapolating
as dexamethasone, because either medication might increase the available data to these individuals.
risk of upper gastrointestinal bleeding.
Acclimatization and Risk of Altitude Illness
NEUROLOGIC DISORDERS Multiple studies from climbing expeditions suggest that the ven-
tilatory and hematologic responses to acute hypoxia, risk of acute
Headaches altitude illness, and summit success rates are similar in well-
A history of nonmigrainous headaches at lower elevation may controlled type 1 diabetic patients and healthy individuals. Pavan
predispose to headaches at high altitude23 and has been associ- and colleagues,125 for example, measured blood gases and hema-
ated with increased severity of headaches when they occur after tologic parameters in well-controlled type 1 diabetic patients at
ascent.142 Hypoxia may trigger migraine headaches at high alti- 3700 and 5800 m (12,135 and 19,025 feet) during an ascent of
tude in patients with a known history of the disorder138 (or a Cho Oyu and noted no difference in PaO2, PaCO2, bicarbonate,
family history of migraine), and these headaches may be of or hematocrit. Multiple studies have reported no difference in
greater severity and associated with focal neurologic deficits.111 the incidence of AMS or Lake Louise AMS scores between dia-
Anecdotal reports67 and systematic studies127 also suggest that a betic and nondiabetic climbers during ascents of Aconcagua
history of migraines may also predispose to acute altitude illness (6962 m [22,835 feet]), Cho Oyu (8201 m [26,890 feet]), or Kili-
after ascent. An important issue for these patients is distinguish- manjaro (5895 m [19,335 feet]).76,110,124 In only one of the studies
ing a migraine headache from headaches associated with AMS, did diabetic climbers fail to summit the mountain, but summit
with the key distinguishing factors being whether the patient has success rates were low in the nondiabetic climbers as well,
36
making it difficult to attribute the lack of summit success to dia- thy. These incidence rates are comparable to those seen in the
37
noninvasive positive-pressure therapy should continue these totomy, but the swelling is more uniform and does not lead to
therapies at high altitude for the duration of electrical power refractive errors.99 Laser-assisted in situ keratomileusis (LASIK) is
access.95 now performed more often than either radial keratotomy proce-
dure. The available data suggest that high-altitude travel, even to
GASTROINTESTINAL DISEASES extreme elevations, is tolerated in these patients. Small myopic
shifts have been demonstrated in controlled studies113 and case
Gastrointestinal Bleeding reports,24,157 but climbers have still been able to reach summit
Several studies have raised concern about the risk of gastrointes- objectives at extreme elevations. In a detailed report by Dimmig
tinal (GI) bleeding at high altitude. Wu and colleagues159 studied and Tabin,43 six climbers ascended above 7900 m (25,910 feet)
more than 13,000 workers between 3500 and 4900 m (11,480 and after LASIK in both eyes, and four reached the summit. Five of
16,070 feet) on the Qinghai-Tibet railroad and noted a 0.49% the six had no visual changes up to 8000 m (26,240 feet), while
incidence of hematemesis, melena, or hematochezia, and Liu86 two climbers reported blurred vision at 8200 and 8700 m (26,900
reported an incidence of 0.8% among Chinese soldiers stationed and 28,535 feet), which improved with descent. Further details
between 3700 and 5380 m (12,135 and 17,550 feet) over a 1-year on this issue are available in a recent review.101
period. Saito134 documented GI bleeding in 5 of 52 Mt Everest
climbers. Fruehauf and associates55 performed upper endoscopy Glaucoma
on 26 asymptomatic individuals before and after ascent to 4559 m The effect of high altitude on intraocular pressure (IOP) is
(14,950 feet) and noted new gastric or duodenal erosions/ulcers, unclear, with studies reporting an increase, decrease, or no
hemorrhagic gastritis or duodenitis, and reflux esophagitis in 28% change in this parameter during exposure to hypoxia.19,27,50 In
and 61% of individuals on the second and fourth days at high one of the better-controlled studies, Somner and colleagues144
altitude, respectively. Although these studies do not definitively examined 76 individuals and found statistically significant but
establish that high-altitude travel increases the risk of GI bleed- clinically insignificant increases in IOP after an exertion-free
ing, they do suggest that individuals with a recent history of GI ascent to 5200 m (17,050 feet), which resolved after 7 days at
bleeding or poorly controlled esophagitis, gastritis, or peptic that elevation. There is no evidence that hypobaric hypoxia
ulcer disease may be at risk for problems at high altitude. It provokes acute narrow-angle glaucoma or worsens open-angle
would be prudent for such individuals to avoid extended use of glaucoma. Acetazolamide would be a useful means for pharma-
MOUNTAIN MEDICINE
aspirin or NSAIDs for prevention of AMS or treatment of other cologic prophylaxis against AMS in glaucoma patients, given its
conditions at high altitude. ability to decrease intraocular fluid production through carbonic
anhydrase inhibition.100
Cirrhosis
No studies have examined how patients with liver cirrhosis fare
at high altitude, but there are strong theoretical reasons to suspect
PREGNANCY
that two groups of cirrhotic patients may be at risk for problems: Because pregnancy-associated hypertension, preeclampsia, and
those with portopulmonary hypertension and those with hepa- small-for-gestational age infants are more common among high-
topulmonary syndrome. As noted earlier, patients with portopul- altitude residents,108,109 the issue arises of whether short-term
monary hypertension, a form of pulmonary arterial hypertension exposure to hypobaric hypoxia poses risks to pregnant lowland
seen in up to 16% of cirrhotic patients,21 may be at risk for HAPE residents during high-altitude travel. Data are sparse, but limited
or worsening right-sided heart function when PAP increases evidence suggests moderate altitude exposure is likely safe.71,72
PART 1
after ascent. Patients with hepatopulmonary syndrome, a disorder There is no evidence that short-term exposures increase the risk
seen in up to 32% of cirrhotic patients136 and marked by hypox- for pregnancy-induced hypertension, spontaneous abortion,
emia from the presence of pulmonary arteriolar vascular dilation, placental abruption, or placenta previa.114 Artal and colleagues7
are at risk for exaggerated hypoxemia. Patients with portopul- performed submaximal and maximal exercise tests on seven
monary hypertension should likely avoid high-altitude travel, or sedentary women at 34 weeks’ gestation at sea level and after 2
if travel is unavoidable, should receive pulmonary vasodilator to 4 days of acclimatization at 1830 m (6000 feet) and docu-
therapy or travel with supplemental oxygen. Hepatopulmonary mented the expected decrease in maximal aerobic work, but no
syndrome patients should travel with plans to monitor pulse difference from sea level in fetal heart rate responses or maternal
oximetry after ascent and fill a prearranged prescription for lactate, epinephrine, or norepinephrine concentration. In another
supplemental oxygen in the event of severe symptoms or hypox- study of 12 pregnant women exercising after ascent to 2225 m
emia. For cirrhotic patients not known to have these disorders, (7300 feet), Baumann and associates17 also found no evidence of
screening for their presence should be considered before any abnormal fetal heart rate responses. Additional studies have
high-altitude travel. demonstrated that the fetus tolerates acute hypoxia at high alti-
Cirrhotic patients should not use acetazolamide for AMS tude, provided that placental fetal circulation is normal.10,34,131
prophylaxis or treatment because this may increase the risk When viewed together, the limited literature suggests that
of hepatic encephalopathy.97 Although development of altered physical exertion during short-term exposure to altitudes up to
mental status at high altitude should always raise concern for 3000 m (9840 feet) is likely safe for women with normal, low-risk
HACE, a broader differential should be considered in cirrhotic pregnancy.71,75 High-altitude travel should be avoided, however,
patients and include the possibility of hepatic encephalopathy in certain groups of patients, particularly after the 20th week of
provoked by infection, GI bleeding, or medication nonadher- pregnancy (Box 3-1).75 Before any high-altitude travel, pregnant
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 BOX 3-1 Contraindications to High-Altitude Travel
evaluation. in Pregnancy
38
women should have a checkup, including ultrasound, to ensure
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.e1
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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. of these mountain ranges include the Wasatch Range in Utah,
In the United States, approximately 100,000 avalanches occur Teton Range in Wyoming, and Columbia Mountains of British
annually, of which about 100 cause injuries, death, or destruction Columbia.
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
PHYSICAL PROPERTIES
injured, and 28 killed.1 The median yearly direct losses to prop- Although snow cover appears to be nothing more than a thick,
erty are estimated at $100,000, although this varies significantly homogeneous blanket that covers the ground, it is in fact one of
from year to year. Annual losses from 2003 to 2013 ranged from the most complex materials found in nature. It often exists con-
a low of about $30,000 to a high of $6 million for destruction currently in solid, liquid, and gaseous phases. Snow is highly
caused by a 2008 avalanche that destroyed a portion of the high- variable; it may go through significant changes during relatively
power transmission lines supplying Juneau, Alaska. This chapter short periods as a result of environmental factors.
describes the properties of the mountain snowpack that contrib- At any single site, the seasonal snow cover varies from top
ute to avalanche formation and discusses avalanche safety tech- to bottom and results in a complex layered structure, the study
niques, rescue, and the physiology and treatment of avalanche of which is referred to as stratigraphy. Individual layers may be
victims. 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
PROPERTIES OF SNOW snow crystals that fall are of the same type, when wind speed
and direction vary little, and when temperature and precipitation
SNOW CLIMATES are fairly constant. Thinner layers that are perhaps only millime-
Snow cover varies on both the broad geographic scale (e.g., ters in thickness often reflect conditions between storms. Exam-
Antarctic snow differs from snow found in the Cascade Moun- ples include a melt-freeze crust or sun crust formed during fair
tains of North America, which is different from the snow in the weather and a hard wind crust formed during a period of strong
southern Rocky Mountains of the United States) and the microscale winds. A brittle, buried surface-hoar layer represents what were
(e.g., snow conditions may vary greatly from one side of a rock once delicate, feather-shaped crystals of surface hoar on the
or tree to the other). All snow crystals are made of water mol- surface of the snow that were deposited from the moist atmo-
ecules, but local and regional environmental conditions control sphere onto the cold snow surface during a clear night. These
the type and character of the snow found at a given location. crystals are fragile and weak; after they are buried by subsequent
To better understand geographic differences that affect ava- snowfalls, they may be persistent and major contributors to ava-
lanche initiation, it is helpful to consider some basic climate lanche formation.
conditions. The character of the snow and avalanche propensity One property of snow is strength or hardness, which is of
in different mountain ranges around the world can be described great importance in terms of avalanche formation. Snow can vary
as one of three types—maritime, continental, or transitional—on from light and fluffy, easy to shovel, and especially suitable for
the basis of the average snow conditions of that particular skiing, to heavy and dense, impossible to penetrate with a shovel,
region. and firm enough to make it difficult for skiing. Arrangement of
Heavy snowfall and relatively mild temperatures characterize the ice skeleton (i.e., the lattice of ice crystals within the snow-
the maritime snow climate. The snow cover is deep, and the pack) and the changing density (i.e., the mass per unit volume,
new snow is dense as a result of moist ocean storms coming typically represented as kilograms per cubic meter [kg/m3])
ashore at lower altitudes. Rain is common and a significant cause produce this wide range of conditions. In the case of snow,
of avalanches when it falls on deep fresh snow. Arctic air intru- density is determined by the volume mixture of ice crystals and
sions are uncommon but can occur each winter. In general, the air. In general, the denser the snow layer, the harder and stronger
snowpack gains strength quickly with time in the maritime snow it becomes, as long as it is not melting.
climate. In North America, examples of maritime ranges include Density of new snow can have a wide range of values. This
the Sierras, Cascade Mountains, and Coast Range of British depends on how closely the new snow crystals pack together,
Columbia. which is controlled by the shapes of the crystals. The initial
Far removed from coastal areas, the continental snow climate crystals that fall from the atmosphere have a variety of shapes,
is characterized by low snowfall, cold temperatures, and higher and some pack more closely together than others (Figure 4-1).
altitudes. Snowfall is light and of low density, and wind is a key For example, needle crystals pack more closely than stellate
instigator of avalanches. Avalanche cycles are often the result of crystals (stellars); thus the density of snow made of compressed
buried structural weaknesses that occur in shallow snowpacks needles may be three to four times greater than that of snow
and may cause avalanche danger to persist for days, weeks, or composed of stellars.
even months. Avalanches released from these old, persistent, Wind can alter the shapes of new snow crystals and break
weak layers are a distinguishing trait of a continental climate. In them into much smaller pieces that pack very closely together
this climate, especially during the early months of winter, the to form wind slabs. Such slabs may possess a density that is 5
shallow snow cover loses strength with time. Continental ranges to 10 times that of new stellars falling in the absence of wind.
include the Canadian Rocky Mountains, southern Rocky Moun- Because these processes occur at different times and locations at
tains, and Brooks Range. the surface of the snow cover and are buried by subsequent
In between the maritime and continental regions is a transi- snowfalls, a varied heterogeneous layered structure results. Minor
tional snow climate that, in North America, is often referred to variations in atmospheric conditions can have an important influ-
as the “intermountain” snow climate. Many mountain regions in ence on the properties of snow on the ground.
this class tend to exhibit intermediate features that reflect both After snow has been deposited on the surface, snow density
maritime and continental snow climates (Table 4-1). Examples increases as the snow layer compacts vertically because of the
40
CHAPTER 4 Avalanches
TABLE 4-1 Characteristics of Maritime, Transitional
(Intermountain), and Continental Snow Climates on the
Basis of 15-Year Means
100
(cm)
F3 Column F8 Graupel 0
Heat supply
from Earth
F4 Needle F9 Ice pellet
41
KINETIC METAMORPHISM
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
Low temperature are described as extending upward from the warm ground
Ice grain
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
Water Heat
flow
centimeters from a warm melt-freeze crust into colder snow.
vapor 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
High temperature effects of alternating incoming solar radiation (short-wave radia-
Ice grain
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)
FIGURE 4-4 In the temperature-gradient process, ice sublimates from in size, have straight sides and sharp angles. Backcountry skiers
the top of one grain, moves upward as water vapor, and then is depos- often describe this snow as “recycled powder,” because it often
ited on the bottom surface of the grain above. If conditions allow this forms on colder and northerly facing slopes with prolonged
process to continue long enough, all the original grains are lost as periods of cold and clear conditions. A temperature gradient
recrystallization produces a layer of new crystals. 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,
in the snow layer are transformed from solid to vapor and back which changes more slowly and may still be under the effects
to solid again; in other words, they recrystallize. The new crystals of daytime warming.
are completely different in texture and shape from their initial In the colder temperatures of continental snow climates,
form. They become loose, coarse crystals with faceting, straight strong temperature gradients often exist just above the warm
MOUNTAIN MEDICINE
sides and sharp angles (also known as faceted crystals or sugar ground and can persist for months when the snow cover remains
snow) and may eventually evolve into a large, striated, hollow- shallow, typically less than 1 m (3.3 feet) deep. The persistent
cup form. Examples of these crystals are shown in Figure 4-5. gradient and warm basal snow layer temperature can cause very
This process is called temperature-gradient metamorphism or large and complex faceted grains to form as well-developed
kinetic metamorphism. Well-developed crystals that typically depth hoar. These large, cup-shaped crystals, typically 4 to
form at the basal layer of the snow cover are commonly known 10 mm (0.16 to 0.4 inch) in size, are characterized by straight
as depth hoar. Depth hoar and faceted crystals are of particular sides, sharp angles, and multiple layers of faceted faces. The
importance to avalanche formation because these crystals are grains can be described as resembling etched crystal glass, and
very weak, with little or no cohesion (bonding) at the grain their organized striations can make them sparkle.
contacts. They can form the weak layer that fails under a slab The strong temperature gradients that drive kinetic metamor-
and causes an avalanche. phism are aided by low-density new snow because the larger
pore spaces allow for easier migration of water vapor. Typical
PART 1
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
A in a more homogeneous manner, rather than showing the pref-
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
B snow force water vapor molecules to form bonds and thus drives
equilibrium metamorphism.
FIGURE 4-5 A, Mature depth-hoar grains. Facets and angles are The previous discussion of kinetic and equilibrium metamor-
visible. Grain size, 3 to 5 mm (0.12 to 0.20 inch). B, Advanced phism provides an overview of what happens to snow layers
temperature-gradient grains attain a hollow, cup-shaped form. Size, after they have been buried by subsequent snowfalls. If the
4 mm (0.16 inch). (Courtesy Doug Driskell.) temperature layer is below freezing and no melting is taking
42
relatively little is known about the processes that cause these
CHAPTER 4 Avalanches
EQUILIBRIUM METAMORPHISM avalanches.
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,
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
Forest Service; Williams K, Armstrong B: The snowy torrents, Jackson, shown in Figure 4-11. Laboratory experiments have shown that
Wyo, 1984, Teton Bookshop, with permission. Top, Courtesy Alexis conditions of warm temperatures and slow application of force
Kelner.) 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
and safe. However, when it rests on a weaker layer that may be when force is applied rapidly, snow reacts like an elastic material.
well below the surface, it may fail under the weight of a skier If enough force is applied, it fractures. We think of such a sub-
and be released as a slab avalanche. Many snow structure com- stance as “brittle”; release of stored elastic energy causes fractures
binations can contribute to slab avalanche formation, but again, to move through the material. In the case of snow cover on a
the prerequisite conditions are a cohesive layer over a weak layer steep slope, forces associated with accumulating snow or the
sitting on a bed surface. Figure 4-10 describes other combinations weight of a skier may increase until the snow fails. At that point,
that result in brittle or cohesive layers of snow on a weak layer. stored elastic energy is released and is made available to drive
brittle fractures over great distances through snow slab.
MECHANICAL PROPERTIES: HOW SNOW The slab avalanche provides the best example of elastic defor-
mation in snow cover. Although the deformation cannot actually
DEFORMS ON A SLOPE be seen, evidence of the resultant brittle failure is clearly present
Almost all physical properties of snow can be easily seen or in the form of the sharp, linear fracture line and crown face of
measured in the field. A snow pit provides a wealth of informa- the slab release (Figure 4-12). The crown face is almost always
44
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
Force
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
Snow 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
Viscous deformation
Elastic fracture decades. Measured data for avalanche velocity and impact pres-
FIGURE 4-11 Depending on prevailing conditions, snow may deform sure are still being studied. Although any environmental measure-
and stretch in a viscous or flowing manner, or it may respond more ment presents its own set of problems, it is clear that opportunities
like a solid and thus fracture. 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
perpendicular to the bed surface, which is evidence that snow 4-14). In the starting zone, which is usually the steepest part of
has failed in a brittle manner. the path, the avalanche breaks away, accelerates down the slope,
A full understanding of the slab avalanche condition or stabil- and picks up additional snow. From the starting zone, the ava-
ity of the snow cover requires consideration of its mechanical lanche proceeds to the track, where it remains essentially con-
state. Snow is always deforming in a downslope manner, but stant and picks up little or no additional snow as it moves. The
throughout most of the winter, the strength of the snow is suf- average slope angle becomes less steep, and frequently the snow
ficient to prevent an avalanche. The snow cover is layered, and cover is more stable than in the starting zone; however, a signifi-
some layers are weaker than others. During periods of snowfall, cant amount of snow can be entrained into the avalanche from
blowing snow, or both, an additional load or weight is being the track. Small avalanches often stop in the track. Larger ava-
applied to the snow in the starting zone, the snow is creeping lanches travel down the track and into the runout zone, where
faster, and these new stresses are beginning to approach the the avalanche motion ends. Most avalanches stop quickly, within
strength of the weakest layers. The weakest layer has a weakest seconds, although very large avalanches tend to decelerate
point somewhere within its continuous structure. If the stresses slowly across a gradual slope, such as an alluvial fan. As a general
caused by the load of the new snow or the weight of a skier rule, the slope angle of starting zones is 30 to 45 degrees, track
reach the level at which they equal the strength of the weakest is 20 to 30 degrees, and runout zone is less than 20 degrees.
point, the snow fails completely at that point (Figure 4-13); this Avalanches may appear to be turbulent rivers of snow with
means that the strength at that point immediately goes to zero. fluid-like characteristics; however, avalanches are granular flows
This is analogous to what would happen if someone on a tug- that move much more like a sliding block than like water. Few
of-war team were to let go of the rope. If the remainder of the actual measurements of avalanche velocities have been made,
team was strong enough to make up for the lost member, not but enough data have been obtained to provide some typical
much would change immediately. The same situation exists with values for the various avalanche types. For highly turbulent dry
snow cover. If the surrounding snow has sufficient strength to powder avalanches, velocities are typically in the range of 34 to
make up for the strength at the weakest point having now gone 45 meters per second (m/s), or 75 to 100 miles per hour (mph),
to zero, nothing happens beyond perhaps a localized movement with rare examples in the range of 67 to 89 m/s (150 to 200
or collapse in the snow, often heard as a “whumpf” sound. If mph). Such speeds are possible for powder avalanches because
the surrounding snow is not capable of compensating, however, large amounts of air in the moving snow greatly reduce the forces
the area of snow next to the initial weak point fails, then at that result from internal friction. As the snow in the starting zone
the next area, and so forth, until a propagating chain reaction becomes dense, the terrain becomes less steep and movement
begins. 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
FIGURE 4-12 The consistent 90-degree angle between the crown face that cannot be easily explained simply by the impact of large
and bed surface of the avalanche shows that slab avalanches result amounts of fast-moving dense snow. Some observers have noted
from an elastic fracture. (Courtesy A. Judson.) 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 utes significantly to the total impact force. Presence of snow
snow. Other reports have indicated that a structure was destroyed crystals can increase air density by a factor of three or more. A
by the “air blast” preceding the avalanche, because there was no powder cloud that is traveling at a moderate dry avalanche speed
evidence of large amounts of avalanche debris in the area. This of 27 m/s (60 mph) could have the impact force of an 80-m/s
damage more likely resulted from the powder cloud, which may (180-mph) wind, which is well beyond the destructive capacity
be composed of only a few inches of settled snow, yet contrib- of a hurricane.
46
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-
Starting
duces many more avalanches than does a slope of 30 degrees.
zone
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
Track 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
Runout zone 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.
FIGURE 4-14 Three parts of an avalanche path: the starting zone, Steep slopes are equally likely to face in any direction. In the
track, and runout zone. (Courtesy B. Armstrong.) 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-
IDENTIFYING AVALANCHE TERRAIN tion with respect to sun and wind. In the southern hemisphere,
The essential ingredients of an avalanche—snow and a steep- more avalanches occur on east, southeast, and south-facing
enough slope—are such that any mountain or even a small slopes. The sun angle in northern hemisphere winters causes
hillside can produce an avalanche if conditions are exactly right. south slopes to receive much more sunshine and heating than
To be a consistent producer of avalanches, a mountain and its north slopes, which frequently leads to radically different snow
weather must work in harmony. 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.
47
that have a curved horizontal profile, such as a bowl or gully, is much more hazardous than the same amount of snow falling
trap blowing snow that is coming from several directions; the over 3 days. As a viscoelastic material, snow can absorb slow
snow drifts over the top and settles as a deep pillow. Alterna- loading by deforming or compressing. Under a rapid load, the
tively, the plane-surfaced slope collects snow efficiently only if snow cannot deform quickly enough and is more likely to crack,
it is being blown directly from behind. A side wind scours the which is how slab avalanches begin. A snowfall rate of 2.5 cm
slope more than it loads the slope. (1 inch) or more per hour that is sustained for 10 hours or more
The surface conditions of a starting zone often dictate the size is generally a red flag with regard to avalanche danger. The
and type of avalanche. A particularly rough ground surface (e.g., danger worsens if the snowfall is accompanied by wind.
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 RAIN
pull out in sections, with the area between two exposed rocks The age of the surface snow is an important factor with regard
running one time and the area between another two other rocks to changes in stability when rain falls. Within hours of light rain
running another. A smooth rock face or a grassy slope provides falling on fresh or recent snow (i.e., within the last several days),
a surface that is usually too slick for snow to grip; therefore full- avalanching can occur for reasons that are not well understood.
depth avalanches are distinctly possible. If the avalanche does The rain somehow causes a loss of strength in the new snow.
not run during the winter, it is likely to run to ground in the Significant rain, usually about 2.5 cm (1 inch), falling on a snow
spring after melt water percolates through the snow and lubri- surface several days or more old produces few or no avalanches.
cates the ground surface. 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
VEGETATION and invariably freezes into an ice crust, which adds strength to
Vegetation has a mixed effect on avalanche releases. Bushes the snow cover. Later, the smooth crust could become a sliding
provide anchoring support until they become totally covered. At layer beneath new snowfall. Heavy rain (usually >2.5 cm) greatly
that point, bushes may provide weak points in the snow cover, weakens the snow cover. It adds weight to the snowpack, but
because air circulates around the bush and provides an ideal adds no internal strength of its own (in the form of a skeleton
MOUNTAIN MEDICINE
habitat for growth of depth hoar. It is common to see that the of ice, as new snow would create). Rain dissolves bonds between
fracture line of an avalanche has run from a rock to a tree to a snow grains as it percolates through the top snow layers, thus
bush, because these are all places of healthy depth-hoar growth. reducing strength even further.
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 NEW SNOW DENSITY AND CRYSTAL TYPE
means of avalanche control. Scattered trees on a gladed slope A layer of fresh snow contains only a small amount of solid
offer little if any support to hold snow in place. Isolated trees material (ice); the majority of the volume is occupied by air. It
may do more harm than good by providing concentrated weak is convenient to refer to snow density as a percentage of the
points on the slope. 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
FACTORS THAT CONTRIBUTE TO
PART 1
48
at Berthoud Pass, Colorado, the wind deposited snow in a gully weather continues, the melt layer becomes thicker, and the
CHAPTER 4 Avalanches
at a rate of 45 cm (18 inches) per hour. potential for wet snow avalanches increases. The conditions that
A speed of 7 m/s (15 mph) is sufficient to pick up freshly are most favorable for wet slab avalanches occur when the snow
fallen snow. Higher speeds are required to dislodge older snow. structure provides the necessary layering. When melt water
Speeds of 9 to 22 m/s (20 to 50 mph) are the most efficient for encounters an ice layer or an impermeable crust, or in some
transporting snow into avalanche starting zones. Speeds of more cases a layer of weak depth hoar, wet slab avalanches are likely
than 22 m/s (50 mph) can create spectacular banners of snow to occur.
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.
DEPTH OF SNOW COVER
Winds also increase the avalanche potential, because blowing Of the snowpack factors that contribute to avalanche formation,
snow is denser after deposition than before transport. Snow the depth of the snow cover is the most basic. When the early-
grains are subjected to harsh treatment in their travels; each col- winter snowpack covers natural anchors (e.g., rocks, bushes),
lision with another grain knocks off arms and rounds sharp the start of the avalanche season is at hand. However, a word
angles, thereby reducing the grain’s size and allowing the pieces of caution is necessary for backcountry travelers in the weak,
to settle and pack together into a denser layer. The net result of depth-hoar–prone, continental snow climate. The early-winter
wind is to fill avalanche starting zones with additional, heavier, avalanche danger starts not when the natural anchors are covered,
and more cohesive snow than if no wind had blown. 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,
TEMPERATURE but another method can be used to determine the time of the
The role of temperature in snow metamorphism occurs over first significant avalanches. Long-term studies show a relationship
days, weeks, and even months. The influence of temperature on between snow depth at a study site and avalanche activity. For
the mechanical state of the snow cover is more acute, with example, along Red Mountain Pass, Colorado, it is unlikely that
changes occurring in minutes to hours. The actual effect of tem- an avalanche large enough to reach the highway will run until
perature is not always easy to interpret. Whereas a temperature almost 90 cm (3 feet) of snow covers the ground at the University
increase may contribute to stabilization of the snow cover in one of Colorado’s snow study site. At Alta, Utah, when 130 cm (52
situation, it might at another time lead to avalanche activity. inches) of snowpack has built up, the first avalanche to cover
In several situations, increased temperature clearly produces the road leading from Salt Lake City can be expected.
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
WEAK LAYERS
as occurs with spring conditions. In the first example, tempera- Any layer that is susceptible to failure and fracture because of
ture at the beginning of a snowfall may be well below freezing, the overburden of additional weight is a weak link. Of the snow-
but as the storm progresses, temperature increases. As a result, pack contributory factors, this is the most important, because a
the initial layers of new snow are light, fluffy, low density, and weak layer is essential to every avalanche. Fracture in the weak
relatively low in strength, whereas the later layers are warmer, layer propagates along what is called the failure plane, sliding
denser, and stiffer. Thus the essential ingredient for a slab ava- surface, or bed surface.
lanche is provided within the new snow layers of the storm: a The most troubling layers are called persistent weak layers,
cohesive slab resting on a weak layer. If the temperature contin- which are usually made of snow crystals and include larger-
ues to rise, the falling snow turns to rain. This situation is seen faceted snow, depth hoar, and surface hoar. These crystals are
in lower-elevation coastal mountain ranges. When this occurs, slow to change shape and gain strength, so they may persist for
avalanches are almost certain. As rain falls, additional weight is days, weeks, months, or even all season. One common weak
added to the avalanche slope, but no additional strength is pro- layer is an old snow surface that offers a poor bond for new
vided, as might be by a new layer of snow. snow. Another weak layer that forms on the snow surface is hoar
The second example may occur after an overnight snowstorm frost or surface hoar (see Physical Properties, earlier). On clear
that does not produce an avalanche on the slope of interest. By and calm nights, this hoar forms a layer of feathery, sparkling
morning, the precipitation stops, and clear skies allow the flakes that grow on the snow surface. The layer can be a major
morning sun to shine directly on the slopes. The sun rapidly contributor to avalanche formation when it is buried by snowfall
warms the cold, low-density, new snow, which begins to deform as a result of its frequent persistence in the snowpack. Many
and creep down slope. The new snow layer settles, becomes avalanches have been known to release from a buried layer of
denser, and gains strength. At the same time, it is stretched surface hoar, and sometimes this layer is more than 1 month old
downhill, and some of the bonds between the grains are pulled and 180 cm (6 feet) or more below the surface.
apart; thus the snow layer becomes weaker. If more bonds are A weak layer that is almost always found deep within the
broken by stretching than are formed by settlement, there is not snowpacks that blanket the Colorado Rocky Mountains (conti-
enough strength to hold the snow on the slope, and an avalanche nental snowpack) is large temperature-gradient snow (facets) or
occurs. depth hoar. One way to decide whether a temperature-gradient
In these first two examples, the complete snow cover gener- layer is near its collapse point is to test the strength of the over-
ally remains at temperatures that are below freezing. A third lying layers and the support provided by specific stability testing
example occurs when a substantial amount of the winter’s snow performed near the edge of the slope. This is no easy task, and
cover is warmed to the melting point. During winter, sun angles results may be unreliable because of the spatial variability of
are low, days are short, and air temperatures are cold enough weaknesses on the slope. In addition, most field stability tests
that the small amount of heat gained by the snow cover during do not test for deep instabilities in the snowpack. Another
the day is lost during the long, cold night. As spring approaches, method is to try jumping on your skis while standing on a
this pattern changes, and eventually enough heat is available at shallow test slope of similar aspect. Collapse is a good indication
the snow surface during the day to cause some melt. This melt that comparable snow cover on a steeper slope will produce an
layer refreezes again that night, but the next day more heat may avalanche. Often, skiers and climbers cause inadvertent collapses
be available, so eventually a substantial amount of melting while skiing or walking on a depth-hoar–riddled snowpack. The
occurs, and melt water begins to move down through the snow resulting “whumpf” sound is a warning of weak snow below.
cover. As melt water percolates slowly downward, it melts the In the past couple of decades, study has focused on the fre-
bonds that attach the snow grains, and the strength of the layers quency of faceted snow layers near the surface of the snowpack
decreases. At first the near-surface layers are affected, with the and their relation to avalanches, particularly in the deeper snow
midday melt reaching only as far as the uppermost few inches cover of the transitional (intermountain) snow climate. Several
and with little or no increase in avalanche hazard. If warm mechanisms involved in the evolution of these layers may
49
account for the majority of avalanches in this region, because possible to trigger an avalanche from below if one is traveling
significant depth-hoar–related avalanches are less common. close to the compression zone, thereby initiating a fracture that
Graupel (pellet-like heavily rimed crystals) can act as ball propagates upward. Slopes of 30 degrees or more should be
bearings after being buried in the snowpack and can be respon- approached with caution. By climbing, descending, and travers-
sible for the layer involved in avalanche initiation. ing only in gentle terrain, avalanche risk can be avoided.
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-
CROSSING AVALANCHE SLOPES
cating that layer and destroying its shear strength. This phenom- Travel through avalanche country always involves risk, but
enon can be seen during the winter months in the maritime snow certain travel techniques can minimize that risk. Proper travel
climate of the West Coast mountains. techniques might not prevent an avalanche release but can
Combining the constellation of contributory factors on a day- improve the odds of survival. The timing of a trip is closely
by-day basis is the avalanche forecaster’s art. Every avalanche involved with safety. Most avalanches occur during and just after
must have a weak layer on which to release, so knowledge of storms. Waiting a full day after a storm has ended can allow the
snow stratigraphy or layering and what level of applied load will snowpack to react to the new snow load and gain strength.
cause a layer to fail form the essence of forecasting. 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
SAFE TRAVEL IN AVALANCHE should be worn normally, because they may afford protection
from back trauma and because the items necessary for survival
TERRAIN after a rescue can be stored inside. If use of a large mountaineer-
The first major decision often faced in backcountry situations is ing pack will make a person top heavy and more likely to fall,
whether to avoid or confront a potential avalanche hazard. A another route should be considered. The skier should remove
group that is touring with no particular goal in mind will prob- pole wrist straps and ski runaway straps, because poles and skis
ably not challenge avalanches. For this group, education to attached to the avalanche victim hinder extremity motions and
recognize and avoid avalanche terrain is sufficient. At the other only serve to drag the victim under. A person who is wearing a
MOUNTAIN MEDICINE
extreme, mountaineering expeditions that have specific goals and rescue transceiver should always be certain that it is transmitting.
are willing to wait out dangerous periods or take severe risks to When crossing potential avalanche slopes, it is always better
accomplish their objective need considerably more information. to cross as high or low as possible and to avoid the middle. All
Traveling safely in avalanche terrain requires special prepara- persons should traverse in the same track, spaced sufficiently
tions, including education and carrying safety and rescue equip- apart to expose only one person at a time. This not only reduces
ment. The group should have the skills required to anticipate the amount of work required but also disturbs less snow, which
and react to an avalanche. 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
IDENTIFYING AVALANCHE TERRAIN moving avalanche will be greater. Invariably the person who is
Because most avalanches release on slopes of 30 to 45 degrees, highest on the slope runs the least risk of being buried.
judging angle is a prime skill for the recognition of potential A person who must climb or descend an avalanche path
PART 1
avalanche areas. An inclinometer can be used to measure slope should keep close to its sides. Should the slope fracture, escaping
angles. Some compasses are equipped for this purpose; a second to the side improves the chance of survival. Only one person at
needle and a graduated scale in degrees can be used to measure a time should cross, climb, or descend an avalanche slope; all
slope angles. A ski pole may be used to judge approximate slope other members should watch from a safe location. Two com-
angle. When dangled by its strap, the pole becomes a plumb monsense principles underlie this advice. First, only one group
line from which the slope angle can be “eyeballed.” member is exposed to the hazard, thereby leaving the others
Evidence of fresh avalanche activity (i.e., the presence of available as rescuers. Second, less weight is put on the snow.
fracture lines and rubble of avalanche snow on the slope or at Snowmobilers all too often fall prey to multivictim accidents
the bottom) identifies avalanche slopes. Other clues are swaths because an additional rider will drive up a steep slope to help
of missing trees or trees that are bent downhill or damaged, a friend who is stuck near the starting zone.
especially with the uphill branches removed. Above the tree line, Skiers, snowboarders, climbers, and snowmobilers should
steep bowls and gullies are almost always capable of producing never drop their guard on an avalanche slope. They should stop
avalanches. 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
ROUTE FINDING person traversing or traveling down a slope may trigger the
Good route-finding techniques are necessary for safe travel in avalanche. Trouble should always be anticipated, and an escape
avalanche terrain (Figure 4-16). Route finding in avalanche route (e.g., moving to the side, grabbing a tree) should be kept
country should avoid avalanches, be efficient, and take into in mind.
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
STABILITY EVALUATION TESTS
and at a distance from them. When taking a route above ava- People who are traveling on snow-covered slopes should perform
lanche terrain, the traveler should choose a ridgeline that is above hands-on tests of snow strength and instability. Testing the
the avalanche starting zones. It is safest to travel the windward strength of snow helps with location of weak layers, and check-
side of the ridge. The snow cover is usually thinner and wind ing for instability demonstrates how well layers are adhering to
packed, with rocks sticking through; this does not make for the one another. Several simple but meaningful tests can be per-
most pleasant skiing, but is safe. Cornice collapses present a very formed without digging holes in the snow, although much more
real hazard; they should be avoided by staying on the roughened information can be learned by digging snow pits.
snow toward the windward side. When ascending a potential A fast and simple test to find significant weak layers is to push
avalanche path, a safe route (e.g., a dense forested area that is a ski pole into the snow; this should be done handle-end first if
well anchored, a low-angle approach) should be selected. the snow is dense. This helps the individual to feel the major
Skiers who are taking a route in the valley below avalanche layering of the snowpack. For example, the skier may feel the
terrain should not linger in the runout zones of avalanche paths. layer of new snow, and stronger or weaker layers in the middle
Although it is unlikely that a skier who is traveling along the of the pack can be appreciated by the ease of the push. Hard-
valley could trigger an avalanche high up on the slope, it is snow layers and ice lenses may resist penetration altogether, but
50
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 and that slopes of similar aspect and elevation, if steeper, would
slowly along the side of the hole. This test reveals only the gross have probably avalanched. Ski cuts can be made on steeper
layers within the reach of the pole. Thin weak layers, such as suspect slopes by starting a diagonal straight path from an area
buried surface hoar or a poor bond between any two layers, of safety in a continuous cut to another planned area of safety
cannot be detected. Although of limited value, the ski pole test on the other side of the slope. This can be a dangerous maneu-
can provide useful information that must then be correlated with ver, but the momentum—even if an avalanche is initiated—
other testing. increases the chances of escaping from the starting zone to a
The simple but useful ski cut test reveals how a similar slope safe position. An experienced snowmobiler can perform a similar
may react to the additional weight of a skier, snowboarder, or test by riding across the test slope.
snowmobiler. On a small slope that is not too steep (and there- A much better way to observe directly and test snowpack
fore probably not avalanche prone), the skier can try a ski cut layers is to dig a hasty snow pit. In a spot as near as possible
by skiing along a shallow traverse and then setting the ski edges to a suspected avalanche slope, without putting the traveler at
in a hard check. Any cracks or collapse noises indicate instability 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
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 Snow pit
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 FIGURE 4-17 Photo and schematic of a shovel compression test.
that is discovered is defined as “easy” (taps 1 through 10), “mod- (From The American Avalanche Association, with permission. Top,
erate” (taps 11 through 20), or “hard” (taps 21 through 30). The Courtesy Doug Richmond.)
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). and well uphill from the isolated block and carefully approaches
Most tests, including the ST and the CT, assess fracture initia- it from above. With skis across the fall line, the skier gently steps
tion (i.e., additional force or stress needed to start fractures), but onto the block, first with the downhill ski and then with the
do not assess fracture propagation (i.e., propensity for fractures uphill ski, so that the person is standing on the isolated block
to spread through a weak layer in the snowpack). Without assess- of snow. If the slab of snow fails at this time, the score is RB2.
ing for fracture propagation, tests may conceal the real problem Gently flexing the knees applies a little more pressure (RB3). The
layer in a weak snowpack. In a stable snowpack, a fracture may tester then jumps and lands in the same compacted spot (RB4).
be easy to initiate, but no avalanche may result because the The jump is then repeated (RB5). If no failure occurs, the skier
fracture does not propagate across the weak layer. In an unstable moves to the middle of the block and repeats the flexing and
snowpack, a fracture may be easy or difficult to initiate. After it jumping (RB6). If no reasonably smooth failure is produced at
has been initiated, however, the fracture can propagate across this time, the test is considered an RB7.
the weak layer and result in an avalanche. The results are interpreted as “extremely unstable” if the block
To better assess fracture initiation, propagation, and instabil- fails while the skier is cutting it, approaching it from above, or
ity, many backcountry travelers and avalanche professionals use merely standing on it (RB1 or RB2); “unstable” if it fails with a
the Rutschblock test (RB). This test is calibrated to the skier’s knee flex or one gentle jump (RB3 or RB4); “moderately stable”
weight and to the stress that the skier would put on the snow. if it fails after repeated jumps (RB5); and “very stable” if it never
A snow pit is dug with a vertical uphill wall. The pit must be fails but merely crumbles (RB6 or RB7). These are somewhat
about 240 cm (8 feet) wide. By cutting into the pit wall, the skier objective results that may help answer the bigger question of
isolates a block of snow that is approximately 210 cm (7 feet) whether the snowpack will fail under the weight of a person,
wide (i.e., a ski length) and that goes back 120 cm (4 feet; i.e., and that may help the mountain traveler with risk evaluation.
a ski pole length) into the pit wall. Both the sides and the back Limitations include the time required to isolate the block; inability
are cut with a shovel or ski so that the block is freestanding. The to test deep, weak layers; spatial variability of the results; and
test receives a score of RB1 if the snow fails while the individual the problem of relying on the RB as a one-step stability
is isolating the block. While wearing skis, the skier climbs around evaluation.
52
A more practical test developed during the late 2000s is the high density. Such snow is extremely difficult to move with hands
CHAPTER 4 Avalanches
extended column test (ECT), which does a remarkable job of or skis.
effectively discriminating between unstable and stable slopes by The shovel should be sturdy and strong enough to dig in
extending the size of the column beyond the size of the loading avalanche debris, yet light and small enough to fit into a pack.
area. Similar to the loading of the CT, stress can be transmitted There is no excuse for not carrying a shovel. Collapsible shovels
across the slab. If conditions are unstable, fracture will propagate made of aluminum are available in mountaineering stores.
across the column’s weak layer. An excellent video tutorial can
be viewed on the Utah Avalanche Center website at https:// Probe
utahavalanchecenter.org/how-do-extended-column-test. Several pieces of equipment are designed specifically for finding
To prepare an ECT, a snow pit is dug with a vertical uphill buried avalanche victims. The first is a collapsible probe pole.
wall and a column isolated that is 90 cm (3 feet) across the slope Organized rescue teams keep rigid poles in 3- to 4-m (10- to
by 30 cm (1 foot) up the slope. The column is then loaded 12-foot) lengths as part of their rescue caches. The recreationist
from one side with use of the same successive tap technique can buy probe poles of tubular aluminum or carbon fiber that
used in the CT. The result reporting emphasizes what happened come in 45-cm (18-inch) sections that attach together quickly by
to the snow column (i.e., whether a fracture propagated across pulling a stiffening cable to construct a full-length probe. Some
the column or not). The coding is recorded as ECTPV (“very ski poles with removable grips and baskets can be screwed
easy”) if the fracture propagates across the entire column during together to make an avalanche probe. Probes are used to search
isolation. As with the CT, the number of taps is reported as for buried victims by spot probing in likely burial areas or to
ECTP## when a fracture initiates and propagates across the entire confirm transceiver findings before shoveling (see Small-Team
column. If a fracture initiates on ## tap but does not propagate Rescue [Companion Rescue], later).
across the entire column, or if more than one additional tap is
required after initiation to cause complete propagation, the result Avalanche Rescue Transceiver
is noted as ECTN##. If no fracture occurs, the result is noted Avalanche rescue transceivers (beacons) are one of the best
as ECTX. personal rescue devices for quickly finding buried companions.
The propagation saw test, developed and tested in Canada With practice and proper use, transceivers are a fast and effective
and Switzerland, has the advantage of being able to assess the way to locate buried victims. Worldwide, these devices have
propensity of a preidentified persistent weak layer and slab become standard gear for ski area patrollers involved in ava-
combination to propagate a fracture. Only a shovel and snow lanche work and for helicopter or other mechanized skiing
saw are needed, and the test’s interpretation is relatively straight- guides and clients. Transceivers are also frequently used by
forward. A column of snow 30 cm (1 foot) wide by at least highway departments and search and rescue organizations and
100 cm (3.3 feet) uphill is isolated. After the persistent weak layer should be used by anyone traveling into avalanche terrain. Since
is identified and marked, the blunt edge of the saw is directed transceivers were first introduced in the United States in 1971,
uphill through the weak layer until a fracture propagates. The they have been credited with saving multiple lives each winter.
spot where the saw was located at the time of the propagation Transceivers act as electromagnetic transmitters that emit a
is marked. Fracture propagation in a similar snowpack is consid- signal on a standard frequency of 457 kHz. A buried victim’s unit
ered “unlikely” if it requires sawing more than 50% of the weak emits this repetitive signal in radial “flux lines,” which the rescu-
layer to initiate propagation, or if the fracture fails to reach the ers’ units receive and analyze when switched to “receive” mode.
end of the column. Propagation would be considered “likely” if The signal carries approximately 30 to 50 m (100 to 150 feet).
the fracture reaches the end of the column, or if it requires When audibly or visibly detected, the signal can guide searchers
sawing less than 50% of the weak layer to fracture. Unlike many specifically to the buried unit in less than 5 minutes.
other stability tests, the propagation saw test allows assessment Transceiver technology has evolved dramatically. Current
of the slab propagation propensity in deep instabilities. transceivers offer a significant technologic advantage over the
Interpreting stability from a single snow pit or stability test is original analog devices. Two major categories of transceivers can
dangerous because of spatial variability. Snow cover is not homo- be found: (1) analog, which processes the receiving signal in a
geneous in its stability; rather, it has a patchwork-quilt–like basic electromagnetic convergence of induction pulses to allow
pattern of stronger and weaker snow. Even within a known for a stronger (visual and audible) signal as the receiving trans-
combination of an unstable slab and a weak layer, there are ceiver approaches the sending unit, and (2) digital, which uses
variations along the slope where one can trigger or not trigger a computer chip to microprocess the receiving analog signal in
an avalanche (i.e., the false-stable rate). The implications of order to display a digital readout of the distance, strength (audible
spatial variability are significant. On a suspected avalanche slope, and visual), and in some units (i.e., dual and triple antenna),
explosives set in an area of strength will not result in an ava- general direction to the buried unit. The newer triple-antenna
lanche. It might then be assumed, incorrectly, that the snow in transceivers not only provide data about distance, direction, and
a ski area is stable and safe, only to have a skier hit a weak spot signal strength, but also can more easily identify multiple burials
and trigger an avalanche. Likewise, a backcountry skier might and their approximate location in relation to each other. The
dig a snow pit and find strong snow, only to trigger an avalanche triple-antenna transceivers reduce occasional misleading signals,
on the entire slope after skiing a few turns. which can be a confusing issue with single-antenna and dual-
All tests are prone to misleading results. Research has shown antenna devices in the final few meters of the search. Transceiv-
that the CT and RB tests, which are favored by most avalanche ers are audiomagnetic-induction devices and not radio devices;
professionals, have a relatively high false-stable rate (i.e., a stable the directional arrows point radially along a flux line of the
test result on an unstable slope) of about 10% to 20%.4 On paper, sending unit’s magnetic field (Figure 4-18). Likewise, the dis-
being correct 80% to 90% of the time may sound encouraging. played distance represents the distance along the flux line rather
In practice, however, the false-stable rate is still too high, because than a direct distance to the sending unit; the closer the distance
the consequences of an error can be fatal. The false-stable rate displayed, the closer the flux line from the sending unit.
of 3% with the ETC is more encouraging, but researchers caution Both analog and digital transceivers operate on the same
that more studies are needed.39 internationally standardized frequency and are compatible with
one another. However, slightly different search techniques may
AVALANCHE RESCUE EQUIPMENT be necessary to use each type most efficiently, and special train-
ing and practice are required before the user attains proficiency.
Shovel Experience has shown that digital units have a significantly faster
The first piece of safety equipment that an individual entering learning curve; these are routinely used by helicopter skiing
avalanche terrain should bring is a shovel, which can be used services and backcountry guides for clients with limited experi-
to dig snow pits for stability evaluation, dig snow caves for ence. Multiantenna digital transceivers have largely replaced pure
overnight shelter, and rescue a buried partner. A shovel is man- analog units because of their relative ease of use and enhanced
datory for digging in avalanche debris because of the snow’s 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
CHAPTER 4 Avalanches
BOX 4-1 Avalanche Transceiver Search
Initial Search 5. When the signal is loud at the minimum volume setting, you
1. Safely access the slide path and debris area, and have everyone should be very close to the victim and can begin the grid
switch their transceivers to “receive” and turn the volume to search.
“high.”
2. If enough people are available, post a lookout to warn others Grid Search
about possible additional slides. 1. When a signal is picked up, stand and rotate the transceiver,
3. Should a second slide occur, have rescuers immediately switch which is held horizontally (parallel with the ground) to obtain the
their transceivers to “transmit.” maximum signal (loudest volume). Maintain the transceiver in this
4. Have rescuers space themselves no more than 30 m (100 feet) orientation during the remainder of the search.
apart and walk abreast along the slope. 2. Turn the volume control down until you can just hear the signal.
5. If a single rescuer is searching within a wide path, he or she Walk in a straight line, down the fall line from where the signal
should zigzag across the rescue zone and limit the distance was first detected. (If the signal fades immediately, walk up the
between crossings to 30 m (100 feet). fall line.) If you are headed in the right direction, the signal will
6. For multiple victims, when a signal is picked up, have one or two increase; turn the volume control down until the signal fades.
rescuers continue to focus on that victim while the remainder of Take an extra couple of steps to be sure that the signal truly
the group carries out the search for additional victims. fades. If the signal increases, continue until it fades.
7. For a single victim, when a signal is picked up, have one or two 3. When the signal fades, mark the point, and then turn 180 degrees
rescuers continue to locate the victim while the remainder of the and walk back toward the starting position. The signal will
group prepares shovels, probes, and medical supplies for the increase in volume and then fade again; take two additional steps
rescue. 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
Locating the Victim
and maximum signal. If you experience two maximum signals, go
With practice, the induction line search is more efficient than the to the midpoint between the two maximums.
conventional grid search for getting close to the sending beacon, 4. At this point, turn 90 degrees in one direction or the other. From
but the conventional grid search is still necessary to fine-search for that position, reorient the transceiver (held parallel with the
the buried victim. A probe pole can be used to pinpoint the victim’s ground) to locate the maximum signal. After orienting the
exact location. The induction line search is very similar to the flux transceiver to the maximum signal, reduce the volume, and begin
line search that is used by digital transceivers. Users should always walking forward. If the signal fades, turn around 180 degrees, and
study the owner’s manual to learn the best techniques for the begin walking again.
specific brand of avalanche rescue beacon that they are using. 5. As the signal volume increases, repeat steps 3 and 4 until you
Induction Line Search (Preferred Method) have reached the lowest volume control setting on the
When an induction line search is used, the rescuer may initially transceiver. (Be sure always to take an extra step or two to
follow a line that leads away from the victim (see Figure 4-18A,B). confirm the fade point.) This time, when you return to the middle
Remember to lower the transceiver volume if it is too loud, because of the fade points, you should be very close to the buried victim
the ear detects signal strength variations better at lower volume and can now begin pinpointing the person.
settings. a. While stationary, orient the transceiver to receive the maximum
1. After picking up a signal during the initial search, hold the signal (loudest volume). At this point, turn the volume control
transceiver horizontally (parallel with the ground), with the front of all the way down.
the transceiver pointing forward (see Figure 4-18C). b. With the transceiver just above the surface of the snow,
2. Holding the transceiver in this position, turn until the signal is continue doing the grid search pattern two to four more times.
maximal (maximum volume), then walk five to seven steps (~5 m Always sweep the transceiver a couple of feet beyond the fade
[16.4 feet]), stop, and turn again to locate the maximum signal point to confirm the fade point.
(see Figure 4-18). When locating the maximum signal, do not turn c. Find the signal position halfway between the fade points (i.e.,
yourself (or the transceiver) more than 90 degrees in either at the loudest signal). At this point, you should be very close to
direction. If you rotate more than 90 degrees to locate the the victim’s position, and you can begin to mechanically probe.
maximum signal, you will become turned around and will follow Speed is essential. With practice, the transceiver will be
the induction line in the reverse direction. accurate to less than one-fourth the burial depth. For example,
3. Walk another five steps, as just described, and then stop and a 4-foot burial should result in about a 1-foot square at the
orient the transceiver toward the maximum signal. Reduce the surface.
volume. d. Depending on the brand, pinpointing with a digital transceiver
4. Continue repeating these steps. You should be walking in a will involve the use of a slight variation or a combination of the
curved path along the induction line toward the victim (see induction line and grid techniques. Be sure to study the
Figure 4-18B). owner’s manual.
studies reported that avalanche airbags reduced mortality from and 3% for noncritically buried victims. Finally, the adjusted
18.9% without an airbag to 2.9% with an airbag.10 This apparent mortality reduction with an inflated airbag dropped from 22%
dramatic reduction in mortality presumably occurs because the without use of the bag to 11% (i.e., mortality was reduced by
avalanche airbag device effectively prevents complete or critical half with inflated airbags). Interestingly, overall noninflation rate
burial, and very few (~3% to 5%) noncritically buried or unburied was 20%, the majority resulting from deployment failure by the
victims die in avalanches. user. These findings, despite inherent limitations of the hetero-
Recent examination of the effectiveness of avalanche airbag geneous data set and the retrospective nature, support that
devices24 used a retrospective, multivariate regression analysis on avalanche airbags are a valuable safety device, although possibly
a comprehensive avalanche accident data set from Europe, of less impact than previously reported.
Canada, and the United States that included avalanches from 1994 The airbag works as a result of granular convection (the
to 2012 with the potential for mortality. Each accident in the “Brazil nut effect,” similar to shaking a large bowl of mixed nuts
analysis involved at least one airbag user compared with either to have the largest nuts rise to the top) (Figure 4-20). An ava-
nondeployed-airbag users or nonusers from the same incident. lanche in motion is composed of many different-sized particles
The multivariate analysis for critical burial and mortality after of snow and other objects moving in layers of granular flow.
protocol exclusions included 189 seriously involved individuals When these particles and objects begin to segregate, smaller
from 61 accidents. The adjusted “risk of critical burial” was 47% particles sink to the lower portion of the flow and larger particles
with noninflated airbags or no airbag compared to 20% with rise to the surface. The process of granular convection depends
inflated airbags. The adjusted mortality was 44% for critical burial primarily on the relative sizes of the particles within this granular
55
Granular convection
FIGURE 4-20 Granular convection. The physical unmixing of flowing FIGURE 4-21 The JetForce Avalanche Airbag Pack (Black Diamond
particles is based on size, which distributes larger particles in the upper Equipment) uses a battery-powered fan instead of a compressed gas
layers and forms the basis for successful functioning of avalanche cylinder. The fan inflates a 200-L (6.9-foot3) airbag in 4 seconds, then
airbag systems. This is similar to the “Brazil nut effect,” where shaking automatically deflates the bag after 3 minutes. This system can be
a bowl of mixed nuts causes the largest nuts to rise to the top. deployed, repacked, and ready for use without having to refill a com-
pressed gas cylinder.
MOUNTAIN MEDICINE
flow. A person who is carried in an avalanche may be a medium Different avalanche airbag device configurations include a
or small particle compared with a particulate slab and therefore pack with two separate airbags, a pack with a single airbag, and
may be buried under the surface. However, the airbag device a vest with a single airbag. Configurations are two approximately
creates a greater surface area (typically a total of 150 to 170 L 75- to 85-L (2.6- to 3.0-foot3) airbags or one 150-L (5.2-foot3)
[5.2 to 6.0 feet3] when inflated) for the avalanche victim, making airbag. These inflate in 2 to 3 seconds with use of the Venturi
the user a large enough particle to allow for greater separation effect. In 2014, one manufacturer released a 200-L (6.9-foot3)
effect toward the surface, thus reducing the risk of full burial. airbag built into a pack that inflates in 4 seconds using an electric-
Buoyancy plays no role in the efficiency of this system. In addi- powered fan instead of a compressed-gas cylinder (JetForce Ava-
tion, during partial burial, the brightly colored balloons may lanche Airbag Pack, Black Diamond Equipment) (Figure 4-21).
be easily visible on the surface, making a transceiver search Avalanche airbags may deploy as a large bag or in a horseshoe
unnecessary. shape around the back of the victim’s head toward the anterior
Since 1995, avalanche airbag devices have undergone signifi- chest. Avalanche airbag systems that cover the back of the neck
PART 1
cant improvements with regard to device size, balloon technol- and head or surround the back and sides of the head and anterior
ogy, and cartridge weight. Avalanche airbags are available from chest (Figure 4-22) have the theoretical advantage of preventing
four companies: ABS (with partners Osprey, Dakine, Ortovox, head trauma and may allow for a greater chance of a head-up
and The North Face), Snowpulse/Mammut, Backcountry Access, partial burial. However, there is no evidence to support preven-
and Black Diamond Equipment. The airbag is usually integrated tion of head or chest trauma with specific avalanche airbag
into a special backpack, and the user deploys it by pulling a system configurations. This is an area for future study.
ripcord-like handle. This action releases a cartridge of com- Unlike the original avalanche airbag system (ABS), none of
pressed air or nitrogen that escapes at high velocity and draws the new systems has been independently tested by the Swiss
in outside air. 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.)
57
minutes by breathing with an AvaLung. Two other skiers buried
SMALL-TEAM RESCUE (COMPANION RESCUE)
in the same avalanche a few feet apart at a similar depth were All backcountry users should carry appropriate avalanche rescue
not wearing the device, and both died of asphyxiation. Rescue equipment to aid a fellow group member or another group. This
times were similar for the three victims, none of whom had suf- includes a transceiver, shovel, and probe, as well as knowledge
fered any trauma.13 of and practice using this equipment. At resorts, ski patrol
The ABS and AvaLung are designed as adjuncts to the basic members monitor the avalanche danger and attempt to trigger
companion (small-team) rescue equipment, which includes a sensitive avalanches. Therefore, avalanches are rare in these
transceiver, probe, and shovel. These devices should never be areas. However, avalanche management is not a perfect science,
used to justify taking additional risks. Surviving any avalanche is and skiers have become caught, injured, and even killed at ski
always uncertain, and no equipment should ever replace sound resorts. Therefore, some skiers wear avalanche transceivers and
judgment. 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
AVALANCHE RESCUE backcountry user should attend a cardiopulmonary resuscitation
INDIVIDUAL RESCUE (SELF-RESCUE) (CPR) course and wilderness-oriented first-aid course.
Escaping to the Side Calling for Help
During the moment that the snow around a person begins to If the accident site may be within the range of cell phones or
move, there is a split second during which that person can other communication methods, a call or text should be attempted
potentially move off the avalanche to more stable snow (see immediately. Search and rescue teams as well as medical assis-
Figure 4-13). Escaping to the side of an avalanche is unlikely, tance can be summoned and can be en route during on-site
however, and should not be considered a viable rescue or safety search for the victim. If team members are certain that no cell
plan. If the skier happens to be next to a tree when an avalanche reception or other communication is possible and that travel to
begins, holding onto the tree may help prevent the person from communications is more than 30 minutes away, all should remain
being carried, but the force of an avalanche usually carries the on-site for the search and rescue. If the accident occurs in or
person. As such, skiing in an area with trees should not be used near a ski area and there are several companions, one person
MOUNTAIN MEDICINE
as a prevention strategy. Trying to outrun an avalanche by can be assigned to leave the scene and immediately notify the
turning the skis or the snow machine downhill is impractical and ski patrol.
dangerous; an avalanche invariably overtakes its victims.
If caught, a victim should shout “Avalanche!” to alert compan- Marking the Last-Seen Area
ions, then close the mouth and breathe through the nose to A companion or eyewitness to an accident needs to act quickly
prevent inhaling a mouthful of snow. If the individual is wearing and positively. Rescuer actions over the next several minutes may
an AvaLung, the mouthpiece should be quickly placed in the mean the difference between life and death for the victim. Com-
mouth, which also helps to prevent oropharyngeal snow impac- panions must assess the terrain to ensure that they and other
tion. If the person is wearing an ABS, the ripcord should be rescuers are safe from secondary slides. The bed surface of an
pulled and the airbag activated. avalanche that has recently run is usually safe to enter. Occasion-
ally, however, an avalanche fracture line has broken at midslope,
Actions during the Slide which leaves a large mass of snow, sometimes called “hang fire,”
PART 1
For years, it was taught to “swim to the surface” (i.e., struggling still positioned above the fracture that could avalanche onto the
with the arms and legs flailing) if caught in an avalanche. The rescuers.
idea is that the victim may be able to climb to the surface as First, the victim’s last-seen area should be fixed and marked
well as increase the apparent surface area. The efficacy of these with a piece of equipment or clothing, tree branch, or any item
actions has been questioned. The process of granular convection that can be seen from a distance downslope. If the victim was
(see Avalanche Airbag, earlier) rather than swimming may be seen riding the avalanche before the last-seen area, a line of
more important in keeping the victim on or near the surface. trajectory can be visualized that could narrow down likely areas
Nevertheless, many survivors claim that “swimming” kept them of burial. Persons equipped with transceivers should travel to the
on or close to the surface. If the victim sees or feels an object, last-seen area to begin their search (see Probing after Transceiver
such as a tree or rock band, the person should make every Search, later). Victims who are fully buried without transceivers
attempt to grab and hang on, allowing some of the avalanche likely face an unsurvivable situation.
forces to bypass.
Skiers should try to discard their skis and poles. With any
luck, the avalanche will strip away the skis. Backpacks should
INITIATE SEARCH AND SCAN FOR CLUES
be kept, if possible, because they make the victim a slightly larger All companions must immediately switch their units to receive
particle for granular convection and increase the likelihood that mode. At the same time as initiating this transceiver search, the
the person will be closer to the surface. Packs might offer some fall line (i.e., the line of trajectory) should be quickly scanned
protection to the thoracic spine. If the victim ends up on the below the last-seen area in the flow line for any clues of the
surface, the equipment will be useful. However, the equipment’s victim. A glove, ski pole, or other object could lead rescuers
fate will usually be decided by the avalanche. Packs slide off directly to the victim. If an obvious clue is seen, shallow probing
easily when a person is turned upside down, even with tight should be done into likely burial spots with an avalanche probe
straps. Snowmobile riders should try to stay on their machine. (i.e., spot probing). All backcountry users should carry a proper
Once separated from the machine, avalanche victims are twice avalanche probe. A ski, ski pole, or tree limb could be used to
as likely to be buried than if they had stayed with the machine. search if necessary or in a ski resort, where probes may not be
Visual clues are the quickest method to find a buried ava- carried. Likely spots are the uphill and downhill sides of trees
lanche victim. If the victim senses that he is close to the surface, and rocks and benches or bends in the slope where snow ava-
he should thrust a hand or a foot toward that direction. Any lanche debris piles up. The toe of the debris should be searched
visual clue on the surface will give rescuers a possible indication thoroughly because many victims are found in this area.
of location and greatly improve odds of survival.
Creating an air pocket is a key to survival. Without an air Rescue Transceivers
pocket, the time to asphyxiation is much more rapid. If the victim While making the quick visual search for clues, companions
is not close to the surface or the position is unknown, the person should search the debris using their transceivers, as described in
should place one or both hands in front of the face to create a Box 4-1 and Figure 4-18. When a signal is detected, companions
space, or air pocket, when the avalanche is slowing. This action must narrow the search area quickly. If they are skilled with a
should be performed early because the avalanche may stop transceiver, companions can pinpoint the burial site in a few
abruptly, at which time no movement will be possible. minutes and should confirm the location with a probe.
58
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
90° 10″ 10″ surface with space to work on the victim, because the air pocket
is not compromised and raising the victim is not necessary.
25 CM 25 CM 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
FIGURE 4-25 Concentric probing method. Probing should proceed motions to clear out snow through the center of the V to create
from inward to outward in concentric circles spaced 25 cm (10 inches) a platform. When nearing the buried victim, an additional shov-
apart. 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
Probing after Transceiver Search chest and use their hands to clear a space for the airway.
When the victim’s location has been pinpointed, probing should Avalanche rescue courses should teach efficient shoveling
begin. The probe should be placed perpendicular to the slope techniques, and the method should be practiced as often as
at the location of the highest transceiver signal and pushed transceiver searches to reduce the total time to extrication.
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 Calling for Professional Resources
removed and probing continued in a spiral or concentric-circle A cell phone or other communication method should have
pattern until the victim is contacted (Figure 4-25). When the already been used to alert outside agencies. If communication
victim is located by a probe strike, the probe should be left in could not be made, on-site rescuers often face a difficult question
place and shoveling should begin. of when to leave the scene to summon outside help. If only one
or two companions are present, the correct choice is more dif-
Shoveling Techniques ficult. The best advice is to search the surface quickly but thor-
Shoveling will, unfortunately, take much longer than the trans- oughly for clues before anyone leaves to notify the patrol or
ceiver search. Depending on the number of rescuers and tech- obtain outside assistance.
nique used, this aspect of the rescue could be the difference If the avalanche occurs in the backcountry far from any pro-
between life and death. Efficient shoveling techniques can make fessional rescue team (organized rescue), all companions should
this process much quicker, increasing the chances of survival. remain at the site. The guiding principle in backcountry rescues
Strategic Shoveling. During companion rescue, only one is that companions search until they cannot or should not con-
to three shovelers might be available. The strategic shoveling tinue. When deciding when to stop searching, safety of compan-
technique14 increases digging efficiency (Figure 4-26). With the ions must be weighed against the decreasing survival chances of
probe left in place, shovelers begin digging downslope about 1 1 2 the buried victim. If a small team (companions) rescues a team
times the burial depth, as determined by markings on the probe. member who has been determined to be dead, the team should
Stand away from the probe, and do not stand above the buried attempt to stay on scene until a professional (organized) rescue
victim, if at all possible. Quickly dig a waist-deep starter hole team arrives or other appropriate arrangements are made. This
about one wingspan wide (i.e., the distance between the finger- allows professional rescue teams and medical examiners to assess
tips when the arms are held out to the sides). If two shovelers the situation and assist in evacuation.
are digging, they should work in tandem and side by side rather
than one digging behind the other. Throw the snow to the sides. PROFESSIONAL RESCUE
Move to the starter hole, and continue digging downward and
forward. As depth increases, snow can be cleared to the back Incident Command System
rather than lifted and tossed to the sides. 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
Snow shoveled to side and rescue operations have four key functional components,
which are often being organized and managed simultaneously.
Burial One component is search, the goal of which is quickly finding
depth 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
1.5 x burial depth system (described later), and basic first-aid equipment. The
immediate search team performs the initial search and looks for
FIGURE 4-26 Strategic shoveling technique for one or two rescuers. clues with the hope of making a quick find. If they have no
(Courtesy Dale Atkins and National Ski Patrol, Lakewood, Colo.) 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 Organized Probing Search Techniques
the accident site, or the reporting person should be returned to Organized probing is a simple but slow method of searching for
the same vantage point from which the accident was witnessed buried victims. For more than 40 years, the traditional probe line
to best guide rescuers to locate last-seen areas. Arriving rescuers (closed course probing) used by rescue teams was composed of
will meet the site leader and continue the immediate search until about a dozen rescuers standing elbow to elbow with a probe
sufficient clues can steer rescuers to positioning probe lines. pole that was 3 to 3.5 m (10 to 12 feet) long. The rescuers probe
The second component is emergency care to provide medical once between their feet, with each probe entering the snow
care for victims who are found. One or two small teams are about 75 cm (30 inches) from the neighbors on either side; the
dispatched with resuscitation, medical, and simple evacuation line then advances 70 cm (28 inches), and the rescuers probe
equipment. Ideally, the medical team should be sent within again. Open course probing involves the rescuers being an arm’s
minutes of fielding the first search teams to ensure that necessary length apart and probing twice (once in front of each foot) before
medical and evacuation equipment reach the site in a timely stepping forward. The probability of detection with these methods
manner. was thought to be about 70%. If the probe line missed the victim
The third component is transportation, which includes travel on the first pass, which tended to happen, the area was probed
for additional rescuers to and from the accident site and for again and again. Behind the probe line, shovelers stood ready
evacuation of victims. The transportation effort must begin im- to check out any possible strike. The line did not stop in such
mediately so that rescuers and equipment can be moved effi- an event but continued to march forward with a methodic “probe
ciently and quickly. Likewise, coordination of helicopters, snow down, probe up, step forward” cadence.
machines, and rescuers is essential to a fast and safe evacuation. The optimal combination of probe-grid spacing and search
The fourth component is support, which sustains the entire time, as determined by computer analysis, is a grid spacing of
operation, especially when a rescue is prolonged. This support 50 cm by 50 cm (20 inches by 20 inches).2 This probe-grid
may include additional rescuers (to take over for cold and tired spacing yields the best combination of probability of detection
searchers), hot food and drinks, tents, warm clothing, and lights and fast search time. For a three-holes-per-step probe, probers
for nighttime searching. stand with their arms out, wrist to wrist. Probers first probe
60
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
50 cm probe lines are time intensive, few victims are found alive using
this technique alone (see Rescue Statistics, later).
50 cm 50 cm
Avalanche Rescue Dogs
Trained search dogs, which are traditionally used in Europe early
FIGURE 4-28 Three-probe spacing for 50-cm by 50-cm, three-hole- during avalanche rescues, are capable of locating buried victims
per-step probe method. 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
between their feet, then probe 50 cm (20 inches) to the right and their owners in the backcountry. Burial depths of avalanche
50 cm (20 inches) to the left (Figure 4-28). At a command from victims found alive ranged from 0.3 to 1.5 m (1 to 5 feet); burial
the leader, the line advances 50 cm (20 inches; i.e., one step). depths of victims killed ranged up to 4.5 m (15 feet).1
This method gives an 88% chance of finding the victim on the The number of trained certified search dogs has increased
first pass, with an estimated time to discovery almost identical to substantially. Search and rescue teams and law-enforcement
that of traditional spacing. Ski patrols and mountain rescue teams agencies work closely with search-dog handlers, and trained
who have adopted the three-holes-per-step style of probe with avalanche dogs are now common fixtures at ski areas in the
a 50-cm by 50-cm (20-inch by 20-inch) grid have noted improved western United States. A trained avalanche dog moving rapidly
efficiency and effectiveness of the probe line. over avalanche debris and using its sensitive nose to scan for
Because these rescuers insert more probes per rescuer, fewer human scent (i.e., rafts or shed dead skin cells) diffusing up
rescuers can be used on a probe line. Short probe lines are easier through the snowpack can search more effectively in 30 minutes
to manage and work faster than long probe lines. Five rescuers than can 20 searchers in 4 hours with the use of course probing.
doing three holes per step at 50-cm intervals form a slightly Dogs are not infallible, and their ability to find buried human
longer probe line than nine rescuers using the traditional method. scent may be affected by several factors, such as the length of
To ensure proper spacing, it is most helpful to use a guidon cord burial, weather, snow density, and contamination of the debris
with marked 50-cm intervals. Suspended between two rescuers, field with spit, urine, cigarettes, or gasoline from snowmobiles
the lightweight guidon cord positions rescuers and probes at the or generators. Dogs have found bodies buried 10 m (33 feet)
correct spots, thereby allowing the line to move smoothly and deep, but have also passed over persons buried only 2 m (6.6
efficiently without interruption. When a guidon cord is not used, feet) deep. Dogs find “scent” and not people, although some-
the probe line must be frequently stopped and reassessed to times they find both. On numerous occasions, dogs signaled an
ensure proper spacing. If the victim is missed on the first pass, alert in the vicinity, which may extend out as far as 9 to 12 m
the second pass increases the probability of detection to 99%. (30 to 40 feet) from a buried victim. These scent clues then led
The third effective organized probe search is called the slalom to searchers finding victims with other technologies.
probing technique (Figure 4-29).17 In this method, organized
rescuers probe three areas in a left-to-right pattern after two RECCO
lateral steps, then step forward, and then probe three areas in a The electronic rescue system called RECCO (www.recco.com)
right-to-left pattern. This pattern is repeated for the debris field enables organized rescue teams to find victims who are equipped
that must be searched. The main advantage of the slalom probing with reflectors (Figure 4-30). The system consists of two parts: a
method is that all probing is performed directly in front of the detector used by the rescue team (either on the ground or from
rescuers, which has been determined to be stronger and more helicopters) and a reflector worn by the recreationist. About the
efficient than probing to the side, as required in the three-hole- size and weight of a notebook computer, the detector is easily
per-step technique. Also, forward steps are more time-consuming transported to the accident site. The detector transmits a direc-
and variable in distance than lateral steps. The main disadvantage tional radar signal. When it hits the reflector, the signal’s fre-
is that it is surprisingly difficult to train novices to perform the quency is doubled and reflected back to the detector, and the
slalom probing technique well. 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
50 cm 50 cm diminished range), such as cell phones, electronic cameras,
radios, and even turned-off avalanche rescue beacons, so RECCO
50 cm 50 cm
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
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 deaths are caused by trauma, especially to the head and neck.
make the avalanche victim easier to locate, available rescue Second, snow burial causes asphyxiation in at least three quarters
equipment, and competence of the rescuers. Body position, of avalanche deaths from either airway obstruction or hypercap-
traumatic injury, snow density, and presence and size of an air nia and hypoxemia as a result of rebreathing expired air. A very
pocket influence risk of asphyxiation. small percentage of avalanche victims succumb to hypothermia
A victim who is uninjured and able to fight on the downhill (see Avalanche Victim Physiology and Medical Treatment after
ride usually has a better chance of being only partly buried, or Rescue, later).
if completely buried, a better chance of creating an air pocket A victim who is swept down in the churning maelstrom of
for breathing. A victim who is severely injured or rendered snow has difficulty breathing. Inhaled snow clogs the mouth and
unconscious will more likely be rolled, flipped, and twisted nose; if the victim is buried with the airway already blocked,
during the slide. Being trapped in an avalanche is a life-and-death asphyxiation will occur more quickly. Snow that was light and
struggle. airy when a skier carved turns becomes viselike in its new form.
Avalanches kill in two ways. First, traumatic injury may occur Where the snow initially might have been 80% air, it might be
as the victim tumbles down the avalanche path. Trees, rocks, less than 50% air after an avalanche and is much less permeable
cliffs, and the wrenching action of snow in motion can produce to airflow, thereby making it more difficult for the victim to
blunt or penetrating trauma. Up to one quarter of all avalanche breathe.
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
RESCUE STATISTICS
100
A buried victim’s chance of survival directly relates not only to
Survival probability (%) Swiss data 1981 to 1998 (N = 638)4 the depth and length of time of burial, but also to the type of
80 Swiss data 1981 to 1991 (N = 422)9 rescue. Table 4-2 shows the statistics for survival as a function
of the rescuer. Buried victims rescued by a small team (compan-
60 ions or groups nearby) have a much better chance of survival
than those who are rescued by professional (organized) teams.
40 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,
20 and 13% were found by a professional rescue team.
Table 4-3 compares the results of rescue by different tech-
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 or an attached object (e.g., ski tip) protruding from the snow,
51% were found alive. In most cases, this was simply good luck,
Time buried under avalanche (min)
but in some cases, it was the result of actively fighting with the
FIGURE 4-34 The solid blue line indicates data from Switzerland for avalanche or of thrusting a hand upward when the avalanche
survival probability for completely buried avalanche victims in open stopped. Either way, this statistic shows the advantages of a
areas from 1981 to 1998 (n = 638) in relation to time (minutes) buried shallow burial: less time required to search, shorter digging time,
under the snow. The median extrication time was 37 minutes. The and the possibility of attached objects or body parts being visible
dashed red line represents survival probability for completely buried on top of the debris. Of the fatalities in this category, many of
avalanche victims in open areas (n = 422) on the basis of the Swiss data the individuals were skiing or snowboarding alone with no com-
for 1981 to 1991. (Data from Falk M, Brugger H, Adler-Kastner L: panion present to identify the hand or ski tip and provide rescue.
Avalanche survival chances, Nature 386:21, 1994. From Brugger H, Organized probe lines have found more victims than any other
Durrer B, Adler-Kastner L, et al: Field management of avalanche method, but because of the time required, most victims (93%)
victims, Resuscitation 51:7, 2001, with permission.) are recovered after they are dead.
MOUNTAIN MEDICINE
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.)
65
TABLE 4-5 Pattern of Injury among 105
10% and the FICO2 increased to about 6% (Figure 4-36). These
changes in O2 and CO2 levels in the air pocket resulted in
Avalanche Victims decreased arterial O2 saturation as measured by pulse oximeter
and increased end-tidal partial pressure of CO2. Most participants
Trauma Frequency (n)
were not able to complete the entire 30 minutes of the study and
had to stop as a result of dyspnea, hypercapnia, and hypoxia,
Cerebral trauma 2
but some reached an equilibrium where FIO2 and FICO2 stabilized
Chest trauma: all 18 and hypoxemia and hypercapnia were tolerable. These few indi-
Chest trauma: sternum or rib fracture (n = 16) viduals lasted the full 30 minutes of the research protocol, dem-
Chest trauma: pneumothorax or hemothorax onstrating how breathing with an air pocket can prolong survival
(n = 6) during avalanche burial.
Spinal fracture: all 7 Hypoxemia and hypercapnia occur as expired air is rebreathed.
Spinal fracture: cervical (n = 3) A smaller air pocket or lower-porosity snow (usually higher
Spinal fracture: thoracic (n = 1) density) causes more rapid development of hypoxia and hyper-
Spinal fracture: lumbar (n = 3) capnia. Larger air pockets and higher-porosity snow (usually
Abdominal trauma 1 lower density) allow for more mixing of expired air with ambient
Pelvic fracture 1 air within the air-filled pore spaces between grains of snow in
Extremity trauma: all 20 the snowpack. This results in longer survival times before hypoxia
Extremity trauma: lower-leg fracture (n = 8) and hypercapnia become severe enough to cause death from
Extremity trauma: shoulder dislocation (n = 6) asphyxiation. Porosity of snow, which is a dimensionless value,
Extremity trauma: femoral fracture (n = 4) 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
From Hohlrieder M, Brugger H, Schubert HM, et al: Pattern and severity of through snow, and roughly correlates to snow density (i.e., the
injury in avalanche victims, High Alt Med Biol 8:56, 2007. mass per unit volume, typically kg/m3; see Physical Properties,
earlier). Higher-density snow generally, but not always, has lower
MOUNTAIN MEDICINE
FIO2 (%)
lization during the rescue and resuscitation period. Avalanche 80
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 15
vulnerable to enormous forces, and these areas appear to be the A
PART 1
RESPIRATORY PHYSIOLOGY OF
AVALANCHE BURIAL 8
Asphyxiation occurs during avalanche burial because inhaled
ETCO2 (kPa)
FICO2 (%)
Rebreathing expired air in an enclosed space results in progres-
sive hypoxia and hypercapnia that eventually causes death from 5
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 0 0
thus survival time is longer before death occurs from asphyxia- 0 5 10 15 20 25 30
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. Time (min)
Because this barrier is impermeable to air, it accelerates asphyxi-
ation by preventing diffusion of expired air away from the air FIGURE 4-36 Curves of individual respiratory parameters in persons
breathing with a tight-fitting face mask connected to respiratory tubing
pocket in front of the mouth.
running into 1- or 2-L air pockets in dense snow (n = 28). The x-axis
The physiology of asphyxiation from breathing with an air represents time in minutes. Some participants did not complete the
pocket in the snow was demonstrated in a study where partici- 30-minute study because of dyspnea or hypoxia. A, Arterial oxygen
pants sat outside a snow mound and breathed through an air- saturation (SpO2 [%]) as measured by a digital pulse oximeter on the
tight mask connected by respiratory tubing to 1- or 2-L (0.9- or left y-axis (red lines) and fraction of inspired oxygen (FIO2 [%]) on the
1.8-quart) air pockets in the snow.12 The snow had a density right y-axis (blue lines). B, Partial pressure of end-tidal carbon dioxide
similar to that of avalanche debris (i.e., 150 to 600 kg/m3 or 15% (ETCO2 [kPa]) on the left y-axis (red lines) and fraction of inspired carbon
to 60% water). The initial fraction of inspired oxygen (FIO2) in dioxide (FICO2 [%]) on the right y-axis (blue lines). (From Brugger H,
the air pocket was 21%, and the initial fraction of inspired carbon Sumann G, Meister R, et al: Hypoxia and hypercapnia during respira-
dioxide (FICO2) was near 0%. As expired air was rebreathed in tion into an artificial air pocket in snow: Implications for avalanche
the air pocket over about 30 minutes, the FIO2 decreased to about survival, Resuscitation 58:81, 2003, with permission.)
66
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 without the device but with a 500-cc (0.45-quart) air pocket in
is very difficult to measure but density is frequently measured in the snow. Mean burial time was 58 minutes when breathing with
the field, the avalanche literature refers to snow density as a the AvaLung and 10 minutes when breathing with a 500-cc air
surrogate value in relation to asphyxiation during avalanche pocket in the snow. Development of hypoxia and hypercapnia
burial.12,20,23 An equilibrium occurs when expired air diffuses out was significantly delayed by breathing with the AvaLung (Figure
of the air pocket and is replaced by fresh air that diffuses in from 4-37). The AvaLung has resulted in survival during actual ava-
the snowpack, depending largely on snow porosity. This results lanche burials.13,34
in FIO2 and FICO2 reaching plateaus within a physiologically toler-
able range, prolonging survival of the avalanche victim. This may MEDICAL TREATMENT AND RESUSCITATION OF
occur even with small air pockets, which has been observed
when extricating avalanche burial survivors of up to 2 hours’
AVALANCHE BURIAL VICTIMS
duration (likely in highly porous snow).8 A published algorithm is available from the International Com-
Even densely packed snow contains sufficient ambient air to mission for Mountain Emergency Medicine (ICAR MEDCOM) for
permit normal oxygenation and ventilation as long as all expired resuscitation of avalanche burial victims.6,9 We recommend an
air is diverted out of the snowpack. This was demonstrated in a algorithm for evaluating an extricated avalanche burial victim that
study of persons who were totally buried in dense snow and incorporates key decision points from the ICAR MEDCOM algo-
who inhaled air directly from the snowpack (density, 300 to rithm for treatment and triage of avalanche victims in cardiac
680 kg/m3 or 30% to 68% water) through a two-way nonrebreath- arrest. However, our algorithm also incorporates recommenda-
ing valve attached to respiratory tubing that diverted all expired tions from the Wilderness Medical Society Practice Guidelines for
air to the snow surface. Participants maintained normal oxygen- the Out-of-Hospital Evaluation and Treatment of Accidental
ation and ventilation for up to 90 minutes.35 This study demon- Hypothermia.44
strated that there is sufficient air for breathing in snow with a Figure 4-38 presents the key points regarding assessment and
density similar to that of avalanche debris as long as expired air treatment of an extricated avalanche burial victim. An initial
is not rebreathed. This is the principle behind the AvaLung (see impression of the level of consciousness is made as the head is
earlier), which has been designed to prolong survival during exposed and cleared of snow. Opening the airway and ensuring
avalanche burial (see Figure 4-23). Although the device prevents adequate breathing are the primary medical interventions. Every
formation of an ice mask, the expired air permeates around the effort should be made to clear the airway of snow as soon as
buried person’s body and through the snow, and it eventually possible and to provide assisted ventilation if breathing is absent
contaminates inspired air. The AvaLung has been well studied or ineffective. These measures should be instituted as soon as
using a human model of burial in snow of similar density to possible and should not be delayed until the entire body is
avalanche debris.18-21 In the initial study,20 breathing with the extricated. If traumatic injury to the spinal column is suspected,
AvaLung while buried in dense snow was compared to breathing or if there is evidence of head or facial trauma, the spinal column
67
Extrication from avalanche burial 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
Normal Yes because of space limitations with the opening of the snow
mental status? leading to the victim. If endotracheal intubation is required for
the unconscious apneic patient who is not yet fully extricated
Treat for Hypothermia I (core temperature >32°C):
from snow burial, the inverse intubation technique may be
No Provide dry warm insulation, hot drink containing sugar,
required.36 With this technique, the laryngoscope is held in the
right hand while straddling the victim’s body and facing the head
medical transport to closest appropriate facility.
and face. While facing the victim, insert the laryngoscope blade
Yes into the oropharynx with the right hand so that the larynx and
Conscious? cords can be visualized by leaning over and looking into the
victim’s mouth. The endotracheal tube is then passed through
Treat for Hypothermia I (core temperature >32°C) or the vocal cords with the left hand.
No Hypothermia II (28 to 32°C): Clear the airway, provide After an adequate airway and breathing are established and
oxygen, dry warm insulation, medical transport to supplemental oxygen is provided, circulation is assessed. The
closest appropriate facility. conscious patient is assumed to have a perfusing rhythm, and
further treatment is directed at treating hypothermia and trau-
Yes matic injuries. A patient who is found unconscious but with a
Breathing?
pulse may have moderate or severe hypothermia and should be
Treat for Hypothermia II (core temperature 28 to 32°C) handled gently to avoid precipitating ventricular fibrillation (VF).
or Hypothermia III (24 to 28°C): Clear the airway, The medical treatment of this patient is focused on (1) ensuring
provide oxygen, assist ventilations, consider intubation adequate oxygenation and ventilation, either noninvasively with
No and ventilation with heated and humidified oxygen, a bag-valve-mask device or with a supraglottic airway device or
dry warm insulation, heated IV fluid. Package and endotracheal tube, as clinically indicated, and (2) immobilizing
transport with spinal column immobilization. Transport the spinal column for transport and treating any obvious signs
MOUNTAIN MEDICINE
68
An air pocket for breathing and a patent airway must be
CHAPTER 4 Avalanches
BOX 4-2 Hypothermia Clinical Prehospital Evaluation:
present for an avalanche burial victim to survive long enough to
develop severe hypothermia. If an air pocket for breathing is not Swiss Society of Mountain Medicine Definitions
present or if the airway is obstructed, the avalanche victim who
Hypothermia I: Patient alert and shivering (core temperature
is extricated from snow burial in cardiac arrest has most likely ≈35°-32° C [95°-90° F])
died from trauma or asphyxiation. This is not meant to discour- Hypothermia II: Patient drowsy and not shivering (core
age initial attempts at resuscitation, but rather to suggest that temperature ≈32°-28° C [90°-82° F])
prolonged CPR may be a futile exercise. It is always warranted Hypothermia III: Patient unconscious (core temperature ≈28°-24° C
initially to start CPR to see if return of circulation can be achieved [82°-75° F])
in a reasonable time. This is because the rescuer can never know Hypothermia IV: Patient not breathing (core temperature <24° C
when the avalanche burial victim went into cardiac arrest; it [75° F])
may have been minutes or hours before extrication. The case of
an 11-year-old boy in Utah who was extricated in cardiac arrest Data from Brugger H, Durrer B, Adler-Kastner L: On-site triage of avalanche
after 40 minutes of full burial demonstrates the importance of victims with asystole by the emergency doctor, Resuscitation 31:11, 1996;
Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche
immediately starting CPR. Return of circulation was achieved 5 victims, Resuscitation 51:7, 2001; and Zafren K, Giesbrecht GG, Danzl DF, et al:
minutes after the initiation of CPR, and the boy went on to full Wilderness Medical Society Practice Guidelines for the Out-of-Hospital
recovery. Evaluation and Treatment of Accidental Hypothermia, Wilderness Environ Med
When laboratory testing equipment is available, serum potas- 25(4 Suppl):S66-S85, 2014.
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 and wet clothing is removed as soon as is practical. If the patient
should be terminated. If the serum potassium is greater than is unconscious, moderate or severe hypothermia is suspected,
12 mmol/L in an adult or a child, resuscitation efforts should be and handling should be gentle to avoid precipitating VF. When
terminated.6 treatment of moderate or severe hypothermia is clinically indi-
cated, IV access is obtained, and warmed (42° C [107.6° F]) iso-
HYPOTHERMIA IN THE AVALANCHE tonic fluid is infused. If the patient is unconscious, endotracheal
intubation is appropriate to provide adequate oxygenation and
BURIAL VICTIM ventilation with heated (40° to 45° C [104° to 113° F]) humidified
In avalanche burial victims who are extricated alive, hypothermia oxygen. The goal of treating moderate to severe hypothermia
is a major medical problem that requires treatment.6,9 Box 4-2 before reaching the hospital is to limit temperature afterdrop
provides clinical definitions of hypothermia severity correlated during medical transport to the location where definitive rewarm-
with core body temperature. As the patient is extricated from ing can occur. The shivering patient with mild hypothermia can
snow burial, warm dry insulation is provided during packaging, 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 adequate diffusion of expired air away from inspired air and
sugar may be given by mouth. If possible, patients with mild prevented asphyxiation. In that same rescue, the survivor’s com-
hypothermia should remain supine until rewarming has occurred, panion was found dead from asphyxiation after 20 hours of burial
to prevent a greater temperature afterdrop from ambulation. with a tympanic core body temperature of 6° C (42.8° F), which
Optimally, the severity of hypothermia is determined by core is an average core body temperature cooling rate of about 1.5° C
body temperature measurement in the field, preferably with use (2.7° F) per hour.
of an esophageal probe, but tympanic membrane sensors or The highest reported rate of core body temperature cooling
rectal probes may also be used. If core body temperature cannot in an avalanche burial victim is 9° C per hour, which was reported
be measured in the field, the severity of hypothermia may be for a 29-year-old man who was buried for 100 minutes and
estimated with use of Swiss hypothermia stages I through IV, as extricated alive with an epitympanic core temperature of 22° C.31
determined by the clinical presentation (see Box 4-2).44 He was endotracheally intubated and ventilated, but went into
Severity of hypothermia may also be estimated from the time VF during helicopter transport and was transported with ongoing
that the victim was buried and the average rate of core tempera- CPR (except for 15 minutes during the initial helicopter evacua-
ture cooling during burial. In a controlled experiment of human tion from the scene to a local hospital). He was in cardiopulmo-
volunteers wearing a lightweight clothing insulation system, nary arrest for 150 minutes before defibrillation on the fifth
fully buried in compacted snow of similar density to avalanche attempt resulted in return of spontaneous circulation after extra-
debris, and breathing with an AvaLung for up to 60 minutes, corporeal rewarming. He made a full recovery.
core body temperature cooling rate was about 1.3° C (2.3° F) per These anecdotal reports demonstrate that core body tempera-
hour.21 ture cooling rates during avalanche burial may vary significantly,
Retrospective studies of core temperature on hospital arrival28 and that survival after long-duration avalanche burial with severe
suggest that the average core temperature cooling rate is 3° C hypothermia is possible. Survival of avalanche victims after
(5.4° F) per hour in survivors (range, 0.75° to 4.75° C [1.4° F to cardiac arrest, however, is possible when the arrest is witnessed
8.6° F]). The higher rate of cooling in this study is based on a after extrication and caused by severe hypothermia. Resuscitation
known time of burial and known arrival time at the hospital efforts should continue, and these victims should be transported
where core body temperature was recorded, and it does not dif- to centers capable of extracorporeal rewarming. Avalanche
ferentiate between core temperature cooling rate during snow victims extricated after unwitnessed cardiac arrest most likely
MOUNTAIN MEDICINE
burial and afterdrop cooling rate during medical transport. were asphyxiated, and resuscitation to a perfusing rhythm is very
Burial cooling rates are accelerated by hypercapnia. Cooling unlikely.29
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,
SUMMARY
total metabolic rate, and respiratory muscle metabolic rate were Asphyxiation is the major cause of death during avalanche burial
greater for the hypercapnic persons. Afterdrop cooling rate and is time dependent. Traumatic injuries can be immediately
increases transiently after extrication from snow burial.18,19 After- fatal or can shorten the time for asphyxiation to occur. Avalanche
drop cooling rate increased up to fourfold for a mean of 12 victims who have not succumbed to a traumatic fatality and who
minutes after extrication in those buried in snow breathing with are extricated within 15 minutes have a greater than 90% chance
an AvaLung for 60 minutes18 (Figure 4-39). Accelerated cooling of survival. However, this “survival phase” decreases to about
rate during and after extrication places avalanche victims at 30% if they are extricated after 30 minutes, thus emphasizing the
PART 1
greater risk for complications caused by hypothermia. Rescue need for small-team (companion) rescue with use of avalanche
personnel should make every effort to prevent further heat loss transceivers, probes, and shovels. Survival beyond 30 minutes of
in avalanche victims as soon as possible during extrication from burial depends on the presence of an air pocket for breathing.
the snow. The larger the size of the air pocket, the longer survival is pos-
Core temperature cooling rate during avalanche burial may sible during burial. Asphyxiation during avalanche burial is
also be estimated from anecdotal reports of prolonged survival caused by rebreathing expired air that contains 16% oxygen and
(Table 4-6). In one case, a 25-year-old male snowboarder with 5% carbon dioxide. A larger air pocket provides more surface
a large air pocket in front of his body survived 20 hours of ava- area for diffusion of expired air away from an avalanche burial
lanche burial.21 At extrication, he had a tympanic core body victim, allowing more ambient air from the snowpack to diffuse
temperature of 25.6° C (78.1° F) in snow at 5° C (23° F) and was into the air pocket for inspiration. Opening the airway, ensuring
spontaneously breathing; he had a Glasgow Coma Scale score adequate ventilation, and providing supplemental oxygen are the
of 8, heart rate of 35 beats/min, and a palpable pulse. Core body primary medical interventions for an extricated avalanche burial
temperature cooling rate in this anecdotal report was about 0.6° C victim. If the victim is conscious, mild hypothermia is most likely,
(1.1° F) per hour. The large air pocket probably allowed for and treatment consists of providing warm, dry insulation and
Locher and Walpoth28 16 survivors (3 cardiac arrest) of Retrospective review, avalanche 2.9° C/hr (range, 0.75°-4.75° C/hr),
(1996) avalanche burial burial victims burial to hospital arrival
Spiegel40 (2002) Case report, 25-yr-old male avalanche 20-hr avalanche burial with a large air 0.6° C/hr
victim pocket
Grissom et al21 (2004) 12 healthy participants with Simulated avalanche burial for up to 1.3° C/hr (range, 0.6°-2.4° C/hr)
lightweight clothing 60 min
Putzer et al33 (2010) Case report, 28-yr-old male avalanche 90-min avalanche burial; 25-min 5° C/hr, burial to hospital arrival
victim transport
Oberhammer et al31 Case report, 27-yr-old male 95-min avalanche burial; cardiac 9° C/hr tympanic membrane
(2008) arrest after extrication temperature, burial to extrication
Paal et al32 (2013) 8 piglets, anesthetized, intubated, Breathing into an air pocket or 4.6° C/hr with air pocket and
buried in a simulated avalanche ambient air 4.8° C/hr with ambient air
Boue et al5 (2014) Two case reports: first case, 17-yr-old First case, complete burial for 6 hr First case, 2.3° C/hr
male; second case, 41-yr-old male Second case, complete burial for 7 hr Second case, 1.8° C/hr
70
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
perfusing rhythm who subsequently have a witnessed cardiac REFERENCES
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Wyo. 25. Hohlrieder M, Brugger H, Schubert HM, et al. Pattern and severity of
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citation: A systematic review. Resuscitation 2010;81(6):645–52. cated in avalanche victims with unwitnessed hypothermic cardiore-
7. Boyd J, Haegeli P, Abu-Laban RB, et al. Patterns of death among spiratory arrest? High Alti Med Biol 2014;15(4):500–3.
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8. Brugger H, Durrer B, Adler-Kastner L, et al. Field management of lanche fatalities. Wilderness Environ Med 2007;18(4):293–7.
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9. Brugger H, Durrer B, Elsensohn F, et al. Resuscitation of avalanche avalanche victim with profound hypothermia and prolonged cardiac
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for Mountain Emergency Medicine (ICAR MEDCOM): Intended for 474–80.
physicians and other advanced life support personnel. Resuscitation 32. Paal P, Strapazzon G, Braun P, et al. Factors affecting survival from
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11. Brugger H, Falk M. Analysis of avalanche safety equipment for back- hour during avalanche burial. Resuscitation 2010;81(8):1043–4.
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12. Brugger H, Sumann G, Meister R, et al. Hypoxia and hypercapnia vival. Wilderness Environ Med 2002;13(2):143–52.
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17. Genswein M, Letang D, Jarry F, et al. Slalom probing—A survival 40. Spiegel RW. Rescuing an avalanche victim alive after 20 hours. Paper
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19. Grissom CK, McAlpine JC, Harmston CH, et al. Hypercapnia effect on 43. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: Cardiac arrest
core cooling and shivering threshold during snow burial. Aviat Space in special situations: 2010 American Heart Association Guidelines for
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20. Grissom CK, Radwin MI, Harmston CH, et al. Respiration during snow Circulation 2010;122(18 Suppl. 3):S829–61.
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71.e1
CHAPTER 5 Lightning-Related Injuries and Safety
CHAPTER 5
Lightning-Related Injuries and Safety
MARY ANN COOPER, CHRISTOPHER J. ANDREWS, RONALD L. HOLLE,
RYAN BLUMENTHAL, AND NORBERTO NAVARRETE ALDANA
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 5-4 Indra, the Hindu god of heaven, lightning, rain, storms,
and thunder.
FIGURE 5-2 Zeus, king of gods who hurls the lightning.
72
because of labor-intensive manual agriculture, mining, and other
73
resuming activity. Although the 30-30 rule is not used as often strike carries a mortality rate of 30% and morbidity rate of 70%.87
as previously, the concept of a rule for both the beginning and A slightly different interpretation of the same data yielded a
end of a thunderstorm is the basis for safety rules used at many mortality rate of 20%.33 Because peer-reviewed publications tend
large venues, such as airports, mines, sports stadiums, and indus- to reflect severe or interesting cases, case reviews likely overes-
trial sites. When objective lightning detection network data timate mortality rate.
provide accurate information on lightning times and locations for A prevalent myth is that the lightning victim retains an electri-
large venues, these data should be used instead of imprecise cal charge and is dangerous to touch because the person is still
colloquialisms.292,295 “electrified.” This myth may have led to unnecessary deaths by
In developed countries, lightning injuries may occasionally delayed resuscitation.89 A person does not retain a charge like a
occur indoors, but they are rarely, if ever, fatal. The causes are battery or a capacitor. However, a person in contact with a live
contact injury or side flashes from plumbing fixtures, computers, electrical power wire may transmit electricity.
hard-wired telephones or electronic devices, and other appli- A myth regarding treatment is that lightning injuries should
ances.11,125,126 With a hard-wired phone, persons may suffer acous- be treated as are other high-voltage electrical injuries. In devel-
tic damage, neurocognitive deficits, death, or other lightning-related oped countries, the injuries seen with lightning are very different
problems.32,277 These occur because the telephone system in most from high-voltage injuries and should be treated differently if
houses is not grounded to the house’s electrical system, but rather iatrogenic morbidity and mortality are to be avoided.23,88
acts as a conduit for lightning either to come into or to exit Although burns are commonly thought to be the major cause
from the home. Cell phones and cordless indoor phones offer of death, this is not the case. Less than one-half of lightning
complete protection from indoor electrical effects of light- survivors have any signs of burns or marks on their skin. The
ning.6,25,140,173,174,274,295 In developing countries where safe housing is “crispy critter” myth, where someone struck by lightning bursts
not available, a dozen or more people may be killed indoors into flames or is reduced to a pile of ashes, is science fiction,
during a single incident. 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
MEDICAL MYTHS AND MISCONCEPTIONS cause of immediate death is from cardiac arrest, sometimes fol-
A persistent myth is that lightning strikes are invariably fatal (Box lowing respiratory arrest.87 Persons who are stunned or lose
MOUNTAIN MEDICINE
5-1). In truth, mortality rate may be as low as 5% to 10%.67 One consciousness without cardiopulmonary arrest are highly unlikely
study of lightning cases occurring since 1900 found that lightning to die, although they may have serious long-term sequelae.90,97,281,320
BOX 5-1 The Most Common Myths and Facts about Lightning
• Burns are a major component of lightning injury.12,26,33,87 • No place outside is safe when thunderstorms are in the area.295
• Nothing is left of a person after a lightning strike except a pile of • It is better to be “proactive” rather than “reactive” with lightning
ashes.87,88 injury avoidance.295
• Lightning victims have “entry” and “exit” points.33,88 • The top activities and places for lightning casualties in the United
• Lightning victims have internal burns.88 States are all outdoors295:
• One can predict the degree of injury from the voltage, amperage, Near trees (or other tall object)
or polarity of the strike. Open fields and elevated locations
• Metal (on the body or not) attracts lightning. Water-related activities (e.g., swimming, boating, fishing)
• Lightning does not hit outside the rainstorm.295 • Safe shelter is a typical house or other fully enclosed and
• It is safe to wait until the rain arrives to evacuate.295 substantially constructed building with properly earthed plumbing
• It is safe to finish the game if lightning is nearby.190,295 and wiring.295
• As soon as the rainstorm passes and rain stops falling, it is safe to • Another safe shelter is a fully enclosed, solid, metal-topped
resume activity.190,295 vehicle, such as a car or bus.90,105,281,295,320
• If you can see blue sky, lightning danger is minimal. • Open picnic, bus, golf, and rain shelters, as well as tents and
• Lightning never strikes the same place twice. other camping cover, offer absolutely no protection from
• It is safe to seek shelter and dryness under a tree.295 lightning and may actually increase the risk for injury.229,292,295
• Tall objects provide a 45-degree “cone of protection.” • Having and following a lightning safety plan can decrease the
• The majority of persons injured are golfers.190,295 number of lightning deaths and injuries.295
• Lightning injuries cannot occur inside a building. • There is nothing that a person can do that will substantially decrease
• Rubber tires (shoes, raincoats, sitting on a backpack) protect a his or her lightning injury risk if “caught” in a thunderstorm.
person from lightning.295 • The lightning crouch does not significantly decrease the chance
• Cell phones, iPods, and other electronic devices attract of injury or death.295,342
lightning.6,25,140,173,174,274,295 • Sitting on a backpack or sleeping pad does nothing to decrease
• Golf, picnic, bus, rain, beach, and other shelters are safe.229,295 an injury.
• Grounding a building or shelter makes it safe for people from • Lying flat on the ground increases injury by increasing ground
lightning injury.229 current effect.104
• Grounding a building makes it safe from structural • The primary cause of death is cardiac and respiratory arrest at the
damage.229,292,325 time of the injury.87
• Lightning victims remain electrified and dangerous to touch. • Ninety percent of lightning victims survive, but often with
• Lightning victims are easier to resuscitate than other cardiac disability.90
arrest victims.372 • Lightning victims are safe to touch and do not retain an electrical
• If there are no outward signs of lightning injury, the damage charge.292,295
cannot be serious.89,90 • Automated external defibrillators (AEDs) have been useful in
• Lightning victims usually require treatments similar to those for some resuscitations.103,106,290
high-voltage electrical injuries, with aggressive fluid resuscitation, • Cell phones, iPods, and other small electronic devices do not
alkalinization, and fasciotomies.88,93 attract lightning.6,19,25,140,173,174,274,295
• Lightning survivors have few permanent problems.90,105,281,320 • Lightning can strike the same place more than once.
74
ropathy, chronic pain syndromes) and neuropsychological symp-
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 FIGURE 5-8 Simulated lightning in a high-voltage laboratory travels
be seeking safety inside a substantial building or fully enclosed across the external metal body of the car, escaping through the axle,
metal vehicle are outside and distracted from paying attention to hubcaps, or other metal closer to ground (arrow). The Faraday cage
the weather while they are talking or texting. 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.
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 itself a significant factor for the propensity to be struck. The
typical of high-voltage electrical injuries. primary factors that affect where lightning will strike follow:
• Wearing rubber-soled shoes is protective. False; similar errone- 1. Height of an object
ous concepts include wearing a raincoat or sitting on a foam 2. Isolation of an object from taller objects
PART 1
pad or backpack. These do not protect a person or reduce 3. Pointed object (not a factor for people)
the severity of the injury. • Lightning always hits the highest object. False; lightning is only
• The rubber tires on a vehicle protect a person. False; electrical affected by objects within approximately 30 to 50 m (98 to
energy travels along the outside of a metal conductor (the car 164 feet) from its leading tip. In addition, several pictures exist
body). It dissipates through the rainwater to the ground or of lightning striking halfway down a flagpole or in a parking
flashes off the axles or bumper of the car (Figure 5-8). Tires lot next to tall, isolated, and pointed light poles. Someone
may be torn or exploded. standing in the middle of a football field will not be protected
• Metal attracts lightning. False; wearing metal does not attract by the goalposts if lightning is coming down directly over-
lightning or increase one’s risk. Metal objects, such as fences head. There are many photographs of lightning branching to
and bleachers, conduct electricity and lightning after they meet the earth in several places. These images portray the
have been struck, but do not inherently attract lightning. Metal immense difficulty in being sure of the path of a cloud-to-
objects worn by a victim may become heated and thereby ground lightning event.
cause burn injuries. Tall objects tend to be made of metal, • Carrying an umbrella increases risk. False; compared with the
which are tall, isolated, and pointed. Their composition is not 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
FIGURE 5-7 Warning on the Great Wall of China. or remember the thunder, but it was there.
76
awareness campaign has been sustained across the United States
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 recent years that summarize lightning fatalities on national scales.
U.S. population data.347 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
GLOBAL LIGHTNING CASUALTIES AND LIGHTNING countries. In addition, it is not uncommon in developing coun-
No reliable complete global information exists regarding fatalities tries for multiple fatalities to occur in what would be considered
or injuries. Two recent global lightning fatality studies estimate an ‘indoor’ environment.
6000 fatalities and 24,000 fatalities per year.59,198 Underreporting Figures 5-12 through 5-17 summarize all published national
of lightning fatalities, and especially injuries, results from a studies of fatality rates, with low lightning fatality rates in yellow,
number of factors, including the situation that many events medium in orange, and red for highest. Fatality rates by decade
involve only one person and may not be reported or considered since the 1800s have been published,189 but no summary over
newsworthy.260 In past population studies, the practice has been recent years has been made. The most common shading is white,
PART 1
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
America, Western Europe, Japan, and Australia. This is probably Figure 5-18 shows Global Lightning Network (GLD360) strokes
because of the availability of more substantial housing, metal for 2011 to 2014.317,318,351 Unlike prior lightning detection net-
vehicles, lightning education, and lower lightning density in works, which did not provide good data over large bodies of
temperate zones. Regional, local, short-period,1 and Internet- water, GLD360 is a real-time network that seamlessly covers
based reports are not included. The most recent published results continents as well as oceans to show lightning on monthly,
include the following: regional, and annual scales. Because 80% of GLD360 lightning
• Africa: South Africa,47 Malawi,282 Swaziland,128 Uganda,5 and events are cloud-to-ground strokes, the actual lightning threat
Zimbabwe81,376 is now much better known around the globe. Land areas
• Asia: China,262,398 India,207 Japan,224a Malaysia,2 and clearly comprise most of the lightning threat to people and
Singapore306 infrastructure.
• Australia84 Lightning is not uniformly distributed. Some locations on land,
• Europe: Austria,231 France,159 Greece,311 Lithuania,149 Poland,256 especially along the slopes of tall mountains and along tropical
Turkey,371 and United Kingdom (including Ireland and coastlines, have much more lightning at certain times of day and
Wales)133,134 year than do others. This knowledge can be useful to improve
• North America: United States,114,200,259 Canada,275 and Mexico322 understanding of lightning threat. Studies have been made in a
• South America: Brazil59 and Colombia288 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.
Timor Leste
Solomon 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
Australia • 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
FIGURE 5-14 Lightning fatality rate per million people per year in may be increasing, which will continue until more people have
Australia. Yellow shading indicates rate <0.5 fatalities/million/yr. White ready access to safe dwellings, structures, and vehicles and spend
indicates no national summaries have been published for data sets less time in labor-intensive agriculture and other outdoor occupa-
ending in 1979 or later. tions. The lightning fatality and injury rates per population are
79
Faroe Is.
Sweden
Estonia
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
El Salvador
Costa Rica
Panama Aruba Barbados
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
CHAPTER 5 Lightning-Related Injuries and Safety
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 “negative.” He went on to prove that lightning is an electrical
published national fatality data shown in Figures 5-12 through phenomenon and that thunderclouds are electrically charged, as
5-17. For example, India is documented to have an average of demonstrated by the famous kite and key experiment.147 Because
1755 deaths per year from 1967 to 2012,207 which represents of the damage he saw to buildings, he invented the lightning rod
78,975 fatalities during this period. 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
CONCLUSIONS them the Means of securing their Habitation and other Buildings from
Mischief by Thunder and Lightning. The Method is this: Provide a small
The impacts of lightning vary greatly between developed and Iron Rod (It may be made of the Rod-iron used by the Nailers) but of
less developed countries. In the United States the population- such a Length, that one End being three or four Feet in the moist Ground,
weighted rate of lightning fatalities and injuries has greatly the other may be six or eight Feet above the highest Part of the Building.
decreased from a maximum approximately a century ago. The To the upper End of the Rod fasten a Foot of brass Wire the Size of a
two priorities in less developed countries to achieve a decrease common Knitting-needle, sharpened to a fine Point; the Rod may be
in lightning deaths and injuries are protecting people working in secured to the House by a few small Staples. If the House or Barn be
labor-intensive agriculture and providing lightning-safe dwell- long, there may be a Rod and Point at each End, and a middling Wire
ings, buildings, and vehicles. Data from global lightning detection along the Ridge from one to the other. A House thus furnished will not
networks can help identify areas with the highest density of be damaged by Lightning, it being attracted to the Points, and passing
lightning. Through a combination of sound science, education, thro the Metal into the Ground without hurting any Thing. Vessels also,
and uniform global lightning data, advances can be made to having a sharp pointed rod fix’d on the Tops of their Masts, with a Wire
reduce the impacts of lightning on people and assets. To achieve from the Foot of the Rod reaching down, round one of the Shrouds, to
improvements, the infrastructure of these countries likely must the Water, will not be hurt by Lightning.
be significantly improved, accompanied by inexpensive lightning
protection systems that can be easily installed and maintained. In the 1750s and 1760s, use of lightning rods became preva-
Initial activities have been taken with regard to education and lent in the United States for protection of buildings and ships.
awareness of lightning threat in several Asian countries through Some scientists in Europe urged installation of lightning rods on
the Centre of Excellence on Lightning Protection (CELP)96,156,157,212 government buildings, churches, and other tall buildings. Reli-
and are beginning in Africa by the newly formed African Centres gious advocates at the time, unfortunately, maintained that it
for Lightning Electromagnetics (ACLE). 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
EARLY SCIENTIFIC STUDIES AND significant destruction and loss of life when the buildings were
struck by lightning.
INVENTION OF THE LIGHTNING ROD Part of the delay in installing lightning rods in England has
The study of electrical phenomena is often traced to publication been attributed to distrust of scientific theories originating in the
of Gilbert’s De Magnete in London in 1600. Experiments in France upstart, newly independent United States. Years and numerous
and Germany and by members of the Royal Society of London unsuccessful trials with English designs were required before the
led to invention of the Leyden jar in 1745. Franklin rod became accepted on Her Majesty’s ships and
Benjamin Franklin is generally regarded as the father of elec- buildings.58
tric science and during his lifetime was known as the American At one time (and still believed by some laymen today), light-
Newton. He was accepted into the French and English courts ning rods were theorized to diffuse electrical charge, neutralizing
around the time of the American Revolution not because he was storm clouds and averting lightning. This may have been an
an ambassador from America but because he was considered one outgrowth of the observation of St Elmo’s fire, an aura appearing
of the foremost scientists of his time. Franklin was elected to around the tip of lightning rods, noses of aircraft, and ships’
every major scientific society at the time and received medals of masts during a thunderstorm, caused by an electron discharge
honor from France and England for his scientific contribu- that results from the strong electromagnetic field induced around
tions.83,325 Before his work, it was thought that two distinct types the glowing object. Properly installed lightning rods and lightning
of electrical phenomena existed. Franklin’s work148 unified these protection systems neither “diffuse” nor “attract” lightning, but
two aspects and is responsible for renaming them “positive” and 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 despite high exposure to lightning, may not be worth the
extensive damage (Figures 5-19 to 5-21). expense, such as for a mountain cabin that is seldom visited.228,295
The first Lightning Rod Conference was held in London in At present, the most important economic impacts from light-
1882. Recommendations from this conference were published ning include electrical utility interruption; interruptions at airports
that year and again in 1905. Several countries developed codes and other outdoor locations; loss or corruption of financial,
of practice for lightning protection (Germany, 1924; United States, security, and other databases and control systems; and downtime
1929; Britain, 1943; British colonies, 1965).115 In the past decade, of industrial equipment. For humans, the impact of being struck
NFPA 780 (U.S. National Fire Protection Act) has been accepted by lightning includes loss of work ability, unemployment, rela-
worldwide as a reliable standard.291 tionship decay, depression, anxiety, and loss of cognition, and
Building codes and industrial standards may require particular this is of economic importance as well. Lightning may pose sig-
structures to have lightning protection systems.52,291 Including a nificant danger not only to individuals, but also to larger groups,
system in the initial design and construction is always easier such as when hundreds of miners are trapped deep underground
PART 1
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-
High-altitude winds
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
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 ground flash is caused by the return strokes, which average three
barely discernible with the unassisted eye. Very-high-speed video to four per flash. Cloud-to-ground flashes contact the surface of
has shown this bright tip and a more faint trailing leader as it the earth at one or more locations, because one of the subse-
travels to the ground.349,353 The leader travels at about one-third quent return strokes often takes a different path to the surface,
the speed of light (1 × 108 m/sec), and the potential difference up to a few kilometers from the first return stroke; the average
between the leader’s lower tip and the earth ranges from 10 to is 1.47 ground contact points per flash.367 The term total lightning
200 million volts (V). The leader ionizes a pathway that contains describes the sum of cloud-to-ground and cloud flashes. An
superheated ions, both positive and negative, and forms a plasma extremely small portion (<0.01 of 1%) of all lightning travels from
column of very low resistance. The leader travels in relatively ground to cloud when this is induced by the special circum-
short branched steps downward about 50 m (164 feet) and then stances of high towers or mountains.
retreats upward. The next time the leader goes downward toward Cloud flashes can travel between clouds, within clouds, from
the ground, it fills the original ionized path but branches at the cloud to cloud, and in all combinations of these paths. The same
end to go down another 50 m and then retreats again. This up- flash can simultaneously strike ground at one or more locations
and-down multiple-branching process continues until the leader and travel a long distance in-cloud (Figure 5-23). There are
comes to within 30 to 50 m (98 to 164 feet) of the ground. several times as many cloud flashes as those that reach the
Because lightning follows this ionized path, its lower tip only ground. Cloud flashes have been measured to extend 305 km
can sense the existence of nearby objects within a radius of about (189 miles) in horizontal length and last 5.7 seconds.244 From the
30 to 50 m, meaning that lightning will not be affected by the point of view of a person on the ground, cloud flashes may
existence of a hill or tower farther away. For human safety, being appear to travel in long streaks across the sky, or the channels
within 50 m (164 feet) of the lowest tip of a cloud-to-ground may be obscured and visible only by the brightening within
lightning flash as it comes to ground is extremely unsafe. 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
DIAMETER AND TEMPERATURE OF LIGHTNING ball lightning. It is usually described as an orange, blue, or white
Although many techniques have been used to measure the diam- globe between the size of a softball and a basketball. It has been
eter and temperature of lightning, all measurement techniques observed to enter planes, ships, or houses and to travel down
MOUNTAIN MEDICINE
have artifact problems. Visual measurements of the lightning narrow spaces such as hallways. Ball lightning very infrequently
stroke using standard photography usually show the diameter of injures people and objects and often exits through a door,
the main body of the stroke to be about 2 to 3 cm (0.8 to 1.2 chimney, or window.313 It may explode with a loud bang or
inches). exhibit other bizarre behavior.
The diameter of the channel is sometimes measured indirectly, Cloud-to-ground lightning flashes usually lower negative
using measurements of holes and strips of damage that lightning charge to the ground.325 The less frequent (5% to 10%) positive
produces when it hits aircraft wings, buildings, or trees. Measure- cloud-to-ground flashes tend to occur during the winter, at the
ments vary from 0.003 to 8 cm (0.001 to 3.15 inches), depending end of thunderstorms, on the U.S. high plains, or in relatively
on the material that was destroyed. Hard metallic structures shallow thunderstorms. Positive flashes usually have one return
sustain smaller punctures than do relatively softer objects such stroke. It is not known if positive cloud-to-ground flashes cause
as trees. The ionized sheath around the tip of the bright leader a different injury profile, although they tend more to have long,
stroke has not been measured but is estimated to have a diameter continuing current that may impart more energy to a person than
PART 1
84
MECHANISMS OF INJURY this happens, a minor amount of current will be conducted
85
Contact voltage
Side flash
MOUNTAIN MEDICINE
A Direct strike B C
PART 1
Upward streamer
Ground
current
D2
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 that after flashover occurs, internal current drops dramatically.
the body. Our understanding of what happens to a lightning- Current can be directed to be conducted within the wood or
struck human is assisted by what happens with conduction in conducted externally over the wood, but not both ways. In wood
wood on telephone and electrical supply poles.118 The consis- pole design, metal implants from outside to inside the wood
tency and resistance of wood are much closer to that of the enhances the ability to swap between these routes. As the current
human body than one might expect. This allows us to conclude continues to increase, the surface flashover bridges the strike
86
point and the ground. When this happens, most of the lightning Earth Potential Rise. Also called “step potential,” “ground
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
B
PART 1
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
PATHOPHYSIOLOGY OF
LIGHTNING INJURY
This section describes the way in which lightning and electric
current produces alterations in human physiology.
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
90
site of a direct strike can also be mechanically or electrostatically the field reached the breakdown strength of air, 4000 V/cm
10 k 0.25 m
10 k
200
10 kW
0.25 mF
200
Key 0.25 m
300
A 300 300
10 k 0.25 m 10 k 0.25 m
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.
91
A
Response
No flashover G4
5 MV VAC 5 kV
F
VAB
4 MV
5 kA
VAF IFH
VEB,DB
G1 5 kA peak
1.11.7 50 Time 500 kV
(msec) 8/20 msec wave
H
With flashover
D E
G2 G3
VAB 500 kV
5 kV 5 kV
B
IFH 800A Physical Earth
MOUNTAIN MEDICINE
<<5 kV 150
VAF
VDB C
True Earth
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 space charge around the victim’s head, under the influence of
is not an index of the severity of injuries sustained within a the electric field resulting from the stepped leader’s downward
PART 1
human. Either may be disproportionately great or small. However, path. Second, once a separate leader from the one affecting the
in unwitnessed situations, forensic evidence of damage to shoes person makes connection with the stepped leader, the electric
and clothing, sometimes accompanied by tympanic membrane field collapses rapidly. In that case, the charge in the unattached
rupture, may be the most important and reliable indicator in upward leader rapidly returns to the earth.
determining whether lightning caused a healthy person’s death The first process is relatively prolonged and regular, and the
when no other cause is apparent.47,218,389 second is rapid and impulsive. In an analysis using a human
The factor that seems most important in separating the effects model and a 30-kiloampere (kA) lightning strike grounding just
of lightning from high-voltage electrical injuries is the duration beyond the striking distance, current rises to approximately 20
of exposure to the current. This conclusion is reached both amperes (A) over 150 microseconds (µsec). At the start of this
because lightning is not present long enough to cause tissue rise, there is an extremely short pulse of about 5 A. This repre-
breakdown in the classic burn sense and because of the results sents a body-charging component before the propagation current
of the mathematic modeling describing the path of the energy for the actual streamer. This is a significant current; however, the
and how long it is in contact with the body. 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
ESTIMATES OF STREAMER CURRENTS effect of this current, conducted internally within a victim for such
Upward streamer mechanism currents have been estimated.8-10,91 a short time, theoretically depends on its timing to the vulnerable
This mechanism recognizes that as a stepped leader steps toward period of the cardiac cycle. For an 80-kA return stroke, the peak
the earth from a cloud, an upward leader will emanate from current is approximately 80 A, which again is significant.
several objects that are possible points of attachment. Of these, Once the aborted leader collapses, there is a current pulse of
a return stroke will evolve from perhaps only one. Alternatively opposite polarity. This is exquisitely short. Little is known about
stated, there will be several upward leaders that dissipate without the collapse of an aborted leader, and assumptions are made
attachment. regarding the time constant of the collapse. This ranges from 0.1
The current needed to establish and maintain any upward to 1 µsec. Cases are examined for a 30-kA and an 80-kA return
leader nonetheless must be supplied from the earth, and if a stroke. The peak current can be large, depending on the size of
person is the source of an upward leader, current must flow the stroke and time constant. The least peak current is computed
through the person. If this streamer meets the downward leader, at about −600 kA, with the least energy deposited being 0.22
a direct strike results. If attachment does not occur, then once kilojoule (kJ). Again, these are highly significant currents that are
the return stroke is established through another upward streamer large enough to produce significant injury and death.
elsewhere, the subject upward streamer collapses back through
the victim. Thus an initial unidirectional current occurs in this
case, followed by a reverse collapse.
BEHAVIOR OF ELECTRIC CURRENT IN TISSUE
Becerra and Cooray41 studied the amount of current to which High-voltage or low-voltage electric current may be carried
a victim of upward leader current may be exposed. They identi- through tissue in a direct conduction manner, obeying simple
fied two processes that are important to model. First, current linear equations such as Ohm’s law. The result is heating of tissues
flows through a victim to establish the upward streamer and under Joule’s law, with thermally-induced cellular death and
92
dysfunction. Simple passage of current may interfere with neural field, it would be wise to be concerned about MRI fields as well,
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 of atrophic spinal paralysis have been reported.26,68,88,104,390a
may or may not have perceived lightning or thunder. At the
scene, they often suffer confusion, amnesia, temporary deafness Severe Injury
or blindness, or temporary unconsciousness.88 They seldom dem- Patients with severe lightning injury may be in cardiac arrest with
onstrate cutaneous burns or paralysis, but may complain of either ventricular standstill or fibrillation when first examined.
confusion and amnesia lasting from hours to days. Paresthesias, Cardiac resuscitation may not be successful if the victim has
muscle pain, and headaches may last for days to months. Victims sustained a prolonged period of cardiac and central nervous
may sustain tympanic membrane rupture from the explosive system (CNS) ischemia. Direct brain damage may occur from the
force of the lightning shock wave. Vital signs are usually stable, lightning strike or blast effect. Tympanic membrane rupture with
although occasionally, victims demonstrate transient mild hyper- hemotympanum and CSF otorrhea is more common in this group.
tension. They may experience soreness for a few days; recovery The prognosis is usually poor in the severely injured group,
is usually gradual and may or may not be complete. Permanent worsening further with any delay in initiating cardiopulmonary
PART 1
neurocognitive damage may occur. Some victims may suffer resuscitation (CPR), thus causing anoxic injury to the brain and
PTSD and other psychological sequelae. other organ systems. There are anecdotal reports of successful
resuscitation of lightning victims with automated external defibril-
Moderate Injury lators (AEDs).159a,290,364
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
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,
BOX 5-4 Lightning Injuries and severity of the clinical situation.
94
Lightning-Linked Secondary Trauma from Falls or Blast zyme, and troponin are used as markers of myocardial damage.
95
Central Nervous System Injury37,68-71,76-80,90,224 Survivors may have persistent sleep disturbances, difficulty
Almost 72% of victims in one study had loss of consciousness.87 with fine mental and motor functions, dysesthesias, headaches,
Nearly three-fourths of these victims also suffer cardiopulmonary mood abnormalities, emotional lability, storm phobias, decreased
arrest. Persons with cranial burns are two to three times more exercise tolerance, and PTSD.90 Centrally derived pain and psy-
likely to sustain immediate cardiopulmonary arrest and have a chological syndromes have been reported.66,69,79,80,297
three to four times greater probability of death. Persons who are Spinal cord injury developing over months after the injury has
stunned or lose consciousness without cardiopulmonary arrest been reported.242,243 Paresthesias are frequently seen, often in the
are highly unlikely to die, although they may still have serious area of keraunoparalysis. There may be evidence of autonomic
sequelae. neuropathy.
The victim of prolonged cardiopulmonary arrest may suffer
anoxic brain injury that is not specific to lightning injury.80a Peripheral Nerve Injury*
Whether by this mechanism or others, cell loss and infarction The peripheral nervous system may be affected. Pain and pares-
of various CNS areas (e.g., cerebellum,37 cerebrum) have been thesias are prominent features of lightning injury, particularly in
reported. Autopsy findings include meningeal and parenchy- the line of presumed current passage, although this is difficult to
mal blood extravasation, petechiae, swelling and herniation ascertain from external burns or other injury. Symptoms may be
of the brainstem, dural tears, scalp hematomas, and skull delayed by weeks to months. Any peripheral nerve can be
fractures).170,265a,284,300,374 involved.
Gross structural changes to the brain have been reported,
including coagulation of brain substance, formation of epidural Autonomic Nervous System Injury85,176,177,323,357,358
and subdural hematomas, paralysis of the respiratory center, and Central hyperadrenergic state with superimposed autonomic
intraventricular hemorrhage. In hemorrhagic injuries, there is a storms and diffuse degeneration of the peripheral autonomic
pattern of compromise to the basal ganglia.4,60,167,305,368 Intracranial system have been reported.309,387 Autonomic dystrophy, also
hemorrhages related to blunt trauma do not tend to occur in the called sympathetic dystrophy or sympathetically mediated pain
basal ganglia, and therefore mechanical trauma is a less likely syndrome, may occur. Such chronic pain syndromes are now
explanation. Studies in animals suggest that direct cellular damage subsumed under the classification of complex regional pain syn-
occurs to basal ganglia, the respiratory center beneath the fourth dromes, which are of type 1 (reflex sympathetic dystrophy) or
MOUNTAIN MEDICINE
ventricle, and the anterior surface of the brainstem. This occurs type 2 (previously causalgia).
because the path of current flow in direct-strike patients is Complex regional pain syndromes are long-term neurologic
through orifices of the head (eyes, nose, ears), and the current sequelae that may be caused by even minor injuries to nerves.
travels caudally from the neocortex toward the basal ganglia, These are characterized by pain, edema, autonomic dysfunction,
pituitary, hypothalamus, and brainstem.12,14 As a result, signs trophic changes (including atrophy secondary to disuse from
and symptoms of endocrine dysfunction, respiratory or cardiac pain), and movement disorder.
arrest, and sleep disturbances can be reasonably expected to
occur. Cerebellar compromise may eventually manifest as par- Posttraumatic Headache93,375
kinsonism, extrapyramidal syndrome, or other involuntary move- Many victims of lightning injury exhibit severe, unrelenting
ment disorders.37,66,69,79,80,297 headaches for the first several months, along with other symp-
Although MRI or CT may show diffuse edema, intracranial toms, including gastrointestinal distress, that resemble postcon-
hemorrhage, or other injuries, they are most often normal.79,80,124 cussion symptoms. Acupuncture may be effective. Many patients
PART 1
Hemorrhage has been found on MRI in a few acutely injured complain of nausea and unexpected, frequent vomiting spells
victims.79,383 early in the recovery period. Dizziness and tinnitus from eighth
Seizures may accompany initial cardiorespiratory arrest as a cranial nerve injury are also common complaints, especially with
result of hypoxia or intracranial damage. Electroencephalography telephone-transmitted lightning strikes.30,90,104,388,392
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-
BURNS†
pitalization. Some victims, including children, develop delayed Most people assume that because of the tremendous energy
seizures (months to 1 or 2 years later), some of which manifest discharge involved, a lightning victim will be “flash-cooked.”58,89
as “absence spells,” memory loss, or blackouts that are often Fortunately, the physics of lightning flashover, as well as the vast
diagnosed as “pseudoseizures.” majority of injuries occurring from indirect strikes, spares most
In Cooper’s study87 of severely injured victims, nearly two- victims from suffering more than minor burns. Less than one-third
thirds had some degree of lower-extremity paralysis (keraunopa- of lightning survivors have any signs of burns or skin marks.
ralysis), usually demarcating around the waist or pelvis, and Although extensive third- and fourth-degree burns may occur in
approximately one-third had upper-extremity paralysis. The combination with skeletal disruption, these are quite rare. The
affected extremities appear cold, clammy, mottled, insensate, and incredibly short period of exposure may explain the lack of
pulseless.26 This is probably the result of sympathetic instability significant burn injury. Burn location provides a prognostic indi-
and intense vascular spasm, similar in appearance to Raynaud’s cator. Cranial and lower-extremity burns are associated with a
phenomenon. It usually clears after several hours.26,88 Fascioto- fourfold and fivefold increase in mortality, respectively, com-
mies are seldom indicated for lightning injuries, because signs pared to burns in other locations.87
of compartment syndrome or distal ischemia usually clear Skin injuries are influenced by amount of moisture on the
with patient observation. Pulses can sometimes be elicited with surface, type of clothing, and presence of metal objects worn or
Doppler examination. Atrophic spinal paralysis has been reported, carried during the strike. Superficial partial- or full-thickness
as have persistent paresis, paresthesias, incoordination, delayed burns can be isolated or combined. The morphology can be
and acute cerebellar ataxia, hemiplegia, aphasia, quadriplegia linear, punctuate, flower-like, tattooing, or imprint burn mark
(immediate or delayed), and progressive muscle atrophy of the from contact with metal objects; feathering; fern-leaf mark; or
upper extremities. classic first, second, or third degree.74,272,385
Whether or not victims have suffered loss of consciousness,
they almost universally demonstrate anterograde amnesia and Entry, Exit, and Types of Burns
confusion, which may last for several days. Retrograde amnesia Discrete entry and exit points are uncommon with lightning. The
is less common. Although victims may carry on a conversation burns most frequently seen may be divided into five categories:
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 *References 66, 68-70, 85, 176, 177, 217, 315, 319, 320, 323, 330, 357,
head or neck. Early after the strike, symptoms resemble postcon- 368, 378, 384, 392.
cussion syndrome. †
References 38, 61, 86, 93,104, 181, 206, 268, 283, 284, 360, 366, 380.
96
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 may be multiple and closely spaced (Figure 5-37). They may be
from ignited clothing or heated metal; and combinations. full thickness and resemble cigarette or cinder burns, and are
Linear burns often begin at the victim’s head and progress usually too small to require grafting.
down the chest, where they split and continue down both legs Particularly useful for forensic investigation is explosion of
(Figure 5-35). The burns generally are 1 to 4 cm (0.5 to 1.5 clothing, such as occurs with vapor explosion of wet socks in
inches) wide and tend to follow areas of heavy sweat concentra- shoes. This may blast shoes off with subsequent contusion and
tion, such as beneath breasts, down the middle chest, and in the avulsion injuries to parts of the foot (see Figure 5-35H). Examina-
midaxillary line.88 Linear burns are usually first- and second- tion of clothing may show singed fibers at the edge of the
degree burns that may be present initially or may develop as late damage and absence of very fine fibers on material, such as
as several hours after the lightning strike. They are not primary cotton, because these were vaporized or burned away (Figures
lightning injuries, but more likely steam burns caused by vapor- 5-38 and 5-39; see also Figure 5-33B). With a handheld 10×
ization of sweat or rainwater on the victim’s skin as flashover magnifier, plasticized or polyester materials may show frank
and current flow occur around the body. In patients wearing thin melting. Even in cotton clothing with no apparent damage to the
or cotton clothing, the steam tends to escape through the cloth- material, examination of the threads joining pieces at the seams
ing, causing less damage than in areas where the clothing is will often show a tiny droplet of plastic, because thread contains
bunched (e.g., axilla, antecubital fossa [see Figure 5-35C], groin) a polyester or nylon core for strength and durability.
or under nonporous material, such as leather jackets or belts Feathering or fern-leaf mark figures are pathognomonic of
(Figure 5-36). lightning and known by such names as Lichtenberg flowers or
Punctate burns are discrete circular burns that individually figures, filigree burns, arborescent burns, ferning, and kerauno-
range from a few millimeters to 1 cm (0.4 inch) in diameter, and 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 Deep burns may be caused by metal worn close to skin.104,215,385
to a strong electric field and has been compared with fractals.181 Figure 5-35E shows a burn resulting from a metal belt buckle or
Sometimes the most superficial skin over the areas will slough athletic supporter worn by a young man who was struck by
or flake off after a few days. Although many pictures exist of lightning while playing softball. Figure 5-42 shows a necklace
these marks, they have never been described histologically. The burned into the skin with permanent tattooing. Another theory
most current theory is that they represent blood cells forcefully for these burns involves discharge of current from metal to
extravasated into the superficial layers of the skin from contract- underlying skin. On rare occasions, clothing is ignited by light-
ing capillaries, similar to a superficial bruise, which is consistent 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
PART 1
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
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
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
FIGURE 5-43 Rondavel in South Africa where this woman’s family
member died by fire. (Courtesy Ronald Holle.)
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-
fractures, including skull, ribs, extremities, and spine, have been tion, macular hole,61,327 optic atrophy, diplopia, loss of accom-
reported in lightning victims.219,255 Unfortunately, these are often modation, and decreased color sense have been reported.
missed, particularly in the workup of persons with chronic pain. Autonomic disturbances of the eye, including mydriasis, Horn-
Rarely, a burst-like injury of soft tissue occurs and discloses er’s syndrome, anisocoria, and loss of light reflexes, may be
MOUNTAIN MEDICINE
extensive underlying injuries, especially in the feet, where boots transient or permanent. Transient bilateral blindness of unknown
or socks may explode as a result of vapor expansion (Figure etiology is not uncommon. Intense photophobia may be present
5-44; see also Figures 5-35H and 5-38). Persistent hypotension as the victim recovers. An interesting paper conjectures that the
should alert the physician to blunt injuries to the chest, spine, conversion of St Paul on the Damascus road and his subsequent
lungs, heart, and intestines that may lead to complications of blindness were caused by lightning.53,54
prolonged coma, pulmonary contusions,365 heart failure, and isch- Dilated or nonreactive pupils should never be used as a
emic bowel. prognostic sign or criterion for brain death in a lightning victim
Other findings, such as hemoglobinuria and myoglobinuria, until all anatomic and functional lesions have been excluded.64,65
are seldom reported.312,314 Multifactor rhabdomyolysis may be
EAR INJURIES‡
Between 30% and 50% of more severely injured lightning victims
PART 1
B *References 56, 62, 127-126, 137, 165, 204, 216, 230, 276, 293, 294, 336,
366, 395.
FIGURE 5-44 The heat from a lightning strike caused water in the wet †
References 56, 126, 127, 137, 165, 168, 230, 276, 336, 366.
boot to instantaneously turn to steam, exploding the boot off the foot ‡
References 42, 44, 57, 141, 153, 158, 163, 216, 238, 277, 285, 298,
(A) and causing burns (B). (Courtesy Sheryl Olson, RN.) 299, 328, 369, 388.
100
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
101
mental abilities, or changes in family dynamics, is almost univer- symptom complexes include linear or punctate burns, tympanic
sal and should be anticipated. Antidepressant medication may be membrane rupture, confusion, and outdoor location. Because
useful. Formal neuropsychological testing may be used to attempt several cases of side flash or contact injury from indoor plumbing
to validate the injury, quantify a functional baseline, and design and telephones have occurred, the physician should suspect
cognitive therapy. Very few studies have formally examined the lightning strike in persons found confused and unconscious
syndrome.320,378 Primeau and co-workers320,321 point to research indoors after or during a thunderstorm.11,26,30,88
difficulties, including sample bias and heterogeneity, methodol- Documentation of lightning activity to support legal or insur-
ogy (cross-sectional rather than longitudinal or prospective), and ance claims is available from commercial sources.
the essential difficulties of determining premorbid status or
current independent psychiatric status. The authors considered INITIAL FIRST AID AND TRIAGE
somatoform disorders as a cause, noting patients’ tendency to be
preoccupied with the injury and to overattribute subsequent
OF VICTIMS26,88,103,106
symptoms to lightning injury. This may result partly from physi- Ensuring scene safety is paramount. Rescuers are at risk if thun-
cians’ general lack of knowledge of the problems and the lack derstorms are in the area.373 If the situation makes it possible,
of longitudinal controlled studies, so victims do not know what the victim is transferred to a safe area quickly, or to a location
to expect in the future. under lesser risk.
Other Behavioral Issues. Conversion reaction may also be If the victim is unresponsive with no breathing or no normal
considered, although it cannot account for the symptomatology breathing (i.e., only gasps), the person has suffered a cardiac
of lightning and electrical disability.90 Good neuropsychological arrest. Rescuers should immediately activate the emergency
testing can detect this facet. One difficulty with neurocognitive response system, if possible. CPR should be started immediately
testing is use and interpretation of the Minnesota Multiphasic with a CAB (chest compressions, airway, breathing) sequence.
Personality Inventory (MMPI). Although it was not developed to AEDs have been helpful in some cases.159a,290 Cardioversion,
characterize patients with chronic problems, particularly those defibrillation, and medications should proceed according to the
with chronic pain, the MMPI has been applied to them, often most recent advanced cardiac life support (ACLS) guidelines.379
resulting in erroneous conclusion of conversion reaction or pre- The victim will probably die unless pulse and respirations
occupation with physical complaints. It should surprise no one resume spontaneously in a short time. The heart may resume
MOUNTAIN MEDICINE
that a person suffering from chronic pain and neurologic injury activity but may slip into secondary cardiac arrest. It is unknown
that hampers normal preinjury activities will rank higher on the whether the secondary arrest is caused by primary brain damage,
“preoccupation with physical complaints” and “conversion” hypoxia from prolonged respiratory arrest, primary cardiac
scales than will uninjured normal individuals. damage, autonomic nervous system damage, or any of a number
Andrews and Darveniza30 recognized three postinjury syn- of other mechanisms. If no pulse is obtained within 20 to 30
dromes in telephone-related lightning injury and correlated these minutes of starting CPR, it is reasonable to stop further resuscita-
with the postinjury periods of 1 week, 1 week to 3 months, and tion efforts; 77% of victims do not respond to CPR.87 If a pulse
3 months to 3 years. Primeau and co-workers320 add a fourth is obtained, ventilation should be continued until spontaneous
syndrome, in persons experiencing longer and perhaps lifetime adequate respirations resume, the victim is pronounced dead,
dysfunction.163 Cherington68 and colleagues80 have further classi- continued CPR is deemed unfeasible because of rescuers’ exhaus-
fied lightning injury by its permanent sequelae. tion, or there is danger to rescuers’ survival.
The first 12 months after injury are crucial to recovery. It is When lightning strike involves multiple victims, resources and
PART 1
during this period that the most recovery is seen, with possible rescuers may not meet the demand, and triage must be instituted.
mild improvement up to 3 years after injury. Van Zomeren and Normally, the rules of triage in multiple-casualty situations dictate
associates378 provide one of the few thorough examinations of bypassing dead persons for those who are moderately or severely
the syndrome in lightning-injured patients. The main complaints injured and can benefit from resuscitation efforts. However,
were fatigue, energy loss, poor concentration, irritability, and “resuscitate the dead” is the rule in lightning incidents,120a,397
emotional lability. Impairment of memory, attention, and visual because victims who show some return of consciousness, or who
reaction times as well as depression and PTSD were documented have spontaneous breathing, are already on the way to recovery.
(p <0.001). The authors stated that the lasting complaints and The most vigorous CPR attempts should be directed to the victims
mild cognitive impairments could not be explained on the basis who appear to be dead, because they may ultimately recover
of anxiety reactions or depression, and summarized their findings if properly resuscitated.106,159a,379 Survivors should be routinely
under the heading of “vegetative dystonia.” stabilized and transported to the hospital for more thorough
evaluation.
The probability that lightning victims can recover after pro-
RECOGNITION AND ACUTE longed CPR is low. No evidence suggests that survival after a
TREATMENT OF LIGHTNING longer period than normal without resuscitation is possible in the
victim of lightning injury. Often, in a remote setting, the rescuer
INJURIES88,90 is emotionally tied to the victim by age and friendship and may
tend to continue resuscitation past the point of futility. In pro-
DIAGNOSIS nouncing a victim dead, the rescuer must ensure that other
Diagnosis of lightning injury may be difficult. The history of problems, such as hypothermia, are not contributing to the vic-
thunderstorms, witnesses who can report having seen the strike, tim’s response to CPR efforts.
and typical physical findings in the victim make diagnosis easier Other procedures, such as airway control or intubation, and
but are not always present. institution of intravenous (IV) fluids and oxygen may be required.
Lightning can strike on a relatively sunny day, thunder may Because lightning victims may suffer traumatic blunt injuries,
not be appreciated, and sometimes the victim is alone when rescuers may need to perform spinal immobilization and splinting
injured. A diligent history taking and careful physical examina- of fractures, if possible, before transport.
tion at the earliest opportunity may help determine the true Most lightning injury victims can be treated and discharged
cause. Any person found with linear burns, mental status from the emergency department (ED), but more complex light-
changes, ruptured tympanic membrane, and clothes exploded ning injuries are considered one of the criteria for being referred
off should be treated as a victim of lightning strike. Tympanic and assessed at a burn unit. If this is not possible because of
membrane rupture may make the diagnostic difference in diffi- geographic location or distance, the receiving institution must
cult cases. have the capacity to treat victims with complex trauma, promptly
Diagnosis is made doubly difficult because burns, which most assemble a multidisciplinary group of specialists and paramedical
people expect to accompany lightning injuries, are often absent. staff with experience in these types of injuries, and access a
Feathering marks, also called Lichtenberg flowers, are pathogno- consolidated group of rehabilitation, physical, and occupational
monic of lightning strike but are rare.73,74,86,129,332,380 Other signs or therapists.
102
developing torsade de pointes ventricular tachycardia (VT) must
103
from abdominal or chest injuries, spinal shock, cardiogenic provides a useful guide to the remote need for surgical interven-
shock, and occasionally deep burns similar to high-voltage elec- tion in lightning injury.
trical burns. As soon as an adequate central blood pressure is
achieved, fluids should probably be restricted because of the Eye Injuries*
incidence of cranial injuries, cerebral edema, and postarrest Eye injuries are myriad. Visual acuity should be measured and
anoxic brain injury. the victim’s eyes thoroughly examined. Cataracts may develop in
Mechanical ventilation is required for the victim who is the first few weeks or months. Eye injuries should be treated in
without spontaneous or adequate respirations until the person standard fashion and may require referral to an ophthalmologist.
resumes adequate ventilation, brain death is declared, or the Case reports exist of successful treatment of optic neuritis with
physician and family decide to cease efforts. high-dose corticosteroids similar to those used with spinal cord
If lightning did not cause immediate cardiac arrest, there is injury, but because there were no controls, it is not known if
very low risk of death. However, observation, cardiac monitoring, recovery would have occurred without drug use.
and serial cardiac marker (e.g., troponin) measurements are in-
dicated if there is any sign of cardiac ischemia or arrhythmia, or Ear Injuries†
if the victim complains of chest pain. The indications for antiar- Loss of hearing mandates otologic evaluation. Blast as well as
rhythmic drugs and pressor agents are the same as for suspected direct injury may occur. Simple tympanic membrane rupture is
myocardial infarction.88 No systematic study has addressed proper usually handled conservatively with observation until the vic-
duration of observation for lightning survivors. tim’s tissues heal. Sensorineural damage to the auditory nerve,
Transient hypertension may be so short-lived as not to require resulting in hearing changes, dizziness, and permanent tinnitus
acute therapy. However, several victims developed hypertension and facial nerve palsies, is not uncommon. Ossicular disruption
12 to 72 hours after lightning strike and seemed to respond well or more severe damage may necessitate surgical repair. Otor-
to antihypertensive medications. No systematic study of antihy- rhea and hemotympanum suggest basilar skull fracture. Com-
pertensive agents has been undertaken for lightning survivors. plaints of pain around the angle of the victim’s jaw may indicate
occult fracture of the styloid process and other musculoskeletal
Central Nervous System Injury* damage.
Every lightning victim should have a screening neurologic exami-
Pregnant Victims144,150
MOUNTAIN MEDICINE
Early seizures are probably caused by anoxia. If there is evi- for survivors to report continuing nausea for several weeks to
dence of CNS damage, or if seizures continue after adequate months.
oxygenation and perfusion have been restored, standard phar- Endocrine dysfunction, perhaps as a result of pituitary or
macologic intervention with diazepam, fosphenytoin, phenobar- hypothalamic damage, including amenorrhea, impotence, hypo-
bital, and other anticonvulsants should be considered. The gonadism, and decreased libido, has occurred in some victims.
response to specific individual drugs has not been studied. Spinal cord or sympathetic nervous system injury or postinjury
If paralysis does not improve, causes other than lightning, depression, as well as side effects of medications, may also cause
including blunt injury from a fall, may be responsible. Spinal impotence, decreased libido, and sexual dysfunction after light-
artery syndrome has been reported, perhaps caused by arterial ning injury.
spasm or undiagnosed fractures. A physical therapy program
should be initiated before discharge. Pronouncing the Victim Dead55,64,65,101,103,106
Dilated pupils should not be taken as a sole sign of brain death
Burns† in the lightning victim. It is always necessary to exclude other
Lightning burns may be apparent at admission but more often causes of pupillary dysfunction and eliminate them before death
develop within the first few hours. Burns occur in less than one- is declared. Hypothermia with lightning injury may cloud end-
half of lightning survivors and are generally superficial, unlike of-life decisions. If the victim has not regained a pulse after 20
high-voltage electrical burns, and seldom cause massive muscle to 30 minutes of resuscitation, it is reasonable to cease CPR.
destruction. Myoglobinuria is infrequently seen, so vigorous fluid
therapy and mannitol diuresis are not usually indicated. In the Long-Term Care‡
rare instance of myoglobinuria, the decision must be made by In the long run, there is no specific treatment for lightning
the treating physician, according to the case. Overzealous hydra- injury. Lightning is a nervous system injury that can involve
tion with resultant cerebral edema following presumption of chronic pain, neuropathy, and brain injury, sometimes compli-
similarity to high-voltage injuries has probably harmed more cated by initially unrecognized musculoskeletal injury. Most
lightning victims than has myoglobinuric renal failure. symptoms can be treated in standard fashion, including cogni-
Lightning burns are generally so superficial that they do not tive therapy, pain management, job retraining, and counseling,
require treatment with topical agents. In the unusual instance of as indicated by the survivor’s signs and symptoms. As with any
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 56 ,62, 126, 127, 137, 165, 166, 204, 216, 230, 276, 293, 294,
336, 366, 395.
†
*References 26, 66, 68, 71, 78-80, 89, 90, 393, 394. References 14, 42, 44, 57, 153, 158, 164, 216, 239, 277, 298, 299, 328,
†
References 38, 86, 93, 104, 129, 181, 206, 268, 283, 284, 359, 360, 369, 388.
‡
366, 380. References 69, 107, 111, 243, 319, 359, 393, 394.
104
A mainstay of treatment is ongoing psychologist consultation
105
Lightning scene investigation can be divided into the tion” and “cuprification,” metal with a lower melting point
following: vaporizes, leaving the other metal behind. Magnetization of
1. Environmental signs of direct lightning strike metallic objects has been mentioned in the literature, although
2. Structural signs of direct lightning strike current thinking is that this may be a myth. Reports of metallic
3. Trace evidence signs of direct lightning strike chains being magnetized and “sticking” to metallic postmortem
trays have yet to be verified.
Environmental Signs of Direct Lightning Strike
• At the scene, there may be damage to nearby trees, such as
splitting or removal of bark. PHYSICAL AND/OR AUTOPSY EXAMINATION
• Arc marks may be present on the walls or nearby A complete postmortem examination of a lightning victim should
structures. be performed.
• The ground may display a fern pattern. • The external examination should include a meticulous descrip-
• Soil may show fulgurite formation—bore or tube-like struc- tion of clothing and any evidence of resuscitation (Figure 5-38).
tures formed in sand or rock by lightning. • Metal objects may have burned underlying skin or may have
• Often a crater will be exposed in the earth, with rock and been marked by the heat of electrical arcing but did not attract
sand being flung far afield. Craters of up to 2 m (6.6 feet) in the lightning strike (Figure 5-45). Figure 5-39 shows damage
diameter have been reported. to clothing and underlying burns. Figure 5-42 shows perma-
• To preserve the case history for scientific purposes, a relevant nent tattooing from a metal necklace burned into skin in a
academic institution or other expert in the field should be nonfatal injury.215
advised of the incident, particularly if there is any indication • Metal objects may show signs of fusing, zincification, or cupri-
of intent to file a lawsuit by a surviving party. fication. Always check for magnetization. Metallic objects,
such as tooth fillings, spectacles, belt, buckles, coins, and
Structural Signs of Direct Lightning Strike pacemakers, should be specifically described.
Jandrell and associates210 described the effects of direct lightning • The type, pattern, and distribution of any cutaneous thermal
strike to housing structures in southern Africa.161,270,271 Figure 5-19 injuries, including clusters of punctuate burns, blisters, or
shows damage to the roof of a clubhouse from direct lightning charred burns, should be noted. Figure 5-44 shows damage
MOUNTAIN MEDICINE
strike. The damage was extensive and included structural and to a hiking shoe with underlying damage to the skin of the
internal damage (see Figure 5-20). Figure 5-21 shows damage to foot.26
curtaining material covering the window. Thatched structures • Determine if there has been tympanic membrane rupture.
have been known to ignite following lightning strike. Thatch is Barotrauma, including pneumomediastinum, has been cited
very combustible, so inhabitants are at greater risk for severe as one of the injuring mechanisms of lightning.169
injury and burns.161,187 • Note singed or scorched hair.
• Ocular injuries, such as retinal detachment, should be deter-
Trace Evidence Signs of Direct Lightning Strike mined. Cataracts may be difficult to demonstrate postmortem.
A direct strike can be very difficult to prove. Cindering on cloth- • Unique arborescent or fern-like injuries (Lichtenberg figures)
ing or arc marks on metallic structures may be seen. In “zincifica- should be noted (see Figures 5-40 and 5-41).
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
• Determine if there are lightning wounds on the bases of the PRECAUTIONS FOR AVOIDING
107
Ready Program covers most outdoor storm threats and is useful lightning.186,397 Summer lightning may linger into the evening in
for camps and hiking programs and in planning for many other almost all regions of the country; unfortunately, this is the time
wilderness or near-wilderness situations (http://www.nws.noaa of day when sports and recreation users are more likely to be
.gov/stormready/).296 outdoors.43
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
AN APPROACHING THUNDERSTORM
by using National Oceanic and Atmospheric Administration Pay more attention to lightning than rain. Approximately 10% of
(NOAA) weather radio, cell phone lightning alerts, websites, and all cloud-to-ground lightning strikes occur without rain at the
tailored information from private weather providers. Because location of the ground strike, so waiting for rain to arrive does
access is available for much of the United States via mobile not provide certain protection from lightning when a thunder-
methods, there should be fewer surprises with regard to storms storm approaches. Thunder can be heard up to about 10 miles
that are growing or moving into an area. Users, however, should away in quiet conditions, but not nearly that far in the presence
be aware that many sources of weather data, particularly free of wind or traffic, or when inside a structure.
ones, may be delayed by several minutes. A simple rule at the beginning of a storm is, “When thunder
Thunderstorm and tornado warnings issued by the NWS indi- roars, go indoors.”182,292,-342-344,346 This rule removes any doubt
cate that thunderstorms are almost certain to occur in the area, about whether it is time to take action and is effective as a thun-
and most likely in surrounding counties. However, most lightning derstorm approaches. Although there is some overwarning
does not occur within a warning area, but appears in less intense, because of distant lightning that may not reach a location, it is
yet frequently nonsevere, thunderstorms.35 an effective and easy way to manage the lightning threat.
Most lightning occurs during the summer months of June, For a more objective approach, use the 30-30 rule developed
July, and August (Figure 5-46A).188 Furthermore, most lightning at the 1998 lightning safety meeting.43,105,132,193,264,384,399 The first 30
occurs between noon and 6 PM (Figure 5-46B).187 These general refers to the time in seconds between seeing lightning and
figures make it much more apparent when to avoid long, risky hearing thunder from that flash (the second 30 refers to the wait
exposure to lightning. Storms begin before noon on some days, time; see next section). If the interval from flash to bang is 30
particularly in locations such as over the high mountains of Colo- seconds or less, people are in danger from lightning and should
MOUNTAIN MEDICINE
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
END OF THUNDERSTORM
FIGURE 5-47 Lightning-unsafe picnic shelter in Tucson, Arizona. Note
Do not underestimate the danger of lightning at the end of a warning sign on roof, which states: “WARNING: This structure is unsafe
thunderstorm. As many people are killed or injured by lightning for shelter during lightning storms. Seek suitable shelter elsewhere.”
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 around people and into the ground. Contact with conducting
the last lightning is seen or thunder is heard before resuming paths of wiring, plumbing, corded telephones, and large open-
outdoor activities.43,105,132,201,399 At night, flashes may be visible low ings, such as garages and doors, can result in injuries. Such
on the horizon inside tall thunderstorms up to 80 km (50 miles) contact needs to be avoided during the presence of lightning to
away, but these are not of much concern unless the lightning avoid potentially serious injury, but these are not known to lead
channel itself is visible to the ground. to fatalities in well-constructed and grounded buildings.
Since the 1998 meeting, it has become apparent that 30 Unsafe indoor locations are small structures such as those
minutes is longer than is needed in most situations because the used as golf, beach, sun, rain, school, agricultural, or bus shel-
lightning threat is minimal after 15 minutes.202 In a large-group ters (Figure 5-47). All these structures should be considered
situation, however, where a long evacuation time is required, the unsafe and must be abandoned for a larger, safe building. It is
full 30 minutes is needed to avoid returning people to a field or possible to make such small structures safe, but their protection
stadium too soon, then needing again to send them to safety a must be designed, installed, and approved by a knowledgeable,
few minutes later when the lightning threat returns. In one’s own experienced, bonded insured lightning protection specialist.229
backyard, a person can wait 15 minutes after lightning and Also on this list of unsafe structures are all tents that only pro-
thunder and be quite safe, although a lingering flash can cause vide rain protection but no barrier to lightning.190 Pads on the
return to a dwelling in a matter of a few seconds if necessary. ground surface inside a tent are of no value for lightning protec-
In practice, most airports and other industrial situations use a tion; composition of the tent structure and poles provides no
warning expiration time of 15 minutes, although local high levels protection.
of safety concerns may make 30 minutes preferable. Less than a In less developed countries, dwellings and workplaces may
10-minute wait time is not recommended. There are exceptions be thatched-roofed huts that provide no protection from lightning
to all rules when a large, overhead thunderstorm lingers for hours because they are often ungrounded and made with nonconduct-
over a location.214 In such a situation, any policy may need to ing material.187 Note that it is possible to provide low-cost light-
balance between efficiency and safety of outside workers. 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
SAFE PLACES INSIDE specialists using internationally accepted, scientifically based
There are two reliable places to be safe from lightning: inside a standards to ensure their efficacy.240
large, substantial building and inside a fully enclosed, metal-
topped vehicle. Vehicles191,214,292,399
Fully enclosed, metal-topped vehicles are safe from lightning and
Buildings should be used as a safe place when no large substantial building
Large, substantial buildings where people live and work are very is available. In a study of hundreds of vehicle incidents, there
safe from lightning in more developed countries. Although such were injuries to vehicle occupants in less than one-half the cases;
structures are often hit directly by lightning, fatalities inside them the majority said the experience was frightening, but they
are extremely rare, considering the amount of time spent by emerged unscathed. There have been no documented “electrical”
people inside them. In a study of U.S. dwellings and buildings, injuries to occupants, with the exception of those involving direct
the only lightning-caused fatalities among many hundreds of wiring, such as from older handheld police radios.191 The only
cases were to older adults, very young persons, or persons with unambiguous fatality was an older adult who was startled or
physical or intellectual disabilities who were unable to leave the incapacitated by a nearby flash and drove into oncoming traffic.
dwelling when a fire broke out, almost always at night.187 There Damage to vehicles ranged from minor, such as antennas vapor-
were no fatalities inside offices, schools, or other large buildings. izing, to a few cases of major engine failure and electrical fires;
As a result, adequate safety is attained by directing people to go nevertheless, all passengers escaped the vehicles.
inside a large, substantial building, including a dwelling, rather Unsafe vehicles are those without the safety of fully enclosed
than staying outside.292 metal surroundings that would otherwise act in a manner con-
The protection in modern buildings is provided by grounded sistent with a Faraday cage.99 Safety is provided from a direct
wiring and plumbing, as well as metal structural members inside vehicle strike by the lightning energy traveling across the outside
the buildings that carry the charge of a strike to the structure shell of the metal vehicle and around anyone inside, with
109
subsequent arcing to the ground through bumpers or axles. This is to stress the direct strike by lowering one’s height, because
path may account for the mistaken impression that tires are the the direct-strike situation is scarce.
safety feature; they are sometimes blown apart by current passing
through the vehicle’s metal frame (nearest to the ground) through The Difficulty of Wilderness Situations
the tires. Unsafe vehicles include those with cloth tops (convert- No action will achieve certain safety from lightning in the wilder-
ibles) or fiberglass or plastic bodies. Others include golf carts ness away from a substantial building or fully enclosed, metal-
and four-wheeled conveyances with open sides. Strikes to such topped vehicle. The two approaches to lightning safety in the
vehicles have no defined path to ground, and it is not safe for wilderness are to avoid the risk in the first place and to accept
people to be inside them. Although it is possible to design light- that a lightning risk exists.
ning protection for unsafe golf carts and other open-sided vehi- The amount of time spent by hikers and climbers in multiday
cles, there is no such commercially available product; such an situations is quite small. The more common situation is a hike
approach requires a specific configuration and correct behavior or climb lasting a day or less, often on a weekend day.190 For
of people inside them.119 this common situation, the first approach of avoiding the risk is
Any place outside such a vehicle is as unsafe as anywhere most manageable, since a vehicle or sometimes a sufficiently
else outside.191 Particularly dangerous is step voltage, when a large building is likely to be available at the trailhead. Pay close
person is in contact with both the vehicle and the ground. This attention to the forecast for the day, and avoid the daytime period
situation occurs when stepping into or out from a vehicle when when lightning is most prevalent. Over high mountains of the
lightning strikes the vehicle, because the step potential between western United States, for example, storms start as early as 10 or
the energized vehicle and the ground is very large. Conversely, 11 AM local time, so hikers should be off the higher parts of the
a nearby ground strike will travel to a person with one foot on mountain by that time. Otherwise, postpone the hike to another
the ground and the other in contact with an unaffected vehicle. day. Such an approach does not necessarily preclude hiking on
Other situations outside a vehicle include frequent cases in most days; a study over Colorado’s Rocky Mountains271 showed
parking lots, waiting for buses, and law enforcement and other that no location had lightning on more than one-third of summer
people near but not inside disabled vehicles. days, and almost none during spring and fall months.194,258 There-
A fully enclosed, metal-topped vehicle can be used as a safe fore, hikers can manage the risk by choosing the time and place
place at a school or sports event. If flashes will strike the ground of a day hike. Once the hike is underway, they should pay atten-
MOUNTAIN MEDICINE
at such a venue, it is an easy choice to be inside such a vehicle tion to evolving cloud formations that indicate future lightning,
rather than outside at the same location. stop the hike or climb, and return to safety when indicated (see
An Approaching Thunderstorm and End of Thunderstorm,
earlier).
ALWAYS UNSAFE OUTSIDE281 The pressure of a schedule or other factors may be such that
There are no reliable places outside to be safe from lightning. a wilderness activity will take place despite the possibility of a
Almost complete safety can be achieved by being inside a large, very real lightning threat. Thus, a hiker or climber has accepted
safe building or a fully enclosed, metal-topped vehicle, as the personal risk in the same manner as risks from dangerous
described in the previous two sections. Some recommendations animals, falls, or other natural hazards. Roeder342 analyzed the
continue to emphasize the speculative and ultimately unsuccess- relative risk when no acceptable buildings or vehicles are nearby.
ful safety approaches outside, at the expense of noting the reli- The five mechanisms of lightning injury discussed earlier help to
able safety that is often present in more developed countries in identify actions that can be taken, such as crouching (minimal
PART 1
nearby substantial buildings and fully enclosed, metal-topped value) and staying away from tall objects. The results of the
vehicles. Roeder analysis show a reduction in risk to about one-half the
One of the most important misconceptions of such outdoor full lightning exposure. In other words, following all precautions
safety advice is the expectation that the direct strike is the most does not prevent half the lightning risk. Because the steps must
common mechanism of lightning injury. As described earlier, it be performed correctly, remembered under duress, and reduce
is estimated that only about 3% to 5% of lightning injuries and the risk for death or injury by only one-half, they are not to be
deaths are caused by direct strikes. The result of this mistaken considered when lightning safety can be readily attained by
direct-strike approach is the recommendation that lowering one’s entering a safe building or vehicle.
height is sufficient to be safe, rather than recognizing the other,
more likely mechanisms and using reliable safety plans and
evacuation.
SAFETY OF LARGE GROUPS
The reliable lightning safety approach is to recognize the An individual can respond to lightning threat quickly by going
lightning threat early and go to the known safe places of build- inside a large, substantial building or fully enclosed, metal-
ings and vehicles. The sooner a person reaches the safety of one topped vehicle. In less than a minute in the backyard of a dwell-
of these locations, the sooner the lightning threat is ameliorated. ing, for example, quick action places the person in safety. When
As a result, the everyday lightning situation encountered by an the threat is over, using a rule such as 15 minutes for the cessa-
individual is to anticipate the lightning threat, know where a safe tion of lightning and thunder, an individual can return to the
building or vehicle is located and how long it will take to reach backyard. If the lightning threat returns, a person can quickly go
that location, and complete the plan by reaching safety before back into the dwelling or a safe vehicle until the threat passes.
lightning arrives. For larger crowds, all these steps are more difficult. Steps
Lightning is not predictable in its path to ground, and exactly include accepting that lightning threat is important, knowing how
what it strikes is not predictable with any certainty. Case reports to identify lightning threat, where safe locations are located and
have indicated that the prior speculative advice of seeking a small how long it will take to reach them, recognizing when the threat
tree among larger ones is unreliable. Recent very-high-speed is over, and who makes important decisions.43,105,117,201,258,264,295,384
video shows lightning traveling toward ground in multiple In the case of a neighborhood youth soccer game, for example,
branches. The first branch that contacts the surface of the earth safety can be reached in minutes inside nearby fully enclosed,
is the only important one, whereas the rest dissipate in the air. metal-topped vehicles. When game officials or others make the
Which branches reach the surface appears to be random within decision to go to safety, players and spectators need to go imme-
the flash.354 diately to the cars, vans, or buses. Note that small venues may
Roeder342 examined the relative value of common advice on have rest rooms or concession stands that are likely to be unsafe
outdoor lightning avoidance according to the five mechanisms from lightning, and people in those locations need to be informed
of lightning injury (see Specific Strike Mechanisms, earlier). It to abandon them for the safety of vehicles commonly located in
was found that if every precaution were to be followed, and parking lots around the field (see Buildings section of Safe Places
some are quite difficult, only a 50% reduction in risk would be Inside, earlier). At a somewhat larger school sporting event,
achieved. The other 50% of the time would result in an injury including practices, there are likely to be nearby lightning-safe
or fatality. As mentioned, one of the least effective approaches large buildings. Sports and custodial staff need to be informed
110
to leave doors unlocked or be available to open doors when accept a long wait. Appropriate signage or inclusion of lightning
111
A
B
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.)
MOUNTAIN MEDICINE
C
Covered
FIGURE 5-48 A, Natural protection zone of a stand. B, The effect of stand
Franklin rods disguised as flagpoles. C, The added effect of a catenary
PART 1
Covered stand
Covered stand
FIGURE 5-50 Use of catenaries to protect several stands. (Redrawn FIGURE 5-52 Open field—a properly installed network of overhead
from Crowd protection strategies: Experience from the Sydney cables that can double for movable cameras can also provide adequate
Olympic Games, 2000. Presented at International Conference on Light- protection. (Redrawn from Crowd protection strategies: Experience
ning and Static Electricity, Blackpool, UK, 2003.) from the Sydney Olympic Games, 2000. Presented at International
Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
112
limitations of present research, and currently debated features reasons. This does not mean the symptoms are imagined, only
113
To separate lightning electrical effects from other etiologies, BOX 5-7 Possible Injuring Forces
it is necessary to obtain relatively recently injured patients (no
more than 6 to 12 months) with an otherwise uncomplicated • Blunt trauma—explosive injury
history. There should be no past history of alcohol or drug abuse, • Structural changes—direct damage
head injury, psychiatric problems, or concurrent medical prob- • Pathway of the injury
lems that cause neuropathic pain or psychiatric symptoms, and • Orifice entry
no blast effect during the injury that would confound investiga- • Flashover—how much goes through versus around
tion of the traumatic effects of lightning. Unfortunately, this • Neurochemical changes
narrows the available participant pool. • Autonomic nervous system effects
• Electrical effects
Experimental Vehicles • Electroporation
Because it is difficult to recruit volunteers, credible animal work • Cellular level mechanical effects
is a reasonable alternative.12,14,208,226,301 Cooper and colleagues107-109 • Cellular level enzymatic effects
have developed a reasonable rat model that demonstrates most • Subcellular organelle damage
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 Awareness of the role of the spinal cord in nociception and
lightning that can reliably reproduce a specific (“standard”) existence of proximally directed neural pathways may provide a
pattern of injury. fruitful connection. Release of humoral transmitters may play a
role. The importance of premorbid personality predisposition is
Equipment Requirements unknown and difficult to measure.
Many hurdles must be overcome in research equipment design, Some note that the neuropsychological constellation resem-
anesthetic choice, animal care, and shock timing and delivery. bles the psychological effects of other syndromes, such as trau-
Monitoring equipment must be electrically isolated from the matic brain injury and the response to autoimmune disorders. It
animal and shocking platform, or the connections may preferen- is possible that the symptom complex represents a “final common
MOUNTAIN MEDICINE
tially transmit the lightning shock to the equipment, not the pathway” of brain injury from many etiologies.17 Box 5-7 lists
animal, clouding the experiment and destroying the equipment. other possible factors yet to be verified.
Some anesthetics are neuroprotective, and others affect cardiac Andrews20,21 and Reisner330,331 have specifically developed
function. Temperature control in anesthetized rats is a significant cogent theories of the psychological injury. To be credible, these
issue. Animals that are studied for neurocognitive injury using theories need to explain several facets, including the constellation
water maze and other behavioral models need a standardized of symptoms, its organicity, symptoms developing over time with
quiet environment, which is not always possible in the cramped some being time-lagged, and the specific underlying organicity
quarters of most animal facilities. In survival or cardiac studies, localizing the injury.
timing of the shock either to target or to avoid the “vulnerable Both theories are similar. Although some current will pass
period” must be done on a statistically predictive basis, because through the brain in any shock, it will often be minute. It is
direct sensing of the specific targeted cardiac cycle would result probable that a chemical generated in the current pathway will
in damage to the equipment. affect the brain; a likely substance is cortisol. The interaction
PART 1
114
This development is paralleled by extension of waveform fre-
115
and electrical wiring in the walls, or within fully enclosed, metal- Availability of safe versus unsafe buildings and vehicles is
topped vehicles.* Although fatalities in these locations are rare important in understanding data that may be collected in less
in developed countries, multiple injuries per incident continue developed areas of the world. It is important that related casualty
to occur in developing countries, where there may be no sub- data be collected concerning activity, location, gender, age,
stantial buildings or metal vehicles for miles in any direction. nearby structures, and other issues related to fatality and injury
Small structures are always problematic, so recommendations data, in order to separate the influences that have been outlined
stress staying away from them, although it is possible to make here and in Roeder’s work.339 Such information can be used to
them safe in certain situations.229 A related question is the develop relevant safety recommendations and strategies.
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.
LIGHTNING DETECTION AND
People may now spend more of their time inside safe buildings DATA APPLICATIONS
and vehicles than in the past. Although social data are extremely
difficult to quantify, knowing the answers may explain a portion
DETECTION
of the steady decrease in lightning fatality rates in developed Cloud-to-ground lightning over the United States has been
countries studied in recent years.189,198 detected and located in real time since the late 1970s. Pulses
In less developed regions, safe buildings and vehicles are from lightning in the very low frequency (VLF) and low fre-
not available to many people much of the time. Lack of such a quency (LF) range that propagate along the earth are used to
safe place nearby is a likely contributor to the higher lightning detect and locate return strokes in cloud-to-ground flashes. Such
fatally rate in such regions compared with more developed sensors can also locate distant lightning in the VLF range because
countries.189 signals propagate thousands of kilometers between the Earth and
ionosphere.113
Safe Distance to Lightning The U.S. National Lightning Detection Network has gone
Real-time cloud-to-ground lightning data have been available through several stages of improvements to combine direction
across the United States since 1989, and monthly maps have been finding and time-of-arrival location methods. Networks with
MOUNTAIN MEDICINE
compiled.112,194 Similar regional or national lightning detection some or most of the NLDN capabilities operate in real time in
network data are also available to a varying extent in many other more than 40 countries; most are owned and operated by national
regions of the world, and a global lightning data set is becoming meteorologic services or electric utilities. The NLDN has been
accessible everywhere.122 These data sets have been considered operating continuously since 1989 and has become the bench-
in some situations for determining the distance between flashes mark for cloud-to-ground lightning detection; typical distances
and the time of day and year when flashes occur.202 between its sensors are 300 to 350 km (180 to 210 miles). NLDN
How long a lead time to seek safety is needed for the general has been calibrated by rocket-triggered lightning, tower strikes,
public, at airports, sports events, and other locations? The lead and camera studies to determine location accuracy over the
time includes identifying the safe places that are nearby and the contiguous United States of 300 to 500 m and flash detection
time to reach them. What amount of risk is acceptable for each efficiency exceeding 90%.45,113,145 The NLDN also provides polarity
application? For example, a munitions depot has no tolerance for and peak current and measures the quality of each flash location.
any direct lightning strike, whereas other situations accept more Approximately 70% of the multiple-return strokes within a cloud-
PART 1
lightning exposure in exchange for economic efficiency. to-ground flash are also located by the NLDN, and half of cloud
The role of cloud lightning in the warning process is also not flashes contain pulses that are strong enough to be detected and
fully understood. Does an overhead flash without a cloud-to- located.113
ground flash demand the same response? What are the safe Direction finding and time-of-arrival methods have been com-
distances to anvil lightning? With development of total lightning bined into an advanced method that allows global coverage to
detection, it is becoming possible to address these questions in detect lightning over extremely long distances.121 The Global
a more systematic way.123 Lightning Dataset GLD360 achieves 70% cloud-to-ground flash
Thunder distancing is often recommended for safety when detection efficiency with a horizontal location accuracy of 2 to
lightning detection network data are not available. Few if any 5 km (1.2 to 3.1 miles). Several lightning detection satellites make
studies of thunder have been made in the last few decades, so twice-daily or regional passes; the new GOES-R lightning sensor
audibility of thunder is not well understood from the practical scheduled for launch in 2016 will cover much of the western
viewpoint of lightning safety. The issues involved are the normal hemisphere at an expected 8-km (5-mile) resolution.
distance that thunder can be heard, effect of nearby noise on In addition to cloud-to-ground lightning detection networks,
that distance, role of cloud lightning in producing thunder to its detailed cloud lightning can be mapped by regional very high
use in warnings, transmission velocity of thunder, and relation- frequency (VHF) networks that use direction finding and/or time-
ship of hearing thunder to the actual lightning threat.339 of-arrival techniques over line-of-sight distances.122,185,235-237,257
These networks track the horizontal branching associated with
Demographics cloud-to-ground flashes, and some provide vertical resolution.
Lightning fatality and injury rates are quite well known in devel- Such cloud lightning networks have closer spacing between
oped countries. The global impact of lightning, however, is not sensors than does the NLDN, because they use line-of-sight
well investigated. Lightning casualty data are beginning to be detection in the VHF range. Some of the cloud flashes seen by
collected systematically in some very populous countries, but these networks are immense and have major implications for
data collection methods are in early stages and will need to be lightning safety. One cloud flash in Texas was measured to have
established over longer periods.333 a continuous horizontal channel measuring more than 300 km
Global lightning impacts were first estimated by Holle and (180 miles) in length and lasting 5.7 seconds.244
López197 to be 24,000 deaths and 240,000 injuries annually around Continued deployment of larger global and smaller regional
the world. This estimate is based on minimal or no data from networks has occurred beyond the medium-area coverage of
Africa, Southeast Asia, and India, where lightning casualty rates wide-area VLF/LF networks. These technologies indicate the
appear to be quite high and flash densities are coincidentally need for different techniques or frequency ranges to meet differ-
often large. Another estimate is 6000 deaths and 60,000 injuries ing demands for lightning information.113
per year globally.59 Local organizations examining lightning are
being established.
APPLICATIONS
The first operational U.S. lightning detection network was de
veloped for early recognition of lightning-caused fires. Eventu-
*References 43, 105, 117, 119, 120, 187, 201, 264, 292, 384. ally, large networks were established to detect cloud-to-ground
116
lightning across the western United States, Canada, and Alaska. and shape; location of frontal boundaries; and when excessively
117
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pocampus. Proc Natl Acad Sci U S A 2001;98(22):12320–2. recreation. J Athl Train 2013;48(2):258–70. errata 38(1):83.
353. Saraive ACV, Campos LZS, Williams E, et al. High speed video and 385. Wankhede AG, Agrawal V, Sariya DR. An injury subjacent to lac
electromagnetic analysis of two natural bipolar cloud-to-ground ornament in a case of lightning. Forensic Sci Int 2009.
lightning flashes. J Geophys Res Atmos 2014. 386. Watanabe N, Inaoka T, Shuke N, et al. Acute rhabdomyolysis of the
354. Saraiva ACV, Saba MMF, Krider E. High-speed video observations of soleus muscle induced by a lightning strike. Skeletal Radiol 2007;
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355. Saukko P, Knight B. Forensic pathology. 3rd ed. Arnold; 2004. p. nomic failure: Coincidence or causally related? J R Soc Med
336–7. 1991;84(11):687–8.
356. Scholz T, Rippmann V, Wojtecki L, et al. Severe brain damage by 388. Weiss KS. Otologic lightning bolts. Am J Otolaryngol 1980;1(4):
current flow after electrical burn injury. J Burn Care Res 2006; 334–7.
27(6):917–22. 389. Wetli CV. Keraunopathology: An analysis of 45 fatalities. Am J Foren-
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358. Schwartzman R, Kerrigan J. The movement dosorder of reflex sym- 390a. Wilbourn AJ. Peripheral nerve disorders in electrical and lightning
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117.e7
PART 2
A warm body has long been recognized as one of the primary substantial vasoconstriction and shivering before dangerous core
conditions of human life. Although humans have physiologic, hypothermia develops. In addition, without this feed-forward
intellectual, and cultural capabilities that equip them to maintain input, when large thermal stresses are encountered, greater devi
viable body temperatures under many climatic conditions, ations in core temperature would be necessary to elicit sufficient
thermal extremes, heavy exercise, and injury can rapidly lead to restorative responses.
dangerous internal temperatures. For a physician who is operat Figure 6-3 illustrates some of the concepts that relate to the
ing in primitive circumstances, maintaining or restoring a patient’s thermoregulatory system and are discussed in this chapter. Under
body temperature can require quick action and ingenuity, both normal conditions, body temperature is relatively constant over
of which are aided by an understanding of the physiology of a range of ambient temperatures, as depicted by trace “a.” The
temperature regulation. breadth of this range of ambient temperature is called the range
Because the thermal environment can be extremely compli of normothermia. The midpoint of this range can be conveniently
cated and the thermoregulatory system of humans is complex, called the regulated temperature, which is shown by the dot in
making decisions about body temperature maintenance in the trace “a.” Toward the upper and lower ends of trace “a,” the core
field can be difficult. This chapter is designed to aid in the temperature inflects up and down. These inflections represent
decision process by providing a basic understanding of the rela ambient temperature extremes at which the regulation begins to
tionships among the ambient thermal environment, thermal char fail. Altered core temperatures can also accrue when there are
acteristics of the body, and physiologic systems that govern alterations in the regulated temperature. Such alterations could
human thermoregulation. First, some overall concepts of tem be caused by the presence of bacterial toxins (e.g., fever) or
perature regulation are reviewed, as well as a way to conceptual starvation, which would cause increases (trace “b”) or decreases
ize the system. Second, the range of normal body temperatures (trace “c”) in the regulated temperature. In addition, under
is covered, along with the consequences of higher and lower various conditions, the effector responses can become compro
body temperatures. Third, methods and potential pitfalls of moni mised, which leads to decreases in the ability to defend against
toring body temperature are outlined, after which the physical low temperatures (dashed line at “d”). This could indicate a
factors that affect heat flow are discussed. Fourth, the neuronal problem with metabolic stores, or high temperatures (dashed line
systems involved in processing thermal information (i.e., sensa at “e”), which may indicate dehydration. Various combinations
tion, integration, and output) are reviewed, followed by a detailed of regulatory changes and altered effector responsiveness occur
description of the effector organ responses involved in the main in conjunction with many threatening situations.
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
BASICS OF CORE TEMPERATURE
capabilities of the thermoregulatory system are noted. In this Typical measurements of core temperature provide a good esti
chapter, when values are given for “a person,” they refer to a mate of the temperature of critical internal organs and are quite
70-kg (154-lb) man. 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)
CONCEPTUALIZING THE and 37.1° C (98.9° F). Core temperature is vigorously defended
by the thermoregulatory system. At low environmental tempera
THERMOREGULATORY SYSTEM tures, regional heterothermy that results from peripheral vaso
Humans are homeotherms and as such are capable of maintain constriction forms an important aspect of this defense. The
ing a relatively constant body temperature across a wide range lowered skin temperature decreases the thermal gradient from
of ambient temperatures. Such constancy is attained through the the skin to the environment and thus decreases heat loss. At
use of behavioral processes that involve maintaining or searching cooler temperatures, there can be a large amount of peripheral
for a preferable environment and physiologic (autonomic) pro tissue that is well below core temperature, which leads to a major
cesses such as dilation of the skin blood vessels, sweating in the decrease in the overall heat content of the body. A nude human
heat, and shivering in the cold. Figure 6-1 provides an overview resting at 35° C (95° F) or 20° C (68° F) exhibits similar tempera
of this process.38 Information about body temperature is inte tures at various locations within the core. However, because of
grated by central nervous system (CNS) structures, which elicit decreased temperatures in the outer shell, a nude person resting
efferent neurogenic responses to correct any changes. Increases at 20° C will have a total heat content that is about 200 kilocalo
in body temperature elicit efferent neurogenic cutaneous vaso ries (kcal) lower than when resting at 35° C.197 If the peripheral
dilation and sweating to increase heat dissipation. Conversely, vessels were suddenly dilated, an immediate drop in core tem
decreases in body temperature elicit cutaneous vasoconstric- perature of about 3.5° C (6.3° F) would result. Because of local
tion (decreased heat dissipation) and shivering (increased heat and systemic influences of temperature on skin blood flow, this
generation). type of extensive vasodilation can happen in a wilderness
Figure 6-2 emphasizes how these responses are controlled— medicine setting if a hypothermic individual is rapidly rewarmed
via negative feedback systems with a primary feed-forward input using surface rewarming methods. In a hypothermic individual,
from skin sensors that monitor ambient temperature.106 The feed- the discrepancy between core and shell temperatures could
forward input from the skin allows for the elicitation of thermo be considerably greater and could result in a dangerous postdila
regulatory responses without an “error signal” from the primary tion drop in core temperature. Such an extensive vasodilation
regulated variable, core body temperature.148 Thus, core tem would also result in a large drop in peripheral vascular resistance,
perature can remain relatively constant under widely varying which would put the individual at risk for dangerous hypoten
environmental conditions. This is particularly helpful in cold sion. Therefore, such methods should be used with caution
environments, where decreases in skin temperature can elicit while carefully monitoring a patient’s vital signs. A method for
120
occur under certain, specialized “man-made” conditions, such as
CHAPTER 6 Thermoregulation
(−) ↑ Heat dissipation during surgery.14
↑ Internal temperature
Cutaneous vasodilation Although an abnormal core temperature is often a signal that
↑ Skin temperature
Sweating “something is wrong,” it is not a very specific signal. A variety
A of conditions can lead to core hyperthermia or hypothermia.
CNS Under some circumstances, the central neural mechanisms that
regulate body temperature may be defending an altered core
POAH 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
↓ Heat dissipation “uncompensable heat stress,” whereas heat exposure in which
↓ Internal temperature (−) Cutaneous vasoconstriction body temperature can be regulated is referred to as “compen
↓ Skin temperature ↑ Heat generation sable.” Finally, CNS control of body temperature could be
Shivering deranged as a result of substance abuse, extreme temperatures,
B side effects of prescription drugs, or other factors. When inter
FIGURE 6-1 Schematic overview of the integrative control of thermo-
preting a particular core temperature, it is important to evaluate
regulation in humans. As shown at A, an increase in internal and/or all these alternatives. Accidents in the wilderness often involve
skin temperature is relayed by neural signals to the central nervous many aspects of thermal balance being compromised, and an
system (CNS) nuclei involved in thermoregulation (primarily the preop- altered body temperature is likely.
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 CONSEQUENCES OF ALTERED
shown at B, a decrease in internal and/or skin temperature is sensed
by the CNS and results in increased cutaneous vasoconstriction
CORE TEMPERATURE
(decreased heat dissipation) and shivering (increased heat generation). When tissue temperatures change, there are immediate and
(From Charkoudian N: Skin blood flow in adult human thermoregula- important effects on metabolism as well as on other physiologic
tion: How it works, when it does not, and why, Mayo Clin Proc 78:603- mechanisms. This effect is characterized by an exponential equa
612, 2003.) 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
Disturbance (Ta) 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
Sensor (18° F), these effects can be calculated with the following
Feed-forward equation197:
signal R 2 = R 1 × Q10 ( [ T2 − T1 ] 10 )
Regulated
Controlled where R2 and R1 are the two rates of physiologic response; T2
Controller variable
system
(Effectors) (Tcore) and T1 are the two temperatures; and Q10 is the increase in rate
(Body mass) caused by a 10° C (18° F) increase in temperature. Thus, if fever
or strenuous exercise were to increase body temperature by 2° C
Sensor (3.6° F), basal metabolic rate would be increased by 22%.
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, °C °F
Crawshaw LI, Nagashima K, et al: Concepts to utilize in describing 39 (102)
thermoregulation and neurophysiological evidence for how the system b
Core temperature
121
Within the normal range of body temperatures, higher tem monitor skin temperature in cold environments. A second elec
peratures favor speed at the expense of tissue resources, whereas tronic thermometer with a wide temperature range is important
lower temperatures conserve resources. Although both high and for measuring skin temperature, as a backup for the standard
low temperature extremes pose a threat to humans, increased clinical thermometer, and for measuring the temperature of other
temperatures greatly accelerate the development of serious com objects such as liquids. Alternate probes and spare batteries for
plications in many wilderness medical situations and therefore both instruments are essential.
pose a much more immediate danger. A deviation of about 2° C Tympanic infrared (IR) radiometers are often used in hospital
(3.6° F) above or below normal core temperature is well tolerated settings. However, even in this relatively predictable environ
by the various regulatory systems of the body, but a discrepancy ment, some controversy exists regarding their ability to assess
of 3° C (5.4° F) begins to disrupt these systems, including those core temperature accurately.160,179 These instruments monitor
involved in temperature regulation. At this level of deviation, if the electromagnetic radiation that emanates from the ear canal;
there is no intervention, physiologic problems compound very various manufacturers make use of different and complicated
rapidly. electronic circuitry to produce a temperature display. An advan
Core hypothermia can also be dangerous to human survival tage is that the reading takes only a few seconds,36 but questions
and recovery from injury. Core temperatures of 34° to 36° C (93.2° remain regarding the overall accuracy of the measurement dis
to 96.9° F) disrupt many important physiologic functions, which, played. In a laboratory situation in which the auditory canal is
taken together, may significantly affect patient outcome. Such plugged with a sponge and the probe measures only radiation
mild hypothermia impairs recovery from surgical procedures as that emanates from the tympanum, IR tympanic thermometry
a result of factors that include impaired peripheral blood flow provides an excellent estimate of the core temperature.203 In
and oxygen availability, increased possibility of cardiovascular clinical settings, the results are less consistent. In one study, IR
complications, decreased antibody and cellular immune defenses, tympanic thermometry produced core temperatures that were
impaired coagulation, and increased metabolic expenditure for much more variable than rectal temperatures. Even after correct
heat production.59,70,118,123 In most situations, it is important to ing for the higher rectal values (0.5° C [0.9° F]), tympanic measure
maintain the patient at normothermic levels. ments still inaccurately displayed one-third of the temperatures
Traumatic brain injury can be present in wilderness accidents, that were more than 37.7° C (99° F). An extended training program
and it may be accompanied by unregulated hyperthermia. did not significantly alter the accuracy of the readings.170
Heightened temperatures can exacerbate cerebral inflammation In one instance, a child who arrived at an emergency depart
and lead to increased neuronal damage.224 There is current inter ment (ED) presented with tachycardia and skin vasoconstriction.
est in invoking mild hypothermia to minimize damage to the CNS Separate tympanic IR thermometers gave core temperatures of
COLD AND HEAT
after neurologic injury.162 However, when this approach is used, 36.4° and 37.6° C (97.5° and 99.7° F); the rectal temperature was
care must be taken to deal with the side effects mentioned determined to be 42.2° C (108° F)182. Alternatively, in a hospital
previously.171 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
MONITORING TEMPERATURE OF THE or the rectum.178
The potential benefits of a continuous and easily applied core
CORE AND OTHER SITES temperature monitor have led to repeated attempts to validate
The overall status of the thermoregulatory system is determined liquid-crystal thermometers, which are typically placed on the
PART 2
by measuring the core temperature. This can be done at a head or neck surface. Unfortunately, the temperature readings
number of sites with several types of instruments (i.e., thermom produced by this method are not reliable.12,130 Because these
eters). In the following paragraphs, the relative merits of locations measurements are compromised by the thermoregulatory vascu
and different types of thermometers are discussed. 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.
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
MEASUREMENT SITES
measuring body temperature, in order of increasing invasiveness, Although the deep internal temperatures of normothermic
include the forehead, axilla, oral cavity, tympanum, rectum, humans are reasonably similar, no specific anatomic site repre
esophagus, bladder, and pulmonary artery. There is no clear-cut sents the “official” core temperature. The temperature at each
choice regarding the best site to monitor; particular situations location is a consequence of a combination of the local metabolic
demand different techniques. Thermometers that have been rate, local perfusion rate, proximity to the outer shell, and prox
employed clinically include mercury-in-glass thermometers imity to other locations that have differing rates of metabolism
(which are now obsolete), electronic thermometers, tympanic and perfusion. Nevertheless, because of the generally high
radiation thermometers, and liquid-crystal thermometers. What overall rates of tissue perfusion in mammals, deep core tem
ever instrument is used should have an accuracy of ±0.1° C peratures rarely differ by more than 0.5° C (0.9° F). The tempera
(0.2° F). The handheld electronic thermometer is a good choice ture of the pulmonary artery is a good reference temperature for
for field emergencies. 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
TYPES OF THERMOMETERS surgical or laboratory setting by trained personnel, esophageal
The handheld electronic thermometer has replaced the mercury- and tympanic temperatures are essentially the same as the tem
in-glass thermometer, and it has been widely used for many perature of the pulmonary artery,178,193 whereas rectal tempera
years. Electronic thermometers can use thermistors or thermo ture averages about 0.4° C (0.7° F) lower, and axillary and oral
couples as sensors, have the requisite degree of accuracy, and temperatures are about 0.2° C (0.4° F) and 0.4° C (0.7° F) lower,
are flexible in application. Although an equilibration time of 1 respectively.12,178
minute is specified for the typical probe, this is largely because Although esophageal temperature is somewhat difficult to
of the need for a stiff casing for ease of insertion; smaller probes obtain, this is the site that is most likely to reflect accurately the
are available that can equilibrate in seconds. The digital display temperature of the pulmonary artery. Measurement at this loca
of these instruments reduces errors, and the probes can be left tion accurately follows changes in core temperature and is rea
in place for continuous monitoring. A quality instrument with a sonably noninvasive. For placement, the probe is lubricated, and
wide range of interchangeable probes is important. Even then, a small amount of local anesthetic is applied. It is then passed
these devices are subject to the usual problems inherent with via a nasal passage into the distal portion of the esophagus to
electronic instruments and rarely have a range low enough to the level of the heart. The probe can be moved up and down
122
slightly to obtain the highest temperature. Although this proce temperature could be made by measuring and weighting the
CHAPTER 6 Thermoregulation
dure is routinely used in physiology experiments, it is somewhat temperature of four skin sites as follows:
unpleasant for conscious patients, particularly those with a 0.3 Chest + 0.3 Arm + 0.2 Thigh + 0.2 Leg
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 PHYSICAL FACTORS THAT GOVERN
has long been controversial. Because the tympanic membrane is HEAT EXCHANGE: THE HEAT
highly vascular and supplied by branches of the external and
internal carotid arteries, it should be an ideal site. Nevertheless,
BALANCE EQUATION
many studies have indicated that tympanic temperature is affected The physical laws that govern heat transfer determine the net
by ambient temperature and local facial cooling.193,223 energy flux into or out of the body.49,85,142,151,197 The heat balance
In steady-state conditions, rectal temperature is a good index equation is a convenient method for partitioning and quantifying
of core temperature.248 However, when the heat content of the the flow of energy between the environment and the body. A
body or of the internal thermal compartments is in flux, rectal high rate of metabolic heat production is critical for maintaining
temperature changes more slowly than temperatures measured a constant body temperature in mammals. This is represented by
in other commonly used sites.178 There is a thermal gradient total heat production (Htot) on the left side of the following equa
along the rectum, so all measurements should be made at a tion. For a person whose body is at thermal equilibrium, the
standard depth; 4 cm (1.6 inches) is recommended,12 although equation is balanced and given as follows:
in a careful study of different depths, sites less deep than 10 cm H tot = ± H d ± H c ± H r ± H e
(4 inches) showed some systematic differences.121 The higher
temperatures recorded in this region may be caused by a com where Htot is the total metabolic heat production; Hd is the con
bination of low perfusion rates, digestive reactions, and bacterial ductive heat exchange; Hc is the convective heat exchange; Hr
activity, but there is not clear evidence of this.130 For assessing is the radiative heat exchange; and He is the evaporative heat
core temperature during outdoor exercise in the heat, the exchange. Htot is always positive. The various modes of heat
National Athletic Trainers’ Association recommends using only exchange from the right side of the equation can be positive or
rectal temperature.33 A subsequent study and review of the litera negative, depending on the situation. Positive values refer to net
ture also concluded that “rectal temperature is the only suitable heat loss from the body. If the equation does not balance, the
and valid index for the monitoring of body temperature in a field body either loses or gains heat. When the sum of the net heat
setting.”73 exchange through the various channels exceeds Htot, heat content
Oral (sublingual) temperature is an excellent index of core of the body will decrease, and MBT will fall. Alternatively, if Htot
temperature, provided that the mouth is kept closed. The sub is greater than the net heat exchange, heat content of the body
lingual pocket is well perfused by blood flow and responds quite will increase, and MBT will rise.
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
CONDUCTIVE HEAT EXCHANGE
precedes the measurement.12,130 The use of an electronic ther Heat transfer between objects that are in direct contact is called
mometer with a rapidly responding sensor makes this measure conduction (Hd). The direction of heat flow is always from the
ment considerably more accurate and rapid than when it is higher to the lower temperature. Because conduction involves a
performed with a mercury-in-glass thermometer. direct interaction (i.e., contact) between molecules, this type of
Although axillary temperature can reflect core temperature, it heat transfer is minimal except under certain circumstances, such
has a number of negative characteristics and should be used only as when sitting on a cold rock with little insulation. Under such
as a last resort. Axillary temperature is affected by local blood conditions, the heat lost to the rock would be similar to that lost
flow as well as by thermal and nonthermal sweating.12 Changes from the remainder of the body surface by radiation and convec
in core temperature are slow to affect the axillary temperature, tion. Adequate insulation should be placed under patients who
and there is high interpatient variability.178 However, this mea are in contact with hot or cold substrates. The equation that
surement has proved to be particularly useful for assessing core governs heat exchange by conduction follows:
temperature in infants.12,130
kA ( Tsk − Ta )
Hd =
ESTIMATING MEAN BODY TEMPERATURE L
Mean body temperature (MBT) provides a mass-weighted where k is thermal conductivity; A is the area of contact; Tsk is
average of body tissue temperature and thus can be related to the skin temperature; Ta is the ambient temperature; and L is the
the heat content of the entire body. For a severely hypothermic distance between the two surfaces.143
patient, MBT provides a way to gauge the potential fall in core The thermal conductivity of several substances is given in
temperature (afterdrop) after vessel dilation caused by rapid Table 6-1. Note that water has 25 times the conductivity of air
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 TABLE 6-1 Thermal Characteristics of Select Substances
estimates was evaluated for patients undergoing various proce
dures, including cardiac surgery during extracorporeal circula Conductivity Specific Volumetric
tion; these studies included core temperatures as low as 18.5° C (cal • s−1• Heat (cal • Heat Capacity
(65.3° F).122 “Peripheral compartment temperatures were esti Substance cm−1 • °C−1) g−1 • °C−1) (cal • L−1 • °C−1)
mated using fourth-order regression and integration over volume
from 18 intramuscular needle thermocouples, 9 skin tempera Air 0.000057 0.24 0.29
tures, and ‘deep’ hand and foot temperatures.”122 The authors Water 0.0014 1.0 1000
concluded that the estimation of MBT from Burton’s original Granite 0.007 0.2 540
formula27 “is generally accurate and precise.”122 That formula is Muscle tissue 0.0011 0.8 850
as follows: Fat tissue 0.00051 0.5 460
MBT = 0.64 ( Core temperature ) + 0.36 ( Mean skin temperature ) Data from Schmidt-Nielsen K: Animal physiology: Adaptation and environment,
ed 4, Cambridge, 1990, Cambridge University Press; Cossins AR, Bowler K:
Ramanathan174 found that a reasonably accurate estimate of Temperature biology of animals, New York, 1987, Chapman & Hall; and
mean skin temperature could be provided by the temperature of Hodgman CD, editor: Handbook of chemistry and physics: A ready-reference
the medial thigh, and that a very accurate estimate of mean skin 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 For temperatures in the physiologic range and where (Tsk − Ta)
the conductivity of fat tissue. The conduction of heat through a is less than 20° C (68.0° F), several authors have noted that IR
tissue is called thermal diffusivity. This expression is obtained radiation heat exchange is about proportional to Tsk − Ta.18,197
by dividing the thermal conductivity by the product of the density Also, the spectrum of emitted radiation depends on the tempera
and the specific heat. The specific heat of various substances is ture of the object. At physiologic temperatures, the predominant
also given in Table 6-1. Water has particularly high specific heat, wavelengths of emitted radiation are longer (IR), whereas at
as does muscle tissue, which consists mostly of water. However, higher temperatures (e.g., the sun’s surface), the predominant
specific heats can be misleading, so volumetric heat capacities wavelengths are shorter (visible radiation) and can be detected
are also listed in Table 6-1. Although the specific heat of water by the human eye. This difference leads to some important con
is four times that of air, it takes about 3500 times as much heat sequences. The middle IR radiation that is emitted by mammals
to raise the temperature of a given volume of water by 1° C is maximal, regardless of skin pigmentation or the color of cloth
(1.8° F) as it does to accomplish the same feat with a similar ing. However, solar radiation peaks in the visible portion of the
volume of air. For a person in the water, the consequence of spectrum and is differentially absorbed. In other words, dark
these properties is that skin temperature is almost always within clothes absorb more heat from solar radiation than do light
1° C of water temperature, and heat transfer to or from the envi clothes, but both types emit similar amounts of radiation energy.
ronment is greatly facilitated. In cool water during rest, skin Incident radiation can vary drastically under different environ
blood flow is minimized as a result of peripheral vasoconstric mental conditions and may severely tax the body’s ability to
tion. Heat loss is importantly determined by the subcutaneous respond. Heat input from solar radiation on a cloudless day may
fat layer; an average-size fat person with 36% body fat by weight exceed by several times the heat produced by basal metabolism;
begins shivering at a water temperature of about 27° C (81° F), on a cloudless night, there can be a significant net loss of radia
whereas a lean person with less than 10% body fat starts shiver tion to the sky. Under the relatively thermoneutral conditions
ing at about 33° C (91° F).153 noted earlier,20 radiant heat loss accounts for about 45% of the
total heat loss.
CONVECTIVE HEAT EXCHANGE
Convection (Hc) can be seen as the facilitation of conduction EVAPORATIVE HEAT EXCHANGE
caused by the movement of molecules in a gas or liquid. This When water changes state, a large amount of energy is either
movement decreases the functional value of L, which is the absorbed or given off. Evaporation of 1 gram (0.035 oz) of water
denominator in the conduction equation. Convection can be at 35° C (95.0° F), which is the usual skin temperature of a person
COLD AND HEAT
either forced or natural (free). Forced convection results from who is sweating,197 requires the input of 0.58 kcal of thermal
gas or liquid movement caused by the application of an external energy. In the field the preferred cooling measure is to splash
force, such as the movement of a fan or the pumping of a heart. water on the patient, coupled with air fanning.81 Heat absorbed
Natural convection results from density changes that are pro by the evaporation of 100 cc of water will lower body tempera
duced by heating or cooling molecules adjacent to the body. ture by about 1° C (1.8° F). In a neutral thermal environment,
These density changes cause the molecules to move with respect active thermoregulatory sweating does not occur, and evapora
to the body surface. For humans, natural convection predomi tion accounts for only 15% of the total heat loss. Of this, slightly
nates at air speeds of less than 0.2 m/sec (0.7 ft/sec), whereas more than one-half is the result of evaporation from the respira
forced convection is more important at greater air speeds.142 tory tract, with the remainder coming from water that passively
PART 2
The relationships that define heat exchange as a result of diffuses through the skin and evaporates.20
convection can be complicated. They depend on surface tem Although it is unusual, the evaporation term (He) of the heat
perature profiles, surface shape, flow dynamics, density, conduc balance equation can become negative, which means that heat
tivity, and specific heat. Any factor that impedes the movement is being introduced into the body. This occurs during airway
of the boundary layer (i.e., the molecules immediately adjacent rewarming, when water-saturated oxygen is introduced into the
to the body) greatly impairs convective heat transfer. respiratory system at about 43° C (109.4° F). Because the patient’s
Brengelmann and Brown20 have noted that, under relatively body is considerably colder than 43° C, water condenses in the
neutral conditions (Ta = 29° C [84.2° F], wind velocity = 0.9 m/sec airways. For every gram (g) of liquid water that is formed, the
[3 ft/sec]), about 40% of heat loss from a nude human is body heat content increases by 0.58 kcal; the formation of 100 g
mediated by convection. Increases in air or fluid velocity greatly of liquid will increase body temperature by about 1° C.
increase convective heat transfer. Fanning a minimally clothed
patient will greatly augment heat loss in a cool environment.
THERMOREGULATORY NETWORK
A regulatory system requires sensing the controlled variable,
RADIATIVE HEAT EXCHANGE comparing it with an ideal value, and producing an appropriate
All objects at temperatures of more than absolute zero emit output signal. The following sections outline the role of the
electromagnetic radiation. This energy transfer occurs through nervous system in maintenance of a stable body temperature.
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.
PERIPHERAL THERMAL SENSORS
The net heat transfer depends on the absolute temperatures, The entire outer surface of the body (i.e., the skin) is well sup
nature of the surfaces involved, and solar input. Surfaces that are plied with sensitive thermoreceptive structures. Because one
effective absorbers of radiation are also effective emitters of radia destination of the output of these thermoreceptors is the sensory
tion. The idealized “black body” illustrates this property; such cortex, many properties of the receptors can be gleaned from
bodies absorb all and reflect none of the incident radiation. direct experience. Afferent thermal information produces both
Conversely, poor absorbers (e.g., a polished silver surface) are hot and cold sensations, and the cutaneous thermoreceptors
also poor emitters. Heat transfer that results from IR (first-term) demonstrate substantial dynamic sensitivity.9,88 Therefore, a
radiation and solar (second-term) radiation is given by the fol change in ambient temperature can be perceived as “cool” or
lowing equation: “warm” simply because of a change from a previous steady level
of temperature (e.g., moving from a warm room to a cooler
H r = σe sk e a ( Tsk 4 − Ta 4 ) + a(1 + r )s
room), even if the absolute temperature is not objectively “cool.”9
where Hr is the radiative heat exchange; σ is the Stefan-Boltzmann In addition to cortical input that arrives via the medial lemniscus
proportionality constant; esk is the emissivity of the skin; ea is the and the ventrobasal thalamus, the brain receives a large amount
emissivity of the environment; Tsk is the skin temperature (given of thermal information from pathways that synapse in the
in kelvins [K]); Ta is the ambient temperature (given in K); a is reticular area.24 Although cortical thermal input is part of the
the absorptance; r is the reflectance; and s is the solar radiation. sensory information used to reconstruct the external thermal
124
CHAPTER 6 Thermoregulation
40
°C
30
A
Shield Shield 1 sec
40
°C
30
Shield Shield
B
W C W C
Thermocouple
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 receptors appear to be involved in local thermal vasodilation
autonomic regulation of body temperature.55 (below the pain threshold), because stimulation of these recep
The structure, location, and properties of peripheral thermo tors with local application of capsaicin shifts thermal responsive
receptors are well documented. Thermal sensors are free nerve ness of the local cutaneous vasodilator response.214 However,
endings and are categorized as warm or cold. Cold receptors are neurogenic vasodilation in response to whole-body heating does
found immediately beneath the epidermis, whereas warm recep not appear to be affected by acute or chronic local capsaicin
tors are located slightly deeper in the dermis. The hallmark of treatment.39 TRP channels are also involved in activation of
both types of receptors is their extremely high rate sensitivity brown adipose tissue thermogenesis during cold exposure, and
(Figure 6-4). Although the static firing rate of cold receptors is as such have been proposed as a target for weight loss with
usually less than 10 impulses per second, under conditions of capsaicin or capsaicin derivatives.243 As examples of the ubiqui
rapid temperature change, firing rates are often higher by an tous, integrative nature of TRP superfamily, TRPM2, TRPM4, and
order of magnitude. Cold receptors are excited by cooling and TRPM5 respond to warm temperatures and are also involved in
inhibited by warming, and they have static maxima at about 25° C insulin secretion226 and taste.220 However, they are not regarded
(77.0° F); these receptors are active from about 10° C (50.0° F) to as warm receptors for thermal sensation, because sensory neurons
40° C (104.0° F). Warm receptors are excited by warming and do not appear to express those subtypes. In addition to TRP
inhibited by cooling, and they have static maxima at more than channels, some members of the TREK/TRAAK K(2P) potassium
40° C; they are active from about 30° C (86.0° F) to 45° C (113.0° F). channel subfamily also appear to be involved in warmth and
At both ends of the spectrum, more extreme temperatures acti cold perception.7,125,155
vate neuronal responses that are subjectively reported as “cold Psychophysical and physiologic studies indicate that thermal
pain” and “warm pain.”87 receptors are not uniformly distributed across the body surface
Over the past two decades, work with the use of cloning and and that there are many more cold receptors.87 Cold receptors
ion channel characterization has provided insight into molecular are abundant in the face and trunk areas, especially in the lips;
mechanisms of central and peripheral temperature transduction. however, they are less numerous in the feet and lower legs. The
A family of related temperature-activated transient receptor face and fingers have a greater number of receptors that respond
potential (TRP) ion channels is highly sensitive to temperature.35 to warmth.176,219 Threshold temperature for the perception of
Although originally identified in the context of noxious heat thermal sensation follows the anatomic distribution and is not
sensation, TRP channels have been found to be ubiquitous and uniform across the body. The face, particularly near the mouth,
have multiple roles in cardiovascular, metabolic, volume regula is exquisitely sensitive because of a high density of thermal
tory, and many other integrative physiologic mechanisms.61,246 receptors, whereas by comparison the extremities have a lower
In terms of thermal sensation, the cloned receptors TRPV3 density of receptors and therefore poor sensitivity. Other regions
and TRPV4 respond over a range similar to that of the warm of the body are intermediate in sensitivity.217
receptors previously described,80 whereas TRPM8 responds simi Because peripheral thermal input is intimately involved in
larly to the cool receptors. TRPM8 also responds to menthol, regulation of body temperature, heating and cooling different
eucalyptol, and icillin.136,169 TRPV1, TRPV2, and TRPA1 respond body sites can differentially affect the magnitude of the restor
similarly to the heat-pain–sensitive and cold-pain–sensitive ative physiologic response produced. In one study, cooling the
neurons. The heat-pain channels (vanilloid receptor 1 [VR1]) also forehead was found to be more than three times as effective (per
respond to low pH, ethanol, and capsaicin, which is the active unit area) for decreasing ongoing sweating as cooling the lower
ingredient in hot peppers.167 In human skin circulation, the TRPV 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
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
CHAPTER 6 Thermoregulation
and TRPV2 channels may be active within the physiologic range understanding of the systems involved in regulation of body
of temperature.109,172 However, some evidence is contrary to the temperature.139,140,244 In this context, the median preoptic nucleus,
proposal of TRPV1 as a thermosensor.181 medullary raphe region, and dorsomedial hypothalamus have
been identified as important areas for integration of thermo
CENTRAL NEURAL STRUCTURES RESPONSIBLE regulatory signals with cardiovascular, volume regulatory, and
FOR CONTROLLING THE LEVEL OF other related physiologic systems.134,137,148 Other notable advances
include demonstration of the relative independence of popula
BODY TEMPERATURE tions of neurons that control separate effector systems107,135,247 and
As mentioned previously, the brain is capable of accurately elucidation of a pathway that conveys cold-sensitive afferent
regulating body temperature under a wide range of conditions. (feed-forward) information to the hypothalamus.149
Although almost all portions of the CNS can potentially be Figure 6-7 presents a schematic model for regulation of body
involved, the most critical neuroanatomic structures for thermo temperature, with credit to many others in the field besides the
regulation include the spinal cord, brainstem, hypothalamus, and authors listed. For ease of understanding, many aspects of the
septum. The preoptic area and anterior hypothalamus are par system’s complexity have been simplified or modified. The mul
ticularly important for both integration and sensing of internal tiple inputs to this system not shown include those mentioned
temperature.15,17,84 Recent advances in neurophysiologic, neuro in the previous discussion of central thermoreceptors (e.g.,
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 cally active organs is convectively distributed to portions of the
covered later in this chapter (e.g., time of day, hormone levels, body where less heat is produced. More frequently appreciated
pyrogen titer, oxygen concentration of blood). In addition, ther are alterations of blood flow patterns that increase or decrease
moreceptors from many locations in the body provide input to the overall thermal conductivity of the body during exposure to
this system. The key sensing elements of Figure 6-7 involve the hot or cold environments, respectively. Some of these alterations
peripheral warm and cold receptors and the central thermodetec in conductivity result from the preferential shunting of peripheral
tors, the latter depicted by solid cell bodies and bold axons. blood flow superficial or deep relative to the subcutaneous fat
Peripheral input originates in the skin and enters the CNS via the layer. Fat has about one-half the tissue conductivity of muscle
spinal or trigeminal dorsal horns; this information ascends to both and typically has a much lower rate of blood perfusion. Never
the midbrain and the thalamus. The thalamic neurons that receive theless, shunting blood away from major portions of the body is
thermal information project to the sensory cortex and subserve at least as important for determining overall conductivity as the
sensory integration and localization of peripheral thermal infor conductive property of the tissue itself. For example, during
mation. They are also likely involved to some degree in learned immersion in cold water, muscle accounts for about 90% of the
behavioral thermoregulatory responses. total tissue insulation of the forearm.60 Thus, directing blood away
Thermal afferent pathways reaching the midbrain are involved from poorly insulated (and more highly conductive) regions
in the feed-forward aspect of regulation.149 Axons of the cell reduces heat loss and preserves core temperature.
bodies in the midbrain synapse on cells in the midline subregion The cutaneous microcirculation is the primary circulation
of the preoptic area. These preoptic cells receive excitatory input responsible for controlling heat transfer to the environment.37,38,101
from peripheral warm and cold sensors, but they inhibit the cells Microcirculatory units contain capillaries, arterioles, venules,
on which they synapse. The systems that subserve heat loss and metarterioles, and arteriovenous anastomoses (AVAs). The skin
cold defense appear to inhibit each other reciprocally and receive has a compliant vascular bed, with the majority of cutaneous
output from a unitary integrating system. However, as mentioned blood volume contained in a plexus of veins just under the
previously, the systems are actually functionally separate to a surface. The slow linear velocity of flow in this venous plexus
large degree. In the schema of Figure 6-7, both systems depend allows for substantial heat transfer to occur between the skin and
on inherently warm-sensitive cells that have a high spontaneous environment, particularly when skin blood flow is elevated.186
firing rate at normal body temperatures. These cells inhibit the The major systemic neural control of skin blood flow occurs
succeeding neurons, but the connections are such that, in a cold through two branches of the sympathetic nervous system: nor
environment or when the body temperature is below normal, adrenergic vasoconstrictor nerves and a non-noradrenergic active
cold defense responses are disinhibited and heat loss responses vasodilator system.37,101 The vasoconstrictor system exhibits tonic
COLD AND HEAT
are further suppressed. The opposite would occur in a warm activity and is responsible for most of the smaller, daily changes
environment or when the body becomes excessively hot. in skin blood flow that occur during minor changes in environ
The output of these systems under different conditions is ment or activity.194 This system is also responsible for the dramatic
illustrated in the panels below the neuroanatomic diagram of decreases in skin blood flow that occur with cold exposure, when
Figure 6-7. The middle graph illustrates the situation for a person skin blood flow can approach zero. Vasoconstrictor nerves
with a body temperature of 37° C (98.6° F) in a thermoneutral release norepinephrine, which interacts primarily on the vascular
environment. At 37° C, both systems are inhibited, and there is smooth muscle with α1- and α2-adrenergic receptors to cause
no effector response. If the body cools or becomes warmer, the vasoconstriction. Glabrous skin (i.e., palms, lips, soles) contains
inherently temperature-sensitive neurons disinhibit either the numerous AVAs and is innervated only by sympathetic vasocon
PART 2
cold defense or the heat loss system. The graph on the left illus strictor fibers. Therefore, all the dramatic changes in skin blood
trates the action of the feed-forward cold neurons in a cold flow that can occur in these regions are controlled by changes
environment. Although the inherently thermosensitive neurons in vasoconstrictor neural activity.
do not change their firing rate as a result of a local temperature Nonglabrous (i.e., hairy) skin is innervated by sympathetic
that stays constant, input from the peripheral cold-sensitive vasoconstrictor and vasodilator fibers and contains few AVAs.
pathway disinhibits the cold defense system. A similar situation— In contrast to the vasoconstrictor system, the active vasodilator
but in reverse—occurs when a person encounters a warm envi system in human skin does not exhibit tonic activity and is only
ronment; this situation is depicted in the right graph. The error activated during increases in internal temperature. The vasodila
signal or output driving force is shown as the difference between tor system operates through cholinergic nerve co-transmission.
the horizontal dashed line and the effector output at a given Although several candidate vasodilators have been studied, the
body temperature. The system is extremely accurate, and the specific vasodilator substance has not been identified; vasoactive
error signal created by peripheral feed-forward input is usually intestinal polypeptide is a likely candidate.8,235 Additionally, nitric
just sufficient to counteract the sensed disturbance and to main oxide has an important role in active vasodilation, contributing
tain body temperature at a constant level. about 30% to the total neurogenic vasodilation seen during
In addition to autonomic responses that are organized and whole-body heat stress.111,112 Active vasodilation accounts for 80%
transmitted from the brainstem (e.g., sweating, shivering), various to 90% of the increases in skin blood flow during heat stress,
complex whole-animal responses are also activated by the ther with about 10% to 20% caused by withdrawal of tonic activity
moregulatory system. Postural reflexes (e.g., huddling, sprawling) of vasoconstrictor nerves.101 Thermoregulatory vasodilation can
and learned behavioral thermoregulatory responses are initiated result in skin blood flow values up to 8 L/min and 60% of cardiac
by cold and warm error signals. Although the mechanism is output, making the skin circulation extremely relevant to systemic
not entirely understood, appropriate behavior reduces the error hemodynamics, particularly during severe heat stress.37,186
signal and activates the reward system, which likely culminates Cutaneous vascular responses to temperature are affected by
in the release of dopamine in the nucleus accumbens of the excessive exposure to ultraviolet B (UVB) radiation. Moderate
septum by cell bodies located in the ventral midbrain.96 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
EFFECTOR RESPONSES disappeared.164
VASCULAR ADJUSTMENTS
Cardiovascular responses to thermal stress are largely geared CENTRAL SIGNAL
toward changing blood flow to the skin surface, thereby increas Vascular changes are bioenergetically the least costly thermo
ing or decreasing convective heat transfer to the skin and to the regulatory autonomic effector response. Because of the high
external environment, as appropriate for the internal and external sensitivity of the vasomotor system, ambient temperatures
thermal environments.20,37,38,101 In general terms, an important between the thresholds for sweating and shivering are often
function of the circulatory system is to maintain a relatively referred to as being in the zone of vasomotor regulation, or the
homogeneous internal body temperature. Heat from metaboli “neutral zone” of human temperature regulation.194 In dogs,
128
manipulation of hypothalamic temperature in this range confirms
CENTRAL SIGNAL
CHAPTER 6 Thermoregulation
a high level of vasomotor activity between the thresholds for By controlling the local milieu at different skin sites, it has been
the activation of panting and shivering.86 Within the vasomotor possible to separate the central thermoregulatory drive to sweat
zone (i.e., skin temperatures of 33° to 35° C [91.5° to 95.1° F]), glands from local effects on the glands themselves. The central
core and skin temperatures linearly combine to control skin thermoregulatory system provides a proportional output that is
blood flow. Skin blood flow responds accurately and rapidly to influenced by both internal and whole-body skin temperatures.
changes in skin temperature, which leads to a very stable core Per each degree increase above thermoneutral values, internal
temperature.21,194 temperature is about 10 times as important as mean skin tem
Although most peripheral arterioles are well supplied with perature for eliciting an output to the sweat glands.144,146
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
LOCAL MODULATION
in other areas; immersing the feet in cold water thus leads to Local effects are also important for determining the output of
marked vasoconstriction in the hands and forearms, but not in sweat glands. Sweat gland temperature exerts a multiplicative
the abdomen or upper arms.78 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
LOCAL MODULATION sweating.145
In addition to systemic (whole-body) stimuli that elicit cutaneous Moderate sunburn disrupts evaporative cooling. This effect is
vasoconstriction and vasodilation through changes in whole- locally mediated and involves decreases in both responsiveness
body temperature, local temperature of the skin can substantially and capacity of the sweat glands.163
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
METABOLIC ADJUSTMENTS
tion when temperature is held at 42° to 44° C for 25 to 30 Heat is an inevitable byproduct of the inefficiencies of the body’s
minutes. This local warming response occurs in two phases: an metabolic reactions. When oxidizing foodstuffs to carbon dioxide
initial peak that occurs within the first few minutes of heating and water during production and transport of adenosine triphos
and that depends on local sensory innervation, and a slower, phate (ATP) to the functional systems of the cells, about 75% of
prolonged phase that reaches a plateau at 25 to 30 minutes. The the original chemical potential energy is given off as heat. With
plateau phase of vasodilation largely depends on nitric oxide the exception of chemical energy sources that are excreted or
(40% to 70%, depending on the population studied).37,101 used to perform physical work, the remaining 25% of the original
Local cooling can decrease superficial cutaneous blood flow energy is also converted to heat when ATP is used in the numer
to almost zero.38,101 Although vascular beds on the skin surface ous metabolic reactions of the body.198 Mammals, compared with
constrict in response to cooling, other vascular beds dilate when poikilotherms such as reptiles or fish, use much more ATP to
cooled.66,67 The specific response to cold shown by cutaneous maintain ionic and electrochemical balances of the cells,216 as
vessels follows from the observed distribution and properties of well as for other necessary functions. This leads to greatly
the α-adrenergic vascular receptors. Local temperature affects the increased metabolic heat production (relative to poikilotherms),
α2- and α1-adrenergic receptors in a reciprocal manner. Although which forms the basis of homeothermy. It also creates the need
cooling augments the response of the α2-receptors, it either to maintain a substantial thermal gradient between the body and
inhibits or does not affect the response of the α1-receptors.46,67 the environment to dissipate the high levels of heat that are
Although initial work was done on canine vessels, subsequent continually produced.
studies that involved α-adrenergic agonists and antagonists An increased rate of metabolism above basal levels is critical
have demonstrated that a similar mechanism exists in human for maintenance of body temperature in cold environments. The
fingers.62,67 elevated heat production is derived from shivering and nonshiv
The responsiveness of cutaneous blood vessels is diminished ering responses. Shivering is muscular contraction for the spe
in people with type 2 diabetes mellitus, both in terms of local cific purpose of producing heat, consisting of simultaneous
responses to temperature and responses to whole-body heat rhythmic excitation of agonistic and antagonistic skeletal muscles.
ing,208,209 resulting in impaired ability to thermoregulate in the Under normal circumstances, carbohydrate oxidation provides
heat. The increased incidence of type 2 diabetes among the the major substrate for shivering. In glycogen-depleted individu
general population may therefore presage a greater number of als, shivering levels are maintained by the greatly increased
patients exhibiting severe hyperthermia.38 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
EVAPORATIVE COOLING tissue and is under strong sympathetic neural regulation in
At high workloads and at environmental temperatures approach humans and other species.139,140 UCP-1 is a transmembrane
ing 37° C (98.6° F), the only way to maintain thermal balance is protein located in the mitochondrial inner membrane, which, on
to augment evaporative cooling by activating the eccrine sweat activation by the sympathetic nervous system, allows for protons
glands. This sympathetic, cholinergically innervated organ system to reenter the mitochondrial matrix without passing through ATP
is spread over the entire body surface, but it is more profuse in synthase. Because energy released during substrate oxidation
some areas than in others. A person who is acclimatized to heat is not conserved as ATP, heat is generated. Although brown
can sustainably produce as much as 1 to 2 L of sweat per hour.2 adipose tissue was previously believed to be of little importance
High rates of sweating occur on the forehead, neck, anterior and in adult humans, recent research has indicated the presence
posterior portions of the trunk, and dorsal surfaces of the hands and physiologic significance of active brown adipose tissue in
and forearms. Lower rates occur on the medial femoral regions, adults.56,139,140,189
lateral trunk areas, and palms and soles.151 Sweat is secreted in Hormonal responses contribute importantly to increases in
these latter two areas in response to a combination of stimuli, metabolism with cold exposure. Evidence shows that both epi
including both nonthermal (emotional, exercise) and thermal nephrine and thyroid hormones are released in humans exposed
inputs.20,187 Because sweating is cholinergically mediated, it can to cold environments.69,211 Both these hormones augment overall
be completely abolished by atropine. Sweat gland activity inter tissue metabolism. Circulating epinephrine and norepinephrine
acts with the regional vasculature; metabolic products of active are increased as part of the overall sympathoexcitatory response
sweat glands increase blood flow in areas of active sweating. In to body cooling. These hormones interact with β-adrenergic
well-hydrated individuals, the degree of anhidrosis is correlated receptors on brown adipose tissue and in skeletal muscle to
with the severity of generalized autonomic failure.78,128 Several increase mitochondrial uncoupling, thereby increasing nonshiv
reviews discuss the many aspects of sweating disorders.44,128,213,229 ering thermogenesis.233,234
129
Thyroid hormone acts by both accelerating ATP turnover these conditions (particularly in cold environments), the choice
and reducing efficiency of ATP synthesis, contributing about of thermal microenvironment and clothing provides a much
30% of resting metabolic heat production.204 Thyroid hormone higher gain than any of the autonomic effector systems discussed
levels are ultimately controlled by thyrotropin-releasing hor previously. Whole-body adjustments are achieved by all motile
mone (TRH), which is synthesized and released in the paraven animals and are particularly well developed in vertebrates.52 In
tricular nucleus of the hypothalamus (PVN). Cold exposure addition to moving the body, the somatic effectors are important
increases biosynthesis, processing, and release of TRH through for optimizing autonomic responses to thermal stress. Thus,
α- and β-adrenergic mechanisms, and a subsequent increase in spreading out the arms and legs during heat stress increases the
thyroid hormone levels appears to increase thermogenesis in surface area available for the autonomic augmentation of conduc
part through binding to thyroid hormone receptors on brown tive, convective, evaporative, and radiative heat losses.
adipose tissue.65 Cabanac28 found that internal body temperature determined
Basal metabolic rate (BMR), when calculated on a weight- whether a particular surface temperature was perceived as pleas
specific basis, decreases with body size. This relationship holds ant or unpleasant. When individuals were hypothermic, a warm
within as well as across species. BMR relates to size according stimulus applied to the hand was experienced as pleasant and
to the following equation.197 a cold stimulus as unpleasant. The opposite responses were
2 = ( 0.676 )M b 0.75 observed in hyperthermic persons. An overall sensation of “ther
VO
mal pleasantness” is obtained when environmental conditions are
2 is oxygen consumption in L/hr and Mb is body mass
Where VO appropriate for maintaining a normal body temperature with no
in kg. 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
CENTRAL SIGNAL tifying the actual peripheral temperature. This study also con
Of the various thermoregulatory outputs, metabolism is the firmed the intimate relationship between the thermoregulatory
easiest to evaluate quantitatively; the most complete documenta network and the pleasure-pain system.165
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 CENTRAL SIGNAL
manipulation of various parts of the brain, body core, and skin. Compared with the knowledge about autonomic thermoregula
This work has made it clear that the thermoregulatory centers tion, we know little about the neural mechanisms that underlie
COLD AND HEAT
act as a proportional controller, and that skin temperature behavioral thermoregulation. As noted in previous sections, the
provides a feed-forward input to the system.84,100 Thus, greater POAH plays a key role in autonomic thermoregulation. It is also
decreases in either core or skin temperature (or both) below important for behavioral thermoregulation, because local heating
neutral values elicit proportionally larger compensatory increases and cooling of this area lead to the appropriate behavioral
in metabolism. In addition to an impaired ability to generate response.31,190 Although animals with lesions of the POAH are
metabolic heat, hypothyroidism is also associated with a decrease severely compromised in their ability to use autonomic thermo
in regulated core temperature of about 1° C (1.8° F).240 regulatory effectors, their ability behaviorally to thermoregulate
Evidence indicates that humans have a control system similar is relatively intact.32,191 These results indicate that the preoptic
to that of medium-sized mammals such as dogs or wolves. In a area is not as crucial for behavioral thermoregulatory processes
PART 2
summary of their data and of that collected previously, Hong and as for autonomic processes. Alternatively, lesions of the lateral
Nadel92 noted that the central output for shivering is augmented hypothalamus, which is involved in various reward systems,
by an increased rate of skin cooling. They also concluded that result in the loss of behavioral thermoregulation.192
a given decrease in core temperature elicits 10 to 20 times the Recent studies involving positron emission tomography (PET)
metabolic response of an equivalent decrease in mean skin and functional magnetic resonance imaging (fMRI) have demon
temperature. Exercise is not incompatible with shivering, but strated that temperature signals from the body surface reach the
increased levels of exercise exert increasing degrees of suppres insular cortex.50,93,161 However, insular activation correlates with
sion on the shivering response, possibly as a consequence of an the discrimination between hot and cold rather than with thermal
increased arousal response.92 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
LOCAL MODULATION ies involving fMRI, it has been shown that activation of the
Although the central and local effects of decreased core tempera amygdala, mid-orbitofrontal and pregenual cingulate cortices,
ture on shivering have not been directly partitioned, both inputs and striatum is correlated with thermally related pleasant and
are important. Slight decreases in core temperature create large unpleasant feelings.107,180
compensatory responses, as delineated previously. However, Because behavioral processes are usually activated by feed-
even moderate hypothermia decreases the metabolic response to forward signals before body core temperature changes, signals
cold, and with severe hypothermia (~30° C [86.0° F] core tempera from the skin are clearly important. In a study involving persons
ture), the shivering response is lost altogether.20 This decrement who were given the choice of moving between 8° C (46° F) and
likely involves impaired transmission of neural signals, because 46° C (115° F), behavior (i.e., moving between environments) was
the muscles themselves are quite responsive below this tempera the primary method of thermoregulation.196 Physiologic (auto
ture. For example, in vitro studies show that limb muscles and nomic) responses occurred but were minimal and secondary to
diaphragm muscles develop peak tensions that are not greatly choice of environment. Furthermore, skin temperature was the
affected by temperatures as low as 25° C (77.1° F), and fatigue primary driver of these behavioral choices, because core tem
resistance is considerably increased at 25° C.173,199 Likewise, alter perature changes were minimal throughout the study.196 Although
ing the local skin and superficial muscle temperature of the feed-forward information from the skin appears to predominate
anterior thigh through a range of temperatures between 12° and in this type of behavioral thermoregulation, severe deviations in
40° C (53.6° and 104.0° F) for 30 minutes had minimal effect on core temperature disrupt ability of feed-forward information to
subsequent isometric peak torque production during isometric contribute to appropriate behavioral responses. When this occurs,
knee extensions to exhaustion.225 Additionally, time to fatigue the person no longer feels too hot or too cold, and the desire
was longer at the coolest temperature. 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
BEHAVIORAL ADJUSTMENTS pleasant experiences during mild heat exposure, whereas during
In most wilderness situations, a variety of ambient temperatures cold exposure, local warming of the chest and abdomen leads
is available, and external insulation is easily adjusted. Under to the most pleasant sensations. This would induce people
130
preferentially to cool the head in the heat and to huddle or add exertion for a standardized task is the greatest, and thermoregula
CHAPTER 6 Thermoregulation
clothing to warm the torso in the cold. 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;
LOCAL MODULATION alternatively, at 11:00 PM, when the body temperature is falling
As with shivering, most problems that involve behavioral tem at the fastest rate, heat loss mechanisms are much more respon
perature regulation probably originate with disruption of central sive.230 Results of studies involving heat dissipation mechanisms
control mechanisms. Skeletal muscle function is fairly resistant to during passive heat exposure or exercise suggest that the thresh
impairment by thermal mechanisms, as described previously. If old for the onset of heat dissipation responses is shifted over the
this occurs, however, a major disruption of the body’s thermal circadian cycle.3-5,215 Sensitivity (responsiveness) of the sweating
defense ensues. 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
IMPORTANT MODIFICATIONS OF studies showing changes3,4 while others did not.215 An excellent
overview of body temperature cycles is available.177
THERMOREGULATORY RESPONSES
In addition to establishing the status of the body temperature Interindividual Differences
when the regulatory system is functioning normally, monitoring Most oral temperature measurements are between 36.0° C (96.9° F)
body temperature provides a significant diagnostic indicator for and 37.1° C (98.9° F) in the early morning. Corresponding values
many pathologic conditions. Whether the goal is to stabilize or for the late afternoon are 36.3° C (97.4° F) and 37.4° C (99.4° F).
monitor the body temperature, it is necessary to understand the On the basis of interindividual differences and diurnal changes,
many conditions that affect both the regulated temperature and it has been suggested that the upper limit for a normal oral
effectiveness of the thermoregulatory system. 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
NORMAL VARIATIONS IN REGULATED and remains at that level until early evening.129 These values
TEMPERATURE AND ABILITY TO MAINTAIN delineate the 99th percentile for body temperature observed
during the respective time periods.
BODY TEMPERATURE Alternatively, it is important to be aware that the normal body
The same body temperature can represent a different set of temperature of some individuals falls outside of population
conditions even under regularly encountered circumstances. norms. We are anecdotally aware of three individuals whose core
Some of these conditions are noted here. 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
Level of Activity fever, but were told by a physician that their temperature of 37° C
Activity normally leads to increases in body temperature. (98.6° F) was normal. For these individuals, however, it was not
However, the level of activity does not appear to provide direct normal; a core temperature of 37° C (98.6° F) in fact represented
input to central thermoregulatory nuclei. Unlike the feed-forward a febrile state. Many individuals with atypical body temperatures
input received from peripheral temperature, the magnitude of are aware of their condition, and it is prudent to ask about this
the error signal for increased heat dissipation is determined possibility.
simply by the increase in body temperature.218 A person who is
exercising heavily (or who has just exercised) in a neutral envi Age
ronment will have an unusually high body temperature, whereas The circadian rhythm of body temperature develops soon after
a person who is sleeping or resting quietly will have a relatively birth. Although newborns display small-amplitude rhythms,
low body temperature. Core temperature increases at the onset the patterns are not circadian. Circadian rhythmicity begins to
of exercise. The time course and magnitude of the temperature develop during the second and third weeks of life, and, after a
increase during exercise depends on several factors, including progressive increase in amplitude, the typical adult temperature
absolute exercise intensity (metabolic heat production), environ rhythms are reached by age 2 years.177 Under thermoneutral
ment, body mass, and body surface area.98 conditions, rectal temperatures of older adults are similar to those
of younger people, whereas oral and axillary temperatures are
Circadian Changes slightly lower.105 A recent overview of circadian temperature and
Body temperature shows cyclic changes throughout the day. aging is available.231
Some of this variation is the result of the daily cycle of activity, Of the major regulatory systems, temperature regulation is
as described previously. However, there also exists a circadian unique in the extent to which the effector organs are shared with
rhythm for the regulated body temperature.3-5 This sinusoidal other systems. This makes developmental assessments difficult
rhythm accounts for much of the observed variations in body because functional changes may be secondary to changes in
temperature. In a study that involved 700 observations of 148 primary systems, such as the skeletal muscles or the blood
healthy individuals, the daily mean oral reading was 36.8° C vessels. Other difficulties, as detailed by Cooper,48 include incon
(98.2° F). However, this was only a midpoint; the mean early- sistencies between chronologic age and physiologic viability and
morning low was 36.4° C (97.6° F), and the mean late-afternoon the increased incidence of interfering disease states and cerebral
high was 36.9° C (98.4° F).153 These diurnal changes definitely microinfarcts as aging progresses.
reflect alterations in the controller, because the body temperature Thermoregulatory capacities of young people show a progres
thresholds for eliciting sweating and peripheral vasodilation are sive increase, but these are not fully developed until after puberty.
significantly lower in the early morning than in the afternoon or Effectors that are more important to infants than to adults include
evening, whereas the sensitivities and maximal response levels certain behavioral responses (including calling for help) and the
remain unchanged.3-5 The body’s biologic clock may directly ability to activate thermogenic brown adipose tissue. Shivering
modulate the body temperature rhythm. The suprachiasmatic is not present in infants; it develops fully only after several years
nucleus in the hypothalamus is the main pacemaker for the cir of nervous system maturation. Metabolism in infants is increased
cadian system of the body. The core molecular mechanisms of to some degree by the increase in motor activity that accompa
the circadian clock consist of autoregulatory transcription and nies cold stress.113
translation loops by the clock genes and show a periodicity of Sweating is present and effective in children, but the typical
approximately 24 hours. Removing the circadian clock abolishes high capacity for evaporative heat loss that is present in adults
the body temperature rhythm as well as the circadian influences is attained only following the changes that occur with puberty.64
on thermoregulatory responses.147,227 Factors that affect loss of body heat during cold stress throughout
Thermoregulatory responses to exercise are affected by the the adult years have been investigated with a multiple regression
circadian clock as well. At the daily low (5:00 AM), the perceived analysis. Fitness, fatness, and age from the 20s to the early 50s
131
were evaluated. Fitness had no effect, but fatness impaired heat sweating, vasodilation, and heart rate.126,127 Heat and exercise may
loss. Aging during this period was correlated with progressive be particularly stressful during and after these episodes. An
weakening of the vasoconstrictor response to cold.25 increase in body temperature caused by heat exposure or exer
Individuals in their late 60s and beyond have a definite cise could also trigger a hot flash.117 The integrative mechanism
decrease in thermoregulatory capacity. Sweating is lessened in for the thermal responses appears to involve estrogen activating
response to passive heating,97 vascular responses to heating and central (POAH) warm-sensitive neurons, which then trigger heat
cooling are significantly reduced,91,110,113 and a distinct shivering dissipation responses.205 Hot flashes may be associated with
tremor is rarely observed.113 In older adults, thermoregulatory activation of the insular cortex,68 as well as circulating serotonin
sympathetic nerve impulses to the skin are reduced by 60%,77 levels.133 Additionally, nitric oxide has been shown to contribute
several mechanisms of cutaneous vasoconstriction and vasodila to the peripheral vasodilator response.94
tion are impaired,91 and resting metabolic rate is lower than in Pregnancy is of special concern to the physician in the wilder
younger individuals.236 ness. This concern does not apply to well-hydrated women who
Young children and older adults are particularly vulnerable to are exercising at submaximal levels, because the thermoregula
thermal extremes and should be given treatment priority when tory system makes adaptive adjustments as pregnancy proceeds.
possible. Both groups are susceptible to climatic heat injury. If In the course of a pregnancy, basal body temperature shows a
core temperatures exceed 40° C (104° F) and are accompanied by continuous decline, and heat loss responses are elicited at pro
an altered mental status, treatment should be immediate, even at gressively lower levels so that, near term, the steady-state tem
the risk of misdiagnosing a febrile condition. As for all such cases, perature during exercise is about 1° C (1.8° F) lower than before
most clothing should be removed; if available, ice should be conception.124 This reduces thermal stress on the fetus, which is
placed around the groin, in the axillae, and around the neck. typically 0.5° C (0.9° F) warmer than the mother.47,212
Cool water should be sprayed on the skin and the individual However, concern is warranted if hyperthermia develops in
then fanned. Blood gas and electrolyte status should be deter pregnant women. Animal experiments and epidemiologic analy
mined and any appropriate treatment measures taken.34 sis both indicate that, during pregnancy, it is dangerous for body
temperature to exceed 39° C (102.2° F). During the first half of
Sex and Reproductive Hormone Status pregnancy, excessive body temperature is likely to produce birth
Women have a number of physiologic and morphologic charac defects; during the latter half, birth weight is more likely to be
teristics that could theoretically produce differences in the regula affected. The fifth week after conception, which is the period of
tion of body temperature. These include smaller blood volume, neural tube closure, is a particularly vulnerable time for the
lower hemoglobin concentration, smaller heart, smaller lean fetus.124 Because women in the early stages of pregnancy may
COLD AND HEAT
body mass, greater percentage of subcutaneous and total body be unaware of their condition, it is critical that heat stress be
fat, greater surface area–to–mass ratio (due to smaller overall promptly treated in women of childbearing age. When exercis
body size), thinner extremities, and cyclic changes in sex hor ing, it is important that pregnant or potentially pregnant women
mone levels. In general, however, historical studies that originally acclimatize gradually to extreme thermal environments, remain
suggested major differences in thermoregulation between men well hydrated, wear loose-fitting clothing, exercise at a comfort
and women were poorly controlled or unclear in data presenta able pace, and avoid swimming in warm water or immersing
tion.43 Most reports have shown that when age, thermal accli themselves in hot tubs.212 A program of water aerobics for preg
mation, body size, maximal aerobic capacity, cardiovascular nant women was reported to decrease requests for analgesia
responses during exercise, and relative workload are matched, when these women gave birth, and it was not found to be det
PART 2
sex differences in thermoregulation are minimal.71 In particular, rimental to the health of the mother or the child.6
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 INDUCED ALTERATIONS OF THE
moregulatory heat dissipation only at very high exercise intensi
ties,72 and the impairment was not such that it would cause an
REGULATED TEMPERATURE
increase in dangerous levels of hyperthermia in women. The optimal body temperature is not always the same. In certain
The menstrual cycle, oral contraceptives, menopause, and conditions of stress or vulnerability, the regulated temperature of
pregnancy are all associated with important effects on the ther the body may be altered; this is often an adaptive response to a
moregulatory system. Relative to the early follicular phase of the particular perturbation or physiologic/pathophysiologic state. In
menstrual cycle, core temperature is typically 0.3° C (0.5° F) lower such circumstances, altered body temperature may be beneficial
during the late follicular (preovulatory) phase, when estrogen is and should not necessarily be manipulated until the underlying
elevated unopposed by progesterone, and 0.5° to 0.7° C (1.0° to condition is improved.
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
FEVER
that heat dissipation responses, including cutaneous vasodilation The association between illness and increased body temperature
and sweating, are initiated at lower temperatures during the has been recognized for thousands of years. Febrile body tem
preovulatory phase and higher temperatures during the midluteal peratures for resting young adults include a morning temperature
phase.40,116,215 These influences are also seen with the exogenous of 37.3° C (99.2° F) or higher, which increases gradually to 37.8° C
hormones in oral contraceptives.40,42 Such data support the idea (100.0° F) for early afternoon and evening. Such elevated tem
that estrogen tends to promote peripheral vasodilation and a perature needs to reflect a regulated increase to be considered
lower body temperature, whereas progesterone tends to promote a true fever.
increased body temperature.41,116 Pathogens that cause fevers interact with components of the
The effects of reproductive hormones on thermoregulation immune system such as macrophages, T cells, monocytes, and
in postmenopausal women undergoing hormone replacement Kupffer cells as well as with glial, epithelial, and many other
therapy are generally consistent with those just described in types of cells. This interaction stimulates the cells to produce
younger women. Administered estrogen acts to lower the core pyrogenic cytokines,131 including interleukin-1 (IL-1), interleukin-6,
temperature at which heat loss effector mechanisms are activated and macrophage inflammatory protein-1. The thermoregulatory
and results in a lowered core temperature.22,222 The addition of “resetting” that results in a regulated increase in body tempera
exogenous progestins reverses these effects.22 Although less work ture is initiated by activation of the complement cascade in the
has been done on the thermoregulatory effects of testosterone, liver, which then initiates afferent neural signaling to the hypo
epidemiologic studies indicate that lower testosterone concentra thalamus via a prostaglandin E2–dependent vagal mechanism.13,185
tion may be associated with a sensation of cold.76 Aspirin and related drugs block fever by inhibiting prostaglandin
During menopause, fluctuating hormone levels are thought to synthesis.13,185 In addition to causing fever, IL-1 and other cyto
contribute to hot flashes or “flushes,” which involve increases in kines have many other effects, including decreased appetite,
132
hypoferremia, activation of B and T lymphocytes, and increased development of hypothermia and decreases the incidence of
CHAPTER 6 Thermoregulation
slow-wave sleep.114 infectious complications.118,201
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
SEVERE HYPOXIA AND ENDOTOXIN SHOCK
feron production are all augmented. The most important aspect When inspired oxygen concentration falls to between 10% and
of fever may be to increase greatly the temperature of the periph 12%, a substantial decrease in the regulated temperature occurs.
eral tissues by selecting a warmer microclimate, adding insula This reaction has been documented with the use of behavioral
tion, and making postural changes. As peripheral temperatures responses in fish, amphibians, reptiles, and mammals.74,237 For
increase from typical levels (i.e., 29° to 33° C [84.2° to 91.4° F]) humans who are exercising in 28° C (82.4° F) water under eucap
to those that approximate core temperature, the activation, pro nic conditions, decreasing inspired oxygen to 12% lowers the
liferation, and effector production in peripheral cells involved in core temperature thresholds for vasoconstriction and shivering
cell-mediated and humoral immunity are greatly increased and and increases the rate of core cooling by 33%.104 The value of
show temperature coefficients (Q10) of 100 to 1000. By contrast, the resultant lowered body temperature is clear: the affinity of
the Q10 for the effectiveness of the newly created effectors them hemoglobin for oxygen is increased, and overall metabolic rate
selves, as well as for antigen-nonspecific defense systems, are is decreased. The mechanism underlying the change in the regu
much lower, at about 1.5 to 5.36.184 lated temperature may involve differential sensitivities of central
The presence and beneficial effects of fever have been docu neurons; hypoxia specifically increases activity of warm-sensitive
mented in a variety of cold-blooded and warm-blooded verte neurons in the POAH.221
brates and even in some invertebrates. Under most conditions, A somewhat similar regulated hypothermic response occurs
it is probably not advisable to alleviate a fever. Exceptions when an animal is exposed to very high levels of pyrogens; the
include malignant hyperthermia and particularly high fevers same response occurs under less extreme conditions in weak or
during pregnancy. In addition, for patients with limited fluid, malnourished animals. The lowered body temperature may serve
oxygen transport, or cardiopulmonary reserves, a febrile re to decrease the energy costs of maintaining a high body tem
sponse should be treated with antipyretics.110 Consequences perature for a severely compromised animal.183
of the decreased immune response can be treated after the
emergency.
ALTERED SYSTEM RESPONSIVENESS
ALCOHOL, ANESTHETICS, AND TOXINS AND CAPACITIES
Increases in the blood concentrations of ethanol, anesthetics, and A number of situations alter responsiveness of the thermoregula
a number of toxic substances lead to substantial decreases in tory system. Awareness of these conditions is important when
body temperature.54,200 In many cases, this fall is caused by a assessing the thermoregulatory capabilities of a particular person
decrease in the regulated temperature. In the case of high con and when determining possible causes for hyperthermia or
centrations of alcohol and certain toxins, the reduction appears hypothermia.
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,
THERMAL ACCLIMATION
mouse studies have shown that lowered body temperature coun Thermoregulation is affected by chronic exposure to very cold
teracts ethanol toxicity.132 In humans as well, a decrease in the or hot environments as well as by chronic exercise in cool or
regulated temperature is caused by increases in blood ethanol warm ambient temperatures. Such exercise in a cool environment
concentration. After ingestion of ethanol (3.0 mL/kg body weight) greatly increases responsiveness of the sweat glands; if exercise
at 33° C (91.4° F), sweat rate increased and body temperature fell. is in the heat, the central temperature at which sweating is initi
Although skin temperature did not increase, individuals reported ated is also lowered. The net consequence of these adjustments
a warm sensation that paralleled the increase in sweat rate.242 At is that a heat-acclimated and exercise-acclimated individual can
18° C (64.4° F), body temperature decreased continuously before work at a given level with far less increase in core temperature.146
and after the drinking of alcohol, with no facilitation of metabolic A regimen of exercise in humid heat appears to decrease resting
heat production. During this period, the thermal discomfort sen core temperature in acclimated individuals.168 Repeated acute
sation became more intense, although the discrimination of cold increases in both core and skin temperatures contribute to
was impaired after the ingestion of ethanol.241,242 However, lower various changes involved in heat acclimation.175 Physical training
blood ethanol levels associated with moderate consumption in also increases skin blood flow at any given increase in core
humans have minimal and inconsistent effects on thermal balance temperature.100 Although acclimation to warm conditions pro
of the whole body.58,103 duces many changes in the cardiovascular system, basic barore
Excellent overviews of the effects of general anesthetics on flex responses are not altered.239
perioperative thermoregulation are available.201,202 Many of these Heat acclimation may result in protective cellular adaptations.
substances (e.g., halothane, fentanyl and nitrous oxide, enflu Intracellular heat shock protein (HSP) 72 is likely involved in
rane, isoflurane) in anesthetic doses act in a similar manner. Heat the maintenance of cellular protein conformation and homeosta
loss thresholds are increased by about 1° C (1.8° F), and heat sis during hyperthermia, inflammation, and injury.141 Consistent
maintenance thresholds are lowered by approximately 2.5° C with this, a 10-day program of heat and exercise acclimation
(4.5° F). Interestingly, in the typical clinical dose range, the gain increased HSP-72 levels in peripheral blood mononuclear
(sensitivity) of the effector responses is near normal. In the con cells.238
ditions under which general anesthetics are normally adminis Chronic cold exposure alters many thermoregulatory systems.
tered, body temperature decreases significantly. An initial rapid These effects can accrue to both evolutionary change and long-
drop is caused by redistribution of heat; cool blood from the term individual thermal acclimation. In many cases, resting meta
periphery lowers central core temperature. A second and slower bolic rate is increased after repeated cold exposure;24 however,
decrease results from a fall in body heat content. Finally, a repeated exposure to very cold environments may produce the
plateau is reached, either because heat production and heat loss opposite effect. For example, eighty 30-minute sessions at 5° C
are passively balanced, or because heat maintenance thresholds (41° F) decreased the metabolic response to a standard cold-air
are reached. During postanesthetic recovery, there is vigorous test and often led to lower internal temperatures in these cold-
shivering. Anesthetic-induced hypothermia is reduced in patients acclimated individuals.89
with higher preoperative systolic blood pressure. This difference On initial exposure of extremities to cold, substantial cutane
is associated with higher preoperative plasma norepinephrine ous vasoconstriction is observed. At some point, however, cold-
levels, which may intensify the vasoconstriction response.108 induced removal of the superficial α-receptor inhibition leads to
Cutaneous warming before and during anesthesia prevents the transient vasodilation of the fingers, which occurs in a cyclic
133
pattern.1,159 This so-called cold-induced vasodilation warms the tion of blood flow from the core to the periphery, and associated
extremities, protects against frostbite, decreases pain, and im decreases in stroke volume maximize cardiovascular strain in
proves manual dexterity during prolonged cold exposure.1,90 This high environmental temperatures. These mechanisms appear to
response has a genetic component; for individuals who are not be as important as the core temperature itself (or more so) with
cold acclimated, this response is very strong among Inuit Eskimos, regard to development of fatigue. The integrative contributions
moderate among whites, and minimal among Chinese from Hong of various mechanisms of fatigue are detailed in a recent
Kong.78 No differences appear to exist between men and women review.156
in the cold-induced vasodilation response.228 Individual differ For maintenance of exercise performance and body tempera
ences in the vasodilation response to cold determine the relative ture in a warm environment, body water status is critical.45,195 It
likelihood of the development of frostbite. An environmental is common for a person who is working in the heat to lose 1 L
influence in this response is also likely; fishermen in northeastern of water per hour. Even when fluids are readily available, main
Canada did not exhibit vasoconstriction of the fingers when taining a euhydrated state may be difficult. For hypohydration
exposed to cold.78 during continued activity, each percent decrease in body weight
leads to a core temperature increase of about 0.15° C (0.27° F).
COMPETITION WITH OTHER This decreased heat dissipation is mediated by two mechanisms.
At a given core temperature, hypertonicity decreases the sweat
HOMEOSTATIC SYSTEMS ing response, and hypovolemia reduces skin blood flow.45,195
In addition to a constant core temperature, the body has many During compensable heat stress, in which a steady-state core
other requirements. When fluid balance or energy requirements temperature can be maintained, hyperhydration has no effect on
are not met, thermoregulatory responses can be compromised. thermoregulation.119 During uncompensable exercise heat stress,
For heat production and heat conservation, an adequate energy in which core temperature continues to rise, hyperhydration
supply, patent nervous system, and functional effector organs are slightly increases the time to exhaustion, but only by delaying
critical. Thus, hypoglycemia decreases the core temperature at hypohydration; thermoregulation is not affected.120 It is important
which shivering is initiated while leaving the thresholds for to be alert to the possibility of dehydration in many atypical situ
sweating and vasodilation unaffected.166 Competition between ations. For example, swimmers training in an outdoor pool with
skin and muscle for blood flow during hyperthermic exercise is a water temperature of 26° C (78.8° F) lost sufficient fluid (2.5%
another consideration. During exercise, cutaneous vasodilation of their body weight) in 3 hours to compromise thermoregulatory
is elicited later, at a higher internal temperature than in resting responses.210
hyperthermia, resulting in lower skin blood flow for a given Exposure to hypoxia can alter thermoregulatory vascular
COLD AND HEAT
internal temperature during exercise than at rest.99 The arterial responses, in part because hypoxia itself is a vasodilator.207
baroreflex is another nonthermal reflex that can alter skin blood During exposure to cold, augmented vasoconstriction appears to
flow responses to thermal stimuli. Activation of the baroreflex defend core temperature such that the rate of body cooling is
using lower-body negative pressure (LBNP) causes decreases unaffected.206 Paradoxically, in a hot environment, hypoxia may
in skin blood flow in both normothermic and hyperthermic reduce the cutaneous vasodilator response for a given level of
individuals.102 hyperthermia.188 This may be caused by the sympathoexcitatory
During exercise, heat is generated by activity of the muscles. influence of hypoxia.82 However, regional differences in the influ
About 80% of the energy consumption is converted into heat, ence of hypoxia on blood flow and vascular tone make mecha
with only about 20% going to the actual work produced by nistic interpretation challenging.
PART 2
134
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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- type of exposure, and a multitude of intoxicants or medications
ties were not scientifically evaluated until the 18th century. The can jeopardize thermostability by decreasing heat production or
hemostatic, analgesic, and therapeutic effects of cold on various increasing heat loss. Physiologic stressors also include dehydra-
conditions were well known. Biblical references cite truncal tion, sleep deprivation, and fatigue. These challenges increase
rewarming of King David by a damsel; various remedies were heat loss through evaporation, radiation, conduction, and con-
mentioned by Hippocrates, Aristotle, and Galen.253 Folklore from vection, and compensatory responses often fail.204 The resulting
Maine still recounts the buggy ride of “Frozen Charlotte.” mortality rates range to well over 50% in many clinical series,
The effects of cold on human performance are perhaps depending largely on the severity of risk factors and on patient
best documented in military history.65,226 Frosty conditions have selection criteria.62,222,270,340
decided many battles. Numerous casualties occur even in train- For safety, experimental investigations of induced hypother-
ing. Most cold injuries currently encountered affect destitute mia in human volunteers usually terminate cooling at about 35° C
urban people and wilderness or sports enthusiasts, such as skiers, (95° F). Naturally, this precludes analysis of some of the more
hunters, sailors, climbers, and swimmers.6,278 The popularity of significant pathophysiologic features of moderate or severe hypo-
Arctic and mountain expeditions increases the number of persons thermia. Design limitations also occur in studies of anesthetized
at risk.3,145 Among those challenging the environment are climb- animals, because the results of these experiments require varying
ers of Mt Everest, Mt Hood, and Denali.122,212,236 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,
EPIDEMIOLOGY particularly in nonporcine animal models. As a result, clinical
In most countries, deaths from primary hypothermia are consid- treatment recommendations must be predicated on the degree
ered violent and classified as accidental, homicidal, or suicidal.41 and duration of hypothermia and on the predisposing factors that
Deaths from secondary hypothermia are usually considered natu- are subsequently identified.34,78,120,229
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 NORMAL PHYSIOLOGY OF
found indoors usually have other serious and diverting medical
illnesses. In addition, delays are common between hospital
TEMPERATURE REGULATION
admission and death, so secondary hypothermia is significantly Warm-blooded animals maintain a precariously dynamic equilib-
underreported. In contrast, death certificate data more accurately rium between heat production and heat loss.152,153 The normal
quantify primary hypothermia.81 diurnal variation in humans is only 1° C (1.8° F). Because physi-
Hypothermia occurs in various locations and in all sea- ologic changes occurring in humans are modified by predispos-
sons.33,222,293,340 In a multicenter survey of 428 cases of civilian ing or contributory factors, the normal responses to severe
accidental hypothermia, 69 occurred in Florida.62,319 Urban set- temperature depression require significant extrapolation.208,237
tings account for the majority of cases in most industrialized Basal heat production usually averages 40 to 60 kilocalories
countries.62,279,309 An annual average of more than 1300 deaths is per square meter (kcal/m2) of body surface area per hour, which
attributed to primary hypothermia in the United States. About approximates the heat from a 100-watt incandescent bulb. This
one-half these fatalities are in patients older than 65, and 67% increases with shivering thermogenesis,220 food ingestion, fever,
are males.17 activity, and cold stress. Normal thermoregulation in vertebrates
The reason for any year-to-year decline in fatalities is unknown. involves transmitting cold sensation to hypothalamic neurons via
Of note, the incidence of secondary hypothermia fatalities is the lateral spinothalamic tracts and the thalamus (Figure 7-1).
much greater, but there are no reliable histologic criteria to Table 7-2 lists the physiologic characteristics of the four zones
confirm that hypothermia is the cause of death. of hypothermia.
CLASSIFICATIONS PATHOPHYSIOLOGY
Accidental hypothermia is best defined as the unintentional
decrease of about 2° C (3.6° F) in the “normal” core temperature NERVOUS SYSTEM
of 37.2° to 37.7° C (99.0° to 99.9° F) without disease in the pre- Numbing cold depresses the central nervous system (CNS),
optic and anterior hypothalamic nuclei (Table 7-1). Classically, producing impaired memory and judgment, slurred speech,
hypothermia is defined as a core temperature below 35° C and decreased consciousness. During cold-weather expeditions,
(95° F).78 Hypothermia is both a symptom and a clinical disease leaders are prone to impaired judgment, risk-taking behavior,
entity. When sufficient heat cannot be generated to maintain and the attendant trauma. Temperature-dependent enzyme
homeostasis and core temperature drops below 30° C (86° F), systems in the brain do not function properly at cold tempera-
the patient becomes poikilothermic and cools to the ambient tures that are well tolerated by the kidneys. As a result, most
temperature.182,61 patients are comatose below 30° C (86° F), although some remain
Among clinical classifications, the most practical division amazingly alert.138
includes healthy patients with simple environmental exposure Neurons are initially stimulated by a 1° C (1.8° F) drop in
(primary), those with specific diseases that produce hypothermia temperature, but the brain does not always cool uniformly during
(secondary), and those with predisposing conditions. Other divi- accidental hypothermia. After the initial increase, there is a linear
sions that reflect the etiology of hypothermia include immersion decrease in cerebral metabolism by 6% to 10% per degree Celsius
versus nonimmersion and acute versus chronic heat loss.204,228 from 35° C (95° F) to 25° C (77° F). Hypothermia can initially
Various physiologic stressors and other factors can impair afford cerebral protection because of the diminished cerebral
thermoregulation.286 Age extremes, state of health and nutrition, 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
Cold exposure
136
CHAPTER 7 Accidental Hypothermia
TABLE 7-2 Characteristics of the Four Zones of Hypothermia
Core
Temperature
Stage °C °F Characteristics
Clinically invisible increased preshivering muscle tone can tive to cold than is the myocardium. As a result, conduction
obscure the P waves; ST-segment and T-wave abnormalities are velocity decreases and electrical signals can disperse. Because
inconsistent.9,326 Of note, standard surface ECG electrodes, when conduction time is prolonged more than the absolute refractory
attached to dry skin, will accurately reflect cardiac electrical activ- period, reentry currents can produce circus rhythms (movements)
ity. Needle electrodes are not necessary to detect weak ECG that initiate ventricular fibrillation (VF).
signals.170 In addition to causing bradycardia, widening the QRS complex,
The J wave (Osborn wave or hypothermic hump; Figure 7-2), and prolonging the QT interval, hypothermia increases the dura-
first described by Tomaszewski in 1938, occurs at the junction tion of action potentials (Figure 7-3).20 During rewarming, non-
of the QRS complex and the ST segment. It is not prognostic but uniform myocardial temperatures can disperse conduction and
is potentially diagnostic.108,177 J waves occur at any temperature further increase the action potential duration, another mechanism
below 32.2° C (90° F) and are most frequently seen in leads II to develop the unidirectional blocks that facilitate reentrant
and V6. When core temperature falls below 25° C (77° F), J waves arrhythmias. At temperatures between 25° and 20° C (77° and
are found in the precordial leads (especially V3 or V4). The size 68° F), myocardial conduction time is prolonged further than the
of the J waves also increases with temperature depression, but absolute refractory period. Another arrhythmogenic mechanism
is unrelated to arterial pH.350 J waves are usually upright in aVL, is development of independent electrical foci that precipitate
aVF, and the left precordial leads.4,158,241 arrhythmias.
J waves may represent hypothermia-induced ion fluxes, result- Various electrolyte abnormalities can further complicate the
ing in delayed depolarization or early repolarization of the left situation during hypothermic conditions, because they exacer-
ventricle, or there may be an unidentified hypothalamic or neu- bate the effects of prolonged action potentials. Most conspicu-
rogenic factor. J waves are not pathognomonic of hypothermia ously, hypothermia-induced cellular calcium loading mimics
but occur also with CNS lesions, focal cardiac ischemia, and digitalis toxicity and may predispose to a forme fruste of torsades
sepsis.158 J waves may also be present in young, healthy persons. de pointes.
When pronounced, J waveform abnormalities can simulate myo- Hypothermia-induced VF and asystole often occur spontane-
cardial infarction. Computer software that can successfully rec- ously below 25° C (77° F). The VF threshold and transmembrane
ognize and suggest the diagnosis of hypothermia is not widely resting potential are decreased. Because the heart is cold, the
available (see Figure 7-2).180,213,234 conduction delay is facilitated by the large dispersion of repolar-
The prehospital capability to differentiate between J waves ization, and the action potential is prolonged. The increased
and injury current is particularly important in rural and wilderness temporal dispersion of the recovery of excitability is linked to
settings with long patient transport times.60 Thrombolysis is VF. Nature’s model of resistance to VF is the heart of hibernat-
unstudied in accidental hypothermia but would be expected to ing animals during rewarming.151 Animals with this capacity
exacerbate coagulopathies.105 seem to be protected by a shortened QT duration and a calcium
Below 32.2° C (90° F), all types of atrial and ventricular arrhyth- channel handling system that prevents intracellular calcium
mias are encountered.45,77 The His-Purkinje system is more sensi- overload.
137
COLD AND HEAT
A
64 ATRIAL FIBRILLATION Req MD:
229 NONSPECIFIC INTRAVENTRICULAR CONDUCTION DELAY Acct No:
PART 2
aVR V1 V4
aVL V2 V5
aVF V3 V6
138
temperature afterdrops occur when participants are rewarmed
139
to be an attempt to compensate for initial relative central hyper- perature at which enzyme activity slows significantly is 34° C
volemia that is caused by vasoconstrictive overload of capaci- (93.2° F).334 In addition, clot strength weakens as a result of
tance vessels. platelet malfunction. Fibrinolysis is not significantly affected at
The diuresis may also be pressure related, caused by impaired any temperature in the range measured (33° to 37° C [91.4° to
autoregulation in the kidneys. Cold diuresis has circadian 98.6° F]) (see Trauma, later).
rhythmicity and correlates with periods of shivering. Cold-water Physiologic hypercoagulability also develops during hypother-
immersion increases urine output 3.5 times, and the presence of mia, with a sequence similar to that seen in disseminated intra-
ethanol impressively doubles this diuresis. vascular coagulation (DIC). This produces a higher incidence of
thromboembolism during hypothermia. Causes include thrombo-
plastin release from cold tissue, simple circulatory collapse, and
COAGULATION release of catecholamines and steroids. Because levels of fibrin
Coagulopathies often develop in hypothermic patients because split products can be normal, bleeding is not always considered
of effects on the enzymatic nature of the activated clotting a hematologic manifestation of DIC.
factors.88 In vivo, clotting prolongation is proportional to the Whole-blood viscosity increases with the hemoconcentration
number of steps in the cascade. For example, at 29° C (84.2° F), seen after diuresis and the shift of fluid out of vascular com
a 50% to 60% increase in the partial thromboplastin time (PTT) partments. Red blood cells (RBCs) simply stiffen and have
would be expected. Kinetic tests of coagulation, however, are diminished cellular deformability when chilled.258 The elevated
performed in the laboratory at 37° C (98.6° F). As the blood warms viscosity of hypothermia is also exacerbated by cryoglobuline-
in the machine, the enzymes between the factors in the cascade mia. Cryofibrinogen is a cold-precipitated fibrinogen occasion-
are activated. The sample of warmed in vitro blood then clots ally seen with carcinoma, sepsis, and collagen vascular diseases.
normally.79 Blood viscosity is increased by the transient increases in platelet
The reversible hemostatic defect created by hypothermia may and RBC counts seen with mild surface cooling. This explains
not be reflected by the reported “normal” prothrombin time (PT), the increased coronary and cerebral thromboses that occur in
PTT,272 or international normalized ratio (INR). This coagulopathy winter.204
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 PREDISPOSING FACTORS
factors.269 When rapid rewarming is difficult, concentrations of The factors that predispose to hypothermia can be separated into
0.01 to 1 nM of desmopressin may partially reverse hypothermia- those that decrease heat production, increase heat loss, and
COLD AND HEAT
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
140
Older adults are physiologically less adept at increasing heat copy, warming the gas before administration helps prevent
141
Pharmacologic or Toxicologic Effects An inverse relationship usually exists between the Injury
Numerous medications and toxins in therapeutic or toxic doses Severity Score (ISS) and core temperature of traumatized patients
impair centrally mediated thermoregulation and vasoconstric- on arrival in the emergency department (ED). This observation
tion.156,352 The usual offenders are barbiturates, benzodiazepines, does not settle whether hypothermia is just another risk factor
antimanic agents, and antidepressants. Reduced core temperature for increased mortality or reflects that the most severely injured
may be a prodrome of lithium poisoning. Organophosphates, patients are in hemorrhagic shock.126,225 One study assessed the
narcotics, glutethimide, bromocriptine, erythromycin, clonidine, impact of hypothermia as an independent variable during resus-
fluphenazine, bethanechol, atropine, acetaminophen, and carbon citation from major trauma.95 Patients not aggressively rewarmed
monoxide (CO) all cause hypothermia. Hypothermia after acute with continuous arteriovenous rewarming (CAVR) had increased
CO poisoning is associated with increased mortality. fluid requirements, increased lactate levels, and increased acute
mortality.
Of the clinical entities associated with hypothermia, traumatic
RECURRENT HYPOTHERMIA conditions causing hypotension and hypovolemia most dramati-
Recurrent and episodic hypothermia are widely reported. The cally jeopardize thermostability. Hypothermia is often obscured
recurrent variety is more common and is usually secondary to by obvious hemorrhaging and injuries. Liberalized indications for
ethanol abuse, with one person having survived 12 episodes.58 Focused Assessment with Sonography for Trauma (FAST) ultra-
Severe, recurrent presentations are also caused by self-poisoning sound examinations can minimize unnecessary computed tomog-
and anorexia nervosa. raphy (CT) imaging. On the other hand, traumatic neurologic
Persons with episodic hypothermia can be divided into two deficits, including paresis and areflexia, can be misattributed to
groups, with significant overlap, as follows: hypothermia. In trauma patients requiring surgery, the mean
Group 1: Diaphoretic episodes precede the temperature decline, temperature loss was greater in the ED than in the operating
which lasts several hours. This group includes those with room.111,112 Thermal insults are often added during a trauma
hypothalamic lesions and agenesis of the corpus callosum resuscitation. The patient is completely exposed for examination,
(Shapiro syndrome) and persons with spontaneous periodic and resuscitative procedures cause further heat loss.287
hyperthermia. Resultant hyperhidrosis and hypothermia When stratifying patients with the anatomic ISS, hypothermic
are successfully treated with clonidine, a centrally acting patients may have a higher mortality rate than similarly injured
α-adrenergic agonist. The hypothermia of corpus callosum patients who remain normothermic. Caution is advised when
agenesis is also seen with hypercalcemia and status epilepti- using trauma revised injury severity score (TRISS) methodology.
It is less valid during hypothermia because the physiologic com-
COLD AND HEAT
days to weeks, rather than hours. These people have more cascade of enzymatic reactions is impaired and plasma fibrino-
seizure disorders, and the central hypothalamic thermostat is lytic activity is enhanced, producing a clinical presentation similar
set abnormally low. to that of DIC. Also, platelets are poorly functional and become
Patients with intermittent hypothermia usually show some sequestered.
characteristics of both groups.204 Circadian rhythm disturbances Hypothermia is protective only when induced before shock
are also seen in persons with neurologic disorders who have occurs. This reduces adenosine triphosphate (ATP) utilization
chronic hypothermia. 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
PREDISPOSING INFECTIONS OR CONDITIONS may synergistically exacerbate the coagulopathy seen in trauma.88
Among the infestations and infections that may elevate or depress The average temperature of 123 initially normothermic trauma
core temperature are septicemia, pneumonia, peritonitis, men patients in whom lethal coagulopathies developed was 31.2° C
ingitis, encephalitis, bacterial endocarditis, typhoid, miliary (88.2° F). Postinjury life-threatening coagulopathy in the seriously
tuberculosis, syphilis, brucellosis, and trypanosomiasis.192 Other injured patient who requires massive transfusion is predicted by
diseases, in addition to cerebrovascular and cardiopulmonary persistent hypothermia and progressive metabolic acidosis.55,89
disorders, that produce secondary hypothermia include systemic The appropriate target core temperature for a hypothermic
lupus erythematosus, carcinomatosis, pancreatitis, and multiple patient with an isolated severe head injury is unclear. The target
sclerosis. Hypothalamic demyelination may explain episodic temperature could help balance neuroprotection against the
hypothermia observed in some patients with multiple sclerosis. adverse hematologic and physiologic consequences of hypother-
Hypothermia can also result from low cardiac output after a mia18,210 (see Cerebral Resuscitation, later.)
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-
PRESENTATION
sium sulfate infusion during preterm labor can produce hypo- The patient’s history may suggest hypothermia.32 Diagnosis is
thermia with fetal and maternal bradycardia, and hypothyroidism simple when exposure is obvious, as with avalanche victims.
can be manifested as hypothermia after preeclampsia (see Subtle presentations, however, predominate in urban settings.
Box 7-2). 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,
TRAUMA immersion, overdose, cerebrovascular accident (CVA, stroke),
Hypothermia protects the brain from ischemia but can result in and psychiatric emergencies (Box 7-3).
arrhythmias, acidosis, and coagulopathies and extracts a high During the head, eye, ear, nose, and throat examination,
metabolic cost during rewarming.95 Hypothermia hinders abnormal findings can include decreased corneal reflexes, mydri-
protective physiologic responses to acute trauma and affects asis, strabismus, flushing, erythropsia, facial edema, rhinorrhea,
pharmacologic and therapeutic maneuvers necessary to treat and epistaxis. Mild hypothermia usually does not depress pupil-
injuries.15,26 lary light reflexes.
142
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- sis.145 Leaders of expeditions can become moody, apathetic,
arrhythmias and hypotension. Heart sounds may be muffled and uncooperative, and risk taking. Older adult patients often with-
distant. Tachypnea, an early respiratory finding, is usually fol- draw in confusion, become silent, and display lassitude and poor
lowed by progressive hypoventilation with bronchorrhea and judgment. A peculiar or flat affect is common, and psychomotor
adventitious sounds. Because the gastrointestinal (GI) tract is impairment can resemble organic brain syndrome.
depressed, abdominal distention or rigidity, ileus, obstipation, Early in hypothermia, simply losing effective use of the hands
and poor rectal tone are often present. Gastric dilation is common can be devastating. Appropriate behavior adapted to the cold,
in neonates and myxedematous adults. Urine output ranges from such as seeking a heat source, is often lacking. An extreme
initial polyuria resulting from cold diuresis to anuria. The inci- example is paradoxical undressing.167 The clothing is removed in
dence of testicular torsion increases because of cremasteric a preterminal effort to address impending thermoregulatory col-
contractions. lapse, and many persons are mistakenly identified as sexual
Diffuse neurologic abnormalities vary widely. Some persons assault victims. This phenomenon is also seen in hypothermic
can still converse at 32° C (89.6° F) and are normoreflexic. The children. Undressing may result from Alzheimer’s disease before
level of consciousness generally declines proportionate to the the patient wanders into the cold.165
degree of hypothermia. The presence of ataxia and dysarthria Musculoskeletal posturing can extend to pseudo–rigor mortis.
may mimic a CVA. Speed of reasoning and memory registration Preshivering muscle tone is increased before core temperature
are also impaired. Amnesia, antinociception, anesthesia, or drops to 35° C (95° F), and muscular rigidity, paravertebral spasm,
hypesthesia can develop. Cranial nerve abnormalities are present and even opisthotonos may occur. Extremity compartment syn-
after bulbar damage from central pontine myelinolysis. These dromes often develop because of associated conditions causing
extraocular muscle movement abnormalities, as with extensor prolonged compression and immobility, in addition to com
plantar responses, do not directly correlate with the degree of partment hypertension seen during reperfusion of frostbitten
hypothermia. extremities.
Hyperreflexia predominates from 35° to 32.2° C (95° to 90° F) Dermatologic presentations of hypothermia include erythema,
and is followed by hyporeflexia. The plantar response remains pallor, edema, and scleral edema. Cold urticaria, frostnip, frost-
flexor until 26° C (78.8° F), when areflexia develops. The knee bite, and gangrene should also cause the clinician to consider
jerk is usually the last reflex to disappear and the first to reappear this diagnosis. Pernio is also observed with chronic myelomono-
during rewarming. From 30° to 26° C (86° to 78.8° F), both con- cytic leukemia.
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 LABORATORY EVALUATION
other CNS lesions may be obscured by depressive neurologic
changes that normally accompany hypothermia.
ACID-BASE BALANCE
Psychiatric presentations and suicide attempts associated with The strategy for achieving and maintaining acid-base balance in
hypothermia often are initially misdiagnosed. Preexisting psychi- hypothermia differs from that of normothermia.68,121,141,162 After
atric disorders can blossom in the cold, even if they were stabi- initial respiratory alkalosis from hyperventilation when a person
lized in temperate climates.29 Mental status alterations include first becomes chilled, a common underlying disturbance is mixed
anxiety, impaired judgment, perseveration, neurosis, and psycho- acidosis. The respiratory component of the acidosis is caused
143
mainly by direct respiratory depression. In addition, as body exhibit this respiratory adaptation and do not depress their respi-
temperature decreases, solubility of CO2 in blood increases. ratory minute volume when cold. This response, termed the
Further contributors to the metabolic component of this acidosis ectothermic, or alpha-stat, strategy, allows them to maintain total
include impaired hepatic metabolism and acid excretion, lactate bicarbonate and CO2 content while increasing pH. Hibernating
generation from shivering, and decreased tissue perfusion.129 mammals are far more acidic because of respiratory acidosis and
Nevertheless, reliable clinical prediction of the acid-base status use an acid-base strategy that suppresses metabolism, termed the
in accidental hypothermia is not possible. In one series of 135 endothermic, or pH-stat, strategy.
patients, 30% were acidotic and 25% alkalotic.222 Induced hypothermia, which clearly differs from accidental
Circulatory changes also prevent adequate mobilization and hypothermia, might benefit from the alpha-stat approach, with
delivery of organic acids to buffer systems. As in normothermia, improved neurologic outcome and myocardial function.69,162,179,268
mixed venous blood may best reflect acid-base status during On the other hand, various animal models suggest that the
resuscitation. Despite flow changes in a canine model of moder- pH-stat strategy may be preferable.76 Accidental hypothermia in
ate hypothermia, a significant correlation persists between arterial a human should not be considered a protective form of hiberna-
and mixed venous pH. The arteriovenous change in pH is 0.03 tion. The ectothermic (alpha-stat) approach appears to ensure
to 0.04 pH unit. adequate alveolar ventilation and acid-base balance at any tem-
The buffering capacity of cold blood is also greatly impaired. perature when the uncorrected pH is 7.42 and the uncorrected
In normothermia, when the arterial partial pressure of carbon PaCO2 is 40 mm Hg.132,162,273
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.
HEMATOLOGIC EVALUATION
The initial assumption was that 7.42 was the ideal “corrected” Severity of blood loss is easily underestimated. Hematocrit value
patient pH at all temperatures and that therapy should be directed increases because of a decline in plasma volume that leads to a
at maintenance of the corrected arterial pH at 7.42.339 A better 2% increase per 1° C (1.8° F) fall in temperature. In addition, total
intracellular pH reference is electrochemical neutrality, at which RBC mass might already be low because of preexisting anemia,
pH equals pOH. Because the neutral point of water at 37° C malnutrition, leukemia, uremia, or neoplasm.
(98.6° F) is pH 6.8, Rahn264 hypothesizes that this normal 0.6 unit The white blood cell count is frequently normal or low, even
pH offset in body fluids should be maintained at all temperatures. if sepsis is present. As a result, systemic leukopenia does not
Because the neutral pH rises with cooling, so should blood pH imply absence of infection, especially if the patient is at either
(Figure 7-5).268 age extreme; is debilitated, intoxicated, or myxedematous; or has
COLD AND HEAT
Relative alkalinity of tissues makes physiologic sense. Intracel- secondary hypothermia.192 The leukocyte count also drops during
lular electrochemical neutrality ensures optimal function of hypothermia because of direct bone marrow depression and
enzyme systems and transport proteins at all temperatures and hepatic, splenic, and splanchnic sequestration.
allows excretion of the neutral intracellular waste product Serum electrolyte levels must be continuously monitored and
urea.13 rechecked during warming. There are no safe predictors of elec-
Depressed metabolism and CO2 generation are physiologic trolyte values.120 Serum electrolytes fluctuate with temperature,
responses to temperature depression, because each temperature duration of exposure, and rewarming technique selected. Both
has its associated metabolic rate. Ventilation is intrinsically membrane permeability and sodium-potassium pump efficiency
adjusted to maintain a net charge on the defended parameter, also change with temperature. Isolated temperature depression
PART 2
the peptide-linked histidine-imidazole buffering system. has no consistent effect on sodium and chloride levels until well
One homeostatic approach to maintain a steady pH is to keep below 25° C (77° F). Plasma electrolyte levels are also affected by
the bicarbonate content constant. This is achievable only if total ongoing fluid shifts, prehydration, rehydration, and endocrine or
blood CO2 content does not change. Because CO2 solubility GI dysfunction.
increases with temperature depression, alveolar ventilation must The plasma potassium level is independent of temperature.
increase to compensate by lowering the PaCO2. Active ectotherms 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
8.0
lood pH changes. Hypokalemia is much more common in prolonged
ected b or chronically induced hypothermia.
corr
n
7.7 ic” u Systemic potassium deficiencies can also be exacerbated
t o t herm by prior diuretic therapy, alcoholism, diabetic ketoacidosis,
“Ec hypopituitarism, and inappropriate antidiuretic hormone (ADH)
“Endothermic” corrected blood
7.4 secretion. Hypokalemic digitalis sensitivity can be masked by
pH
144
CHAPTER 7 Accidental Hypothermia
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 may or may not be shivering and often have a distant gaze and
utilization. In addition, insulin release and activity are greatly slurred speech.98
reduced below 30° C (86° F). Because target cells are insulin The type of power available in the transport vehicle deter-
resistant, hyperglycemia is frequently seen initially. Markedly mines the options for active rewarming. These include forced-air
elevated glucose levels often correlate with hyperamylasemia and warming devices, heated IV fluids, and resistive and combustive
increased cortisol secretion.340 heat.99,101,106
Acute hypothermia initially elevates the serum glucose level Comatose patients require careful handling because they are
through catecholamine-induced glycogenolysis. Chronic expo- extremely likely to develop VF and asystole with rough handling
sure after exhaustion and glycogen depletion leads to hypogly- (Figure 7-6). Gurneys should be carried or rolled slowly to avoid
cemia.305 The symptoms often resemble those of hypothermia. jostling, and “code 3, full lights and sirens” transport should be
Cold-induced renal glycosuria is common and does not imply avoided if patients are perfusing spontaneously.
normoglycemia or hyperglycemia. When hypoglycemia and It is often impossible for rescuers to separate primary from
central neuroglycopenia are present, correction improves the secondary hypothermia when an unwitnessed cardiac arrest
level of consciousness only to that expected for the current core patient is found in a frigid environment. Patients with cold, stiff,
temperature. Cholesterol and triglyceride levels are also often and cyanotic primary hypothermia and fixed and dilated pupils
below normal. have been “reanimated.” A succinct summary of prehospital care
Hyperglycemia that persists during and after rewarming of the hypothermic patient is rescue, examine, insulate, and
should suggest diabetic ketoacidosis or hemorrhagic pancreatitis. transport.
Insulin is ineffective until the core temperature is well above 30° The initial rescuer and first responder often encounter obsta-
to 32° C (86° to 89.6° F) and therefore should be withheld to cles to preventing further heat loss.224,335 In certain imposing
avoid iatrogenic hypoglycemia after rewarming. Although prior geographic settings, treatment protocols are helpful to standard-
renal disease should be a consideration, blood urea nitrogen ize treatment while tacitly acknowledging that available health
(BUN) and creatinine concentrations are often elevated because care facilities may offer limited expertise and equipment. All
of decreased nitrogenous waste clearance by the cold diuresis. treatment recommendations must be adapted to local rescue
Ongoing fluid shifts render the BUN a poor reflection of circula- systems and facilities.78,274 Aeromedical transport is often ideal in
tory volume status.97 these circumstances.347 In difficult environments, proper proto-
The relationship between primary accidental hypothermia and cols with rehearsal and critique of mass casualty plans in the
hyperamylasemia appears to correlate with the severity of tem- cold are very important.
perature depression, but preexisting or hypothermia-induced The history obtained at the scene helps determine optimal
pancreatitis is present in up to 50% of patients. The abdominal treatment. The pertinent medical history regarding prior cardio-
examination is frequently unreliable. Therefore, lipase levels pulmonary, endocrinologic, and neurologic conditions is par
should be measured, except in minor cases.51 Ischemic pancre- ticularly helpful. The circumstances of discovery, duration of
atitis is attributable to microcirculatory collapse in hypothermia. exposure, associated injuries or frostbite, and obvious predispos-
Decreased pancreatic blood flow activates many proteolytic ing conditions should be recorded. No prognostic neurologic
enzymes. 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-
TREATMENT cult.306 The International Commission for Mountain Emergency
Four decisive factors should be considered when assessing non- Medicine recommends tympanic or esophageal field measure-
perfusing, severely hypothermic patients at the site. Rescuers ments, although these have significant limitations. Never insert
should reconsider the decision to resuscitate if there is evidence an esophageal probe unless the patient is already tracheally
of asphyxia or lethal injuries. A rigid thorax precludes closed- intubated.62,274
chest cardiopulmonary resuscitation (CPR), and a probable field Prolonged field treatment should be avoided whenever pos-
core temperature below 10° to 12° C (50° to 53.6° F) is ominous. sible, although the rescuer must attempt to prevent further heat
Pulses are difficult to palpate in vasoconstricted and extremely loss (Box 7-4). The rescuer should anticipate the presence of an
bradycardic patients. If possible, check for an organized rhythm irritable myocardium, hypovolemia, and a large temperature gra-
on a cardiac monitor. Bedside echocardiography is an ideal tool dient between the periphery and the core.353
to assess cardiac activity.28,229 The crux of the prehospital quandary surrounds the safety of
The combination of cold and exhaustion is a common cause providing prehospital heat. On the one hand, the original “meta-
of hypothermia in the field.142,223,224 The individual’s cold tolerance bolic icebox” concept223,224 implies that the risk of inducing a
depends on temperature, wind, clothing worn, and wetness. It nonperfusing rhythm in a hostile environment justifies simple
does not take an extremely cold temperature to produce hypo- stabilization of the core temperature; on the other hand, the
thermia after energy depletion. As mental function decreases, the warmer the heart, the better. Core temperature can decrease
hypothermic patient cannot respond to the rising threat. Judg- beyond reversal. Operant factors impacting the decision whether
ment is impaired, and the patient seldom takes necessary precau- or not to provide prehospital heat include core temperature, fluid
tions to prevent further disaster.24 status, predisposing factors, extent of frostbite, length and type
Field presentation of patients who are awake covers a wide of exposure, available expertise and position of transport, and
spectrum. Some persons are obtunded but conscious. Patients type of active rewarming available.
145
BOX 7-4 Preparing Hypothermic Patients for Transport
cerns regarding these agents before warming include precipita-
tion of acute withdrawal, seizures, and markedly increased
1. The patient must be dry. Gently remove or cut off wet clothing, oxygen utilization.
and replace it with dry clothing or a dry insulation system. Keep Most patients are volume depleted. Nevertheless, iatrogenic
the patient horizontal, and do not allow exertion or massage of volume overload should be avoided, because myocardial con-
the extremities. tractility is impaired. Improvisation during transport is often
2. Stabilize injuries (i.e., the spine; place fractures in the correct helpful. For example, a plastic IV container can be placed under
anatomic position). Open wounds should be covered before the patient’s back, shoulders, or buttocks to add warmth and
packaging. infusion pressure. Taping heat-producing packets to IV bags is
3. Initiate heated intravenous infusions (IVs) if feasible; bags can another option. These heating agents may be chemical packets
be placed under the patient’s buttocks or in a compressor or phase-change crystals, which produce heat for up to several
system. Administer a fluid challenge. hours. A variety of hot-pack hypothermia devices are commer-
4. Active rewarming should be limited to heated inhalation and cially available.
truncal heat. Insulate hot-water bottles in stockings or mittens, Intravenous fluid compressors are bulb-inflating cuffs that
and then place them in the patient’s axillae and groin. surround IV pouches to maintain flow. The Israeli army has a
5. The patient should be wrapped. Begin building the wrap by spring steel compressor system for IV bags. Portable IV fluid
placing a large plastic sheet on the available surface (floor, heaters are commercially available. The devices fit in-line and
ground), and on it place an insulated sleeping pad. A layer of
are DC powered. Commercial heaters are available that are
blankets, a sleeping bag, or “bubble wrap” insulating material
is laid over the sleeping pad. The patient is then placed on the
powered by a battery or from a DC converter plugged into an
insulation. Heating bottles are put in place along with IVs, and AC outlet.
the entire package is wrapped layer over layer, with the plastic Some warmers run on 12 volts from any vehicle or portable
as the final closure. The patient’s face should be partially battery. The current drain can be 4 amperes, and the insulation
covered, but a tunnel should be created to allow access for case may lose only 0.5° C (0.9° F) over 10 minutes. In a study
breathing and monitoring. 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.
The rescuer should stabilize injuries, protect the spine, splint Peripheral vessels may be difficult to locate, and IV lines are
fractures, and cover open wounds. Rescuer safety concerns typi- difficult to maintain during transport. Ideally, IV fluids should be
COLD AND HEAT
cally include unstable snow or ice and falling rocks.263 warmed to body temperature or slightly higher, but total body
Passive external rewarming with dry insulating materials warming is not accomplished with IV fluids in the field. Using
minimizes conductive, convective, evaporative, and radiant heat intraosseous infusions may provide a reasonable pathway for
losses. Remove any wet clothing from awake patients, and insu- fluid replacement in the field when peripheral vessels have
late them with sleeping bags, insulated pads, plastic “bubble collapsed.
wrap,” metallized or regular blankets, or even newspaper. One The methods selected to stabilize core temperature should be
device has a nylon shell and a polyester-pile liner to wick mois- tailored to the severity of hypothermia and the field circum-
ture. In a survey of common field rewarming methods used by stances.313 Gently removing or cutting off wet clothing while the
mountain rescue teams, the most common techniques included patient remains prone may be the best option to limit heat loss
PART 2
chemical pads, sleeping bags, body-to-body contact, and hot- and prevent orthostasis. Passive external rewarming with water-
water bottles.118 proof insulation suffices for mild chronic hypothermia. The addi-
If extrication will be delayed, give mildly hypothermic patients tion of a vapor barrier will reduce evaporative heat loss.127,128
warm, sweet drinks, warm gelatin (Jell-O), Tang, juice, tea, or Other common equipment types include duvets and plastic
cocoa, because carbohydrates fuel shivering. Avoid heavily caf- bubble wrap.159
feinated drinks. A significant diuresis is usually associated with In a series of patients requiring cardiopulmonary bypass
the cooling process, so the patient’s fluid balance must be reas- (CPB), hypothermia was maintained during transport.332 Whether
sessed. Once mildly hypothermic patients are well hydrated, they supplemental active field rewarming should be initiated en route
can be walked out to safety. to the ED, and in which subsets of patients, is not definitively
Handle severely hypothermic patients gently, immobilizing established. Intentionally maintaining hypothermia during gentle
them to prevent exertion. Although exercise can rewarm a person transport seems wise only for patients with an isolated closed-
more rapidly than shivering, it also greatly increases afterdrop.97,100 head injury. For long helicopter or ambulance transports, the
Patients must be kept in a horizontal position whenever possible ideal ambient temperature in the vehicle is unclear. Rescue per-
to minimize orthostatic hypotension. Vigorously massaging cold sonnel comfort is important to maximize performance, and it is
extremities is also contraindicated, because skin rubbing, as with unlikely that heating the interior above 25° C (77° F) will acceler-
ethanol, suppresses shivering thermogenesis and increases cuta- ate the rate of rewarming or induce vasodilation.
neous vasodilation. “Field rewarming” is a misnomer, because adding much heat
Field management of the comatose patient first involves ven- to a hypothermic patient in the field is difficult.82 Warmed IV
tilation to raise oxygen saturation. Rescue breathing may be solutions, heated sarongs, or heated humidified oxygen can
difficult because of chest stiffness and significant resistance to provide only a small amount of heat input. Hot-water bottles or
diaphragmatic motion. Forced ventilation increases oxygenation, heat packs can be placed in the axillae, in the groin, and around
which helps stabilize cardiac conduction. The single greatest the neck. Casualty evacuation bags are available in many models
factor in maintaining perfusion during severe hypothermia is and designs. Some have more insulation than others, and some
oxygenation.98 At altitude, a portable hyperbaric chamber may have specialized zippers and openings that allow access to the
prove useful.42 victim during transport. Most bags are windproof and waterproof.
During a storm, prolonged field rewarming may be the only Experimentally, convective air warming is more effective than
viable option until meteorologic conditions become more favor- resistive heating147 and might be a viable option in some transport
able for land or, preferably, aeromedical evacuation.347 Many situations.
prehospital medications freeze in solution. If this occurs, their Inhalation therapy is safe for active rewarming of patients with
pharmacologic activity after thawing is indeterminate (see Appen- profound hypothermia in the field.120 It helps prevent respiratory
dix at the end of this book). heat loss, which represents an important percentage of heat
The rescuer should administer an IV fluid challenge with 250 production when the core temperature is below 32° C (89.6° F).
to 500 mL of heated (37° to 41° C [98.6° to 105.8° F]) 5% dextrose Technical difficulties can occur while using inhalation rewarming
in normal saline solution. Empirical 50% dextrose is indicated devices in volunteers, illustrating the importance of proper
only in select cases. The safety of several reversal agents, such instruction for the rescuer.302 Under certain conditions, the impact
as naloxone or flumazenil, used in the field is unknown. Con- of field inhalation therapy on the rate of rewarming may not be
146
significant.106 In shivering, mildly cold patients the thermal advan- convective warming is more efficient than resistive heating.147 The
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
(6 inches) is fairly reliable unless adjacent to cold feces. Rectal inaccurate if the canal is full of cerumen or snow, or is not
temperature lags behind core temperature fluctuations and is also adequately sealed.85
affected by lower-extremity temperatures (Table 7-3).341 Although bladder temperature measurement devices can be
Esophageal temperature measurements are far preferable in incorporated into the urinary drainage catheter, the readings
severe cases when airway protection is provided with endotra- are frequently unreliable. Measurements are falsely elevated with
cheal intubation. Esophageal temperature approximates cardiac heated peritoneal lavage and, more often, low as a result of
temperature. Because the upper third of the esophagus is near cold-induced diuresis and crystalloid resuscitation.
the trachea, the probe may read falsely high during heated inha-
lation therapy if the probe is positioned too proximally. The Initial Stabilization
probe does not have markings but should be placed 24 cm (9.5 After core temperature measurement, all clothing should be
inches) below the larynx into the lower third of the esophagus. gently removed or cut off with minimal patient manipulation.251
The greatest discordance between rectal and esophageal tem- Immediately insulate the patient with dry blankets. Apply a
peratures is noted during the transition phase between cooling cardiac monitor, and insert IV catheters as needed. Arterial cath-
and rewarming. eter insertion may help in managing select, profoundly hypother-
Tympanic temperature theoretically approximates hypotha- mic patients. Pulmonary artery catheters can precipitate cardiac
lamic temperature and can be accurately measured with ther- 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
BOX 7-5 Resuscitation Requirements arrhythmias. A better option is temporary catheterization of the
femoral vein.
Thermal Stabilization The accuracy of pulse oximetry during conditions of poor
• Conduction perfusion is unclear, because there are no studies in accidental
• Convection hypothermia.172 In one study of hypothermic patients on CPB,
• Radiation the finger probes were inaccurate.46 The probe may be more
• Evaporation reliable if a vasodilating cream is applied first. In addition, there
• Respiration is a lag time in pulse oximetry with hypoxic desaturation in
Maintenance of Tissue Oxygenation anesthetized hypothermic individuals. There is less failure with
• Adequate circulation forehead pulse oximetry compared to fingertip readings.205
• Adequate ventilation In theory, combining pulse oximetry with near-infrared spec-
Identification of Primary vs. Secondary Hypothermia troscopy could provide tissue perfusion information during hypo-
Rewarming Options
thermic vasoconstriction. More practically, an accurate core and
peripheral muscle temperature would prove just as useful. The
• Passive external rewarming
• Active external rewarming
value of end-tidal CO2 measurements to assess adequacy of tissue
• Active core rewarming 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
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/
Treatment modalities
Forced-Air Surface Rewarming
FIGURE 7-8 First-hour rewarming rates from a large multicenter Forced-air surface warming systems efficiently transfer heat.11,99,176
survey. ACR, Active core rewarming; AER, active external rewarming; Hot air is circulated through a blanket. The air exits apertures
ECR, extracorporeal rewarming; ETT, endotracheal tube; GBC, gastric- on the patient side of the cover, permitting the convective trans-
bladder-colon; IV, intravenous; NT, nasotracheal tube; P, peritoneal; fer of heat.215 In one study that rewarmed accidental hypothermia
PER, passive external rewarming. (Data from Danzl DF, Pozos RS, patients in the ED, rewarming shock and core temperature after-
Auerbach PS, et al: Multicenter hypothermia survey, Ann Emerg Med drop were not noted299 with the use of heated inhalation and
COLD AND HEAT
16:1042, 1987.) 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
to minimize the normal mechanisms of heat loss. When the wind than passive metallic-foil insulation.115
is blocked, less heat escapes through radiation, convection, and A study of full-body forced-air warming compared a com-
conduction. Conditions with higher ambient humidity slightly mercially available convective blanket with simple air delivery
limit respiratory heat loss. beneath bedsheets.163 Directed 38° C (100.4° F) warm air under
Aluminized body covers also reduce heat loss.83 Nevertheless, the sheets warmed standardized thermal bodies containing water
PART 2
endogenous thermogenesis must generate an acceptable rate of very efficiently. Commercially available convective air rewarming
rewarming for PER to be effective.239 Humans are functionally devices are also effective. Another option is conductive warming
poikilothermic below 30° C (86° F), and metabolic heat produc- with a warm-water–filled heat exchange blanket.
tion is less than 50% of normal below 28° C (82.4° F). Shivering The use of forced-air surface warming systems is most practi-
thermogenesis is also extinguished below 32° C (89.6° F). This cal in the ED.174,189 Although these devices decrease shivering
thermoregulatory neuromuscular response to cold normally thermogenesis, afterdrop is minimized and heat transfer can be
increases heat production from 250 to 1000 kcal/hr unless gly- significant. Thermal injury to poorly perfused, vasoconstricted
cogen is depleted before or during cooling. skin using some of the other external heat application techniques
Older adult patients in whom mild hypothermia develops is a hazard in both adults and children.118 In particular, avoid
gradually are less acceptable candidates for PER. When rewarm- resistance-heat electric blankets on which a patient lies, because
ing times are markedly prolonged (more than 12 hours), com- vasoconstricted capillaries are compressed and burns occur
plications tend to increase. easily.
Patients who are centrally hypovolemic, glycogen depleted, Another AER option is a thermoregulatory system that circu-
and without normal cardiovascular responses should be stabi- lates warm water through energy transfer pads placed on the
lized and rewarmed at a conservative rate. In a multicenter chest and lower limbs.48 The core temperature measured via
survey, the rewarming rates for older adults in the first (0.75° C probe is fed back to the control module.
[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 Immersion
mortality rate (Figure 7-8).62 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
ACTIVE REWARMING afterdrop. In normothermic men with coronary artery disease,
Active rewarming, which is the direct transfer of exogenous heat the cardiovascular stress and arrhythmogenic response to immer-
to a patient, is usually required with temperatures below 32° C sion in a hot tub are mild, less than those induced by exercise.
(89.6° F).185 Rapid identification of any impediment to normal In contrast, placing the hands and feet in warm water theoreti-
thermoregulation, such as cardiovascular instability or endocri- cally opens arteriovenous shunts and accelerates rewarming in
nologic insufficiency, is essential.186 Intrinsic thermogenesis may acute hypothermia. Scandinavian palmar heat packs may capital-
also be insufficient after traumatic spinal cord transection or ize on this physiology.
pharmacologically induced peripheral vasodilation. Some patient
populations generally require active rewarming.66 For example, Arteriovenous Anastomosis Rewarming
aggressive rewarming of infants minimizes energy expenditure The original description of this noninvasive AER technique is by
and decreases mortality. In these circumstances, vigorous moni- Vangaard.324 Exogenous heat is provided by immersion of the
toring for respiratory, hematologic, metabolic, and infectious distal extremities (hands, forearms, feet, calves) in 44° to 45° C
complications is essential.329 (111.2° to 113° F) water. The heat opens arteriovenous anasto-
When active rewarming is needed, heat can be delivered moses (AVAs). These structures are 1 mm (0.04 inch) below the
externally or to the core. Active external rewarming (AER) epidermal surface in the digits.16,220 Countercurrent heat loss is
150
minimized because the superficial veins are not close to the arte-
O2 (% saturation)
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 50 NORMAL
during peripheral vasoconstriction. In combination with localized T 37° C
heat application, application of subatmospheric pressure theoreti- pH 7.40
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 0
neoprene collar. After a vacuum pressure of −40 mm Hg is
0 50 100
created, heat is applied over the dilated AVAs. The thermal load
can be provided by an exothermic chemical reaction or a heated PO2 (mm Hg)
perfusion blanket.
The clinical efficacy of AVA rewarming in accidental hypo- FIGURE 7-9 Oxyhemoglobin dissociation curve at 37° C (98.6° F). At
thermia is unclear.39,56 The potential for superficial burns of colder temperatures, the curve shifts to the left.
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 ventricular contractions (PVCs) may reappear during rewarming,
rewarming increased dramatically,109 but another study compar- there is no evidence that inhalation rewarming precipitates new,
ing negative-pressure rewarming with forced-air warming failed clinically significant ventricular arrhythmias. Vapor absorption
to replicate these results.308 does not increase pulmonary congestion or wash out surfactant.
When the pulmonary vasculature is heated, warmed oxygenated
Active Core Rewarming blood that returns to the myocardium could attenuate intermittent
Various techniques that can effectively deliver heat to the core temperature gradients. The amplitude of shivering is also lowered,
include heated inhalation, heated infusion, diathermy, lavage an advantage in more severe cases. This suppression could
(gastric, colonic, mediastinal, thoracic, peritoneal), and extracor- decrease heat production in mild hypothermia, although experi-
poreal rewarming. Figure 7-8 lists average first-hour rewarming mentally the core temperature continues to rise.56
rates reported with some of these techniques in one multicenter There are numerous oxygenation considerations in hypother-
study. Although hemodynamic instability impacts the rewarming mia (see Box 7-1). The “functional” value of hemoglobin at 28° C
strategy, noninvasive techniques often succeed unless significant (82.4° F) is 4.2 g/10 g in patients on CPB. The oxyhemoglobin
comorbidities exist.269,323 dissociation curve also shifts to the left (Figure 7-9). This impairs
release of oxygen from hemoglobin into the tissues. Although
Airway Rewarming some patients can self-adjust their respiratory minute volume
The effectiveness of the respiratory tract as a heat exchanger (RMV) for current CO2 production, this may not be possible if
varies with technique and ambient conditions.218 Dry air has low there are additional toxins or metabolic depressants.58
thermal conductivity, and complete humidification coupled with Most humidifiers are manufactured in accordance with Inter-
an inhalant temperature of 40° to 45° C (104° to 113° F) is national Standards Organization (ISO) regulations. The humidifier
required.267 The main benefit of airway rewarming is prevention will not exceed 41° C (105.8° F) close to the patient outlet with
of respiratory heat loss. Heat yield can represent 10% to 30% of a 6-foot (180-cm) tubing length.331 If the decision is made to alter
the hypothermic patient’s heat production when respiratory equipment, carefully monitor the temperature and do not exceed
minute volume is adequate.27 45° C (113° F). The only report of thermal airway injury was in
The rate of rewarming is greater using an endotracheal tube a patient ventilated by ETT for 11 hours with 80° C (176° F)
(ETT) than by mask. In one series, the reported rewarming rate inhalant.
with a 40° C (104° F) aerosol was 0.74° C (1.33° F) per hour by Strategies to circumvent the 41° C ceiling include reduction
mask and 1.22° C (2.2° F) per hour by ETT.222 In a multicenter of tubing length, adding additional heat sources, disabling the
survey,62 the average first- and second-hour rewarming rates in humidifier safety system, and placing the temperature probe
severe cases were 1.5° to 2° C (2.7° to 3.6° F) per hour. The outside the patient circuit.331 Label all modified equipment to
decremental efficiency at higher temperatures slows the rate avoid routine use. A volume ventilator with a heated cascade
(10 kcal/hr) in mild cases.62 humidifier can also deliver CPAP or positive end-expiratory pres-
Thermal countercurrent exchange in the cerebrovascular bed sure (PEEP) if needed during rewarming. The airway rewarming
of humans67 affects the efficiency and influence of heated-mask rates clinically range from 1° to 2.5° C (1.8° to 4.5° F) per hour.58
ventilation during hypothermia. Known as the rete mirabile, this In stable patients, circumventing the 41° C ceiling may not be
system could preferentially rewarm the brainstem. Heated inhala- worth the effort because the clinical benefit is modest.162
tion by face mask continuous positive airway pressure (CPAP) Heat and moisture exchangers function as artificial nares by
may correct the ventilation-perfusion mismatch.40 Heated humidi- trapping exhaled moisture and then returning it. The exchangers
fied oxygen by face mask is not feasible in some patients with provide inadequate humidification to treat accidental hypother-
coexistent midface trauma. mia. With prolonged use, ETT occlusion and atelectasis are both
Heat liberated during airway rewarming is produced mainly problems.49
from condensation of water vapor. The latent heat of vaporiza- Airway rewarming is indicated in the ED when core tempera-
tion of water in the lungs is slightly lower than 540 kcal/g H2O. ture is lower than 32.2° C (90° F) on arrival. Although airway
This is multiplied by the liters per minute (L/min) ventilation to rewarming provides less heat than other forms of active core
calculate the quantity of heat transfer. When core temperature is warming, it prevents normal respiratory heat and moisture loss
28° C (82.4° F), the rate of rewarming with heated ventilation at and is safe, fairly noninvasive, and practical in all settings.
42° C (107.6° F) equals endogenous heat production. Although
the effect on overall thermal balance can be minimal, there may Heated Infusions
be preferential rewarming of thermoregulatory control centers.58 Cold-fluid resuscitation of hypovolemic patients can induce
Heated humidified inhalation ensures adequate oxygenation, hypothermia. In one series of previously normothermic patients
stimulates pulmonary cilia, and reduces the amount and viscosity with major abdominal vascular trauma, the average temperature
of cold-induced bronchorrhea. Although preexisting premature 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
dental hypothermia. bladder heat exchange are also very limited.336,337 Aesthetic obsta-
In summary, IV solutions and blood should be routinely cles aside, heat transfer through colonic irrigation is negligible.
heated during hypothermia resuscitations. Various blood warmers
are available commercially, but countercurrent in-line warmers Mediastinal Lavage
are the most efficient.148 A mathematic model indicates that infu- Mediastinal irrigation and direct myocardial lavage are alterna-
sion heating devices are essential in trauma patients with high tives in patients lacking spontaneous perfusion. A standard left
fluid requirements.26 thoracotomy is performed while CPR is continued. Opening the
pericardium is unnecessary unless an effusion or tamponade is
HEATED LAVAGE 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),
Gastrointestinal Lavage then suctions and replaces warm fluids.36
Heat transfer from irrigation fluids is usually limited by the avail- The physician may attempt internal defibrillation after myo-
able surface area. The irrigant should not exceed 45° C (113° F). cardial temperature reaches 26° to 28° C (78.8° to 82.4° F). Unless
Direct GI irrigation is less desirable than irrigation via intragastric a perfusing rhythm is achieved, lavage and all available heating
or intracolonic balloons because of induced fluid and electrolyte techniques are continued until myocardial temperature exceeds
fluxes. Exceeding 200- to 300-mL aliquots may force fluid into 32° to 33° C (89.6° to 91.4° F). A standard post-thoracotomy tube
the duodenum; therefore frequent fluid removal by gravity drain- in the left side of the chest could provide an avenue for contin-
age minimizes “lost” fluid. A log of input and output is essential. ued rewarming via thoracic irrigation.
This facilitates estimation of fluid balance during resuscitation A median sternotomy also allows ventricular decompression
and helps determine if irrigation should be abandoned in antici- and direct defibrillation.190 One potential disadvantage of both
pation of dilutional electrolyte disturbances. these techniques is that open cardiac massage of a cold, rigid,
To avoid these limitations, a double-lumen esophageal tube and contracted heart may not generate flow.5,57 Unless immediate
is available, as are other modified tubes. Patients should be tra- CPB is an option, mediastinal irrigation and direct myocardial
cheally intubated before gastric lavage. Because of the proximity lavage are indicated only if cardiac arrest has occurred. In this
of an irritable heart, overly vigorous placement of a large gastric circumstance, personnel skilled in the technique should also initi-
tube is not advised. In a multicenter survey, gastric, bladder, and ate all other available rewarming modalities.
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 Thoracic Lavage
3.6° F) for the second hour.62 Irrigation of the hemithoraces is a valuable rewarming
Commercially available kits designed for gastric decontamina- adjunct.37,171,317 An important semantic issue is that closed thoracic
tion are convenient (Figure 7-10). The use of a Y connector and lavage via two thoracostomy tubes differs from open mediastinal
clamp simplifies the exchanges. Ideal dwell times for thermal and direct myocardial lavage. With the latter, closed-chest CPR
exchange depend on flow rates and may average several minutes. is not possible. Two large-bore thoracostomy tubes (36 French
In direct gastric lavage, warmed electrolyte solutions, such as [36F] to 40F in adults; 14F to 24F, ages 1 to 3; 20F to 32F, ages
normal saline or Ringer’s lactate, are administered via nasogastric 4 to 7) are inserted in one or both of the hemithoraces. One is
tube.191 After 15 minutes the solution is aspirated and replaced placed anteriorly in the second to third intercostal space at the
152
Warmed
Saline
Rib
2
AA S 3
Heat exchanger V
C
RB Lung
4
Fluid T6
Air
warmer eliminator Midclavicular 5
line
6
Saline out
Postaxillary
line B
Autotransfusion
bag
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 massage of a rigid, contracted heart may not be possible in severe
the fourth to fifth intercostal space. Normal saline heated to 40° cases before bypass, which is a problem with mediastinal
to 42° C (104° to 107.6° F) is then infused via a nonrecycled sterile irrigation.5,57,61
system (Figure 7-11A).169 Various complications should be considered. Left-sided tho-
A high-flow countercurrent fluid infuser heats to 40° C (104° F) racostomy tube insertion into patients who are perfusing could
and delivers normal saline in 1-L or preferably 3-L bags into the easily induce VF. Patients with pleural adhesions or a history of
afferent chest tube.260 Ideally, connect into the tubing with stan- pleurodesis have poor infusion rates, and subcutaneous edema
dard 0.19-inch internal-diameter suction connection tubing and may develop. If the fluids are infused under pressure without
a sterilized plastic graduated two-way connector, because this adequate drainage, intrathoracic hypertension or even a tension
facilitates adaptation to any size of chest tube (Figure 7-11A). hydrothorax can develop and cause expected adverse cardiovas-
The effluent is then collected in a thoracostomy drainage set. cular effects.157,256
The reservoir must be emptied frequently. Alternatively, when a
single chest tube is used, 200- to 300-mL aliquots are used for Peritoneal Lavage
irrigation, and suctioning is achieved through a Y connector. The Heated peritoneal lavage is a technique available in most facilities
Y connector is also useful for irrigating both hemithoraces with (Figure 7-12). Heat is conducted intraperitoneally via isotonic
a single fluid warmer (Figure 7-11B). dialysate delivered at 40° to 45° C (104° to 113° F).327
Fluid can be infused into the anterior higher chest tube (affer- Before lavage is initiated, imaging should be obtained because
ent limb) and suctioned or gravity drained out the lower posterior subsequent films may reveal subdiaphragmatic air introduced
tube (efferent limb) into a water-seal chest drain.117 Infusion during the procedure. The bladder and stomach must be emptied
inferoposteriorly with suction anteriorly can increase dwell before insertion of the catheter. The two common techniques for
times.148 The efficiency of thermal transfer varies with flow rates introducing fluid into the peritoneal cavity are the mini-laparotomy
and dwell times. Once the patient is successfully rewarmed, the and the percutaneous puncture.
upper tube should be removed and the lower tube left in place The “minilap” requires an infraumbilical incision through the
to allow residual drainage. linea alba. A supraumbilical approach is necessary if previous
Closed sterile thoracic lavage is a natural choice in the ED surgical scars, a gravid uterus, or pelvic trauma is identified. The
during potentially salvageable cardiac arrest resuscitations.346 peritoneum is punctured under direct visualization and dialysis
Thoracic lavage is an option either as a bridge to CPB or when catheter(s) inserted. A much simpler and more rapid technique
CPB is initially unavailable. In patients who are perfusing, this is the guidewire, or Seldinger, variation of the percutaneous
technique should be considered hazardous unless extracorporeal puncture. The site is infiltrated if necessary with lidocaine, and
rewarming capability is immediately available. Many hypothermic a small stab incision is made. An 18- to 20-gauge needle pene-
trauma patients are irrigated successfully during surgery. trates the peritoneum, and a guidewire is introduced. Entry into
The clinically reported infusion rates range from 180 to the peritoneum is usually recognizable by a distinct “pop.” Dis-
550 mL/min. The overall rate of rewarming should easily equal posable kits are available. The 8F lavage catheter is inserted over
or exceed that achievable with peritoneal lavage and is often the wire and advanced into one of the pelvic gutters. Double-
3° to 6° C (5.4° to 10.8° F) per hour. The surface area of the catheter systems with outflow suction speed rewarming.
pleural space is well perfused. An added benefit is preferential Normal saline, lactated Ringer’s solution, or standard 1.5%
mediastinal rewarming. In addition, closed-chest compressions dextrose dialysate solution with optional potassium supplementa-
during cardiac arrest can maintain perfusion. Open cardiac tion can be used. Isotonic dialysate is heated to 40° to 45° C (104°
153
14F catheter
Peritoneum
Fascia of
linea alba
Wire
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-
C loop catheter has a temperature control element at the tip.
FIGURE 7-12 Peritoneal lavage. A, Mini-laparotomy for peritoneal Available models have a fail-safe feature on the console that must
lavage. B, The catheter in place with the needle removed and the wire be circumvented to allow rewarming if the core temperature is
introduced. C, An 8F catheter is introduced over the wire, and the wire below 30° C (86° F).181
is then removed.
EXTRACORPOREAL BLOOD REWARMING
Table 7-4 summarizes the techniques for extracorporeal blood
rewarming.
154
In another variation of the extracorporeal venovenous circuit,
155
Oxygenator
and
vortex pump Arterial line
Portable Heat 16-20F
bypass exchanger
machine
Venous line
16-30F
rewarming (ACR) techniques, and it reduces the high blood affected electroencephalographic (EEG) regeneration. The other
viscosity associated with severe cases. CPB should also be con- theoretical concern is the possibility of increased bubbling if high
sidered when severe cases do not respond to less invasive perfusate temperature gradients are used. Most investigators use
rewarming techniques, in patients with completely frozen 5° C (9° F) gradients21or 10° C (18° F) gradients.22 Neuromonitoring
extremities, and when extensive rhabdomyolysis is accompanied during rewarming is advised. In severe cases, evoked cerebral
by major electrolyte disturbances.154 responses before EEG regeneration could help assess the recov-
Various extracorporeal rewarming techniques can be lifesav- ering brain.284
ing in select profound cases of hypothermia.122 A 65-year-old A variety of techniques decrease the need for IV anticoagula-
woman survived sequela free after 520 minutes of cardiac arrest tion with heparin, which previously limited clinical applicabil-
PART 2
treated with CPR and CPB.221 Complete recovery was also ity.168 Heparin-coated perfusion equipment can be considered
reported in three severely hypothermic tourists after prolonged without systemic heparinization in patients with hypothermic
periods of cardiac arrest and CPR.5 In a review of 17 cases, there cardiac arrest and intracranial trauma. The use of nonthrombo-
were 13 survivors.297,332 In another series rewarming 32 patients genic pumps, coupled with enhanced physiologic fibrinolysis
with CPB, 15 are long-term survivors. The average age was 25.2 seen in the first hour of CPB, should be considered. ECMO
years. Their mean presenting esophageal temperature was 21.8° C requires lower levels of anticoagulation in addition to the pos-
(71.2° F), and the mean interval between discovery and CPB was sibility of prolonged extracorporeal-assisted resuscitation; these
141 minutes. factors may explain the published mortality reduction compared
The standard femoral-femoral circuit includes arterial and with CPB.33
venous catheters, mechanical pump, membrane or bubble oxy- Complications with the standard technique include vessel
genator, and heat exchanger (Figure 7-15). A 16F to 30F venous damage, air embolism, hemolysis, DIC, and pulmonary edema
cannula is inserted via the femoral vein to the junction of the right (Box 7-8). ECMO appears to decrease the incidence of severe
atrium and the inferior vena cava. The tip of the shorter 16F to pulmonary edema in some patients.33 Endothelial leakage
20F arterial cannula is inserted 5 cm (2 inches) or proximal to the increases compartment pressures and exacerbates frostbite. If
aortic bifurcation. Consider use of 32F venous and 28F arterial adequate flow rates of 3 to 4 L/min (50 to 60 mL/kg/min) cannot
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 BOX 7-8 Extracorporeal Rewarming: Complications
surgical technique insertion and may help decompress the dilated,
nonbeating heart. Transesophageal echocardiography can help and Contraindications
evaluate ventricular load and valve function.
Complications
Heated, oxygenated blood is returned via the femoral artery.19
• Vascular injury
Femoral flow rates of 2 to 3 L/min can elevate core temperature
• Air embolism
1° to 2° C (1.8° to 3.6° F) every 3 to 5 minutes. In one review, • Pulmonary edema
the mean CPB temperature increase was 9.5° C (17.1° F) per hour. • Coagulopathies (hemolysis, disseminated intravascular
Most pumps can generate full flow rates up to 7 L/min.297 Con- coagulation)
sider the use of vasodilator therapy with IV nitroglycerin to • Frostbite tissue damage
facilitate perfusion.199,200 Initiate bypass flow rates at about 2 L/ • Extremity compartment syndromes
min and gradually increase to 4 to 5 L/min. Vasoactive agents
Contraindications
may be needed to maintain the cardiac index at 30 L/min/m2 or
• Futile resuscitations
more and a (low) systemic vascular resistance of 1000 dynes/sec
• Lack of venous return
× cm−5 or less.207 • Intravascular clots or slush
The optimal temperature gradient and bypass rewarming rates • Complete heparinization would be hazardous*
are unknown. One study of rewarming via CPB in a swine model • Cardiopulmonary resuscitation is contraindicated (see Box 7-9)
cooled to 23° C (73.4° F) addresses this concern. An excessive
temperature gradient between brain tissue and circulant adversely *Unless with athrombogenic tubing or adequate physiologic fibrinolysis.
156
Diathermy
Yes Responsive
No
Respirations
Yes No
Cardiac monitor
Cardiac monitor
PER
ACR and truncal AER
157
patients with hypothermia.303 The optimal rate and technique compression rate that allows maximal left ventricular end-diastolic
remain unclear. Definitive prehospital determination of cardiac filling. Interestingly, transesophageal echocardiography in a
activity requires a cardiac monitor or portable ultrasound, because canine model demonstrates mitral valve closure during chest
misdiagnosis of cardiac arrest is a hazard. Peripheral pulses are compression except during low-impulse (downstroke momen-
difficult to palpate when extreme bradycardia is present with tum) compressions. Compression of a cold, stiff chest wall may
peripheral vasoconstriction.124,249,343 be equivalent to low impulse.57
Asystole may be as common a presenting rhythm as VF. In In hypothermia, the role of a “thoracic pump” with the heart
the field, differentiating VF from asystole may be impossible. as a passive conduit is an attractive hypothesis. The phasic altera-
Possible causes of VF include acid-base fluxes, hypoxia, and tions in intrathoracic pressure generated by compressions are
coronary vasoconstriction with increased blood viscosity. Chest equally applied to all the cardiac chambers and thoracic vessels.
compressions and various therapeutic interventions are also The mitral valve remains open during compression, and blood
implicated.116,245 The role of acid-base fluxes is not clear. Mild continues to circulate through the left side of the heart.
alkalosis appears somewhat protective against VF during con- Myocardial compliance can be severely reduced in hypother-
trolled, induced hypothermia.179 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
RESPIRATORY CONSIDERATIONS cardiac massage could have been.” Open cardiac massage can
When cardiopulmonary arrest develops during resuscitation, be combined with mediastinal irrigation when immediate CPB is
noncardiac causes are often pulmonary emboli or progressive an option.36,37,38
respiratory insufficiency. Provision of adequate oxygen supply is Chest wall elasticity is also decreased with cold, as is pulmo-
essential during rapid rewarming. For each 1° C (1.8° F) rise in nary compliance. If the abdominal muscles are not kneadable,
temperature, oxygen consumption increases up to three times the clinician should anticipate that the stiff chest wall will prevent
(see Box 7-1). Eventually, regional cerebral oxygen saturation adequate ventilation. Lastly, more force is needed to depress the
monitoring may help differentiate shockable VF and ventricular chest wall sufficiently to generate intrathoracic vascular compart-
tachycardia (VT).1 ment pressure gradients.
Endotracheal intubation and ventilation decrease atelectasis Despite these potential physiologic explanations, a large
and ventilation-perfusion mismatch. Complete airway protection number of neurologically intact survivors are reported after pro-
averts aspiration, which is otherwise common with depressed longed closed-chest compressions. The explanation lies in mea-
airway reflexes, bronchorrhea, and ileus. CO2 production also suring intrathoracic pressures during hypothermic closed-chest
COLD AND HEAT
tiple operators in various settings.62 No induced arrhythmias were Mechanical thoracic compression devices should be consid-
recognized, which is consistent with several reports.186,222 Poten- ered during prolonged resuscitations with limited availability of
tial arrhythmogenic factors include hypoxia, mechanical jostling, personnel. In addition, an automatic mechanical chest compres-
and acid-base or electrolyte fluctuations. sion device may serve as a bridge while establishing the capabil-
The indications for endotracheal intubation in hypothermia ity for CPB.343
are identical to those in normothermia.103 Ciliary activity is During hypothermic cardiac arrest in swine, cardiac output,
depressed in hypothermia, frothy sputum produces chest conges- cerebral blood flow, and myocardial blood flow averaged 50%,
tion, and bronchorrhea resembles pulmonary edema. Fiberoptic 55%, and 31%, respectively, of those achieved during normother-
or blind nasotracheal intubation may be preferable to cricothy- mic closed-chest compressions. Blood flow to these areas did
roidotomy when cold-induced trismus or potential cervical spine not decrease with time, unlike in the normothermic group. Hypo-
trauma is present. Oral rather than nasal intubation is advisable thermic rheologic changes, including increased viscosity, also
in patients with coagulopathy, to avoid major epistaxis. affect flow. Peripheral vascular resistance is expected to increase
Rapid-sequence intubation may be impossible when severe during vasoconstriction, but in the swine there was no difference
cold-induced trismus is present and the mandible will not move. in systemic and organ vascular resistance between normothermic
In the milder cases, hypothermia prolongs the duration of neu- and hypothermic CPR.209
romuscular blockade. Drug metabolism is also prolonged with In a multicenter survey of 428 cases, 9 of the 27 patients
vecuronium and atracurium. As a result, neuromuscular blockade receiving CPR initiated in the field survived, as did 6 of 14
should be avoided.162 Efficacy, metabolism, and clearance are patients with ED-initiated CPR62 (see Box 7-9).
very unpredictable, and assessment of sedation adequacy is Cardiac output is the product of heart rate and stroke volume;
difficult. 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
BLOOD FLOW DURING CHEST COMPRESSIONS recovered after 220 minutes at half the normal compression
During normothermic conditions, blood flow partially results rate.243 A patient at 16.9° C (62.4° F) recovered neurologically after
from phasic alterations in intrathoracic pressure and not just 307 minutes of intermittent CPR. At 3-month follow-up, she
from direct cardiac compression. Antegrade flow occurs without showed a good physical and neurologic recovery.23 The optimal
left ventricular compression in a normothermic canine model.240 rate probably has a direct linear relationship with the degree of
Closed-chest compressions increase intrathoracic pressure.206 hypothermia.
When thoracic inlet venous valves are competent, the resultant Tissue decomposition, apparent rigor mortis, dependent livid-
pressure gradient between arterial and venous compartments ity, and fixed, dilated pupils are not reliable criteria for withhold-
generates supradiaphragmatic antegrade flow. ing CPR. In addition, intermittent flow may provide adequate
The “cardiac pump” model is predicated on closure of the support during evacuation. CPR should not be withheld only
mitral valve and opening of the aortic valve during chest com- because continuous chest compressions cannot be ensured.44,78
pression. This allows a forward stroke volume. During release of Intermittent flow may be preferable to no flow. The lowest tem-
compression, transmitral flow can fill the left ventricle. Optimal perature documented in an infant survivor of accidental hypo-
cardiac output is thus generated by achieving the maximal thermia is 15.2° C (59.4° F); in an adult, 13.7° C (56.7° F); and in
158
induced hypothermia, 9° C (48.2° F).102,237,244 One patient recov- Second messengers in the cascade are signals during ischemia
159
7-year, 30° C (86° F) slumber. Ironically, so was a quiescent oat
VENTRICULAR ARRHYTHMIAS
cell carcinoma. Preexisting chronic ventricular ectopy may be suppressed in a
Cold induces stimulation of the hypothalamic-pituitary-thyroid cold heart. Ectopy developing during rewarming is problematic.
axis. Unless myxedema is suspected, empirical therapy is not The history from the hypothermic patient may be unproductive,
recommended. A history of neck irradiation, radioactive iodine, and the past cardiac history is often unavailable.
Hashimoto’s thyroiditis, or surgical treatment of hyperthyroidism Transient ventricular arrhythmias should generally be left
should heighten the clinician’s suspicion of myxedema. Failure untreated. In one study of 22 continuously monitored patients
to rewarm despite an appropriate course of therapy is a further with hypothermia, supraventricular arrhythmias were common
clue.204 (nine cases) and benign.266 Ventricular extrasystoles developed
Myxedema coma is usually precipitated in older adult patients in 10 patients, but none experienced VT or VF during rewarming.
with chronic hypothyroidism who are stressed by trauma, infec- The terminal rhythm in the eight patients who died while being
tion, anesthesia, or medication ingestion. Typical nonspecific monitored was asystole and not VF. The energetics of the fibril-
laboratory abnormalities include hyponatremia, anemia, and liver lating hypothermic ventricle suggest that asystole may consume
function tests and lipid elevations. If myxedema coma is sus- less energy and may be more protective.
pected, thyroid function studies, including serum thyroxine (T4) Pharmacologic options are limited because hypothermia
by radioimmunoassay, triiodothyronine (T3) resin uptake, and induces complex physiologic changes that result in abnormal
thyroid-stimulating hormone level, should be obtained and serum responses.349 Drug metabolism and excretion are both progres-
cortisol level measured. sively decreased. In normothermia, class IA ventricular antiar-
Considering the previous discussion, administer 250 to rhythmics have negative inotropic and indirect anticholinergic
500 mcg of levothyroxine (T4) intravenously over several minutes, effects and moderately decrease conduction velocity (Box 7-10).
without waiting for confirmatory laboratory results. Daily injec- Procainamide increases the incidence of VF during hypothermia.
tions of 100 mcg are required for 5 to 7 days. The clinician should Quinidine has been useful during induced profound hypother-
consider adding at least 100 to 250 mg of hydrocortisone to the mia, preventing VF during cardiac manipulation at 25° to 30° C
first 3 L of IV fluid. Absorption of T4 is erratic if the drug is given (77° to 86° F). The efficacy and safety of disopyramide are
orally or intramuscularly. The onset of action of T3 is more rapid, unknown.
which jeopardizes cardiovascular stability; therefore T3 is avoided The role of the class IB agent lidocaine for prophylaxis or
in acute replacement therapy. The onset of action of T4 is 6 to treatment is unresolved. In animal studies, lidocaine and pro-
12 hours, evidenced by continuous improvement of the vital pranolol have minimal hemodynamic effects in hypothermia. If
signs during rewarming. Up to one-half the T4 is eventually con- normothermic effects persist during hypothermia, the class IB
COLD AND HEAT
verted by the peripheral tissues into T3. 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
CORTICOSTEROIDS animal studies and ineffective in others.80,304 It is not commercially
Acute cold stress and many coexisting disease processes stimu- available. This class of agents seems most ideal pharmacologi-
late cortisol secretion. The free active fraction of cortisol decreases cally because it possesses direct antifibrillatory properties. The
as the temperature drops because of increased protein binding, ability to prolong the APD is temperature dependent. Ideally, a
and cortisol utilization is similarly decreased. The increase in drug would lengthen the APD only in warmer regions of the
adrenocorticotropic hormone (ACTH) and adrenal steroid secre- myocardium to reduce dispersion (Box 7-11). Two cases of
PART 2
tion may also be a neurogenic or an emotional response in the chemical ventricular defibrillation after infusion of bretylium
conscious person to an unpleasant environment. (10 mg/kg) in accidental hypothermia are reported.58,173
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. BOX 7-10 Antiarrhythmic Agents
Serum cortisol levels are usually elevated. Secondary adrenal
insufficiency resulting from panhypopituitarism may also coexist Class I. Sodium Channel Blockers
with myxedema. Empirical administration of corticosteroids is IA. Conduction and depolarization moderately slowed, and action
indicated if hypoadrenocorticism is suspected on the basis of a potential duration (APD) and repolarization prolonged
previous history of corticosteroid dependence, suggestive physi- • Disopyramide
cal findings, or an inexplicable failure to rewarm. • Procainamide
The use of narcotic antagonists in hypothermia is reported. • Quinidine
Naloxone may reduce the severity of hypothermia in drug over- IB. Conduction and depolarization minimally slowed, and APD
doses and in spinal shock and appears to have activity at the and repolarization shortened
µ-opioid receptor sites.58 • Lidocaine
• Mexiletine
• Moricizine
RESUSCITATION COMPLICATIONS • Phenytoin
• Tocainide
ATRIAL ARRHYTHMIAS IC. Conduction and depolarization markedly slowed, and APD and
repolarization prolonged
All atrial arrhythmias, including atrial fibrillation (AF), should have • Encainide
a slow ventricular response during temperature depression. AF is • Flecainide
typically noted below 32° C (89.6° F). AF usually converts sponta-
Class II. β-Adrenergic Blockers
neously during rewarming, and digitalization or other pharmaco-
logic intervention is not warranted. Electrophysiologic studies Class III. Antifibrillatory Properties (APD Prolonged)
show that the interval prolongation present on His bundle elec- • Amiodarone
trocardiography is unresponsive to atropine. Mesenteric emboli- • Bretylium
zation and embolic stroke are potential hazards when the rhythm • D-sotalol
converts back to sinus rhythm. Hypothermia renders the negative Class IV. Calcium Channel Blockers
inotropic effects of calcium channel blockers redundant.58 • Diltiazem
In summary, all new atrial arrhythmias usually convert • Verapamil
spontaneously during rewarming and should be considered Unclassified
innocent. Attention is directed toward correcting acid-base, fluid, • Adenosine
and electrolyte imbalances and avoiding administration of atrial • Magnesium sulfate
antiarrhythmics.
160
infants, more than half were septic. Although there were no reli-
161
Excellent physical conditioning with adequate rest and nutri- significant predictors of outcome after multivariate analysis.59,161
tion is paramount. Hikers and skiers must be accompanied by a Reporting unusual cases to a hypothermia registry could stimulate
partner and should wear effective thermal insulation. Wet inner advances in treatment.143,221
garments must be changed promptly. Persons who exert them- In a multiple regression analysis of 234 cases in Swiss clinics,198
selves, including long-distance skiers, should switch garments the most common negative survival factors were asphyxia, slow
depending on current exertional heat production.139 Dehydration rate of cooling, invasive rewarming, asystole, and development
must be avoided, and drinking from a cold stream is preferable of pulmonary edema or adult respiratory distress syndrome. The
to snow ingestion. Significant energy is needed to convert ice at largest single-hospital series of adult hypothermic cardiac arrest
0° C (32° F) into water. patients rewarmed with CPB is reported from Finland. Patients
All areas with a large surface area–to–volume ratio should be with cold exposure or immersion without suffocation or asphyxia
well insulated. Excellent synthetic insulating materials include tolerated prolonged CPR before CPB.292 Positive predictors of
Gore-Tex, Flectalon, Thinsulate, and taslanized nylon. survival include rapid cooling rate, presence of VF during cardiac
Under certain circumstances, insidious hypothermia may arrest, and narcotic or ethanol intoxication. In a study of 29
develop during exposure to cold water because of the effects of patients below 30° C (86° F), mode of cooling was the only inde-
increased insulation on compensatory physiologic events.12 The pendent risk factor.255
U.S. Army mnemonic COLD, in reference to insulation with cloth- In a study of CPB survivors, 15 of the 32 patients are
ing, means clean, open during exercise to avoid sweating, loose long-term survivors.332 Their neuropsychological functioning after
layers to retain heat, and dry to limit conductive heat losses. prolonged prehospital circulatory arrest is encouraging. These
Prevention of urban accidental hypothermia requires continu- patients were not asphyxiated before becoming hypothermic. A
ous public education. For example, the optimal safe indoor literature review on the outcomes of 68 patients resuscitated with
temperature recommendation for older adults has risen to 21.1° C CPB notes the survival rate was 60%, and the coldest survivor
(70° F). Energy assistance and temporary sheltering are effective was 15° C (59° F).330 In a series of 26 patients given extracorporeal
measures, and selective heating of sleeping quarters and use of rewarming, those with nonasphyxiated deep accidental hypo-
electric blankets are economic suggestions. Prewarming the bed thermia had a reasonable prognosis.86
and bedroom at night may be the best overall advice to older A valid triage marker of death is needed because vital organ
adults. 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
OUTCOMES fruitless.276 A serum potassium below 7 mmol/L may be a valu-
Partially in reaction to the dramatic reports of reanimations, the able indicator for survival.25 In the Mt Hood tragedy, the non
historical standard of care has been that “no one is dead until survivors were also hyperkalemic (serum potassium level
they are warm and dead.” Clearly, some victims are indeed “cold >10 mmol/L).122 Although a serum potassium level of 10 mmol/L
and dead,” and it would be useful to identify them safely.10,275 appears to be a reasonable ceiling for viability, a child at 14.2° C
Survival is difficult to predict because human physiologic (57.6° F) with a potassium level of 11.8 mmol/L did well.34,73 In
responses to temperature depression vary so widely.214,217,255,333 both these reports, asphyxia and compression injury may have
The type and severity of the underlying or precipitating disease been contributory. Do not attempt resuscitation if an avalanche
process are two determinants.325 Age extremes, although not victim is buried longer than 35 minutes with a snow-obstructed
statistically correlated with survival, are often associated with airway.353 Other indicators of a grave prognosis include a core
severe illnesses. In a multicenter survey, however, there were no temperature below 12° C (53.6° F), arterial pH below 6.5, or evi-
significant age differences in mortality.62 dence of intravascular thrombosis (direct visualization; fibrino-
Gender, trauma, infection, and toxin ingestions affected sur- gen <50 mg/dL).
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-
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PART 2
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255. Pillgram-Larsen J, Svennevig JL, Abdelnoor M, et al. Accidental hypo- 284. Seiji M, Sadaki I, Shigeaki I, et al. The efficacy of rewarming with
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316. Tsokos M, Rothschild MA, Madea B, et al. Histochemical and immu- 336. Weinberg AD. Hypothermia. Ann Emerg Med 1993;22:370.
nohistochemical study of Wischnevsky spots in fatal hypothermia. 337. Weinberg AD. The role of inhalation rewarming in the early manage-
Am J Forens Med Pathol 2006;27:70. ment of hypothermia. Resuscitation 1998;36:101.
317. Turtiainen J, Halonen J, Syvaoja S, Hakala T. Rewarming a patient 338. Weiss SJ, Muniz A, Ernst AA, et al. The physiological response to
with accidental hypothermia and cardiac arrest using thoracic lavage. norepinephrine during hypothermia and rewarming. Resuscitation
Ann Thorac Surg 2014;97(6):2165–6. 1998;39:189.
318. Tveita T. Rewarming from hypothermia: Newer aspects on the patho- 339. White FN. Reassessing acid-base balance in hypothermia: A com-
physiology of rewarming shock. Int J Circumpolar Health 2000;59:260. parative point of view. West J Med 1983;138:255.
319. Tyndal CM Jr, Rose MW, McFalls RE, et al. Profound accidental 340. White JD. Hypothermia: The Bellevue experience. Ann Emerg Med
hypothermia in the Deep South: Clinical exposure. Perfusion 1996; 1982;11:417.
11:57. 341. White JD, Butterfield AB, Almquist TD, et al. Controlled comparison
320. Udy AA, Ziegenfuss MD, Fraser JF. Deep accidental hypothermia of humidified inhalation and peritoneal lavage in rewarming immer-
during the Queensland summer. Crit Care Res 2007;9(4):341. sion hypothermia. Am J Emerg Med 1984;2:210.
321. Vaagenes P, Gundersen Y, Opstad PK. Rapid rewarming after 342. White JD, Butterfield AB, Nucci RC, et al. Rewarming in accidental
mild hypothermia accentuates the inflammatory response after acute hypothermia: Radio wave versus inhalation therapy. Ann Emerg Med
volume controlled haemorrhage in spontaneously breathing rats. 1987;16:50.
Resuscitation 2003;58:103. 343. Wik L, Kiil S. Use of an automatic mechanical chest compression
322. Reference deleted in proofs. devise (LUCAS) as a bridge to establishing cardiopulmonary bypass
323. Van der Ploeg GJ, Goslings JC, Walpoth BH, Bierens JJ. Accidental for a patient with hypothermic cardiac arrest. Resuscitation 2005;
hypothermia: Rewarming treatments, complications and outcomes 66:391.
from one university medical centre. Resuscitation 2010;81:1550–5. 344. Willekes T, Naunheim R, Lasater M. A novel method of intravascular
324. Vangaard L, Eyolfson D, Xu X, et al. Immersion of distal arms and temperature modulation to treat severe hypothermia. Emerg Med J
legs in warm water (AVA rewarming) effectively rewarms mildly 2006;23:56.
hypothermic humans. Aviat Space Environ Med 1999;70:1081. 345. Wilson E, Waring WS. Severe hypotension and hypothermia caused
325. Vassal T, Benoit-Gonin B, Carrat F, et al. Severe accidental hypo- by acute ethanol toxicity. Emerg Med J 2007;24:7.
thermia treated in an ICU: Prognosis and outcome. Chest 1998; 346. Winegard C. Successful treatment of severe hypothermia and pro-
120:2001. longed cardiac arrest with closed thoracic cavity lavage. J Emerg Med
326. Vassallo SU, Delaney KA, Hoffman RS, et al. Prospective evaluation 1997;15:629.
of the electrocardiographic manifestations of hypothermia. Acad 347. Wisborg T, Husby P, Engedal H. Anesthesiologist-manned helicop-
Emerg Med 1999;6:1121. ters and regionalized extracorporeal circulation facilities: A unique
327. Vella J, Farrell J, Leavey S, et al. The rapid reversal of profound chance in deep hypothermia. Arctic Med Res 1991;50:108.
hypothermia using peritoneal dialysis. Ir J Med Sci 1996;165:113. 348. Wollenek G, Honarwar N, Golej J, et al. Cold water submersion and
COLD AND HEAT
328. Vince SC, Flint NJ, Hall AP. A novel non-invasive warming technique cardiac arrest in treatment of severe hypothermia with cardiopulmo-
in severe accidental hypothermia. Resuscitation 2008;77(1):144. nary bypass. Resuscitation 2002;52:255.
329. Vionnet M, Mueller X, von Segesser LK. Unusual complications after 349. Wong KC. Physiology and pharmacology of hypothermia. West J
rewarming for deep accidental hypothermia. Thorac Cardiovasc Surg Med 1983;138:227.
2004;52:185. 350. Wong FW. J wave and hypothermia. Dynamics 2005;16:17.
330. Vretenar DF, Urschel JD, Parrott JC, et al. Cardiopulmonary bypass 351. Ying CL, Tsang SF, Ng KF. The potential use of desmopressin to
resuscitation for accidental hypothermia. Ann Thorac Surg 1994; correct hypothermia-induced impairment of primary haemostasis: an
58:895. in vitro study using PFA-100. Resuscitation 2008;76(1):129.
331. Wallace W. Does it make sense to heat gases higher than body 352. Young DM. Risk factors for hypothermia in psychiatric patients. Ann
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PART 2
332. Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcome of sur- Practice Guidelines for the Out-of-Hospital Evaluation and Treatment
vivors of accidental deep hypothermia and circulatory arrest treated of Accidental Hypothermia. Wilderness Environ Med 2014;25(4):
with extracorporeal blood warming. N Engl J Med 1997;337:1500. 425–45.
333. Wanscher M, Agersnap L, Ravn J, et al. Outcome of accidental 354. Zandstra D: Extracorporeal rewarming. Immersion Hypothermia
hypothermia with or without circulatory arrest: Experience from Task Force, World Congress on Drowning. Amsterdam, June 26–28,
the Danish Praesto Fjord boating accident. Resuscitation 2012;83: 2002.
1078–84. 355. Zehner WJ, Terndrup TE. Ear temperatures during rewarming from
334. Watts DD, Trask A, Soeken K, et al. Hypothermic coagulopathy in hypothermia. Ann Emerg Med 1994;23:901.
trauma: Effect of varying levels of hypothermia on enzyme speed, 356. Zell SC, Kurtz KJ. Severe exposure hypothermia: A resuscitation
platelet function and fibrinolytic activity. J Trauma 1998;44:846. protocol. Ann Emerg Med 1985;14:339.
335. Watts DD, Roche M, Tricarico R, et al. The utility of traditional pre- 357. Zhong H, Qinyi S, Mingjlang S. Rewarming with microwave irradia-
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Care 1999;3:115.
162.e6
CHAPTER 8
Immersion into Cold Water
GORDON G. GIESBRECHT AND ALAN M. STEINMAN
The authors of this chapter hail from two different countries that conversion chart to allow neighbors from either side of the
view and measure temperature differently. The United States uses border to get on the same thermal wavelength (Box 8-1).
° F (Fahrenheit), whereas the country up north uses ° C. (Some Immersion in cold water is a hazard for anyone who partici-
people think that the letter C stands for “Celsius,” but it actually pates in recreational, commercial, or military activities in the
means “Canadian.”) The author from up north has provided a 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
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 abandon ship, the vessel capsized, throwing most of the men
RESCUE 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;
During winter 1988, two men died of hypothermia when their as in the Ocean Ranger case, the crewmembers were incapaci-
nine-man rowing scull sank during a winter storm on a small tated by the cold water and unable to maintain airway freeboard
lake in western Canada. The nine rowers were immersed in the heavy seas.
in 4° C (39.2° F) water. They struggled to hang on to their The Marine Electric disaster had one beneficial outcome.
overturned vessel in 0.6- to 1.0-m (2- to 3.3-foot) waves and Despite the loss of 31 lives in this case, the disaster resulted in
30 km/hr (18.7 mile/hr) winds for more than 50 minutes before establishment of the now-famous U.S. Coast Guard (USCG)
rescuers could reach them. One man drowned just before Rescue Swimmer program. USCG helicopters were on scene
rescue; the others were all conscious when they were pulled within about 2.5 hours of the Marine Electric’s capsizing, but
from the water. However, during the 13-minute boat transport without rescue swimmers, they could not recover possible sur-
to shore, three of the thinnest victims lost consciousness, and vivors from the water because of the high seas and cold-water–
one of these men suffered cardiopulmonary arrest. His core induced incapacitation of the crew. USCG Rescue Swimmers have
temperature (Tco) in the hospital 44 minutes after rescue was saved thousands of lives since their creation after this disaster.
23.4° C (74.1° F); subsequent resuscitation efforts were unsuc-
cessful. The remaining seven survivors were resuscitated from MILITARY ACTIVITIES AND COLD WATER
Tco as low as 25° C (77° F). This case illustrates the rapidity of
onset of immersion hypothermia in lean subjects and the poten- The extensive use of combat ships and aircraft in World War II,
tially serious consequences of cardiovascular instability, circum- particularly in the north Pacific and north Atlantic oceans, pro-
rescue collapse, and post-rescue Tco afterdrop in individuals vided many examples of accidental immersion in cold water.
with immersion hypothermia (see Physiologic Responses to Molnar124 reviewed several hundred of these cases, including the
Cold-Water Immersion with the Head Above Water, later).58 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
Case Study 8-5 DANGERS OF FISHING IN
on to ropes couldn’t let go and rescuers had to cut frozen rope to release
COLD WATER
COLD AND HEAT
them. It appears miraculous how the survivors could have endured such
cold water. Most of those who were rescued were in an unconscious
In December 2004, the fishing vessel Northern Edge capsized
state and, when they became conscious, complained of numbness of
near Nantucket, Massachusetts, in 4° C (39.2° F) water and 3- to
extremities and hands.
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 The Falklands War in 1982 provided further examples of
fishermen on three different vessels lost their lives during a immersion hypothermia related to naval combat. The Argentinian
30-day period in the winter of 2004-2005.181 In June 2003 the cruiser General Belgrano sank in approximately 5° C (9° F) water,
charter fishing vessel Taki Tooo, which was carrying 17 pas- which resulted in the deaths of many sailors. Some of the deaths
sengers and crew, capsized in the turbulent waters of the Til- from cold occurred even after the sailors had managed to emerge
PART 2
lamook River bar on the Oregon coast, with the loss of 11 lives. from the water into life rafts.
The water temperature was 10° C (50° F).183 In April 2001 the Maritime military operations are not the only source of hypo-
fishing vessel Arctic Rose sank in the Bering Sea of Alaska, with thermia casualties in the armed forces; land operations, either
a loss of 15 crewmembers.184 The vessel sank so quickly that during combat or training, also have immersion hypothermia
there was no time for either a distress call to be made or the risks. In March 1995, four U.S. Army Rangers died and four others
crewmen to don survival suits. 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,
Fishing vessel mishaps are a common cause of immersion much of the time partially immersed in the 15° C (59° F) water.
hypothermia. Case Studies 8-5 and 8-6 illustrate the problems Night conditions and difficulties encountered during the medical
that face the commercial fishing industry (Figure 8-4). evacuation of the accident victims contributed to the hypothermia
Another commercial maritime disaster involving mass casual- deaths.17,186
ties from immersion hypothermia and drowning was the capsiz- In March 2001, two USCG crewmen drowned after immersion
ing and sinking of the collier Marine Electric off the coast of in cold water, when their four-man vessel capsized in the waves
Virginia in the early-morning hours of February 12, 1983 (Video of the Niagara River bar in Lake Ontario. The water temperature
8-2) (www.uscg.mil/history/docs/casrep/1983marineelectric.pdf). was 2° C (3.6° F). All the crewmen were wearing dry suits with
The vessel began taking on water in gale-force winds and seas insulation as well as PFDs, but they were without insulated
up to 11 m (35 feet) in height. Before the crew of 34 could 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
Case Study 8-6 COLD-WATER FISHING FATALITIES subsequent drowning.182
A 1999 U.S. Coast Guard Fishing Vessel Casualty Task Force The relatively high fatality rate from accidental immersion in
Report181 found that, in just 2 months (December 1998 and cold water in various military, commercial, and recreational set-
January 1999), 20 commercial fishing vessels were lost at sea. tings has stimulated technologic advances in protective clothing
During these mishaps, 21 persons on board died, mainly from and rescue devices. The current availability of commonplace items
exposure to cold water as a result of the vessel sinking or cap- of survival equipment (e.g., wet suits, dry suits, survival suits,
sizing or from persons falling overboard. From 1994 to January inflatable life rafts) is primarily a response to the needs of people
1999, U.S. Coast Guard statistics show that 396 fishermen lost who work in cold-water environments. The value of various types
their lives while fishing. Of these, 298 died from cold-water of protective clothing is examined later in this chapter.
immersion as a result of falling overboard or of the vessel
sinking, capsizing, or flooding. In 1998, mortality rate for fisher- VEHICULAR ACTIVITIES ON ICE
men was 179 per 100,000 workers; this is 16 times higher than
the averaged rates for firefighters and police officers. Motor vehicle submersions account for approximately 10% of
all drownings, including approximately 400 fatalities in North
166
CHAPTER 8 Immersion into Cold Water
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 problems for both primary victims and the persons trying to
open water during spring, summer, or fall, many also occur rescue them.
during the winter, when vehicles break through the ice while The primary pathophysiologic effects of hypothermia are a
traversing either makeshift (e.g., ice fishing) or official (e.g., decrease in tissue metabolism and the gradual inhibition of
winter roads) transport routes. In 2005, a heavy-machine operator neural transmission and control. However, during the initial
was maintaining an ice road when his snowplow broke through stages of cooling of an intact and conscious victim, secondary
the ice, and he drowned.91 The ice-cold-water temperature was responses to skin temperature cooling predominate. Sudden
cited as a contributing factor to his death. immersion in cold water results in an immediate decline in skin
In summary, numerous case histories and statistical evidence temperature, which in turn initiates shivering thermogenesis
document the significance of cold-water immersion as a cause with increases in metabolism, ventilation, heart rate, cardiac
of the environmental emergencies of drowning and hypothermia. output, and mean arterial pressure. As body temperature declines
Although drowning is relatively easy to prevent (e.g., with the and shivering ceases, metabolism, heart rate, mean arterial
use of PFDs, water safety training, and restriction of alcohol use), pressure, and cardiac output decrease proportionally with the
hypothermia is not easy to prevent. Hypothermia is now more fall in core temperature (Tco), whereas hematocrit and total
widely recognized than in the past, but the prevention of immer- peripheral resistance increase. Renal diuresis and extravascular
sion hypothermia is still a difficult and often expensive proposi- fluid shifts can lead to a considerable loss of intravascular
tion. Therefore, in regions with cold water (which includes most volume, thus decreasing systemic perfusion. A more detailed
of the North American continent), cold-water safety, knowledge description of the pathophysiologic effects of systemic hypother-
of cold-water risks, and the use of appropriate flotation and mia is provided in Chapter 7. This section pragmatically describes
protective clothing are essential (Video 8-3). 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-
PHYSIOLOGIC RESPONSES TO water immersion can be divided into four phases: (1) initial
COLD-WATER IMMERSION WITH immersion and the cold shock response, (2) short-term immer-
sion and the loss of performance, (3) long-term immersion
THE HEAD ABOVE WATER and the onset of hypothermia, and (4) circum-rescue collapse
The effect of sudden cold-water immersion on humans is poorly just before, during, or after rescue. Each phase is accompanied
understood by the general public as well as by medical and by specific survival hazards for the immersion victim that origi-
rescue personnel. Many believe that an individual who falls into nate from or are influenced by a variety of pathophysiologic
ice water will die of hypothermia within minutes, even if that mechanisms. Deaths have occurred during all four phases of
person is dressed in winter clothing. In a series of surveys of immersion.
continuing medical education attendees,47 72% of respondents
thought that, under these conditions, a victim would experience PHASE 1: THE COLD SHOCK RESPONSE
life-threatening hypothermia in less than 10 minutes. As dis-
cussed later, most adults can survive for 1 hour or more if they
(0 TO 2 MINUTES)
take appropriate action. The improper assumption of rapid and The cold shock response occurs during the first 1 to 2 minutes
impending death only serves to induce panic, poor decisions, of cold-water immersion and depends on the extent and rate of
and exhaustion as a result of thrashing about, thereby causing skin cooling. The responses are generally those that affect the
167
respiratory system, heart, and the body’s metabolism (Figure Sudden death can occur either immediately or within minutes
8-5).36,175 Rapid skin cooling initiates an immediate gasp response, after immersion as a result of syncope or convulsions, which can
an inability to hold one’s breath, and hyperventilation. The gasp lead to drowning, vagal cardiac arrest, or VF in susceptible
response may cause drowning if the head is submersed during individuals.23,44,103,118,167
the initial entry into cold water. The subsequent inability to hold Cold shock can occur in water colder than 20° C (68° F), with
one’s breath may further potentiate drowning in high seas. Sub- symptoms increasing as water temperature decreases to freezing.
sequent hyperventilation will normally diminish within seconds Staged entry into cold water attenuates respiratory responses
to minutes, but it could be increased and exaggerated indefinitely because of a gradual increase in thermal stimulation. The best
as a result of emotional stress and panic. Uncontrolled hyperven- advice to combat this phenomenon is, when possible, to control
tilation can cause numbness, muscle weakness, or fainting, which entry into cold water by entering slowly and most importantly
may lead to drowning. Any of these respiratory responses can by keeping the head from being submersed. One should never
lead to pulmonary aspiration of water. Panic may ensue, with dive into cold water. After cold-water immersion, it is important
subsequent drowning (Videos 8-4 and 8-5). to focus on surviving the first minute by not panicking and by
Skin cooling initiates peripheral vasoconstriction as well as consciously getting one’s breathing under control. Figure 8-6
increased cardiac output, heart rate, and arterial blood pressure. shows that minute ventilation and breathing frequency increase
Increased workload on the heart may lead to myocardial isch- dramatically with rapid immersion in cold water. These responses
emia and arrhythmias, including ventricular fibrillation (VF). are blunted by more than 50% with graded immersion.
STIMULATION OF
PERIPHERAL RECEPTORS
COLD AND HEAT
↑ 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
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
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)
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 Most people greatly underestimate the amount of time required to
1 minute—10 minutes—1 hour.* become hypothermic in very cold water. This is important, because
• You have 1 minute to get your breathing under control, so if a victim thinks that hypothermia will set in very quickly, panic is
don’t panic. more likely. A proper understanding of the fact that cold shock is
• You have 10 minutes of meaningful movement to get out of initially the greatest threat will help the victim to focus more on
the water or to attain a stable situation. controlling the gasp reflex and to get control of his or her breathing.
• 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.
rescue periods, despite the survivor being recovered in an appar-
*Times are subject to individual variability and factors such as body size, water
temperature, and amount of the body immersed.
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
thermogenesis), clothing and insulation, water temperature, and that deaths can occur either shortly before rescue, during rescue,
sea conditions90,163,197,202,207 (see Cold-Water Survival, later). or after rescue, and they have used the term circum-rescue col-
Even in ice water, a victim may not drown when he or she lapse to describe these events. Deaths have occurred within
becomes unconscious as a result of hypothermia (≈30° C [86° F]) minutes before rescue, while climbing out of the water, while
if a PFD is worn or if some other factor prevents the need for being hoisted onto a helicopter, within a few minutes of entering
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 CAUSE OF DEATH IN COLD (NO FLOTATION)
are not necessarily going to die if they are suddenly immersed
in cold water (Box 8-2). 100.0
COLD AND HEAT
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–
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
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 may also cause sudden collapse. Pulling a victim out of the water
rescue, in a hospital after transport, and during the 24-hour in a vertical position removes hydrostatic squeeze around the
period after rescue.71,73,100,116 lower limbs and may cause blood pooling in these extremities,
Three causes of circum-rescue collapse have been proposed: with subsequent decreased blood pressure. Extra cardiac work
(1) afterdrop, which is a continued drop in Tco after recovery; or rough handling may induce reflex cardiac arrest of the
(2) collapse of arterial pressure (Figure 8-11); and (3) factors cold heart.
that potentiate the risk of VF (e.g., hypoxia, acidosis, rapid Afterdrop is a well-known phenomenon that occurs after the
changes in pH). These causes are discussed further later in this removal of a victim from cold-water immersion. Tco continues to
chapter. decline (i.e., afterdrop) in both animate and inanimate objects,
When rescue is imminent, mental relaxation and the decreased even after cold-water immersion has ended.2,13,20,57,75,141,147,194 After-
output of stress hormones may result in a drop in blood pressure, drop of as much as 5° to 6° C (9° to 10.8° F) has been observed
which may cause fainting and drowning. The act of rescue itself 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 of blood to the extremities (especially the lower extremities) may
further cooling of the heart might result in a temperature at which cause collapse as a result of decreased blood pressure and car-
VF or cardiac arrest could occur.13 diovascular instability, sudden return of metabolic byproducts to
Golden and colleagues73 discount the importance of this phe- the irritable heart, or continued decrease in temperature (after-
nomenon and propose the collapse of arterial pressure as the drop) of an irritable heart. The Tco will continue to drop, and the
cause of death during rescue. They correctly note that afterdrop heart will react with profound tachycardia or fibrillation. Up to
occurring in victims who were hypothermic yet warm enough to 20% of persons who are recovered alive die as a result of circum-
climb on board a ship without assistance would be unlikely to rescue complications, either before or during rescue, or within
cause enough myocardial cooling to result in cardiac arrest or hours after rescue.
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 FACTORS THAT AFFECT COOLING OF
mechanism is likely the main factor in both pre-rescue collapse
and collapse that occurs during rescue. A fall in blood pressure
THE BODY’S CORE
before removal from the water may be the result of reduced Normal body core temperature fluctuates around 37° C (98.6° F).
sympathetic tone or catecholamine secretion when rescue is The clinical definition of hypothermia is a Tco of 35° C (95° F) or
imminent. Hypotension during and shortly after rescue may be lower; however, any exposure to cold that lowers the Tco to less
caused by a sudden decrease in hydrostatic pressure on the than a normal level results in the body becoming hypothermic.
body (i.e., removal of the hydrostatic squeeze of water pressure Although various temperatures and terms have been used to
that exists during immersion), hypovolemia, or impaired barore- classify different levels of hypothermia, the following classifica-
ceptor reflexes. However, this mechanism cannot fully account tions are used here (Figure 8-13). With mild hypothermia
for all the other deaths that occur 20 minutes to 24 hours after (Tco = 32° to 35° C [89.6° to 95° F]), thermoregulatory mechanisms
rescue. continue to operate fully, but ataxia, dysarthria, apathy, and even
The importance of continued myocardial cooling cannot amnesia are likely. With moderate hypothermia (Tco = 28° to 32° C
be discounted. Fibrillation of a cold heart can be initiated by [82.4° to 89.6° F]), effectiveness of the thermoregulatory system
mechanical stimuli, hypoxia, acidosis,131 and rapid changes in (i.e., shivering thermogenesis) diminishes until it fails; there is a
pH.101 In dogs, myocardial cooling from 30° to 22° C (86° to continued decrease in the level of consciousness, and cardiac
71.6° F) caused a fivefold decrease in the electrical threshold for dysrhythmias may occur. With severe hypothermia (Tco <28° C
VF.25 Also, an increase in the rate of myocardial cooling may [82.4° F]) consciousness is lost, shivering is absent, acid-base
COLD AND HEAT
likely stimulate fibrillation. On the basis of the large afterdrop disturbances develop, and the heart is susceptible to VF or asys-
values described previously, it is plausible that continued Tco tole. Death from hypothermia is generally a result of cardiore-
cooling in significantly hypothermic patients could result in VF, spiratory failure.
caused primarily by spontaneous fibrillation of the cold myocar- If a victim of cold-water immersion can avoid drowning
dium or secondary to a cold-induced increase in sensitivity to during the initial few minutes after water entry, the prevention
other fibrillation stimuli. of hypothermia becomes an important problem. Survival time
Death may occur within minutes to hours after rescue. A in cold water, which is based on the pathophysiologic effects
rescued victim may be severely compromised with cold alkaline of decreasing Tco, is not a precise calculation. Large individual
or acidic blood returning from the extremities, a heart that is variations among survivors with regard to body morphology
PART 2
extremely prone to failure, a decrease in or a loss of conscious- and state of health and fitness, in combination with many exog-
ness, or low blood volume (hypovolemia). Sudden redistribution enous variables that affect cooling rate (e.g., clothing, water
Patient’s ability to
Core rewarm without
Classifications temperature external heat source Clinical presentation
172
temperature, sea state, flotation, behavior), preclude exact pre-
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 caused by the flushing of cold water through the garments.
males dressed in the various types of protective clothing shown However, even the tight-fitted full “wet” suit allowed for a 30%
in Figure 8-15 in both calm and rough waters at approximately faster cooling rate in rough water than that seen in calm water.
10° C (50° F).158 The most dramatic differences occurred in the The “dry” suit, which did not leak, showed no significant differ-
loose-fitted “wet” protective clothing (e.g., float coat, insulated ence between calm and rough seas.
coveralls), where cooling rates almost doubled in rough seas Estimated survival times in rough seas, on the basis of experi-
compared with those seen in calm seas. This was primarily mental data, were published for thin males wearing different
COLD AND HEAT
PART 2
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
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])
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
The advantage of body fat as an insulator against cold is
Flotation discussed earlier. With the use of an extrapolation of a linear
High thermal protection 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-
Core temperature
Flotation
Moderate thermal protection 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-
Flotation thermia is highly improbable, cold water still potentiates death
No thermal protection 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-
No flotation cusses only calm-water survival times. Because rough-water con-
No thermal protection ditions decrease survival times, as discussed later, Figure 8-17
may be useful for estimating maximum survival times for an
Time
individual who is immersed in cold water. Search and rescue
organizations might find such a maximum survival time helpful,
FIGURE 8-18 Schematic estimation of core temperature and survival
because they often use the longest possible survival time to
times with varying flotation devices and thermal protective clothing.
decide when to terminate a search effort.
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
177
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.
COLD AND HEAT
178
been determined, but the implications are clear for manufacturers
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
vigorous extremity movements that are necessary to maintain
BOX 8-5 Controversy Box: You Lose Most of Your
airway freeboard in rough seas).
Heat Through Your Head Hayward and colleagues86 demonstrated that minimizing both
voluntary activity and exposure of major heat loss areas of the
This common belief has caused many incorrect and even
skin to cold water are the most effective ways to minimize a
dangerous actions, such as going to extreme lengths to retrieve
hats or to removing clothing when immersed to place it on the
decline in Tco. They showed that treading water and drownproof-
head for thermal protection. In a cold-water immersion scenario, ing significantly increased the cooling rate. Despite increased
90% to 95% of heat loss occurs through the cold-exposed body. metabolic heat production during exercise, the increased surface
It has been demonstrated that, under similar thermal stresses, heat loss resulted in faster Tco cooling during exercise in cold
relative heat loss from the head (per unit of surface area) is not water. They also developed two well-known cold-water survival
that much higher than that from other areas of the body. However, techniques: HELP and the group huddle (see Figure 8-8). These
under certain conditions, increased heat loss from the head can adaptive behaviors reduce Tco cooling by 69% and 66% of that
cause a disproportionate decrease in body core temperature. of control conditions, respectively.82 When the sea is not calm,
Thus, head contact with cold water should be minimized whenever it may be difficult to perform the group huddle with complete
possible by changes in posture and maximum practical insulation. 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
BEHAVIOR AND POSTURE OF THE BODY may be individual variations.
IN COLD WATER
Behavioral variables also affect Tco cooling rate. Hayward and EXERCISE
colleagues85 used infrared thermography to demonstrate that, Normally, the advice is not to exercise while awaiting rescue in
despite marked peripheral vasoconstriction, heat losses are high cold water. Although metabolic heat production will increase,
in the groin, the lateral and central thorax, and the neck. In the exercise increases blood flow to muscles and causes increased
groin and neck, which are regions with relatively thin layers of heat loss to the water, with a net result of increased Tco cooling.
peripheral soft tissue, blood flow through the large and relatively Færevik and colleagues39 studied participants wearing neoprene
superficial femoral vessels, carotid arteries, and jugular veins survival dry suits in a wave tank with water temperature of 0° C
COLD AND HEAT
potentiates heat flow to the cold water. In the lateral and central (32° F) and air temperature of −5° C (23° F). When they remained
thorax, the relative absence of tissue (muscle and subcutaneous still, Tco dropped more during 3 hours of immersion than it did
fat) insulation in combination with the high thermal conductivity during 6 hours of immersion during which they performed leg
of rib bone potentiates heat loss from the relatively warm lungs exercises for 5 minutes every 20 minutes (Figure 8-33). Thus, if
to the cold environment. Furthermore, exercise or excessive enough insulation is worn, the heat of exercise can be contained
movement in the water greatly increases heat loss from active within the insulation, which attenuates the drop in Tco.
muscles.
The effect of activity on total heat balance depends on the
balance among the many factors illustrated in Figure 8-32. In
SHIVERING
PART 2
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
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
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)
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 including ability to control the cold shock response; ability to
rate of Tco cooling of up to twofold under these conditions. In a swim and maintain airway freeboard; availability and type of a
separate study, this group demonstrated qualitatively similar PFD; availability of a life raft or other floating object to increase
effects of insulin-induced hypoglycemia.137 buoyancy; behavior of the survivor in water; decision to swim for
Hypercapnia and hypoxia may also be present in various shore or to wait for rescue; availability of signaling devices (e.g.,
underwater scenarios. Hypercapnia has been shown to lower whistles, flares, dye, smoke, strobe lights, radios, mirrors) and the
the shivering threshold94 and transiently inhibit shivering. Both ability to use them; and proximity of rescue personnel.154,155,159
hypercapnia94 and hypoxia95 have also been shown to accelerate
Tco cooling. ABILITY TO CONTROL THE COLD
Alcohol consumption is frequently associated with immersion
hypothermia, because ethanol impairment of mental and motor
SHOCK RESPONSE
performance is often the cause of accidental immersion. Social As previously discussed, sudden immersion in cold water initiates
drinking can result in carelessness. Intoxicated mariners or others a cardiorespiratory cold shock response that significantly potenti-
near water often fall from a boat, ship, gangway, wharf, or bridge ates the risk of drowning. This response and the resulting inca-
into the water. Drunken drivers capsize or collide. On the basis pacitation have been suspected as the primary causes of drowning
of the frequency of occurrence alone, the consequences of after short-term (<10 minutes) immersion in cold water.165 Abrupt
alcohol ingestion warrant special considerations. tachycardia and hypertension induced by sudden immersion in
Studies of the effects of moderate doses of ethanol (i.e., blood cold water can produce incapacitating cardiac dysrhythmias in
alcohol levels of 50 to 100 mg/dL, which is the range associated susceptible individuals and myocardial infarction or cerebrovas-
with legal impairment) on cold stress have established the cular accident (stroke) in persons with arterial disease or hyper-
following: tension.165 In addition, reflex gasping and hyperventilation165,174
1. The rate of heat loss is not significantly increased. Alcohol significantly shorten the duration of breath holding.84,88,165 Figure
has a primary vasodilatory effect under normothermic condi- 8-35 illustrates this phenomenon. Loss of breath-holding capacity
tions.38,83,100 Under hypothermic conditions, where vasocon- can have severe consequences for survivors attempting under-
striction predominates, alcohol lowers the vasoconstriction water egress from a submerged vehicle or from a capsized vessel
threshold during the moderate cold stress of 28° C (82.4° F) or aircraft, or for survivors who are simply trying to maintain
water immersion, but does not affect the shivering threshold airway freeboard in a rough sea or white-water river.88,144,169
or the rate of Tco cooling.93
2. The rate of heat production is slightly decreased. For immer-
COLD AND HEAT
182
Respiratory difficulties induced by the cold shock reflexes waves are present, it is usually necessary for a survivor to actively
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
Raft
Boat
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
CHAPTER 8 Immersion into Cold Water
Accidental cold-water immersion
Don’t panic,
breathing under control
PFD on No PFD
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 protective clothing. There is no uniformly correct answer to the
question, “Should I swim for it?” Each survival situation must be
WAIT FOR RESCUE evaluated individually (Figure 8-38 and Box 8-6).
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
SURVIVAL MODELING
movement in the water (e.g., swimming, performing the vigorous When a rescue organization is tasked with searching for victims
extremity movements necessary to maintain airway freeboard in in cold water, it is important to have an accurate estimate of how
rough seas). long the victims might survive and thus continue to warrant
The decision to swim for shore or to wait for rescue is crucial search resources. Various prediction models have been devised
for a survivor of cold-water immersion. The increased cooling to assist with these difficult estimates.
rate associated with swimming might lead one to conclude that The Cold Exposure Survival Model was devised by Tikui-
holding still is preferable to an attempt to swim for safety. sis162,163 to provide a sophisticated set of survival-time estimates
However, if the survivor can make it to shore or even to shallow for individuals who are immersed in cold, rough seas and for
water, survival is likely to be prolonged, despite the risk of lower survivors who are partially immersed or exposed to cold wind
Tco. Ducharme and Lounsbury32 specifically evaluated this issue under wet conditions. The model was developed on the basis of
by comparing the cooling rates and swimming distances for both experimental data about cooling with different types of flotation
novice and expert swimmers in a swimming plume. Experimental devices and thermal protective clothing (Figure 8-39),158,159 shiver-
participants, who were wearing average clothing (i.e., no specific ing control and capacity,38 body composition (Figure 8-40), and
insulation against cold-water immersion) and PFDs, were other factors.
immersed in 10° C (50° F) water and either remained still in a The Cold Exposure Survival Model has been used for many
HELP position or swam against a current that was matched with years by both the Canadian and U.S. Coast Guards. Recently, the
their swimming ability. Swimming resulted in a 17% faster rate USCG started using a new decision tool: the Probability of Sur-
of Tco cooling compared with holding still. The novice swimmers vival Decision Aid (PSDA), which was developed by Xu and
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 BOX 8-6 Controversy Box: Always Stay with Your Boat
the probability of a successful survival outcome depended on
the decision to swim for safety early during a survival event. For many scenarios in which warmer water temperature allows for
If the participants had cooled for 30 minutes before attempting longer survival and in which rescue is likely to occur, this is good
to swim, the likelihood of success was significantly reduced. advice. However, in colder water in secluded areas, the decision is
The decision to swim or to remain still ultimately depends on 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
the immersed individual’s understanding of the many variables
personal flotation device, if the likelihood of rescue is low, and if
that affect a successful outcome, including body morphology and the victim can reach shore within 45 minutes. With a PFD, if swim
cooling rate; water temperature; wave conditions and currents; failure occurs, the victim will still remain afloat. Without a PFD,
proximity of shore; proximity of rescue personnel; swimming swim failure will result in drowning (see Figure 8-38).
ability; and availability of signaling devices, flotation devices, and
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)
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)
0
colleagues. 205
Although the Cold Exposure Survival Model is –10 5 0 5 10
based on a one-cylinder model, which assumes that most heat B Ta (° C)
loss comes from the torso in cold victims, the PSDA includes six
cylinders that represent the head, torso, arms, hands, legs, and FIGURE 8-40 Predicted survival time (ST) for individuals wearing boat-
feet. For example, Figure 8-41 shows predicted survival times for crew coveralls (see Figure 8-15) for A, immersion in rough seas versus
victims in varying water temperatures. Presently, the PSDA pre- water temperature; and B, exposure to air at 20 km/hr (12.4 miles/hr)
dicts the time required for Tco to drop to 34° C (93.2° F) (i.e., under wet conditions (i.e., clothing wetness of 1550 g/m2) versus air
functional time) and to 30° C (86° F) (i.e., survival time). temperature. The lower and upper boundaries of the shaded regions
When the PSDA was applied to the four football players represent predictions for lean and fat individuals, respectively. (From
whose boat capsized (as described previously in Recreational Tikuisis P: Predicting survival time at sea based on observed body
Activities and Cold Water), the survival-time predictions for the 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)
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
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
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.
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
190
professional rescuer should follow the policies and procedures
A B
C D
FIGURE 8-48 Single (A) and double (B and C) sling techniques affect A B
how vertical the victim is during extraction from the water. The rescue
slings provide a leverage advantage, especially when there is high FIGURE 8-50 Comparison between single (A) and double (B) sling
freeboard (A and B). A wet victim is wrapped in a makeshift vapor methods for hoisting to a helicopter or boat. The double sling method
barrier to minimize evaporative and convective heat loss during boat places the patient in a more horizontal position. (Courtesy Garrick
transport (D). (Courtesy Gordon G. Giesbrecht.) Kozier.)
191
The patient’s Tco may continue to decline—depending on the BOX 8-9 Controversy Box: Afterdrop Is an Artifact
quality of insulation provided, the patient’s endogenous heat
production, active or passive manipulation of extremities, and and Is Unimportant
the site of Tco measurement—even after the person has been
Rescuers and emergency medical personnel should be aware that
rescued as a result of the physiologic processes described earlier core temperature will continue to drop after an individual has
as “afterdrop.” To diminish this effect, the patient’s physical activ- been removed from the cold stress (see Figure 8-12). Although
ity must be minimized. Conscious patients should not be required some decrease is inevitable, the understanding is that anything
to assist with their own rescue (e.g., by climbing up a scramble that increases blood flow to cold tissue (e.g., the legs) will increase
net or a ship’s ladder) or to ambulate when they are out of the afterdrop. Thus, patients should be kept from walking and should
water (e.g., by walking to a waiting ambulance or helicop- remain horizontal, and the arms and legs should not be rubbed or
ter).49,122,157 Physical activity increases afterdrop, presumably massaged in an effort to warm the patient.
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- of definitive medical care.33,79,105,112,152,157 Aggressive rewarming in
geal temperatures of 33° C (91.4° F) demonstrated a threefold the field has been contraindicated in the past, because the means
greater afterdrop during treadmill walking than while lying to diagnose or manage the many potential complications of
still.10,56 Such an exercise-induced enhancement of afterdrop severe hypothermia are unavailable in this setting.122 However,
could precipitate post-rescue collapse. Throughout the rescue in the prehospital scenario of cold-water immersion, there is no
procedures and during subsequent management, hypothermic source of heat that could be considered too aggressive. Figure
patients must be handled gently.3,77,122 Excessive mechanical stim- 8-51 indicates the levels of aggressiveness and effectiveness of
ulation of the cold myocardium is another suspected cause of various sources of heat for hypothermia and frostbite treatment.
death after rescue.110,192 When transportation to a site of definitive care will take more
Several extraction techniques are presented in Figure 8-48 and than 30 minutes or is impossible, rewarming in the field with the
Videos 8-7 and 8-8. The technique depends on the number of use of the principles and techniques of management described
rescuers, the design of the boat platform and the resultant free- next may be appropriate (Box 8-9).
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
192
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 √√√√ –
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 cardiac arrest, because management beyond BLS differs from that
normothermic CPR protocols, when chest compressions may be used for normothermic patients.3,29 Defibrillation and pharmaco-
indicated if bradycardia fails to provide sufficient cardiac output logic interventions are usually ineffective for myocardial tempera-
or systolic blood pressure.3 Because the metabolic requirements tures of less than 30° C (86° F).3,7,29 Furthermore, repeated
of hypothermic patients are reduced, bradycardia and bradypnea defibrillatory shocks may damage the myocardium.3,156 Defibril-
may still meet tissue oxygen requirements.29,49 Inappropriate lation should be limited to three shocks at 200, 300, and 360
administration of chest compressions in an attempt to augment joules, consecutively, for patients who are colder than 30° C
cardiac output may precipitate VF from mechanical stimulation (86° F).3 Administered medications are ineffective, and they may
of the irritable myocardium29 (Box 8-10). accumulate to toxic levels, because drug metabolism by the
If a victim of cold-water immersion is found floating face- hypothermic liver and kidneys is reduced.29,196 For hypothermic
down, drowning should be suspected and managed accordingly patients with a Tco of more than 30° C (86° F), normal ACLS pro-
(see Chapter 69). In this case, correction of anoxia is paramount, tocols may be used.3 All intravenous (IV) fluids should be warmed
and consideration of hypothermia is of secondary importance.3,130 before administration. However, it may be necessary to extend
Normal advanced cardiac life support (ACLS) protocols should the recommended interval for IV medications because of the
not be routinely applied to severely hypothermic patients in 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-
BOX 8-10 Controversy Box: Cardiopulmonary ing VF, but prior ventilation with 100% oxygen has been associ-
Resuscitation (CPR) Should Be Started Rapidly if a ated with a decreased risk for VF.27,28 Rescuers should not
Pulse Cannot Be Found Quickly withhold endotracheal intubation, if indicated, for fear of pre-
cipitating VF.3
A hypothermic patient has been cooling for a long time, and it will If the patient does not require immediate life support interven-
likely not affect the outcome if a few minutes are taken to ensure tion, a thorough and systematic examination must be performed
that the heart is not functioning before commencing CPR. as quickly as possible before the initiation of treatment for hypo-
Premature chest compressions can cause an irritable heart to thermia. Because severely hypothermic patients may have a
fibrillate. An initial pulse check should be done for 60 seconds. If greatly depressed mental status, they may not respond normally
no pulse is found, 3 minutes of rescue breathing might oxygenate to painful stimuli. Victims of immersion hypothermia may have
the heart enough to strengthen contractions. If a pulse still cannot
suffered trauma before entering or while in the water. Central
be found after another 60-second check, it can be assumed that
the heart is not functioning, and chest compressions can be
nervous system (CNS), skeletal, and soft tissue injuries may be
started in accordance with local jurisdiction protocols (see overlooked unless a careful examination occurs.
Figure 8-52).152 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
194
most hypothermia treatment protocols continue to recommend
195
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
FIGURE 8-55 Placement of a charcoal heater on the chest. Warming
ducts are wrapped over the shoulders and touching the neck, under
Forced-air warming (FAW) is derived from a treatment modality
the axillae, and over the chest. This configuration provides heat to used to prevent or reverse hypothermia in surgical patients.106,149
important areas for heat transfer (surrounding or near the heart) to a Convective heat transfer is provided by warm air blown into
cold patient. 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,
Particularly when applied to the patient’s thorax, including during the initial 35 minutes of rewarming, shivering patients
axillae, chest, and upper back, (areas with high potential for experienced net heat loss of 30 to 50 W, compared with net heat
conductive heat transfer),85 hot-water bottles, chemical and char- gain from FAW of 163 to 237 W.61 In moderately to severely
COLD AND HEAT
coal heat packs (Figure 8-55), heating pads, and other warmed hypothermic patients with a mean rectal temperature of 28.5° C
objects have been used to attempt to stabilize the patient’s Tco. (83.3° F) who were treated in an emergency department, FAW
If a patient is shivering vigorously, Tco will warm at a similar rate (in conjunction with warmed IV fluids and inhalation warming)
as with external heat.21,56,80,113,160 For more severely hypothermic achieved a rewarming rate of 2.4° C/hr (4.3° F/hr), which was
patients who are not shivering, these types of external heat almost twice that of patients treated only with warmed IV fluids
sources would help to stabilize and even increase the patient’s and inhalation warming (1.4° C/hr [2.5° F/hr]).153
Tco, which would likely remain low if no heat were added. A In another series of human experiments, a FAW device
recent study demonstrated that charcoal heating provides a sig- designed for field use was associated with a significantly higher
nificant rewarming advantage for hypothermic individuals when Tco rewarming rate (5.8° C/hr [10.4° F/hr]) than with shivering
PART 2
shivering was pharmacologically inhibited.92 alone (3.4° C/hr [6.1° F/hr]), but it showed no advantage over
Rescuers should be aware of several potential hazards with shivering with regard to decreasing afterdrop.35 When shivering
this rewarming technique. Hypothermic skin is very sensitive to was inhibited with meperidine in volunteers,57 FAW was associ-
heat and easily injured. All sources of external heat must be ated with a 50% decrease in afterdrop and a 600% increase in
separated from direct contact with the patient’s skin to prevent rewarming rate compared with spontaneous rewarming alone.67
severe thermal burns.156 Third-degree burns have resulted from A different prototype FAW device that used a collapsible rigid
the application of a lukewarm hot-water bottle directly to a patient cover and that was evaluated experimentally on non-
hypothermic child’s skin.129 Furthermore, heat packs that make shivering volunteers was associated with a smaller afterdrop
use of burning charcoal as a heat source can create a carbon and faster rewarming rate than with spontaneous rewarming
monoxide hazard within an enclosed space.160 alone.60
In summary, FAW has shown significant promise as both a
Arteriovenous Anastomoses Rewarming field and a hospital treatment modality. It is a safe, noninvasive
The arteriovenous anastomoses (AVA) rewarming technique technique that can both decrease afterdrop and increase the Tco
relies on the physiologic AVAs that exist in human digits and on warming rate of immersion hypothermic patients. Figure 8-56
the superficial venous rete in the forearms and the lower legs. schematically illustrates Tco responses to various rewarming meth-
Warming these areas opens the AVAs and increases superficial odologies under mild (i.e., shivering intact) and severe (i.e.,
venous return via the rete. Warmed venous blood thus reaches shivering absent) hypothermic conditions.
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
TRANSPORTATION
proposed AVA rewarming, the Royal Danish Navy has been using Stabilization, insulation, and rewarming of the hypothermic
this technique since 1970.187 Experimental studies have confirmed patient should be started during transport of the patient to an
the efficacy of this technique.188 Mildly hypothermic participants appropriate medical center for definitive rewarming. If possible,
with an esophageal temperature of 34.2° C (93.6° F) whose hands, the receiving facility should be selected on the basis of its knowl-
forearms, feet, and lower legs were immersed in either 42° C edge of and experience with management of hypothermic
(108° F) or 45° C (113° F) water had a smaller postcooling after- patients. In the same manner that victims of multiple trauma are
drop than with shivering alone (0.4° C [0.7° F] vs. 0.6° C [1.1° F]) most appropriately managed in trauma centers, severely hypo-
and a significantly faster rate of rewarming (6.6° C/hr [11.9° F/hr] thermic patients are best managed in hospitals equipped to
and 9.9° C/hr [18° F/hr]) than with shivering alone (3.4° C/hr handle potential complications and provide core rewarming
[6.1° F/hr]). Although this technique may be difficult to implement therapies. For example, a hospital with cardiac bypass rewarming
in some field settings, it may be practical for mildly hypothermic capabilities may be a better choice for management of a severely
victims on rescue vessels or other locations where a source of hypothermic patient than a hospital without such qualifications,
warm water is available. even if the former may require a longer transport time.
As with heating pads and other sources of external heat, During transport to a site for definitive medical care, emer-
however, rescuers should be concerned about the possibility of gency medical personnel should frequently monitor the patient’s
thermal burns. In the previously described study, no burns were Tco and other vital signs. In addition, they should attach an
196
REWARMING
Shivering
Start or
40 cooling High moderate
Core temperature (° C)
197.e1
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COLD AND HEAT
PART 2
197.e4
CHAPTER 9 Frostbite
CHAPTER 9
Frostbite
LUANNE FREER, CHARLES HANDFORD, AND CHRISTOPHER H.E. IMRAY
197
viewed by Larrey; soldiers with cold injuries rapidly rewarmed
their extremities over roaring fires (65° to 75° C [149° to 167° F]) ANATOMY AND PHYSIOLOGY
after long marches, only to renew the trek and refreeze their Physiologically, humans are tropical animals, better suited to
extremities the next day. Larrey recognized that warming was losing heat than retaining it. When naked and at rest, a per-
good, but cautioned against the use of excessive heat and ulti- son’s neutral environmental temperature is 28° C (82.4° F). With
mately recognized the freeze-thaw-freeze cycle. Napoleon left an environmental drop of 8° C (14.4° F) to 20° C (68° F), the
France with 250,000 men and returned 6 months later with only metabolic rate must double to avoid lowering of body
350 effective soldiers. The remainder were casualties to cold or temperature.
starvation.105 The rate at which heat is lost by radiation is a function of
During both world wars and the Korean conflict, at least 1 the temperature of the cutaneous surface, which in turn is pri-
million cases of frostbite occurred.142,181,198 High-altitude frostbite, marily a function of the rate of blood flow through the skin.
first described in 1943, was recognized from the treatment of Heat is poorly conducted from warmer internal tissue to the
aviators in World War II, when gunners of aircraft flying between cutaneous surface because adipose tissue is a good heat
7620 and 10,668 m (25,000 and 35,000 feet) fired machine guns insulator.
through open ports, removing their bulky mittens and jackets to As a result, cutaneous circulation is key to development of
improve the dexterity that they thought was crucial to saving frostbite. Because of its role in thermoregulation, normal blood
their lives.198 flow of skin far exceeds its nutritional obligation. The skin holds
Until the 1950s, treatment of cold injuries basically followed a complex system of capillary loops that empty into a large,
Larrey’s guidelines. In 1956, experimental laboratory work subcapillary venous plexus containing the majority of the cutane-
encouraged Meryman, the U.S. Public Health Service district ous blood volume. Under normothermic conditions, 80% of an
medical officer in Tanana, Alaska, to try rapid rewarming at extremity’s blood volume is in the veins of skin and muscle. Skin
37.8° C (100° F) on a patient with frostbite and hypothermia.25,131 blood volume depends in part on tone in resistance and capaci-
This was the genesis and has become the cornerstone of the tance blood vessels, and tone in turn depends largely on ambient
method currently used in Alaska and popularized by Mills.130,131 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
EPIDEMIOLOGY temperature at 41° C (105.8° F), this may increase to 7000 to
No comprehensive statistical data are available on the incidence 8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may
of frostbite, but it is much more prevalent during military cam- diminish it to 20 to 50 mL/min.
COLD AND HEAT
paigns and is a known hazard for mountain climbers and polar Blood flow through apical structures, such as the nose, ears,
explorers. The typical frostbite patient is either working or rec- hands, and feet, is most variable because of richly innervated
reating in cold and/or high-altitude environments, is homeless, arteriovenous connections. Blood flow to hand skin can be
or is accidentally trapped outdoors in the winter.98,101,146 The increased from a basal rate of 3 to 10 mL/min/100 grams (g) of
patient is typically 30 to 49 years old, and in more than half of tissue to a maximum of 180 mL/min/100 g of tissue. This cutane-
urban cases, is intoxicated. 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
CIVILIAN warming results in vasodilation dominated by local effects. When
PART 2
In the nonadventurer U.S. civilian population, Mills129-131 had col- both types (central and peripheral) of heating or cooling are
lected 500 cases in Alaska by 1963, Cook County Hospital in present, their effects are additive.
Chicago recorded 843 cases from 1962 to 1972, and Detroit Cutaneous vessels are controlled by sympathetic adrenergic
Receiving Hospital reported on 154 patients treated between 1982 vasoconstrictor fibers, and vascular smooth muscles have both
and 1985.17,74,102 The incidence of frostbite in Finland calculated α-adrenergic and β-adrenergic receptors. Vasodilation in the
in a 9-year retrospective query of hospital admissions was 2.5 hands and feet is passive, so maximal reflex vasodilation occurs
cases per 100,000 inhabitants.87 after sympathectomy.
When the hand or foot is cooled to 15° C (59° F), maximal
vasoconstriction and minimal blood flow occur. If cooling
MILITARY AND OCCUPATIONAL continues to 10° C (50° F), vasoconstriction is interrupted by
The mean annual incidence of frostbite in the Finnish military periods of vasodilation and an associated increase in blood and
was reported as 1.8 episodes per 1000 persons, with the head, heat flow. This cold-induced vasodilation (CIVD), or “hunting
hands, and feet most often affected.107 In a more recent study of response,” recurs in 5- to 10-minute cycles and provides some
almost 6000 Finnish military recruits, 44% reported at least one protection from the cold. There is considerable individual varia-
episode of frostbite during their lifetime, and the annual inci- tion in the amount of CIVD, and it is believed this might explain
dence was 2.2%; the head, hands, and feet were the sites most some of the variation in susceptibility to frostbite. Prolonged
frequently afflicted.47 Among refugees navigating a high-altitude repeated exposure to cold increases CIVD and offers a degree
military line of control during December 1988 to March 2003, of acclimatization. Inuit, Sami, and Nordic fishermen have a
2564 cases of frostbite were treated at local hospitals in Muzaf- strong CIVD response and very short intervals between dilations,
farabad, Azad Kashmir.92 which may contribute to maintenance of hand function in the
cold environment.66
Normal skin maturation and tissue function rely on mainte-
MOUNTAINEERING nance of permeability and integrity of all tissue membranes. A
A 10-year retrospective review of medical records of the British steady-state relationship of prostaglandins, particularly pros
Antarctic Survey revealed that the incidence of frostbite was taglandin E2 (PGE2, vasodilator) and PGF2α (vasoconstrictor),
approximately 65.6 cases per 1000 persons per year.28 During a is crucial for normal skin function. Imbalance may disrupt
10-year period in the Karakorum Mountains, 1500 cases of frost- cell membrane equilibrium. This relationship is controlled
bite were treated at tertiary care medical facilities; all victims were through PGE2–9-ketoreductase and nicotinamide adenine dinu-
males age 17 to 43 years. The incidence is unknown because the cleotide phosphate (NADPH). Low concentrations of PGE2–9-
total number of potential exposures was unrecorded.71 In a ketoreductase found in normal skin emphasize an active biologic
questionnaire-based study of 637 mountaineers, the mean inci- presence.
dence of frostbite was 366 cases per 1000 persons per year,70 It is not difficult to imagine why frostbite tends to affect tissues
and of 2219 south-side Mt Everest climbers in 7 years (2001– that are acral (e.g., fingers, toes, ears, nose) and that receive
2007), the base camp medical clinic at Mt Everest saw 35 cases diminished blood supply as a result of vasoconstriction, thereby
of frostbite (and estimates at least a comparable number of conserving heat for the core. The nose and corneas may be dif-
patients not brought for treatment at the facility).56 ficult to protect from cold wind and are particularly vulnerable;
198
face coverings such as a balaclava and goggles should be con-
CHAPTER 9 Frostbite
INDIRECT CELLULAR DAMAGE/PROGRESSIVE
sidered in extreme conditions. In addition, men who jog, ski, or
otherwise exercise in the cold may be prone to penile frostbite,
DERMAL ISCHEMIA
especially if fast speeds create a headwind. Clothing becomes Indirect cellular damage secondary to progressive microvascular
moist with sweat in the groin, and the tip of the penis is vulner- insults is more severe than the direct cellular effect. This is sup-
able, especially if unprotected by a wind-resistant or windproof ported by the observation that skin tissue subjected to a standard
outer layer.56,76 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-
PATHOPHYSIOLOGY OF FROSTBITE treated with the same freezing injury. Thus, direct skin injury is
The pathophysiology of frostbite has been categorized in several reversible. The progressive nature of injury is probably secondary
different ways, illustrating the numbers of variables that affect to microvascular changes.
the extent and depth of tissue damage. Frostbite may be divided Approximately 60% of skin capillary circulation ceases in the
into four pathologic phases: prefreeze, freeze-thaw, vascular temperature range of 3° to 11° C (37.4° to 51.8° F), while 35%
stasis, and late ischemic. Overlap occurs among these phases. and 40% of blood flow ceases in arterioles and venules, respec-
The changes during each phase vary with rapidity of freezing tively.161 Capillary patency is initially restored in thawed tissue,
and duration and extent of injury. but blood flow declines 3 to 5 minutes later. Three nearly simul-
Some believe that it is conceptually more clear to divide taneous phenomena occur after thawing: momentary and initial
pathologic changes occurring in frostbite into two categories: vasoconstriction of arterioles and venules, resumption of capillary
those resulting from direct cellular injury and those from indirect circulation and blood flow, and showers of emboli coursing
cellular effects, or progressive dermal ischemia,138 a similar patho- through microvessels.212 Ultimately, there is progressive tissue
physiology described in thermal burn patients.119,120,163 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
DIRECT CELLULAR INJURY effect of arachidonic acid metabolites, oxygen free radicals have
Regardless of the classification scheme, researchers agree that the been shown to be detrimental and contribute to tissue loss. It
changes caused by direct injury include the following211,212: has been proposed that this may be the case with frostbite
• Extracellular ice formation injury.24
• Intracellular ice formation Emerging concepts, perhaps including the deleterious role of
• Cell dehydration and shrinkage protein kinase C in mitochondrial dysfunction during reperfusion
• Abnormal intracellular electrolyte concentrations injury and the role of nitric oxide production and activation, will
• Thermal shock no doubt be incorporated into our understanding of frostbite
• Denaturation of lipid-protein complexes injury as scientific understanding evolves.
Cells subjected to a slow rate of cooling (over hours) develop Considerable evidence indicates that the primary alteration
ice crystals extracellularly in the cellular interspaces. Rapid caused by cold injury is to vascular endothelium.210 At 72 hours
cooling (over seconds to minutes) produces intracellular ice after a freeze-thaw injury, vascular endothelium is lost in capillary
crystals, which are more lethal to the cell and less favorable for walls, accompanied by significant fibrin deposition. The endo-
cell survival. In a clinical cold injury, the slower rate of freezing thelium may be totally destroyed, and fibrin may saturate the
does not produce intracellular crystals;124,125 however, the extra- arteriole walls.134,210,212 Ultrastructural derangement of endothelial
cellular ice formed is not innocuous. It draws water across the cells after the thaw period has been observed by electron micros-
cell membrane, contributing to intracellular dehydration. The copy in capillaries of the hamster cheek pouch following subzero
theory of cellular dehydration was originally proposed by Moran temperatures.156 The endothelial injury was confirmed by dem-
in 1929 and subsequently supported by Meryman’s study of onstrating fluid extravasation from vessels almost immediately
“ice-crystal nucleation.”124,125,127,136 Cellular dehydration produces after thawing.212 As in other forms of trauma, vascular endothelial
modification of protein structure because of high electrolyte cells swell and protrude inward into the lumen until they lyse.
concentrations, alteration of membrane lipids, alteration of cel- Venules appear more sensitive to cold injury than do other
lular pH, and imbalance of chemical activity.116,118,128 This phe- vascular structures, partly because of lower flow rates. Arterioles,
nomenon subsequently permits a marked and toxic increase of with a rate of flow almost twice that of venules, are less damaged
electrolytes within the cell, leading to partial shrinkage and col- by freezing and develop stasis later than do venules. Capillaries
lapse of its vital cell membrane. These events are incompatible manifest the fewest direct effects of cold injury, but their flow is
with cell survival. quickly arrested as a result of their position between arterioles
Not all the water within a cell is freezable. A small amount and venules. Generalized stasis and cessation of flow are noted
of unfrozen water, “bound water,” constitutes up to 10% of the at the point of injury within 20 minutes after freeze and thaw.
total water content and is held tightly in the protein complex “White thrombi” (blood cells and fibrin) appear after platelet
within the cell. Regardless of how rapid or marked the cold thrombi as blood flow progressively slows. Sludging and stasis
injury, this bound water remains liquid. At temperatures below result in thrombosis. Microangiography after cold injury shows
−20° C (−4° F), approximately 90% of available water is frozen.208 that although spasm of the arterioles and venules exists, it is not
Although the theory of ice crystal disruption of cell structure is marked enough to completely account for the decreased flow of
attractive, it has yet to be conclusively proven. progressive microvascular collapse.4 In the 1950s, Kulka99,100
“Thermal shock” is the phenomenon of sudden and profound observed that vascular thrombosis after cold injury advanced
temperature change in a biologic system. Precipitous chilling has from the capillary level to that of the large vessels and ultimately
been theorized to be incompatible with life, but the severity of resulted in ischemic death of progressively larger areas. Viable
this phenomenon is debatable. Another poorly understood dermal cells may be observed histologically in cold-injured
concept is the manner in which subzero temperatures produce tissues for up to 8 days or until occlusion of local vessels occurs.
denaturation of lipid-protein complexes. One proposed theory This emphasizes that vascular insufficiency plays a major role,
hypothesizes detachment of lipids and lipid protein from cell and that direct injury to cellular structures and mechanisms may
membranes as a consequence of the solvent action of a toxic be reversible. It also suggests other mechanisms, such as reperfu-
electrolyte concentration within a cell.42,110 No direct evidence sion injury.
supports an alteration of enzyme activity during freezing, but Because Cohnheim had shown changes in cold injury to be
DNA synthesis is inhibited.85 On the other hand, there is indirect similar to changes seen in other inflammatory states, Robson and
evidence of ox liver catalase inactivation caused by denaturation Heggers163 postulated that the progressive ischemia seen in frost-
and structural alteration of lactic acid dehydrogenase after freez- bite might be caused by the same inflammatory mediators
ing and thawing.112,179 responsible for progressive dermal ischemia in the burn wound.
199
They evaluated blister fluid from patients with hand frostbite, As early as 1991, Manson and co-workers111 proposed that
measuring levels of PGE2, PGF2α, and thromboxane B2 (TXB2). frostbite is characterized by acute tissue injury induced by freez-
Levels of the vasoconstricting, platelet-aggregating, and leukocyte- ing and thawing. Initial complete ischemia is followed by reper-
sticking prostanoids (PGF2α and thromboxane A2 [TXA2]) were fusion and later by tissue necrosis. The authors suggested that
greatly elevated. The investigators postulated that massive edema the vascular events supported the hypothesis that free radical–
after cold injury was caused either by leakage of proteins from mediated reperfusion injury at thawing might contribute to tissue
release of these prostanoids or by leukocyte sludging in the necrosis after frostbite in a manner similar to that seen after
capillaries and increased hydrostatic pressure. Studies have con- normothermic ischemia. Supporting evidence included electron
firmed the similarity between cold injury and the burn wound.24 micrographs showing the appearance of severe endothelial cell
Severe endothelial damage was observed by researchers injury, beginning during freezing and extending through early
studying a minimal cold-injury model in the hairless mouse.18 In reperfusion. Later, neutrophil adhesion, erythrocyte aggregation,
addition, the sequence of endothelial damage, vascular dilation, and microvascular stasis were seen.
vascular incompetence, and erythrocyte extravasation was con-
firmed. This led to speculation that arachidonic acid metabolites,
which may originate from severely damaged endothelial cells,
DEFINITIONS AND CLASSIFICATIONS
are important in progressive tissue loss. Significantly absent from Classically, frostbite has been described by its clinical presenta-
in vivo and microscopic observations were vascular spasm, tion, but this can be difficult to predict in the field and before
thrombosis, and fibrin deposition, all of which had previously rewarming.97,131 Mills136,139 favors the use of two simple classifica-
been implicated as pathophysiologic mechanisms. A rabbit ear tions: mild (without tissue loss) and severe (with tissue loss).
model demonstrated increased tissue survival after blockade of Historically, and following the classification of thermal burn
the arachidonic acid cascade at all levels.157 The most marked injury, frostbite has been divided into “degrees” of injury based
tissue salvage resulted when specific TXA2 inhibitors were on acute physical findings after freezing and rewarming.
used. This has now been shown to be effective in clinical Frostnip is superficial and associated with intense vasocon-
situations.74 striction. It is characterized by discomfort in the involved parts
Reports in the 1940s documenting the histopathology of frost- (Figure 9-1; see also Figure 9-8). Symptoms usually resolve spon-
bite injury to the skin were not comprehensive. Historically, taneously within 30 minutes, and no tissue is lost. There is some
studies by several investigators have been limited to skin biopsies question whether this qualifies to be called an injury, because
without documentation of location, exposure time, temperature, neither frozen extracellular water nor progressive tissue loss is
or time elapsed since the injury.174 routinely demonstrated.
COLD AND HEAT
More recently, experimental studies have been able to docu- First-degree frostbite injury shows numbness and erythema.
ment the histopathology of skin changes under controlled condi- There may initially be a firm, white or yellowish plaque in the
tions. In 1988, Schoning and Hamlet176,177 used a Hanford area of injury. There is no tissue loss, although edema is common
miniature swine model for frostbite injury (−75° C [−103° F] expo- (Figure 9-2). Second-degree injury results in superficial skin vesic-
sure for up to 20 minutes) to note progressive epithelial damage. ulation (Figure 9-3). Clear or milky fluid is present in the blisters,
Early changes included vacuolization of keratinocytes; loss of surrounded by erythema and edema. Third-degree injury shows
intercellular attachments and pyknosis occurred over 1 week or deeper blisters, characterized by purple, blood-containing fluid
more. This subsequently progressed to advanced cellular degen- (Figure 9-4). This indicates that the injury has extended into the
eration and formation of microabscesses at the dermoepidermal reticular dermis and beneath the dermal vascular plexus. Fourth-
PART 2
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
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
FIGURE 9-2 Nordic skier with first-degree frostbite (central pallor
healing. Grade 3 lesions are connected with a significant risk for
having cleared after rewarming) of the abdominal skin. This skier amputation and require rapid rewarming, antibiotics, aspirin, and
reported having skied for 90 minutes in −23.3° C (−10° F) temperature, intravenous (IV) vasodilators. Grade 4 lesions have high risk for
unaware that his shirt, underneath a parka, had come untucked from amputation and complications such as thrombosis, sepsis, and
his trousers. (Courtesy Luanne Freer, MD.) 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
FIGURE 9-3 Climber with second-degree frostbite of the fifth finger
sustained after only several seconds’ exposure to −45.6° C (−50° F)
when the body is unable to conserve heat or protect against
windchill when gloves were briefly removed to handle placement of a heat loss.
carabiner to the fixed rope. Clear bullae developed after rewarming.
(Courtesy Luanne Freer, MD.)
201
TABLE 9-1 Proposed Classification for Severity of Frostbite Injuries of the Extremities
Extent of initial lesion at day Absence of Initial lesion on distal Initial lesion on intermediary Initial lesion on carpal/tarsal
0 after rapid rewarming initial lesion phalanx (and) proximal phalanx
Bone scanning at day 2 Useless Hypofixation of radiotracer Absence of radiotracer Absence of radiotracer uptake
uptake area area on the carpal/tarsal
Blisters at day 2 Absence of Clear blisters Hemorrhagic blisters on the Hemorrhagic blisters over
blisters digit carpal/tarsal
Prognosis at day 2 No amputation Tissue amputation Bone amputation of the Bone amputation of the limb
digit ±systemic involvement ±sepsis
Sequelae No sequelae Fingernail sequelae Functional sequelae Functional sequelae
From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ
Med 12:248, 2001.
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
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.
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 rest of the body. In fact, any uncovered part of the body loses
body into the environment, because water is a thermal conductor heat in proportion to the body surface area exposed; appropriate
superior to air by a factor of about 25.97 Clothing that transmits protection is important for all exposed skin.153
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;
SKIN WETNESS/UNWASHED SKIN
COLD AND HEAT
otherwise, clothing will still become moist. Clothes that decrease Development of frostbite does not depend only on ambient
the amount of surface area may decrease frostbite risk. Mittens temperature and duration of exposure. Windchill, humidity, and
are more protective than gloves, because gloves have a greater wetness predispose to frostbite. Skin wetting adds an increment
surface area and prevent air from circulating between fingers. of heat transfer through evaporation and causes wet skin to cool
Poorly fitted boots notoriously generate frostbite injuries, even faster than dry skin.135 More important, water in the stratum
when worn with excess socks (Figures 9-10 and 9-11). corneum can terminate supercooling by triggering water crystal-
Although up to 40% of total body heat loss can occur through lization not only in this layer but also in underlying tissue. Skin
exposed head and neck areas,3 a study has refuted the widely wetness is therefore conducive to frostbite because it allows
held belief that the head loses proportionally more heat than the crystallization to terminate supercooling after approximately one-
PART 2
FATIGUE
FIGURE 9-11 Climber on South Col, Mt Everest (7950 m [26,083 feet]) During World War II and the Korean conflict, clinical studies
with excess socks in hand, about to descend. Caudwell Xtreme Everest indicated that cold injuries occurred with higher frequency
Expedition. (Courtesy Christopher H.E. Imray, MD.) among soldiers in retreat.142,207 Fatigue and apathy increase the
204
incidence of cold injury. When warfare is proceeding toward
GENETIC PREDISPOSITION
CHAPTER 9 Frostbite
defeat, or in conditions of starvation, soldiers often become indif- The deletion genotype (DD) for the angiotensin I–converting
ferent to personal hygiene and clothing, and the frequency of enzyme (ACE) has been associated with increased vascular reac-
frostbite increases.95 Overexertion increases heat loss. A large tivity in vivo and in vitro.23,75 Kamikomaki88 proposed that a case
amount of body heat can be expended by panting, and perspira- of frostbite in a climber with ACE DD allele was caused by
tion further compounds the problem of chilling. Both panting genetic propensity for vasoconstriction.
and sweating consume energy, which compounds the fatigue Civilian clinical studies are inadequate for statistical evalua-
factor. 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
TOBACCO SMOKING (measured by oxygen consumption [ VO 2 ] and rectal tempera-
Impaired local circulation is a primary contributor to frostbite. ture) after acute cold exposure, and researchers suggest this
Cigarette smoking causes vasoconstriction, decreased cutaneous group may be at greater risk for cold injury.49 Military studies
blood flow, and tissue loss in random skin flaps.106 Reus and suggest that women and blacks may be more susceptible to
colleagues160 documented that smoking induced arteriolar vaso- cold injury.37,61 One author postulates that blacks are three to six
constriction and decreased blood flow in a nude subject. Although times more susceptible to frostbite than are whites because
red blood cell velocity increased, the net effect was decreased blacks tend to initiate shivering at lower core temperatures and
blood flow in cutaneous microcirculation during and immediately tend to have long, thin fingers and toes, as well as thin arms
after smoking. Curiously, habitual heavy smokers show higher and legs, which do not conserve heat as efficiently as do their
scores on the Resistance Index of Frostbite (RIF), which corre- white counterparts. In testing, black fingers cool faster when
lates with lower risk for frostbite.36 Empirically, one could con- immersed in cold water and reach a lower temperature before
clude that smoking, which induces vasoconstriction, should place the hunting response ensues.61 Individuals with type O blood
one at increased risk for frostbite, and research supports this.37,47,71 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
COMORBIDITIES 6000 military recruits with cold-provoked white finger syndrome
Drugs known to have vasoactive properties may predispose to and in those with hand/arm vibration.47,141
or worsen frostbite injury. Disease states that alter tissue perfu- A low RIF, determined in a simple laboratory test, may be
sion, such as diabetes, atherosclerosis, arteritis, and Raynaud’s indicative of increased risk for cold injuries during operations in
disease, predispose to frostbite (Figure 9-12).41,100 the field.36
205
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
A spontaneous rewarming. Anticipate that frostbitten areas will rewarm
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.
B All constrictive and wet clothing should be replaced by dry, loose
wraps or garments. The extremity is padded and splinted for
protection, and oral ibuprofen, 400 mg twice daily, may be initi-
COLD AND HEAT
assess the severity of the injury. transport is not feasible, rapid rewarming should be instituted
After the extremity is rewarmed, edema appears within 3 (goal is to see blush of rewarming and/or 15 minutes immersed
hours and lasts 5 days or longer, depending on the severity of in rewarming fluid) and the patient transported with protective,
the case. Vesicles or bullae appear 6 to 24 hours after rapid dry, and nonadherent dressings to prevent refreezing. Appropri-
rewarming. Clear bullae confer a better prognosis than hemor- ate adequate analgesia should be administered; an IV or intra-
rhagic bullae, which indicate deeper injury. During the first 9 to muscular (IM) opiate may be required. Blisters should be left
15 days, severely frostbitten skin forms a black, hard, and usually intact. Patients with long transport times are at greater risk for
dry eschar, whether or not vesicles are present (Figure 9-13). (refreezing) recurrent injury. All efforts should be made to
Mummification forms an apparent line of demarcation in 22 to
45 days.142
206
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
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
A or clear blisters, which represent more superficial injury, are
debrided to prevent further contact of PGF2α or TXA2 with the
damaged underlying tissues. Unlike the clear blisters, 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
COLD AND HEAT
208
and potentially salvageable. Weeks after injury, the interface zone
CHAPTER 9 Frostbite
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 FIGURE 9-17 Vascular imaging at 7950 m (26,083 feet) using a
patient, so immediate discharge is rarely prudent. portable battery-powered SonoSite MicroMaxx duplex ultrasound
Overall goals of hospital treatment include keeping the patient machine. Caudwell Xtreme Everest Expedition. (Courtesy Christopher
calm, well nourished, suitably hydrated, and pain free. Wound H.E. Imray, MD.)
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 portability, and the ability to make repeat examinations give the
be treated with clean dressings and twice-daily whirlpool baths technique certain advantages over other imaging modalities.
with an antiseptic such as chlorhexidine or povidone-iodine. Many remote research stations and even large expeditions may
Topical Aloe vera gel should be applied every 6 to 8 hours have portable ultrasound machines. Duplex imaging has been
through resolution of blisters. This encourages the eschar created used in the field at altitudes as high as 7950 m (26,083 feet)
by the blisters to separate from underlying healthy tissue. (Figure 9-17). Ultrasound has been used to determine the need
Although patients may be housed anywhere that these objectives for sympathetic blockade after frostbite.158
can be achieved, vascular surgery or plastic surgery/burns wards
(with multidisciplinary input) tend to be most appropriate for Magnetic Resonance Angiography
more severe injuries. The MRI/MRA investigation has a theoretical advantage over
99m
Frostbite blisters have been shown to contain high concentra- Tc bone scanning because it allows direct visualization of
tions of the vasoconstricting metabolites of arachidonic acid, vessels (both patent and occluded), as well as imaging of sur-
PGF2α and TXB2, which are known to mediate dermal ischemia rounding tissues. Some suggest that it shows a more clear-cut
in burns and pedicle flaps. It is suggested that these may play a line of demarcation of ischemic tissue.14 The other advantage of
role in the pathogenesis of frostbite.163 Debate continues about MRA over angiography is that it is noninvasive. However, there
management of such blisters and the risk versus benefit of poten- are relatively few accounts of its use in frostbite evaluation in
tial introduction of infection. Current thinking is that clear/cloudy the literature.14,159
blisters should be drained by needle aspiration (especially if the
bullae restrict movement), and that hemorrhagic (presumably Technetium-99m Scanning
deeper) blisters should be left alone.123 In general, our view is The first description of 99mTc scanning for assessment of bone
to support aspiration of all blisters. Optimally, large-blister viability in patients with frostbite injuries was in 1976.109 The
aspiration/deroofing will be carried out in a controlled environ- degree of accretion of the 99mTc was found to depend on integrity
ment using sterile procedures and anesthetics as needed. 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
TECHNIQUES TO EVALUATE TISSUE PERFUSION was not as accurate an indicator of the ultimate extent of tissue
Over the years, several diagnostic tests have been used to attempt loss as scanning at 5 days after injury. They also noted that
to predict severity and prognosis of frostbite injury. These include lesions appeared to fluctuate in extent over a 3-week period.
plain radiographs, infrared thermography, angiography,65 triple- Cauchy and colleagues30,31 recognized that existing frostbite
phase bone scanning,33 laser Doppler, digital plethysmography,158 classifications were based on retrospective diagnoses and were
and magnetic resonance imaging/magnetic resonance angiogra- not useful for predicting the extent of final tissue loss and prog-
phy (MRI/MRA). The most promising approaches seem to be nosis for frostbite patients. The 3- to 6-week waiting period
triple-phase bone scanning15,33 and MRI/MRA.14 Early diagnostic often necessary to determine severity of the lesion and resultant
digital subtraction angiography (before administration of tissue need for amputation often caused considerable distress for
plasminogen activator) is an essential first-line investigation for patients. The authors suggested a new classification system that
the patient presenting acutely with severe frostbite injury without begins at day 0 (just after rewarming) and is based mainly on
significant comorbidities, where thrombolysis is an available the topography of the lesion and on early bone scan results.
treatment modality and option.178 This appears to be a very useful classification for the physician
and patient, in that it allows accurate determination at a very
Duplex Ultrasonography early stage of the likely extent of subsequent tissue loss (see
Duplex ultrasonography uses B-mode, pulsed-wave Doppler Tables 9-1 to 9-3).
ultrasonography to visualize blood flow within vessels and color An interesting insight into some of the possible mechanisms
flow Doppler imaging to visualize the structure and hemodynam- involved in certain frostbite injuries was described by Salimi
ics within vessels. In modern vascular units, there is a move and co-workers,171 who designed an experimental model to
toward using duplex ultrasound examination as the first-line study pathogenesis and treatment of frostbite. Using 99mTc radio-
investigative examination, reserving angiograms for situations in nuclide imaging, they monitored evolution and extent of tissue
which a therapeutic intervention is required. Ease of access, 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
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*
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, 250 mg of aspirin and 400 mg of IV buflomedil, and who were
suppresses platelet aggregation, and activates fibrinolysis. Its then randomized to receive 250 mg of aspirin per day, plus
intraarterial use has been effective in treating ischemic peripheral buflomedil, iloprost, or recombinant tissue plasminogen activator
vascular disease. with iloprost. The iloprost group had the lowest overall amputa-
The potentially beneficial effect in treating frostbite injuries tion rate. Although the ideal dose is undetermined, these encour-
with intraarterial PGE1 was first assessed in an animal model.209 aging data offer hope to frostbite victims.
PGE1 reduced the magnitude of frostbite injury when the injured Iloprost is best given as an IV infusion through a peripheral
limb was slowly rewarmed. The data suggested a possible or central line in a monitored vascular or general surgical unit.
role for the use of PGE1 in frostbite patients who have not under- The diluted iloprost should be delivered by an accurate rate
PART 2
gone rapid rewarming. Since the first description of its use in delivery system, such as a syringe driver. The infusion is started
patients,68 PGE1 has been used with some success in frostbite at a rate of 2 mg/hr and incrementally increased up to 10 mg/
injuries.79,197 hr, titrated against the side effects of facial flushing, headache,
Further experimental evidence implicates an inflammatory nausea, and flulike symptoms. The infusion is usually run for 5
process in the underlying mechanism of tissue injury. It has been to 8 days for 6 hours a day.79,81 A practical guide and stepwise
postulated that progressive ischemic necrosis is secondary to algorithm was recently produced to aid clinicians (Figure 9-23).69
excessive TXA2 production, which upsets the normal balance Reserpine. Reserpine is a powerful vasodilator that acts by
between prostacyclin (prostaglandin I2) and TXA2.144 inhibiting uptake of norepinephrine into storage vesicles.150 For
Cauchy and co-workers29 showed a promising decrease in the frostbite, it is used intraarterially. The first description in the
digit amputation rate with the use of IV iloprost in severe frostbite treatment of frostbite was by Snider and colleagues.183 An animal
injuries. The clinicians compared results of a controlled trial of 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
FIGURE 9-22 Aloe vera cream being applied at the Everest Base controlled study of pentoxifylline in the management of frostbite
Camp Medical Clinic. Note the care being taken to apply nonconcen- has yet to be performed.
tric dressings to allow for edema formation. (Courtesy Suzanne Boyle, Buflomedil. Buflomedil hydrochloride is a vasoactive drug
MD.) that may have a number of effects, including inhibition of
212
CHAPTER 9 Frostbite
Iloprost
administration
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- that the use of 1 L of IV 6% dextran on the day of injury, fol-
cyte deformability, nonspecific and weak calcium antagonistic lowed by 500 mL on each of 5 successive days, might be of
effects, and oxygen-sparing activity.35,115,117 A case series of 20 benefit.164 The extent of tissue necrosis was also found to be
patients reported that early administration of IV buflomedil significantly less than in controls, when hemodilution with
appeared to reduce the risk for subsequent amputation.54 dextran was combined with water bath rewarming.
However, buflomedil has not been shown to reduce microcircu- With our present understanding of the etiology of frostbite
latory damage from acute, experimentally induced freeze injury.45 and introduction of newer interventions (e.g., iloprost, t-PA),
Although buflomedil does not have U.S. Food and Drug Admin- there appear to be fewer cases when LMW dextran may have
istration (FDA) approval, it has been used extensively in France benefit.
to treat frostbite, with considerable beneficial effect.31
ENDOVASCULAR INTERVENTIONS
Blood Viscosity: Low-Molecular-Weight Dextran
It has been observed that shortly after thawing, cold-injured Thrombolysis with Tissue Plasminogen Activator
vessels become dilated and filled with clumps of erythrocytes. In 1963, Fogarty and co-workers52 reported treating acute occlu-
These clumps can be easily dislodged by gentle manipulation sion of a peripheral vessel with an embolectomy catheter tech-
and do not represent true thrombosis. Although the mechanism nique. More recently, catheter-directed thrombolysis has been
that leads to erythrocyte clumping is not completely understood, used to clear distal arteries and the microvasculature using a
it may reflect cold-induced increase in blood viscosity. This sug- thrombolytic agent such as tissue plasminogen activator (t-PA).
gests that use of low-molecular-weight (LMW) dextran may be Found in vascular endothelial cells, t-PA has fibrinolytic action and
beneficial for early treatment of frostbite. Although no controlled plays an important role in the dynamic balance between clot for-
clinical trial of LMW dextran has been reported, experimental mation and lysis. Plasminogen and t-PA bind to the fibrin surface
evidence supports its use. Weatherly-White and colleagues204 of the thrombus, resulting in production of plasmin and subse-
demonstrated that LMW dextran, 1 g/kg/day, protected against quent dissolution of the thrombus. t-PA has been used extensively
tissue loss in the rabbit ear model. This led to the suggestion 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
214
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
A causes elevation of intracellular cyclic adenosine monophosphate
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
B amputation rate was observed in the buflomedil group, at
39.9%. No amputations were observed in the iloprost group,
FIGURE 9-26 Repeat images of the hands of the patient in Figures whereas those treated with iloprost/IV t-PA had an amputation
9-24 and 9-25 after 24 hours of intraarterial catheter-directed throm-
rate of 3.1%.
bolytic therapy with tissue plasminogen activator show greatly
improved perfusion at all levels. (From Sheridan RL, Goldstein MA,
Iloprost has some advantages compared with t-PA. Radiologic
Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia intervention is not needed during its administration, which can
and frostbite, N Engl J Med 361:2654, 2009.) 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
FIGURE 9-27 Appearance of right hand of the patient in Figures 9-24 BOX 9-3 Proposed Screening and Treatment Tool for
to 9-26 at approximately 30 days. (From Sheridan RL, Goldstein MA,
Use of Thrombolysis in Frostbite Patients
Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia
and frostbite, N Engl J Med 361:2654, 2009.)
Treatment Screen (Four “Yes” Answers Required to Proceed
to Angiography)
Are the patient’s gas exchange and hemodynamics stable?
is not recommended because it may not be possible to detect Is flow absent after rewarming (no capillary refill or Doppler
and treat bleeding complications. signals)?
The Hospital Unit. The hospital unit needs intensive care Was the cold exposure time less than 24 hr?
monitoring capabilities, and clinicians should be familiar with Is the warm ischemia time less than 24 hr?
IA angiography and t-PA. A review of absolute and relative Treatment Protocol
contraindications of t-PA should be undertaken. The Massachu- Perform angiography with intraarterial vasodilators.
setts General Hospital group has proposed a screening and treat- If there is still no flow after angiography with vasodilators, infuse
ment tool for thrombolytic management of frostbite, including a tissue plasminogen activator (t-PA) with systemic heparinization,
protocol (see Box 9-3).178 with priority to the hands—other sites receive a systemic dose.
Choice of Imaging in the Patient Presenting within 24 Repeat angiography every 24 hr.
Hours of Injury. Angiography or 99mTc scanning should be Indications for Stopping the Infusion of t-PA
used to evaluate the initial injury and monitor progress after t-PA
When restored flow has been confirmed by angiography or clinical
administration per local protocol and resources. Angiography is examination
an invasive procedure that allows both diagnostic and therapeutic If a major bleeding complication occurs
measures to be carried out, unlike 99mTc scanning, which is only After 72 hr of treatment
diagnostic. Logical practice dictates that angiography be used to
monitor IA t-PA and 99mTc scanning used to monitor IV admin- Postlysis Anticoagulation
istration of t-PA. No evidence demonstrates superiority of one One month of subcutaneous low-molecular-weight heparin at a
imaging modality over the other. prophylactic dose
Choice of Imaging in the Patient Presenting after 24 From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A
Hours of Injury. In patients with delayed presentation (>24 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.
215
Hospital
management
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 protection against subsequent cold injury appears to be the only
benefit of surgical sympathectomy for frostbite.19
Sympathectomy Because surgical sympathectomy is irreversible, great caution
Cutaneous vessels are controlled by sympathetic adrenergic vaso- should be exercised when considering its use, particularly with
constrictor fibers, and vascular smooth muscles have both the advent of alternative IV vasodilators. Many would argue there
α-adrenergic and β-adrenergic receptors. Because vasodilation of is now no role for its use in the early management of frostbite.
extremities is passive, maximal reflex vasodilation occurs after However, some interest in a potential role for more selective
sympathectomy. chemical sympathectomy remains.34,145
The use of sympathectomy (open or minimally invasive
surgery) has yielded mixed results. Surgical sympathectomy per- Hyperbaric Oxygen Therapy
formed within the first few hours of injury increases edema Evaluating the effectiveness of use of hyperbaric oxygen therapy
formation and leads to increased tissue destruction. However, if (HBOT) in the management of frostbite is difficult. Although
performed 24 to 48 hours after thawing, sympathectomy is several animal studies have demonstrated no benefit,138 two
believed to hasten resolution of edema and decrease tissue loss. recent human studies have yielded excellent results.50,199 Multiple
Surgical sympathectomy may have a role in preventing certain mechanisms of action are proposed, but the major changes are
long-term sequelae of frostbite, such as pain (often caused by postulated to occur in the microcirculation. HBOT reportedly
vasospasm), paresthesias, and hyperhidrosis.188 increases erythrocyte flexibility, decreases edema formation in
In a study of 66 patients with frostbite, 15 patients with acute, postischemic tissues, and is bacteriostatic. Such actions may
bilaterally equal, severe injuries were treated with immediate IA counteract vascular congestion, platelet aggregation, and infiltra-
reserpine in one limb and ipsilateral surgical sympathectomy. tion of leukocytes seen in the microcirculation of frostbite
Efficacy of therapy was assessed by comparison of the sympa- patients. Finderle and Cankar50 report successful HBOT of a
thectomized limb with the contralateral untreated limb. There patient at 2.5 atm for 90 minutes daily for 28 sessions in a multi
was no conservation of tissue, resolution of edema, pain reduc- place chamber, without significant tissue loss; this treatment
tion, or improved function in sympathectomized limbs compared started 12 days after injury. HBOT may also act as an antioxidant.
with those treated with IA reserpine. One patient demarcated A series of case reports suggests significant beneficial effects from
more rapidly, and another patient appeared to be protected from HBOT.11,53,140,199,201
recurrent injury. Sympathectomy was not effective therapy for Cauchy and colleagues32 have recently suggested a novel use
acute frostbite, even when achieved early with IA reserpine. Late 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
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 The role of HBOT in all stages of frostbite therapy warrants
conditions in acute mountain sickness when true descent is not further investigation because it is a relatively safe and inexpen-
possible. The authors note that altitude itself exaggerates cold- sive treatment.90,202
induced vasospasm and hypothesize that placing a frostbite
patient in a field hyperbaric chamber may dampen this response Epidural Spinal Cord Stimulation
and improve tissue perfusion. Although there is no evidence for An anecdotal case series that described epidural spinal cord
HBOT at altitude for frostbite, it warrants further investigation stimulation versus conventional treatment reported good thera-
because of its simplicity and likely availability during high- peutic effects in four young patients with frostbite of the lower
altitude expeditions. 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.
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.
FIGURE 9-30 Axial fasciotomies on the dorsum of the left hand. (Cour- Following amputation, primary skin cover is usually preferred.
tesy Christopher H.E. Imray, MD.) 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
but the treatment is reported to have resulted in rapid recovery, weight-bearing stump. Split grafts inserted directly onto bone
reduced pain, and more peripheral level of amputation.7 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-
SURGICAL TREATMENT propriate attempts at preserving long bone length restrict use of
COLD AND HEAT
The conventional teaching is that early surgical intervention has modern “intelligent” prosthetic limbs; preoperative consultation
no role in the acute care of frostbite. However, early surgical with the rehabilitation/prosthetic team is strongly advised.
intervention in the form of fasciotomy is required for compart- The patellar tendon–bearing orthosis technique was originally
ment syndrome in the immediate post-thaw scenario or for designed to support body weight for treatment of the below-knee
ischemia from a constricting eschar or subeschar infection.62 segment that is structurally inadequate or causes severe pain.168,189
Decompressing escharotomy incisions are rarely necessary to The technique allows unloading of the leg at the below-knee
increase distal circulation. If such escharotomies are necessary to level while retaining full knee movement. It is beneficial in
decompress digits and facilitate joint motion, incisions along the
transaxial line may be the most appropriate.121 However, many
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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,
219
those at risk would be helpful to assess risk for people planning toward fats, with carbohydrates of intermediate importance
to work or travel to high altitude or into extreme cold, as well and proteins least important. As altitude increases above
as those who may be particularly valuable to military recruiting 3048 m (10,000 feet), carbohydrates become most important
and planning. It would also be especially helpful when trying to and proteins remain least important.
advise persons who have sustained previous cold injury. • Do not climb under extreme weather conditions, particularly
The RIF finger skin temperature response, determined in a at high altitudes on exposed terrain, or start too early in cold
simple laboratory test, may be related to the risk for cold injuries weather. The configuration of a mountain can help a climber
during operations in the field.36 The reproducibility of the time find maximal shelter and solar warmth.
course of CIVD suggests this methodology may be of value for • Avoid tight, snug-fitting clothing, particularly on the hands
further studies examining the mechanism of the response.139 and feet. Socks and boots should fit closely, with no points
Kamikomaki88 proposed that a case of frostbite in a climber with of tightness or pressure. When donning socks and boots, a
ACE DD allele was caused by genetic propensity for vasoconstric- person should carefully eliminate all wrinkles in socks. Old,
tion. Perhaps we will see the evolution of testing for genetic matted insoles should be avoided.
predisposition to frostbite as a screening tool. • Avoid perspiration under conditions of extreme cold; wear
Thermography is an easy, noninvasive method for monitoring adequately ventilated clothing. If perspiring, remove some
thermal changes after experimental frostbite, but its clinical value clothing or slow down.
is as yet unknown.45,86,173 Laser Doppler techniques have been • Keep the feet and hands dry. Even with vapor-barrier boots,
used to assess efficacy of HBOT of frostbite. The number of socks must not become wet. All types of boots must be worn
visible nutritive capillaries in frostbitten areas was shown to with great care during periods of inactivity, especially after
increase.50 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
PREVENTION increasing the danger of other foot injuries, such as blistering.
In 1950, Herzog and Lachenal made a successful lightweight bid Extra socks and insoles should always be carried. Light,
without oxygen for the summit of Annapurna, the first 8000-m smooth, dry, and clean socks should be worn next to the skin,
(26,247-foot) peak to be climbed. Herzog77 lost his gloves near followed by one or two heavier outer pairs.
the summit, and the summit team spent a night in a crevasse. • Wear mittens instead of gloves in extreme cold, although
Both climbers suffered severe frostbite to their hands and feet. gloves can be worn for short intervals when great manual
In a heroic retreat, Dr. Jacques Oudot first gave intraarterial dexterity is required for specialized work such as photography
COLD AND HEAT
vasodilators and then performed field amputations without or surveying. In these situations, a mitten should be worn on
anesthetic. one hand and a glove temporarily on the other. If bare-finger
Eleven of the 210 deaths on Mt Everest between 1921 and dexterity is required, silk or rayon gloves should be worn, or
2006 were attributable to hypothermia,51 and a significant pro metal parts that must be touched frequently should be covered
portion of climbers attempting to climb to extreme altitude with adhesive tape. Occasionally, the thumbs should be
develop frostbite,56 suggesting that climbing above 8000 m pulled into the fists and held in the palms of the mittens to
(26,247 feet) carries significant risk for permanent cold injury (see regain warmth of the entire hand.
Figure 9-7). • Be careful while loading cameras, taking pictures, or handling
stoves and fuel. The freezing point of gasoline (−57° C
PART 2
220
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
FIGURE 9-33 Selection of gloves and mittens used on a frostbite-free H.E. Imray, MD.)
summit day on Mt Everest. (Courtesy Christopher H.E. Imray, MD.)
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.)
221
less benefit44 and thus to increase the need for secondary inter-
TUMOR NECROSIS FACTOR-α
ventions, such as fasciotomies for reperfusion injuries, or subse- Evidence indicates that tumor necrosis factor (TNF)-α–induced
quent amputations.81 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
ULTRASOUND-ACCELERATED THROMBOLYSIS injuries after ischemia and reperfusion injury suggests that these
In vitro work has shown that ultrasound accelerates transport of processes may be modified.184 This particular approach might
recombinant t-PA into clots.55 Ultrasound is believed to reversibly offer improved outcome in early frostbite.
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
VACUUM-ASSISTED CLOSURE THERAPY
and complete thrombolysis has been reported with the use of Vacuum-assisted closure therapy has been shown to be beneficial
this technique than with standard catheter-directed thrombolysis. in accelerating wound healing in partial diabetic foot amputa-
Results of one study suggest that percutaneous ultrasound- tions.6 This therapy can be used in community and specialty
accelerated thrombolysis is more effective at clearing clots than hospitals, and in many tertiary care hospitals it is being admin-
is catheter-directed thrombolysis in patients with acute massive istered through specialist tissue-viability nurses. One report has
pulmonary embolism.108 shown a good outcome with frostbite.152
CHAPTER 9 Frostbite
of 70 cases of severe frostbite lesions: A proposed new classification
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COLD AND HEAT
PART 2
222.e4
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 hazards innate to the cold environment should mean that NFCI
that results from the damage caused to tissues exposed to cold is preventable in most circumstances.
temperatures at or above freezing point (0° to 15° C [32° to 59° F). This chapter explores the history, epidemiology, pathophysi-
NFCI does not involve tissue freezing, which distinguishes it both ology, and current prevention and treatment of NFCI and spe
clinically and pathologically from frostbite.45 The earliest descrip- cifically discusses pernio (chilblains), cryoglobulinemia, cold
tions of this syndrome originated in the military. Baron Domi- urticaria, and Raynaud’s phenomenon.
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
EPIDEMIOLOGY
Russia.115 Historically, infantry regiments have been decimated by Individuals with cold and wet extremities for extended periods
cold and wet conditions, and many medical advances in under- are at risk for nonfreezing cold injuries. During the 1800s, NFCI
standing the pathophysiology and clinical course of NFCI have was observed more frequently when the temperature hovered
occurred after wars.1,44, However, the continuity of research tends around the freezing point—when the ground was muddy rather
to lag during the periods between major military campaigns.123 than frozen.54,114 Standing or sitting for long periods, wearing
Developments in the prevention of cold injury have flourished constrictive footwear, malnutrition, fatigue, or the blunt trauma
as new clothing and footwear are designed, but little progress of marching on cold, wet feet all added to the severity of injury.115
has been made in the treatment of NFCI. Original animal studies that modeled NFCI demonstrated that
An increasing number of people are pursuing recreational cold temperatures near the freezing point were more likely to
activities in harsh environments, and as a consequence, civilian cause injury when the extremities were wet than when they were
NFCIs are becoming more prevalent. However, because many dry.13,114 Ambient temperature and wind speed can both influence
physicians are unfamiliar with these injuries, they may go undi- cooling.39,140
agnosed during assessment of the cold-exposed patient.123 This In “shelter limb” (dependency without cold) and “paddy foot”
results in unnecessary hospital admissions and potentially harmful (wet but not cold), there is an injury that has no apparent dis-
and expensive therapy.49 Proper education and awareness of the tinguishing differential features from NFCI. This would suggest
222
that neither cold nor wet is a prerequisite required to develop a 4-year period, the reporting rate increased from 9 to 30 per
223
hypothalamic via the sympathetic nervous system and direct local cold-air exposure (r = 0.83; p <0.01), showing that a weak CIVD
control, dilating under warm conditions and constricting in reac- response in the hand is related to a weak response in the foot.131
tion to a cold stimulus. The two effects are additive. Cutaneous Felicijan and associates40 found evidence for significant enhance-
vessels are controlled by sympathetic adrenergic vasoconstrictor ment of the CIVD response after brief high-altitude acclimatiza-
fibers, and vascular smooth muscles have both α- and β- tion; these changes were especially prominent in the feet of
adrenergic receptors. When core temperature exceeds 37.5° C Alpinists compared with controls.
(99.5° F), the hypothalamus reduces vasoconstrictor drive to Temperatures of the extremities can drop surprisingly quickly
AVAs and vasodilation occurs. As a result, a low-resistance shunt in the field. Toe temperature of 10 individuals was monitored in
in the dermal venous plexus opens, which in turn increases local the field in Arctic Norway (minimum air temperature, −27° C
heat loss. Under cold conditions, sympathetic tone increases, [−16.6° F). The lowest skin temperature recorded was 1.9° C
resulting in local arteriovenous vasoconstriction and reduced (35.4° F). The mean estimated time for toe temperature to cool
cutaneous blood flow. from 25° C (77° F) to 5° C (41° F) was 109 minutes (standard devia-
Under basal conditions, a 70-kg (154-lb) person has total tion [SD], 10.2) at an ambient temperature of −21° C (−5.8° F).
cutaneous blood flow of 200 to 500 mL/min. With external One person experienced a toe temperature below 5° C (41° F) for
heating to maintain skin temperature at 41° C (105.8° F), this may 2.9 hours during a 27-hour period. Surprisingly, none of the
increase to 7000 to 8000 mL/min, while cooling the skin to 14° C participants demonstrated clinical signs of cold injury, but this
(57.2° F) may diminish it to 20 to 50 mL/min. does not mean that this exposure was without risk.127
Cutaneous vascular tone is inversely related to ambient The cutaneous microcirculation of skin was assessed in
temperature. Cold-induced vasoconstriction is attenuated by α2- patients with sequelae from local cold injuries. All patients
adrenergic blockers and by sympathetic inhibition. Reduction in reported cold intolerance 3 to 4 years after the primary CWI,
ambient temperature results in insertion of more α2-adrenergic sustained during military service.7 Transcutaneous oxygen tension
receptors from the myocyte Golgi apparatus into the plasma was decreased, but oxygen reappearance time, oxygen recovery
membrane, raising the affinity for the sympathetic neurotransmit- index, postocclusive reactive hyperemia, and venoarterial reflex
ter norepinephrine. At the same time, endothelial nitric oxide were normal. No capillary nailfold abnormalities were found.
synthase (eNOS) activity declines, resulting in vasoconstriction of Local cold injuries appear to cause disturbances in the CIVD and
the AVAs. Core temperature has a strong influence over cutane- impair cold tolerance and may increase the risk for future cold
ous sympathetic vasomotor activity. injuries. Evidence suggests disturbances of reflex mechanisms
The vascular endothelium regulates local vascular tone by mediated by the central nervous system. Neurophysiologic factors
secreting vasoactive agents, including the vasoconstrictor endo- seemed more important than ischemic mechanisms in the patho-
COLD AND HEAT
thelin and the vasodilators nitric acid and prostacyclin. Endothe- physiology of late sequelae with peripheral CWI.
lin causes long-lasting vasoconstriction and is elevated in hypoxia,
preeclampsia, and hemorrhagic stroke.
PATHOPHYSIOLOGY
Continuous exposure to a cold, wet environment causes break-
ORTHOSTASIS down of skin, directly cools nerves in the area of exposure, and
Orthostasis (standing upright) or lowering a limb below heart causes prolonged vasoconstriction. NFCI is primarily caused by
level causes immediate reduction in local blood flow; cutaneous prolonged vasoconstriction, which in turn causes direct injury to
perfusion is reduced by approximately two-thirds as a result of the vessels (and endothelium) that supply nerve, fat, and muscle
PART 2
the poorly understood venoarteriolar response. It is thought that cells.62,92,123 Pain, fear, constrictive footwear, and immobility inter-
this response helps maintain central arterial pressure during act in maintaining vasoconstriction through a heightened sympa-
standing and also reduces dependent edema formation. Long thetic nervous system response or by mechanically limiting blood
periods of sitting or standing tend to exacerbate this response. 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-
COLD-INDUCED VASODILATION perature and directly proportional to duration of insult.13,124
When the hand or foot is cooled to 15° C (59° F), maximal vaso- Lengthy exposure to a temperature of about 10° C (50° F) will
constriction and minimal blood flow occur. If cooling continues result in similar injury as a short exposure to a temperature of
to 10° C (50° F), vasoconstriction is interrupted by periods of 1° C (33.8° F). Repeated exposure is likely to cause a more sig-
vasodilation and an associated increase in blood and heat flow. nificant injury than a single exposure of longer duration.72
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 Local nerve Swelling and
Cold-wet
and offers some degree of acclimatization. Eskimos, Lapps, and cooling breakdown of
exposure
Nordic fishermen have a strong CIVD response and short inter- skin
vals between dilations, which may contribute to maintenance of
hand function in the cold environment.55 CIVD responses are Vasoconstriction Pain and fear
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 Constrictive
Cheung and colleagues21 investigated if CIVD responses of one ↓ Local blood flow footwear
finger can predict the responses of other fingers, as well as Immobility
whether the CIVD of fingers could predict CIVD responses of
the feet and toes. They found that CIVD is highly variable across Local nerve Ischemia
the fingers and is not a generalizable response across either digits damage
or limbs. Paradoxical CIVD will normally prevent tissue damage,
but in conditions such as Raynaud’s phenomenon, the vessels of Endothelial
the toes and fingers exhibit an exaggerated and sustained vaso- damage
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- Sensory Loss of Cold
water immersion of the fingers in a laboratory setting have a impairment vasodilation sensitization
higher risk for local cold injuries when exposed to cold in real
life.30 A strong correlation exists between the mean temperature FIGURE 10-1 Schematic of factors and mechanisms that contribute to
of the fingers during cold-water immersion and toes during nonfreezing cold injuries.
224
VASCULAR INJURY
ANIMAL MODELS
Animal models have been developed to understand the underly-
NERVE INJURY ing pathophysiology of NFCI. Thomas and colleagues124 devel-
Nerve cooling has been suggested as contributing to the etiology oped a rat model of NFCI by immersing the tail in 1° C (33.8° F)
of NFCI. Large myelinated fibers (C fibers) are most susceptible water for 6 to 9 hours and characterized the loss of CIVD as a
to prolonged cold exposure.67,75,76,110 In severe NFCI, characteristic prolonged decrease in tail blood flow followed by increased
peripheral nerve damage and tissue necrosis occur.68 Clinical blood flow above baseline. This pattern is similar to that clinically
sensory tests indicate damage to both large- and small-diameter observed in humans during the prehyperemic phase followed by
nerves. The prolonged cold injury affects blood vessels serving the hyperemic phase.
these large myelinated fibers, with subsequent ischemia causing Stephens and associates118 recently used the rat tail model in
a decrease of oxygen to the nerve, resulting in the appearance an attempt to elucidate possible mechanisms that cause vascular
of a primary nervous system injury71,72 (Figures 10-2 to 10-5). endothelial damage. Their preliminary data suggest that acute
In NFCI, nerve injury is ultimately likely to be multifactorial, cold-water exposure causes loss of nitric oxide–dependent endo-
consisting of both direct nerve fiber damage and a vascular thelial function and possibly a change in smooth muscle contrac-
component.73 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
cold-water immersion damaged large myelinated fibers while acidophilic and hyalinized (Zenker’s hyaline degeneration). The
sparing small myelinated and unmyelinated fibers. myoplasm within muscle loses its cross-striation, and the healing
Nonfreezing cold injuries affect many different types of tissue. muscle then appears to undergo fibrous tissue replacement.
Pathologic examination of specimens displays a variety of lesions One of the major pathologic processes in NFCI is progressive
to the skin, muscle, nerve, and bone.11,12,46 Muscles exhibit separa- microvascular thrombosis following reperfusion of the ischemic
tion of the cells and damage of the muscle fibers, described as 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
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
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 10-11 Hyperemic phase in moderately severe nonfreezing
cold injury. Swelling, redness, and persistent pain in the feet of an
FIGURE 10-8 Hyperemic phase of nonfreezing cold injury. This person infantry soldier from the Falklands War. (British Crown Copyright/
spent 18 hours in winter bailing out a boat that threatened to capsize MOD.)
in Prince William Sound, Alaska. (Courtesy James O’Malley, MD.)
COLD AND HEAT
swollen, red, and painful. (British Crown Copyright/MOD.) 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
may be unbearable.57 After 7 to 10 days, the nature of the pain Crown Copyright/MOD.)
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 color, whereas blanching occurs when the limb is raised. Tense
is reduced or lost, whereas proprioception is usually retained. edema becomes marked during this stage. Blisters containing
Anhidrosis coincides with the extent of sensory loss.123 serous or hemorrhagic fluid may form, indicating more severe
Vascular injury is evident in vessel reactivity. Skin tempera- injury.123 The superficial epidermis becomes thick, indurated,
ture gradients are absent, with digits often as warm as or and desquamated. Eschars form (Figures 10-13 and 10-14) and
warmer than the groin or axillae. When the affected limbs are eventually slough, leaving a pink dermis (Figure 10-15). In more
lowered, blood pools, turning the extremity a deep purple-red 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 10-10 Hyperemic phase of immersion foot. The characteristic FIGURE 10-13 Severe nonfreezing cold injury. This Argentinian soldier
redness of the stage is absent due to the pigmented skin, but the feet had been unable to care for his feet for many weeks. (British Crown
are swollen and painful. (British Crown Copyright/MOD.) Copyright/MOD.)
228
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.)
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.)
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
FIGURE 10-15 Severe nonfreezing cold injury in a British sailor during the functional biomechanics of the foot. Since this is often associ-
World War II. (Courtesy M. P. Hamlet.) ated with alterations in the sensory nerve supply to the feet,
disabling problems can persist64 (Figure 10-20).
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
229
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
FIGURE 10-19 Magnetic resonance imaging scan of the patient in studied this in NFCI, it is advisable to consider starting a neu-
Figures 10-17 and 10-18, 24 months after nonfreezing cold injury, with ropathy agent as early as possible.
chronic discharging sinuses from osteomyelitis of the first metatarsal
head. (Courtesy Christopher H.E. Imray, MD.)
OCCUPATIONAL MEDICINE
Depending on the patient’s profession, occupational medicine
TREATMENT review may be required. This will be the case if patients work
in environments that put them at risk of repeated NFCI.
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
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 B
appraisal of the injury is required if optimal treatment is to be
given. FIGURE 10-20 A guillotine transmetatarsal amputation of left foot was
undertaken 6 months after severe nonfreezing cold injury. The patient
DRUGS was treated with delayed primary split-skin grafting. This photo was
taken 12 months after the original injury. The graft has taken but is
The diagnosis of an NFCI is often difficult or delayed. In view now ulcerated as a result of the shear forces generated by walking on
of involvement of the α-adrenergic receptors in control of the the insensate tissue. (Courtesy Christopher H.E. Imray, MD.)
230
although used extensively by the UK military, IR thermography
28 PREVENTION
The simplest way to prevent NFCI is to avoid prolonged exposure
26 to cold, wet environments. This can be difficult to implement
because of varying conditions and individual susceptibility. In
24 military conflicts, completing the assigned mission is most impor-
20.9° C 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
FIGURE 10-21 Infrared thermography in the assessment of the con-
save others that they do not take adequate care of themselves.
sequences of nonfreezing cold injury (NFCI). The upper sequence of
three images was taken from an uninjured, asymptomatic control; the
Prevention can be achieved by encouraging people to remain
lower sequence from a patient who had sustained NFCI and was sub- active and increase blood flow to the feet, rotating personnel out
sequently complaining of sensitivity to the cold. In both control and of cold-wet environments on a regular basis, keeping feet dry by
patient, the first (left) image was taken after resting in an ambient air early changing of wet socks, maintaining body core temperature
temperature of 30° C (86° F). The second (center) image was taken by limiting sweat accumulation into clothing and dressing in
immediately after the foot had been immersed in water at 15° C (59° F) layers, and educating personnel about the early signs and symp-
for 2 minutes. The final (right) image was taken 5 minutes after removal toms of NFCI. Changing socks two or three times throughout the
from the water, again in 30° C (86° F) air. The upper series shows feet day is mandatory in cold, wet environments. Military sources
that were warm at rest, which rewarmed briskly after mild cold stress, suggest that optimal care entails air drying feet for at least 8 hours
recovering almost completely within 5 minutes after removal from the of every 24 hours.17,143 Vapor-barrier boots do not allow sweat
water. The lower series shows a severe degree of cold sensitization; from the foot to evaporate, and in some situations, this increases
the feet were much colder than the surrounding air at rest, and once maceration.4 Boots should be taken off each day, wiped out, and
cooled, took a long time to rewarm, remaining much cooler than the dried. Footwear should not constrict blood flow; sizing is impor-
control foot at 5 minutes after immersion. The scale at far right indi- tant, as is educating the user not to tie shoelaces too tightly. To
cates the color-temperature relationship. (British Crown Copyright/ achieve an adequate level of self-care, education must impart a
MOD. Reproduced with the permission of Her Britannic Majesty’s sense of individual responsibility, while expedition leaders still
Stationery Office. From Thomas J, Oakley H. Nonfreezing cold injury. monitor and ensure that standards are maintained.
In Pandolf KB, Burr RE, editors: Textbook of military medicine: Medical
Prophylactic treatment with silicone preparations has proved
aspects of harsh environments. Vol 1. Washington, DC, 2002, Office
of the Surgeon General, Borden Institute, pp 467-490.)
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
ASSESSING INJURY SEVERITY ointment applied only to the sole of the foot instead of to the
Following the initial injury, increased sensitivity to cold develops. entire foot (thus reducing surface area exposed to dirt retention,
There are often surprisingly few objective clinical signs. A careful amount of material transported by the soldier, and dollar cost)
history of appropriate cold-weather exposure, clear history of the was sufficient to prevent NFCI.35
typical rewarming symptoms and signs, detailed examination, Because of the apparent increasing incidence of NFCI in
and special investigations all build a picture consistent with NFCI. the British military, a number of additional preventive steps
Corroborative evidence from medical records is vital. have been taken, including improved education of personnel
about prevention measures, equipment, and early recognition
(Figure 10-22).
SPECIAL INVESTIGATIONS The severity of the injuries affecting the military appears to
Infrared (IR) thermography can be used to assess the individual’s be relatively mild compared with civilian NFCI injuries (see
response to a standardized cold stress and may be helpful in Figures 10-17 to 10-19) and military historical controls (see
confirming the diagnosis, assessing injury severity, and monitor- Figures 10-13 to 10-16). This raises the question as to whether
ing recovery (or otherwise) from NFCI (Figure 10-21). However, there is (1) a continuous spectrum of disease, (2) a bimodal
231
distribution of the disease with milder and more severe forms of winter horseback riding, and hiking.101 Pernio can be caused by
NFCI, or whether (3) the commonly presenting form now seen brief cold exposure (30 minutes), often appearing several hours
is the same disease process investigated in the past. Part of the after exposure, with the skin lesions fully developed within 12
problem may lie in the UK military’s decision to use IR thermog- to 24 hours.99 Characteristic locations for these lesions are the
raphy as one of the bases on which the diagnosis, severity, and feet, hands, legs, and thighs. Single or multiple, erythematous,
progression of NFCI are determined. purplish, edematous lesions form, with vesicles in severe cases.
One approach to the high levels of NFCI noted would be to Symptoms include intense pruritus, burning, or pain, often wors-
consider screening potential recruits. This requires a test with ened by subsequent warmth. The lesions of acute pernio are
high sensitivity and specificity. However, individual variation in self-limited and usually resolve within a few days to 3 weeks,100
the control of peripheral blood flow is so great that none of the occasionally leaving residual hyperpigmentation.25 Although the
assessments currently available meets these requirements.15,28,30,123 healing process appears to occur as the plaques resolve, pain
Reducing the incidence of cold injury in military training often persists. Subsequent mild cold exposure may trigger par-
requires striking a delicate balance between training realism and esthesias, edema, and skin scaling.57
safety. While training in demanding environments runs real risks Chronic perniosis usually progresses over several winters after
of injuring personnel, the benefits to them in the development repeated episodes of acute pernio, rarely progressing from the
of field-craft skills are vital if they are to avoid NFCI.123 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
MORE SEVERE INJURIES formation. The nodules are firm and painful, ultimately rupturing,
Nonfreezing cold injury can vary in severity from mild to severe. which provides pain relief and leaves a shallow ulcer with pig-
In severe cases, cold sensitization is so serious that individuals mented atrophic skin. These ulcers may grow larger and coalesce,
are unable to work outside. Edema and hyperhidrosis often remaining open, which leads to permanently swollen extremities,
occur, making the individual susceptible to fungal infections. scaly pigmented skin, and unremitting pain aggravated by light
Chronic pain resembling causalgia or reflex sympathetic dystro- pressure.
phy may occur. The profound sensory loss may lead to minor Pernio is thought to be caused by prolonged cold-induced
or major lower-limb amputation. Ongoing care within a specialist vasoconstriction with subsequent hypoxemia and vessel wall
foot clinic using custom-made shoes and insoles appears to inflammation.49,69 Subcutaneous arterial vasoconstriction is docu-
improve functional outcome. Multidisciplinary team approaches, mented by both pathologic81 and arteriographic studies.116 Histo-
such as healing of the ulcerated neuropathic foot using patella logic examinations show lymphocytic vasculitis and papillary
COLD AND HEAT
tendon–bearing orthoses, have been described.77 NFCI pain is dermal edema with pervasive inflammatory changes.49,69,81 The
often so severe as to require tricyclic antidepressants, which differential diagnosis includes lupus erythematosus, Raynaud’s
should be instituted at an early stage.66,123 Failure to do so phenomenon, polycythemia vera, atheromatous embolization,
increases the risk of developing severe chronic pain resistant to erythema nodosum, and livedo vasculitis with ulcerations.
all subsequent treatment modalities. Early involvement of pain Treatment of pernio is accomplished by drying and gently
specialists is important. 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
TRENCH FOOT (IMMERSION FOOT) ultraviolet irradiation,61 thymoxamine,70 intravenous calcium com-
PART 2
Trench foot and immersion foot are clinically and pathologically bined with intramuscular vitamin K,42 corticosteroids,47 and sym-
indistinguishable but have different etiologies. The term trench pathectomy in severe cases,81 few have proved to be either
foot originated during the trench warfare of World War I,136 when effective or universally accepted. Nifedipine (20 mg three times
soldiers wore wet boots and socks for prolonged periods.8 daily) has been effective for treatment of severe perniosis.
Immersion foot was first medically documented during World Patients treated had a significantly reduced time for clearance of
War II among shipwreck survivors whose feet had been continu- lesions, decreased pain and irritation of existing lesions, and less
ously immersed in cold water.27 Both injuries occur when tissue development of new pernio.49,108
is exposed to cold and wet conditions at temperatures ranging Preventing pernio is relatively simple. Recommended prophy-
from 0° to 15° C (32° to 59° F). Colder temperatures decrease the lactic measures include minimizing cold exposure with suitable
time required to induce NFCI.13,115 Severe nerve damage from clothing when outdoors and maintaining adequate warm tem-
immersion foot has been seen after exposure periods of 14 to peratures indoors.
22 hours.128,130 Immersion foot injury may extend proximally and
involve the knees, thighs, and buttocks, depending on the depth
of immersion.137
RAYNAUD’S PHENOMENON
This eponymous phenomenon was first identified by Maurice
Raynaud in 1862, who described “local asphyxia of the extremi-
PERNIO (CHILBLAINS) ties.” Raynaud’s phenomenon is a paroxysmal vasospastic and
Pernio (perniones) or chilblains are localized, inflammatory, subsequently vasodilatory arteriolar response to temperate or
bluish red lesions caused by an abnormal reaction to a cold, occasionally emotional stressors. This can include changes in
damp environment. This mild form of cold injury is prevalent in temperatures, not only cold exposure,52 and is essentially arterial
the temperate climates of northwestern Europe81 and is found hyperresponsiveness and vasoconstriction in susceptible indi-
worldwide throughout temperate and northern zones.49,87,88,99 viduals.59 The classic observed color change, common in digits,
Pernio is less common in very cold climates, where well-heated is white (following the initial vasospastic response) to blue
houses and adequate warm clothing are common.100 (indicating hypoxia) and finally to red, with subsequent vasodila-
In a recent study of 111 patients, 67 (60.4%) were males and tion on rewarming. The final stage is often associated with
44 (39.6%) females; 89 (80.2%), 90 (81.1%), and 90 (81.1%) burning pain.
patients had onset in relation with lower temperature (<10° C Broadly, Raynaud’s can be divided into primary and second-
[50° F]), relatively low atmospheric pressure (<1500 kPa), and ary. Raynaud’s phenomenon is the primary form, typically affect-
higher relative humidity (>60%), respectively. Susceptibility to ing women in their 20s to 30s, with no obvious underlying cause.
chilblains appeared to increase when ambient temperature was Raynaud’s syndrome, or secondary Raynaud’s, is when the phe-
less than 10° C (50° F) and relative humidity was more than 60%.105 nomenon has an underlying cause, sometimes presenting as
Acute pernio has a seasonal incidence, with reversible symp- the first sign of a systemic condition, such as systemic sclerosis.52
toms more common in cold weather. The acute form is seen The vascular defect in primary Raynaud’s is thought to be primar-
primarily in schoolchildren and young adults younger than 20, ily functional with a hyperresponsiveness causing symptoms,
with the highest incidence in adolescent females.81 It can occur whereas secondary Raynaud’s often has underlying vascular and
in mildly cold settings such as logging, kayaking, snowmaking,57 microvascular abnormalities.59
232
Primary Raynaud’s is unlikely to cause digital ischemia and tive dihydropyridine for treatment and prophylaxis, and meta-
233
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-
FIGURE 10-23 Cold urticaria. The hive occurred within minutes of cal, a cold-water immersion test of submerging a forearm for 5
holding an ice cube against the skin. (From Habif TP: Clinical dermatol-
to 15 minutes in water at 0° to 8° C (32° to 46.4° F) establishes
ogy, ed 4, Philadelphia, 2004, Mosby.)
the diagnosis.
Treating cold urticaria with antihistamines is the most effective
option. To reduce symptoms sufficiently requires dosing up to
object) to cold111 (Figure 10-23). It most frequently affects young four times the recommended dose.95,111,112 In addition, other thera-
adults, although primary cold urticaria can occur at any age. pies include leukotriene antagonists, cyclosporine, corticoste-
Women are twice as likely to be affected.112 The incidence rate roids, and anti-IgE.112 Individuals with severe reactions should
is about 0.05% of the population. have an emergency kit containing corticosteroids, antihistamines,
Symptoms are usually limited to cold-exposed skin areas.111 and epinephrine. Based on the finding that infectious disease
Local symptoms include redness, itching, wheals, or edema of may be a trigger for cold urticaria, treatment with antibiotics may
exposed skin. The wheals last approximately 30 minutes. Sys- also be warranted.112
temic reactions include fatigue, headache, dyspnea, and hypoten-
sion. Swimming in cold water is the most common trigger of
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87. Mills W, Pozos R. Low temperature effects on humans. In: Ency 116. Spittel J, Spittell P. Chronic pernio: Another cause of blue toes. Int
clopedia of human biology. New York: Academic Press; 1991. Angiol 1992;11(1):46–50.
p. 117–28. 117. Steinhard MJ, Fisher GS. Essential cryoglobulinemia. Ann Intern Med
88. Mills WJ Jr, Mills WJ III. Peripheral non-freezing cold injury: immer- 1955;43:848–58.
sion injury. Alaska Med 1993;35(1):117–28. 118. Stephens D, Saad AR, Bennett LA, et al. Damage to vascular endo-
89. Mitchell J, Simpson R, Whitaker J. Cold injuries in contemporary thelium and smooth muscle contribute to the development of non-
conflict. J R Army Med Corps 2012;158(3):248–51. freezing cold injury n the rat tail vascular bed in vitro. 13th
90. Mohan JS, Marshall JM, Reid HL, et al. Comparison of responses International Conference on Environmental Ergonomics; 2009;
evoked by mild indirect cooling and by sound in the forearm vas- Boston; 2009. pp 177-81.
culature in patients with homozygous sickle cell disease and in 119. Summaries NIfHaCECK. Raynaud’s phenomenon: NICE; 2014.
normal subjects. Clin Auton Res 1998;8(1):25–30. 120. Tedeschi A, Barate C, Minola E, Morra E. Cryoglobulinemia. Blood
91. Mohr WJ, Jenabzadeh K, Ahrenholz DH. Cold injury. Hand Clin Rev 2007;21(4):183–200.
2009;25(4):481–96. 121. Teixeira F, Pollock M, Karim A, Jiang Y. Use of antioxidants for the
92. Montgomery H. Experimental immersion foot: Review of the phys- prophylaxis of cold-induced peripheral nerve injury. Mil Med 2002;
iopathology. Physiol Rev 1954;34(1):127–37. 167(9):753–5.
93. Moran DS, Heled Y, Shani Y, Epstein Y. Hypothermia and local cold 122. Tek D, Mackey S. Non-freezing cold injury in a Marine infantry bat-
injuries in combat and non-combat situations: The Israeli experience. talion. J Wilderness Med 1993;4:353–7.
Aviat Space Environ Med 2003;74(3):281–4. 123. Thomas J, Oakley H. Nonfreezing cold injury. In: Pandolf KB, Burr
94. Neittaanmaki H. Cold urticaria: Clinical findings in 220 patients. RE, editors. Textbook of military medicine, vol. 1. Medical aspects
J Am Acad Dermatol 1985;13(4):636–44. of harsh environments. Washington, DC: Office of the Surgeon
95. Neittaanmaki H, Myohanen T, Fraki JE. Comparison of cinnarizine, General, Borden Institute; 2002. p. 467–90.
cyproheptadine, doxepin, and hydroxyzine in treatment of idiopathic 124. Thomas JR, Shurtleff D, Schrot J, Ahlers ST. Cold-induced perturba-
cold urticaria: Usefulness of doxepin. J Am Acad Dermatol 1984; tion of cutaneous blood flow in the rat tail: A model of nonfreezing
11(3):483–9. cold injury. Microvasc Res 1994;47(2):166–76.
96. Nukada H, Pollock M, Allpress S. Experimental cold injury to periph- 125. Thompson AE, Pope JE. Calcium channel blockers for primary Rayn-
eral nerve. Brain 1981;104(Pt 4):779–811. aud’s phenomenon: a meta-analysis. Rheumatology 2005;44(2):
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112–19. Cold-induced cutaneous vasoconstriction is mediated by rho kinase
234.e2
in vivo in human skin. Am J Physiol Heart Circ Physiol 2007; 135. Webster D, Woolhouse F, Johnson J. Immersion foot. J Bone Joint
234.e3
CHAPTER 11
Polar Medicine
MARTIN RHODES AND HANS CHRISTIAN SØRENSON
As with much of wilderness medicine, polar medicine is largely within an extreme cold environment, distinguished by a scarce
derived from its setting. Polar, however, can be defined in several population, limited resources, and challenging logistics.” It is the
different ways. Geographically, the Arctic and Antarctic circles, cold, remoteness, hostility, and unforgiving nature of the environ-
at latitudes 66 degrees, 33 minutes north and south, delimit areas ment in which humans struggle to survive, let alone work, that
in which the sun does not rise or set on at least 1 day of the make medicine in polar areas, and in particular Antarctica, so
year, and determine the North Polar region (“The Arctic”) and challenging.69
South Polar region (“The Antarctic”). A definition based on tem- The environment itself defines polar medicine in another
perature is the 10° isotherm, which joins those areas in which sense. So harsh are the poles that the simplest of mistakes can
the average temperature in the warmest month of the year is lead to harm. The average temperature at the South Pole in winter
10° C (50° F); this correlates roughly with the tree line. is −60° C (−76° F). At this temperature, exposed skin freezes within
For medical purposes, the definition of polar is more complex. minutes. Prevention is everything, and thus polar medicine can be
Although climate and geography are clearly important, the salient seen as example of preventive medicine in practice.
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. THE DISTINCTION BETWEEN ARCTIC
High-altitude medicine is a medical field because of the environ-
ment’s effect on the human organism, but polar medicine is
AND ANTARCTIC MEDICINE
largely medical practice within a particular environmental setting. Although the polar regions share the predominant attributes of
Medical practice in isolated settings is paradigmatic of wilder- cold, dark, isolation, and severe weather, they display many
ness medicine; the patient population is essentially, if not literally, important contrasts. The Arctic has been described as a frozen
a small demographic island. A broad definition of polar medicine, sea nearly surrounded by land, whereas Antarctica is a land and
therefore, could be “the practice of medicine in isolated settings ice mass circumscribed by ocean. The moderating effect of the
234
surrounding North Polar waters contrasts with the cooling effect enlarged by several remarkable expeditions, and recent stunning
235
been important in both polar regions. With increasing exploration half-life of radioactive fallout deposits,120,129 and increased chemi-
of mineral and oil reserves and fishing potential, migrating humans cal contamination, particularly in animals high on the food chain,
will continue to bring medical problems with them. Although the with persistent organic compounds, heavy metals, and other
Antarctic Treaty of 1959 prohibits territorial or commercial claims, contaminants affecting the environment and food supply.71,129
seven nations have made sectoral claims on the continent. Some Widening of the Antarctic ozone hole (discovered by BAS scien-
of these claims overlap and in the future may lead to a less-than- tists in 1985) carries implications of increased ultraviolet (UV)
peaceful resolution. In early 2010, however, Australia failed to radiation. As occupational and environmental health issues draw
pursue Japan legally for ramming and sinking an antiwhaling boat more attention, this aspect of polar medicine assumes greater
in Antarctic waters supposedly governed by Australia. The most importance.30,31
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. BRIEF HISTORY OF HUMAN
In 2007, the Russian minisubmarines Mir-1 and Mir-2
descended to 4300 m (14,108 feet) in the Arctic Ocean and HABITATION IN POLAR REGIONS
placed a Russian flag on the seabed under the North Pole. The A perspective on the contrasts between Arctic and Antarctic
Russians were hoping that soil samples would prove that its medicine may be sharpened by a brief summary of human habi-
Siberian ridge was directly connected to the Lomonsov Ridge, an tation in polar areas. Humans are known to have inhabited Arctic
underwater crest 1996 km (1240 miles) long running across the regions for at least 4500 years. Anthropologists have uncovered
Arctic, and would lend credence to their territorial claim. evidence for several waves of population migration from Siberia
Concern about the environmental impact of increasing human through northern Canada to Greenland. Each of these migrations
activity in polar regions seems to be tempering the pace of was probably linked to climatic conditions, and each resulted in
development. As national resources diminish, however, the Ant- a distinct set of cultures. The general pattern was of a nomadic
arctic may come under increasing pressure to open up to extrac- life with population densities of approximately one person per
tion industries, similar to the situation in the Arctic. 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-
INCREASES IN RESEARCH ACTIVITIES matically during the second half of the 19th century, when the
Scientific research has been a part of polar exploration through- whaling industry moved into Hudson Bay, leading to sustained
out this century. There are scientific and medical journals devoted contact between Europeans and the Inuit. In the early part of
COLD AND HEAT
to the polar regions, and thousands of articles are indexed each the 20th century, religious missions, trading company posts,
year in the Antarctic Bibliography (http://www.coldregions.org/ government stations, church missions, and eventually medical
antinfo.htm). The International Journal of Circumpolar Health clinics and schools began to encourage permanent settlements,
(http://ijch.fi/Issues.htm) is a richer source for health issues in roughly quadrupling the population density.55 In some areas,
polar regions. Antarctic research continues to expand. All the such as Eurasia, large industrial and mining cities arose. This
continent’s permanent stations are primarily there to support change in population distribution has at times led to conflict
research. The largest study is the IceCube project at the South between indigenous and European cultures, and it has had sig-
Pole station, which uses a series of downward-looking detectors nificant environmental and medical consequences.130
spread over a square kilometer to look for traces of the notori- The known history of human exploration of Antarctica, unlike
PART 2
ously elusive neutrinos. Neutrinos are produced when neutrons that of the Arctic, is quite recent. Recorded sightings of the con-
transform into protons during nuclear reactions. The detectors tinent date only to around 1800, and “winter-over” sojourns did
do not detect the neutrinos themselves, but rather the blue light not occur for another century. Waves of settlement also occurred
emitted by the breakdown particle (a “muon”) produced when in Antarctica: sealing in the early 19th century, whaling in the
a neutrino collides with an ice molecule. The source of these early 20th century, and scientific exploration since the mid-20th
neutrinos coming up through the ice to the detectors may be century.123 The heroic era of Antarctic exploration occupied the
black holes, gamma ray bursts, or supernova remnants and other early years of the 20th century, with exploits such as the highly
extragalactic events. The muon preserves the direction of the publicized race for the South Pole between Roald Amundsen and
original neutrino and thus points back toward its cosmic source. Robert Scott in 1911; the extraordinary survival of the crew of
The IceCube project is at the forefront of astronomy and particle the 1914 Endurance expedition, led by Ernest Shackleton;64 and
physics research. In 2014, a report on 3 years of analysis dem- the heroic survival of Douglas Mawson, an Australian geologist
onstrated a total of 37 high-energy neutrino strikes. The largest who wintered alone after other expedition members perished.75
of these, detected on December 4, 2012, is nicknamed “Big Bird” Perhaps because of these and other dramatic events, and the
and is the highest-energy neutrino interaction ever observed.1 absence of an indigenous population and a scarcity of easily
The South Pole also hosts two large telescopes. exploited resources, human activities in the Antarctic have
Another huge project involving many countries at multiple retained a somewhat more expeditionary flavor than in the Arctic.
sites across the Antarctic continent is ice-core drilling, designed This has helped shape the contrasts in medical practice between
to catalog climate change over tens of thousands of years. Other the northern and southern polar regions.
scientific endeavors include marine biology and ocean dynamics
research; atmospheric and climatologic research, including air
cleanliness monitoring and ice sheet movements; medical re- ARCTIC MEDICAL PROBLEMS
search (primarily at Japanese and Chinese stations)84; biologic EFFECTS OF CULTURAL AND
research (ecosystems, penguins, seals, bacteria, lichen); seismic
monitoring; aerial and sea floor mapping with unmanned vehi-
DEMOGRAPHIC TRANSITION
cles in the harsh environment; paleontology; meteorite searches; The Arctic is not a homogeneous region. Although the population
and demonstrations of alternative power in extreme circum- is only approximately 4 million, it is very diverse, with few fea-
stances (e.g., wind generators at New Zealand’s Scott Base). tures in common except the latitude of residence and hours of
Some observers have discerned a north-south split, perceiving daylight. Medical problems among indigenous populations in the
research in Antarctica as having more of a political motivation Arctic, approximately 10% of the total population, are character-
and that in the Arctic as being more practical. For both scientific istic of displaced aboriginal people elsewhere in the world. The
and political reasons, an important part of scientific research in wide-ranging interrelated factors include demographics, socio-
polar regions concerns environmental issues. The remoteness of economic and physical environments, personal health practices,
these regions enhances their value as benchmarks for studies of and availability of good-quality and culturally appropriate health
pollution. Indeed, several worrisome facts have been revealed care services.13,56 Although increased contact with industrialized
about the contamination of formerly pristine wilderness, such as cultures has brought benefits, it has also brought many problems.
widespread radioactive contamination, the prolonged effective Some of the benefits include greatly improved life expectancy,
236
largely because of a decrease in morbidity and mortality from the endocrine-disrupting effects of PCBs may have changed the
237
Most other studies suggest that this figure may be low. One study There is increasing acknowledgment that isolated Inuit com-
among Inuit found that 22%, or one in five, experience depression munities offer rich grounds for research. For example, a 2014
during the winter months, and 7% appeared to have seasonal study from Greenland demonstrated that bacille Calmette-Guérin
affective disorder.39 Cultural stress, erosion of traditional lifestyles, (BCG) vaccination significantly lowered the incidence of Myco-
and substance abuse are all contributory factors.13 Studies inves- bacterium tuberculosis infection and tuberculosis in Greenlandic
tigating scientific staff at Arctic research stations are relatively children and young adults. This study was possible because the
uncommon but show patterns of sleep disturbances, depression, BCG vaccination, introduced there in 1955, was temporarily
and alcohol use reminiscent of those in Antarctic stations. halted from 1991 to 1996 because of nationwide policy changes.78
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-
ANTARCTIC MEDICAL PRACTICE
land, one in three Inuit dies a violent death, and about 25,000 Medical practice, problems, and their study in the Antarctic are
adults consume 28 million cans of beer a year, one of the highest somewhat different from those in the Arctic. Extreme isolation
per capita consumptions of alcohol in the world. Prevalence of makes Antarctic medicine unique. Because of the remoteness, it
“binge drinking” among Arctic peoples ranges from 12% to 39%, may not be possible to medically evacuate (medevac) a patient
with male greater than female rates. Fetal alcohol syndrome is for weeks or even months. It might be easier to medevac from
13% higher in Alaska than in the continental United States.13 One the International Space Station than from some of the more
study compared alcohol consumption by the Greenland Inuit remote Antarctic stations.36 In general, the population residing at
with nonindigenous local inhabitants and found that alcohol national Antarctic programs is adult, relatively young, and physi-
consumption was less among the Inuit. However, other studies cally and mentally healthy. As previously, noted, however, the
found the reverse.63 number of tourists of all ages visiting the Antarctic has increased
Accidents are the leading cause of death in the Arctic, and dramatically, bringing with them a broad range of acute and
one-third of these are estimated to be alcohol related. In the chronic medical conditions.
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,
NATIONAL ANTARCTIC PROGRAMS
for boys and men ages 15 to 29, suicides are the most common There are approximately 30 summer-only and 42 year-round
form of injury leading to death. It should be no surprise that life national Antarctic program bases spread around the Peninsula
expectancy is lower, and infection rates for many diseases (e.g., and continent. The newest of these is the Chilean summer-only
COLD AND HEAT
In summary, indigenous populations of the Arctic show lower respective sovereignty claims. All stations have some form of
life expectancy, higher rates of infectious diseases, higher infant medical care, usually a station physician. The more temporary
mortality, and higher rates of injuries and suicides compared with camps have varied medical support, ranging from first-aid wilder-
norms in their respective countries.51 Fortunately, there are ness responders to paramedics or midlevel providers with limited
encouraging signs related to Arctic health care. The incidence of medical supplies. In general, the permanent year-round bases
low birth weight, 5.5% in the central Canadian Arctic, has have more sophisticated facilities, with radiographic, laboratory,
decreased, although it is still higher than that among non-Arctic surgical, and dental provisions and a reasonably well-stocked
dwellers.13 Tuberculosis, which incapacitated up to 20% of the pharmacy for expected emergencies. There is at least one physi-
Canadian Inuit by 1950, has largely been brought under control, cian and sometimes nurses and ancillary medical personnel.
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
MEDICAL STATIONS IN ANTARCTICA
in 1975, it decreased to 25 per 1000 in 1995 and 15 per 1000 in Medical facilities in the Antarctic polar regions can be conve-
2009.16 This is as a result of national guidelines, improved train- niently divided into permanent and expeditionary facilities. As a
ing, and introduction of ultrasound screening. High-risk pregnan- result of community expectations and long-term commitment to
cies are identified as early as possible, with childbirth planned research in Antarctica, a notable shift from an expeditionary to
to occur in the main hospital in Nuuk, West Greenland. Despite an operational attitude has occurred in many of the Antarctic
these improvements, perinatal mortality is still significantly higher programs. Figures 11-1 to 11-3 show the expeditionary facilities
than for the rest of the developed world. This is the inevitable at Union Glacier field camp. This unit can be flown in and out
consequence of life in the polar regions. With long transfer-to- of Antarctica by cargo plane.
hospital distances, weather-dependent logistics, and limited What type of physician is needed? To paraphrase Grant,36 the
medical resources, a sudden unexpected premature birth or physician cannot be too specialized in approach; broad knowl-
obstetric complication is at high risk for a poor outcome. Trends edge and a wide range of practical skills are necessary to provide
in environmental and occupational health problems show good Antarctic medical care. Specialization in emergency medi-
increased monitoring, intervention, and improvement. Unfortu- cine or the equivalent seems to be a suitable choice, especially
nately, the age-adjusted incidence of diabetes mellitus is dramati- to deal with emergencies. Bases usually have no room for anes-
cally rising among First Nations populations.28 thetists, surgeons, dermatologists, or psychiatrists; one person
An important development in recent years has been the insti- covers these roles. However, huge advances in satellite and video
tution of trauma registries to track and target significant causes teleconferencing (VTC) enable polar physicians to access advice,
of morbidity and mortality. Recent research emphasizes that counsel, and guidance. For a significant proportion of the Ant-
injury prevention is not solely a function of safer design of equip- arctic population, it is still extremely difficult and costly to evacu-
ment but also a complex interplay of environment, activity, and ate patients.36
people, notably including personal risk-taking behavior. If current The following is a description of the personnel and facilities
trends continue toward greater economic independence and in the U.S. Antarctic Program; other nations maintain similar
education of Arctic peoples, such potentially modifiable adverse facilities. McMurdo Station (MCM) (Figures 11-4 to 11-8) has the
health behaviors may recede in importance in coming years.61,62 largest population: about 200 in the winter and 1200 in the
238
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.)
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
240
Pregnancy
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%
Cardiovascular
8% Altitude related
possible. A historic medical evacuation from the South Pole was Gastrointestinal
undertaken in winter 2001 with the first successful landing of a 5%
10%
twin Otter aircraft in full darkness at a temperature of −68.9° C
(−92° F) (Figure 11-10). This event, while fraught with danger, FIGURE 11-11 Evacuations for medical reasons, with percentages of
5-year totals (1998-2003). (From Mahar H [Safety and Health Officer,
has opened new possibilities and has been repeated.18,21
OPP/NSF]: Medical clearance criteria: Revalidation study. Personal
To increase further the ability to provide medical assistance, communication, 2003.)
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 completely clothed, from a 93.3° C (200° F) sauna to the Pole
through careful screening of candidates and increased use of outside at an ambient temperature of −73.3° C (−100° F) or lower.
telemedicine as a way to avoid medevacs still remains the ulti- Similarly, the quintessential polar first-aid story involves creative
mate goal. solutions to the problem of finding warm fluids,3 but it would
To reduce the number of medical crises and need for urgent be reckless to forget the ever-present danger of such a hostile
medical evacuations, all participants must pass a “physical quali- environment. Windchill typically drops the effective temperature
fication test.” Medical clearance criteria are used as a screening on exposed skin far below −73° C. It has been estimated that
tool. To establish appropriate guidelines, evidence-based criteria under the most severe winter conditions, an inactive person in
from the medical literature, historical data of the U.S. Antarctic full polar clothing could undergo a life-threatening drop in core
Program, and guidelines from other programs, such as the temperature in only 20 minutes. Airplane refueling crews and
National Aeronautics and Space Administration (NASA), the others working with liquids at polar ambient temperatures are
Peace Corps, and the U.S. Navy, that have activities in remote constantly reminded that even a small splash can mean instant
areas were used. What appears to be lacking is screening for frostbite.34
body mass index and alcoholism. However, up to 30% of all Rescue and treatment are complicated by the additional
medical evacuations (both emergent and urgent) have been for need for both victim and rescuer to avoid hypothermia and
trauma; that is, they were not related to the evaluation criteria. frostbite.55,57 Disorientation and confusion from hypothermia,
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 MEDEVACS BY LOCATION
a chart showing the number of medevacs from MCM and the
South Pole station. 100%
241
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
FIGURE 11-13 Clothing is an important topic in polar medicine. expeditions. Early expeditions in both polar regions provided
A researcher prepares to leave the station for an extended time at several examples of nutritional illnesses, including scurvy and
−56.7° C (−70° F). The total weight of his clothes is 11.5 kg (25.4 lb). possible hypervitaminosis A and lead poisoning. More sophisti-
COLD AND HEAT
Notice the multiple layers for each area of the body. (Courtesy Stephen
cated nutritional analyses have been possible during recent expe-
Warren.)
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
clumsiness from bulky clothing, and degraded performance char- without loss of lean body mass.73 Although many prolonged,
acteristics of equipment and intravenous (IV) fluids can compli- unsupported expeditions include an element of malnutrition or
cate otherwise straightforward procedures. A recent case report even starvation, protein synthesis is still active.121,122
describes almost immediate freezing of fluid in IV lines and shat- During a Canadian-Soviet transpolar ski trek, participants
tering of the plastic IV tubing despite vigorous attempts to warm skiing approximately 20 km/day (12.4 miles/day) at a speed of
PART 2
them.57 Simple devices commonly used in warmer settings, such about 3.5 km/hr (2.2 miles/hr) while carrying 37- to 45-kg (81.6-
as air splints and pneumatic antishock garments, would be simi- to 99.2-lb) packs showed increased strength, decreased body fat,
larly unusable. In more sophisticated equipment, batteries rapidly and increased high-density lipoprotein cholesterol. A paradoxical
fail, unwinterized mechanical moving parts seize up, and metal drop in aerobic power was noticed, perhaps because of intensive
objects become dangerous sources of frostbite. pretraining and conditioning, as well as increased efficiency of
Clothing, not normally considered a medical topic, assumes skiing as the trip progressed. More recently, in a nonsupported,
special importance in the polar environment76,104 (Figure 11-13). two-man, 86-day trans-Greenland trip, well-trained and experi-
Although the clothing used for many polar research programs in enced skiers eating an adequate caloric diet had little if any
the summer seems adequate, a strong argument can be made for significant impairment. Their average energy intake in rugged
specialized winter gear, possibly adapted from the space program, terrain was 28 to 34 kilojoules (kJ) per day (6688 to 8121 calories/
that would allow relatively delicate manipulation of scientific day) and in level terrain 14 to 16 kJ/day (3344 to 3822 cal/day).34
equipment while offering protection from the cold. In fact, at Although applicability of these figures to more sedentary polar
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. FIGURE 11-14 Frostbite on thigh with eschar. Newer phase-change
materials would have prevented this injury. This skier across Antarctica
Altitude Illnesses suffered frostbite when he removed one layer of insulating clothing to
Altitude illness can be a major issue at many Antarctic stations, avoid sweating on a calm sunny day. When a wind came up, it caused
camps, and research locations, including the South Pole, Vostok, frostbite through the wind pants and light insulation. (Courtesy Borge
and Mt Erebus. A literature-based approach to preventing altitude Ousland.)
242
sojourners is probably limited, work is being done to alter the chronobiotic and is used as a supplement to treat circadian
243
personnel (2000 person-years), there were four medical deaths, National Programs’ Responsibilities for Tourist Safety
two myocardial infarctions, one case of appendicitis, one perfo- As transportation increasingly opens up previously inaccessible
rated gastric ulcer, and one cerebral hemorrhage. The remainder areas, this image attracts growing tourist traffic and, with it,
of the events were accidents involving falls, head injuries, hypo- heated debate from both legal and environmental viewpoints.116
thermia, drowning, crush injury, and burns.68,70 The essential medicolegal issue is the extent of governmental
There have been 60 deaths in the U.S. Antarctic Program since organizations’ responsibility for medical care of participants in
1946.2 These can be ranked by cause: aviation, 61%; vehicles, nongovernmental activities, whether scientific, political, or com-
11%; ships, 7%; recreational, 7%; station/industrial, 5%; field mercial. Although this discussion started much earlier, it is
activities, 5%; and other, 4%.72 Although it is difficult to adhere ongoing.81 When a tourist group requires aid beyond its own
to standard occupational safety practices when in a remote loca- capabilities, whose responsibility is it? To what extent should a
tion, new guidelines and serious efforts in some of the programs research station with limited medical supplies be required to
have led to improved worker and participant safety. divert some of those supplies to an individual who presumably
A review of data for the Australian National Antarctic Research bears responsibility for planning his or her own medical cover-
Expedition (ANARE) 2002-2003 season listed the following age? By default, stations provide what assistance they can,
reasons for medical consultation: medical (e.g., upper respiratory, although they often try to bill tourist companies and their insur-
GI), 39%; injuries (sprains, strains, dermatologic, lacerations, frac- ance agencies for costs involved in patient treatment or transport.
tures), 27%; follow-up visits, 24%; and preventive (immuniza- The Antarctic Treaty Consultative Meeting XXXI provided attend-
tions, midyear examinations, wellness programs), 10%.19 For the ees with a list of guidelines recommended before trips to Ant-
2004-2005 season, Antarctica New Zealand (ANZ) reported mus- arctica, including travel insurance, contingency plans, and other
culoskeletal, 42%; medical (e.g., upper respiratory infections, GI), necessary equipment.4
22%; other injuries, 20%; dermatologic, 15%; and preventive,
dental, and other, 8%.103 Usually, most visits are related to injuries, Air Safety
and the next most frequent medical clinic visits are attributable As in the Arctic, reliance on aircraft for transportation has high-
to upper respiratory infections. Environmental problems include lighted the critical importance of air safety. The worst Antarctic
dry skin and fissures, particularly on fingertips as a result of cold air accident was the crash of an Air New Zealand tourist “flight-
and very dry conditions. Cyanoacrylate glue hastens healing of seeing” DC-10 on Mt Erebus in November 1979.87 This accident
disabling fingertip and heel fissures.8 Cold-induced urticaria, killed all 257 people aboard and temporarily ended such flights,
frostnip, and frostbite are frequently underreported, except for although IAATO records indicate that overflights are now hap-
moderate to severe cases. Small nasal bleeds occur frequently, pening with new guidelines in place. There have been 35 air-
COLD AND HEAT
but they rarely require treatment beyond instruction to use pet- related fatalities in the U.S. Antarctic Program since 1946 from
rolatum or antibiotic/antiseptic ointment once or twice daily to crashes related to either fixed-wing or rotor aircraft.72,116 A ski-
protect the delicate nasal epithelium, which easily becomes dehy- equipped LC-130 Hercules crashed at the remote D-59 camp in
drated or can sustain frostnip. Although the bulk of care is limited 1971 (Figure 11-15). Fortunately, none of the 10 crew members
to routine visits, the pathologic conditions encountered even aboard was injured. During a salvage operation in 1987, however,
among this carefully screened population have included myocar- another LC-130 bringing supplies to D-59 crashed nearby, killing
dial infarctions, massive GI bleeds, unreported Crohn’s disease, two and injuring nine. More recently, a helicopter crash occurred
bowel obstructions, acute cholelithiasis with pancreatitis, pulmo- in the dry valleys; both the pilot and passenger were seriously
nary emboli, massive head injuries, fractures, crush injuries, injured. After a weather delay, they were extricated and evacu-
PART 2
newly diagnosed schizophrenia, and cancer. ated to New Zealand for definitive care.19,85 With better weather
prediction and increased safety standards, the accident profile is
Fire Safety improving. However, in 2010, there was a fatal helicopter crash
In light of the extreme cold, it is somewhat counterintuitive that near the Dumont d’Urville station that killed four persons. In
fire is a major concern and significant danger at all Antarctic January 2013, a Kenn Borek Air DHC-6 Twin Otter crashed near
stations. This surprising assessment rests on a number of factors. the summit of Mt Elizabeth in the Queen Alexandra range on a
Cold temperatures severely limit the utility of water for fire flight from the South Pole to the Italian base at Terra Nova Bay.
suppression. Firefighting equipment may become inoperative All three crew members perished.
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 FIGURE 11-15 LC-130 Hercules partially stuck in a hidden crevasse,
Comandante Ferraz base on King George Island. In Antarctica, demonstrating the inherent hazards of working in Antarctica. (Courtesy
fire is an ever-present threat. National Science Foundation photo archive.)
244
PSYCHOSOCIAL HEALTH PROBLEMS mission or even those primarily motivated to earn money. In
245
winter-over in the dark latitudes.96 Further studies indicate that Tourist visitors can be broadly divided into two groups, “sight-
S-SAD may be part of the T3 syndrome.99 Correlations with mela- seeing” and “expedition/adventure sport.” Ship-based sightseers
tonin levels have been shown to be associated with the frequent make up approximately 98% of the visitor total. A very small
sleep disturbances at higher latitudes, both with advanced or number travel to the continent itself, to visit, for example, the
delayed phases and with increased latency.6,133 In some studies, South Pole or emperor penguin colonies. There is little if any
melatonin’s chronobiotic properties are used to resynchronize medical screening of ship-based tourists, and persons of all ages
the individual’s sleep.6 Other studies have demonstrated the may travel. The financial expense of these cruises means that
effectiveness of light therapy in helping resynchronize the there is bias toward the older traveler who has accumulated
body.133 SAD may be no more prevalent in Antarctica than at wealth and has the time to spend it. A recent paper showed that
lower latitudes; some of the depressive symptoms may well be more than half the respondents on an Antarctic cruise ship were
the result of social isolation or related to seasonal changes.100 older than 50, and 25% were over 60.136
Medical facilities on board ship vary widely, as do the experi-
Beneficial Effects of Isolation ence and competence of accompanying medical professionals.
An interesting point is that isolation may have positive as well The American College of Emergency Physicians published com-
as negative effects.100 Isolation is not synonymous with loneliness prehensive guidelines to enhance medical care on board cruise
and depression, as Amundsen reported from his sojourn at Fram- ships, including specific requirements for physicians, such as
heim. In fact, a subset of “professional isolates” may actually 3 years of postgraduate/postregistration experience in general
prefer polar stations to “normal” society.125 In some cases, reentry and emergency medicine. These are only guidelines and not
and adaptation to the rest of the world can take up to 6 months. requirements.3a
The positive effect of isolation may be reflected in a 1992 study The medical problems encountered mirror those found in an
of somatic complaints that compared U.S. Navy volunteers who urban setting, with additional risks of trauma (usually minor)
qualified for winter duty in Antarctica and wintered-over, with from, for example, falls in the unfamiliar environment.
those who were physically qualified but were assigned elsewhere The expedition/adventure sport group is primarily involved
because of the limited number of winter assignments. Those who in ski or mountaineering expeditions, with most professionally
spent the winter in Antarctica had fewer illnesses and hospitaliza- guided. These visitors are generally a fitter and younger popula-
tions after the winter-over period. These volunteers were fol- tion. In line with adventure sports worldwide, age and (lack of)
lowed an average of 5.4 years after the winter period. It was also experience are bars to participation. Other visitors are involved
noted that the complex psychophysiologic symptoms experi- in sailing, kayaking, and scuba-diving trips. Some expeditions
enced during the winter-over period were probably adaptive deploy motorized vehicles. At Union Glacier in 2014, there were
COLD AND HEAT
coping mechanisms. Coping led to a process of negotiation two marathon and two ultramarathon running events.
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
MEDICAL PROBLEMS
completing a long-term contract in an isolated environment.92,100 Many medical problems of activity in the extreme cold, including
frostbite and hypothermia, are discussed elsewhere (see Chapters
Screening and Selection 6 through 10). Clinical entities particularly associated with polar
Based on the preceding findings, several attempts have been ski expeditions include polar thigh, skier’s thumb, and kite
made to refine the selection and screening processes for success- skier’s toe.
PART 2
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. FIGURE 11-16 Polar thigh. (Courtesy Ian Davis.)
246
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
247
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
FIGURE 11-21 Kite skier’s toe. A recurrent medical issue in polar stations involves con
tingency planning and the optimal level of inventory. This ques-
Reflection on some of the issues raised previously suggests tion applies equally to drugs, equipment, training, and personnel
several common areas of linkage and directions for future work. and is faced immediately by any incoming physician. “Just
in time” principles of inventory management are unlikely to be
ISSUES OF METHODOLOGY AND appropriate.9,116
Combined improvements in communications systems, the
MEDICAL EPISTEMOLOGY Internet, and the powerful tool of telemedicine with its many
The state of knowledge about the human factors involved in modalities have transformed what was once an extremely iso-
living in the Antarctic is still rudimentary, although renewed lated practice of medicine. The advantages of rapid access to
interest by NASA and ESA in Antarctica as a space analog has organized databases and remote consultations for radiology and
COLD AND HEAT
led to increased research funding and should lead to better other specialties via video are realities. Telemedicine is in place
information. Studies in polar settings are often handicapped by and functioning in many northern Arctic regions. The Australian,
extremely difficult research conditions and may never achieve British, Italian, and U.S. Antarctic Programs and many others have
the statistical power and validity expected of counterparts in been using it successfully for a number of years.36,59,67,108 Physi-
more forgiving climes. Common methodologic problems most ologic, psychological, and occupational health data can be moni-
notably include small sample sizes, unknown effect sizes, mea- tored or retrieved, ultimately linking geography and information
surement of proxy variables, and multiple confounders. 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.
FOURTH WORLD MEDICAL DECISION MAKING
PART 2
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, [email protected].
REFERENCES
Complete references used in this text are available
online at expertconsult.inkling.com.
FIGURE 11-22 Leonid Rogozov.
248
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248.e3
CHAPTER 12
Pathophysiology of
Heat-Related Illnesses
LISA R. LEON AND ROBERT W. KENEFICK*
Heat illnesses exist along a continuum, transitioning from heat occurs between tissues in direct contact with one another but is
exhaustion to heat injury and the life-threatening condition of limited by poor conductivity of the tissues. For example, subcu-
heatstroke. Environmental heat exposure is one of the most taneous fat has approximately 60% lower conductivity than the
deadly natural hazards in the United States, with about 200 heat- dermis and impedes conductive heat loss.329 Convection is a
stroke deaths per year. The majority of heatstroke deaths are mechanism of dry heat transfer that occurs as air or water moves
observed in the very young and elderly populations during over the skin surface. The windchill index is an example of the
annual heat waves, whereas fit, young athletes typically succumb convective cooling effect of wind velocity. The rate of convective
to heatstroke during strenuous exertion in hot or temperate heat transfer depends on the temperature gradient between the
environments. Multiorgan system failure is the ultimate cause of body and environment, thermal currents, bodily movements, and
heatstroke death as a result of complex interplay among the body surface area exposed to the environment, which can vary
physiologic and environmental factors that compromise an indi- dramatically with different clothing ensembles. Within the body,
vidual’s ability to respond adequately to heat stress. The patho- convective heat transfer occurs between blood vessels and tissues
physiology of heatstroke is thought to be caused by a systemic and is most efficient at the capillary beds, which are thin-walled
inflammatory response to endotoxin leakage across ischemic, and provide a large surface area for heat exchange. Radiative
damaged gut membranes, although our understanding of the heat transfer is electromagnetic energy exchanged between the
mechanisms causing morbidity and mortality remains limited. body and surrounding objects and occurs independently of air
This chapter provides an overview of the pathophysiologic velocity or temperature. Radiation is effective even when air
responses observed in patients and experimental animal models temperature is below that of the body. All objects within our
at the time of heatstroke collapse and during long-term recovery. environment absorb and emit thermal radiation, but clothing can
A brief discussion is provided on current clinical heatstroke treat- reduce radiant heat impinging on the skin from various environ-
ments as well as promising avenues of research that may aid in mental sources.
the development of more effective interventions and treatments Evaporation represents a major avenue of heat loss when
to prevent this debilitating illness. 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
HEAT STRESS AND vaporized and removes heat from the skin surface, with approxi-
mately 580 kilocalories (kcal) of heat lost for each liter (L) of
THERMOREGULATION evaporated sweat.104 The most important environmental variables
affecting evaporative cooling are ambient humidity and wind
FOUR AVENUES OF HEAT EXCHANGE velocity. Sweat is converted to water vapor and readily evapo-
Mammals and other homeotherms are capable of maintaining rates from the skin in dry air with wind, whereas the conversion
body temperature within a fairly narrow range, approximately of sweat to water vapor is limited in still or moist air. If sweat
35° to 41° C (95° to 105.8° F), despite large fluctuations in envi- accumulates and fails to evaporate, sweat secretion is inhibited
ronmental temperature. Environmental variables that have the and the cooling benefit is negated. Small mammals, such as
largest impact on heat exchange are temperature; humidity; rodents, do not possess sweat glands but achieve evaporative
radiation from the air, water, or land; and air or water motion.98 cooling by grooming nonfurred and highly vascularized skin
To maintain stable body temperature, organisms rely on four surfaces, such as the ears, paw pads, and tail, with saliva that
avenues of heat exchange: conduction, convection, radiation, evaporates in a manner similar to that of sweat in humans.114,295
and evaporation.
Dry heat exchange is achieved by conduction, convection,
and radiation. Effectiveness of these mechanisms depends on
BODY TEMPERATURE CONTROL
differences between the skin and environmental temperature. Regulation of a relatively constant internal temperature is critical
Dry heat loss occurs when skin temperature exceeds that of the for normal physiologic functioning of tissues and cells. For
environment, and dry heat gain occurs when environmental example, membrane fluidity, electrical conductance, and enzyme
temperature exceeds that of the body. Conduction occurs when functions are most efficient within a narrow temperature range.
the body surface is in direct contact with a solid object and By convention, thermal physiologists describe body temperature
depends on thermal conductivity of the object and the amount control with a two-compartment model that consists of an inter-
of surface area in contact with the object. Conduction is typically nal core (viscera and brain) and an outer shell (subcutaneous fat
an ineffective mechanism of heat exchange because of behavioral and skin) (Figure 12-1).81
adjustments that minimize contact with an object. For example, The skin is the final barrier between the body and the envi-
wearing shoes is an effective behavioral adjustment that mini- ronment and functions as a conductive pathway for heat transfer,
mizes conduction of heat from a hot or cold surface (e.g., desert while also serving as the primary site to sense changes in envi-
sand to the foot). Within the body, conductive heat transfer ronmental temperature. Skin temperature may fluctuate because
of changes in environmental temperature, relative humidity, wind
velocity, and radiation. Heat transfer mechanisms are evoked in
*The opinions or assertions in this chapter are the primary views of the response to changes in body heat storage (S), which depends
authors and are not to be construed as official or reflecting the views of on metabolic rate, work, and the four avenues of heat exchange,
the U.S. Army or Department of Defense. Any citations or trade names as follows:
do not constitute an official endorsement of approval of the products or
services or these organizations. S = M − ( W ) − ( E) − (C) − ( K ) − ( R )
249
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
37° C 36° C 37° C 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
Core 32° C Core 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
Shell for thermoregulatory control because it receives and integrates
synaptic afferent inputs and evokes corrective autonomic and
28° C 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
34° C 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
31° C 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).
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 Heat stress Exercise
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.)
↑ Temperature
PART 2
250
Many species exploit regulated hypothermia as a means of
251
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
A 12-1). Heat cramps are often mistaken as a form of heat illness
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
COLD AND HEAT
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
PART 2
252
CHAPTER 12 Pathophysiology of Heat-Related Illnesses
100 100
r = 0.53 r = −0.76
−100 −100
−200 −200
−300 −300
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 increased surface area–to–body mass ratio (accelerates heat
of heatstroke severity; injury to the gut, kidney, lung, spleen, gain), limited effective mechanisms of thermoregulation (e.g.,
liver, and skeletal muscle (specific to exertion) often occurs suppressed behavioral adjustments), increased risk for dehydra-
within days or weeks of clinical presentation. tion (e.g., lack of water availability), and preexisting respiratory
Heatstroke may be classified as “classic” or “exertional” infections. On the other hand, older individuals have preexisting
depending on the etiology of the condition. Classic heatstroke is conditions, such as mental illness, prescription drug use (e.g.,
observed in very young or elderly persons who are often immu- diuretics, anticholinergics), or infections, that predispose to
nocompromised before heat exposure and experience high mor- passive heatstroke10,69,315 (Box 12-1).
tality during annual summer heat waves. Classic heatstroke Exertional heatstroke (EHS) occurs primarily in young, physi-
occurs at rest during exposure to high environmental tempera- cally fit individuals who collapse during exercise from heat
ture, with patients often presenting with hot, dry skin caused by stress.333 Physical effort unmatched to physical fitness is a signifi-
failure of the normal sweating response (e.g., anhydrosis). Up to cant risk factor for EHS.256 Anhydrosis is an uncommon finding
60% of patients with classic heatstroke are hospitalized or found in these patients; rather, continuation of sweating after cessation
dead within 1 day of the reported onset of illness, underlying of exercise facilitates spontaneously cooling of EHS patients after
the life-threatening nature of this condition.145 Several intrinsic collapse. Behavioral influences may increase the risk for EHS;
factors may predispose infants to heatstroke death, including highly motivated individuals may ignore the physiologic signs of
Heat cramps Brief, painful skeletal muscle spasms Rest; replacement of electrolytes; avoid salt tablets.
Heat rash (miliaria rubra) Blocked eccrine sweat glands Cool, dry affected skin area; topical corticosteroids, aspirin
Heat exhaustion Mild to moderate illness with inability to sustain Move supine individual to cool, shaded environment, and
cardiac output; moderate (>38.5° C [101.3° F]) elevate legs; loosen or remove clothing, and actively
to high (>40° C [104° F]) body temperature; cool skin; administer oral fluids.
often accompanied by dehydration
Heatstroke Profound CNS abnormalities (agitation, delirium, Ensure an open airway, and move to a cool environment.
stupor, coma) with severe hyperthermia (>40° C Immediately cool to <39° C (102.2° F) using ice packs,
[104° F]) 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 HEATSTROKE EPIDEMIOLOGY AND
Heat Illness RISK FACTORS
The ability to perform strenuous work in a hot environment is
Environmental Factors
inversely related to the heat stress level, which can be assessed
High ambient temperature
using the wet bulb globe temperature (WBGT) index. The WBGT
High humidity
Lack of air movement
for indoor or outdoor environments is determined as follows:
Trees and shrubbery Indoor WBGT = 0.7 Tw + 0.3 Tamb
Access to air-conditioning
Lack of shelter Outdoor WBGT = 0.7 Tw + 0.2Tbg + 0.1Tamb
Heat wave (≥3 days of temperatures >32.2° C [90° F])
where Tw is the natural wet bulb temperature, Tbg is the black
Individual Factors
globe temperature, and Tamb is the dry bulb temperature. Tbg
Age (small children, older adults)
determines the radiant heat load with a specialized thermometer
Obesity
Poor physical fitness level
that is surrounded by a 15-cm (6-inch)–diameter blackened
Lack of acclimatization sphere. The WBGT is the most widely used index to determine
Dehydration safe limits of physical activity and establish strategies that will
minimize the incidence of heat illness during military, athletic,
Drug Use or occupational tasks. The WBGT index does not take into con-
Diuretics sideration different clothing ensembles or exercise intensities, so
Anticholinergics (e.g., atropine) the most practical and safe application of this measurement
β-Adrenergic blockers (e.g., propranolol)
requires adjustment for these factors.
Antihistamines
Amphetamines (e.g., Ecstasy)
Heat waves are defined as three or more consecutive days
Ergogenic aids (e.g., ephedra) during which the environmental temperature exceeds 32.2° C
Antidepressants (90° F).50 In summer 2003, Europe experienced 22,000 to 45,000
Alcohol consumption 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
Compromised Health Status
continent has experienced an increase in minimum daily tem-
Viral infection (e.g., pneumonia, mononucleosis) peratures over the last 30 years, and this trend will likely increase
COLD AND HEAT
may occur in temperate conditions because of high physical 253% increase in annual heatstroke deaths in the United Kingdom
demand or clothing that inhibits cooling (e.g., firefighter uni- by 2050.74
forms). Mortality from EHS is relatively low (~3% to 5%) com- The impact of climate change is not equally distributed across
pared with classic heatstroke (~10% to 65%), which is likely a the globe because of regional variability in thermal tolerance that
consequence of preexisting medical conditions and chronic use influences the incidence of heatstroke mortality. A study of
of medications in the classic form that increase thermoregulatory 11 U.S. cities showed that threshold temperatures for heatstroke
and cardiovascular strain.49,281,284,286 mortality are higher in warmer southern cities than in cooler
northern cities.63 A comparison of temperature-mortality relation-
COMPENSABLE VERSUS UNCOMPENSABLE ships in southern Finland, southeastern New England, and North
Carolina indicated that lower temperature thresholds in cooler
HEAT STRESS climates are coupled with steeper temperature-mortality relation-
Heat stress refers to conditions that increase body temperature, ships.73 Similarly, the upper safety limit of environmental tem-
whereas heat strain refers to the physiologic consequences of peratures in The Netherlands, London, and Taiwan are 16.5°, 19°,
heat exposure. Heat stress is typically described as compensable and 29° C (61.7°, 66.2°, 84.2° F), respectively.193 A case study of
heat stress (CHS) or uncompensable heat stress (UCHS), with 15 Marine Corps recruits who collapsed from heatstroke during
both these conditions affected by biophysical (environment, training exercises in South Carolina showed that 73% previously
clothing) as well as biologic (hydration status, acclimatization) resided in northern states and that 60% of cases occurred during
factors. CHS occurs when the rate of heat loss maintains balance the second week of training during the hottest summer months.229
with heat production, and steady-state body temperature can be From 1980 to 2002, the highest EHS incidence in military recruits
sustained during physical activity or heat exposure. A physically was in unacclimatized individuals from northern, cold-climate
fit individual wearing light clothing while exercising in moderate states who were enlisted for less than 12 months.49 During July,
heat and low humidity would typically experience CHS. Under many regions of the world have a WBGT index that is greater
these conditions, elevated body temperature (<40° C [104° F]) can than 29° C (84.2° F), and military training often occurs in environ-
be sustained for a relatively long period until dehydration or ments with a WBGT index that is greater than 35° C (95° F).
energy depletion occurs. During peacetime exercises, approximately 25% of fatal military
Uncompensable heat stress is a consequence of an individu- EHS cases occur during the hottest summer months in recruits
al’s evaporative cooling requirements being ineffective because who have been in training camp less than 2 weeks.197 Individuals
of environmental or other conditions that impede cooling. For from northern states are expected to be less acclimatized to hot,
example, an individual wearing heavy protective clothing while humid summer conditions than those from southern states. Heat
exercising in a hot, humid environment would be expected to acclimatization improves thermotolerance but requires several
experience UCHS. Under UCHS conditions, body temperature days to weeks of exposure to similar heat stress and exercise
will increase to the point of exhaustion. Even for individuals at conditions to be fully effective. This likely accounts for hot days
low risk for UCHS, the physiologic demands for increased heat early in the summer showing a greater impact on heatstroke
dissipation during prolonged exercise and heat stress cannot be morbidity and mortality than those cases occurring later in the
endured indefinitely and often lead to circulatory insufficiency training process, after the protective effects of heat acclimatiza-
and collapse at relatively mild temperatures. tion have been realized.115
254
Humanity’s impact on the landscape in conjunction with blood mononuclear cells (PBMCs) from these recruits expressed
255
individuals are acclimatized to uniforms and environmental Climatic heat stress and exercise
temperatures.108,263
SKIN DISORDERS
Heat strain
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 Cardiovascular Heat cytotoxicity
reaction consisting of redness and blister-like lesions. Miliaria responses
rubra can increase body heat storage, reduce exercise perfor- (Intestine, kidney,
mance in the heat (with as little as 20% of the body surface Gut Skin spleen, endothelium)
affected), and persist for up to 3 weeks after the rash appears to constricts dilates
have resolved.241,242 If heat illness is expected, the affected area Ischemia HSPs
of the skin should be cooled and dried to control infection.
Topical corticosteroids or aspirin may be effective in reducing
swelling and irritation. ↑ Gut epithelial Systemic inflammatory
Sunburn is a common reaction to ultraviolet (UV) radiation membrane permeability response syndrome
that causes epidermal and dermal injury and limits efficiency of Increased tight (fever, DIC, rhabdomyolysis,
the sweating response.105 Sweating sensitivity as well as sweat junction permeability tissue injury)
rates on the forearm and back were significantly reduced 24
hours after artificial sunburn compared to responses observed in Endotoxin Anergy
body regions that were protected from UV exposure.240 Severe (Th1 > Th2
sunburn to major portions of the body can cause systemic toxicity response)
that manifests as chills, fever, nausea, and delirium.132 Sunburn
effects on sweating are locally mediated at the sweat glands and Innate immune system
dermal vasculature and can persist after the skin appears to be Multiorgan
completely healed.240 If the sunburn covers more than 5% of the
COLD AND HEAT
256
CHAPTER 12 Pathophysiology of Heat-Related Illnesses
TABLE 12-2 Clinical Characteristics of Exertional Heat Illness Cases
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 reminiscent of Liebermeister’s experimental observations of the
thought to represent a loss of thermoregulatory control after recurrence of fever after experimental cooling of the POAH of
heat-induced damage to the POAH. However, evidence in rats.185 This suggests that fever may provide protection against
support of this hypothesis is lacking. That is, histology and some aspect of the SIRS and development of multiorgan dys-
magnetic resonance imaging (MRI) studies have failed to detect function. The argument against this hypothesis is that recurrent
damage to the POAH despite extensive damage in other hyperthermia in heatstroke patients has been anecdotally associ-
organs.5,180,197,235,298,340 In experimental animals, hypothermia is a ated with poor outcome.197,210,285 For example, an amateur long-
natural heatstroke recovery response associated with behavioral distance runner was hospitalized for 10 days after collapsing
and autonomic thermoeffector responses that support a decrease from EHS during a 9.6-km (6-mile) foot race. This patient dis-
in core temperature. Mud puppies are ectothermic species that played moderate fever (>38° C [100.4° F]) during the first 4 days
rely on behavioral adjustments, such as the selection of differ- of hospitalization, but on the 10th day, convulsions induced a
ent microclimates, to control body temperature. Mud puppies rapid increase of body temperature to 41° C (105.8° F). Rapid
heat-shocked to about 34° C (93.2° F) behaviorally selected a cooling and aspirin therapy were ineffective in reducing body
cooler microclimate and maintained a significantly lower body temperature, and the patient died.210 NSAIDs are potent inhibi-
temperature than did nonheated controls during 3 days of tors of prostaglandin production within the POAH, which is the
recovery.137 This study did not determine the impact of hypo- mechanism by which these drugs normally inhibit fever during
thermia on survival, but the association of decreased body tem- infection. Lack of an effect of aspirin on recurrent hyperthermia
perature with the selection of cool microclimates indicated this suggests this was not a true fever response, but rather a patho-
was a regulated response to a decrease in the temperature set logic response to increased metabolic heat production induced
point. Small rodents, such as mice, rats, and guinea pigs, by convulsions. Indomethacin is an NSAID with potent anti-
showed reductions greater than 1.0° C (1.8° F) in body tempera- pyretic actions in mice, but it failed to reduce fever during
ture that were associated with improved survival after passive heatstroke recovery.24 Unfortunately, prostaglandin production
heatstroke. In mice, hypothermia was associated with a 35% within the POAH has never been examined in animal heatstroke
decrease in metabolic heat production and with the behavioral models, so it remains unknown if activation of these signaling
selection of microclimates that precisely regulated the depth pathways is associated with development of recurrent hyperther-
and duration of this response.180 Exposure of mice to warm mia during heatstroke recovery. Physicians may attempt to treat
ambient temperatures that prevented heat-induced hypothermia recurrent hyperthermia episodes with NSAIDs, but these drugs
caused increased intestinal damage and mortality.179,331 Hypo- are toxic to the liver and have been associated with the need
thermia likely provides protection against heat-induced tissue for liver transplantation.102,123,124,271,318
injury in a manner similar to that shown for protection against
other extreme environmental insults based on the temperature
coefficient (Q10) effect.
IMMUNE RESPONSES
A common heatstroke recovery response observed in patients During heat stress, blood flow to the skin is increased to facilitate
and animal models is recurrent fever during the days and weeks heat loss to the environment and reduce the rate of total body
of recovery.14,179,197,210 In mice, fever was observed within a day heat storage. Increased skin blood flow is accompanied by a fall
after passive heatstroke collapse and was associated with a 20% in splanchnic (i.e., visceral organ) blood flow as a compensatory
increase in metabolic heat production and increased plasma mechanism to sustain blood pressure. Endotoxin is normally
levels of the proinflammatory cytokine interleukin-6.177,179,180 IL-6 confined to the gut lumen by tight junctions of the epithelial
is an important regulator of fever during infection and inflam- membrane, but these junctions can become “leaky” following
mation and may regulate fever during heatstroke recovery, prolonged reductions in blood flow that cause ischemic stress.117,170
although this hypothesis remains to be experimentally tested.175 Several lines of evidence support the hypothesis that endotoxin
In patients, fever is reestablished after clinical cooling.197 This is 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
trophils that use pattern recognition receptors (PRRs) on their marrow, PBLs
cell surfaces to recognize pattern-associated molecular patterns TLR9 CpG DNA B cells, DCs
(PAMPs) on the cell surface of endotoxin and other invading Spleen, lymph node, bone
pathogens.144,310 Toll-like receptors (TLRs) are a class of PRRs that marrow, PBLs
have been widely studied in the immune response to infec- TLR10 Unknown B cells
tion.209,310 Ten mammalian TLRs have been identified, and the Spleen, lymph node,
specific pathogenic ligands that activate these PRRs are known thymus, tonsil
(Table 12-3).
Toll-like receptor 4 (TLR4) is the principal receptor for LPS Data from Medvedev AE, Sabroe I, Hasday JD, et al: Tolerance to microbial TLR
that stimulates gene transcription factors, such as nuclear factor ligands: Molecular mechanisms and relevance to disease, J Endotoxin Res
(NF)–κB, to increase the synthesis of a variety of immune modu- 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.
lators in response to endotoxin. Endotoxin infection (i.e., sepsis) CpG, Deoxycytidylate-phosphate-deoxyguanylate; DC, dendritic cell; DNA,
is associated with increased expression of TLR4 on circulating deoxyribonucleic acid; NK, natural killer; PBL, peripheral blood leukocyte; RNA,
human PBMCs, as well as on mouse liver and spleen macro- ribonucleic acid.
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 the SIRS. The actions of cytokines depend on the nature of the
mortality during the SIRS to bacterial infection, which was caused danger signal, the target cells with which they interact, and the
by inability to induce the full complement of immune responses.113 cytokine “milieu” in which they function. Th1 and Th2 cytokines
These mice also experienced more severe classic heatstroke function in a negative feedback pathway to regulate each other’s
responses than did wild-type mice. These included profound and production and maintain a delicate balance of inflammatory reac-
sustained hypothermia, rapid induction of circulating IL-1β, IL-6, tions. Anergy is thought to be a consequence of inadequate Th2
tumor necrosis factor (TNF)–α, high-mobility group box 1 cytokine production late in the SIRS. For example, increased
(HMGB1), more severe liver damage, and increased mortality patient mortality from peritonitis is associated with the inability
through 3 days of recovery.67 HMGB1 is a classic alarmin that to mount a Th2 cytokine response127 (see Figure 12-6).
binds a wide range of molecules to dictate the resulting immune Alarmins are endogenous PAMPs released from stressed or
response. On binding LPS, HMGB1 induces a SIRS composed of injured tissues that initiate restoration of homeostasis after an
elevated IL-1β and IL-6 secretion.135 Given that TLR4 polymor- infectious or inflammatory insult.23 HMGB1 is a highly conserved
phisms exist in humans, this may be one of several genetic factors nuclear protein that functions as an alarmin after release from
that predispose to mortality during the SIRS to heatstroke.7,85 necrotic (but not apoptotic) cells.273 Necrosis is premature death
Specificity of immune responses is provided by B and T cells of cells in a tissue or organ in response to external factors, such
of the adaptive immune system. These cells respond to antigens as pathogens and toxins. Because necrosis is detrimental to the
by secreting cytokines, which are intercellular immune signals host, it is associated with an inflammatory response. Apoptosis
that elicit proinflammatory (T helper type 1 [Th1]) and antiinflam- refers to genetically programmed cell death that does not elicit
matory (T helper type 2 [Th2]) actions during the progression of 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
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 renal failure, coagulopathy, and death if not rapidly detected and
as an indication of impaired renal function, although BUN levels treated.15,96,190,244,322 Not all cases of rhabdomyolysis are associated
may be altered by conditions unrelated to heat illness, including with myoglobinuria; many patients can be asymptomatic. Clinical
malnutrition, high-protein diets, burns, fever, and pregnancy.2,270,321 markers of rhabdomyolysis include elevated myoglobin, CK,
AST is released by the liver and skeletal muscle and may be a aldolase, lactate dehydrogenase, ALT, and AST, which are influ-
clinical sign of congestive heart failure, viral hepatitis, mononu- enced by a variety of factors (type, intensity, and duration of
cleosis, or muscle injury. ALT is released by the liver, red blood exercise; gender; temperature; altitude) and released by more
cells, cardiac muscle, skeletal muscle, kidneys, and brain tissue. than one organ or tissue.58,211,270 If a clinical diagnosis of rhabdo-
AST and ALT are common clinical markers of liver function in myolysis is confirmed, immediate medical attention is imperative
PART 2
260
because 50% mortality rates from acute renal failure have been cooling correlate with heatstroke severity, tissue injury, and
261
IL-6
sIL-6R
IL-6 IL-6
IL-6R sIL-6R
gp130 gp130 gp130
Signal Signal
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 murine macrophages, HSP 70 inhibited IL-12 (Th1) and stimulated
human PBMCs, inhibition of TNF-α, IL-1β, IL-10, and IL-12 in IL-10 (Th2) production in response to LPS.324 The shift from Th1
response to LPS was specific to HSPs 70 overexpression.71 A lack to Th2 cytokine production may be a mechanism by which HSP
of effect of HSP 70 on IL-6 gene transcription may be an indirect 70 protects against bacterial infection.
mechanism of protection, because IL-6 functions in a regulatory Heat strain is a consequence of the time and intensity of heat
feedback loop to inhibit IL-1 and TNF production, which are exposure. These factors interact in vivo to influence the magni-
Th1 cytokines with potent proinflammatory activities.71,82,83,324 In 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
PART 2
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 some resistance because it is thought that cooling of the skin will
263
Cell membrane blood plasma substitute that exerts high colloidal pressure to
stimulate movement of fluid from the interstitial space into the
Phospholipids blood vessel lumen for plasma volume expansion.238,334,341 Small-
NSAIDs
PLA2 volume treatment with HES protected against heatstroke mortality
Acetaminophen Arachidonic acid (AA)
Salicylic acid
in rats, but use of HES in other heatstroke animal models and
Ibuprofen COX LOX humans has not been validated.192 Because of severe dehydration
and acute renal failure with heatstroke, fluid shifts from the
Liver toxicity interstitial fluid into the vessel lumen may mean HES will not be
Prostaglandins
Leukotrienes well tolerated in patients with severe heatstroke patients (see
Thromboxanes
Leukocyte aggregation
Chapter 13).
Fever
Vascular permeability
Platelet aggregation
Vasomotor changes
Induce IFNγ, IL-1, IL-2 ANTICOAGULANTS
Inhibit IL-1, IL-2 Anticoagulants (e.g., heparin, aspirin) have been examined for
FIGURE 12-10 Eicosanoid metabolism is initiated when cell mem- heatstroke protection, with mixed results. Heparin therapy has
brane phospholipids are converted to arachidonic acid (AA) by enzy- been associated with positive heatstroke outcome in patients,
matic actions of phospholipase A2 (PLA2). Cyclooxygenase (COX) although it is difficult to dissociate the direct effects of this
converts AA to prostaglandins and thromboxanes, whereas the lipo- therapy from other clinical treatments.247,292 The mechanisms of
oxygenase (LOX) pathway is responsible for production of leukotri- heat-induced DIC may include prostaglandin synthesis, because
enes. Nonsteroidal antiinflammatory drugs (NSAIDs) block the action aspirin has shown protection against platelet hyperaggregation
of COX enzymes with potential toxic effects on the liver. IFNγ, in vitro and in animal models. In human volunteers, ingestion of
Interferon-γ; IL-1, interleukin-1; IL-2, interleukin-2. 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,
respectively. In a mouse model of heatstroke, an acute oral dose even though complete inhibition of the arachidonic acid pathway
of indomethacin (a potent antipyretic NSAID) provided immedi- was achieved.97 The ability of aspirin to protect guinea pigs from
ately before heat exposure resulted in a 40% increase in heat- DIC induced by Staphylococcus aureus suggests that similar
stroke mortality because of extensive gut hemorrhaging.178 activities function in vivo to control platelet reactivity.225 However,
Increased mortality was also observed in heat-exposed rats there is currently insufficient evidence to support the use of
COLD AND HEAT
injected peripherally with aspirin.153 Aspirin has also been shown aspirin as a preventive measure in heatstroke patients. Given the
to attenuate protective, reflexive skin blood flow responses hormonal and metabolic alterations that accompany heatstroke,
required for adequate heat dissipation.131,206 Aspirin will therefore including dehydration, increased catecholamine levels, and
predispose to heatstroke collapse. Given that NSAIDs do not hypoxia, the mechanisms responsible for DIC extend beyond
attenuate hyperthermia and that organ (e.g., gut, liver) toxicity those mediated by prostaglandins alone. Furthermore, aspirin
of these drugs is exacerbated with heat, they are contraindicated and other antiinflammatory drugs can cause liver damage if con-
for prophylaxis or treatment of heatstroke patients. sumed in large quantities, as previously mentioned.
Alcohol sponge baths are inappropriate under any circum- Recombinant activated protein C (APC) is an effective antiin-
stances, because transcutaneous absorption of alcohol may lead flammatory drug for treatment of sepsis and may also hold
PART 2
to poisoning and coma. 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
FLUID RESUSCITATION (See Chapter 89) (benefit not apparent if failure of only one organ), and the pres-
One of the first lines of defense against permanent tissue damage ence of shock at infusion, which improves its efficacy.326 In rat
is treatment with resuscitation fluids. The objective of IV fluid heatstroke models, the efficacy of APC depends on the time of
administration is to restore intravascular volume and rehydrate treatment. A single dose of recombinant human APC provided
the interstitium to stabilize cardiovascular functioning, improve at the onset of heatstroke inhibited inflammation and coagulopa-
tissue perfusion, and maintain immune function. The resuscita- thy, prevented organ failure, and improved survival; however, if
tion fluid optimally needs to be safe, efficacious, and easy to treatment was delayed for 40 minutes after onset of heatstroke,
transport for use in military or athletic settings and have the there was no beneficial effect on survival time.54 The efficacy of
capability to restore tissue oxygen perfusion and minimize cel- APC was less obvious in a baboon heatstroke model. Infusion
lular and tissue injury. Blood provides oxygen-carrying capacity for 12 hours after heatstroke onset attenuated plasma IL-6, throm-
and volume, but supply is limited, with a risk for allergic or bomodulin, and procoagulant components but had no effect on
infectious reactions, difficulties with crossmatching, and potential mortality.35 APC is the first biologic agent approved in the United
for high hemoglobin levels to increase blood viscosity and reduce States for the treatment of severe sepsis based on two decades
nutrient flow to the tissues.259 Balanced salt solutions, such as of research,326 but there is insufficient evidence to justify use of
saline and lactated Ringer’s, have a long shelf life and are inex- this treatment in heatstroke patients.
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
ANTICYTOKINE THERAPIES
edema and makes frequent transfusions necessary to maintain As previously described, attenuations in splanchnic blood flow
adequate plasma volume.119,152,307 Tissue edema increases the during heatstroke contribute to increased gut permeability and a
distance from blood vessels to tissue mitochondria and limits rise in circulating endotoxin. This series of events is hypothesized
oxygen delivery to the tissues. There is a greater risk for edema to stimulate the increased plasma cytokine levels implicated in
in heatstroke patients because of increased capillary permeability the adverse consequences of SIRS. Based on these findings, the
and lack of muscle movement that limits lymph flow following question arises: Do anticytokine therapies represent an effica-
collapse. cious treatment strategy for heatstroke? No controlled studies
To minimize the adverse consequences of balanced salt solu- have examined the efficacy of anticytokine therapies on patient
tions, these fluids may be replaced with colloid solutions. Natural outcome with heatstroke. However, clinical sepsis trials indicate
colloids, such as albumin, possess antioxidant properties that that potential protective effects of anticytokine therapies need
reduce tissue injury during times of oxidant stress, but carry a to be viewed with cautious optimism. Sepsis patients display
risk for infection.94,341 Dextran is an artificial colloid that was used high circulating IL-1 levels that correlate with morbidity and
after World War II until adverse hemostatic effects restricted its mortality, but IL-1ra treatment has been unsuccessful in reducing
use to specific clinical conditions, such as deep vein thrombosis mortality.236,257 A comparison of 12 randomized, double-blind
and pulmonary embolism.21,66 Hydroxyethyl starch (HES) is a multicenter trials of more than 6200 sepsis patients showed
264
no significant benefit of antiendotoxin antibodies, ibuprofen,
265
That is, whereas nonacclimated individuals require de novo HSP
160 72 synthesis for cellular protection, individuals who reside in hot
climates maintain elevated HSP 72 levels.194 The cellular mecha-
circles, Values before start of the first exercise period each day; small human leukocyte antigen (HLA) haplotypes that encode cell
circles, successive values; squares, the final values each day. Controls surface antigens. Coinheritance of these genes may ultimately be
of exercise in cool environment before and after acclimation. (Modified responsible for poor sepsis outcome.146,297
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.) 20
experiencing syncope
266
MALIGNANT HYPERTHERMIA most common experimental animal is a porcine MH model that
Malignant hyperthermia (MH) is a genetic disorder that causes possesses a single mutation in the skeletal muscle RyR1 gene.
muscle rigidity, hyperthermia, tachycardia, and metabolic acido- These animals develop the MH syndrome in response to inhala-
sis during exposure to volatile anesthetics or depolarizing skeletal tional anesthetics, exercise, heat, and other stressors.313 Mild
muscle relaxants. Exercise, heat stress, and emotional stress also exercise exacerbates MH symptoms in response to anesthetics in
trigger reactions in 5% to 10% of MH patients.70,325 MH reactions MH pigs, suggesting that inflammatory mediators released by
result from massive release of calcium from the type 1 ryanodine skeletal muscle may contribute to the MH syndrome.313 MH
receptor (RyR1) of the sarcoplasmic reticulum, which overwhelms patients show an approximately fivefold higher expression of
cellular mechanisms of calcium homeostasis and activates actin- IL-1β when stimulated with caffeine and 4-chloro-m-cresol com-
myosin filaments to cause muscle rigidity and hyperthermia.230 pared with control cells.103 Recent development of a transgenic
RyR1 is the most common mutation in skeletal muscle, but addi- mouse model that overexpresses the RyR1 receptor has proved
tional isoforms have been identified in B and T cells, thalamus, useful to study the MH/EHS link and could shed light on the
hippocampus, and heart.169,208,302 Activation of RyR1 by a variety role played in this syndrome by inflammatory cytokine produc-
of pharmacologic compounds, including caffeine, halothane, and tion from skeletal muscle or other organs.79 Association of RyR1
the muscle relaxant 4-chloro-m-cresol, has led to development mutations with EHS incidence suggests that screening young,
of an in vitro contracture test of skeletal muscle biopsies to healthy individuals (e.g., athletes, military personnel) for the MH
identify MH individuals.268,342 Dantrolene is used to treat MH reac- mutation could be a powerful tool to determine heatstroke
tions by lowering intracellular calcium stores, decreasing muscle susceptibility.
metabolic activity, and preventing hyperthermia. Using dan-
trolene, in combination with improved monitoring standards and
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267.e6
CHAPTER 13 Clinical Management of Heat-Related Illnesses
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 Individuals susceptible to heat cramps are often believed to be
management from the field through hospital discharge, return- profuse sweaters who sustain large sodium losses.16,114 Heat
to-activity considerations, and prevention of heat-related ill- syncope (fainting) is characterized by dizziness and weakness
nesses. The spectrum of injuries ranges from milder conditions during or after prolonged standing or after rapidly standing up
such as heat cramps to fatal manifestations such as arrhythmias. from a lying or sitting position during heat exposure. Heat
Heat-related illnesses generate complications such as rhabdomy- syncope results from blood pooling in the cutaneous and skeletal
olysis and multiorgan dysfunction syndrome and may result in vasculature and occurs most often in dehydrated and inactive
death from overwhelming cell necrosis caused by a lethal heat persons who are not acclimated.101 Erythromelalgia is character-
shock exposure. Exertional heatstroke (EHS) is usually character- ized by pain and swelling of the feet and hands, triggered by
ized by development of mental status changes or collapse during exposure to elevated temperatures.70
physical activity in a warm environment. Severity of heat illness Serious illnesses include exertional heat injury (EHI) and EHS.
depends on degree and duration of elevation in core temperature These illnesses have many overlapping diagnostic features; it has
(Tco). Heatstroke is an extreme medical emergency that can be been suggested that they exist along a continuum on the severity
fatal if not treated promptly with rapid cooling. To prevent and scale.20 Heat exhaustion is characterized by inability to sustain
minimize complications and save lives, proper prevention, man- cardiac output in the presence of moderate (>38.5° C [101° F]) to
agement, and clinical care are essential. 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,
EXERTIONAL HEAT ILLNESS gut, muscle) and usually (but not always) involves a high Tco of
Dehydration and heat exposure can impair exercise performance more than 40° C (104° F). EHS is a severe illness characterized by
and contribute to various illnesses. Exertional heat illnesses central nervous system (CNS) dysfunction (e.g., confusion, dis-
include both minor and serious disorders. Minor heat and orientation, impaired judgment) and is usually accompanied by
dehydration-related illnesses include heat cramps, erythromelal- a Tco above 40.5° C (105° F). EHI and EHS can be complicated
gia, and heat syncope. Heat cramps are characterized by intense by cardiac arrhythmia, liver damage, rhabdomyolysis, coagulopa-
muscle spasms, typically in the legs, arms, and abdomen. Heat thy, fluid and electrolyte imbalances, and kidney failure. Rhab-
cramps result from fluid and electrolyte deficits and occur most domyolysis is most often observed with novel and strenuous
often in persons who have not been fully acclimated to a com- overexertion. Clinical evidence suggests that dehydration in-
bination of intense muscular activity and environmental heat. creases the likelihood or severity of acute renal failure associated
267
with rhabdomyolysis.22,99 Among U.S. soldiers hospitalized for normal Tco. After a return to normothermia, persistence of coma
serious heat illness, 25% had rhabdomyolysis and 13% had acute is a poor prognostic sign.62,110 Other symptoms include fecal
renal failure.25 incontinence, flaccidity, and hemiplegia. Cerebellar symptoms
Exertional heatstroke is usually associated with prolonged may persist beyond the acute phase.77,110,124
exertion in a warm climate; in many cases, however, EHS occurs Other common disturbances during the acute phase occur in
within the first 2 hours of exercise and not necessarily at high the gastrointestinal (GI) and respiratory systems. GI dysfunction,
ambient temperatures.20,40 This is because exertion and environ- including diarrhea and vomiting, often occurs. However, the
mental heat stress during the 72 hours that precede such an event vomiting may reflect translocation of toxic gram-negative bacte-
strongly influence the individual’s susceptibility to heat illness.43 rial lipopolysaccharide from the lumen of the intestines because
Using Tco of 40.5° C (104.9° F) as a critical temperature initially to of poor splanchnic perfusion as a result of hypotension caused
diagnose EHS is arbitrary. Mental status changes in an individual by increased skin blood flow and from CNS impairment.21,44,110
performing exertion in the heat should be the defining charac- Hyperventilation and elevation of Tco primarily lead to respiratory
teristic of heatstroke unless the individual has sustained head alkalosis, which in EHS may be masked by metabolic acidosis
trauma. At the stage of collapse, profuse sweating is still likely as a result of increased glycolysis and hyperlacticacidemia.29,82
to be present unless heatstroke develops in an already anhidrotic Hypoxemia may be present in patients with respiratory complica-
individual. Dry skin may be evident either in situations where tions.31,82,113 Also, oxygen consumption is elevated during hyper-
the climate is very dry and sweat evaporates easily or when thermia, with a 10% to 13% increase for every degree Celsius
heatstroke coincides with a severe degree of dehydration.39 above euthermia.35
Heatstroke is often categorized as either classic or exertional, Exertional heatstroke shares many common findings with
with the classic form primarily observed in elderly individuals or systemic inflammatory response syndrome (SIRS).20,105 Endotox-
otherwise sick or compromised populations and EHS in appar- emia, hyperthermia, and other risk factors (e.g., preexisting infec-
ently healthy and physically fit persons. 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-
CLINICAL MANIFESTATIONS ture less than 36° C (98.6° F) or more than 38° C (100.4° F); heart
Clinical manifestations of heatstroke vary, depending on whether rate greater than 90 beats/min, tachypnea, or an arterial partial
the person experiences classic heatstroke, which is a common pressure of carbon dioxide (PaCO2) less than 4.3 kPa (32 mm
disorder of older adults during heat waves and occurs in the Hg); and white blood cell count less than 4000 cells/mm3 (4 ×
form of epidemics, or EHS,1 which occurs when excess heat 109 cells/L) or of more than 12,000 cells/mm3 (12 × 109 cells/L),
COLD AND HEAT
generated by muscular exercise exceeds the body’s ability to or the presence of more than 10% immature neutrophils. When
dissipate it (Table 13-1). Some overlap in presentation may occur; two or more of these criteria are met, SIRS can be diagnosed.
treatment with a medication (e.g., antihypertensive or antipsy- The presence of systemic inflammatory response markers during
chotic) that places an older adult at risk for classic heatstroke the acute phase predicts the severity of subsequent phases.
also places an exercising individual at risk for EHS. The clinical
picture of heatstroke usually follows a distinct pattern of events Hematologic and Enzymatic Phase
with three phases: (1) acute, (2) hematologic or enzymatic, and Hematologic and enzymatic disorders peak 24 to 48 hours after
(3) late.41 collapse. In the hematologic and enzymatic phase of EHS, hema-
tologic, enzymatic, and other blood parameters are altered. In
Acute Phase
PART 2
268
split products increased, with a fall in thrombocytes.41 Clotting the poor and limited results of liver transplantation after heat-
269
should be kept wet by applying large quantities (20 to 30 L [5.3 The Tco reported in the field for heatstroke patients may be
to 7.9 gal]) of tap water or water from any source, and the per- significantly higher (e.g., 41.1° C [106.9° F]), than those docu-
son’s body should be constantly fanned. Cooling blankets are mented in the hospital ED (e.g., 37.8° C [100° F]) because Tco may
generally ineffective as a single modality for inducing rapid low- fall during transport to the hospital.107 Documenting only a mild
ering of body temperature required for treating heatstroke. 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
EMERGENCY MEDICAL SERVICES TREATMENT infection, sepsis, or other disease process. Other diagnoses
During evacuation, CWI is often not a viable method for treat- should be considered when the patient does not regain normal
ment. Iced sheets and ice packs can be easily used en route mental status after the Tco is normalized in less than 30 minutes.
during transport. Many EMS vehicles now carry refrigerated intra- When Tco remains elevated longer, there is a decreased likelihood
venous (IV) fluid to initiate induction of therapeutic hypothermia that mental status will normalize with euthermia.20
in cardiovascular emergencies. When used, chilled IV fluid (4° C Core temperature can be measured at several anatomic sites,
[39° F]) should be peripherally administered.68 Vascular access but oral, tympanic, esophageal, and rectal temperatures show
should be established without delay by inserting a 12- or 14-gauge regional variations as a result of differences in tissue metabolic
IV catheter. Administration of normal saline or lactated Ringer’s activity, local blood supply, and temperature gradients between
solution should be started. Recommendations vary regarding neighboring tissues. During exercise, active skeletal muscle tem-
administration rate of fluids. Some clinicians advise a rate of perature differs dramatically from that of other areas of the body
1200 mL (1.26 qt) over 4 hours,87 whereas others encourage a not directly involved in the activity. Oral temperature is consid-
2-L (2.11-qt) bolus over the first hour and an additional liter of ered to be similar to blood temperature as a result of the rich
fluid per hour for the next 3 hours.106 Patients should be placed blood supply of the tongue, but it is also influenced by hyper-
on a cardiac monitor. Administration of supplemental oxygen ventilation and drinking fluids. Rectal temperature is a highly
may help to meet the patient’s increased metabolic demands and reliable indicator of body temperature, but it has a slower
may also be used to treat the hypoxia often associated with response rate and gives slightly higher readings than do other
aspiration, pulmonary hemorrhage, pulmonary infarction, pneu- sites in the body.
monitis, or pulmonary edema.37,73 Blood glucose determination The comparison of oral and rectal temperature values in heat-
should be performed, and adults with blood sugar level less than stressed underground miners showed a difference of approxi-
60 mg/dL should be treated with one ampule of 50% IV dextrose mately 1° C (2° F), with oral temperatures underestimating rectal
solution. Children should be treated with 2 to 4 cc/kg of 25% IV values.116 Tympanic temperature responds more rapidly to
COLD AND HEAT
dextrose solution. cooling or heating than does rectal temperature, but it is influ-
Antipyretics are not effective and may potentially be harmful enced by changes in the skin temperature of the head and
to heatstroke patients. Aspirin and acetaminophen lower Tco by neck.47,74 The ear should be insulated from the environment to
normalizing the elevated hypothalamic set point that regulates prevent cool ambient temperatures (<30° C [86° F]) from affecting
the fever response caused by pyrogens; in heatstroke, the set this measurement. Esophageal temperature is the most accurate
point is normal, with Tco elevation reflecting a failure of normal and responsive to changes in blood temperature, but its instru-
cooling mechanisms. Furthermore, acetaminophen may induce mentation is impractical in severely injured or unresponsive
additional hepatic damage, and administration of aspirin may patients.
aggravate bleeding tendencies. Aspirin has also been shown to If airway control was not previously established and the
PART 2
attenuate protective, reflexive skin blood flow responses that are patient is still unconscious, a cuffed endotracheal tube should be
required for adequate heat dissipation,57,75 which will predispose inserted to protect against aspiration of oral secretions. Supple-
to heatstroke collapse. In a mouse model of heatstroke, an acute mental oxygen should be provided, as well as PPV when hypoxia
oral dose of indomethacin (a potent antipyretic nonsteroidal (PaO2 <55 mm Hg) or hypotension is present. Overvigorous fluid
antiinflammatory drug [NSAID]) provided immediately before resuscitation may precipitate pulmonary edema, so careful moni-
heat exposure resulted in about a 40% increase in heatstroke toring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid
mortality because of extensive gut hemorrhage.69 Similar results should be administered during the first hour after collapse, and
were observed in rats injected peripherally with aspirin.61 Because additional fluids should be administered until satisfactory urine
NSAIDs do not attenuate Tco during environmental heat exposure, output (0.5 cc/kg/hr in adult and 1.0 cc/kg/hr in child) is estab-
and their toxicity on the gut and liver is exacerbated with heat, lished.41 Most heatstroke patients arrive with a high cardiac index,
using these drugs prophylactically or for treatment of heatstroke low peripheral vascular resistance, and mild right-sided heart
patients is not warranted. Alcohol sponge baths are inappropriate failure with elevated central venous pressure (CVP). Only moder-
under any circumstances, because transcutaneous absorption of ate fluid replacement is indicated if effective cooling results in
alcohol may lead to poisoning and coma. vasoconstriction and increased blood pressure. Providers should
In a comatose patient, airway control should be established consider noninvasive intravascular volume monitoring or the
by inserting a cuffed endotracheal tube. Positive-pressure ventila- minimally invasive monitoring of systolic volume variation and
tion (PPV) is indicated if hypoxia persists despite supplemental pulse pressure variation. If these methods are not adequate, a
oxygen administration. Swan-Ganz pulmonary artery catheter may be necessary to assess
The patient’s altered mental status may adversely affect the appropriate fluid supplementation. Some patients have a low
ability of emergency department (ED) personnel to obtain a cardiac index, hypotension, and elevated central venous pres-
detailed history of precipitating events. Lack of such information sure. These persons have been successfully treated with an
may delay diagnosis. EMS transport personnel should attempt to isoproterenol drip (1 mg/min).87 Patients with low cardiac index,
obtain this history before evacuating the patient and should com- low CVP, hypotension, and low pulmonary capillary wedge
municate the information to medical staff. Of particular impor- pressure should receive fluid. Unless the patient has rhabdomy-
tance is the duration, and when available, maximum degree of olysis, aggressive fluid hydration is seldom required after initial
hyperthermia. treatment.
Cardiac monitoring should be maintained during at least the
first 24 hours of hospitalization. Arrhythmia is most likely to occur
HOSPITAL EMERGENCY MEDICAL TREATMENT during hyperthermia, but it may also occur as a result of elec-
Patients with suspected heatstroke should be placed in a large trolyte abnormalities. Using norepinephrine and other α-adrenergic
treatment room to accommodate the needed number of staff. drugs should be avoided because they cause vasoconstriction,
Patients are often combative and disoriented before reestablish- thereby reducing heat exchange through the skin. Anticholinergic
ing their baseline mental status. Aggressive cooling measures drugs that inhibit sweating (e.g., atropine) should also be avoided.
should continue until mental status returns to normal and Tco is Cooling techniques are ineffective when the patient has sei-
39° C (102° F).27 After discontinuation of cooling, Tco should be zures that increase body heat storage; therefore, convulsions
monitored every 5 minutes to ensure that it does not increase. should be controlled. IV benzodiazepines are preferred for their
270
efficacy and renal clearance. Initial dosing is either 4 to 8 mg of cooling by depressing Ca2+ entry into the sarcoplasm; this led to
271
• Ability to perform safely with equipment modification, bracing, coaches continue to use physical or psychological methods to
and orthoses force athletes to compete or train under intolerably hot condi-
• Compliance with applicable federal, state, local, school, and tions. This practice should be viewed as irresponsible, dangerous,
governing-body regulations and possibly criminally negligent.
The cornerstone assessment in the RTP decision requires The importance of recognizing milder forms of heat illness
fundamental understanding of the anatomic as well as functional cannot be overstated. Any time heat injuries occur, coaches and
healing of the particular disorder that affects the athlete. Exer- trainers should reassess all athletes and determine what other
tional heat illness RTP is especially challenging because there measures can be implemented to prevent occurrence of addi-
is incomplete understanding of the pathophysiologic processes tional or more serious injuries.
involved in development of and recovery from EHI.26,76
Despite the frequency of EHI, current civilian and military RTP Awareness of Host Risk Factors
guidelines for a particular athlete are largely based on anecdotal Shapiro and Moran104 studied 82 cases of EHS in Israeli soldiers
observation, prudence, and caution.76,86 At this time, no evidence- and concluded that at least one factor that predisposes an indi-
based guidelines or recommendations exist for returning indi- vidual to heatstroke (e.g., diarrhea, lack of acclimatization, poor
viduals, athletes, or soldiers to play or duty. Most guidelines are fitness) was associated with each case. Correcting individual risk
commonsense recommendations that require an asymptomatic factors should lead to strategies that can prevent heatstroke. Any
state and normal laboratory parameters, coupled with a cautious underlying condition that causes dehydration or increased heat
reintroduction of activity and gradual heat acclimatization. Current production or that causes decreased dissipation of heat interferes
suggestions range from 7 days to 15 months before EHS patients with normal thermoregulatory mechanisms and predisposes an
return to full activity.8 This lack of consistency and clinical agree- individual to heat injury. Older individuals are less tolerant to
ment can negatively impact athletes and soldiers and makes it EHI than younger persons and are more susceptible to classic
difficult for medical providers to determine the best solution for heatstroke because of decreased secretory ability of their sweat
each individual; the inconsistencies also can directly impact mili- glands and decreased ability of their cardiovascular systems to
tary readiness. Additionally, whereas current guidance states that increase blood flow to the skin. When healthy young adults
EHS patients may return to practice and competition when they exercise strenuously in the heat, EHS may occur despite the
have reestablished heat tolerance, no evidence-based tools are absence of host risk factors.
available to assess when the body’s thermoregulatory system has Elite and professional athletes, the general public, and the
returned to normal.76 military have widely used ergogenic aids (e.g., the herb ephedra
This lack of clear evidence-based guidance has allowed some
COLD AND HEAT
recover fully from EHS; indeed, this occurs in the vast majority sweat glands per area of skin than adults and overall greater
of cases when the athlete is treated promptly with aggressive sweat rates per unit area.58 Any reduction in the rate of sweating
cooling strategies (i.e., ice-water immersion).11,26,95 puts children especially at risk. The primary mechanism for heat-
stroke in young children is hot-vehicle entrapment. Between
Current Civilian Recommendations 1998 and 2010, 462 children died from heatstroke as a result of
In our opinion, the consensus RTP guidelines set forth by the vehicular hyperthermia.
ACSM are clear and succinct and provide a rational process for The primary means of heat dissipation is production and
guiding athletes who have sustained an EHI. Current recommen- evaporation of sweat. Any condition that reduces this process
dations from the ACSM for returning an athlete to training and places the individual at risk for thermal injury. Poor physical
competition follow8: conditioning, fatigue, sleep deprivation, cardiovascular disease,
1. Refrain from exercise for at least 7 days following release from and lack of acclimation all limit the cardiovascular response to
medical care. heat stress.43,60 Obesity places an individual at risk as a result of
2. Follow up about 1 week after the incident for a physical reduced cardiac output, the increased energy cost of moving
examination and laboratory testing or diagnostic imaging of extra mass, increased thermal insulation, and altered distribution
the affected organs, based on the clinical course of the of heat-activated sweat glands.80 Older adults and younger indi-
heatstroke. viduals show decreased efficiency of thermoregulatory functions
3. When cleared for RTP, begin exercise in a cool environment and increased risk for heat injury.
and gradually increase the duration, intensity, and heat expo- Several congenital or acquired skin abnormalities affect sweat
sure over 2 weeks to demonstrate heat tolerance and to initi- production and evaporation. Ectodermal dysplasia is the most
ate acclimatization. common form of congenital anhidrosis. Widespread psoriasis,
4. If RTP is not accomplished over 4 weeks, a laboratory poison ivy, sunburn, scleroderma, miliaria rubra (“prickly heat,”
exercise–heat tolerance test should be considered. caused by the plugging of sweat ducts with keratin), deep burns,
5. Clear the athlete for full competition if heat tolerant between and prior skin grafting may also limit sweat production.
2 and 4 weeks of full training. 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
PREVENTION volume. In an otherwise healthy adult, GI infection with vomiting
Prevention of heat illness relies on an awareness of host risk and diarrhea may cause sufficient dehydration to place the indi-
factors, a change in behavior and physical activity to match these vidual at risk for EHS.
risk factors and environmental conditions, and a requirement for Chronic conditions that may contribute to heat illness include
appropriate hydration during physical exercise in the heat. More diabetes mellitus, diabetes insipidus, spinal cord injury, eating
aggressive educational activity that explains heat illness and its disorders (especially bulimia), and mental retardation. Alcohol-
prevention to the public should be strongly promoted. Primary ism and illicit drug use are among the 10 major risk factors
care physicians should incorporate this information into the for heatstroke in the general population.63 An important effect
anticipatory guidance of routine health assessment. Despite a of alcohol consumption is inhibition of antidiuretic hormone
wealth of medical literature about heat injury, some athletic secretion, which leads to relative dehydration. Autonomic
272
during the first week of training and during times of high heat
CLOTHING
TABLE 13-2 Determination of Wet Bulb Globe
Different regions of the body are not equivalent with regard to
sweat production.56 The face and the scalp account for 50% of Temperature Heat Index
total sweat production, whereas the lower extremities contribute
only 25%. When exercising under conditions of high heat load, Temperature (T [°F]) Factor Example
maximal sweat evaporation is facilitated by maximal skin expo-
sure. Clothing should be lightweight and absorbent. Although Wet bulb T ×0.7 78 × 0.7 = 54.6
significant improvement has been made in fabrication of athletic Dry bulb T ×0.1 80 × 0.1 = 8.0
uniforms, uniforms and protective gear required by certain Black globe T ×0.2 100 × 0.2 = 20.0
branches of the military and public safety officers continue to Heat index 82.6
add to the risk of heat injury. Developing protective clothing that Wet bulb reflects humidity, dry bulb reflects ambient air temperature, and black
permits for more effective heat dissipation is indicated. Uniforms globe reflects radiant heat load; the heat index is the sum of the three.
should be modified to decrease the amount of extra protective Alternative equation: Wet bulb globe temperature = (0.567 Tdb) + (0.393 Pa) +
equipment and head gear needed as much as is safely possible 3.94, where Tdb is dry bulb temperature and Pa is water vapor pressure.
273
TABLE 13-3 Modification of Sports Activity Based on
tions and not individual factors, which emphasizes the impor-
tance of proper guidelines and safety measures in a warm climate
Wet Bulb Globe Temperature for preventing EHS fatalities. It follows that a combination of
predisposing factors that were already found to impair heat toler-
Index Limitation
ance43 is a strong predictor of a poor prognosis. Dehydration was
found in only two of the six fatal cases reported.
<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. CONDITIONING
18.3°-22.8° C (65°-73° F) There is a moderate risk toward the The contribution of cardiovascular conditioning to thermoregula-
end of the workout. tion is discussed in Chapter 6. Ideally, an individual should train
22.8°-27.8° C (73°-82° F) Those at high risk for heat injury should under temperate or thermoneutral conditions before exercising
not continue to train; all athletes in the heat. For the previously sedentary individual, an exercise
should practice in shorts and T-shirts regimen that incorporates 20 to 30 minutes of aerobic activity
during the first week of training. 3 to 4 days a week will improve cardiovascular function after
27.8°-28.9° C (82°-84° F) Care should be taken by all athletes to 8 weeks.
maintain adequate hydration. It is important to remember that even physically active indi-
28.9°-31.1° C (85°-88° F) Unacclimated persons should stop viduals may lack physical conditioning relative to a particularly
training; all outdoor drills in heavy stressful competition or activity. Heat illness in runners usually
uniforms should be canceled. occurs when novices exceed their training effort during races or
31.1°-32.2° C (88°-90° F) Acclimated athletes should exercise when well-trained athletes increase their pace above normal
caution and continue workouts only at during long-distance events.
reduced intensity; they should wear
light clothing only. ACCLIMATIZATION
≥32.2° C (90° F) Stop all training.
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-
COLD AND HEAT
yearly and are not left out in the heat for long periods without stroke deaths are most likely to occur during the first 4 days of
use. Care should also be taken to ensure that the device measures practice.95 Children and teenagers require 10 to 14 days to achieve
radiant heat, humidity, air movement, and shaded temperature an appropriate acclimatization response. Acclimatization can be
to calculate WBGT. Devices that measure the heat stress index, induced by simulating hot environmental conditions indoors.
relative humidity, and wind speed should not be used to estimate Aerobic activity should be conducted during exposure to the hot
WGBT. Current recommendations from the ACSM for preventing environment so that the individual can achieve optimal acclima-
EHI during workouts and competition are based on the WBGT.4 tization.98 If symptoms of heat illness develop during the acclima-
Most heat injuries occur during cooler WBGT periods as a result tion period, all physical activity should be stopped and appropriate
of cumulative heat exposure from preceding days. Some clini- interventions begun. Acclimatization is not facilitated by restrict-
PART 2
cians propose that heat-warning systems base their alerts on ing fluid intake; in fact, conscious attention to fluid intake is
cumulative heat stress rather than solely on the current WBGT.121 required to prevent dehydration. As with physical conditioning,
Other clinicians suggest using syndromic surveillance to help there are limits to the degree of protection that acclimatization
alert the public about periods of high heat stress.14 provides from heat stress. Given a sufficiently hot and humid
Table 13-3 presents a suggested modification of sports activity environment, no one is immune to heat injury.
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
RESEARCH
cautioned that the highest humidity of the day is usually early Areas for future research include improved clarification of when
morning. In 1999, Montain and co-workers78 updated fluid athletes can safely return to play; role of autonomic nervous
replacement guidelines for warm-weather training (see Chapter system dysfunction in EHS; benefit of induced hypothermia for
89, Table 89-5). It is important to note that compliance with these EHS treatment; and roles of clonidine, activated protein C, and
recommendations does not remove all risk of heat injury. The antibiotics during initial treatment.
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
ACKNOWLEDGMENTS
cases of EHS in the Israeli Defense Forces and examined the The authors extend much appreciation to the previous authors of
circumstances that led to the deaths. A significant association this chapter, Daniel S. Moran and Stephen L. Gaffin.
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- REFERENCES
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fatality factors primarily concerned organizational training regula-
274
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PART 2
274.e2
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 Saturday, February 7, 2009, Australia experienced a bushfire
on the Mann Gulch Fire near Helena, Montana, on August 5, disaster of unparalleled portions491:
1949, Norman Maclean285 wrote in his award-winning 1992 book In the wake of a long drought, and on a day of high temperatures, strong
Young Men and Fire, “They were still so young they hadn’t winds and low humidity, bushfires swept through residential and farming
learned to count the odds and to sense they might owe the communities in Victoria. Some 430,000 hectares [one million acres] of
universe a tragedy.” Three years later, Canadian folksinger- forest and farmland, countless homes and other buildings were burnt,
songwriter James Keelaghan, inspired by Maclean’s book, paid and hundreds of millions of dollars damage were done to economic and
tribute to the fallen firefighters in a haunting ballad entitled “Cold community assets. Far more tragically, it was Australia’s worst civil disas-
Missouri Waters.” The Mann Gulch Fire has been called “the race ter: 173 lives were lost. February 7th 2009 has become Black Saturday,
that couldn’t be won.”418 Although the crew increased their pace to be (one imagines) seared into the Australian psyche for generations
ahead of the fire, the fire accelerated faster than they did until to come.
fire and people converged. Miraculously, three people were able
to survive the fire’s wrath. Smoke jumper foreman Wagner Dodge On the fatal day, more than 300 fires were reported across
ignited an “escape fire” by burning off a patch of cured grass,26 the state. Fifteen of these developed into major incidents, with
into which he tried to move all his crew, while two others found the most extensive damage and loss of life resulting from four
a route to safety and escaped injury on a nearby rockslide. fires.142,203,311 The Kilmore East Fire alone was responsible for 70%
Many improvements in a firefighter’s odds of surviving an of the 173 deaths that occurred.162 A royal commission was estab-
entrapment or burnover encounter with a wildland fire have lished soon afterward to investigate the causes and responses
occurred since 1949. These advances include improved under- to these fires (www.royalcommission.vic.gov.au/). The commis-
standing of fire behavior, increased emphasis on fire safety and sion’s final report, issued at the end of July 2010, sets out 67
fire training, and development of personal protective equip- recommendations for protecting human life, “designed to reflect
ment.143 However, as incidents such as the 14 firefighter fatalities the shared responsibility that governments, fire agencies, com-
on the 1994 South Canyon Fire in western Colorado (Figure 14-1) munities, and individuals have for minimizing the prospect of a
and in 2015 in Washington have shown, tragedies can and con- tragedy of this scale ever happening again.”477 In their report, the
tinue to occur.178 Norman Maclean’s son, John, would in turn commissioners offered a warning: “It would be a mistake to treat
write about this fatal fire 50 years later.286 Grief over lost loved Black Saturday as a ‘one-off’ event” because “the risks associated
ones can sometimes lead to further tragedies. For example, one with bushfires are likely to increase.”
of the smoke jumpers killed on the 1949 Mann Gulch fire, Stan Given the occurrence of other major wildfire disasters involv-
Reba, had been married less than a year. His widow grieved for ing significant loss of life among civilian populations in recent
him and never remarried, then 10 years later took her own years—for example, Greece in August 2007 (84 fatalities),545,546
life.247,299 western Russia during the 2010 summer fire season (63 fatali-
The latest major multiple-casualty wildland firefighter fatality ties),218 Mount Carmel in northern Israel in December 2010 (44
event to occur, the Yarnell Hill Fire in central Arizona, took place fatalities),531 and Valparaiso, Chile, in April 2014 (15 fatalities)412—
on the last day of June 2013. Nineteen members of the 20-person this prediction has global application.
Granite Mountain Hotshots perished during the fire’s major run.532 This chapter describes the current look at fire as a historical
Wildland fires are a threat to human life, property, and natural force and discusses fire management policies, the nature and
resources in many regions of the world (Figure 14-2). Although scope of wildland fire hazards, behavior of fires, typical injuries,
the total number of deaths among the general public caused by fatality fire statistics, several fatal fire incidents, and survival
wildland fires in modern times pales in comparison with the techniques. Although the emphasis is on North America, refer-
death toll and destruction from other natural hazards (e.g., hur- ence is made to other regions of the globe, most notably Aus-
ricane, tornado, flood, earthquake, tsunami, avalanche)86 and tralasia and Europe. Wildland fire, like many other disciplines
human-made disasters, the fatalities are frequent and nevertheless and subjects, has its own unique terminology, so readers may
devastating.488 need to consult glossaries.198,313,359,456
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 WILDLAND FIRE MANAGEMENT
unique.353 Statistics on the number of civilian or wildland fire-
fighter fatalities from being trapped or overrun by wildland fires
AND TECHNOLOGY
on a global basis are unfortunately not kept in any systematic Programs for dealing with the overall spectrum of fire are col-
manner.245 It is, however, well known that more than 300 deaths lectively termed fire management.58 They are based on the
caused by bushfire entrapments and burnovers occurred in the concept that fire and the complex interrelated factors that influ-
state of Victoria in Australia alone during the 20th century.259 On ence fire phenomena can and should be managed to the extent
276
Idaho, in 1992; Garnet Fire near Penticton, British Columbia, in
277
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.
278
• Ensuring that necessary firefighting resources and personnel
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
280
and fire survival principles must be readily available to emer- region, including the Peshtigo and area fires (www.peshtigofire
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
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.
Tok, Alaska, July 1, 1990, 15 to 30 minutes after the lightning strike The girls loaded their cars with personal items. Mine was loaded
that started the Tok Fire. (Photo by D. Blasor-Bernhardt.) 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
July 1, 1990, started out like any other Sunday, but it quickly turned near and we had to evacuate, the plan was for the girls and I to
Tok, Alaska, into a near raging inferno. I was working at the load our pets while the boys quickly cut the trees down around the
Chamber of Commerce Main Street Visitor Centre when an cabins, hopefully providing a bare, wet perimeter between them
otherwise beautiful day suddenly turned black and foreboding. and the fire.
Blowing in, a huge thundercell hung just southeast of town. Fully loaded, we assembled in the driveway, ready for word to
I stepped outside just in time to see a long, crooked finger of come. Besides myself, six young adults, a baby, half a dozen dogs,
electricity split from an ominous cloud and drill its way into Earth. numerous cats, a snake, six vehicles, and a trailer comprised the
Minutes later, where the lightning had hit, a mushroom-shaped Bernhardt entourage. We were ready. We waited in the foul air, our
cloud began to grow. I grabbed my camera and snapped a few eyes smarting from the smoke. An ember hit me on the shoulder,
shots. burning a hole though my shirt. Sadly, I turned to look at our homes
Five days later, and in spite of several thousand firefighters and one last time. Tomorrow they would be gone.
equipment from all over Alaska, Canada, and the States, Tok was Imperceptibly at first, a slight shift in the wind began. I held my
completely under siege and at risk of being cremated. The breath. “Mom?” my son said. “Yes,” I answered, “but I’m afraid to
wind-blown inferno licked greedily at several unoccupied dwellings, hope.” The wind, definitely shifting now, was no longer blowing
then consumed them. East-side residents were evacuated. We, on toward us. A sweet, light rain began to fall. While the eight of us
the west side, were told to pack our things, to be ready to leave, stood together, soaking wet in the rain, a trooper came by to tell us
and to await further instructions. the worst was over.
Tok was enveloped on two sides by fire—from the eastern and In all, the fire burned 109,501 acres (44,314 hectares) at a cost of
northern directions. My log home was about a mile from the north over $35 million (U.S.), yet not one person had been injured, not
front of the fire. I stood on the cabin’s sod roof, watching the fire, one occupied dwelling destroyed, and Tok had been spared by a
when the kids and extended family converged there about the same miracle wind.
From Blasor-Bernhardt D: A town that nearly went . . . up in smoke, Guide to the Goldfields and Beyond (Harper Street Publishing, Dawson City, Yukon Territory)
Summer: 52, 1997.
281
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
BURNS, FIRE, AND RADIATION
282
The area had not experienced any rain for 67 days before the people taking risks in their lives provided that they also bear the
Scenario
House and Surrounding Fuel Conditions A B C D
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
283
defend or “fight” for their homes, or “flee” in the hopes of escap- a wildfire, preparing one’s family for evacuation, and finally,
ing an advancing fire.539 leaving earlier. The program is now endorsed by the International
In the late 1990s, the Tasmania Fire Service had a policy that Association of Fire Chiefs (www.iafc.org/displaycommon.cfm?an
provided guidance on bushfire safety and evacuation decision =1&subarticlenbr=1229).
making called “Prepare, Stay, and Survive.”213 When there was a In many regions of the world, people are warned that wild-
threatening wildfire, people were told to go home and assist in fires are dangerous and that they always need to evacuate. This
the protection of their property. Because human lives and prop- “scare tactic” approach reinforces the concepts that wildland fires
erty values are at risk when threatened by wildfires, exemplary are always dangerous and that people must leave their homes.
cooperation and teamwork are required to ensure adequate Perhaps one solution to dealing with fires in the WUI in the
safety margins. Team members identified for reducing the loss future would be to embrace the concept of “A Dream, a Team,
of life and property include state agencies, local government, the and a Theme.”335 The “dream” would be one where houses are
communities, and individuals. able to survive fires even when fire services personnel are not
The “Stay or Go” policy concerning evacuation was advocated available. The “team” would consist of the effective partnership
by the Australasian Fire Authorities Council (AFAC)48 as a funda- between the fire services and home dwellers. The “theme” would
mental component of community bushfire safety in Australia.233 comprise the dual strategy of adequate defensible space coupled
Variants to this general theme exist (e.g., “prepare, leave early, with the home dweller’s motivation to remain on site as an
or stay and defend”). However, the essence of the approach important factor in suppressing fires initiated by ember attack.
urges people to make the decision to prepare themselves and In order for this approach to work, rural homeowners must
their properties to “stay” and defend when a wildfire is likely, or understand that although wildfires can be dangerous, with proper
to “go” well before a fire is likely to arrive. Although early evacu- precautions, people can remain with their homes and be an
ation may contribute to increased personal safety, bushfire prop- important part of the solution to the WUI fire problem. Empow-
erty losses are likely to increase. Conversely, late evacuation may ering communities at risk from wildfire to play an active part in
put people at greater risk than had they stayed in the house as their own protection is viewed as a viable long-term strategy to
BURNS, FIRE, AND RADIATION
the fire passed around them. enable safe and harmonious coexistence with fire as an element
An evaluation of this policy was the focus of Project C 6— of nature.121
Evaluation of Stay or Go Policy undertaken by the Australian During the 2000 fire season in western Montana, some indi-
Bushfire Cooperative Research Centre (www.bushfirecrc.com/), viduals opted to stay with their homes as flame fronts advanced.
led by co-project leaders John Handmer, RMIT University, and They created defensible space, installed sprinkler systems,
Alan Rhodes, Country Fire Authority of Victoria. Fire management engaged in fire suppression activities, and provided local intel-
agencies and the public alike will find the final results of this ligence to incoming fire service personnel. No home was lost as
research project of great interest. The preliminary results gener- people demonstrated responsibility for their personal well-being.
ally supported the 2005 AFAC position, while recognizing that A similar “prepare, stay, and defend” action was successfully
implementation issues remained.90,92,231,236,278,482 However, the fires carried out during the 2003 fire season on the Wedge Fire along
of February 7, 2009, in Victoria, Australia, and in turn the Royal the North Fork of the Flathead River in western Montana. The
Commission’s report477 have changed the context for this approach property was prepared in advance to be “fire safe,” the home-
quite significantly. There are a number of emerging issues (e.g., owner remained with volunteer fire department officials, and
limit of validity), so the policy is most likely to evolve in coming the home survived the passage of a high-intensity crown fire
years414 in the aftermath of the Black Saturday fires, as evidenced (Figure 14-11).
PART 3
by AFAC’s revised position on bushfire community safety based Wildland fires that threaten human lives and property are not
on emergency risk management principles.52 exclusively located in southern California because the exodus
The 2009 Black Saturday fires have placed an urgent emphasis to wildland regions has become a national phenomenon. Fires
on the continuing debate over what constitutes the safest strate- burned about 81,000 hectares (about 200,000 acres) in Maine
gies for survival in the WUI. The Victorian fires led to the creation in October 1947, killing 16 people;93,180 another area of about
of a catastrophic, or “Code Red,” level of fire danger. When this 81,000 hectares (about 200,000 acres) burned in New Jersey in
category of fire danger is forecast for the next day, it is recom- April 1963.55 Wildland fire disasters have not always been large
mended that people in a high-risk bushfire area leave the night in size. On September 26, 1936, most of the coastal town of
before or in the early morning (www.cfa.vic.gov.au/warnings- Bandon in western Oregon was destroyed, and 11 people were
restrictions/). At the next two lower levels (“Extreme” and killed by a wildfire that covered probably no more than about
“Severe”), it is recommended to stay only if one’s home is well 4000 hectares (10,000 acres).243 The prevalence of gorse, a non-
prepared, well constructed, and can be actively defended. native plant, was considered a key contributing factor to the
Testimony by John Handmer before the 2009 Victorian resulting devastation (Figure 14-12). On July 16, 1977, the Pattee
Bushfires Royal Commission,477 coupled with analyses pro- Canyon Fire that occurred near Missoula, Montana, destroyed six
duced by his research team,230 indicate that only a small per- homes and charred about 500 hectares (1200 acres) of forests
centage of homes and property were adequately prepared to and grasslands in only a few hours.195 Similarly, more than 70
be fire resistant. Without preparing a fire-resistant home and homes were damaged or destroyed by fires in the southern Cape
property in advance, the only prudent course of action is to Peninsula region of South Africa that burned about 8000 hectares
evacuate early. (about 19,800 acres), during January 16 to 20, 2001.109,504 A host
This issue of whether to “prepare, stay, and defend” or evacu- of other cases have occurred in North America242 and are steadily
ate early is a subject considered worthy of more open debate accumulating.
and discussion in North America.17,307,339,379,459 Two communities Fires at the WUI are also increasing internationally. For
in the United States—Painted Rocks in Montana and Rancho example, the Ash Wednesday fire disaster in southeastern Aus-
Sante Fe in California—have adopted variations of the original tralia on February 16, 1983 burned about 340,000 hectares
Australian model of “Prepare, Go Early or Stay and Defend.”339 (840,000 acres) of urban, forested, and pastoral lands in the states
Both communities have had the “Stay and Defend” practice suc- of Victoria and South Australia, killing 77 people, injuring about
cessfully tested by wildfires. Both U.S. communities are carefully 3500, and destroying more than 2500 homes.59,237,366 Phenomenal
monitoring the lessons learned from the 2009 Black Saturday fires fire spread rates in both forests and grasslands occurred,254,407 and
to determine if any change is needed in their approach. Mean- flame heights of almost 200 m (650 feet) were observed.472 In
while, Ready, Set, Go! (RSG) was rolled out as a full-scale pilot May 1987, wildfires in northeastern China425 added a new per-
program by the Ventura County Fire Department and the Orange spective regarding the devastating impact wildland fires may
County Fire Authority for the 2009 fire season in Southern Cali- have on human lives, property, and natural resources. These fires
fornia. Other fire departments, such as Los Angeles County,156 reportedly burned about 1.34 million hectares (3.31 million
Los Angeles City, San Bernardino County, Riverside County, Santa acres), killed 212 people, seriously injured another 226, and left
Barbara County, and Cal Fire, have adopted the basic approach. about 56,000 homeless.173 Clearly, it was a disaster of major pro-
The RSG approach involves preparing one’s house to withstand portions. These fires resulted from a combination of plentiful
284
were killed in Mexico as a result of the fires,486 and ecosystems
285
serious nature of worldwide vegetation fires.199 Participants at the BOX 14-2 Recommendations to Reduce Loss of Life
conference in Rome concluded that governments needed to enact
more sustainable land use policies and practices to reduce the and Property in the Wildland-Urban Interface (WUI)
impacts of wildfires on people and natural resources. Fire Protection Services
It is becoming increasingly rare to have a wildland fire situa-
Remember that firefighter and public safety is the first priority in
tion or incident that does not involve people and their homes. every fire management activity.
However, people are not fully aware of the fire risks and hazards Ensure that all personnel receive regular cross-training in fighting
of living and traveling in or near wildlands.65,224 “Risk,” in the wildfires and structural fires.
jargon of the wildland fire specialist, is the probability that a fire In urban departments, in particular, recognize the need to
will occur. “Hazard” is the likelihood that a fire, once started, extinguish fires in wildland fuels by using thorough mop-up
will cause unwanted results. Risk deals with causative agents or procedures.
ignition sources; hazard deals with the fuel complex.205 The Recognize the need for close coordination of response efforts
results of two surveys carried out in the western United States among neighboring departments or agencies.
during the 1970s indicated a general feeling of overconfidence Develop specific mutual-aid plans for coordinating resources to
by most residents toward the potential danger or threat of a attack fires in the WUI.
wildland fire. About 80% of Seeley Lake, Montana, forest resi- Schedule and conduct regular mutual-aid training exercises.
dents interviewed thought that the forest fire hazard was low to Regularly schedule and conduct fire prevention and fire
moderate in their area.204 About 75% of Colorado residents inter- preparedness education programs for the general public and
viewed thought that the forest fire hazard was low or moderate homeowners.
in mountain subdivisions of their state.244 Forest fire hazards in Conduct an assessment of fire risks, and prepare a strategic plan
these two areas were much higher than these public estimates. to reduce these risks.
A survey of attitudes toward bushfires in the Dandenong Ranges Work effectively with lawmakers and other government officials to
help prevent unsafe residential and business development.
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 Legislators
people without such experience.183 However, the survey also Examine existing laws, regulations, and standards of other
revealed that 40% of the people with recent severe bushfire jurisdictions that are applicable locally in mitigating hazards
experiences still did not rate bushfires as one of the three most associated with wildland fires.
important environmental problems in their area. Dr. Sarah McCaf- Adopt National Fire Protection Association (NFPA) guidelines in
frey,306 a research social scientist with the USDA Forest Service the form of NFPA 1144 (formerly NFPA 299, 1991 edition),
who has studied the social dynamics of fire management for Standard for the Protection of Life and Property from Wildfire.344
The purpose of this standard is to provide criteria for fire
many years, suggests that the general public is much better
agencies, land use planners, architects, developers, and local
informed of the issues dealing with the WUI fire problem than government for fire-safe development in areas that may be
during the 1970s and 1980s.304,305 She attributes this fundamental threatened by wildfire. NFPA 1144 provides minimum planning,
change to programs such as Firewise, fire safe councils, and construction, maintenance, education, and management
media coverage. No doubt the large number of conflagrations in elements for the protection of life, property, and other values
the past 25 years has also contributed to an increased awareness that could be threatened by wildland fire. It is designed to
regarding the realities of wildland fire. assist local, state, and federal fire agencies in dealing with the
In more recent surveys carried out in Florida and Minnesota362 escalating challenges presented by the proliferation of WUI
PART 3
of homeowners’ preferences for vegetation and defensible space communities and the monetary losses of structures in WUI
near their homes, people recognized the wildfire threat but areas. These guidelines address the following topics:
varied in their perceptions of effective wildfire prevention mea- assessment and planning; access, ingress, egress, and
sures and willingness to take actions to reduce the potential evacuation; fuel modification area; water supply; and residential
threat to themselves and their homes. Most supported the use of development design, location, and construction.
planned fire to reduce fire potential, especially if wildland fire Provide strong building regulations that restrict untreated wood
experts who understand the local ecology and fire behavior shingle roofs and other practices known to decrease the fire
conducted the prescribed burns. In-depth interviews conducted safety of a structure in the wildlands.
with homeowners along the northern part of the Colorado Front Planners and Developers
Range revealed that these people face difficult decisions regard- Create a map of potential problem areas based on fuel type and
ing implementation of wildfire mitigation measures.79 Perceptions known fire behavior.
of wildfire mitigation options were found to be possibly as Evaluate all existing or planned housing developments to
important as perceptions of risk in determining likelihood of determine relative wildland fire protection ratings, and advise
implementation. These mitigation options were often viewed as property owners of conditions and responsibilities.
trade-offs between wildfire risk and preferred landscapes. The Ensure that all developments have more than one ingress-egress
study participants also reported, however, that one-on-one infor- route.
mation sharing with wildland fire experts, as well as increased Offer options for fire-safe buildings.
understanding of the flexibility of mitigation options, encouraged Provide appropriate firebreaks, fuel breaks, or greenbelts in
developments.
implementation. Personalized contact appears to be a key factor
Ensure that adequate water supplies exist in developments.
in educating homeowners about the realities of living in a wild- Follow specifications in NFPA 1144 Standard for the Protection of
land environment.303 Life and Property from Wildfire.344
Participants in a survey conducted in Michigan541 considered
wildland fires as inherently uncontrollable and the resulting Public and Homeowners
damage essentially random. Thus, they only weakly supported Determine the wildfire hazard potential of the immediate area
investments in fire suppression infrastructure but strongly sup- before buying or moving into any home.
ported fire prevention programs that reduced the number of fire Contact federal, state, and local fire services for educational
programs and materials regarding fire protection.
starts, were unlikely to take all possible steps to safeguard their
Provide a fuel-modified area or defensible space around
own properties, and exhibited a negative view of prescribed vulnerable structures to reduce the likelihood of ignition by an
fire to the extent that it could preclude its use as a risk manage- advancing wildfire.
ment tool. Design and build nonflammable homes.
There is a growing need for the general public, emergency Urge lawmakers to respond with legislative assistance to require
medical personnel, and fire suppression organizations to be well appropriate fire safety measures for communities.
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
have demonstrated that community firefighting resources are
287
responsible for fire protection. Firewise Communities workshops
help define responsibilities for a network that includes many C
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 B
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 A
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 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
Oregon University, and University of Florida. Sixteen community
firefighters took refuge in the fire line, in the foreground at point A.
preparedness case studies were completed between 2002 and Affected by intense convective and radiant heat and dense smoke, one
2004 in a variety of locations throughout the continental U.S. individual ran into the fire and died at point B. Another individual ran
(jfsp.fortlewis.edu).527,534 about 300 m (1000 feet) down the ridge, where his body was found
In 1990, Partners in Protection (PiP) of Alberta, Canada, was at point C. The third fatality was a person who remained at point A;
established. PiP is a coalition of professionals representing he died a short time after this position was overrun by fire. The only
BURNS, FIRE, AND RADIATION
national, provincial, and municipal associations and organiza- survivor also remained in a prone position at point A with his face
tions committed to raising awareness, providing information, and pressed to the ground. At one point he reached back and threw dirt
developing forums to encourage proactive, community-based on his burning pants legs. The survivor sustained severe burns to the
initiatives regarding fires at the WUI. In 2008, PiP was invited by backs of his legs, buttocks, and arms. The deaths of the other three
the Canadian Council of Forest Ministers to develop a proposal individuals were attributed to asphyxiation. (Courtesy USDA Forest
for a nationally oriented effort. In response, PiP developed the Service.)
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 WILDLAND FIRE BEHAVIOR
This well-illustrated guide focuses on how individuals and com-
munities can work together to reduce the risk for loss from
URBAN AND WILDLAND FIRE THREATS
wildfires in the WUI. It provides practical tools and information Safety precautions for wildland firefighting crews are continually
for use by residents and by individuals and organizations that upgraded as new knowledge is gained about fire behavior and
operate in the WUI. The primary topics are description of human behavior. The sites where people were injured or killed
PART 3
interface issues, evaluation of hazards, mitigation strategies and by fire are routinely examined afterward to assess fuel conditions,
techniques, emergency response for agencies and individuals, terrain features, probable wind movements at the time of the fire,
training for interface firefighters, community education programs, and actions of firefighters294,329,530 (Figure 14-14). In this regard,
and regional planning solutions. The manual, available in both Maclean285 has noted:
book form and CD-ROM, can be viewed online (www.firesmart It is hard to know what to do with all the detail that rises out of fire. It
canada.ca/resources-library/protecting-your-community-from- rises out of a fire as thick as smoke and threatens to blot out everything.
wildfire) and covers almost every facet of fire preparations in the Some of it is true but doesn’t make any difference. Some of it is just
WUI. In the chapter on communications and public education, plain wrong. And some doesn’t even exist, except in your mind, as you
for example, the following principles are cited for effective slowly discover long afterwards. Some of it, though, is true—and makes
communication: all the difference.
• Begin with clear, explicit objectives.
• Do not make assumptions about what people know, think, The information gleaned from past wildland firefighter fatali-
or want done. Take time to find out what people are thinking ties, as well as data about hazards in the WUI, are now included
by using surveys, focus groups, or other research. in training programs and safety briefings.
• Involve all parties that have an interest in the issue. Identify In reviewing many past wildland fire tragedies, a sobering
and address the particular interests of different groups. observation is that crew members are almost always experienced
• Identify with your audience. Put yourself in their place, and and well-equipped firefighters, trained to anticipate “blowup” fire
recognize their emotions. conditions (i.e., a temporary escalation in fire behavior). However,
• Take time to coordinate with other organizations or groups. when visibility is lowered to 6 m (20 feet), noise levels preclude
• Choose your spokespeople carefully, and ensure they have voice communication, eyes fill with tears, and wind blows debris
the training to communicate your messages effectively. in all directions, a person’s judgment is greatly impaired. For
• Practice and test your messages. many members of the general public, the first wildland fire they
• Do not either minimize or exaggerate the level of risk. may experience will in all likelihood be a high-intensity confla-
• Promise only what you can do. Do what you promise. gration. As Cheney122 notes:
• Plan carefully, and evaluate your efforts.
Kumagai and colleagues261 also offer some excellent advice The approach of a major fire can appear ominously threatening to those
with respect to wildland fire education and communication with directly in its path, but is often viewed with curiosity and with little
the general public. concern if it appears that the wind will direct the fire past their proper-
Most local, state, provincial, territorial, and federal fire man- ties. Thus, when a combination of circumstances, often associated with
agement agencies now have some type of outreach program a frontal wind passage, exposes residents to a high-intensity fire environ-
related to the WUI. For example, the State of Alaska offers ment, they are very much unprepared. Their senses are assaulted by
teachers both face-to-face wildland fire workshops and an sudden darkness, thick blinding and choking smoke, buffeting winds and
online training course.468 In 1993 the Country Fire Authority of unexpected calm periods, searing heat and flames which illuminate the
Victoria, Australia, developed a program called “Community Fire- smoke-obscured scene and a roaring noise of wind and explosive com-
guard,” which assists communities in developing wildfire survival bustion. In all this activity they observe flames which change from a
strategies.74 metre or two to engulfing whole trees. In such a dramatic and emotional
288
situation, many people are apt to invent phenomena (such as, houses
289
behavior guidelines and experienced judgment35,57 based on BOX 14-3 Requirements for Wildland Fire Spread
current and expected fire weather conditions in relation to local
fuel type information, topographic conditions, and moisture Certain universal principles apply to all spreading fires in
levels.88,273,475 This is also referred to as situational awareness, vegetation, living or dead. These really have nothing to do with
that is, understanding what the fire is doing and what you are biology but are based purely on the physics and chemistry of
doing in relation to the fire and being able to predict where the combustion:
fire and you will be in the future.391 1. There must be sufficient fuel of appropriate size and
In the conclusions to their detailed case study report on the arrangement in space.
1994 South Canyon fire in Colorado, USDA Forest Service fire 2. This fuel must be of sufficient dryness to support a spreading
researchers98 noted: combustion reaction.
3. There must be an agent of ignition.
None of the findings and observations discussed in this study represent
In practical terms, the primary requirement is a continuous layer
new breakthroughs in wildland fire behavior understanding. Rather, the of finely divided fuel or minor vegetation on the surface of the
findings support the need for increased understanding of the relations ground. This material may be conifer needles, hardwood leaves,
between the fire environment and fire behavior. We can also conclude grass, lichen, moss, finely divided shrubs, or other minor
that fire managers must continue to monitor and assess both present fire vegetation. However, it must be present and it must be
behavior and potential future fire behavior given the possible range of continuous, or the possibility of spreading fire does not really
environmental factors. exist. The second requirement is that the material be dry enough.
The maximum moisture content at which fire will spread is hard to
The emergency medical person, backcountry recreationist, specify; for any given fuel or vegetation complex, it will depend on
and wildland homeowner must also understand certain basic fire the amount of fuel, its arrangement in space, and the wind speed.
behavior principles to provide for adequate personal safety. A Thus, fire spreads poorly or not at all in surface litter of various
cardinal rule in wildland fire suppression is to base all actions kinds at moisture contents over 25% or 30% (dry weight basis),
on current and expected fire behavior.300,322 Attention to simple whereas fine shrubby fuels or conifer foliage may support
BURNS, FIRE, AND RADIATION
principles, indicators, and rules should enable wildland users to fast-spreading fires at moisture contents of 100% or more.
anticipate and avoid wildfire threats. The two limiting criteria common to all spreading fires are as
Heat, oxygen, and fuel are required in proper combination follows:
before ignition and combustion will occur57,209 (Figure 14-16). If 1. The fire must transfer enough heat forward to dry out the
any one of the three is absent, or if the three elements are out unburned fuel and raise it to ignition temperature by the time
of balance, there will be no fire (Box 14-3). Fire control actions the flame front arrives.
are directed at disrupting one or more elements of this basic fire 2. Enough fuel must pass through the moving flame front to
triangle.14 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
PHYSICAL PRINCIPLES OF HEAT TRANSFER energy flowing in and out of the flame zone. However difficult this
Heat energy is transferred by conduction, convection, radiation, whole process may be to describe and predict, the above two
criteria run like threads through the whole range of fires in
and spotting, but generally only the last three processes are
vegetation, whether the fuel itself is dead or live.
significant in a wildland setting.106 Although conduction through
solid objects is important in the burning of individual logs,57 this From Van Wagner CE: Fire behaviour in northern conifer forests and shrublands.
PART 3
process does not transfer much heat outward from a flaming In Wein RW, MacLean DA, editors: The role of fire in northern circumpolar
front, unless there is a substantial accumulation, such as is found ecosystems, Chichester, England, 1983, John Wiley & Sons.
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 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
Heat 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
O2 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
Oxygen Fuel wildland fires87 and in fact could cause serious burn injuries.
FIGURE 14-16 Combustion is a process involving the combination of Similarly, “emergency evacuation smoke hoods,” intended for use
heat, oxygen, and fuel. An understanding of the variations of these in urban situations or other human-made environments (e.g.,
three factors is fundamental to an understanding of wildland fire airplanes), have absolutely no application in a wildland fire
behavior. (Modified from Barrows JS: Fire behavior in Northern Rocky environment despite manufacturers’ suggestions to the contrary.
Mountain forests, Station Paper No 29, Missoula, Mont, 1951, USDA Spotting is a fire spread or mass-transport heat transfer mecha-
Forest Service, Northern Rocky Mountain Forest and Range Experi- nism by which wind currents carry flaming firebrands or glowing
ment Station.) embers land beyond the main advancing fire front to start new
290
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 rence with high-intensity crown fires.30 Longer-range spotting
very quickly, unexpected new fire starts can occur, and fire occurs very infrequently in most fuel types. Firebrand material
intensity and in-draft winds can dramatically increase as spot fires being transported up to 16 km (10 miles) from its source has
coalesce (Figure 14-21) and directly increase a fire’s rate of been reported in North America.41 The native eucalyptus forests
spread. High-density, short-range spotting up to 100 m (328 feet) of Australia have a notorious reputation when it comes to spot-
is a common feature of many wildfires, especially when fine fuels ting behavior because of the bark characteristics of many species,
are very dry.39 Low-density, intermediate- to medium-range spot- including an authenticated spot fire distance of 30 km (19 miles)
ting up to about 1 to 2 km (0.6 to 1.2 miles) is a common occur- 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
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)
FIGURE 14-20 Fires can easily cross narrow canyons. Fuels and people in a single day7,420 and for grass fires to travel correspondingly
on the slope opposite a fire in a narrow canyon are subject to intense even farther.528
radiant heat and spot fires from airborne embers. (Modified from The threat to life and property largely depends on a fire’s
BURNS, FIRE, AND RADIATION
Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station residence time (Table 14-2). This represents the length of time
Paper No 29, Missoula, Mont, 1951, USDA Forest Service, Northern any object overrun by a fire will be heated by direct flame
Rocky Mountain Forest and Range Experiment Station.) 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
PART 3
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
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)
*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- factors, and observed fire behavior. After the fire’s probable
mined by the size and geometry (e.g., height, depth, and tilt direction and rate of spread are estimated, travel routes that avoid
angle) of the flame front. Radiation levels coupled with residence hazards to human life can be planned (see Figure 14-24). The
times determine the nature of burn injuries.87,181 direction of the main body of smoke is often a good indicator
of the direction the fire will take.
Environmental Factors Influencing Wildland Fire Behavior Fuel. Because wildland fuels vary so widely in their distribu-
A wildland fire behaves according to variations in the fire envi- tion, their physical characteristics or properties (i.e., moisture
ronment (i.e., fuels, weather, and topography). Box 14-4 lists content, size and shape, compactness or arrangement, load,
some of the fire environment factors associated with adverse horizontal and vertical continuity, chemical content), and their
burning conditions that can signal the potential or onset for effect on fire behavior, some means of classification is needed
severe fire behavior. These factors or indicators are subject to for their systematic assessment. Fuels are commonly classified
assessment, observation, and measurement. into four groups or strata (Figure 14-26). Some fuel types may
When a person encounters a wildland fire, the first step exhibit only one or two of the strata (e.g., grasslands, shrublands,
should be to review the principles and indicators of fire behavior, and logging slash lack the ladder and crown fuel stratum).
sizing up the situation in terms of fuel, weather, topographic 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:
BOX 14-4 Early-Warning Signals or Indicators 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
Associated with Extreme Fire Behavior Potential
with which the fire fighter must cope, and that largely determines the
Fuel 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
• Continuous fine fuels, especially fully cured (dead) grasses
• Large quantities of medium and heavy fuels (e.g., deep duff in relation to fuels. In short, no fuel, no fire!
BURNS, FIRE, AND RADIATION
layers, dead-down logs) Certain types of fuel, such as chaparral, pine, and eucalyptus,
• Abundance of bridge or ladder fuels in forest stands (e.g., burn more intensely because their foliage contains flammable oils
branches, lichens, suspending needles, flaky or shaggy bark, and resins (see Figure 14-12). The size and arrangement of fuel
small conifer trees, tall shrubs extending from ground surface also influence fire behavior. Small, loosely compacted fuel beds,
upward)
such as dead grass, long pine needles, and shrubs, burn more
• Tight tree crown spacing in conifer forests
• Presence of numerous snags rapidly than does tightly compacted fuel. Large fuels burn best
• Significant amounts of dead material in elevated, shrubland fuel when they are arranged so that they are closely spaced, such as
complexes logs in a fireplace. Scattered logs with no small or intermediate
• Seasonal changes in vegetation (e.g., frost kill) fuel nearby seldom burn unless they are decomposed. Seasonal
• Fire, meteorologic or insect and disease impacts (e.g., changes in the moisture content and live-to-dead ratio (e.g.,
preheated canopy or crown scorch; snow-, wind-, or ice- degree of curing in grasslands) of conifer tree foliage, shrubs,
damaged stands; drought-stressed vegetation; or mountain grasses, and other herbaceous plants can result in gradual
pine beetle–killed stands) changes in fuel flammability over the course of a fire season.153,281
Weather Wildland fire research has identified a wind speed threshold
PART 3
• Extended dry spell in fuel types with a discontinuous, combustible surface layer
• Drought conditions (e.g., caused by the presence of areas of bare, mineral soil).85,89
• High air temperatures In these discontinuous fuel types, fire spread is exceedingly
• Low relative humidity limited until a certain or threshold wind speed level is attained,
• Moderately strong, sustained winds and then the rate of advance can be quite unexpectedly rapid207
• Unstable atmosphere (visual indicators include gusty winds, dust (Figure 14-27). This type of situation could lead a person into a
devils, good visibility, and smoke rising straight up) false sense of security regarding fire potential, until unfortunately
• Towering cumulus clouds it is often too late.
• High, fast-moving clouds Various weather phenomena (e.g., wind, hail, snow, ice, frost)
• Battling or shifting winds and insect and disease epidemics can drastically elevate the flam-
• Sudden calm mability of a fuel complex, creating decidedly new fire safety
• Virga (i.e., a veil of rain beneath a cloud that does not reach the concerns.34 For example, on July 9, 1999, heavy rains and winds
ground) in excess of 145 km/hr (90 miles/hr) blew down about 181,000
Topography hectares (447,000 acres) of sub-boreal forest in northeastern Min-
• Steep slopes nesota, resulting in heavy, dead and downed, woody fuel loads.208
• South- and southwest-facing slopes in the northern hemisphere Weather. The greater the wind, the more rapid is the spread
• North- and northeast-facing slopes in the southern hemisphere of fire. Thunderstorm downdrafts and winds associated with dry,
• Gaps or saddles cold frontal passages can be especially hazardous.129,427 Low rela-
• Chutes, chimneys, and narrow or box canyons tive humidity and high ambient air temperatures decrease the
Fire Behavior moisture content of fine, dead fuels and thereby increase ignition
• Many fires that start simultaneously ease and rate of spread. Prolonged drought makes more medium
• Fire that smolders over a large area and heavy fuels, such as duff and deep organic layers, available
• Rolling and burning pine cones, agaves (a desert plant found in for combustion, leading to increased intensity levels. When fuels
the southwestern U.S.), logs, hot rocks, and other debris igniting reach critically dry levels, fires become very responsive to minor
fuel downslope changes in wind and slope. Fires tend to burn more vigorously
• Frequent spot fires developing and coalescing under unstable atmospheric conditions.
• Spot fires occurring out ahead of the main fire early on The North American continent has been classified into 15 fire
• Individual trees readily candling or torching out climate regions based on geographic and climatic factors427
• Fire whirls that cause spot fires and contribute to erratic burning (Figure 14-28). Major fire seasons, or periods of peak fire activity,
• Vigorous surface burning with flame lengths starting to exceed can be used to warn emergency medical personnel and wildland
1 to 2 m (3 to 6 feet) users of the most probable times for life-threatening situations.
• Sizable areas of trees or shrubs that begin to readily burn as a Exceptions occur. For example, rapidly spreading grass and
“wall of flame”
• Black or dark, massive smoke columns with rolling, boiling
forest fires can occur during the winter months in the northern
vertical development latitudes, as occurred in Alberta, Canada, on December 14, 1997,
• Lateral movement of fire near the base of a steep slope under Chinook conditions and no snow cover.223 A wildfire near
the town of Hinton in the mountainous region of the west-central
294
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.)
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
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
Inches
Inches
Inches
2 2 2 2 2
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
297
crowning is significant from both a safety and suppression per- ately at the head, or downwind side, of the fire, although
spective. At a minimum, when a fire crowns, the rate of spread medium- and long-distance spot fires can also pose an unex-
and intensity doubles, and the area burned quadruples.12 pected risk.5,69
Maclean284 gives an indication of how crown fires were Plume-Dominated or Convection-Dominated Crown
handled in the early part of the 20th century by the USDA Forest Fire. An alternative form of crown fire develops with relatively
Service: low wind speeds or when wind speed decreases with elevation
By the time they reached the fire, it had spread all over the map, and above the ground. This type of crown fire is referred to as plume
had jumped into the crowns of trees, and for a lot of years a prospective dominated or convection dominated because it is characterized
ranger taking his exam had said the last word on crown fires . . . When by a towering convection column that stands vertically over the
asked on his examination, “What do you do when a fire crowns?” he fire (Figure 14-33). This type of fire poses a unique threat to
had answered, “Get out of the way and pray like hell for rain.” people because it can produce spot fires in any direction around
its perimeter. It can also spread rapidly as the combustion rate
This wisdom seems still valid today. Rothermel417,419 described accelerates.
the conditions that produce a crown fire: One form of a plume-dominated crown fire that can be espe-
1. Dry fuels cially dangerous is when a downburst of wind blows outward
2. Low humidity and high temperatures near the ground from the bottom of the convective cell. These
3. Heavy accumulations of dead and downed fuels winds can be extremely strong226 and can greatly accelerate a
4. Small trees in the understory, or “ladder fuels” fire’s spread. This type of wind event occurred during the major
5. Steep slope run of the Dude Fire near Payson, Arizona, on June 26, 1990,
6. Strong winds when six firefighters were killed.216
7. Unstable atmosphere Some indicators help signal the onset of a downburst from a
8. Continuous crown layer plume-dominated crown fire. The surest indicator is the occur-
The two most prominent behavior patterns of crown fires are rence of precipitation of any amount, even a light sprinkle, or
BURNS, FIRE, AND RADIATION
wind driven and plume (or convection) dominated. Each type of the appearance of virga (evaporating rain) below the base of a
crown fire poses a distinct set of threats to people. Free-burning cloud formation.417,427 Another indicator is rapid development of
wildland fires are seldom uniform and well behaved, so these a strong convection column above the fire, or nearby thunder
descriptions of wind-driven and plume-dominated crown fire cells. A third and very short warning is the calm that develops
behavior may not be readily apparent. The behavior of these when the in-draft winds stop before the turnabout and outflow
types of fires can be expected to change rapidly as environmen- of wind from the cell. This brief period of calm may be accom-
tal, fuel, and topographic conditions change.417 panied by a humming sound just before the reversing wind flow
Wind-Driven Crown Fire. A running crown fire can arrives. If any of these indicators is present, the area should
develop when winds increase with increasing elevation above quickly be evacuated and a safe refuge area sought. The down-
the ground, driving flames from crown to crown (Figure 14-32). burst may also break or uproot trees, creating an additional
Steep slopes can produce the same effect. Spread rates in conifer hazard for people.417
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 Value of Fire Danger Ratings
especially in open forest or nonforested or shrubland fuel Forest fire control in the early days before organized protection
types.98,133 A running crown fire is accompanied by showers of was relatively simple. As Williams533 explains:
PART 3
Wind
1 2 3 3 2 1
Ignition
point
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
circumstance was the general feeling that, as it was late October, the fire
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
FIGURE 14-33 Cross-sectional view of a plume-dominated or
regularly. In the United States, statistics for wildland fire–related
convection-dominated crown fire. People are at risk around the com- serious injuries and deaths have now been maintained for several
plete perimeter of this type of fire, because it has the potential to decades and have provided useful data in developing protocols
spread intensely or spot in any direction around its perimeter with little for safe firefighting practices. The nature of these fatalities can
or no warning. This form of crown fire develops when wind velocities be broadly categorized as deaths directly by fire in burnover or
are relatively low or when velocities decrease with elevation above the entrapment situations and deaths resulting from fire suppression
ground coupled with critically dry and abundant fuel conditions. The activities.
convective plume associated with this type of fire may rise to 7600 to Most fatalities in wildland fire burnover situations occur on
9100 m (25,000 to 30,000 feet) above the ground. (Modified from days of extreme fire danger when people are exposed to abnor-
Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain mally high heat stress caused by weather or proximity to fires.
Press Publishing Co.) Loss of life is dramatically highlighted under extreme burning
conditions; however, many more people are injured than are
killed by fires.
specific plans for fire control action became an obvious necessity. To One of Australia’s worst bushfire disasters occurred on Febru-
form the basis for such plans, a reliable measure of the day-by-day state ary 7, 1967, when 62 people died in Tasmania.301,529 Analysis of
of forest flammability was needed. the locations and ages of 53 individuals at the time of death are
instructive (Tables 14-3 and 14-4). Most people whose bodies
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 *www.researchgate.net/profile/Domingos_Viegas/publication/229042984
or less uninterrupted since that time.22,83 _Comparative_study_of_various_methods_of_fire_danger_evaluation_in_
Fire management agencies employ fire danger rating systems Southern_Europe/links/0c96051a8bbd686302000000.pdf.
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 TABLE 14-3 Location of Bodies of 53 Persons Who
knowledge garnered from research.23,281,474 Such systems have Died in Tasmanian Fires, February 7, 1967
been demonstrated to be of value in accurately predicting fire
behavior in the WUI.10 In commenting on the historic fatality fires No. of
around the turn of the 20th century, Brown and Davis83 pointed Location Deaths
out that in general terms, these situations reflected the public’s
indifference to forest fires that had persisted for so many years Mustering stock 2
and still lingers to some degree today: Firefighting 11
Traveling in a vehicle 2
The Maine fires of 1947 were a sobering reminder in this respect. They Escaping from and found at some distance from houses 11
occurred at a time when fire danger measurement was well understood
Within a few meters of houses 10
and means for mass public dissemination of this information were well
In houses 17
developed. Responsible officials were aware of the mounting fire danger.
Nonetheless, some fifty fires were reported to have been burning in From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7
Maine at the time the major break occurred on October 23. A contributing February 1967, Hobart, Australia, 1967, Government Printer.
299
TABLE 14-4 Age Distribution of 53 Persons Who Died
with a “can-do” attitude who are willing to work through many
hardships that would cause workers in a general workforce to
in Tasmanian Fires, February 7, 1967 take time off for rest. Second, the vast majority of the care
happens informally either on the fire lines as work continues or
Age Group (yr) No. in Group Average Age (yr) at base camps at temporary, low-level medical facilities where
formal records are not maintained. Firefighters will often wait
1-25 1 23
until they leave a fire to seek treatment from a private provider
26-50 13 38 for an ongoing problem, and the injury or illness will not be
51-75 26 64 tracked as a workplace-related incident.
76-88 13 82 The U.S. Bureau of Land Management has guidelines outlining
From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7
the nature of burn injuries that require transport to and evaluation
February 1967, Hobart, Australia, 1967, Government Printer. 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-
were found within or near houses were old, infirm, or physically dent. Fire suppression crews frequently have one or two medics,
disabled. More than one-half of the houses vacated by the 11 usually trained to the Emergency Medical Technician (EMT)–
people who traveled some distance before being killed were not Basic level, among their members. The skill set of these medics
burned. Most of these victims would probably have survived if depends on whether they are active, professional medical provid-
they had remained in their homes. Most of the 11 firefighters ers when they are not fighting wildland fires, or if they maintain
who died were inexperienced. Many might have survived if they the certification solely for the position on the crew. Larger inci-
had observed fire behavior and safety rules. dents may employ additional medical personnel to survey per-
Krusel and Petris259 investigated the circumstances surround- sonnel on the fire lines or at portable medical tents/trailers in
BURNS, FIRE, AND RADIATION
ing the 32 civilian deaths that occurred during the 1983 Ash the base camp. Midlevel providers, such as paramedics, nurse
Wednesday bushfires in Victoria. As a result, they identified three practitioners, and physician’s assistants, usually staff these facili-
categories of victims, suggesting ways to address the deficiencies ties. The availability of a medical command physician varies by
in the manner in which individuals respond to the wildfire threat: region in the United States.
• Victims who recognized the real threat to their safety with When a firefighter requires evaluation and care outside the
enough time to save their lives, but chose an ineffective sur- scope of first responders, the patient must be transported from
vival strategy the incident. The nature of the problem dictates if this transport
• Victims who did not recognize the real threat to their safety requires specialized care at a trauma or burn center or if the local
in time to implement an effective survival strategy hospital closest to the incident can provide care. When large fires
• Victims who were physically incapable of implementing an require hundreds to thousands of personnel, a small local hos-
effective survival strategy pital in a rural area may be overburdened by the temporary
Similar situations have been reported around the world. For additional population. Transport protocols are determined on a
example, during the 1993 fire season in the Tarragona Province regional basis and may use ground ambulances or air medical
of eastern Spain, five people were killed trying to escape from service (via rotary- or fixed-wing aircraft) depending on the
their home, built in the woods and surrounded by a fire; four of nature of the incident and availability of resources.
PART 3
the victims were older adults who dared not flee until it was
impossible to escape.505 COMMON DENOMINATORS OF FIRE BEHAVIOR
In 2007 the National Wildfire Coordinating Group published
an analysis of 310 wildland firefighter fatalities that occurred in
ON FATALITY FIRES
the United States from 1990 to 2006.295 During this 17-year period, A review of wildland firefighter fatality records between 1926
burnover situations constituted only the fourth most common and 1976 shows that 145 men died in 41 fires from fire-induced
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 BOX 14-5 21st-Century Common Denominators for
(22.9%) were caused by vehicle accidents, and 64 wildland fire- Wildland Fire Fatalities
fighters (21.9%) died from heart attacks. The remaining percent-
ages were classified as deaths resulting from falling trees, snags, More than 20% of fatalities during wildand firefighting operations
or rocks (3.9%), other medical causes (2.9%), and miscellaneous continue to concur in burnovers and entrapments. Carl Wilson’s
causes (4.5%). Thus, the three leading causes of deaths related original common denominators536 are just as important in the 21st
to wildland firefighting activity were not the result of individuals as they were in the 20th century. However, as the major causes of
being burned over or entrapped by a wildland fire, although five firefighter fatalities shift, it has suggested that additional factors
need to be considered:
firefighters were killed at a single location on the 2006 Esperanza
• Firefighters are most likely to die in an aircraft accident. Before
fire in southern California.500 Reports for 2007-2009, in which 49 every flight, fire managers must ask, “Is this flight essential?”
wildland firefighters died, showed similar trends.297 Interventions and “Is everyone onboard essential to the mission?”
are possible to reduce the number of firefighter fatalities associ- • Firefighters are nearly as likely to die in a motor vehicle accident
ated with aircraft and vehicle accidents, as well as those linked as in an aircraft accident. Driving too fast for the conditions,
to heart attacks292,296 (Box 14-5). failure to wear seat belts, rushing to a fire, and driving home
There have been more than 160 wildland fire suppression– while exhausted from firefighting kills firefighters.
related fatalities in Canada during the 70-year period between • Firefighters can reduce their risk for dying from heart attack on
1941 and 2010.25 The names of many of these wildland firefight- the job by staying fit, maintaining their ideal body weight, and
ers are listed, along with their structural brethren, on the Cana- having regular medical checkups.
dian Fallen Firefighters Foundation website (www.cfff.ca/EN/ • Unexpected events such as falling snags, rolling rocks, downed
index.html). Although the causes for all these firefighter fatalities power lines, and lightning strikes cause more than 8% of
are not precisely known, certainly aircraft-related fatalities have fatalities during wildland firefighting operations. Firefighters and
been far more common in recent decades compared with earlier fire managers can reduce fatalities by learning to expect these
years of recordkeeping. unexpected events.
It is much more difficult to gather accurate information regard- Modified from Mangan R: Wildland firefighter fatalities in the U.S.: 1990-2006,
ing the incidence of minor to moderate injuries and episodes of National Fire Equipment System Publication PMS 841, Boise, Idaho, 2007,
illness among wildland firefighters. These statistics do not exist National Interagency Fire Center, National Wildfire Coordinating Group, Safety
for several reasons. First, in general, the field draws individuals and Health Working Team.
300
injuries.353,354,536 Besides the 1949 Mann Gulch and 1990 Dude
Number of deaths
California (29 deaths and 150 others injured),182 the Blackwater 30
Fire in Wyoming in 1937 (15 deaths),78 the Pepper Hill Fire in
Pennsylvania in 1938 (8 deaths),429 the Hauser Canyon fire 20
in California in 1943 (11 deaths),114,446 the Rattlesnake Fire in
California in 1953 (15 deaths),287 the 1956 Inaja Fire in California 10
(11 deaths),428,492 the 1966 Loop Fire in California (12 deaths),148
0
and the 1968 Canyon Fire in California (8 deaths).154 Wilson’s
review536 of people killed by wildfires in areas protected by other
90
91
92
93
94
95
96
97
98
federal, state, county, and private agencies indicated 77 fire-
19
19
19
19
19
19
19
19
19
induced fatalities in 26 fires during this same time period. The Year
United States is not the only country to have had firefighters
killed by entrapments and burnovers. For example, 25 soldiers FIGURE 14-34 Annual death toll for persons who died from all causes
were killed while involved in wildland firefighting operations while involved in fighting wildland fires in the United States from 1990
near Lisbon, Portugal, on September 6, 1966.245 Australia has to 1998 (133 total deaths). (From Mangan R: Wildland fire fatalities in
experienced a number of firefighter fatality incidents.119,245 For the U.S.: 1990-1998, Technical Report 9751-2817-MTDC, Missoula,
example, on December 2, 1998, five volunteer firefighters were Mont, 1999, USDA Forest Service, Missoula Technology and Develop-
killed near the town of Linton, Victoria, when the tanker they ment Center.)
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: for example, from thunderstorm downdraft winds,129,427 a change
1. Most of the incidents occurred on relatively small fires or in fuel types,53 fire whirl development as the fire reaches a ridge-
isolated sectors of larger fires. line with an opposing gradient wind,150 or a “slope reversal” (e.g.,
2. Most of the fires were innocent in appearance prior to the fire slowly backs down a northerly aspect, crosses the drainage,
“flare-ups” or “blow-ups.” In some cases, the fatalities occurred and then rapidly spreads up the south-facing slope),402 such as
in the “mop-up” stage. documented with time-lapse photography on the 1979 Ship
3. Flare-ups occurred in deceptively light fuels. Island fire in central Idaho.350 As the moisture content of dead
4. Fires ran uphill in chimneys, gullies, or on steep slopes. and live fuels decreases, fires become increasingly more respon-
5. Suppression tools, such as helicopters or air tankers, can sive to slight changes in wind strength and slope steepness. Once
adversely modify fire behavior (helicopter and air tanker vor- “critically” dry levels are reached, fire behavior becomes exceed-
tices have been known to cause flare-ups). ingly unstable.29,88,281
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
NATURE OF INJURIES AND FATALITIES
was relatively quiet just before the incident, even in the cases Fire-related injuries and fatalities are a direct consequence of
involving aircraft.154,168,225 Many have been led to believe that it heat, flames, smoke, critical gas levels, or indirect injuries293,330
is the conflagration or large, high-intensity crown fire in timber (Figure 14-34). Injuries and fatalities associated with wildland
and heavy brush that traps and kills firefighters. With some fires fall into one of these five categories:
exceptions, however, most fires were innocuous appearing just 1. Heat: direct thermal injury, inhalation, and heat stress
before the fatal moment. Case studies of wildland firefighter disorders
fatality incidents from other regions of the world suggest similar 2. Flames: direct thermal injury and inhalation
patterns and circumstances, for example, the 25 fatalities at 3. Smoke: inhalation and mucous membrane irritation
Puerto Madryn, Argentina, on January 21, 1994;171 10 fatalities in 4. Critical gas levels: oxygen and carbon monoxide (CO)
the Sabie district of the Mpumalanga Province of South Africa in 5. Indirect effects: acute and chronic medical disability and
1994;172 and five fatalities associated with three different incidents trauma
in Portugal during the 1999 and 2000 fire seasons.508 Wildland Intense fires that produce very high temperatures are gener-
firefighter fatalities have been reported in Italy, Spain, Portugal, ally brief. The duration of intense heat increases with fuel load,
and Croatia in the last decade.507,511 being greater in a forest fire where heavy fuels471 are burning
Wilson536 concluded that the hairline difference between fatal than in a grass129 or shrub fire (see Table 14-2). Temperatures
fires and near-fatal fires was determined by the individual’s reac- near the ground are lower because radiant heat is offset some-
tion to a suddenly critical situation. Escapes were the result of what by inflow of fresh air, and gases of combustion rise and
luck, circumstances, advance planning, a person’s ability to avoid are carried away by convection.118 Close to the ground, within a
panic, or a combination of these factors. Frequently, poor visibil- few meters of flames reaching up to 11 m (36 feet), air tempera-
ity and absence of concise fire information threatened survival tures may be less than 15° C (59° F) above ambient levels. The
opportunities by creating confusion and panic. For many years, breathing of heated air can be tolerated for 30 minutes at 93° C
Wilson’s findings were summarized in a popular booklet, pub- (199° F) and for 3 minutes at 250° C (482° F).281 Death or severe
lished initially by the USDA Forest Service and in later years by pulmonary injury occurs when these limits are exceeded. Thermal
the National Wildfire Coordinating Group.352 Beginning in 2010, injuries of the respiratory tract frequently contribute to the clinical
this information has now been incorporated into the Incident picture of smoke inhalation. People trapped in a fire may have
Response Pocket Guide, published by the U.S. National Wildfire no choice but to breathe flame or very hot gases. This usually
Coordinating Group.360 injures the tissues of the upper airway and respiratory tract, most
The British Columbia Forest Service found many of the same often the nose, nasopharynx, mouth, oropharynx, hypopharynx,
factors identified by Wilson in their investigation of a number of larynx, and upper trachea. These injuries may result in edema
close calls or near misses that occurred during the 1994 fire that obstructs the airway and produces asphyxia or that causes
season.53 The few wildland firefighter fatalities in Canada caused tracheitis and mediastinitis.
by entrapments or burnovers37,480 are also in alignment with Wil- Signs of thermal injury to the airway include thermal injuries
son’s findings.64 to the head, face, and neck; singed facial hair; burns of the nasal,
Most fatality fires are the result of a temporary escalation in oral, or pharyngeal mucosa; and stridor or dysphonia.326,467,548
fire spread, an increase in flame dimensions, crowning and spot- Associated with a history of exposure to flame and hot gases in
ting activity, or the development of large fire whirls, often occur- a closed space, these clinical findings strongly suggest the pres-
ring suddenly and with very little warning. A gentle surface fire ence of a thermal injury to the airway. With the potential for
will rapidly develop into a high-intensity fire. This could result, 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
pharyngitis and vomiting. Keratitis, conjunctivitis, and chemosis Service; photo by J.B. Halm.)
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 Safety and Health (NIOSH): 35 ppm over an 8-hour period.483
space associated with wildland fires usually contributes to con- However, more recent measurements of CO levels and particu-
tinual mixing of air. Misconceptions or myths about lack of lates made on wildfires between 1992 and 1995408 indicate that
oxygen or excessive CO and CO2 in a wildland fire abound in wildland firefighters are seldom exposed to smoke that exceeds
the popular literature.129 U.S. Occupational Safety and Health Administration (OSHA) per-
Flaming combustion can be maintained only at oxygen levels missible exposure limits.409
that exceed 12%, a level at which life can also be supported.118,281 Decreased ambient oxygen may contribute to hypoxia and
With continued in-drafts of air that feed the flames, a fresh the overall picture of smoke inhalation (Table 14-5). This mecha-
source of oxygen is usually present. Even mass fires, in which nism is at least variably operant. When standing gasoline was
large tracts of land are burning, rarely reduce oxygen to hazard- ignited in a closed bunker, the fire self-extinguished, whereas
ous levels. Low oxygen levels may occur, however, where there the ambient oxygen level remained at 14%, a survivable level.324
is little air movement, such as in caves or mine shafts (Figure Injecting burning gasoline or napalm into bunkers produced
14-35) or in burned-over land that continues to smoke from nearly complete and prolonged exhaustion of ambient oxygen.
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 TABLE 14-5 Human Response to Decreased Ambient
because of air movement. High CO concentrations appear to be Oxygen at Sea Level
associated with smoldering combustion of heavy fuels, such as
accumulations of fallen tree stems or of slash piles, and CO Ambient
may also collect in low-lying areas or underground shelters (e.g., Oxygen
root cellars).120 Outdoors, the danger lies in continual exposure (%) Human Response
to low concentrations that can increase blood carboxyhemoglo-
bin levels. Prolonged exposure affects the central nervous system, 20.9 Normal function
resulting in headache, impaired judgment, progressive lethargy, 16-18 Decreased stamina and capacity for work
decreased vision, and other psychomotor deficits.536 12-15 Dyspnea with walking; impaired coordination; variable
Carbon monoxide levels of 50 ppm were measured close to impaired judgment
a prescribed burn in grass.149 In another estimate, CO concentra- 10-12 Dyspnea at rest; consciousness preserved; impaired
tions of 30 ppm were found about 61 m (200 feet) from the fire judgment, coordination, and concentration
front. Studies on the 1974 Deadline and Outlaw forest fires in 6-8 Loss of consciousness; death without prompt reversal
Idaho showed that firefighters were exposed to CO levels above <6 Death in 6 to 10 minutes
the standards proposed by the National Institute of Occupational
302
Conflicting data make it difficult to classify definitively situations options can be exercised. One of these studies suggested that
303
sparse, either for analysis of short-term outbreak situations or
long-term health and wellness.
Lookout(s) Hazard
ing the threat posed by fire-line hazards and determining the best Harry Luke and Alan McArthur281 state in their seminal reference
course of action to follow (Figure 14-36). book Bushfires in Australia, fire suppression “must at all times
Some fire management agencies have added an “A” to LCES, start from an anchor point.”
thus LACES, for a variety of meanings—attitude, awareness, and The wildland fire environment’s basic hazards are lightning,
anchor points.262,479 The Australasian Fire Authorities Council, for 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.
BOX 14-6 Ten Standard Firefighting Orders Adapted
LCES should be viewed from a “systems” point of view, stress-
for the General Public ing their interdependence. For example, the best safety zone is
worthless if the escape route does not offer access at the point
1. Keep informed of fire weather conditions, changes, and of need. People must be familiar with the LCES plan well before
forecasts and how they may affect the area where you are
it is needed. In addition, the nature of wildland fires dictates that
located.
2. Know what the fire is doing at all times through personal
LCES be redefined in pace with changing conditions. The LCES
observations, communication systems, or scouts. wildland fire safety system is implemented as follows:
3. Base all actions on current and expected behavior of the fire. Lookout(s): Fixed lookouts or roving lookouts must be where
4. Determine escape routes and plans for everyone at risk, and both the hazard and the people can be seen. A lookout is
make certain that everyone understands routes and plans. trained to observe the wildland fire environment and to rec-
5. Post lookouts to watch the fire if you think there is any danger ognize and anticipate changes in fire behavior. When the
of being trapped, of increased fire activity, or of erratic fire hazard becomes a potential threat or danger, the lookout
behavior. relays this information so people can depart for the safety
6. Be alert, keep calm, think clearly, and act decisively to avoid zone.
panic reactions. Communication(s): Communication refers to alerting people to
7. Maintain prompt and clear communication with your group, the approaching or pending hazard. Promptness and clarity
firefighting forces, and command and communication centers. are essential.
8. Give clear, concise instructions, and be sure that they are Escape routes: These paths lead from a currently threatened posi-
understood. tion to an area free from danger. More than one escape route
9. Maintain control of the people in your group at all times. must be available. Escape routes are probably the most elusive
10. Fight fire aggressively, but provide for safety first. component of LCES because they change continuously. Timely
(Nonqualified or untrained and improperly dressed or access to safety zones is the most important component.66
equipped persons should engage in firefighting operations Research on wildland firefighter travel rates28,60,102,424 suggests
only when it is absolutely necessary to assist injured persons.
that, although civilians could momentarily advance at a rate
Wildland firefighting is a physically demanding task and
should not be attempted by persons who are not in good
in excess of what most wildland fires are capable of achieving,
physical condition.) even the most fit individuals would not be able to sustain
such a pace for more than a few minutes before being burned
304
over by an advancing fire, especially on steep slopes— Territories,18,463 one of the authors (MEA) was able to informally
305
dangerous because of proximity to intense heat, smoke, and Vehicles
flames, along with limited escape opportunities. Wildland firefighters have survived severe fire storms or the
10. Spot fires occur frequently across the fire line. Generally, passage of fire fronts by taking refuge in vehicles.291,302,375,376
increased spotting indicates increased fire activity and inten- Unfortunately, there are reported cases where civilians would
sity. The danger is that of entrapment between coalescing have survived or avoided serious injury had they remained in
fires. their vehicles.245,372 Bereska68 has indicated that he and two
11. The main fire cannot be seen, and you are not in commu- others were forced to drive a 3 4 -ton Dodge 4 × 4 truck at a mod-
nication with anyone who can see it. If you do not know erate speed (25 to 30 km/hr [16 to 19 miles/hr]) through the
the location, size, and behavior of the main fire, planning flame front of a grass fire during a prescribed burning operation
becomes guesswork, which is an unfavorable response. in north-central Alberta in early April 1980. Winds at the time of
12. An unclear assignment or confusing instructions have been the incident were light (<12 km/hr [7 miles/hr]), and the flames,
received. Make sure that all assignments and instructions are although high (3 to 4 m [10 to 13 feet]), were not deep (1 to 2 m
fully understood. [3 to 7 feet]). “It got very hot instantly and as we came out of
13. You are drowsy and feel like resting or sleeping near the the flames we opened the windows and appreciated the cool
fire line in unburned fuel. This may lead to fire entrapment. fresh air.”68
No one should sleep near a wildland fire. If resting is abso- The following three U.S. case histories serve as examples of
lutely necessary, choose a burned area that is safe from intense burning situations where lives were saved because
rolling material, smoke, reburn, and other dangers, or seek people stayed inside vehicles while the fire front passed by their
a wide area of bare ground or rock. location.449
14. Fire has not been scouted and sized up. • In 1958, a veteran field section fire warden and two young
15. Safety zones and escape routes have not been identified. men were fighting forest fires that burned in heavy fuels near
16. You are uninformed on strategy, tactics, and hazards. the Bass River State Forest in southern New Jersey. A 90-degree
17. No communication link with crew members or supervisors wind shift transformed the flank fire into a broad head fire,
BURNS, FIRE, AND RADIATION
has been established. with the advancing flames reaching up to 12 m (40 feet) in
18. A line has been constructed without a safe anchor point. height. The men entered their vehicle, a Dodge W300 Power
Each of these situations has come about as a result of one or Wagon, which stood in the middle of a 4-m (13-foot)–wide
more wildland firefighter fatalities (http://wlfalwaysremember. sand road. Simultaneously, the engine and radio failed. The
org). Artwork has been developed to help illustrate or visualize fire warden repeatedly admonished the crewmen, who wanted
the 10 standard fire orders and 18 “Watch Out!” situations.331 to flee, to stay in the truck. Subsequently, the truck was
rocked violently by convection currents and microclimatic
FIFTEEN STRUCTURAL “WATCH changes generated by the flames. The men could neither see
OUT!” SITUATIONS FOR THE nor breathe because of smoke, and the cab began to fill with
sparks that ignited the seat. The men stayed with the truck
WILDLAND-URBAN INTERFACE for only 3 or 4 minutes during passage of the head fire, but
Continuing development creates ever more WUI area; therefore, they indicated later that the interval involved seemed more
fires are tending to occur more often in that interface. These 15 like 3 or 4 hours. At the first opportunity, all of them left the
structural “Watch Out!” situations have been defined to increase vehicle on the upwind side and crouched beside it to escape
awareness of structural fire dangers484: the searing heat and burning seats. The warden proceeded to
PART 3
1. Access is poor (e.g., narrow roads, twisting, single lane with burn his hand severely while disposing of a flaming gas can
inadequate turning). located in the truck bed. Although the young men escaped
2. Load limits of local bridges are light or unknown; the bridges virtually unscathed, the older man suffered lung damage and
are narrow. remained on limited duty for 5 years. He eventually recovered
3. Winds are strong, and erratic fire behavior is occurring. completely and subsequently retired.
4. The area contains garages with closed, locked doors. • In a 1962 California Division of Forestry fire in Fresno County,
5. You have an inadequate water supply to attack the fire. three men, followed by a flank fire that had turned into a
6. Structure windows are black or smoked over. head fire, raced back to their truck only a few feet ahead of
7. There are septic tanks and leach lines. These are found in the flames. The truck would not restart. After the main body
most rural situations. of flames passed over the vehicle, the men jumped out to
8. A house or structure is burning with puffing rather than breathe because the truck was burning. Almost completely
steady smoke. blinded by smoke and heat, they stumbled headlong into
9. Inside and outside construction of structures is wood with matted fuels, and two received first- and second-degree burns.
shake-shingle roofs. One man was not burned but had to be treated for smoke
10. Natural fuels occur within 9 m (30 feet) of the structures. inhalation. The truck was a loss.
11. Known or suspected panicked individuals are in the • In 1976 a firefighter died while fighting a grass fire near the
vicinity. town of Buhler in Reno County, Kansas. A flashover occurred
12. Structure windows are bulging, and the roof has not been from buildup of gases on the lee side of a windbreak. A fire
vented. truck was caught in the flashover, and the firefighter working
13. Additional fuels can be found in open crawl spaces beneath from the back of the vehicle ran and was killed. Although the
the structures. truck burned, the driver was not seriously hurt.
14. Firefighting is taking place in or near chimney or canyon Sitting in a vehicle during a passing fire front is often perilous,
situations. but when a person is trapped, it is almost certain doom to attempt
15. Elevated fuel or propane tanks are present. escape by running from the fire. The preceding case histories
These are also known as the “Wildland-Urban Watch illustrate the following facts about vehicles and fire, which, if
Outs!”360 remembered, may prevent panic-like reactions:
1. The engine may stall and not restart.
TAKING REFUGE IN VEHICLES, BUILDINGS, 2. The vehicle may be rocked by convection currents.
AND PROTECTIVE FIRE SHELTERS USED BY 3. Smoke and sparks may enter the cab.
4. The interior, engine, or tires may ignite. (Tires exploded
WILDLAND FIREFIGHTERS during the Crank Fire burnover in California in August 1987
The radiant energy of a fire, although highly intense at a given involving several wildland fire engines.348 This is obviously
location, typically lasts for only a short time. Because radiant heat unsettling in an already stressful situation that could lead to
travels in straight lines, does not penetrate solid substances, and panic-like reactions.)
is easily reflected, seeking refuge in vehicles, buildings, or pro- 5. Temperatures increase inside the cab because heat is radiated
tective fire shelters should be viewed as a lifesaving solution. through the windows.
306
6. Metal gas tanks and containers rarely explode.
307
left their houses as fire approached. All died, and some were be to retreat to a room with an exit door that opens onto a
within a few meters of the buildings. Many houses did not burn region with little fuel. Turn on a light in each room to make
and would have served as safe refuges. the house more visible in heavy smoke. Have a backup plan
When taking refuge in a building, give people useful jobs, for when the electricity supply fails by having flashlights
such as filling vessels with water, blocking cracks with wet blan- handy.
kets, and tightly closing windows and doors. If possible, assign • Turn off the main gas supply to stoves and furnaces.
lookouts to keep watch for spot fires on and within the building • If you have time, take down drapes and curtains. Close all
throughout the fire event. Venetian blinds or noncombustible window coverings to
Before fire approaches the house, plan to have taken the fol- reduce the amount of heat radiating into the house. This
lowing precautions269,449: provides added safety in case the windows give way because
• If you plan to stay, evacuate your pets and livestock and all of heat or wind.
family members not essential to protecting the home well in • As the fire front approaches, go inside the house. Stay calm;
advance of the fire’s arrival. you are in control of the situation. Continually move around
• Be properly dressed to survive the fire. Wear long pants and inside the house, monitoring its state and the progress of the
leather boots, and carry for protection a long-sleeved shirt or fire outside. Avoid spending time in the areas that have only
jacket made of cotton fabrics or wool. Synthetics should not one way of exiting the space. If practical, include monitoring
be worn because they can ignite and melt. Wear a hat that can of the roof cavity. Goggles will prove handy in dealing with
offer protection against radiation to the face, ears, and neck any smoke that enters the house.
areas. Wear leather or natural-fiber gloves, and have a hand- • After the fire passes, check the roof immediately. Extinguish
kerchief handy to shield the face, water to wet it, and safety any sparks or embers. Then check the attic for hidden burning
goggles, if possible. sparks. If you have a fire, enlist your neighbors to help fight
• Remove combustible items from around the house, including it. For several hours after the fire, recheck for smoke and
lawn and poolside furniture, umbrellas, and tarp coverings. If sparks throughout the house.
BURNS, FIRE, AND RADIATION
they catch fire, the added heat could ignite the house. It is worth noting the research in this area by the Australian
• Ensure that anything that might be tossed around by strong Bushfire Cooperative Research Centre is continuing under Project
fire-induced winds is secured (e.g., sheet metal, lumber, D1—Building and Occupant Protection under the leadership of
plywood). Justin Leonard, CSIRO Land and Water.
• Ensure that the areas around any external propane tanks are If a person expects to take refuge in his or her home and in
fuel free for a considerable distance. Ensure that the tanks are turn survive to ensure its defense, it is critical that steps are taken
properly restrained and the pressure relief value is directed to reduce the ignition potential of the structure as much as pos-
away from buildings and access ways. sible. Recent research on home ignition involving field experi-
• Close outside attic, eave, and basement vents to eliminate the ments, coupled with modeling and observations of recent WUI
possibility of sparks blowing into hidden areas within the fire incidents, has provided valuable new insights into the means
house. Close window shutters. of ensuring home survival.134,135,137 The research has shown that
• Place large plastic trash cans or buckets around the outside the characteristics of the home (e.g., exterior building materials)
of the house and fill them with water. Soak burlap sacks, small and in an area referred to as the “home ignition zone” located
rugs, and large rags to use in beating out burning embers or within 30 to 60 m (100 to 200 feet) of the home (e.g., surface
small fires. Inside the house, fill bathtubs, sinks, and other fuel accumulations immediately adjacent to the structure that
PART 3
containers with water. Toilet tanks and water heaters are an would be receptive to ignition by airborne firebrands) principally
important water reservoir. determines its ignition potential and thus its survivability during
• Place garden hoses so that they will reach any place on the exposure to a wildland fire (Figure 14-37); videos that summarize
house. Use the spray gun type of nozzle, adjusted to spray. this research are available from Firewise Communities.136,193,194 For
Avoid laying the hose over or adjacent to combustible example, a home could have little or no natural surface fuel
objects. within the immediate vicinity of the dwelling, but because cedar
• If you have portable gasoline-powered pumps to take water shake shingles were used in the roof construction, it is vulnerable
from a swimming pool or tank, make sure they are operat- to ignition from airborne embers or firebrands from an approach-
ing in place and well protected from nearby combustible ing wildfire. If such a burning structure is not handled soon after
elements. ignition, it can contribute to the demise of neighboring houses
• Place a ladder against the roof of the house opposite the side if left unattended,328 or push the limits of fire protection to keep
of the approaching fire. If you have a combustible roof, wet up effectively if too many structures become involved.138
it down or turn on any roof sprinklers. Turn on any special The use of external sprinkler systems on a home146,363,453
fire sprinklers installed to add protection. Do not waste water. should not be viewed as a panacea for a lack of fuel treatment
Waste can drain the entire water system quickly. Where pos- in the home ignition zone and beyond or the use of flammable
sible, divert water from gutters back into the firefighting building materials. There is a perception that sprinklers should
supply. be capable of providing thermal protection from a high-intensity
• Back your car into the garage, and roll up the car windows. wildfire assault when in fact their real value is in preventing
Disconnect the automatic garage door opener (otherwise, in ignitions from airborne firebrands,318 direct flame contact, and
case of power failure, you cannot remove the car). Close all radiation. The FPInnovations–Feric Wildland Fire Operations
garage doors, and seal them with wet rags where possible. Research Group has been engaged in a number of research
Avoid storing combustible elements in a garage that cannot studies related to the use of sprinkler systems for home and cabin
adequately be sealed from ember attack. protection since 2002, including outdoor field trials, using simu-
• Place valuable papers and mementos inside the car in the lated structures, involving both prescribed and experimental
garage for later departure following passage of the fire, when fires.513,514 The group’s leader, Ray Ault,46 maintains that the great-
it is safe and may become necessary to do so. In addition, est use of commercially available Rain Bird types of sprinklers
place all pets in the car. and small portable pumps for individual home structure protec-
• Close windows and doors to the house to prevent sparks from tion is in applying water in sufficient quantities and locations to
blowing inside. Close the damper on the fireplace to prevent inhibit external ignitions from airborne firebrands by an approach-
smoke and embers from entering the house. Leave the doors ing or passing wildfire well in advance. If the presoaking or
inside the house open. This will enable occupants to remain application of water for wetting down fuels is applied for too
vigilant throughout the exposure. If a room or area in the long, it can lead to other problems (e.g., flooded basements).
house ignites and develops beyond the occupants’ ability to Irrigation systems have also been occasionally applied to the
contain it, doors can be closed in the house to manage smoke task of WUI protection. Other, more elaborate systems have been
spread. Begin to plan an exit to the outside, bearing in mind devised. For example, the Saskatchewan Fire Management and
the state of the fire outside the house. The approach should Forest Protection Branch has successfully adapted and applied
308
CHAPTER 14 Wildland Fires: Dangers and Survival
Home destruction
Yes No
Yes
High-intensity wildfire
Expected Not expected
No
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 they could be handled only with gloves. After leaving the shel-
task of creating wet “breaks or belts” in values protection or to ters, some firefighters showed symptoms of possible carbon
facilitate backfiring or burnout operations.260 monoxide poisoning, including vomiting, disorientation, and dif-
ficulty breathing. Emergency medical technicians administered
PROTECTIVE FIRE SHELTERS USED BY oxygen to several individuals before evacuation from the site
after the incident. Five firefighters were hospitalized overnight
WILDLAND FIREFIGHTERS for heat exhaustion, smoke inhalation, and dehydration. The
The concept of a protective fire shelter for wildland firefighters consensus of those interviewed was that without the shelters,
described earlier (see Figure 14-19) was originally conceived by none would have survived.347
Australian bushfire researchers in the late 1950s.256,281 The USDA It should be emphasized that the fire shelter was intended to
Forest Service equipment development center in Missoula, be used as a last resort when it became impossible to escape to
Montana (now the MTDC) initiated research and development of a safety zone before being overrun by a fire. However, despite
protective fire shelters about the same time as the Australians,493 the emphasis placed on this basic tenet and extensive training
and this work has continued to this day,104,394 with a view to in entrapment avoidance over the years,320,322,349,355,480 the results
reducing the number of serious burn injuries and fatalities among from a study of possible risk taking as a consequence of being
firefighters who become entrapped while fighting wildland provided with fire shelters77 suggest a possible link to what has
fires.42 Shelters designed in the shape of a pup tent protect the been suspected for many years—that some firefighters are likely
firefighter by reflecting radiant heat. Constructed of an aluminum- to engage in behavior that neutralizes the gain in safety afforded
foil and fiberglass cloth laminate, the shelter reflects about 95% by fire shelters. In other words, fire shelters can lead to additional
of the radiant heat emanating from a fire. These shelters were risk taking426 or what’s called “risk homeostasis.”210
never designed for direct flame contact. Fire shelters were first Putnam392 maintains that “you are always better with a fire
introduced operationally on the wildland fire scene in the United shelter in an entrapment situation than not.” This seems fair
States in the mid- to late 1960s and became a required PPE item advice. Fire shelters are, after all, relatively light to carry—the
for federal wildland firefighters in 1977. More than 1200 U.S. current model weighs 1.9 to 2.2 kg (4.2 to 4.8 lb), depending on
wildland firefighters have deployed their fire shelters to date (up the size43,381—and a minor inconvenience. Even when fire shelters
to and including the 2010 fire season).384 The fire shelter is cred- become compromised, they still provide some protection. One
ited with having saved the lives of more than 320 firefighters and of the entrapment survivors of the 1990 Dude Fire, Dave LaTour,
preventing at least 315 serious burn injuries,384 although it is not deployed his fire shelter before the arrival of the fire front and
known with any degree of certainty how many would have actu- stayed under his shelter even after a hole was kicked in it by
ally survived and suffered no burn injuries without the fire one of the firefighters who got out of his shelter and attempted
shelter. Some personal accounts of fire shelter deployments have to evade the flames.357 This allowed hot gases to enter his shelter.
been published116,411 (Box 14-8). Despite this development, LaTour stayed down on the ground
Why protective fire shelters work well was demonstrated as flat as possible. He did sustain some burn injuries but fully
dramatically on August 29, 1985, when 73 firefighters were forced recovered. LaTour was able to concentrate his attention on his
to take refuge in their shelters for about 1.5 hours following family to help him through the ordeal of being burned over by
passage of a high-intensity, active crown fire that swept over and the passage of a high-intensity flame front.
around their location.8,340,421 The incident took place during the Alexander11 believes that the main issue regarding use of
Butte Fire in the Salmon National Forest in central Idaho. Observ- shelters, beside not knowing what constitutes an adequate
ers described the crown fire that overran the firefighters as a clearing size for a shelter deployment in a particular situation,258
standing wall of flame that reached about 60 m (about 200 feet) is the time taken for their efficient deployment.67 In trying to
above the treetops. Within the shelters, firefighters experienced avoid a wildland fire entrapment or burnover, seconds can
extreme heat for as long as 10 minutes. Shelters were so hot that 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?
The Shelley fire was started by lightning on June 16, 1989 but I the radiant heat from the shelters and I was really glad that we had
didn’t visit the fire site until June 23. I initially went out to the Sheep them. There were many comments about being done on one side
Corral area toward Goose Lake to photograph the slurry bombers and “could we turn over to the other?”
dropping fire retardant but decided to return the next day and get The fire finally moved on down the canyon, but we stayed in the
on the line. Jim Turner from the Shasta Ranger District in California shelters for an hour it seems. Finally we stuck our heads out to a
was assigned to go with me and we headed up to the Snow Creek smoke-filled environment where it was difficult to see more than 10
spike camp being manned by the local National Guard. The troops feet. I continued to take photographs as I thought folks wouldn’t
had a water tender and some miscellaneous stores with which to really believe it if I just told them about this. A few of the crew were
resupply the firefighters. We left our vehicle at the spike camp and having some respiratory problems, but everyone was mobile. The
headed down the fireline in a northeasterly direction. The fire had cubitainers had been stripped of their cardboard casings and cases
been turned over to a Class I Incident Command Team and an of MREs (meals ready to eat) were burnt to the ground. The handles
infrared imaging aircraft had been brought in to determine the on the fire tools were history, but the chainsaws and fuel bottles
location of hotspots. There was major concern down the valley near were intact.
Lake Roberts about the many structures that could conceivably be The deployment zone was still smoldering. I’m amazed how small
in the path of the fire if the current fire suppression efforts were to it felt during the peak period of fire activity. Our shelters were fairly
fail. I photographed many of the hotshot crew members as they well spent and we tossed them into a pile—an unwise decision if we
built fireline and felled snags near the line. It is hot, dirty work, had had to deploy later again that day—and we headed down to
especially when air temperatures are already high and there is little the spike camp.
or no humidity. General observation: cool heads keep a situation from escalation.
formalized training program, carried out under realistic environ- EMERGENCY PROCEDURES DURING A WILDLAND
mental conditions, the precious time taken to deploy a shelter
might be better spent attempting to evade the fire’s encroachment
FIRE ENTRAPMENT OR BURNOVER
on one’s position to reach a safer location.11 The danger of being entrapped or burned over and possibly
The British Columbia Forest Service is the only Canadian fire killed or seriously injured by a wildfire is a very real threat for
management agency to have ever formally included protective people living, working, or visiting498 in rural areas subject to
fire shelters as part of a firefighter’s PPE. In 2005, it undertook wildfires. Arnold “Smoke” Elser,188 an accomplished Montana
an associated risk analysis62 and as a result decided to have its outfitter, described how he helped guests avoid entrapment by
firefighters no longer carry fire shelters,234 relying instead on situ- a forest fire in the mid-1960s:
ational awareness and entrapment avoidance. The Australasian
Fire Authorities Council has adopted a similar position on the The fire began at the bottom of the canyon and proceeded up canyon
grounds that fire shelters cannot guarantee firefighter survival and as fires do. However, the wind currents carried the smoke to the east
may result in firefighters placing themselves at greater risk in the and not up the drainage to the north; therefore, we received no warning
belief that a fire shelter will protect them.50 of the fire. The Monture Creek trail goes through some very old mature
310
timber which was not burning as we approached. As my stock, the
311
3. Hunker in place. feet) once the “race” had started. Chandler and colleagues116 state,
4. Pass through the fire edge into the burned-out area. “In most firefighter fatalities . . . the unsuccessful strategy has
These four survival options are presented in no particular been to try and run away from the fire and continue running
order of priority. Such factors as the size of the fire, fire environ- until exhaustion or the radiant heat load from the fire front fells
ment, size and location of safety areas or zones, prevailing fire the victim and allows the flame front to pass over him or her.”
behavior, and location of the person with respect to the head of Thus, trying to outpace a fire for any significant distance, but
fire will ultimately dictate which option or options (should the especially uphill, is “courting disaster.”281 For this reason, escape
first one of these options selected become compromised) should routes involving travel upslope should generally not be selected.
be selected. Each of these options has its own unique advantages
and disadvantages. Survival Option 2: Burn Out a Safety Area
Burning out fuels to create an area of safety or to enlarge an
Survival Option 1: Retreat From the Fire and Reach a existing burned area is a viable survival technique or option in
Safe Haven some situations (e.g., light fuels and having sufficient time to
When people are under pressure, they fall back on habitual, implement). As Luke and McArthur281 have noted, “Carrying a
first-learned, and overlearned responses.522 The natural tendency box of matches is part of survival planning” (in this regard, a
when a person is threatened by a hazard such as a wildfire is to windproof type of matches would be ideal, although a fuse
try and move away from the danger as quickly as possible to a would be infinitely more reliable and effective than a match).
place of safe refuge. If the distance between the fire and safe Undoubtedly the most publicized example of this survival
area is short, the fire’s advance slow, the path to the safe area strategy being used in modern times occurred on the 1949 Mann
easily traversed, and the person able bodied, then selection of Gulch Fire, discussed earlier.285,418 However, the technique was
this survival option is appropriate. Bear in mind that a safe refuge known to have been used by American Indians in the early
may be nearby, so one should not avoid the most obvious place, 1800s395,494 and undoubtedly by aboriginal peoples in other parts
even though it may temporarily be uncomfortable to reach of the world, as depicted, for example, in the 1989 movie The
BURNS, FIRE, AND RADIATION
because of, for example, smoke or low to moderate radiation Gods Must Be Crazy II. Wag Dodge described his escape fire
levels. In some cases, this might mean just taking a few steps during his testimony at the board of review investigation into the
into the “black” or recently burned-over ground. The question 1949 Mann Gulch fire as follows:
of whether a previously burned area will serve as a safety zone After setting a clump of bunch grass on fire, I made an attempt to start
will depend not only on the size of the area but also on the another one, but the match had gone out and upon looking up, I had
degree of completeness of fuel consumption, both vertically and an area of 100 feet square that was ablaze. I told the man nearest to me
horizontally.98,380 Furthermore, a recently burned-over area may that we would wait a few seconds to give it a chance to burn out inside,
not immediately serve as a safe refuge because of the burnout and then we would cross through the flames into the burned area, where
time of woody fuels and duff,471 in contrast to grassland fuels, we could make a good stand and our chances of survival were more
where a person can enter the recently burned area in a few than even.
seconds.129
Firefighters have escaped injury and death in many cases by Interestingly, Dodge’s statement was printed in the letters to
being able to outpace or outmaneuver a spreading fire.380,480 the editors section of the September 1949 issue of Life magazine
There have also been many well-publicized cases or incidents after publication of an article on the Mann Gulch Fire entitled
during which attempting initially to outpace and then ultimately “Smokejumpers Suffer Ordeal by Fire” from the previous issue.
PART 3
outrun an advancing flame front have ended in tragedy, includ- In that letter, the reader stated, “I am sure that there are many
ing several mentioned earlier (e.g., 1938 Pepper Hill Fire, 1949 people throughout the country who would appreciate and
Mann Gulch Fire, 1953 Rattlesnake Fire, 1956 Inaja Fire, 1966 perhaps benefit sometime by a more detailed account of how
Loop Fire, 1968 Canyon Fire, 1994 South Canyon Fire). Sadly, Foreman Wagner Dodge, who kept calm and did not become
there are many other examples,413 including the 2003 Cramer Fire panic-stricken, saved himself.” It has been estimated that Dodge’s
in central Idaho involving two firefighter fatalities.133 For informa- escape fire was about 37 m (121 feet) long and 26 m (85 feet)
tion on many of these incidents, consult www.fireleadership.gov/ wide at the time that his “island” of survival was engulfed by
toolbox/staffride/. 3-m (10-foot)–tall flames associated with the main fire front.26
Dr. Ted Putnam,393 a retired wildland fire safety specialist with
the USDA Forest Service, considers that many of these fatality Survival Option 3: Hunker in Place
fires were in fact escapable had better decision making been As mentioned previously, when caught in the open, survival may
employed (e.g., dropped tools and packs earlier to maximize rate depend on taking advantage of every possible source of cover
of advance, put the fastest pacesetters at the lead, and used fire or protection from radiant and convective heat (e.g., depressions
shelters as shields against radiant and convective heat). in the ground, large rocks or logs).201 If a cave (see Figure 14-35)
Incidents similar to those experienced by firefighters involving or root cellar538 is used as a refuge, it is important to vacate
civilians have also taken place. For example, on November 30, into the open at the earliest opportunity because of potential
1957, four members of a group of nine young hikers perished problems associated with accumulations of smoke and carbon
while trying to outrun a bushfire in the Blue Mountains of New monoxide.
South Wales, Australia, as it advanced upslope.201,281 Another In selecting this option, the importance of staying as flat as
incident occurred on August 26, 1995, near the community of possible with one’s nose and mouth pressed down into the
São Domingos in the district of Sandtarém, Portugal.510 Three ground cannot be overemphasized, because the reduction in
civilians who had been assisting local firefighters in suppression radiation received is considerable.27 Lying prone not only mini-
operations eventually ended up being killed while trying to run mizes one’s radiation profile, but cooler, denser air will always
ahead of the fire when it blew up. A fourth individual received be present at ground level. In selecting this option, also bear in
severe burns to his feet, which eventually led to them being mind the following advice125:
amputated, and he died some months later. When a fire passes over a point, the air temperature near the ground is
Simulations carried out by the FPInnovations Wildland Fire higher than the air above it and remains higher for longer. So if someone
Operations Research Group based on their research on firefighter is sheltering from radiation at ground level, they need to stand up as
travel rates,164 coupled with case study information gleaned from soon as possible after the fire passes to breathe cool, fresh air. This is
the 1949 Mann Gulch and 1994 South Canyon fires,102 clearly most apparent in grass fires where air at ground level is hot and smoky
indicate that a person is not able to sustain a maximum pace for for several minutes whereas at 2 m [6.6 feet] it is cool and breathable
even a relatively short time without being overrun by a rapidly within 10 to 15 seconds of the flames passing.
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% Although there have been reported cases of firefighters surviv-
slope would, depending on the fuel type, overrun someone in ing on large rockslides during a wildfire entrapment or burnover,
about 6 to 7.5 minutes or after about 360 to 460 m (1200 to 1500 most notably two smoke jumpers on the 1949 Mann Gulch
312
Fire,285,418 there have also been instances in which these appar- require ideal running conditions (e.g., good footing, no obstruc-
313
Convection 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
Weak have to burn down across a little saddle before it went uphill any more.
indraft
One crew member was reported to have been taking photo-
Strong graphs of the fire less than 10 minutes before the first fatalities
indraft 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).
Flame detached
Even on the major run of the Thirtymile Fire in north-central
from slope
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
A SHALLOW SLOPE 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
BURNS, FIRE, AND RADIATION
314
CHAPTER 14 Wildland Fires: Dangers and Survival
BOX 14-10 Envisioning the Worst
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.
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-
A intensity flame front approaches (Figure 14-41). This is a poten-
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,
B underwear made of synthetic materials does melt. Wearing exces-
FIGURE 14-40 Fires in fully cured grasslands are very responsive and sive layers of clothing generally contributes to heat stress.
can attain exceedingly rapid rates of spread. The flank of a grass fire, As little skin as possible should be exposed to fire. Long
with a change in wind direction, can quite quickly become the head trousers and a long-sleeved shirt should be worn. For maximum
and catch unwary persons off guard. This scene from the multifire situ- protection, the shirt should be kept buttoned with the sleeves
ation that occurred in the Spokane, Washington, area on October 16, rolled down.
1991 (A), reinforces the importance of having well-established escape Brightly colored (yellow or orange) coveralls or shirts are
routes that can be easily navigated (B) to a designated safety zone. worn by organized firefighting crews. These colors improve
(Courtesy Spokane Statesman Review/WorldPictureNews; photos by safety and communications because they are visible in smoke,
K. King.) vegetation, and blackened landscapes.
315
• 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.
FIGURE 14-41 An inappropriately clad and positioned homeowner
attempting to defend his property from ember attack during a wildfire PORTABLE FIRE EXTINGUISHERS
in Rancho Penasquitos, San Diego, California, on August 25, 1995. The
fire at the moment appears largely dominated or supported by a People should know which extinguisher to select for a specific
plentiful fuel source. However, given the capricious nature of fire and hazard in the home or recreational vehicle and be trained in its
winds, this fire could have easily turned into a more wind-dominated use. When a fire is discovered, first evacuate occupants to safety
event at any time. Thus, this individual could have been incapacitated and promptly report the fire to the appropriate authorities. If the
by a momentary blast of superheated air from the convection or fire is small and poses no direct threat, an extinguisher should
BURNS, FIRE, AND RADIATION
radiant heat produced by the spreading fire. In the absence of any be used to fight it.
outside assistance, this would then have left him vulnerable to burning The three major classes of fires are as follows:
by direct flame contact along with his home. Fortunately for this indi- Class A fires: Fueled by ordinary combustible materials, such
vidual, shortly after the photo was taken, an air tanker dropped a load as wood, paper, cloth, upholstery, and many plastics
of fire retardant near the advancing flames and effectively nullified the Class B fires: Fueled by flammable liquids and gases, such as
fire’s spread and intensity. (Courtesy California Chaparral Field Insti- kitchen greases, paints, oil, and gasoline
tute; photo by R.W. Halsey.) 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
Other essential apparel includes a safety helmet (hard hat), fire. Water extinguishers control class A fires by cooling and
gloves (leather or natural fiber), leather work boots, woolen or soaking burning materials. Carbon dioxide or dry chemical extin-
cotton socks, a warm jacket for night wear, goggles, and a hand- guishers are used to control class B fires by smothering flames.
kerchief. Clothing, backpacks, tents, and other camping equip- Multipurpose dry chemical or liquefied gas extinguishers control
ment made of synthetic materials should be discarded when a class A, B, and C fires by a smothering action. Liquefied gas
person is close to a fire. extinguishers also produce a cooling effect. A dry chemical
PART 3
316
BASIC WILDLAND FIRE MATERIALS, Wildfire Today (www.wildfiretoday.com) and the Global Fire
317
have survived, although they did sustain minor injuries, had they they need to be fully aware of the full potential for fire behavior
not joined up with the firefighters just before (~14 minutes) their and what can be done to protect themselves and their assets.
location was overrun.498 “They must be individually persuaded to recognize what consti-
Many years of practical experience with wildland fires allow tutes the fuel for a forest fire and be convinced that, since they
us to conclude the following: own the fuel, they also own the fire it produces and are respon-
• Many indicators show that financial support and programs that sible for the damage they or others nearby incur.”122 The public
address only emergency responses to wildfires will result in and fire management agencies themselves must fully appreciate
more damaging and expensive wildfire emergencies in the that fuel management is not a panacea for conflagration miti
future. Public policies and public education that link sustain- gation, but rather a prerequisite to aid in successful fire sup
able land use practices with emergency preparedness are pression.20,75,126,490 An excellent source of information on fuel
likely to be most successful in the long run. management is the USDA Forest Service Fuels Synthesis Project
• Residential shifts to the WUI will increase exposures to life- (www.fs.fed.us/rm/pubs/rmrs_rn019.pdf).499
threatening situations. After the 1983 Ash Wednesday fires in southeastern Australia,
• Expanded use of fire in managing national parks and wilder- the editor of Australian Forestry commented on what could be
ness areas will increase the likelihood that backcountry rec- learned from studying such wildland fire disasters184:
reationists will encounter free-burning fires. Advances in technical areas will be of great value. It would be valuable
• By and large, the general public tends to underestimate exist- too to make comparable advances in the areas of public policy. People
ing fire hazards and for the most part is usually not experi- forget, community attitudes change and policies erode. Perhaps one of
enced in avoiding wildfire threats. the greatest challenges, given the realities of southeastern Australia, is to
• In some cases, attempted fire exclusion practices have con- learn how to ensure the permanence of public interest policies where
tributed to development of hazardous wildland fuel situations permanence is required.
in terms of quantity and continuity, setting the stage for
extreme fire behavior in some plant communities. The national Twenty years later and following the bushfires that engulfed
BURNS, FIRE, AND RADIATION
ecosystem health issue has compounded this problem by Canberra, Australia, in 2003 (https://en.wikipedia.org/wiki/2003
producing vast expanses of dead and dying forests, increasing _Canberra_bushfires), Cheney124 offered some advice on this
the threat to people from fast-moving, high-intensity fires. matter:
• Knowledge of fire behavior principles and survival guidelines . . . I believe that there is strong evidence that the policies and institu-
will prepare people to take appropriate preventive measures tional arrangements of organizations, both those directly related to fire
in threatening situations. management and those completely unrelated, will have the result of
The general public must share responsibility with suppression perpetuating major fire disasters. I also believe that the legal framework
organizations to minimize fire hazards created by humans. Care in which we’re working is one that [militates against] individuals taking
with fire, proper cleanup of debris, fuel reduction efforts on responsibility for their own actions and lifestyle choices. In this country
wildland property, fire-safe construction guidelines, and applica- wildfire is inevitable but the impact of disastrous fires can be reduced.
tion of survival skills will minimize fire threats. Such precautions But this will only be achieved if policies focus on the physics of fire
should become as commonplace in the wildland environment as spread and foster a climate of awareness where fuel reduction, from the
smoke alarms and fire extinguishers have become in urban set- backyard to beyond, is encouraged and supported by legislation.
tings. Every community should undertake, as part of the risk
management process associated with the wildfire threat, an At the end of the day, though, what can an individual do to
PART 3
assessment of their fire environment in terms of potential fire improve matters when it comes to living with fire? Kaufmann and
behavior. A good example of this type of analysis has been colleagues249 offer some very practical advice:
completed for over a hundred communities in northern Saskatch- • Get involved in a community-based conservation group
ewan, Canada.165 working on local landscape restoration projects.
Unfortunately, major disasters are often required for funda- • Educate yourself about the role of fire in your local
mental changes to occur. Disasters do not simply happen.488 ecosystems.
They usually involve an “incubation period” that involves “the • Provide feedback on agency land management plans.
accumulation of an unnoticed set of events that are at odds with • Consult with regional experts on how to safely reintroduce
the accepted beliefs about hazards and the norms for their fire on to your land holding.
avoidance.”487 • Participate in local workshops (e.g., Firewise Communities) to
Wildland fire suppression agencies will continue to provide learn how to treat fuels around your home and create defen-
fast, safe, and energetic initial attack responses to protect human sible space.
life, property, and natural resources.14 Many fires will start and Their final suggestion: “Start simply. But start.” Local forestry
burn under environmental conditions that permit their control at and fire management agencies are more than willing to offer
a very small size. However, in certain situations (e.g., critically technical advice and information. Just give them a call to get
dry fuels or strong winds), some fires9,32,33 will defy control until started today, before wildfire comes knocking!191
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
ACKNOWLEDGMENTS
examples of this type of fire behavior and associated suppression The authors hereby thank the following individuals for their
problems. No radically new concept of fire suppression for stop- candid comments on various sections of the chapter: M. Acker-
ping the head of a hot, fast-running wildland fire should be man, A. Beaver, K. Brauneis, B. Butler, D. Campbell, P. Cheney,
anticipated in the future.152 In An Introduction to Fire Dynamics, J. Cohen, M. DeGrosky, T. Greer, M. Heathcott, J. Leonard, T.
Drysdale181 states, “Further major advances in combating wildfire Leuschen, S. McCaffrey, J. McLevin, B. Mottus, P. Murphy, S.
are unlikely to be achieved simply by continued application of Otway, G. Proulx, T. Putnam, D. Quintilio, A. Rhodes, B. Sharkey,
the traditional methods. What is required is a more fundamental R. Smith, D. Thomas, R. Thorburn, K. Weick, and T. Zimmerman.
approach which can be applied at the design stage. . . . Such an The assistance of the following individuals in the preparation
approach requires a detailed understanding of fire behavior.” of this chapter is also duly noted: B. Bereska, M. Campbell, M.
Strategic fuel management and land use planning could Cruz, M. Erickson, J. Handmer, T. Petrilli, G. Pearce, and O.
reduce the total number and size of wildfire occurrences, as well Spencer.
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-
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BURNS, FIRE, AND RADIATION
PART 3
318.e10
CHAPTER 15
Emergency Care of the
Burned Patient
MICHAEL J. MOSIER, ROBERT L. SHERIDAN, AND DAVID M. HEIMBACH
319
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
most common cause of burns. Water at 60° C (140° F) creates a Flame burns are the next most common burn injuries after scalds.
deep partial-thickness or full-thickness burn in 3 seconds. At Although injuries in house fires have decreased with the advent
68.9° C (156° F), the same burn occurs in 1 second. Freshly of smoke detectors, a significant number of burn injuries still
brewed coffee from an automatic percolator is generally approxi- result from careless smoking, improper use of flammable liquids,
mately 82° C (179.6° F). Boiling water always causes deep burns. automobile accidents, and clothing ignited from stoves or space
Soups and sauces, which are thicker in consistency, remain in heaters. Patients whose bedding or clothes have been on fire
contact longer with skin and often cause deep burns. Exposed rarely escape without full-thickness burns. Outdoor misadven-
areas typically tend to be burned less deeply than areas covered tures result from spilled hot water while cooking, fuel fires from
with thin clothing. Clothing retains heat and keeps liquid in cooking stoves and lanterns, fabric fire (e.g., taking lanterns into
contact with skin for a longer time. tents), smoking in a sleeping bag, tripping and falling into a
Immersion scalds are deep and severe burns21,31,105 (Figure campfire, and application of accelerants (e.g., gasoline, charcoal
15-2). Although water may be cooler than with a spill scald, lighter fluid) to wood or charcoal fires. Most accelerants, whether
duration of contact is longer. These burns frequently occur in gasoline, kerosene, propane, or diesel, have ignition tempera-
small children or older adult patients with thin skin. Conse- tures of 210° to 280° C (410° to 536° F) and cause rapid tissue
quently, many states have passed legislation to set home and 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
CHAPTER 15 Emergency Care of the Burned Patient
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 FIGURE 15-6 This patient suffered deep localized burns to fingers
accidents typically have severe contact burns and crush injuries, from a 220-volt power source. Electricity passing through smaller body
because these accidents are often caused by direct contact with parts generates more intense heat, so less is dissipated. Fingers,
hands, forearms, feet, and lower legs are frequently destroyed. (Cour-
presses or hot, heavy objects. Toddlers may receive contact burns
tesy Rob Sheridan, MD.)
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 abdomen or chest (Figure 15-6). Although cutaneous manifesta-
against a radiator) or individuals dealing with molten materials, tions may appear limited, massive underlying tissue destruction
are frequently fourth degree.19,59,92 In wilderness settings, the most may be present because muscle, nerves, blood vessels, and
common contact burns are from hot coals, which are often as bones can be burned beyond recovery.18,36,37,77
hot as 537.8° C (1000° F). These burns may occur when intoxi- Arc burns occur when current takes the most direct path rather
cated campers dance around and then into campfires, architects than the path of least resistance. Arcs create extremely high
of “river saunas” mishandle hot rocks, children fall into fires, and temperatures. These deep and destructive wounds occur at joints
beach walkers sustain deep burns when coals are buried in sand that are in close apposition at the time of injury. Most common
overnight. Coals buried in “extinguished” campfires can remain are burns from forearm to arm (i.e., when the elbow is flexed)
dangerously hot for days. Falling into such ashes can cause very and from arm to axilla (i.e., current passes from the upper
deep burns (Figure 15-5). Even though injured areas may be extremity to trunk) if the shoulder was adducted.
small, they can be deep and debilitating when the hiker must Electrical burns cause a particular set of other injuries and
walk a considerable distance on burned feet.27 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
ELECTRICAL BURNS fractures of lumbar vertebrae, humerus, or femur, and dislocate
Electrical burns are thermal burns from very-high-intensity heat. shoulders or hips.
As electrical energy encounters body tissue resistance, it is con- Electrical cardiac damage presents with symptoms similar to
verted to heat. This occurs in direct proportion to current’s those of a myocardial contusion or infarction. The conduction
amperage and electrical resistance of body parts through which system may be deranged. There can be rupture of a heart wall
it passes. The smaller the body part through which electricity or of a papillary muscle leading to sudden valvular incompetence
passes, the more intense the heat and the less it is dissipated. and refractory heart failure. Household current (in the U.S., 110
Therefore, fingers, hands, forearms, feet, and lower legs are volts) typically causes no damage or induces ventricular fibrilla-
frequently totally destroyed, whereas larger-volume areas (e.g., tion. Alternating current (AC) is more likely to induce fibrillation
trunk) usually dissipate the current sufficiently to prevent exten- than is direct current (DC). After exposure to shocks of 110 to
sive damage to viscera, unless the contact point is on the 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
FIGURE 15-5 Coals buried in extinguished campfires will stay danger-
ously hot for days. This toddler stumbled into the ashes of a fire Chemical burns, usually caused by strong acids or alkalis, most
extinguished 24 hours earlier. (Courtesy Rob Sheridan, MD.) 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.
burn size.
A reasonably accurate estimate of burn size is provided by
the “rule of nines.” In adults, each upper extremity accounts for
FIGURE 15-7 Evidence of myoglobinuria with “cola-colored” urine. 9% TBSA, each lower extremity accounts for 18%, anterior and
Myoglobin pigment released from damaged muscle by electrical posterior trunk each account for 18%, head and neck account
trauma will cause renal failure if not cleared. Administering intravenous for 9%, and perineum accounts for 1% (Figure 15-8). Although
crystalloid to an end point of 2 to 3 cc/kg/hr urine output reduces risk the rule of nines is rapid and effective, a number of more precise
of renal failure. Intravenous bicarbonate (1 mEq/kg) may enhance charts have been developed. To establish TBSA, draw a diagram
clearance of these pigments. (Courtesy Rob Sheridan, MD.) 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
cleaners, improper use of harsh solvents, and assaults.26,38,67,70,84,87,94 in proportion to body size than do adults. In an infant, the head
Chemical burns cause progressive damage until chemicals are accounts for approximately 18% of TBSA. Body proportions do
inactivated by reaction with tissue or by dilution (e.g., flushing not fully reach adult percentages until adolescence. To further
with water). Typically, acid burns tend to be more self-limited increase accuracy in burn size estimation, especially when burns
PART 3
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
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
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
FIGURE 15-11 Deep partial-thickness burn. Note the cherry-red color.
CARE AT THE SCENE
Flame Burns
but in pigmented individuals, healed burns may never completely The first responder must remove the injured person from the
match the color of surrounding normal skin. source of heat. Because of potential dangers of smoke inhalation
BURNS, FIRE, AND RADIATION
inevitable. heat. Any wet clothing should be removed, because fabric retains
moist heat and may continue to burn skin that is in contact with
Full-Thickness Burns hot material. Accidents resulting from cooking indoors with
Full-thickness burns involve all layers of dermis and can heal grease are particularly hazardous. The startle response to a grease
only by wound contracture, epithelialization from the wound splatter may cause the victim to drop a pan of grease onto the
margin, or skin grafting (Figure 15-12). Full-thickness burns are fire and so ignite a kitchen fire that can rapidly become a dwell-
classically described as leathery, firm, insensitive to light touch ing fire.
and pinprick, and depressed compared with the adjoining normal
skin. Difference in depth between a deep partial-thickness burn Airway
and a full-thickness burn may be less than 1 mm (0.04 inch). Once flames are extinguished, direct primary attention to the
Full-thickness burns are easily misdiagnosed as deep partial- airway. Any person rescued from a closed space or involved in
thickness burns, because both have many of the same clinical a smoky fire should be considered at risk for smoke inhalation
findings. Both may be mottled in appearance. They rarely blanch
with pressure and may have a dry, white appearance. Burns may
324
injury. If supplemental oxygen is not available, a patient who is cutters. Once the patient is removed from the source of current,
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 prevents burned skin from tightening and assists with pain
cotton clothing can be used to improvise many effective burn control and prevention of edema.
dressings. Clean, white cotton T-shirts can be used to good effect. These principles are much more important than the choice of
Oversize clean cotton socks can be used to reinforce dressings topical agent to cover the burn. Commonly used topical agents
on hands and feet. Simple dressings (i.e., topical cream, plain that might be carried in first-aid kits include antiseptic and anti-
gauze) are sufficient. Some patients prefer nonadherent dressings biotic ointments and creams (e.g., bacitracin, double antibiotic
(e.g., Telfa or Adaptic, the latter sometimes known as “greasy [Polysporin: polymyxin B, bacitracin], triple antibiotic [Neosporin:
gauze”), because they are less likely to stick to wounds during bacitracin/gramicidin, neomycin, polymyxin B], silver sulfadia-
dressing changes. The same effect can be achieved by soaking zine) and nonantibacterial ointments (e.g., Aquaphor, Vaseline,
(with water) a plain gauze dressing that appears stuck to wound, A+D). Any of these agents is acceptable. Using a topical antimi-
waiting a few minutes, and then removing the dressing with crobial is not essential in early postburn care.
additional water if necessary. Other dressings (e.g., hydrogels, Technique of Burn Wound Debridement. Small, intact
silver-coated dressings, silicone gel sheets, calcium alginate) blisters do not need debridement (Figure 15-15). Blisters serve
designed to minimize frequency of dressing changes and promote as sterile biologic dressings to minimize desiccation and pain.
healing are available but not necessary. To stock first-aid kits, Protect intact blisters from trauma, and observe every few hours
PART 3
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
living patient who has normally functioning kidneys and does
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 If the abdomen is involved with burn, the inferior margins of
of the high incidence of septic thrombophlebitis, lower extremi- escharotomy may be connected transversely (Figure 15-20).
ties should be avoided as IV portals. Upper extremities are Fasciotomies are rarely needed in patients with thermal burns.
preferable, even if the IV line must pass through burned skin. However, if distal pulses do not return after medial and lateral
Patients with burns larger than 50% TBSA or who have associated escharotomies, fasciotomy should be considered. Fasciotomies
medical problems, are at the extremes of age, or have concomi- can generally be done through the initial escharotomy incisions
tant smoke inhalation should have additional central venous (Figure 15-21). In contrast, patients with electrical injuries fre-
pressure monitoring. Because of extreme hemodynamic instabil- quently need fasciotomies. Careful monitoring is mandatory for
ity in patients with burns over 65% TBSA, these patients should all patients with electrical burns and with burns associated with
be monitored in an intensive care unit (ICU) setting with a Swan- soft tissue trauma or fractures. In these circumstances, loss of
Ganz catheter to measure pulmonary capillary wedge pressure pulses is a strong indication for urgent fasciotomy under general
and cardiac output. anesthesia in the operating room.
Presence of myoglobinuria alters the resuscitation plan. Myo- Need for escharotomy in the burned hand is controversial.
globinuria results from destruction of muscle cells leading to Fingers burned severely enough to require escharotomy are
myoglobin (red muscle pigment) release. This is most often frequently mummified, and lack of muscles in the fingers puts
PART 3
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
cedures are necessary, general anesthesia and operating room
329
blisters form, because wound management then becomes more tap water and reapply a topical agent and light dressing. During
important because of potential for infection and subsequent dressing changes, and as often as possible, put all involved joints
scarring. through a full range of motion. The dressing may be unnecessary
while the patient is at home, but he or she should dress the
Superficial Partial-Thickness Burns wound before leaving the house. This method is highly success-
Treatment of superficial partial-thickness burns presents little ful, but is inconvenient, may be fairly painful, and requires good
problem. If the wound is kept clean, patient kept comfortable, patient cooperation.
and joints kept active, these wounds heal in less than 3 weeks The “exposure” method has little to recommend it. This
with minimal scarring and no joint impairment. method involves leaving the wound open, allowing wound drain-
First, clean and debride the wound as described previously. age to desiccate and form a scab. Controlled studies in animals
Small blisters may be left intact. Biochemical analysis using poly- have shown that desiccation and crust formation interfere with
acrylamide gel electrophoresis of burn blister fluid has shown it wound healing. Our experience has also shown that crusts
to be similar to that of serum.101 We suggest that blister fluid is crack over joints, cause considerable discomfort, and can hide
an exudate mainly from the vascular system, provides a good infection.
environment for fibroblasts in the damaged site, and facilitates
healing. Larger blisters are difficult to protect, however, and Deep Partial-Thickness and Full-Thickness Burns
blister fluid is a rich culture medium for bacteria that live in skin Treatment of deep partial-thickness and full-thickness burns is a
appendages. Therefore, large blisters and small blisters in large matter of grave concern. Full-thickness burns heal only by con-
burns should usually be totally removed with forceps and scis- traction and epithelialization from the periphery. Epithelium
sors. In some instances, blister fluid can be aspirated with a does not begin to migrate until eschar is removed, and the
large-bore needle, allowing blistered epidermis to remain on the growth rate is only approximately 1 mm (0.04 inch) per day.
wound as a biologic dressing. This dead epidermis is fragile, Healing of even a small full-thickness burn may involve many
tends to contract, and rarely stays intact except over small areas. weeks of discomfort and disability. Deep partial-thickness burns
BURNS, FIRE, AND RADIATION
After debridement, the most common treatment is wound may take 4 to 8 weeks to heal and then leave an unacceptable
coverage with silver sulfadiazine and application of a light dress- scar. If a joint is involved, some loss of joint function is the rule.
ing to promote active range of motion. Some wounds can be We have adopted a policy of early excision and grafting for such
managed with synthetic dressings that contain elemental silver wounds.
(e.g., Aquacel Ag, Acticoat, Mepilex Ag). These can be applied Initial outpatient treatment can be followed by elective surgery
and left in place for 1 week or until the burn is healed at approxi- as soon as it can be scheduled. Small wounds can be treated
mately 2 weeks (Figure 15-25). Some very small burns do not through day surgery. Larger wounds located over dynamically
require topical agents. For small facial burns, bacitracin ointment important areas can be closed with only 1 or 2 days of hospital-
may be a better choice than silver sulfadiazine cream because it ization. Excision and grafting procedures should be done by a
is less drying. surgeon experienced in tangential wound excision. Advantages
Pain is managed as for first-degree burns. Patient usually of this aggressive approach are a pain-free patient with normal
should return every 2 to 3 days until the wound heals or the joint function, better cosmetic result, and a rapid return to work
patient has demonstrated ability to manage the wound without or school. These more than compensate for the brief hospitaliza-
supervision. tion and very small risk associated with minor surgery.
If silver sulfadiazine is used, an appropriate home treatment Should excision and grafting be unacceptable to the patient
PART 3
regimen is to have the patient cleanse the wound once daily with 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-
FIGURE 15-25 Many new silver-releasing membranes are available mately 1 year to fade, soften, and mature. Physical therapy may
that provide antiseptic coverage of wounds for several days. They need be required throughout this period or longer. Pressure garment
to be monitored for development of submembrane infection. (Cour- therapy may be used in certain cases in an attempt to prevent
tesy Rob Sheridan, MD.) hypertrophic scar formation. The reader is referred to books
330
dealing with acute burn care, reconstructive plastic surgery, and mia or arrest).34,95 A large, multicenter trial of sufficient size to
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 FIGURE 15-27 View of the proximal airway on bronchoscopy, demon-
on the patient’s clothes should raise suspicion. Rescuers are strating moderate erythema and carbonaceous debris, consistent with
often the most important historians and should be carefully a grade 2 inhalation injury by bronchoscopic criteria. (From Kim CH,
questioned. Wool H, Hyun IG, et al. Pulmonary function assessment in the early
Perform early, careful inspection of the mouth and pharynx. phase of patients with smoke inhalation injury from fire. J Thorac Dis
Hoarseness and expiratory wheezes are signs of potentially 2014;6(6):617-624.)
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 is anticipated, endotracheal intubation should be performed.
levels should be obtained. Elevated COHb or any clinical symp- Oxygen at 100% can then be administered by ventilator.
toms of CO poisoning are presumptive evidence of associated Mucosal burns of mouth, nasopharynx, and larynx respond
smoke poisoning. In very smoky fires, COHb levels of 40% to with edema formation and may lead to upper airway obstruction
50% may be reached after only 2 to 3 minutes of exposure.100 at any time during the first 24 hours after the burn. Red or dry
Arterial blood gases (ABGs) are drawn from patients with mucosa or small mucosal blisters should alert the observer to the
suspected smoke poisoning. One of the earliest indicators of possibility of subsequent airway obstruction. These signs also
PART 3
smoke poisoning is an improper ratio of arterial partial pressure should raise suspicion that significant smoke inhalation may have
of oxygen (PaO2) to fraction of inspired oxygen (FIO2). This P/F occurred. Carefully inspect the mouth and pharynx of any patient
ratio is typically 400 to 500. Patients with impending pulmonary with facial burns. If abnormalities are found, the larynx should
problems have a ratio of less than 300 (e.g., PaO2 <120 mm Hg be examined immediately on arrival at the hospital. Presence of
with FIO2 of 0.40). A ratio less than 250 is an indication for vigor- significant intraoral and pharyngeal burns is a clear indication for
ous pulmonary therapy, not for merely increasing inspired emergency endotracheal intubation. Progressive edema may
oxygen concentrations. make later intubation extremely hazardous, if not impossible.
A number of authorities suggest routine use of fiberoptic Mucosal burns are rarely full thickness and can be successfully
bronchoscopy for airway assessment11,57,82,88 (Figure 15-27). It is managed with good oral hygiene.
inexpensive, quickly performed by an experienced clinician, and Pulmonary functions early in the course of smoke poisoning
useful for accurately assessing edema of the upper airway. Aside may be variably affected. Typical findings include decreased lung
from establishing evidence of tracheal erythema, it may not volume (i.e., functional residual capacity) and vital capacity,
materially influence treatment for smoke poisoning. evidence of obstructive disease with reduction in flow rates,
We have conducted a multivariate analysis of a constellation increased dead space, and rapid decrease in compliance. Much
of history, signs, and symptoms with bronchoscopic findings in of the variability in pulmonary response appears to correlate with
100 consecutive patients admitted with suspected smoke inhala- severity of the associated cutaneous burn.12 Without associated
tion. If the patient had the combination of history of exposure burns, mortality from smoke poisoning is low, disease rarely
to closed-space fire, carbonaceous sputum, and COHb level progresses to ARDS, and symptomatic treatment usually leads to
greater than 10%, there was a 96% correlation with positive complete resolution of symptoms in a few days. In the presence
bronchoscopy. Presence of two of the above features dropped of burns of any size, smoke poisoning appears approximately to
correlation to 70%, and if only one was present, to 36%. As double the mortality rate. Pulmonary symptoms (e.g., hypoxia,
discussed previously, upper airway edema was best correlated rales, rhonchi, wheezes) are seldom present on admission but
with an explosion (i.e., flash burn) that involved the face and may appear 12 to 48 hours after exposure. In general, earlier
upper torso. Almost 50% of such patients had significant upper onset of symptoms is associated with more severe disease.98
airway edema and underwent prophylactic airway intubation. No standard treatment has evolved to ensure survival after
smoke poisoning. Each recommended treatment modality is tem-
Therapy pered by the opinion and individual experience of the treating
All patients burned in an enclosed space or having any sugges- physician. In the presence of increasing laryngeal edema, naso-
tion of neurologic symptoms should be given 100% oxygen while tracheal or orotracheal intubation is indicated. A tracheostomy is
awaiting measurement of COHb levels. This should be adminis- never an emergency procedure and certainly should be avoided
tered through a tight-fitting mask in the field. If the patient as initial airway management in patients with burns to the face
demonstrates labored breathing, or if a prolonged transport time 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-
*References 10, 17, 39, 42, 55, 56, 83, 91, 106, 109. fied air, vigorous pulmonary toilet, and bronchodilators as
332
needed. ABGs are drawn at least every 4 hours, and the P/F ratio serum sodium and potassium levels becomes important. High
333
BOX 15-2 Burn Center Referral Criteria
availability, local terrain, weather, and distances involved. For
distances of less than 80 km (50 miles), a ground ambulance is
A burn center may treat adults, children, or both. typically satisfactory. For distances between 80 and 241 km (50
Burn injuries that should be referred to a burn center include the and 150 miles), helicopter transport may be preferred. Monitor-
following: ing, airway management, and changes in therapy are more dif-
1. Partial-thickness burns of greater than 10% of the total body ficult to achieve in a helicopter. All patients transported by air
surface area should have a nasogastric tube inserted and be placed on depen-
2. Burns that involve the face, hands, feet, genitalia, perineum, dent drainage, because nausea and vomiting usually result during
or major joints the flight. Two large-bore IV lines should be established in case
3. Third-degree burns in any age group one stops working. For distances greater than 241 km (150
4. Electrical burns, including lightning injury miles), fixed-wing aircraft are usually satisfactory. Air ambulances
5. Chemical burns may function as well-equipped, flying ICUs, and personnel are
6. Inhalation injury typically trained for both critical care and peculiarities of advanced
7. Burn injury in patients with preexisting medical disorders burn care during a flight (see Chapter 58).
that could complicate management, prolong recovery, or The referring physicians must ensure that patient’s condition
affect mortality is suitable for a long transport and prepare the patient for flight.
8. Any patients with burns and concomitant trauma (such as Secure the patient’s airway. At 9144 m (30,000 feet), planes
fractures) in which the burn injury poses the greatest risk of
can be pressurized to an altitude of about 1676 m (5500 feet).
morbidity or mortality. In such cases, if the trauma poses
the greater immediate risk, the patient’s condition may be
Although supplemental oxygen can be administered during flight,
stabilized initially in a trauma center before transfer to a if the patient’s oxygenation is marginal, performing endotracheal
burn center. Physician judgment will be necessary in such intubation and initiating mechanical ventilation before transport
situations and should be in concert with the regional is preferred. In-flight endotracheal intubation is difficult. If there
medical control plan and triage protocols. is any question of upper airway edema, intubate the patient
BURNS, FIRE, AND RADIATION
9. Burned children in hospitals without qualified personnel or before transport from the referring hospital. Wrap patients to
equipment for the care of children keep them warm because burned patients have difficulty main-
10. Burn injury in patients who will require special social, taining body temperature. Bulky dressings, blankets, and a Mylar
emotional, or rehabilitative intervention sheet (usually available from the flight team) can help maintain
body temperature. If the patient has any cardiac irregularities,
Excerpted from Guidelines for the Operation of Burn Centers (pp 79-86), advanced cardiac monitoring must be available. In-flight noise
Resources for Optimal Care of the Injured Patient 2006, Committee on Trauma,
American College of Surgeons.
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
knowledge to ensure a good result. Adoption of early excision burn wounds alone. They should calculate burn size for resuscita-
and grafting or creative use of local tissue rearrangement to tion purposes and monitor pulses distal to circumferential full-
achieve early wound closure have made burn care more complex. thickness burns. Wrap the patient in a clean sheet and keep him
An increasing number of patients with small but significant burns warm until arrival at the definitive care center.
PART 3
334
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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335.e1
69. Moylan JA. Supportive therapy in burn care, smoke inhalation, diag- 90. Shangraw RE, Jahoor F, Miyoshi H, et al. Differentiation between
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70. Mozingo DW, Smith AA, McManus WF, et al. Chemical burns. 91. Sharar SR, Heimbach DM, Howard M, et al. Cardiopulmonary
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72. Narita H, Kikuchi I, Ogata K, et al. Smoke inhalation injury from Pediatrics 1987;80:18.
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Burns Incl Therm Inj 1987;13:147. patients. J Trauma 1988;28:171.
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335.e2
CHAPTER 16 Exposure to Radiation from the Sun
CHAPTER 16
Exposure to Radiation from the Sun
ANDREW C. KRAKOWSKI AND ALINA GOLDENBERG
Adverse effects of sunlight overexposure are well documented.84,139 noma skin cancer formation.139 Beneficial effects of UVB in-
Public attention is increasingly focused on the adverse effects of clude vitamin D production from a cutaneous precursor, 7-
sun exposure, but sun-protective strategies are still debated. dehydrocholesterol, to form previtamin D3, which is quickly
These issues are of particular concern to wilderness enthusiasts. converted to vitamin D3 (cholecalciferol). Cholecalciferol is first
Salutary effects of sun protection against acute phototrauma (e.g., hydroxylated in the liver into 25-hydroxyvitamin D3, then in the
sunburn) are more easily judged than are sequelae of chronic kidneys into the active metabolite 1,25-dihydroxyvitamin D3,
phototrauma (e.g., cataracts, photoaging, photocarcinogenesis). which stimulates calcium absorption from the gut.122 Approxi-
These chronic effects are increasingly relevant given the state of mately 90% of 25-hydroxyvitamin D3 is formed in this manner.234
demographically aging populations. Economic concerns are stag- At Earth’s surface, approximately 10% of UVR is UVB and 90%
gering; billions of dollars are spent annually in the cosmetic and is ultraviolet A (UVA; 320 to 400 nm). This ratio can vary with
medical industries to prevent and repair photodamage, photoag- season and time of day. UVA is divided into “near UVA,” or UVA
ing, and skin cancer. With improvements in sunscreens and II (320 to 340 nm), and “far UVA,” or UVA I (340 to 400 nm).
photoprotective clothing, limiting skin damage while remaining These categories are based on photobiologic responses. UVA
active outdoors is increasingly simpler. 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
SOLAR RADIATION stratum corneum and epidermis.
ELECTROMAGNETIC SPECTRUM
ENVIRONMENTAL INFLUENCES ON ULTRAVIOLET
The sun produces a continuous spectrum of electromagnetic
radiation (Figure 16-1). The most energetic rays are those with
RADIATION EXPOSURE
wavelengths that are shorter than 10 nm: cosmic rays, gamma Exposure to UVR varies substantially by latitude, altitude, season,
rays, and x-rays. These do not penetrate the atmosphere to reach time of day, solar zenith angle, albedo (reflectivity), clouds,
Earth’s surface. Phototrauma is primarily the result of ultraviolet atmospheric pollution, ozone levels, and individual factors (e.g.,
radiation (UVR). UVR (10 to 400 nm) accounts for approximately occupation and personal behaviors). Most UVR reaches Earth
10% of the incident radiation at Earth’s surface; visible light (400 around midday when the sun is at its zenith: 80% between 9 AM
to 760 nm) approximately 50%; and infrared (IR; 760 to 1700 nm) and 3 PM and 65% between 10 AM and 2 PM.84 UVB peaks at
approximately 40%.84 Longer-wavelength visible light and IR midday.176 UVB is absorbed, reflected, and scattered by the atmo-
may also cause cutaneous phototrauma. Solar urticaria has been sphere. During early morning and late afternoon, when the sun
reported to occur with exposure to visible wavelengths. IR may nears the horizon, UVB decreases considerably. Latitude and
produce epidermal and dermal alterations.145 season have similar effect; peak UVB exposure is approximately
Ultraviolet radiation has four components. Vacuum UVR (10 100 times greater in June than in December.176 For each degree
to 200 nm) is readily absorbed by air and does not penetrate of latitude away from the equator, UVB intensity decreases an
Earth’s atmosphere. Ultraviolet C (UVC; 200 to 290 nm) is almost average of 3%. UVA varies considerably less than does UVB with
entirely absorbed in the stratosphere 15 to 50 km (9.3 to 31.1 latitude, time of day, and season, as predicted by Rayleigh’s law:
miles) above Earth’s surface by oxygen and ozone. Man-made Atmospheric light scattering ∝ 1 λ
sources of UVC (e.g., germicidal lamps, arc-welding devices) are
rarely medically relevant. where λ is the wavelength. A shorter wavelength results in
Ultraviolet B (UVB; 290 to 320 nm) is biologically active greater atmospheric scattering. UVB is scattered much more
and principally responsible for tanning, burning, and nonmela- 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
Vacuum
UVR UVC UVB UVA
UVA II UVA I
BURNS, FIRE, AND RADIATION
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
UVR exposures a risk. approximately 75 years.302 Each Cl− ion may destroy 100,000
Wind augments sunburn. In mice, exposure to wind plus UVR molecules of ozone.302 Above Antarctica, molecular halogens coat
results in more erythema than does exposure to UVR alone.223 In the surface of ice clouds, making them even more reactive and
humans, wind reduces heat perception and encourages longer able to degrade ozone.117
exposure. Altitude profoundly influences UVB exposure. Until Ozone losses were first reported in 198574 by the British Ant-
recently, UVB exposure was thought to rise 4% for each 305-m arctic survey. Ozone above Antarctica showed large declines in
(1000-foot) rise above sea level. However, recent research dem- the austral springtime (September/October), and decreased 35%
onstrated an 8% to 10% increase in UVB for each 305-m (1000- during the springs from 1975 to 1984.117 Ozone depletion is now
foot) rise above sea level.240 This study found that UVB exposure documented at all latitudes except the equator. This depletion is
readings in Vail, Colorado (latitude 39 degrees North) at 2591 m uneven, with more loss at the poles and less at the middle lati-
(8500 feet) approximated readings at Orlando, Florida (latitude tudes.302 Waxing and waning occurs with the seasons. Docu-
28 degrees North, elevation 18 m [60 feet]), 772 miles nearer the mented ozone depletion exists over continental Europe, North
equator. and South America, South Africa, New Zealand, and Australia.160
Significant increases in UVB caused by ozone depletion have
OZONE DEPLETION AND ULTRAVIOLET been documented, even near the middle latitudes. In Toronto
from 1989 to 1993, Kerr and McElroy144 documented surface UVB
RADIATION EXPOSURE increases of 35% per year in winter and 7% per year in summer,
Stratospheric ozone, which lies 15 to 50 km (9.3 to 31.1 miles) corresponding with ozone decreases of 4% per year and 1.8%
above Earth’s surface, provides a thin and fragile shield against per year, respectively. In Scotland, similar increases in ground-
UVR. Ozone attenuates UVB and modestly reduces UVA II, but level UVB caused by decreased stratospheric ozone have been
allows transmission of all UVA I.313 Natural physicochemical documented.208 In the northern hemisphere’s middle latitudes,
processes continuously create and remove ozone from the strato- ozone losses are greater during winter (~6% per decade) than
sphere. Man-made pollution accelerates ozone degradation. summer (~3% per decade).117 Pollution (e.g., smog, particulates)
Molina and Rowland206 first suggested that chlorofluorocarbons may mitigate UVR increases by absorbing UVB.302
(CFCs) could cause ozone depletion. Developed during the 1970s Ozone depletion affects the biosphere and human skin cancer
as refrigerants, CFCs contain carbon, chlorine, and fluorine. CFCs rates. Data suggest that every 1% decrease in ozone causes an
have been used in air-conditioning systems, insulation, cleaning increased incidence of skin cancer: 1% for melanoma, 2% for
solvents, degreasing agents, and metered-dose inhalers. Halons, basal cell carcinoma, and 3% for squamous cell cancer.59,302 Given
related compounds containing bromine, also deplete strato- the paucity of direct sunlight, even if UVB triples near the poles,
spheric ozone. Halons arise from seawater, fire extinguishers, as suggested in worst-case scenarios, polar areas will still receive
and various industrial processes.117 CFCs and halons are halocar- less UVB than current equatorial levels.302 Ozone depletion may
336
have its greatest effects on nonhuman biosystems. Plant and skinned individual in San Diego, 1 MED of UVB would require
337
BOX 16-1 Skin Types
benzocaine, diphenhydramine). Refrigerating topical anesthetics
before application provides added relief. Topical remedies
I. Always burns; never tans include aloe, baking soda, and oatmeal, but controlled studies
II. Often burns; tans minimally are lacking. Topical corticosteroids, with their vasoconstrictive
III. Sometimes burns; tans moderately effects, are often considered “first-line” treatment for acute
IV. Burns minimally; tans well sunburn; however, their efficacy remains controversial. A trial
V. Rarely burns; tans deeply; moderately pigmented (brown) comparing erythema reactions in skin treated with either topical
VI. Never burns; deeply pigmented (black) 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-
Chronic suberythemal UVA exposures also cause photodam- roid 30 minutes before UVB exposure.76 When applied after
age. Repetitive low-dose exposures to UVA result in histologic exposure, diclofenac gel, a topical nonsteroidal antiinflammatory
changes174: thickening of the stratum corneum, granular and drug (NSAID), alleviates pain, erythema, and edema for up to 48
stratified cell layers; decreased elastin, vascular dilation, and hours.145 Oral NSAIDs provide analgesia and may reduce sunburn
inflammation. erythema.84 Combined use of topical corticosteroids and oral
Intrinsic mechanisms of photoprotection include antioxidants NSAIDs slightly decreases erythema during the first 24 hours if
(e.g., glutathione peroxidase-reductase system mitigates damage administered before sunburn becomes clinically apparent.235 A
from UVR-induced reactive oxygen species), DNA repair enzymes recent metastudy found no therapy to be consistently effective,
(correct most UVR-induced mutations), and carotenoids (stabilize and no consensus could be made regarding treatment of
biologic membranes from singlet oxygen attack). sunburn.110
SUNBURN TANNING
BURNS, FIRE, AND RADIATION
Sunburn reflects a local vascular reaction. The causes are multi- As with sunburn, tanning is caused by UVR. Persons who seek
factorial; DNA damage, prostaglandin activation, cytotoxicity, and a tan risk sunburn. Tanning is biphasic. There is immediate
other mechanisms are implicated. Onset of UVB erythema occurs pigment darkening within minutes (caused by UVA), followed
2 to 6 hours after exposure, peaks at 12 to 36 hours, and fades by delayed pigment darkening (DPD) in 3 days (primarily a re-
after 72 to 120 hours.84,127,139 Acute histologic changes accompany- sponse to UVB). Immediate pigment darkening results from
ing UVB exposure include edema with vasodilation of the upper action of UVA on preformed melanin precursors and occurs as
dermal vasculature127 and endothelial cell swelling, most likely soon as 5 minutes after exposure, peaks in 60 to 90 minutes, and
caused by release of vasoactive mediators.102 Delayed histologic then fades quickly. DPD represents new melanin synthesis within
changes include appearance of sunburn cells within 30 minutes melanocytes and subsequent spread of richly melanized melano-
after exposure. These dyskeratotic cells have enlarged nuclei and somes into surrounding keratinocytes. DPD is notable by 72
vacuolated cytoplasm. Initially, sunburn cells localize in the epi- hours after UVB exposure, peaks after 5 to 10 days, then slowly
dermis’s lower half; after 24 hours, they are also found in the fades. Most tanning studies have been performed with erythemal
upper half. Sunburn cells may represent proliferating basal cells doses of UVR. Multiple suberythemal UVA exposures are signifi-
that cannot adequately repair UVR-induced DNA lysosomal cantly more melanogenic than is similarly dosed UVB.17 The
PART 3
damage.55 Stainable Langerhans cells (i.e., cutaneous antigen- mechanism of DPD is multifactorial. UVB stimulates tyrosinase
presenting cells) decrease rapidly: at 1 hour by 25% and at 72 release and arachidonic acid metabolites, and releases α-
hours by 90%.127 In mice exposed to repetitive suberythemogenic melanocyte-stimulating hormone from keratinocytes.8 UVB in-
doses of UVB, normal numbers of Langerhans cells return by 8 creases binding affinity of melanocytes for melanocyte-stimulating
days. Vacuolization of melanocytes is seen after 1 hour and hormone, resulting in increased melanocyte proliferation, mela-
returns to normal 4 to 24 hours after exposure. Mast cells decrease nization, and arborization.24 UVB increases melanocytes in both
in number and granularity within 1 hour, returning to normal exposed and protected skin,276 suggesting a UVR-stimulated cir-
after 12 to 72 hours.127 By 24 to 48 hours after exposure, there culating factor that promotes melanocyte proliferation.
are increases in melanin synthesis, epidermal proliferation, and
thickening of stratum corneum.
Biochemical changes that accompany sunburn include in-
PHOTOAGING
creased levels of histamine,127 which return to normal within 74 Repetitive long-term exposures to sunlight result in photoaging.80
hours. Histamine is unlikely to be the principal mediator of The process termed dermatoheliosis is clinically and histologically
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 BOX 16-2 Sunburn Treatments
blister aspirates immediately after UVB exposure, and peak after
18 to 24 hours.127 Topical and intradermal indomethacin (a pros- Pain Control
taglandin inhibitor) blocks UVB-induced erythema for 24 hours Acetylsalicylic acid
after exposure,268 supporting the thesis that eicosanoids (PGs Nonsteroidal antiinflammatory drugs
and leukotrienes) are significant mediators of UVR-induced
Skin Care
inflammation.151
Cool soaks and compresses
Nonmedicated moisturizers
SUNBURN TREATMENT Topical anesthetics
Pramoxine (Prax) lotion
Sunburn is self-limited. Treatment is largely symptomatic and Menthol plus camphor (Sarna) anti-itch lotion
involves local skin care, pain control, and antiinflammatory Anti-itch concentrated lotion (pramoxine) plus camphor plus
agents (Box 16-2). Studies of sunburn therapies include agents calamine (Aveeno)
used immediately after UV exposure (i.e., before symptoms Lidocaine plus camphor (Neutrogena Norwegian Formula)
have manifested) and agents for treatment of acute sunburn soothing relief moisturizer
reactions.110 Corticosteroids
Cool-water soaks or compresses may provide immediate relief
Topical agents (e.g., triamcinolone 0.1% cream applied twice daily
from sunburn. Topical anesthetics are sometimes useful; use when erythema first appears)
nonsensitizing anesthetics (e.g., menthol, camphor, pramoxine, Systemic agents
lidocaine) rather than potentially sensitizing anesthetics (e.g.,
338
There is increased demand for treatments to manage photoag-
339
(e.g., decreased DNA repair, UVR-induced immunosuppression) “sun-worshiping” lifestyle (sunbathing, tanning), poor preventive
likely play a permissive role. Patients with xeroderma pigmento- behaviors (e.g., insufficient use of sunscreen, hats, and covering
sum (XP) have increased numbers of p53 mutations,32 defective bathing suits), aging population, and depletion of the ozone
gene repair mechanisms, and greatly increased NMSC incidence. layer.
Cutaneous lymphomas show a higher frequency of UVR signature Exposure to UVR causes the majority of precancerous actinic
p53 mutations.193 In mycosis fungoides, mutations are found in keratoses and true skin cancers (Figure 16-3). Laboratory data
the tumor stage but not the plaque stage,193 suggesting that UVR confirm UVR induces and promotes NMSC in mammalian animal
promotes clinical progression of this lymphoma. Epidemiologic models.139 Ninety percent of all NMSC are attributed to sunlight
data demonstrate increased incidence of non-Hodgkin’s lym- exposure alone.251 NMSC has a much greater incidence in whites
phoma among persons who live closer to the equator.1 than in blacks and occurs primarily on sun-exposed areas. Risk
Other TSGs are less well studied but have increasingly defined for NMSC increases with increasing sun exposure. Repeated
roles in photocarcinogenesis. In melanoma, p16 is frequently sunburn is an independent risk factor.155 Patients with XP have
inactivated130 and increasingly downregulated as melanoma pro- impaired ability to repair UVR-induced DNA damage and
gresses.271 Another TSG, PTCH, which is also located on chromo- 1000-fold greater risk of developing NMSC, typically at a very
some 9, is frequently mutated in both familial and sporadic BCCa. early age.151
Mutations of PTCH are especially notable in patients with XP and Development of NMSC in humans is related to time and
multiple BCCa130 intensity of UVR exposure. British immigrants to Australia assume
In addition to downregulating TSGs, UVR can activate proto- the much higher Australian risk of NMSC only if they emigrate
oncogenes (e.g., bcl-2, c-fos, and ras) to form functional onco- before age 18 years; after that time, immigrants retain the lower
genes.130 In response to UVR, bcl-2 protein is overexpressed, British risk.187 Another study suggests NMSC risk decreases for
suppressing apoptosis and permitting expansion of malignant UVR exposure after age 10 years.154
clones. UVR alters c-fos, disrupting transcription of nuclear pro-
teins involved in cell proliferation. UVB causes mutations in ras, Basal Cell Carcinoma
BURNS, FIRE, AND RADIATION
disrupting mitogenic signaling pathways. Mutations in BRAF, a Basal cell carcinoma is associated with sun exposure up to the
critical component of the ras protein kinase pathway, are found age of 19 years but is not associated with mean annual cumula-
in a large percentage of nevi158 and melanomas,227 especially tive summer sun exposure.87 Risk for BCCa is associated with fair
melanomas that arise on intermittently sun-exposed skin.182 BRAF complexion and freckling. Intermittent (rather than continuous)
mutations occur only rarely in melanomas arising in chronically sun exposure in poor tanners may be the most important factor
sun-exposed or completely sun-protected skin,182 suggesting mul- in development of BCCa.155
tiple genetic pathways for melanoma induction. Mutations of Basal cell carcinoma includes a heterogeneous group of low-
BRAF and p53 may interact to form melanoma.227 grade malignant cutaneous tumors characterized by markers
UVR-related oxidative damage is another mechanism contrib- associated with hair follicle development. BCCa is the most
uting to photocarcinogenesis. Although UVA causes fewer direct common cancer in the United States and is most often found on
mutations than does UVB, it is a more potent cause of cellular the head and neck (Figure 16-4). In contrast with SCCa, BCCa is
oxidative damage, producing reactive molecular oxygen and relatively uncommon on the dorsal surface of the hand, where
nitrogen species. Oxidative damage to DNA, proteins, and lipids solar radiation exposure is high. While locally aggressive, BCCa
contributes to carcinogenesis through inflammation, immunosup- is rarely metastatic. Several clinical morphologies of BCCa exist;
pression, and ultimately mutation.109 The MMPs, a group of zinc- diagnosis depends on the astute clinician. Nodular BCCa, the
PART 3
dependent enzymes, increase in response to UVR to favor tumor most common form, manifests as one or a few small, pearly
invasion and spread.34,130 papules with a central depression. Telangiectasias may be seen.
Lesions are usually friable and frequently bleed when rubbed
Photoimmunology vigorously with a cotton-tipped swab. Pigmented BCCa is similar
Ultraviolet radiation produces local and systemic immunosup- to nodular BCCa but appears brown or black because of pig-
pression.216 UVB depletes immunocompetent antigen-processing mentation. Cystic BCCa manifests as bluish gray, dome-shaped
cells (Langerhans cells) for up to 2 weeks after exposure.204 UVB cystic papules or nodules similar in appearance to hidrocystomas.
alters Langerhans cells by interfering with their ability to present Morpheaform BCCa manifests as a white sclerotic plaque, usually
antigens to T cells.101 UVB diminishes type 1 helper T cell without the characteristic findings of a pearly border, leading to
responses (which promote contact hypersensitivity) while pre- this morphologic lesion often being overlooked or misdiagnosed
serving type 2 helper T cell responses (which suppress contact as a benign scar. Superficial BCCa, the most common pattern in
hypersensitivity), converting Langerhans cells from immunogenic patients with human immunodeficiency virus (HIV), favors the
to tolerogenic. As a consequence, UVR exposure diminishes trunk and distal extremities. It typically manifests as superficial,
contact hypersensitivity and mixed-lymphocyte reactions. This dry, scaly lesions that may resemble patches of slow-growing
may explain why UVR-induced skin cancers, which are antigenic, eczema or psoriasis; close examination typically reveals the char-
progress to clinical lesions. UVR-induced immunosuppression acteristic raised border. “Rodent ulcer” is a neglected BCCa that
can be transferred in mice with irradiated T lymphocytes.216 has ulcerated; consequently, the “rolled” border of the lesion may
Immunoregulatory failure contributes to formation of skin not be present or recognizable (Figure 16-5).
cancer.156 In immunosuppressed patients, skin cancer is often
more aggressive and occurs at an earlier age.71 In kidney trans- Squamous Cell Carcinoma
plant patients in Australia, 45% develop skin cancer within 11 Both UVC and UVB are effective inducers of SCCa in mice.127
years and 70% within 20 years.28 For heart transplant patients in SCC may begin as an actinic keratosis, appearing clinically as an
Australia, the incidence of skin cancer is 31% at 5 years and 43% irregularly bordered, pink, rough papule or plaque. Actinic kera-
at 10 years. In immunosuppressed patients, the ratio of SCCa to toses may be successfully treated with cryotherapy, topical
BCCa is 4 : 1, the opposite of the ratio in immunocompetent imiquimod, topical 5-fluorouracil (5-FU), and surgical removal.
patients.72 Of note, although kidney transplant patients are taking True SCCa, the second most common form of skin cancer,
higher doses of immunosuppressive drugs than are heart trans- may manifest clinically as dull-red, superficial, indurated, well-
plant patients, skin cancer rates appear higher in heart transplant demarcated papules and plaques arising on sun-exposed areas
patients. Chronic sun exposure and fair complexion further (i.e., the face and dorsal surfaces of the hands). Lower-lip lesions
increase risk of skin cancer in transplant patients, possibly as a may develop with actinic cheilitis; a history of repeated sunburns
result of overexpression of p53.93 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
NONMELANOMA SKIN CANCER crust that, when removed, reveals a discrete, indurated, and
Americans240 have a 20% lifetime risk of developing NMSC. The elevated base. Careful examination of regional lymph nodes is
incidence continues to rise.98 Factors that play a role include a warranted in suspected cases. Rate of metastasis ranges from
340
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 risk increases with chronic occupational exposure, especially
the temple, scalp, ear, or lip; recurrence after prior treatment; during the 10 years before diagnosis.87 SCCa risk factors include
size and depth of the primary lesion; aggressive histologic find- periodic recreational exposure, pale complexion, and red hair.
ings; and host immunosuppression. In select mouse models, suberythemal UVR has caused SCCa,
The relationship of photoexposure and SCCa is different than and gradual suberythemal exposures may be more carcinogenic
that between photoexposure and BCCa. SCCa and cumulative than erythemal doses.86,213 This may explain why persons with
lifetime photoexposure do not appear to be associated, but SCCa 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
increased to 92% in 2003, from 49% in the 1950s.238 The total hyperplasia, atypia, and melanoma in newborn human foreskin
estimated cost of treating melanoma was $2.36 billion in 2010.280 xenografts on RAG-1 (immunodeficient) mice.8
Melanoma includes different clinicopathologic types. Nodular Melanoma incidence increases with proximity to the equator
melanomas are typically smooth, dome-shaped, and friable in white populations142 in the United States, Australia, Scandina-
lesions occurring most frequently on sun-exposed areas of the via, and the nonwhite population of India.157 Intermittent intense
head, neck, and trunk. They are twice as common in men as in exposures pose a particularly high risk for melanoma.69 A 2005
women. Lentigo maligna manifests as a tan macule on sun- meta-analysis of 57 studies associates increased risk of melanoma
damaged skin that may darken and spread so slowly that patients with a history of intermittent sun exposure and sunburn.89 There
are often unaware of changes (Figure 16-7). It typically occurs is only a small increased risk for total sun exposure, and a
among older patients who live in sunny climates. Superficial decreased risk with heavy occupational exposure.70,89 Patients
spreading melanoma has no preference for sun-damaged skin with melanoma are twice as likely to relate a history of prior
and affects adults of all ages. Color variegation (i.e., dark brown, sunburn than are age-matched controls, and are three times as
black, red, white, blue) is common (Figure 16-8). Lesions may
arise de novo or in association with preexisting nevus. A new
342
likely to relate a history of multiple prior sunburns.70 Persons
343
absorber but provokes contact and photocontact dermatitis in Eight different UV filters (e.g., quinolone derivatives and novel
approximately 4% of exposed persons and can permanently stain UVA filters) are currently in the FDA application process. Already
fabrics a dull-yellow color. PABA has been largely replaced by in use in Australia and Asia, these filters will greatly broaden the
PABA esters (e.g., amyl dimethyl PABA [padimate A] and octyl U.S. sunscreen market if approved.37,231,287,298
dimethyl PABA [padimate O]). These absorb UVB well and are
less staining and less allergenic. Sunscreen Vehicles
Cinnamates are the next most potent class of UVB absorbers, Sunscreen vehicles affect efficacy and acceptability. The ideal
often replacing PABA in PABA-free sunscreens. Octyl methoxy- vehicle spreads easily, maximizes skin adherence, minimizes
cinnamate (octinoxate; Parsol MCX) is an order of magnitude less interaction with active sunscreening agent, and is noncomedo-
potent than padimate O.167 Octocrylene, which is a cinnamate genic, nonstinging, nonstaining, and inexpensive. The best
derivative, is a weak UVB absorber that also absorbs UVA mod- vehicle is highly dependent on personal preference. Creams
estly up to 360 nm. Cinnamates may cause contact dermatitis. and lotions (emulsions) are most popular. Lipid-soluble sun-
Cinoxate is the most frequent contact sensitizer, with cross- screening agents result in an objectionable greasy feel. “Dry
sensitization to related cinnamates in coca leaves, balsam of Peru, lotions” minimize the lipid component(s) and often include
and cinnamon oil.64 water-soluble sunscreening agents to reduce oiliness.167 Sun-
Salicylates (e.g., homosalate, octyl salicylate [octisalate]) are screen oils contain only a lipid phase and are cosmetically less
relatively weak absorbers of UVB. They are most often used in acceptable.
combination with other sunscreening agents. Salicylates are non- Gels tend to be nongreasy but wash or sweat off easily. Gels
sensitizing and water insoluble and help to solubilize benzophe- produce more stinging and irritation. Sticks typically incorporate
nones in commercial products.84 sunscreening agents into wax bases but are difficult to apply to
Anthranilates (e.g., methyl anthranilate [meradimate]) are simi- larger areas. Aerosols cover large areas quickly but tend to dis-
larly weak UVB absorbers, which also filter UVA. They display perse spray into the air and form an uneven film.167 Aerosols
peak absorption at 340 nm.167 need to be rubbed in to provide uniform protection.14 Sunscreens
BURNS, FIRE, AND RADIATION
Phenylbenzimidazole sulfonic acid (ensulizole) is a unique are increasingly being incorporated into cosmetics (e.g., founda-
UVB absorber, in that it is water soluble. It is increasing used in tions, lipsticks, moisturizers).
oil-free cosmetic sunscreens.167
Benzophenones (e.g., oxybenzone, dioxybenzone, sulisoben- Sun Protection Factor
zone) are broader-spectrum sunscreening agents, with good A sunscreen’s ability to protect skin from UVR-induced erythema
absorption in the UVB and UVA ranges up to 360 nm.167 is measured by the sun protection factor (SPF). SPF is defined
As UVA photodamage is increasingly appreciated, UVA- as the ratio of UVR required to produce minimal erythema (1
blocking agents (e.g., avobenzone, ecamsule) have been MED) in sunscreen-protected versus unprotected skin.139,284 Mul-
introduced. Avobenzone (Parsol 1789, butyl methoxydibenzoyl- tiplying the time required to burn an individual’s unprotected
methane) is a potent UVA absorber and the only organic filter skin by the sunscreen’s SPF factor provides the time skin would
approved as a long-range UVA protectant.167 Its absorption be protected from burning with sunscreen. It can be represented
peak at 358 nm falls almost to zero at 400 nm.243 Photodeg by the following formula:
radation may limit its effectiveness. Under simulated solar
light, avobenzone can be degraded 36% within 15 minutes,250 MED of sunscreen-protected skin
but a patented complex known as Helioplex, a combination SPF =
MED of unprotected skin
PART 3
344
in vitro test to demonstrate broad-spectrum protection. Perfor-
8 87.5 ∫ A ( λ ) d λ = 0. 9 ∫ A ( λ )d λ
15 93.3 290 290
345
sunscreens are truly surf resistant. The concerns about saltwater There are few published data regarding packaging, storage,
substantivity have led to marketing of “surf shop” sunscreens. and shelf life of sunscreens. Packaging may affect sunscreen
Few published data indicate whether these products are more acceptability and stability. Shelf life of at least 1 year is presumed
substantive. for most commercially available sunscreens. Sunscreens exposed
The PABA and PABA esters are intrinsically substantive as a to extremes of temperature for long periods (e.g., glove compart-
result of bonding to stratum corneum proteins. Other sunscreens ments) may be degraded.
must be incorporated into vehicles that confer substantivity.
Substantivity can be increased by applying sunscreen 15 to 30 Sunscreen Prevention of Chronic Photodamage
minutes before water exposure. Reapplication after swimming Sunscreens prevent sunburns and mitigate UVR-induced histo-
or sweating increases protection. Affordable UVA- and UVB- logic damage, UVR-induced immunosuppression, photoaging,
protective water-resistant sunscreens are widely available and photocarcinogenesis. Sunscreens reduce UVR-induced DNA
(Table 16-3). damage,41 decreasing pyrimidine photoproducts in humans41 and
UVR-induced p53 mutations and skin cancer in mice.5 Sunscreen
Stability nearly eliminates overexpression of p53 in mice after acute233 and
Photostability is a sunscreen’s ability to remain intact and chronic88 UVR exposure. In humans, an SPF 15 sunscreen reduces
effective after sun exposure. Questions regarding photostability p53+ cells by 33% after chronic UVR exposure.18
have been raised about avobenzone, octyl dimethyl PABA, and Published effects of sunscreen on immunosuppression are
octyl methoxycinnamate. Photodegradation of octyl methoxycin- contradictory, largely resulting from the complex relationships of
namate allows histologic and enzymatic injury to the skin.188 UVR dosing and sensitivity in different experimental models.
Failure of a photolabile sunscreen may result in genotoxicity.189 Overall, sunscreens mitigate UVR-induced immunosuppression.
In a study of 27 photoprotective lipsticks, 14 became partially SPF is not a reliable measure of a sunscreen’s ability to block
photoinactive after moderate UVR exposure.181 Twelve were pho- UVR-induced immunosuppression; two sunscreens with identical
tolabile in the UVA range, one in the UVB range, and one in SPF values may vary considerably in their immunoprotectant
BURNS, FIRE, AND RADIATION
both UVA and UVB ranges. effects.16,237,314 A broad-spectrum SPF 15 sunscreen prevents the
Photostability can be improved by using combinations of UVR-induced suppression of contact hypersensitivity to dinitro-
sunscreening agents. Octocrylene stabilizes avobenzone in a chlorobenzene, a potent topical allergen, in humans.259 In suscep-
number of sunscreen formulations; 4-methylbenzylidene camphor tible mice injected with melanoma, sunscreens fail to adequately
stabilizes octyl methoxycinnamate.25 Vehicle formulations also suppress UVB enhancement of melanoma growth.305 This finding
affect stability.25 has been used to support a peculiar antisunscreen stance. A
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
CHAPTER 16 Exposure to Radiation from the Sun
FIGURE 16-10, cont’d
reasonable interpretation is that sunscreens by themselves are not age 18 years would reduce the lifetime risk of NMSC by 78%,
sufficient to prevent all immunosuppressive sequelae of UVR but did not show a significant decline in BCCa.275
exposure.
Sunscreens reduce sunburn cell formation and solar elastosis29 Sunscreens and Melanoma
in humans. Histologic changes of photoaging in mice are pre- Controversy exists regarding the effects of sunscreen use on
vented by pretreatment with SPF 15 sunscreen.146,147 Higher-SPF melanoma incidence. Previous epidemiologic studies have failed
sunscreens provide increasing protection against UVB-induced to demonstrate conclusive evidence of decreased melanoma inci-
wrinkling in mice.22 Histologic and clinical signs of UVA-induced dence with sunscreen use. Several studies have suggested an
photoaging are prevented by broad-spectrum sunscreens.114 increased risk of melanoma with sunscreen use.12,62 A 1996 meta-
analysis evaluated melanoma risk in sunscreen users;62 one study
Sunscreens and Nonmelanoma Skin Cancer showed decreased risk,124 and seven showed increased risk.
Daily sunscreen use is associated with prevention of AKs, SCC, Subsequent studies have continued to show contradictory results.
and melanoma.103,56 Confounding these studies are the following:
Actinic Keratoses and Squamous Cell Carcinoma. Sun- • Persons at the highest risk for melanoma (i.e., those with fair
screen use reduces formation of precancerous actinic keratosis complexions who burn easily) may be the same persons who
and promotes resolution of preexisting lesions.48,212 In a 2-year use sunscreens.
trial of sunscreens, persons who benefited most had the greatest • Prior sunscreen products were inferior (e.g., lower SPFs and
number of keratoses at enrollment,212 underscoring the value of narrower spectra). Modern sunscreens are more substantive,
continuing sunscreen use in adults. A trial in Australia comparing with higher SPFs and substantially broader and better UVA
an SPF 16 sunscreen (2% avobenzone and 8% octinoxate) against protection.
a sunscreen of the participants choosing, found a 24% reduction • Because sun exposure during childhood appears to be the
in actinic keratosis development and acquisition at 4.5 years and most provocative for melanoma, surveying adults about their
a 38% reduction in SCCa.104 Liquid-base makeup provides an current sunscreen habits may be irrelevant and misleading.
approximate SPF 4 because of pigments used in the founda- A large, community-based 2011 study in Australia provides
tion.167 Women who use lipstick have a lower incidence of SCCa strong evidence that daily application of sunscreen may directly
than those who do not use lipstick.120,167 reduce melanoma risk.103 During 15 years of follow-up, in persons
Basal Cell Carcinoma. Daily use of SPF 15 sunscreen in provided with broad-spectrum (SPF 16) sunscreen for daily
adults reduces the incidence of SCCa but not of BCCa.104 One use, risk for any first primary melanoma was reduced by 50%
study estimated that using an SPF 15 sunscreen from birth until (p = 0.051) and for invasive melanoma by 73% (p = 0.045).
347
TABLE 16-3 Select Sunscreen Products
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
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 well established in the literature.138 Extraskeletal effects of vitamin
349
for all-cause mortality, cardiovascular disease, vascular calcifica- reduces formation of skin cancers in patients with XP.17 Wearing
tion, pancreatic cancer, falls, frailty, and fractures. The recom- long sleeves was associated with lower 25(OH)D levels.169
mended UL for vitamin D follows131: However, 100% cotton clothing transmits 15% of UVR. Adequate
• 9 years and older, 4000 IU per day vitamin D levels can be achieved even if only the face and palms
• 4 to 8 years, 3000 IU per day are exposed.269
• 1 to 3 years, 2500 IU per day Ladies’ hosiery provides surprisingly low SPF: black hose have
• 6 to 12 months, 1500 IU per day SPF of 1.5 to 3, and beige hose SPF of less than 2.262 Hat protec-
• 0 to 6 months, 1000 IU per day tion varies as a function of brim diameter and style. Small-
These recommendations have been upheld by the U.S. Pre- brimmed (<2.5 cm [1 inch]) hats adequately protect the forehead
ventive Services Task Force Unit in its 2013 recommendations, and the upper nose; medium-brimmed (2.5 to 7.5 cm [1 to 3
with a goal of 800 IU for asymptomatic adults older than 65.209 inches]) and wide-brimmed (>7.5 cm [3 inches]) hats protect
proportions of the nose, cheeks, chin, and neck.60 Wide-brimmed
OTHER SOURCES OF SUN PROTECTION 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.
Clothing Protection They protect the forehead well, allowing sunscreen application
Clothing provides substantial sun protection to broad surface below the cheekbones, thus mitigating the risk of stinging from
areas. The United States has the most stringent UV-protective application near the eyes.
clothing standards in the world and assesses fabrics using the Glasses, contact lenses, and sunglasses protect the corneas
ultraviolet protection factor (UPF). UPF measures both UVB and from most UVB and from variable amounts of UVA.247 A complete
UVA radiation blocked. Approved fabrics must undergo 40 simu- discussion of this is provided in Chapter 48.
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
SUN AVOIDANCE
BURNS, FIRE, AND RADIATION
Although the FDA was initially involved, the Federal Trade Com- An indoor lifestyle is undesirable for most persons. More practical
mission now reviews clothing applications. is avoidance of excessive midday sun (i.e., 10 AM to 3 PM), which
Several manufacturing strategies are used to achieve high significantly reduces UVB exposure.172 Shade provides variable
SPFs. Solumbra is made of tightly woven nylon with an SPF of protection. In one study, shade beneath leafy trees provided SPF
30 or more (Figure 16-11). In hairless mice, this fabric is signifi- of less than 4.225 Shade cloths allow significantly more UVB
cantly better than cotton for reducing formation of UVR-induced exposure than does clothing of the same fabrics, largely because
SCCa.197 SolarKnit uses chemically treated cotton and cotton- of atmospheric scattering and surface reflection.306
synthetic blends to achieve an SPF of 30 or more. Rayosan, a Automobile windshields block UVB and some UVA. Side
UVR-absorbing agent, bonds to various fabrics and increases the windows typically block only UVB.282 This may explain why
SPF by up to 300%.176 Tinosorb FD, a unique organic UVR pro- photodamage is more prominent on the left side of the face of
tectant, may be incorporated into detergents to increase the SPF Americans (and on the right side of the face of Australians) who
of clothing with each wash. drive a great deal.58 Factors that affect UV-protective properties
Unregulated clothing varies considerably in ability to block of glass include color, type, coating, and interlayers between
UVR. The SPF fabrics range from 2 (polyester blouse) to 1000 layers of glass. Transparent plastic films that meet legal require-
(cotton twill jeans).242 A typical dry white cotton T-shirt has SPF ments in all 50 states can be applied to block more than 99% of
PART 3
of 5 to 9.242 The most important factors for determining SPF are UVR (e.g., LLumar UV Shield).
tightness of the weave176,242 and the actual fabric. Lycra is an
extreme example of this; it blocks almost 100% of UVR when lax SUNLESS TANNING
and only 2% when maximally stretched.176 Other determinants
include wetness and color. Dry and dark fabrics have a higher Bronzers
SPF than do wet and white fabrics. Most artificial tanners and bronzers contain dihydroxyacetone
Clothing prevents chronic photodamage and is associated (DHA). DHA reacts with amino groups of keratin proteins by the
with fewer nevi.10 Blue denim reduces UVR-induced p53+ cells Maillard reaction to form brown-pigmented products known as
twice as effectively as does an SPF 15 sunscreen.18 Denim greatly 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.
A B These stimulate melanin synthesis, but are tumorigenic in mice.45
Psoriasis patients treated with psoralen plus UVA (PUVA) have
FIGURE 16-11 Photoprotective clothing. A, Solumbra hiking apparel. a higher incidence of SCCa275 and melanoma.274 Psoralen-
B, Coolibar swimwear. (A courtesy Sun Precautions; B courtesy containing sunscreen is associated with increased risk of subse-
Coolibar.) quent melanoma.12 Oral carotenoids (e.g., canthaxanthin) are
350
potentially toxic and consequently not approved in the United topical vitamin E) may provoke contact sensitization and serve
351
tan is the index of chic” characterized the times. This attitude led BOX 16-3 Common Oral Photosensitizing Medications
to dangerous behaviors and created cultural norms that remain
challenging to overcome. Numerous recent studies document Antihistamines
continued skepticism toward photoprotection.15,149,194,318 Fluoroquinolones
Even patients with sun-related problems often do not adopt Nonsteroidal antiinflammatory drugs
adequate sun protection habits. One study documented that Oral contraceptives
patients with dysplastic nevus syndrome, at high risk for mela- Phenothiazines
noma, do not avoid sunburning.30 Among patients 1 year after Sulfonamides
treatment for BCCa, only 49% wore hats or long sleeves in the Sulfonylureas
summer, and 62% used less than two bottles of sunscreen per Tetracyclines
year.115 Studies found that organ transplant recipients did not Thiazides
considerably improve sun-protective behaviors after their Tricyclic antidepressants
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 identifying the specific causative agent is crucial, and discontinu-
survey of American adults, 42% were aware of the term mela- ation or substitution should be considered.
noma, and 34% knew it was a type of skin cancer.199 Some use Treatment for polymorphous light eruption includes super- or
sunscreens in the belief that sunscreens will promote tanning. high-potency topical corticosteroids for several daily to weekly
More education is needed. In college students in Southern Cali- pulses, frequently in combination with systemic antihistamines
fornia, a 12-minute videotape about photoaging in conjunction (e.g., diphenhydramine, hydroxyzine, doxepin). Hardening of
with UV facial photography resulted in improved sun-protective the skin in the spring with UVB, narrow-band UVB, or PUVA
behaviors 1 month after the education.180 In Australia, where can be very effective. Systemic antimalarials (e.g., 200 to 400 mg/
there are significant educational efforts about UV-related skin day of hydroxychloroquine sulfate, started in late winter) are
BURNS, FIRE, AND RADIATION
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- streaks and postinflammatory hyperpigmentation after exposure
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FIGURE 16-12 Phytophotodermatitis on a teenager after a “lime online at expertconsult.inkling.com.
fight” that took place during an outdoor summer picnic.
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PART 3
353.e6
CHAPTER 17
Volcanic Eruptions, Hazards,
and Mitigation
JOANNE FELDMAN AND ROBERT I. TILLING
Volcanic eruptions are spectacular, violent, and often quite dan- years, the average is two to four fatal volcanic events per year.
gerous expressions of Earth’s dynamic internal processes (Figure Causes of death and number of fatalities are not well docu-
17-1). More than 80% of the earth’s surface above and below sea mented.73 As the most deadly volcano hazards, pyroclastic flows
level is of volcanic origin, and gaseous emissions from volcanoes have claimed the most lives, whereas tephra is the most common
helped form Earth’s oceans and atmosphere.24 On average, about killer (Box 17-1). Long after the eruption, famine and disease
60 to 70 eruptions occur worldwide each year; half of these are epidemics are responsible for up to one-third of the total fatalities
continuations of previously erupting volcanoes, and the others attributed to explosive eruptions73 (Tables 17-2 and 17-3).
are new eruptions.70,79 There are approximately 600 active volca- Compared with other natural disasters, volcanic eruptions
noes in the world and probably another 800 that have erupted occur infrequently, affect few people, and are responsible for
at least once during the past 10,000 years.79 Some volcanoes erupt only a small percentage of fatalities. Only about 2% of all natural
only once in their lifetime, whereas others erupt repeatedly or disasters are from volcanic activity.38,74 The deadliest volcanic
even continuously. The largest explosive eruptions occur infre- eruption in history, Tambora, Indonesia in 1815, killed approxi-
quently; in general, the longer the time interval between erup- mately 60,000 people, whereas 1 million people were killed in
tions, the larger the next eruption tends to be. Some of the worst the worst hurricane (Ganges Delta in Bangladesh, 1970) and
volcanic catastrophes in history have occurred at volcanoes 830,000 were killed in the worst earthquake (Shaanxi earthquake
believed to be extinct, including the famous eruption of Vesuvius in China, 1556).41,71,79 Nevertheless, volcanoes have the potential
in AD 79, which destroyed the cities of Pompeii and Herculaneum to unleash one of the most destructive forces on Earth. Approxi-
(see later).79 In fact, in the past two centuries, 12 of the 17 largest mately 74,000 years ago, an Indonesian volcano named Toba
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
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
FIGURE 17-1 Eruption of Mt St Helens on May 18, 1980. (Courtesy summit caldera. (A, MODIS/NASA image, May 3, 2008; B courtesy
Robert M. Krimmel, U.S. Geological Survey.) John Pallister, U.S. Geological Survey.)
354
CHAPTER 17 Volcanic Eruptions, Hazards, and Mitigation
TABLE 17-1 Some Notable Historical Volcanic Eruptions
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.
355
TABLE 17-2 Causes of Fatalities from Notable Volcanic Disasters Since 1000 AD
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/.
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.)
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
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.)
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
Oc
Isl ea
an nic
Tre
d
ar Tr Shield rid spre nc
c ge ad h
volcano ing
en
Strato-
ch
te Hotspot ting e
M
pla plat
e
ting
uc
bd Mantle
Su
Mantle plume ?
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
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
e
au
ng
ra
late
ain
nt
hp
ou
Hig
Continental crust
Continental crust
Lithosphere Lithosphere
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 are Long Valley Caldera in California and Valles Caldera in New
boundaries (e.g., Hekla in Iceland, Mt Kilimanjaro in Tanzania) Mexico. Outside the United States, very large calderas include
or at hot spots (e.g., Mt Erebus in Antarctica, Tenerife of the Campi Flegrei in Italy, Kamari Caldera on the island of Kos in
Spanish Canary Islands).65,66 The steep-sided shape results from the eastern Aegean Sea, and Rabaul Caldera in Papua New
deposition of viscous lava flows alternating with pyroclastic flows Guinea. Fortunately, very large caldera-forming eruptions were
and ashfall deposits. The explosive nature of composite volca- rare events, occurring approximately once in hundreds of thou-
noes comes from high viscosity and volatility of the magma sands of years (Figure 17-17).66
(Figure 17-15).
GENERALLY NONEXPLOSIVE VOLCANOES
Calderas
Formed by collapse of a volcanic structure, calderas are circular Shield Volcanoes
or elliptical depressions, generally more than 1 km (0.62 mile) Shield volcanoes have gentle slopes and are formed almost ex-
in diameter. Crater Lake in the U.S. Cascade Range is a large, clusively of layers of lava that have often flowed great distances
partially filled caldera 10 km (6.2 miles) in diameter and 600 m from the eruptive vents. The magma, unlike that of explosive
(1970 feet) deep, formed when Mt Mazama exploded 7700 years volcanoes, is predominantly of low viscosity and low volatility.
ago. Krakatau, in Indonesia, was created by an 1883 eruption Shield volcanoes are mostly formed at hot spots, although some
that involved rapid emptying of the magma chamber and subse- are located at convergent or divergent plate boundaries—for
quent collapse of the volcano.65 Kilauea Crater is another well- example, Erta Ale in Ethiopia and Mt Etna in Italy. The largest
known caldera (Figure 17-16). volcanoes on Earth, Mauna Loa and Mauna Kea of Hawaii, are
Very large calderas fed by huge active magma chambers have classic examples of shield volcanoes (Figure 17-18).
been called supervolcanoes and are capable of producing enor-
mously explosive eruptions. Yellowstone Caldera, 85 km (53 Subglacial Volcanoes
miles) long by 45 km (28 miles) wide, the largest and most wor- Historically active volcanoes located under glaciers, called sub-
risome in the United States, has a magma chamber that is 40 km glacial volcanoes, are known only in Iceland and Antarctica. They
(25 miles) long, 20 km (12 miles) wide, and 10 km (6 miles) can erupt explosively, but thick glacial ice cover generally inhib-
deep.66 Yellowstone has produced explosive eruptions 1000 its material from being ejected high into the atmosphere. Instead,
times larger than the 1980 Mt St Helens eruption. Two other lava generally is erupted effusively, forming flows that often melt
geologically young, large calderas located in the United States 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
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 injury from lightning or ionizing radiation injury from radon gas
Some volcanic eruptions cause injury, death, and destruction (Figure 17-22).4 Most volcano-related deaths, injuries, and psy-
within minutes to hours. Others produce hazards that pose risks chosocial effects occur because the volcano erupts violently and
to human life, livestock, and the environment for months to years rapidly, leaving little or no time for people to escape or take
after the eruption. Explosive and nonexplosive volcanoes gener- shelter.57 However, significant fatalities have been associated with
ate unique hazards, but explosive eruptions are usually associ- mudflows and release of toxic gases during noneruption periods.
ated with much larger numbers of deaths. Unfortunately, global distribution of explosive volcanoes, mostly
along convergent plate boundaries, places them in densely popu-
lated areas.7 Fortunately, explosive eruptions occur infrequently,
HAZARDS FROM EXPLOSIVE VOLCANOES and technologic advances have increased the ability of volcanolo-
Volcanoes with explosive characteristics are extremely danger- gists to predict an eruption. Before the 1980 and 2004 eruptions
ous. They can cause thermal injury from hot gases and ash; of Mt St Helens, 1991 eruption of Mt Pinatubo, and 2010 eruption
mechanical injury from mudflows, debris avalanches, and falling of Mt Merapi, high-risk zones around the volcanoes were evacu-
tephra; chemical injury from toxic gases; and rarely, electrical 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- surrounding air, it collapses and falls back toward the ground.
tubo, which was the largest eruption in the world in the 20th Such gravitational collapse of the cloud leads to formation of a
century. hot, high-speed avalanche of ash, volcanic gases, lava fragments,
and heated air, called a pyroclastic flow.65 Pyroclastic surges are
Pyroclastic Flows and Surges similar to flows but are more dilute and less dense and can travel
Typically, when an explosive volcano erupts, a volcanic cloud farther4 (Figure 17-23).
of gas, ash, and lava fragments rises vertically into the atmo- There is little chance for survival in the direct path of a pyro-
sphere. If this rising eruption cloud becomes denser than the clastic flow or surge traveling at 300 km/hr (186 miles/hr) or
PART 3
364
Ice cap Subglacial lake Skin should be completely covered, the head swathed in cloth,
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
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
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.)
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 FIGURE 17-28 Early in the morning on April 1, 1946, an earthquake
prolonged. (magnitude 7.1) in the Aleutian Islands off Alaska sent large, destruc-
tive waves toward the Hawaiian Islands. Five hours later, the waves
Tsunamis struck the Big Island, killing 159 people, including many curious school-
Tsunami, the Japanese term for harbor wave, is a seismic sea children who ventured into the exposed reef area, not knowing the
wave triggered by an earthquake or by volcanic activity. Specific receding water was a sign of an approaching tsunami. Pictured are
people fleeing the approaching tsunami (seen in background) in Hilo,
BURNS, FIRE, AND RADIATION
although it is difficult to know the exact figure (Figure 17-27). 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
FIGURE 17-27 Hundreds of dead bodies and debris are piled along Northeastern Atlantic, the Mediterranean and Connected Seas
the coast, a dramatic demonstration of devastation caused by tsunamis Tsunami Warning System—have been established but are still in
affecting the Indian Ocean basin, this one triggered by the Banda Aceh the planning stages and not yet fully operational. The United
earthquake, December 26, 2004. (Photographer unknown.) Nations Intergovernmental Oceanographic Commission, through
368
CHAPTER 17 Volcanic Eruptions, Hazards, and Mitigation
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 Ballistic Ejecta. An erupting volcano can eject huge ballistic
four systems. fragments at high velocities (Figure 17-30). These can travel
Evacuation to higher ground is essential to reduce morbidity kilometers away from the volcanic vent and can cause significant
and mortality associated with tsunamis, and effective evacuation damage (skull injuries, lacerations, blunt trauma of the chest and
depends on public education of the officials and inhabitants of abdomen) to humans on impact.4,66 The zone of damage from
coastal communities. Emergency medical personnel need to be volcanic ballistics is generally limited to about 5 km (3 miles)—
prepared to treat drowning victims, the effects of trauma, and the maximum recorded range—so this is rarely a major human
disease epidemics. health hazard.4 However, in Italy in 1944, three men were killed
at Terzigno by falling volcanic rocks from Mt Vesuvius 5 km (3
Debris Avalanches miles) away. In 1924, an explosive eruption at Kilauea knocked
Volcanoes, especially steep-sided composite volcanoes, can be a photographer down with flying stones and severed his leg. He
the site of catastrophic debris avalanches at any time.65 In 1792 died later that day, probably from toxic gas exposure.10 Fire is a
at Mt Unzen, mentioned previously, it was a debris avalanche more common hazard, because hot flying ejecta can set fire to
that swept down the side of the volcano, killing thousands before wooden structures, forests, or grassland.
emptying into the sea and setting off a devastating tsunami. Also Volcanic Ash. Smaller-sized tephra, especially ash, pose a
in Japan, in 1888 an avalanche from the north flank of Bandai much greater danger than do blocks and bombs. Drifting volcanic
volcano sent 1.5 km3 (0.36 cubic mile) of debris down the moun- ash can be deposited hundreds to thousands of kilometers down-
tainside, killing 400 people below.65,66 A debris avalanche also wind from a volcano. Heavy accumulations of ashfall can col-
contributed to the eruption of Mt St Helens in 1980. Triggered lapse roofs, interfere with driving, clog machinery, and damage
by an earthquake, a debris avalanche on the north flank of the vegetation (Figure 17-31).
mountain removed rock overlying a shallow magma chamber. A layer of ash only 10 cm (4 inches) thick is enough to col-
Pent-up volatile gases in the magma, no longer contained by the lapse a flat roof, especially if it is wet with rainfall.60,66 Approxi-
overlying pressure of the rock, quickly expanded, causing explo- mately 10,000 fatalities have been directly associated with ashfall,
sive fragmentation of the magma and the first eruption. and the majority of these are from collapsed roofs. In 1991, Mt
Mitigation. Mitigating danger from debris avalanches in- Pinatubo in the Philippines erupted during an untimely typhoon.
cludes mapping the zones of potential slope collapse and avoid- Subsequent ash mixed with rain collapsed roofs and killed at
ing travel to and high-density development within those areas. least 300 people.66
Fatalities and injuries are associated with blunt trauma and burial Decreased visibility from airborne ash and slippery ash-coated
beneath rock debris. A victim caught in a rock fall should im- roads pose danger to drivers of motor vehicles. During and after
mediately seek some sort of shelter and roll into a ball to protect an eruption, the incidence rises of motor vehicle crashes and
the head. Health care professionals need to be prepared for associated injuries. Moderate amounts of ashfall can also directly
victims of blunt trauma. damage motors and other machinery, because fine ash clogs
engine filters and lubrication systems.66 Damaged machinery is
Tephra rarely a risk to human health, except in the case of jet engines.
Tephra is the general term for fragmented rock of any size (vol- Volcanic ash clouds contain a combination of fine rock and
canic blocks, glass shards, pumice, ash) ejected into the air by glass particles. If a jet aircraft flies into a volcanic ash cloud, even
volcanic explosions. Tephra can range in size from large ballistic thousands of kilometers away from the eruption site, the ash can
ejecta (>1 m [3.3 feet]) to ash (<2 mm). The largest tephra fall damage engines, avionics, and airframes. Ash particles can block
back to the ground at high speeds in the immediate vicinity of fuel nozzles, air filters, and external navigational equipment.
the volcano. Smaller fragments stay airborne longer, and the Abrasion damage can severely scratch cockpit windows, landing
smallest are carried away by prevailing winds before ultimately lights, and turbine blades. Volcanic glass sucked into the engine
being deposited, even at distances of many hundreds of kilome- will melt in the heat, accumulate, and solidify into a glassy layer
ters from the volcano. 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
with sensors, leading to reduced engine performance and ulti- 11, 2001, terrorist attacks on the United States. An ash cloud from
mately total engine failure. High levels of static electricity in the 2011 eruption of Grimsvötn caused a similar crisis for com-
volcanic material can also interfere with radio communication. mercial aviation. This time, however, even though the Grimsvötn
Comprehensive summaries of the damage and impacts of volca- plume was very large, it lasted for a relatively short time. Equally
nic ash on aircraft operating and support systems have been important, the international civil aviation agencies had learned
described.14,53 valuable lessons from the Eyjafjallajökull experience in how to
Since the mid-1950s, more than 80 commercial aircraft have better manage a volcanic ash crisis. These two factors combined
accidentally flown into eruption clouds, and seven of these to greatly reduce the impact of the Grimsvötn eruption on global
encounters caused in-flight loss of jet engine power.28,55 In 1982, air travel.76
two jetliners flew into the eruption cloud from Galunggung Heavy ash can strip vegetation from plants and coat surviving
volcano on Java. The first, a British Airways jumbo jet carrying leaves. Destroyed vegetation and crops result in starvation of
240 people, lost all four engines and plummeted 7500 m (24,600 animals and can ultimately lead to famine in areas dependent on
feet) in 16 minutes before cold air chilled and shattered the agriculture for subsistence. Famine from ash-related destruction
volcanic glass and the engines could be restarted. The jet made of crops was the number-one cause of fatalities associated with
an emergency landing at Jakarta airport with three functioning volcanic eruptions before the 20th century. With global com-
engines and flying blind because the windshield was opaque munication and world relief organizations, famine is now less
from ash abrasion. A few weeks later, a Singapore Airline jumbo common.
jet flew into a volcanic ash cloud from the same volcano, lost Most volcanic ash poses little direct danger to humans. Eye
three engines and dropped 2400 m (7874 feet) before one engine irritation may cause conjunctivitis and corneal abrasion, espe-
restarted, and the aircraft was able to make an emergency landing cially in persons wearing contact lenses.39,60 Nose and throat irrita-
(Figure 17-32).10 Fortunately, to date no lives have been lost from tion are common in persons not wearing a mask. Inhalation of
aircraft–volcanic ash encounters. However, in mid-April 2010, the ash, typically thought to be a significant health hazard, is for the
high eruption cloud from the Eyjafjallajökull eruption (Figure most part benign, except for people with preexisting lung disease
17-33A) and its easterly drift over northern Europe (Figure and heavily exposed workers, such as gardeners, road workers,
17-33B) raised serious concerns of possible damaging encounters and police.6,8,11,15,26,50,67,86 Most ash particles are too large to be
between commercial aircraft and volcanic ash. As a precautionary respired, high dust concentrations are of brief duration, and ash
measure, aviation officials closed many airports and grounded is biologically inert.60,83
flights in the United Kingdom, France, Germany, Norway, However, fine ash particles less than 10 µm in diameter can
Sweden, Finland, and Spain; many Europe-bound flights from irritate the lungs. This is especially dangerous for people with
the United States were also cancelled. The many airport closures asthma and chronic bronchitis and results in increased visits to
and flight cancellations (>107,000) resulted in the largest disrup- emergency departments (EDs) for exacerbation of chronic lung
tion in commercial aviation since that caused by the September disease.54,68 For example, after Mt St Helens erupted in 1980,
370
Mitigation. To prevent injury from large-size tephra, danger
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 A
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.)
371
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
A asphyxiant, and at concentrations higher than 20%, even a few
breaths can very quickly lead to unconsciousness and death
from acute hypoxia, severe acidosis, and respiratory paralysis.
H2S, the colorless gas that smells like rotten eggs, is so toxic that
a high-level exposure can kill a human after a single breath.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
BURNS, FIRE, AND RADIATION
Lake
Nyos
w
flo
gas
2
CO
372
was erupting at the time.35,66 Chronic low-level H2S exposure may
373
caused the death of an estimated 60,000 people in Indonesia and
Vog free 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
A the lymphatic system, causing inflammation, lymphatic fibrosis,
and ultimately blockage. As the lymphatics are obstructed, the
lower extremities swell, resulting in elephantiasis. Podoconiosis
Heavy vog 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-
BURNS, FIRE, AND 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 RISK REDUCTION FROM
sulfur oxides, into the air. Introduced vegetation, such as Kona coffee
plants, can be scorched, and downwind of Kilauea, only native species
VOLCANIC HAZARDS
PART 3
tolerant of the natural acid rain survive. The two images compare Humans are vulnerable to severe, unpreventable volcanic erup-
atmospheric clarity between a volcanic-smog (vog)–free day (A) and a tions. Risk reduction starts with comprehending the seriousness
heavy-vog day (B). (Courtesy Jeff Sutton, U.S. Geological Survey.) 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,
of hydrogen chloride, and 15 MT of HF were released into the sometimes on the volcano slopes or on the remains of a previ-
atmosphere.84 HF poisoned most of Icelandic sheep and destroyed ous pyroclastic flow, lahar, or debris avalanche.60,66 Fortunately,
crops, contributing to the death of nearly a quarter of Iceland’s most volcanic eruptions are preceded by premonitory events,
entire population from famine.64 In addition, the Laki eruptions such as earthquakes and other measurable phenomena, far
were probably responsible for the death of more than 10,000 enough in advance to enable scientists and emergency workers
people in England during summer 1783 and winter 1784. Noting to plan for disaster. However, a few of the most severe erup-
that the mortality rate was 16.7% above normal for this time tions have occurred with little or no warning, and most of the
period, experts in the United Kingdom suggest that a cloud of world’s dangerous volcanoes are in densely populated coun-
volcanic gases and particles swept south from Laki into England tries that lack the resources or political interest to monitor
and was responsible for the very hot 1783 summer and subse- them.5,79
quent severe winter.64,84 Climatic data, burial records, and written Nevertheless, emergency planning for an eruption, including
accounts describe a summertime “volcanic haze” or “dry fog” that creation of hazard-zone maps and hazard evaluation, should be
shrouded the moon and sun, reduced visibility, withered vegeta- routine for all populated areas near volcanoes, regardless of their
tion, and caused health problems.22,64 As with smog, the dry fog location or apparent state of activity.5 Risk reduction includes
caused headache and eye irritation, exacerbated lung disease, volcano monitoring, eruption prediction, and effective coordina-
and irritated mucous membranes. Wintertime deaths were associ- tion between volcanologists, scientists, health care professionals,
ated with unusually cold temperatures. Benjamin Franklin, U.S. and the community at risk. In addition, with tourism increasing
ambassador to France in Paris at the time, was the first to link to volcanic destinations, the tourist industry, practitioners of
the effect of Laki’s eruption on climate and presented a scientific travel medicine, and adventure travelers need to educate them-
paper on the topic. selves and others about the potential health hazards of volcanic
Eruption clouds that penetrate the upper atmosphere can environments.29
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.
VOLCANO MONITORING
The 1991 eruption of Mt Pinatubo in the Philippines created a Scientists monitor volcanoes for seismic activity (earthquakes),
large volcanic cloud that drifted around the world and caused a changes in volcano shape (ground deformation), surface tem-
temporary average global temperature drop of 0.5° C (0.9° F).40 perature, magma level, gas emissions, and other chemical and
The largest eruption in recorded history in 1815 at Tambora, physical attributes (Figure 17-38).57 Earthquakes and ground
Indonesia, reduced the average global temperature by 3° C deformations are the most reliable diagnostic observations for
(5.4° F) for several years.40 This eruption directly or indirectly helping scientists predict when a volcano might erupt or when
374
Additional eruptions took place over the next 2 days. On June
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.
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
376
REFERENCES 34. Hooper PR. Flood basalt provinces. In: Sigurdsson H, Hougthon BF,
376.e1
66. Rothery DA. Volcanoes: Teach yourself. Chicago: McGraw-Hill; 2001. 79. Tilling RI. Volcanic hazards and their mitigation: Progress and prob-
67. Searl A, Nicholl A, Baxter PJ. Assessment of the exposure of islanders lems. Rev Geophys 1989;27:237.
to ash from the Soufriere Hills volcano, Montserrat, British West 80. Tilling RI, Heliker C, Swanson DA. Eruptions of Hawaiian volcanoes—
Indies. Occup Environ Med 2002;59:523. Past, present, and future, US Geological Survey General Information
68. Shimizu Y, Dobashi K, Hisada T, et al. Acute impact of volcanic ash Product 117, 2010.
on asthma symptoms and treatment. Int J Immunopathol Pharmacol 81. Tilling RI, Topinka L, Swanson DA. Eruptions of Mount St. Helens:
2007;20:9. Past, present, and future. Washington, DC: US Geological Survey;
69. Shojima J, Ikushima S, Ando T, et al. [A case of volcanic ash lung: 1993.
Report of a case]. Nihon Kokyuki Gakkai Zasshi 2006;44:192. 82. Wanji S, Tendongfor N, Esum M, et al. Elephantiasis of non-filarial
70. Siebert L, Simkin T, Kimberly P. Volcanoes of the world. Tucson: origin (podoconiosis) in the highlands of north-western Cameroon.
Smithsonian Institution/University of California Press, Berkeley; Ann Trop Med Parasitol 2008;102:529.
2010. 83. Weinstein P, Patel A. The Mount Ruapehu eruption, 1996: A review
71. Sigurdsson H. Introduction. In: Sigurdsson H, Hougthon BF, McNutt of potential health effects. Aust NZ J Public Health 1997;21:773.
SR, et al., editors. Encyclopedia of volcanoes. San Diego: Academic 84. Witham CS, Oppenheimer C. Mortality in England during the
Press; 2000. 1783-1784 Laki Craters eruption. Bull Volcanol 2005;67:15.
72. Sigurdsson F. Eruption in Eyjafjallajökull. 2010. <http://www2.norvol 85. Yakob B, Deribe K, Davey G. Health professionals’ attitudes and
.hi.is/page/ies_Eyjafjallajokull_eruption>. misconceptions regarding podoconiosis: Potential impact on integra-
73. Simkin T, Siebert L, Blong R. Disasters: Volcano fatalities—Lessons tion of care in southern Ethiopia. Trans R Soc Trop Med Hyg 2010;
from the historical record. Science 2001;291:255. 104:42.
74. Smith K. Environmental hazards. New York: Routledge; 2001. 86. Yano E, Yokoyama Y, Higashi H, et al. Health effects of volcanic
75. Smithsonian: SI/USGS weekly volcanic activity report, 3-9 November ash: A repeat study. Arch Environ Health 1990;45:367.
2004. <http://www.volcano.si.edu/reports/usgs/index.cfm?content 87. Zeballos JL, Meli R, Vilchis A, et al. The effects of volcanoes on
=archive&year=2004&week=nov_3-9_04>. health: Preparedness in Mexico. World Health Stat Q 1996;49:204.
76. Stevenson JA, Loughlin SC, Font A, et al. UK monitoring and deposi- 88. Zeilinga de Boer J, Sanders DT. Volcanoes in human history: The
tion of tephra from the May 2011 eruption of Grímsvötn, Iceland. far-reaching effects of major eruptions. Princeton, NJ: Princeton
J Appl Volcanol 2013;2:3. University Press; 2002.
BURNS, FIRE, AND RADIATION
376.e2
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 WILDERNESS TRAUMA
and health care workers with a logical approach to management
of trauma and surgical emergencies that may be encountered in
EMERGENCIES OVERVIEW
the wilderness environment. The focus is on health care profes- All classic mechanisms of trauma (penetrating, blunt, and thermal)
sionals who will be responsible for the urgent management of occur in the wilderness environment and are discussed in this
such emergencies for all expedition members. chapter. Blast injury is also mentioned briefly because its treat-
Wilderness expedition health care providers have varied expe- ment in combat situations has led to some important advances
riences and capabilities. In this environment, the location, dis- in wilderness medicine. Blunt trauma remains the most common
tance from medical facilities, conditions, and available resources cause of injury in an austere environment; it can often be difficult
are the most influential factors in patient outcome. It is often to definitively diagnose. Delays in diagnosis in the wilderness
impractical to perform complex interventions in the field, but it can substantially increase complications and deaths.
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
HISTORY OF WILDERNESS MEDICINE
of survival.40,104 The key to successful management of wilderness The medical literature is limited regarding the incidence of injury
emergencies is preparedness. Advanced Trauma Life Support during wilderness-related activities. It is estimated that more
(ATLS) protocols can provide a template for preparation for than 10 million Americans participate in wilderness backpacking
wilderness travel. The principles embodied in ATLS concepts are and camping activities annually. A study by Gentile and col-
well suited to management of wilderness emergencies, especially leagues57 documented the injury and evacuation patterns
in circumstances where scant resources are available and, thus, recorded by the National Outdoor Leadership School over a
a prompt response is essential for the victim’s survival. The 5-year period. Injuries occurred at a rate of 2.3 per 1000 person-
American College of Surgeons has formulated the Rural Trauma days of exposure, with orthopedic and soft tissue injuries most
Team Development Course, which emphasizes the ATLS princi- frequent. Montalvo95 analyzed case incident report files from
ples in situations where a small trauma team, typically two eight California National Park Service parks and found an injury
or three rescuers, is in charge. The course is applicable to the incidence of 9.2 nonfatal events per 100,000 visits, with 78 fatali-
wilderness environment.135 ties reported in a 3-year period. In a prospective surveillance
When team members are planning an expedition, the role for study evaluating 38,940 days of wilderness exposure on the
each member should be explained clearly. Teamwork is essential Appalachian Trail,18 foot blisters and diarrhea were the most
for solving problems, communicating, executing procedures, common reasons for premature discontinuation of hikes. Leemon
transporting a patient, and continually improving the skills of and Schimelpfenig89 showed that more than 50% of evacuated
team members. The medical director (director) of an expedition participants in the National Outdoor Leadership School were
takes on significant responsibility during preparation. The direc- able to return and finish their courses. The Rocky Mountain
tor must screen participants to make sure they can tolerate the Rescue Group reported on their rescue experiences from 1998
expedition and must tell the expedition leader of the findings. It to 2011 in Boulder County, Colorado, where they had a total of
is important to know the medical and surgical history of each 2198 rescues over that time period.83 These studies document a
expedition member. The director must also know wilderness low risk for injury but highlight the possible morbidity resulting
medical protocols. For lengthy expeditions, the director should from wilderness injury or illness and the need for rapid, uniform
consider carrying diagnostic modalities such as a portable ultra- intervention.
sound unit and point-of-care testing equipment. Communication A 2001 study from the University of Arizona61 highlighted
with appropriate rescue facilities prior to starting the trip is wilderness deaths over 13 years. Alcohol was the most common
essential. The director should also have a plan for transfer of causative factor, involved in 40% of the 59 unintentional trauma
information to the next level of care. When an emergency occurs, deaths. In addition, 80% of these victims died immediately or
the director will likely be placed in a position of authority, so it before evacuation could be completed. This emphasizes the
is essential to clarify the command structure and role of each importance of sound judgment and preparedness of rescuers
member. The specifics of wilderness preparation, equipment, and and expedition members in maximizing care. A recent study
medical supplies are presented in Chapter 102. of emergency medical services (EMSs) in the California state
parks emphasizes the difficulty of providing care to wilderness
participants.65
*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. ESTABLISHING PRIORITIES IN THE WILDERNESS
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 There are three immediate priorities in managing wilderness
U.S. Government). This work was prepared as part of my official duties. trauma:
Title 17, USC, §105 provides that “Copyright protection under this title is 1. Control oneself. It is normal to feel anxious when con-
not available for any work of the U.S. Government.” Title 17, USC, §101 fronted with an injured victim. However, anxiety must not
defines a U.S. Government work as a work prepared by a military service be transmitted to the victim or other members of the expe-
member or employee of the U.S. Government as part of that person’s ditionary team. One must be in control of oneself to take
official duties. control of the situation.
378
2. Control the situation. The first priority in controlling the Packaging the victim for evacuation is the final step. The
379
CIRCULATION Hypoxia, hypovolemia, and hypothermia should be promptly
Circulation is evaluated by assessing the cardiac output and corrected.
controlling any major external hemorrhage. Manometric blood
pressure measurement is not easily performed in the field,
although it may provide useful data. Important information
EXPOSURE AND ENVIRONMENTAL CONTROL
regarding perfusion and oxygenation can be obtained rapidly by The victim should be fully undressed and exposed, if possible
determining level of consciousness, assessing peripheral and in a protected environment. Garments and gear should be
central pulses, looking at skin color, and evaluating capillary refill removed if necessary by cutting them away, unless the garments
time. can be dried and are essential for future protection from the
Pulses should be assessed first. Although the following are environment. Wet clothing must be removed early to prevent
only general estimates and carry some inaccuracy, approxima- hypothermia. It is mandatory to visualize the entire victim to
tions of the minimum systolic blood pressure can be used if a document and assess injury. However, this step of the primary
palpable pulse is present: survey should be performed with caution. First, it is imperative
Radial artery: 80 mm Hg to cover the victim immediately after removal of clothing. Hypo-
Femoral artery: 70 mm Hg thermia and its effects on mental status, cardiovascular function,
Carotid artery: 60 mm Hg and coagulation are among the most underappreciated entities
If hypovolemia is suspected on the basis of absent pulses or in care of the trauma victim. The possibility of hypothermia
prolonged capillary refill, the examiner should immediately should be entertained in all environments. A victim with hypo-
assess the neck veins. Distended neck veins, although a nonspe- thermia may not be able to use stored energy to carry on normal
cific sign, may suggest tension pneumothorax or pericardial metabolic processes. A severely injured patient may become
tamponade in the context of hypotension. Flat neck veins may hypothermic in any ambient environment. Second, clothing and
suggest hypovolemia and hemorrhagic shock. gear should not be removed unless complete immobilization of
Major hemorrhage can occur in five anatomic areas: injuries can be achieved. Assessment of an area of injury should
Chest be performed, but clothing should be left to cover the patient to
Abdomen ensure that the body temperature is maintained. A patient may
Retroperitoneum be wearing a variety of gear and clothing, including a helmet for
Thigh biking, skiing, or climbing; the helmet should be removed, with
External environment in-line stabilization of the cervical spine.
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
SECONDARY SURVEY
direct pressure or a tourniquet. Proper stabilization of long bone The secondary survey is an extension of the primary survey and
TRAUMA
(femur) fractures minimizes blood loss into soft tissues. In the should not be undertaken until the primary survey is complete
wilderness, little can be done about significant intrathoracic or and the victim has been stabilized. In addition, resuscitative regi-
intraabdominal hemorrhage. Survival of patients with significant mens, if available, should have been initiated. The secondary
blunt injuries is likely if basic ATLS principles are followed. 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
DISABILITY AND NEUROLOGIC ASSESSMENT
PART 4
380
be placed as adjunctive measures. This degree of resuscitation is advances in prehospital care can and should be applied to trauma
A B C
FIGURE 18-1 A, FAST1 intraosseous infusion system. B, Bone Injection Gun (BIG). C, EZ-IO.
381
The Israel Defense Forces doctrine has mandated use of prehos- BOX 18-2 Tourniquet Use Recommendations
pital tourniquets for control of extremity hemorrhage since the
late 1980s. Medical personnel demonstrated that tourniquets were Apply the tourniquet early, before the onset of shock.
safe, easily applied (by medical and nonmedical personnel), and Use scientifically designed, laboratory-tested, clinically validated
potentially lifesaving.84 Use of tourniquets was not effectively or tourniquets.
widely taught in the U.S. military at the beginning of Operation Using an improvised tourniquet is acceptable if a commercially
Enduring Freedom and Operation Iraqi Freedom. However, injury available tourniquet is not available.
patterns from these and previous conflicts demonstrate that most Continuing education on the use of tourniquets is essential for
injuries sustained by combatants are of the extremities.9 Kragh personnel who will be expected to use them.
and colleagues from the U.S. Army Institute of Surgical Research The goal of the tourniquet is to stop bleeding and stop the distal
(USAISR) prospectively evaluated the use of tourniquets at the pulse.
busiest Combat Support Hospital in Iraq in 2006. They concluded Avoid placement over Hunter’s canal (≈ 5 cm above the femoral
that tourniquets can be lifesaving, especially when used early in condyle).
the prehospital setting prior to the onset of shock.82 A tourniquet Side-by-side use of tourniquets is acceptable if single tourniquet
is defined as a limb-constricting device that is placed in an attempt application does not arrest hemorrhage.
to arrest extremity hemorrhage; the device can be improvised or Effectiveness of the tourniquet will be inversely proportional to the
one of the many commercially available devices. The author’s girth of the extremity.
Tourniquets should be applied directly on the skin.
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). applied, and the mechanism of action is not complicated. When
the rescuer identifies bleeding that cannot be controlled with
Hemostatic Dressings direct pressure or a tourniquet, application of a hemostatic dress-
The high-tempo combat operations of Operation Iraqi Freedom ing can potentially be lifesaving. Remove the product from its
and Operation Enduring Freedom accelerated development of packaging, place it on the bleeding area, and hold it with direct
hemostatic dressings. Both civilian and military data show that pressure for at least 3 minutes. Once hemorrhage has been con-
the most common cause of potentially preventable death in trolled, the dressing stays in place. The dressing works by being
trauma patients is exsanguinating hemorrhage.49,118 Almost 20% of in direct contact with the bleeding source, so piling further hemo-
these lethal hemorrhages will be from junctional anatomic loca- static dressings on top is not productive. The hemostatic dressing
tions, primarily the groin and axilla.49 To facilitate use in austere must be removed eventually, but this can be done in a delayed
locations or combat operations, the ideal hemostatic dressing fashion once the victim reaches definitive care (Figure 18-3).
would be rapidly available, simple to use, lightweight, and rela-
TRAUMA
tively inexpensive and have a long shelf life.109 Several products Junctional Tourniquet
are on the market, with the largest reported experience being Another product for the control of lethal hemorrhage is the junc-
with the mucoadhesive Chitosan-based HemCon (HemCon tional tourniquet. Several types exist, with the basic premise being
Medical Technologies, Portland, OR) and the procoagulant sup- that the belt encircles the pelvis or torso and has pressure devices
plementor, kaolin-based product QuikClot Combat Gauze62 to occlude the axillary or external iliac vessels. The devices use
(Z-Medica, Wallingford, CT). Case reports from combat operations either direct mechanical or pneumatic pressure to achieve occlu-
PART 4
and civilian EMS support the preclinical data that have shown sion. There are limited data to support use of these tourniquets,
that these products are effective in arresting hemorrhage in the but laboratory investigations of the SAM Junctional Tourniquet
prehospital environment.24,111,140 Hemostatic dressings are easily (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
A and that one clamp will not provide adequate closure of a large
or nonlinear wound (see Figure 18-3).
382
CHAPTER 18 WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
A B C
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- has been a paradigm shift toward use of blood products in
line to address hypothermia prevention at all levels of care. In trauma resuscitation and limiting crystalloid infusion.69 During
the austere environment, this should be the goal of the wilder- Operation Iraqi Freedom, Borgman and associates showed the
ness medical team. A team or individual will use everything utility of a high or nearly equivalent ratio of red blood cells to
available (e.g., jackets, blankets, improvised coverings) to protect plasma to platelet resuscitation.16 Most experts recommend deliv-
the patient from the environment. Several lightweight compact ery of these blood products in a ratio that resembles the normal
adjuncts can be used to assist with prevention of hypothermia. composition of whole blood, with 1 unit of red blood cells:1 unit
These essential items can easily be packed as part of the team’s of plasma:1 unit of apheresis platelets.100 The complexity of
kit. Injury in a hot environment does not prevent hypothermia massive transfusion protocols may not apply to every austere
in a seriously injured patient. One commercially available product situation, primarily due to lack of resources. The medical team
is the Hypothermia Prevention and Management Kit (North should consider the ability to establish a walking blood bank as
American Rescue, Greer, SC), which is a self-contained, self- part of the medical kit.
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
FRESH WHOLE BLOOD
guideline.48 Prehospital providers need to be proficient in iden- Primarily a tool of the military, fresh whole blood has been used
tifying casualties who require the DCR approach. It may be dif- in combat theaters dating back to World War I.103 The U.S. military
ficult for a rescuer to rapidly identify this group of patients. has continued the use of fresh whole blood extensively in ongoing
Although there are no uniformly accepted criteria for identifying conflicts.130 Fresh whole blood is warm, the volume is close to
patients who will benefit from DCR, several groups have devel- 500 mL, the hematocrit is 38% to 50%, there are 150,000 to 400,000
oped scoring systems (using a variety of anatomic, physiologic, platelets per microliter, there is 100% coagulation activity, and
and laboratory variables) for identifying patients who will likely 1500 mg of fibrinogen is included. Fresh whole blood does not
require massive transfusion and thus be more likely to enter the possess the “storage lesion” of banked blood. Fresh whole blood
vicious cycle of hypothermia, coagulopathy, and acidosis.94,99,137,145 has the ultimate 1 : 1 : 1 ratio. There are several downsides to using
Each of these scoring systems is quite accurate, but two that are fresh whole blood: It must be type specific, and there are the
most applicable to EMS are the shock index and the ABC system potential for transmission of blood-borne disease, a limited donor
(Boxes 18-3 and 18-4). In the austere environment, the shock pool, and potential deleterious effects on the donor (who in the
index by Vandromme and colleagues is most useful due to its austere environment may have a job to do that prevents taking
simplicity.99,137 the time to donate blood). Even with these known risks, we
The tenets of DCR are limited crystalloid resuscitation, permis- strongly encourage use of fresh whole blood in certain austere
sive hypotension, hemostatic resuscitation, and proper patient locations from which the patient cannot be easily transported or
selection.8,10,35,69,99,137 Limited crystalloid resuscitation has become at which blood products are not readily available.130
an accepted tenet for care of hemorrhaging patients. The EAST
guidelines35 on prehospital resuscitation state that there is a need Organization of Walking Blood Bank
to (1) embrace permissive hypotension in penetrating torso The process of obtaining fresh whole blood requires superb
patients; (2) base resuscitation on mental status and presence of planning and coordination. It is helpful to have a prescreened
radial pulse; (3) give patients a bolus with smaller aliquots of IV donor pool; questionnaires are available to help determine a safe
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 BOX 18-4 Assessment of Blood Consumption (ABC)
particular expedition, early use of blood products needs to be Score for Massive Transfusion
discussed, including a “walking blood bank” (using whole blood
donated by locally available personnel). In the past 15 years there The presence of two or more of the following factors identifies
patients at risk for massive transfusion:
Systolic blood pressure < 90 mm Hg
BOX 18-3 Shock Index Heart rate > 120 beats per minute
Penetrating mechanism
Shock index = Heart rate/Systolic blood pressure Positive FAST signs (Face drooping, Arm weakness, Speech
Shock index > 0.9 identifies patients at risk for massive transfusion difficulty, Time to call 9-1-1)
383
donor pool. This must be done prior to the team’s expedition. Management guidelines specific for head injuries in a wilderness
Trying to do this when a casualty has arrived would cause a setting do not exist, and a wide range of clinical approaches are
dangerous delay in the initiation of hemostatic resuscitation. The used in hospital settings.58 However, the literature suggests that
beginning donor pool is all of the persons on the expedition. morbidity and mortality can be reduced by means of a protocol
The plan must include a predetermined method to activate and that includes early airway control with optimization of ventilation,
operate the walking blood bank. A responsible individual must prompt cardiopulmonary resuscitation, induced hypothermia, and
have access to the blood donor pool and be able to manage the rapid evacuation to a trauma care facility.63,131
walking blood bank. The authors recommend using the rapid Initial management of head injury in the wilderness should
screening kits to evaluate for human immunodeficiency virus, follow established ATLS protocols. Prompt attention must then be
hepatitis, and human T-lymphotropic virus.130 These rapid immu- given to victim triage, evacuation strategies, and ongoing resus-
noassays may not be as accurate as desired, but a positive result citative needs to prevent or minimize secondary brain injury from
can be helpful. hypoxia and hypotension. Expeditious evacuation to a trauma
center in which neurosurgery can be performed is essential.
Collection of Fresh Whole Blood Multiple clinical and experimental studies have demonstrated
When the decision to use fresh whole blood has been made the detrimental effects of hypoxia on the injured brain. A defini-
because blood components are unavailable or the normal blood tive airway should be established if any degree of neurologic or
bank has been exhausted, the preassigned individuals mobilize respiratory compromise exists, but not at the expense of risking
the donors and begin to collect the fresh whole blood. The basic severe hypoxia to accomplish it in an otherwise well-ventilated
procedures require proper identification of individuals in the patient.55 Cervical spine injuries are common in patients with TBI.
donor pool, confirmation of an up-to-date screening question- Therefore, cervical spine immobilization is paramount to prevent
naire, and selection of individuals that have not recently donated. devastating neurologic injury.
If one is able to screen for blood-borne infectious diseases, this After immobilization, attention is directed to prevention of
should be done. Once a person has been deemed physically fit secondary brain injury. Given adequate resources, all efforts
to provide a donation (this should be done quickly), the walking should be made to avoid oxygen saturation levels of less than
blood bank personnel should crossmatch the donor to the recipi- 90% and to maintenance of blood pressure of more than
ent, check the donor for significant anemia, and proceed with 90 mm Hg.55 The purpose of the wilderness head injury protocol
collection of up to 500 mL of whole blood into a commercial is to allow individuals with widely varying levels of experience
collection bag with anticoagulant citrate phosphate dextrose and expertise to identify signs of significant head injury, begin
adenine. The collection area should be as calm as possible, proper resuscitation in the context of prevention of secondary
because chaos breeds errors. A clerical error leading to transfu- brain injury through airway maintenance and hemodynamic
sion of the incorrect blood type could create a devastating support, and evacuate appropriately.
hemolytic reaction. The collection area may be within a few feet
TRAUMA
of the patient, but the collected blood must nonetheless be Anatomy of the Head
properly labeled. After labeling, the unit of blood is “walked The scalp has five layers of tissue that cover the calvaria: skin,
over” to the patient and infused. This entire process can take less connective tissue, galea aponeurotica, loose areolar tissue, and
than 25 minutes. 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-
INJURIES TO THE HEAD, FACE,
PART 4
384
based on current recommendations.21,135 At a MAP of between 50
385
level of suspicion and clinical signs and symptoms. After atten- TABLE 18-1 Interpretation of Pupillary Findings in
tion to the primary survey, including airway provision and spinal
immobilization, the physical examination component of the sec- Victims with Head Injury
ondary survey is imperative and can provide information about
Pupil Size Light Response Interpretation
the presence of a TBI.
Head Injury Classification Unilaterally Sluggish or fixed Third nerve
Intracranial injuries have a wide range of causes, with variable dilated compression
severity. In order to simplify evaluation of the head-injured secondary to
patient, the GCS has been used.134 The initial GCS score of the tentorial herniation
patient assists the treatment team in developing a treatment plan. Bilaterally dilated Sluggish or fixed Inadequate brain
Mild injury is classified as a GCS score of 13 to 15; moderate, 9 perfusion; bilateral
to 12; and severe, 3 to 8. Patients with an initial GCS score of 8 third nerve palsy
or less in the field have a predictive value for a poor outcome Unilaterally Cross-reactive Optic nerve injury
of at least 40%, and need urgent medical attention.7 This risk dilated or equal (Marcus Gunn pupil)
increases proportionally with a lower GCS score. These individu- Bilaterally Difficult to determine; Opiates
als should be evacuated to a trauma center as soon as possible constricted pontine lesion
if a favorable outcome is possible. Patients with mild TBI should Bilaterally Preserved Injured sympathetic
be assessed for limitations that would preclude them from con- constricted pathway
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 compression of the corticospinal tract in the midbrain. Ipsilateral
more than 13 do not necessarily need to be transferred to a pupillary dilation associated with contralateral hemiplegia is a
trauma center but should be evaluated and undergo CT scanning classic and ominous sign of tentorial herniation. Deep tendon
at the earliest and safest moment.7,71 Moderately injured patients reflex changes in the absence of altered mental status or lateral-
with a GCS of 9 to 12 or 13 are the ones in whom the outcome izing signs are not indicative of TBI. Detailed evaluation of
can be affected by early, correct interventions. Avoidance of brainstem function cannot be undertaken in the wilderness
hypotension in isolated head injury is paramount. As in combat- setting. Evaluations of the gag and corneal reflexes may provide
related head trauma, use of mannitol, hypertonic saline, hy some information helpful in triage and evacuation planning, but
perventilation, and antibiotics is indicated for prophylaxis in the findings would not automatically obviate the need for
penetrating head trauma.20 prompt evacuation.
TRAUMA
GCS score aids in recognition of TBI and should be regularly ABCDE sequence, IV access should be established. It is not advis-
reassessed to provide a mechanism for quantifying neurologic able to administer fluids orally to the victim with head injury
deterioration. Physical signs that may denote underlying brain because of the likelihood of vomiting, airway compromise, and
injury include significant scalp lacerations or hematomas, contu- aspiration. In the patient with suspected head injury without
sions, facial trauma, and signs of skull fracture. Findings specific confirmatory imaging, the use of hypertonic IV fluids or mannitol
for basilar skull fracture include ecchymosis behind the ears will effectively reduce the ICP.56,125
(Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood Individuals sustaining head trauma have a high incidence of
behind the tympanic membrane on otoscopic examination concomitant injuries, and many of these individuals, especially if
(hemotympanum), frank bleeding from the ears, and CSF rhinor- the injury is related to combat, have persistent postconcussive
rhea or otorrhea also suggest skull fracture and underlying TBI. symptoms for 6 months or longer.85,90 A victim who does not
The pupillary examination may provide valuable data in have a palpable peripheral pulse or presents with other signs of
assessing an underlying TBI. Herniation of the temporal lobe of hypotension in the context of suspected head injury must not be
the brain may be heralded by mild dilation of the ipsilateral pupil assumed to have a neurogenic cause of shock, so other causes
with sluggish response to light. Further dilation of the pupil fol- must be thoroughly and aggressively investigated. Recognition of
lowed by ptosis (drooping of the upper eyelid below its normal additional injuries is critical in the setting of head injury for mul-
level), or paresis of the medial rectus or other ocular muscle, tiple reasons. Management of a head injury should be secondary
may indicate third cranial nerve compression by a mass lesion to other life-threatening injuries, which, if not addressed, may
or herniation. Table 18-1 relates pupillary examinations to pos- lead to hemorrhagic shock and preclude survival. As previously
sible underlying brain lesions. discussed, maintenance of the MAP (and thus the CPP) and
Most dilated pupils (mydriasis) are on the ipsilateral side adequate oxygenation are critical in preventing secondary brain
to the mass lesion. With direct globe injury, traumatic mydriasis injury.
may result, making evaluation of TBI more difficult. Also, 5% to The type of resuscitative fluid administered to trauma victims
10% of the population has congenital anisocoria (a normal differ- continues to be controversial. Previously, recommendations
ence in pupillary size between the eyes); however, the pupil will warning of the dangers of overhydration in head injury led to
maintain a response to light. Casual inspection may overlook a recommendations for restricting fluids. The need for resuscitation
prosthetic eye, which is mistaken for a fixed pupil. Neither direct and intravascular volume support has been well established.
trauma nor congenital anisocoria should be assumed in a head- Possible resuscitative fluids include isotonic crystalloid, hyper-
injured victim exhibiting mental status change in the wilderness. tonic crystalloid, or colloid solution. Osmotic agents, such as
After quantification of the GCS score, pupillary examination, hypertonic saline, have been shown to increase hypoperfused
and examination of the head and face for signs of external regions of the brain after TBI.121 Hypotonic fluids, however, are
trauma, a concise neurologic examination should be performed. not appropriate in TBI secondary to an increase in whole-brain
The goal in the field is to identify motor or sensory focal deficits water content and subsequent elevation in ICP. Data from animal
suggestive of intracranial injury. Sensory deficits follow the studies of TBI suggest that colloid solutions offer no advantage
general dermatome patterns shown in Figure 18-6. over isotonic crystalloids, such as lactated Ringer’s solution, in
Unilateral hemiplegia may signify uncal herniation resulting terms of augmenting cerebral blood flow or preventing cerebral
from mass effect in the contralateral cortex because of edema.146 As previously noted, no prospective trial has clearly
386
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)
Sural (S1,2)
Superficial peroneal (L4,5,S1)
Deep peroneal (L4,5)
documented an advantage of colloid over crystalloid administra- Inability to measure or titrate the PaCO2 in the wilderness man-
tion in the victim with multiple systemic injuries. Evidence is dates that respiration be controlled to approximate near-normal
accumulating that hypertonic solutions, particularly mannitol minute ventilation while maintaining oxygen saturation of more
or hypertonic saline, may be beneficial in TBI.56 However, an than 95%.
advantage has not been demonstrated in trauma victims overall, All bleeding from the scalp or face should be controlled with
especially with concomitant injuries. The recommended resusci- direct pressure. Scalp hematomas, regardless of size, should not
tative fluid for the head-injured victim in the wilderness setting be decompressed. Open wounds, particularly skull fractures,
is isotonic crystalloid in the form of lactated Ringer’s solution, should be irrigated and covered with the most sterile dressing
with a target MAP of 80 to 90 mm Hg based on cuff blood pres- available. Fragments of displaced cranium overlying exposed
sure determinations or extrapolation from evaluation of distal brain tissue should not be replaced. If signs of skull fracture are
pulses. present, broad-spectrum antibiotic prophylaxis and immunization
against tetanus are administered. Although diuretics have been
Further Management of Head Injury widely used in the intensive care management of intracranial
Numerous adjuncts exist for management of the head-injured hypertension, no rationale exists for their use in the field. The
victim, few of which are applicable in the wilderness setting. wilderness trauma victim may have many injuries that are impos-
Once the primary and secondary surveys are complete, the sible to evaluate fully in the field. In this setting, particularly in
airway is secured, resuscitation has been initiated, and spine the presence of hemorrhagic shock, attempts to induce osmotic
immobilization has been achieved, the victim should be placed diuresis to decrease ICP may be life-threatening. Diuretics such
in a 30-degree head-up position. This position assists in control as furosemide or mannitol may exacerbate hypotension, cause
of ICP, and thus CPP, through augmentation of venous outflow. metabolic alkalosis, and induce renal complications in the
This maneuver should not be attempted if the spine cannot be absence of physiologic monitoring.4 Corticosteroids have no role
adequately immobilized. in head injury in the field or intensive care unit. Studies have
If endotracheal intubation is possible, ventilation should be documented no beneficial impact on ICP or survival. Attempts
optimized without hyperventilating the victim. Hyperventilation at brain preservation by slowing the metabolic rate and oxygen
has been used aggressively in the past to promote hypocarbia- consumption have no role in the wilderness setting. Barbiturates
induced cerebral vasoconstriction and, theoretically, to decrease have been used for elevated ICP refractory to other measures,
brain swelling. However, if the PaCO2 falls below 25 mm Hg, but they may induce hypotension, depress myocardial function,
severe vasoconstriction ensues, effectively reducing cerebral and confound the neurologic examination.4 Feasibility of these
blood flow, promoting ischemia, and possibly augmenting sec- advanced interventions may not be advisable in the wilderness,
ondary brain injury. Studies have demonstrated worse outcomes especially if skilled providers are not available. The use of
in victims with severe head injury who were hyperventilated.98 hypertonic saline empirically in the treatment of TBI has little
387
likelihood of complication and is often deployed in combat by status that may or may not involve loss of consciousness. The
today’s military embedded medical technician.47 neurologic impairment is short lived and resolves spontaneously
Approximately 50% of persons with severe head injury experi- without any structural injury to the brain. These individuals
ence posttraumatic seizures.21 Phenytoin, valproate, or levetirace- should not be allowed to return to activity until they are asymp-
tam, if available, can be safely administered in the field. tomatic and are no longer taking any medications. The following
Prophylactic administration has not been shown to change long- signs indicate that more advanced medical care is necessary:
term survival rates, but seizure prophylaxis may benefit patients (1) inability to be awakened; (2) severe or worsening headaches;
with TBI by reducing additional accidental injury, psychological (3) somnolence or confusion; (4) restlessness, unsteadiness, or
effects, and loss of driving privileges. Controlling seizures may seizures; (5) difficulties with vision; (6) vomiting, fever, or stiff
reduce secondary injury due to hypertension, increased ICP, neck; (7) urinary or bowel incontinence; and (8) weakness or
changes in oxygen delivery, and excess neurotransmitter release.21 numbness involving any part of the body. No prospective vali-
dated guidelines for return to activity have been established,
Skull Fracture although level III evidence recommends a graded plan for return
Skull fracture in the wilderness mandates evacuation. Therapeutic to activity.60 Generally, one should not return to an environment
options in the field are few, with intervention limited to identify- in which concussion is a risk (e.g., contact sports) until symptoms
ing the injury and arranging rapid transport. Skull fractures may have been absent for 14 days and the individual is no longer
be open or closed, linear or stellate, and may occur in the vault taking medications.
or skull base. These fractures are associated with a high incidence The group for which the evacuation decision is most difficult
of underlying intracranial injury. Skull fractures with depression is the moderate-risk group. These persons have a history of a
greater than the thickness of the skull may require elevation. No brief loss of consciousness or change in consciousness at the
attempt at elevation should be made in the field. Any exposed time of injury, or a history of progressive headache, vomiting, or
brain surface should quickly be covered with the most sterile posttraumatic amnesia. If any of these signs is present in the
covering available, preferably moistened with crystalloid solu- face of concurrent systemic injury, the victim should be evacu-
tion. Loose bone or brain fragments should not be manipulated. ated immediately. Studies associating clinical variables and
If a broad-spectrum antibiotic is available, it should be adminis- abnormal results on CT scan have demonstrated the significance
tered. After attention to the wound and stabilization of associated of a decreased GCS score, presence of symptoms, and loss of
injuries, the victim should be rapidly evacuated. consciousness. If these signs are present in isolation and the
evacuation can be completed in less than 12 hours, the evacua-
Penetrating Head Injuries tion should proceed. If the evacuation is impossible or will
Most penetrating head injuries in the wilderness are gunshot require longer than 12 hours, the victim should be closely
wounds; knives and arrows may also penetrate the cranium. Such observed for 4 to 6 hours. If the examination improves to nor-
penetrating injuries are usually catastrophic; more than 60% of mality during the observation period, it is reasonable to con-
TRAUMA
patients with gunshot wounds to the head succumb prior to tinue observation.
reaching a medical treatment facility.115 Some persons have sur-
vived small-caliber, low-velocity injuries and tangential wounds NECK INJURIES
that need only local debridement or antimicrobial therapy without
an operation.115 As with closed-head injury, management priori- Blunt Neck Injuries
ties consist of maintenance of the airway, prevention of second- Injuries to the neck may be classified as blunt or penetrating.
PART 4
ary brain injury, and rapid evacuation. If the cranium has been Significant blunt injuries include cervical spine injuries and laryn-
violated, the victim should receive antibiotics and tetanus immu- gotracheal injuries. The neck is divided into three distinct zones
nization in the same manner as for open skull fracture. In the that help predict injury and guide management (Figure 18-7).
rare instance that the projectile is embedded in the skull, no Fracture of the larynx and disruption of the trachea usually
attempt at removal should be undertaken. If the length of the require surgical intervention that is unavailable in the wilderness.
projectile makes immobilization or transport cumbersome, the The sooner laryngeal repair is accomplished, the better the
excess length may be removed but only if this can be done outcome with respect to phonation.39 Victims present with a
without displacement of the intracranial segment. history of a significant blow to the anterior neck. Physical exami-
nation findings include difficulty with phonation, subcutaneous
Evacuation of Patients with Head Injury emphysema that may extend as far inferiorly as the abdominal
Survival and outcome of head injury in the wilderness correlate wall, stridor, odynophagia, and often acute respiratory distress.
directly with rapidity of evacuation. Certain situations dictate Blunt cerebrovascular injuries pose unique challenges in the
immediate evacuation. Any person with evidence of an open or wilderness because they are difficult to diagnose. Practice
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 III
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 II
GCS score of 14 or greater includes persons who have suffered
a blow to the head but are asymptomatic, did not lose conscious- I
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 FIGURE 18-7 Zones in neck trauma.
388
management as well as diagnostic and surveillance guidelines
389
Mechanism of injury suggestive of cervical spine injury?
expedition members and rescuers that may ensue when the
victim is immobilized. If a rigid litter is not available, the victim
Yes/unknown
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
Alert and oriented, no distracting injury, not intoxicated?
amount of immobilization.51 The Philadelphia collar allows 44%
of normal rotation and 66% of normal lateral bending.92 To
Yes
achieve 95% immobilization, a halo and vest are necessary. Any
number of materials may be used to improvise an immobilizing
Tenderness, pain spontaneously or with movement? device (see Chapter 46). Restriction of flexion, extension, and
rotation must be achieved to the greatest degree possible. Optimal
No immobilization consists of a long spine board or litter, rigid collar,
bolsters to the sides of the head, and tape or straps restricting
Normal neurologic exam? movement (see Figure 18-8B).
Treatment. Because little definitive treatment for cervical
Yes spine injury can be accomplished in the field, survival and
outcome depend on speed of transport and maintenance of the
A Immobilization unnecessary? 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.
TRAUMA
390
Most rib fractures can be managed with oral analgesics. Deep
391
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
A first-aid kit.
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
B as midazolam, will help with pain and anxiety relief during the
insertion period. A 2- to 3-cm incision is made through the skin
FIGURE 18-10 A, Ultrasound image demonstrating fluid in Morison’s and subcutaneous tissue down to the ribs and intercostal space.
TRAUMA
pouch. B, Fluid around the spleen. 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-
Pneumothorax sected away from the pleura, so that chest tube insertion will be
As air enters the pleural cavity, causing the intrapleural pressure done properly. For a simple pneumothorax, a 20 or 22 French
PART 4
to equal the atmospheric pressure, the lung collapses (pneumo- tube is used, or a pigtail catheter if available. The catheter or
thorax). The three types of pneumothorax are simple, tension, chest tube should be directed posteriorly and apically, and
and open pneumothorax. secured with a suture or tape. If possible, the tube should
In simple pneumothorax, symptoms include tachypnea, dys- be connected to suction or an underwater seal. The tube can be
pnea, and hyperresonant breath sounds in the affected hemi left open to the atmosphere to accomplish decompression and
thorax. Treatment of a simple pneumothorax, depending on its the end of the tube covered with a rubber glove, finger cot, or
symptoms and size, is decompression of the pleural cavity.41 In plastic bag modified to permit unidirectional egress flow of air.
the wilderness, tube thoracostomy can be difficult to perform. A Preinsertion antibiotics, oral or parenteral, to cover gram-positive
small pneumothorax can often be managed without placing a skin flora will reduce the chance of a subsequent pleural
chest tube, especially if the patient can ambulate with adequate infection.38
analgesia. Frequent rest breaks may be necessary. Suspicion of
a pneumothorax alone on physical examination does not neces- Hemothorax
sitate placement of a catheter or chest tube.22,128 However, if the A hemothorax is the presence of blood in the pleural space,
patient develops incapacitating symptoms, decompression may usually associated with an overlying major chest wall injury with
be necessary to avoid a life-threatening situation. Portable ultra- multiple rib fractures. The most common cause is a direct blow
sound can be used to make the diagnosis (see Chapter 109). The to the chest that causes laceration of the lung, intercostal vessels,
patient should be monitored with physical examination and pulse or pulmonary vasculature. Tenderness, inspiratory pain, and
oximetry. dyspnea can be associated with a hemothorax. In the wilderness,
Tension pneumothorax develops when the intrapleural pres- a tube thoracostomy is rarely required or feasible, but can be
sure increases, so that the heart and great vessels are shifted away placed if the equipment is available and the patient is symptom-
from the pneumothorax. This commonly impedes venous return atic, especially with prolonged evacuation. A 32F to 36F chest
from the superior and inferior venae cavae, decreases cardiac tube should be inserted if a hemothorax is suspected. If more
output, and causes hypotension leading to shock. The patient than 1500 mL is evacuated after placement of the chest tube, this
may have distended neck veins and tracheal deviation away from is indicative of a massive hemothorax. This mandates rapid
the side of the lesion. Other physical findings are absent breath evacuation and ongoing resuscitation in anticipation of operative
sounds, hyperresonance on percussion, respiratory distress, cya- intervention. The major goal in treatment is to evacuate the
nosis, and cardiovascular collapse. This life-threatening injury pleural space and allow expansion of the lung, which helps
demands immediate chest decompression, followed by evacua- appose the lung pleura and visceral pleura and potentially
tion. A temporizing treatment is to insert a needle or catheter into decreases bleeding from the lung and other low-pressure
the pleural space, which converts the tension pneumothorax into sources.51
a simple pneumothorax. This is done by inserting a 14-gauge
catheter percutaneously over the second rib in the midclavicular Flail Chest
space or laterally in the anterior axillary line in the fifth intercostal When two or more ribs are fractured in two or more places, that
space.72 The needle is placed over the anterosuperior surface of segment of the chest wall has lost bony continuity with the rest
the rib through the intercostal muscles to avoid the inferiorly of the bony thorax. An unstable segment will have paradoxic
located neurovascular bundle. If successful, a rush of air is usually motion inward upon inspiration. This is often associated with an
392
underlying pulmonary contusion, which may blossom only after
PENETRATING CHEST WOUNDS
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
kidneys or pancreas may be referred to the back. However,
INJURIES TO THE ABDOMEN referred pain is usually a late finding and is not helpful in evalu-
Intraabdominal injuries in the wilderness setting are difficult to ation of acute trauma.
recognize. Once recognized, all require appropriate resuscitation Gross hematuria that does not clear immediately or that is
and immediate evacuation. The abdomen is the most frequent coupled with an associated injury, such as pelvic fracture or
site of life-threatening hemorrhagic shock; however, in the wil- abdominal or back pain, requires immediate evacuation. To
derness setting, few diagnostic and treatment options exist. 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
BLUNT ABDOMINAL TRAUMA little to the evacuation decision when evaluating for abdominal
Blunt intraabdominal injury is commonly associated with falls. trauma. The unstable pelvic fracture associated with rectal and
Abdominal injuries are often associated with fractures or closed- vaginal injuries is usually the determinant for evacuation.
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
PENETRATING ABDOMINAL TRAUMA
occult injury. Penetrating intraabdominal injuries may result from blast, gun-
shot, stab, or arrow wounds. The social context in which these
Anatomy of the Abdomen injuries occur (accidental, intentional, or self-inflicted) makes
For descriptive purposes, the abdomen may be divided into little difference in the wilderness setting. Recrimination, guilt,
thoracic, true, and retroperitoneal compartments. The thoracic and blame only interfere with the paramount goal of immediate
abdomen contains the liver, spleen, stomach, and diaphragm. evacuation.
The liver, spleen, and, more rarely, stomach may be injured by
direct blows to the ribs or sternum. Twenty percent of persons Gunshot Wounds
with multiple left lower rib fractures have a ruptured spleen. A A low-caliber gunshot injury often manifests with a small entrance
direct blow to the epigastrium may result in increased intraab- wound and no exit wound. A high-caliber, high-velocity gunshot
dominal pressure, with subsequent rupture of the liver or dia- injury may have a relatively innocuous entrance wound but a
phragm. The true abdomen contains the small bowel, large large, disfiguring exit wound and extensive internal injuries. No
bowel, and bladder. Isolated bowel injuries are rare in the wil- matter what the caliber or trajectory and no matter where the
derness setting. Blunt bladder or rectal injury usually occurs in entrance and exit wounds, all gunshot wounds from the nipple
conjunction with severe pelvic fracture and carries a high risk of line to the inguinal ligament should be presumed to have pen-
death. The retroperitoneal abdomen contains the kidneys, ureters, etrated the abdominal cavity and created an intraabdominal
pancreas, and great vessels. It is notoriously difficult to evaluate injury. These injuries mandate immediate surgical intervention.
TRAUMA
by physical examination. Life-threatening hemorrhage can occur A victim of gunshot wounds to the head, neck, chest, abdomen,
into the true abdomen or retroperitoneal space. or groin should undergo immediate evacuation and should
receive a single-agent broad-spectrum antibiotic, such as an oral
Diagnosis fluoroquinolone, second-generation cephalosporin, or extended
The wilderness physician must have a high index of suspicion beta-lactam drug. Hunting injuries are discussed in Chapter 26.
and perform a superlative history and physical examination. With
Shotgun Injuries
PART 4
394
decreasing in most trauma centers. The practice of nonoperative
395
hemorrhage. The victim of trauma may die in short order from BOX 18-7 Vascular “Hard Signs”
a major vascular injury. Ideally, control of hemorrhage can be
accomplished without resultant ischemia of the distal extremity. Pulsatile bleeding
Hemorrhage from an extremity wound can almost always be Palpable thrill
controlled with direct pressure and pressure dressings. These Audible bruit
measures permit circulation to and from the extremity outside Expanding hematoma
the area of pressure application. In some circumstances, a tour- Six Ps of regional ischemia
niquet may be required. Pain
Pulselessness
History of the Injury Pallor
A complete history of the time and mechanism of injury is invalu- Paralysis
able in planning further management. Although no absolute Paresthesia
ischemia time has been established, a goal of less than 6 hours Poikilothermia
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; suspicion is high, and evacuation can be accomplished safely,
however, minimal morbidity has been achieved with longer the victim should be transported and observed in a medical
applications.80,81 The amount of blood present at the scene should facility.
be quantified. A history of pulsatile bleeding of bright-red blood Although not feasible in the wilderness, the use of vascular
that abates suggests arterial injury. Thirty-three percent of victims shunts has been shown to be a viable option for increased limb
with arterial injuries have intact distal pulses. salvage without an increasing risk of death.28 Based on recent
military conflict data, the use of battlefield temporary vascular
Physical Examination shunts does not lead to increased limb loss rates.17 Porcine
Vascular examination in the field can be difficult. Hypovolemia, models have demonstrated safety of temporary vascular shunt
hypothermia, and hostile conditions make accurate examination use without increased thrombosis rates within 48 to 72 hours of
challenging. Skin color and extremity warmth should first be placement.29 Additionally, the more proximal the shunt on the
assessed. Distal pallor and asymmetric hypothermia suggest vas- extremity, the better the patency. This is also true of shunted
cular injury. Pulses should be palpated. In the upper extremity, venous injuries.112
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-
TRAUMATIC AMPUTATION
tion of the wound, amount of hemorrhage, and presence of In the wilderness, amputation victims require immediate evacu-
TRAUMA
hematomas or palpable thrill should be noted. ation. Hemorrhage is controlled during the primary survey with
A neurologic examination that quantifies motor and sensory direct pressure, and resuscitation is instituted. Tourniquets are
deficits is critical. Because of the high metabolic demands rarely required. The victim should be kept warm and calm. Reas-
of peripheral nerves, disruption of oxygen delivery makes neu- surance and analgesics should be administered. Amputations
ronal cells highly susceptible to ischemic death. Conversely, should be completed only if minimal tissue bridges exist and it
skeletal muscle is relatively resistant to ischemia. Loss of sensa- is clear that the neurovascular supply has been interrupted.
PART 4
tion or limb paralysis is an alarming sign of impending anoxic Amputation of a mangled extremity, defined as an extremity
necrosis. with a high-grade open fracture and significant soft tissue injury,
should not be carried out in the wilderness except to free a
Treatment of Vascular Injuries trapped victim to avoid further severe injury or even death, or
All external hemorrhages should be identified during the primary in the case of uncontrollable hemorrhage threatening the life of
survey and controlled with direct pressure at the site of injury. the victim, and then only by experienced surgical personnel. All
Tourniquets should be applied only when direct pressure fails other severely injured extremities should be wrapped in available
to control bleeding or cannot be applied (as while a casualty is sterile materials, splinted, and kept moist.
being evacuated by hoist to an aircraft). Tourniquets should be Amputated extremities should be cooled if possible, optimally
released every 5 to 10 minutes to attempt to limit ischemia, unless in a plastic bag in ice or ice water. Avoid placing the extremity
severe hemorrhage continues when the tourniquet is loosened. in direct contact with ice. Without cooling, the amputated extrem-
In this case, it should be left tightened. Efforts to control bleed- ity remains viable for only 4 to 6 hours; with cooling, viability
ing with pressure should be undertaken. Direct pressure permits may extend to 18 hours. The amputated extremity should accom-
collateral flow to provide some perfusion to the distal extremity. pany the victim throughout the course of the evacuation.
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-
CRUSH INJURIES AND RHABDOMYOLYSIS
vascular examinations are mandatory. Rhabdomyolysis is a potentially fatal syndrome that results from
Once bleeding is controlled and the wound is covered with lysis of skeletal muscle cells. In its fulminant form, rhabdomyoly-
a sterile but nonconstrictive dressing, completion of the primary sis can affect multiple organ systems. Compartment syndrome,
survey, identification and stabilization of associated injuries, and renal failure, and cardiac arrest are the major complications.
appropriate resuscitation with normal saline should follow. After Any condition resulting in significant acute or subacute stri-
hemostasis is achieved, a nonconstrictive dressing will obviate ated muscle damage can precipitate rhabdomyolysis. Crush inju-
the chance for unintended venous outflow obstruction. The ries of the extremities and pelvis, revascularization of ischemic
extremity should be splinted to prevent movement. The need tissue, ischemic extremities, animal bite and snakebite, frostbite,
for evacuation depends directly on the results of the physical and traumatic asphyxia can all result in rhabdomyolysis in a
examination. Examination results can be grouped into “hard wilderness setting. Crush injuries are frequently results of ava-
signs,” indicative of ischemia or continued hemorrhage, and “soft lanches, falls from heights, or rock slides.
signs,” suggestive of, but not indicative of, ischemia (Boxes 18-7
and 18-8).
All victims with hard signs should be evacuated emergently. BOX 18-8 Vascular “Soft Signs”
Based on current data, an isolated soft sign may warrant observa-
Injury in proximity to major vessel
tion alone, depending on the remoteness of the expedition and Diminished but palpable pulses
the risks of evacuation. The data for observation of soft signs Isolated peripheral nerve deficit
have emerged from hospital settings and must be applied with History of minimal hemorrhage
great caution in the wilderness. If soft signs are present, clinical
396
The pathophysiology of rhabdomyolysis remains controver- spider bite or mushroom ingestion, both of which can simulate
Associated
Location of Pain and Mode of Onset and Gastrointestinal
Disease Prior Attacks Type of Pain Problems Physical Examination
Acute appendicitis Periumbilical region or Insidious to acute and Anorexia common; Low-grade fever; epigastric
localized generally to right persistent nausea and tenderness initially; later, right
lower abdominal quadrant vomiting in some lower quadrant pain
Intestinal Diffuse Sudden; crampy Vomiting common Abdominal distention;
obstruction high-pitched rushes
Perforated Epigastric; history of ulcer in Abrupt; steady Anorexia; nausea and Epigastric tenderness; involuntary
duodenal ulcer many vomiting guarding
Diverticulitis Left lower quadrant; history Gradual; steady or Diarrhea common Fever common; mass and
of previous attacks crampy tenderness in left lower quadrant
Acute cholecystitis Epigastric or right upper Insidious to acute Anorexia; nausea and Right upper quadrant pain
quadrant; may be referred vomiting
to right shoulder
Renal colic Costovertebral or along Sudden; severe and Frequently nausea Flank tenderness
course of ureter sharp and vomiting
Acute pancreatitis Epigastric penetrating to Acute; persistent, dull, Anorexia; nausea and Epigastric tenderness
back severe vomiting common
Acute salpingitis Bilateral adnexal; later, may Gradually becomes Nausea and vomiting Cervical motion elicits tenderness;
be generalized worse may be present mass if tuboovarian abscess is
present
Ectopic pregnancy Unilateral early; may have Sudden or intermittently Frequently none Adnexal mass; tenderness
shoulder pain after rupture vague to sharp
397
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
A to an hour, and then abates. It is occasionally associated with
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-
B floxacin 750 mg twice a day) to cover gram-negative enteric
bacteria and Streptococcus species.27
FIGURE 18-13 A, OPTION-vf (female) catheter. B, OPTION-vm (male)
catheter. (Courtesy Practica Medical Manufacturing, Inc, Dublin, Ohio.)
PEPTIC ULCER DISEASE
initiated to counteract potential sepsis and hypovolemic shock. Peptic ulcer disease is on the decline in the United States, espe-
Decompressing the stomach with a NG tube may alleviate severe cially with the advent of acid-reducing agents and the treatment
nausea and vomiting if antiemetics are ineffective, which is often of Helicobacter pylori infection. Duodenal ulcer perforation is a
the case with a small bowel obstruction. Confirmation of proper serious complication and should be in the differential diagnosis
placement of a NG tube is made by aspirating gastric contents of upper abdominal pain in the wilderness. Patients often have
TRAUMA
or oscillating gastric air when one insufflates the stomach through a history of peptic ulcer disease, which is much more common
the tube. Monitoring the urine output is a good estimate of intra- in males than females. The use of nonsteroidal antiinflammatory
vascular volume status. Therefore, placing an indwelling urinary drugs and smoking are the most common risk factors. These
catheter in circumstances of major volume depletion may be patients have an acute onset of constant epigastric pain that radi-
helpful to determine the adequacy of the resuscitation (Figure ates to the midback. There is tenderness and tympany of the
18-13). Portable ultrasound can also be used to diagnose certain upper abdomen. Signs of peritonitis mandate evacuation. Tem-
PART 4
intraabdominal conditions and is valuable in determining the size porizing measures may include insertion of a NG tube and
of the vena cava as an estimate of intravascular volume. 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-
ACUTE APPENDICITIS testinal bleeding. The differential diagnosis may include pancre-
About 7% of people have a chance of developing acute appen- atitis, acute cholecystitis, myocardial infarction, or a perforated
dicitis during their lifetime.1 In normal circumstances, early diag- viscus.
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
DIVERTICULITIS
carefully assess and evacuate the patient early if acute appendi- Most patients with diverticulitis remain asymptomatic. Patients
citis is suspected. The most common differential diagnosis with that present with uncomplicated diverticulitis usually have non-
acute appendicitis is mesenteric adenitis, which is often preceded specific symptoms, including vague, colicky, left lower quadrant
by an upper respiratory tract infection and associated with vague abdominal pain. Diverticulitis can involve the entire lower
abdominal pain beginning in the right lower quadrant. Pelvic abdomen and is occasionally associated with diarrhea and fever.
inflammatory disease in young women usually occurs within a Classically, the patient is in moderate discomfort with left lower
week of menses. With gastroenteritis, vomiting often precedes quadrant pain with or without localized guarding. Perforation
abdominal pain and is often associated with diarrhea. and abscess formation can present with minimal symptoms if the
Clinical presentation of acute appendicitis revolves around the perforation is contained in the retroperitoneum. However, if the
associated abdominal pain. Classically, the pain is initially achy perforation extends into the peritoneal cavity, it can present with
in nature and located in the periumbilical area. As the disease generalized peritonitis. Treatment in the wilderness for diverticu-
progresses, the pain becomes sharper and localized in the right litis includes hydration, bowel rest, and broad-spectrum antibiot-
lower quadrant. It is associated with fever, anorexia, and malaise. ics; if evacuation is delayed, IV antibiotics covering gram-negative
In later stages, the patient often remains still, occasionally with enterics and anaerobes are given. Oral antibiotic coverage with
the right hip flexed, complaining of pain on passive hip exten- ciprofloxacin and metronidazole may be adequate for mild cases
sion (psoas sign). The patient may have indirect tenderness in of diverticulitis. Because of the unpredictable response to anti-
the right lower quadrant upon palpation of the left lower quad- biotics and potential for progression, evacuation is most often
rant. As mentioned, if acute appendicitis is suspected, evacuation indicated when patients develop diverticulitis.
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
MECHANICAL SMALL BOWEL OBSTRUCTION
and initiation of broad-spectrum antibiotics covering anaerobic Small bowel obstruction is a common surgical condition; in the
and gram-negative bacteria (e.g., cefoxitin 2 g, or piperacillin- wilderness, it is a true emergency. The most common cause is
tazobactam 3.375 g). If only oral antibiotics are available, a fluo- postoperative adhesions, followed closely by an incarcerated
roquinolone, such as oral ciprofloxacin 750 mg twice a day, is abdominal wall incisional hernia. The clinical presentation varies
recommended. between patients according to the level of obstruction, the time
398
course, and the presence of or potential for strangulation. Initially
399
maintenance, induced nausea, and vomiting.138 Any person Testicular torsion can occur at any age, but it is more likely
whose symptom complex cannot be controlled must be evacu- near puberty. The likelihood of testicular salvage is inversely
ated. Additional indications for evacuation include calculus proportional to the elapsed time from torsion; this is a true surgi-
anuria, evidence of obstruction-induced infection, and signs of cal emergency. Acute onset of severe testicular pain is the hall-
systemic infection. 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
URINARY RETENTION have testicular torsion. In addition, nausea and vomiting may
Urinary retention is a painful experience in which the patient is accompany torsion, whereas fever, dysuria, and frequency are
unable to voluntarily urinate. This condition requires immediate associated with epididymitis.
medical, and sometimes surgical, intervention.123,141 Causes of Physical examination reveals a patient in extreme discomfort
urinary retention can be categorized as obstructive, infectious, with a swollen scrotum and a tender testicle; the affected testicle
inflammatory, pharmacologic, or neurologic.123 Twenty-three may be higher than normal and have a horizontal lie.36 Scrotal
percent of men reaching 80 years of age will experience acute skin may be edematous and discolored. Unilateral scrotal swell-
retention at some time.19 Acute urinary retention can lead to ing without skin changes is more indicative of a hernia or hydro-
incapacitating symptoms in the wilderness; prompt recognition cele. In testicular torsion, the affected testis is often larger than
and intervention are necessary and can be addressed with limited the unaffected testis. Prehn’s sign (relief of pain accomplished
resources.136 by elevation of the testicle) may be helpful to some degree in
Principal symptoms are bladder distention and pain that may differentiating testicular torsion from acute epididymitis.119 With
mimic acute abdomen, overflow incontinence, dribbling, and torsion, which twists the spermatic cord and elevates the testicle,
hesitancy. Physical examination findings include prostatic enlarge- pain is not relieved by elevation (negative Prehn’s sign); with
ment in men and lower midline abdominal tenderness and epididymitis, pain is relieved by elevation (positive Prehn’s sign).
distention. If painful distention of the bladder is present, decom- This maneuver has low sensitivity in distinguishing the two con-
pression should be undertaken. ditions, but may be helpful in conjunction with other findings.119
Medical therapy may be considered before complete obstruc- Treatment consists of surgical detorsion, which should be
tion to urinary flow. Third-generation α-adrenergic blockers may accomplished within 12 hours of torsion.36 Manual detorsion is
provide some relief. The α-adrenergic blockers such as terazosin not the treatment of choice; however, remoteness of the wilder-
promote bladder neck and prostatic urethral relaxation.59 ness environment may mandate manual attempts. Studies of
Bladder decompression should be initially attempted with a manual detorsion are scant and the cohorts small.36
standard Foley catheter. In men with prostatic hypertrophy, If manual detorsion is necessary, the victim should be placed
passage of the catheter may be challenging, and a large catheter supine. The procedure can be assisted with IV sedation with or
or coudé catheter should be used if a standard Foley catheter without local anesthetic. Classic teaching has suggested that tes-
TRAUMA
cannot be passed.123 Instrumentation of the urethra with hemo- ticular torsion typically occurs in the medial direction. Therefore,
stats or dilators is dangerous and should not be attempted in the detorsion is initially attempted with outward rotation of the testis
field. (toward the ipsilateral thigh). Simultaneous rotation in the caudal
There are several valved urinary catheters that eliminate the to cranial direction may be necessary to release the cremasteric
need for the urine drainage bags and connecting tubes normally muscle.114
required with Foley catheters. These catheters incorporate a The surgical treatment of testicular torsion includes pexing the
PART 4
manually activated valve at the end of the catheter that allows testes to prevent recurrent torsion. Thus, although detorsion may
the patient to store urine in the bladder and to mimic normal be a temporary treatment for an acute situation in the field, all
voiding behavior.141 The catheters may be used with a continuous victims must be evacuated for definitive treatment.
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
PROSTATITIS
severe, needle decompression is indicated. The skin of the supra- A number of forms of prostatitis have been defined, including
pubic region should be anesthetized, if possible. The distended viral, bacterial, nonbacterial, and chronic forms. The acute bacte-
bladder is palpated to guide aspiration. If ultrasound is available, rial form may potentially lead to severe infection.
it can be used to guide the decompression. A 22-gauge needle Bacterial prostatitis is an infection of the prostate caused pri-
attached to a syringe is introduced through the skin of the lower marily by gram-negative bacteria, with 80% attributable to Esch-
abdomen two fingerbreadths above the pubic symphysis and erichia coli. It is an acute, febrile illness characterized by perineal
directed at the anus. The needle is advanced with simultaneous pain radiating to the low back, chills, malaise, and voiding symp-
aspiration of the syringe until free-flowing urine is visualized. toms, such as urgency, frequency, and dysuria. Urinary retention
Palpation of the bladder in combination with adherence to this is common, and cystitis frequently accompanies the infection. On
technique should lead to successful decompression. rectal examination, the prostate gland is usually boggy, warm,
Complications related to decompression can occur. Drainage and tender, and enlargement is variable.
of more than 300 mL/hr can induce mucosal hemorrhage. A small In an ideal situation, treatment is individualized to the cause,
number of victims develop obstructive diuresis that may lead to which may be difficult to discern in the wilderness. The infection
dehydration, in which case aggressive oral hydration or crystal- may respond to an oral antibiotic such as ciprofloxacin (750 mg
loid repletion should be undertaken.105 Finally, surgical decom- orally twice a day), ampicillin (500 mg orally 4 times a day), or
pression is temporizing, and retention will recur. Treatment may trimethoprim (160 mg) with sulfamethoxazole (800 mg) orally
need to be continued or repeated. Drainage of the bladder twice a day. Penetration of prostatic secretions has been shown
acutely relieves symptoms and may allow ambulatory evacuation, to be best achieved by trimethoprim/sulfamethoxazole. The
but the underlying cause must be addressed once the patient is chosen antibiotic should be administered for 30 days. If retention
undergoing definitive care. is present, catheterization or suprapubic aspiration should be
undertaken.
Acute bacterial prostatitis can escalate in severity to systemic
ACUTE SCROTUM toxicity. Persons with evidence of systemic toxicity unresponsive
Acute onset of scrotal pain and swelling requires immediate to a trial of oral or parenteral antibiotic therapy should be
attention. Causes are multiple, but the three that should be con- evacuated.
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,
URINARY TRACT INFECTION
when all aspects are taken as a whole, they frequently suggest Urinary tract infections (UTIs) are extremely common and in-
the cause of the scrotal pathology.36 clude episodes of acute cystitis and pyelonephritis occurring in
400
otherwise healthy individuals. These infections predominate in despite treating with antibiotic therapy could be related to an
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.)
401
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
with community-acquired S. aureus (CA-MRSA), which is resis- One of the major disadvantages of operative procedures in the
tant to beta-lactam antibiotics. CA-MRSA can spread by contact austere environment is inability to sterilize instruments and estab-
with an infected person or by exposure to a contaminated object lish a sterile field. The goal is to decrease the risk for bacterial
or surface. Sharing personal items, such as towels or razors, is a contamination as much as possible.
common mode of spread. Antiseptics are agents used to decontaminate skin. Chlorhexi-
About 80% of MRSA infections involve the skin and soft tissue dine is an antiseptic with excellent antimicrobial activity and
PART 4
(Figure 18-16). MRSA infection can also involve bones and joints, prolonged length of activity. In many health care facilities,
leading to severe sepsis. Outbreaks have been reported during chlorhexidine has replaced iodophors as the antiseptic of choice.
wilderness excursions. Areas of skin violation that are most vul- Isopropyl alcohol may be used if no other antiseptic is available.
nerable include lacerations, burns, blisters, abrasions, and insect It is particularly ineffective on dirty skin and has little persistent
bites. Areas of increased body hair, such as the buttocks, axillae, activity. If nothing is available, soap and water may be of benefit.
back of the neck, and beard, are more likely to be infected. The Soap removes unattached bacteria from the surface of skin, but
most frequent presenting sign is a red, swollen, painful lesion does not remove adherent bacteria.
resembling an infected spider bite. Subsequent yellow or white If sterile fluid is not available for wound irrigation, potable
central pustules or boils may drain spontaneously. The spectrum water may be used. Boiling water before irrigation does not rid
of CA-MRSA infections includes cellulitis, furuncles, carbuncles, the water of spores. If water is to be boiled, the boiling should be
and cutaneous abscesses. “rolling” for 20 minutes to be effective. Any fluids used should
CA-MRSA has been found in 75% of cutaneous abscesses in be removed from the wound as best as possible. Wounds should
the community. The mainstay of treatment is adequate drainage. be managed to ensure that no devitalized tissue or foreign bodies
Oral antibiotics that have been effective include clindamycin and remain in them.
trimethoprim/sulfamethoxazole. These infections can occasion- If preparations are made for the possibility of surgical proce-
ally disseminate and become life-threatening, with associated dures during an expedition, instruments taken into the field
bacteremia, septic arthritis, or endocarditis. Avoidance of dis- should be packed sterile in durable containers. Paper wrappers
semination is best accomplished with preventive measures, can become perforated, permitting contamination. A disinfectant
which include washing the hands on a regular basis, using a is an agent that will decontaminate inanimate objects. If surgical
hand sanitizer with 60% alcohol, wearing long pants and protect- instruments are not sterile, disinfectants can be used to decrease
ing the skin from injury, and not sharing personal items such as the bacterial count on the surface. Of course, all instruments
towels and clothing. If skin injuries occur, keep them covered should be clean of debris. Unfortunately, many of the disinfec-
and clean and report all suspected skin infections promptly.42,132 tants used in health care facilities are not practical for the austere
These life-threatening conditions are caused by virulent toxins environment. Ortho-phthaladehyde, peracetic, and glutaralde-
produced by bacteria, the most common being group A beta- hyde are effective disinfectants, but hazardous for personnel and
hemolytic Streptococcus, with or without Staphylococcus present. the environment and impractical in the field environment.43 The
Frequently these infections are caused by multiple mixed flora antiseptic chosen, such as chlorhexidine, for skin preparation
of both anaerobic and facultative aerobes, especially C. perfrin- may be applied to the instruments.
gens and Bacteroides. The depth of tissue involvement may Placing instruments into boiling water decreases the bacterial
include subcutaneous tissue, fascia, or even muscle. These infec- count but will not completely eliminate bacterial spores. Apply-
tions most commonly occur in the extremities, abdominal wall, ing flame to instruments may kill bacteria but leave products of
or perineum and occur within a week of the inciting event. combustion on the instruments that are then left in the wound
Necrotizing infections occur with increased frequency in immu- as foreign material.
nosuppressed patients, including those with diabetes, peripheral The U.S. Army has developed a field sterilization system that
vascular disease, and chronic renal failure; drug abusers; and is lightweight and does not require an external energy source.
persons of advanced age. The area of cellulitis spreads progres- The system is the size of a suitcase and has the capacity to
402
accommodate a surgical tray. A mixture of water and dry reagents monitoring, and the capability of establishing a definitive airway
controllably generates chlorine dioxide. The chlorine dioxide should be immediately available. Common agents used to sup-
kills all vegetative cells and bacterial spores within 30 minutes.43 plement local or regional anesthesia are opioids and benzodiaz-
Although the specific system used by the army may not be avail- epines. Should these agents be used, reversal agents of naloxone
able to the public, there are a number of commercially available and flumazenil should be available. Ketamine is an excellent
products that can be easily found on the Internet for the purpose agent for providing dissociative sedation and pain reduction.
of field sterilization.
403.e1
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403.e3
CHAPTER 19 Emergency Airway Management
CHAPTER 19
Emergency Airway Management
ANDREW J. EYRE AND CALVIN A. BROWN III
Emergency airway management skills are crucial in the care of anteriorly by the anterior pharyngeal wall. The base of the val-
critically ill or injured patients. Airway management consists of lecula contains the hyoepiglottic ligament. This structure is key
a structured patient assessment, methodical approach, and effec- to successful visualization during direct laryngoscopy with a
tive oxygenation and ventilation, typically by inserting a cuffed curved blade. Engaging the hyoepiglottic ligament with the
endotracheal tube. Effective airway management takes prece- bulbous end of a MacIntosh laryngoscope blade elevates the
dence over all other clinical considerations. epiglottis and reveals the glottic aperture. Failure to fully engage
In resource-limited, austere environments, airway manage- the hyoepiglottic ligament can result in a poor glottic view and
ment is by definition challenging. Many resources that are readily intubation failure. The laryngeal inlet is the opening to the larynx
accessible in a hospital or emergency department setting are that is bounded by the epiglottis, aryepiglottic folds, and aryte-
not available in remote settings. Improvisation may prove noid cartilages. The glottis is the vocal apparatus. The glottis
invaluable. 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).
AIRWAY ANATOMY Externally identifiable landmarks are important for airway
The airway consists of the mouth, nasal and oral cavities, pharynx, assessment and management (Figure 19-2). The mentum is the
nasopharynx, hypopharynx, glottis, and tracheobronchial tree anterior aspect of the mandible that forms the tip of the chin.
(Figure 19-1). It begins at the oral and nasal apertures. The nasal The hyoid bone forms the base of the floor of the mouth. The
cavity extends from the nostrils to the posterior nares (i.e., thyroid cartilage forms the laryngeal prominence (Adam’s apple)
choanae). Due to anatomic features (e.g., turbinates), resistance and thyroid notch. The cricoid cartilage, which lies inferior to
to nasal airflow is approximately twice that of oral airflow. The the thyroid cartilage, forms a complete ring that provides struc-
nasopharynx extends from the posterior nasal cavity to the level tural support to the lower airway. The cricothyroid membrane
of the soft palate. Primary impediments to airflow through the lies between the thyroid and cricoid cartilages and serves as an
nasopharynx are the tonsils. The oral cavity is bounded by the access point during surgical airway management.
teeth anteriorly, the hard and soft palates above, and the tongue Knowledge of anatomic differences between adults and
and floor of the mouth below. The oropharynx communicates infants is integral to effective pediatric airway management.
with the oral cavity and nasopharynx and extends from the soft These important differences are summarized in Table 19-1 and
palate to the tip of the epiglottis. Figure 19-3.
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 DECISION TO INTUBATE
the laryngopharynx and trachea, and serves as the organ of A decision to intubate is based on three criteria: (1) failure to
phonation. The larynx and epiglottis serve to protect the lower maintain or protect the airway, (2) failure of ventilation or oxy-
airway from aspiration. The larynx is made up of muscles, liga- genation, and (3) the patient’s anticipated clinical course and
ments, and cartilages (i.e., thyroid, cricoid, arytenoids, cornicu- likelihood of deterioration.23
lates, and epiglottis).
The epiglottis is flexible. It originates from the hyoid bone
and base of the tongue and covers the glottis during swallowing.
FAILURE OF AIRWAY PROTECTION
During laryngoscopy, the epiglottis is an important landmark A patent airway is essential for ventilation and oxygenation. If a
because it serves as a guidepost for the glottic inlet and laryn- patient is unable to maintain an unobstructed airway, the pro-
goscopic blade placement. The vallecula is the space at the base vider should establish patency by repositioning, performing a
of the tongue that is bounded posteriorly by the epiglottis and chin lift and/or jaw thrust, or inserting an oral or nasopharyngeal
403
Nasal
cavity
Hyoid bone
Thyroid
Thyroid membrane cartilage
Nasopharynx
Thyroid notch
Laryngeal
Oral Cricothyroid prominence
cavity membrane
Oropharynx Cricoid cartilage Thyroid
gland
Vallecula Tracheal rings
Laryngeal inlet
Laryngopharynx FIGURE 19-2 External airway anatomy.
Epiglottis
Glottis
Larynx
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
FIGURE 19-1 Lateral airway anatomy. indicate the need for airway management.
airway. The patient must be able to protect against aspiration of ANTICIPATED CLINICAL COURSE
gastric contents. The presence of a gag reflex is neither sensitive Patients with a moderate to high likelihood of airway deteriora-
nor specific for predicting the need for intubation. A patient’s tion often require endotracheal intubation despite airway patency,
ability to swallow or handle secretions is a more reliable indica- adequate oxygenation, and normal vital signs. For instance, a
tor. The recommended approach is to evaluate the patient’s patient with significant blunt trauma from a climbing accident
mental status, phonation, response to verbal commands, and may require intubation due to pain severity and likelihood of
ability to manage secretions. If a patient has pooling secretions, deterioration. Assess the structural integrity of the central face
has difficulty phonating, is comatose, or cannot respond to and mandible. Injuries to these structures may lead to airway
TRAUMA
simple verbal cues, the patient likely cannot adequately protect distortion and compromise. Inspect the anterior neck and chest
against aspiration. Intubation is required. In most patients, if a for penetrating wounds, asymmetry, or swelling that may herald
maneuver for establishing an airway is needed, definitive airway impending airway compromise. Anticipating deterioration or pro-
management is also required. gression of disease that may confound subsequent intubation
attempts is crucial.
In children, visual signs of airway compromise and respiratory
FAILURE OF VENTILATION OR OXYGENATION
PART 4
Large intraoral tongue that occupies a relatively large portion of High anterior airway position of glottic opening compared with that of
oral cavity adult
High tracheal opening: C1 in infancy; C3 or C4 at age 7 years; Straight blade preferred over curved blade to push distensible anatomy
C4 or C5 in adulthood out of the way to visualize larynx
Large occiput may cause flexion of airway; large tongue easily Sniffing position is preferred; large occiput elevates head into sniffing
collapses against posterior pharynx position in most infants and children a towel may be required under
shoulders to elevate torso relative to head in small infants
Cricoid ring is the narrowest portion of the trachea as compared Uncuffed tubes provide an adequate seal because they fit snugly at the
with vocal cords in adults level of the cricoid ring; correct tube size is essential because variable
expansion cuffed tubes are not used
Airway anatomy varies consistently by patient age; there are Age less than 2 years, high anterior airway
fewer abnormal variations related to body habitus, arthritis, or Age 2 to 8 years, transitional airway
chronic disease Age older than 8 years to small adult; “normal” adult positioning of airway
Large tonsils and adenoids may bleed; more acute angle Blind nasotracheal intubation not indicated for children; nasotracheal
between epiglottis and laryngeal opening results in intubation failure
nasotracheal intubation attempt failures
Small cricothyroid membrane Needle cricothyroidotomy difficult and surgical cricothyroidotomy
impossible in infants and small children
Modified from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, 2nd ed, Philadelphia, 2004, Lippincott Williams & Wilkins.
404
HEAD POSITIONING
405
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
FIGURE 19-5 Head tilt with chin lift. 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
TRAUMA
(Figure 19-8). The NPA is inserted through the nose. The NPA
has a distal flange to prevent insertion beyond the nostril. The
FIGURE 19-6 Jaw thrust without head tilt.
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
PART 4
quite effective. If cervical spine injuries are not suspected, it can obstacles preclude OPA placement. NPAs are contraindicated in
be used in combination with a head tilt/chin lift. 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
MECHANICAL AIRWAY ADJUNCTS varying designs and sizes to accommodate patients of all sizes.
After a patent airway has been established, it is critical that the The sizes (as indicated by the internal diameter) range from 12
airway remain open. This requires continual reassessment of to 36 French. The proper NPA length is determined by measuring
airway patency. An oropharyngeal airway (OPA) or nasopharyn- the distance from the tip of the patient’s nose to the tragus of
geal airway (NPA) device can be placed to create a patent the ipsilateral ear.
conduit for spontaneous or assisted ventilation. Each device has After selecting the appropriate size, the NPA is lubricated with
specific indications and contraindications and must be properly a water-soluble lubricant. Insert it gently into the nostril with its
selected to avoid causing harm. Although OPAs and NPAs help beveled end pointed toward the nasal septum. Continuing to act
to maintain airway patency, they do not protect against aspira- gently, advance the NPA along the floor of the nasal passage and
tion. They serve as temporizing measures until a definitive airway into the nasopharynx. If resistance is met, gently rotate the NPA,
can be established or the patient’s condition improves. select a smaller size, or attempt to insert it through the other
nostril. In position, the flange should rest against the patient’s
Oropharyngeal Airway nostril. The distal end should rest behind the tongue in the pos-
The OPA is a curved, rigid device designed to hold the tongue terior pharynx. Ensure that the NPA has created a patent airway.
away from the posterior pharyngeal wall (Figure 19-7). When If necessary, an NPA can be placed in each nostril.
406
becomes essential to create and maintain a patent airway and to
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 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
open airway with the head tilted. Alternatively, the thumbs and a
similar to that for mouth-to-mouth ventilation. Open the airway portion of the rescuer’s palms can anchor the mask, and the index and
in a similar fashion, and then close the mouth using the thumb remaining fingers can lift the jaw and hold it against the mask. (Redrawn
and forefinger to seal the lips. The patient’s nostrils are left open, from American Heart Association: Guidelines 2000 for cardiopulmo-
and the rescuer’s mouth is sealed around the patient’s nose. nary resuscitation and emergency cardiovascular care. Circulation
Breaths are delivered until chest rise is observed. 102:I95, 2000.)
PART 4
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 tilation include traits that prevent an adequate mask seal (e.g.,
or a similar barrier device allows the rescuer to provide ventila- beard, facial trauma) or limit flow to gas-exchanging portions of
tion without making direct contact with the patient’s mouth and the lungs (e.g., chronic obstructive pulmonary disease, airway
nose. The mask has a one-way valve in the stem to prevent obstruction, morbid obesity).12,13 The MOANS mnemonic outlines
exhaled gases and bodily fluids from reaching the health care predictors of difficult bag-and-mask ventilation (see Box 19-2).
provider. A disposable filter may be added to trap infectious air Face mask fittings are interchangeable with distal ETT adapters.
droplets and secretions. The same bag can be used after intubation.
The pocket face mask is made of pliable plastic material and Competence with a BVM device is a vital emergency skill and
can be easily carried. Some masks have an oxygen inlet so that a prerequisite for the use of paralytic agents for endotracheal
supplemental oxygen can be administered. Devices are available intubation. Whenever possible, use a two-handed and two-
in a number of sizes. If an infant mask is not available, an adult person technique. Holding the mask with a thenar grip results
mask can be turned upside-down for a better fit. To use a pocket in more effective ventilation, even by novice airway managers.
mask, first open the airway and clear any obvious obstruction With thumbs pointed toward the patient’s chest, place the thenar
using the head tilt/chin lift or jaw thrust. Take a position behind eminences against the lateral walls of the mask. Wrap the other
the patient’s head. In an unresponsive patient, insert an OPA or fingers around the mandibles and pull the jaw up into the mask.
NPA to help maintain a patent airway. Stretch the mask and apply Ensure an even mask seal.9 If a single-handed mask hold is
it to the patient’s face. Apply pressure to both sides of the mask required, the operator must remain vigilant to prevent mask
with the thumbs and base of the palm to create an air-tight seal. leakage and ineffective ventilation. When rescue ventilating a
As with a jaw thrust, place the remaining fingers underneath the supine, apneic, and unresponsive patient, an oral airway is
patient’s jaw and apply upward pressure. Provide breaths directly imperative because the tongue falls against the posterior pharynx
to the mask, ensure adequate chest rise, and allow for passive and occludes the airway. During prolonged mask ventilation,
exhalation between breaths. 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
BAG-VALVE-MASK VENTILATION regulates the volume of air transferred, the amount of air trans-
A self-inflating ventilation bag with face mask (i.e., bag-valve- ferred by a BVM is a clinical estimate based on the patient’s
mask [BVM] device) allows for emergency ventilation with a high weight, approximately 5 to 7 mL/kg, or enough to create visible
concentration of oxygen. Devices are equipped with several chest rise.
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
ADVANCED AIRWAY MANAGEMENT
(15 L/min), BVM devices can supply approximately 100% oxygen. A definitive airway requires patency and protection provided by
Patient characteristics associated with difficult rescue mask ven- a stabilized, inflated cuffed structure in the trachea attached to
408
predictive of a challenging intubation. Providers should always
409
BOX 19-2 MOANS Mnemonic for Challenging Rescue BOX 19-4 SMART Mnemonic for Evaluation
Bag-and-Mask Ventilation of Difficult Cricothyrotomy
Mask seal (beard or altered anatomy) Surgery
Obstruction or Obesity Mass (head and neck cancer, hematoma)
Aged (> 55 years old) Access/anatomy problems (obesity, edema)
No teeth Radiation
Stiffness (resistance to ventilation or intrinsic lung pathology) Tumor
Adapted with permission from The Difficult Airway Course: Emergency and Adapted with permission from The Difficult Airway Course: Emergency and
Walls RM, Murphy MF, editors: Manual of emergency airway management, Walls RM, Murphy MF, editors: Manual of emergency airway management,
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins. 4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
Predicting Difficult Bag-Mask Ventilation with the intubation is unsuccessful (e.g., due to residual muscular contrac-
MOANS Mnemonic tion and limited mouth opening), a neuromuscular blocking
Attributes of difficult BMV are well validated. They are reflected agent (NMBA) (e.g., succinylcholine [1.5 mg/kg intravenously])
in the mnemonic MOANS (Box 19-2).12,13 Patients in whom rescue can be administered, followed by another intubation attempt. If
ventilation by face mask is difficult or impossible typically have an ETT has not been placed after three attempts, place an EGD.
features that interfere with an adequate mask seal (e.g., patients If at any point the oxygen saturation drops and cannot be main-
with beards or altered lower craniofacial anatomy) or qualities tained with an EGD or rescue ventilation technique, a failed
that impair adequate delivery of oxygen to gas-exchanging por- airway has developed and the operator should move quickly to
tions of the lungs. This can be due to advanced age, morbid create a surgical airway.
obesity, airway obstruction, or intrinsic lung pathologic condi-
tions (e.g., asthma, chronic obstructive pulmonary disease).
The difficulty with BVM management of the edentulous
RAPID SEQUENCE INTUBATION
patient is the basis of the advice, “Teeth out to intubate; teeth in If a patient does not require an immediate (crash) airway inter-
to ventilate.”6 In patients without teeth, place the mask or a rolled vention and assessment does not predict a sufficiently difficult
gauze inside the lower lip to limit air leakage and eliminate the airway such that neuromuscular blockade might be contraindi-
risk of aspiration associated with dental prosthetics. cated, pursue RSI. RSI follows a coordinated series of steps to
allow safe and effective airway management without interposed
Predicting Difficult Extraglottic Device Placement with BVM. It is the method of choice for most acutely ill or injured
TRAUMA
tion with an EGD is predicted by the mnemonic RODS (Box RSI is described in discreet steps termed the seven Ps of RSI
19-3). If the LEMON and MOANS assessments have been com- (Table 19-2).25
pleted, only the D (distorted anatomy) remains to be evaluated.
Distorted upper airway anatomy may result in an incomplete seal Preparation
and air leakage that cause ineffective ventilation. Restricted Prior to the intubation attempt, gather the proper equipment and
mouth opening, airway obstruction, and intrinsic lung pathologic medications for use during airway management. This may include
conditions can make ventilation difficult with a mask or EGD. pretreatment, induction, and paralytic agents (see below). Attach
cardiac and oximetry monitors. In an austere environment, this
Predicting Difficult Cricothyrotomy with the process may be quite limited.
SMART Mnemonic
Predicting difficult cricothyrotomy is outlined by the SMART Preoxygenation
mnemonic (Box 19-4). Difficult cricothyrotomy occurs when The goal of preoxygenation is to prolong the period of safe
there is limited access to the anterior neck or when laryngeal apnea (from the onset of paralysis to desaturation below 90%)
landmarks are obscured. Inspect and palpate the neck for signs by creating an oxygen reservoir in the patient’s lungs. This is
of prior surgery, hematoma, tumor, abscess, or radiation changes. typically accomplished by supplying nonrebreather face mask
oxygen at approximately 100% for 3 minutes of normal, tidal
IMMEDIATE ORAL INTUBATION volume breathing. In a healthy patient, this may allow 6 to 8
minutes of safe apnea. This time will be much less in children,
(“CRASH” INTUBATION) obese patients, and patients with critical illness or injury for
Patients in cardiorespiratory arrest or with agonal vital signs whom oxygen use is increased. Preoxygenation is essential to
require immediate oral intubation. These patients often have little the “no bagging” approach of RSI. If time is insufficient for a full
or no muscular tone and can be intubated without the need for
RSI drugs. Attempt immediate intubation without medications. If
TABLE 19-2 The Seven Ps of Rapid Sequence
Intubation
BOX 19-3 RODS Mnemonic for Potentially Difficult Time Action
Extraglottic Device Placement and Use
Zero minus 10 minutes Preparation
Restricted mouth opening Zero minus 5 minutes Preoxygenation
Obstruction or Obesity
Zero minus 3 minutes Pretreatment
Distorted anatomy
Stiffness (resistance to ventilation) —Time zero— Paralysis with induction
Zero plus 20-30 seconds Positioning
Adapted with permission from The Difficult Airway Course: Emergency and Zero plus 45 seconds Placement with proof
Walls RM, Murphy MF, editors: Manual of emergency airway management, Zero plus 1 minute Postintubation management
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
410
CHAPTER 19 Emergency Airway Management
TABLE 19-3 Clinical Characteristics of Induction Agents*
*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 Principal induction agents used in the emergency setting are
high-flow oxygen can achieve oxygen saturations and apnea etomidate, propofol, and ketamine. In North America, more than
times that match or exceed those obtained with traditional pre- 90% of inductions in adult patients in the emergency department
oxygenation. For an obese patient, if contraindications do not involve etomidate, indicating widespread familiarity and confi-
exist, preoxygenation should be performed with the patient dence with this drug.3 Previous controversy regarding the poten-
upright. After neuromuscular blockade, passive oxygenation is tial harmful effects of etomidate in septic patients has not been
accomplished by continuing supplemental oxygen by nasal substantiated.10 Clinical characteristics of the most commonly
cannula (at a flow rate of 2 to 6 L/min) during laryngoscopy, used induction agents and their typical doses are summarized in
and the time to 95% desaturation is extended from 3.5 to 5.3 Table 19-3.
minutes.16,26 Neuromuscular Blockade. NMBAs induce rapid, transient
paralysis to facilitate laryngoscopy and ETT placement. These
Pretreatment agents do not provide analgesia, sedation, or amnesia. The ideal
Laryngoscopy may have detrimental physiologic effects (e.g., NMBA has a rapid onset and short duration of action and few
increased intracranial pressure, heart rate, blood pressure, vascu- adverse side effects. Succinylcholine, a depolarizing NMBA,
lar sheer forces, and bronchospasm). Pretreatment agents are comes closest to fulfilling these traits. It is the most commonly
used to mitigate these effects. Pretreatment regimens have used NMBA, although rocuronium is becoming increasingly
evolved, and many formerly traditional methods (e.g., defascicu- popular.3 At the neuromuscular junction, succinylcholine binds
lating doses of competitive neuromuscular blockers before tightly to acetylcholine receptors that control potassium channels.
administering succinylcholine; routine use of atropine in chil- Efflux of potassium ions results in motor end-plate depolarization
dren) have largely been abandoned. Patients who may still be and muscle contraction. Succinylcholine prevents repolarization,
considered for pretreatment are those with reactive airway causing flaccid paralysis. Clinically, this manifests as muscle fas-
disease, elevated intracranial pressure, or a cardiovascular or ciculations (10 to 15 seconds following IV bolus administration)
neurovascular condition for which increased vascular sheer followed by complete muscle relaxation and paralysis (at 45 to
forces might be dangerous. In patients with asthma, lidocaine 60 seconds). It has a short duration of action. Patients may
has been recommended as a pretreatment drug to limit the bron- resume spontaneous breathing within 3 to 5 minutes.
chospastic response to laryngoscopy. Given that data are limited Succinylcholine is administered at a dose of 1.5 mg/kg via
and beta agonists are universally recommended for acute asthma rapid IV bolus. It is contraindicated in patients with postsynaptic
exacerbations, lidocaine is unlikely to confer benefit. It is reason- receptor upregulation following neurologic injury (i.e., stroke or
able to administer lidocaine (1.5 mg/kg) as a pretreatment drug spinal cord injury). In this population, succinylcholine depolar-
for asthmatic patients who have not received albuterol. Lidocaine ization can cause severe hyperkalemia. This risk presents 3 days
is no longer indicated for pretreatment in head-injured patients after a discreet neurologic insult and lasts approximately 6
with presumed elevated intracranial pressure. A patient intubated months. Nondepolarizing NMBAs (e.g., rocuronium) cause paral-
in the setting of a vascular emergency (e.g., ischemic coronary ysis by competing with acetylcholine for receptors at the neuro-
disease, aortic dissection) may benefit from a sympatholytic dose muscular junction. Rocuronium is the most commonly used
(3 µg/kg) of fentanyl to blunt the release of catecholamines competitive NMBA for emergency airway management. It is
caused by laryngeal manipulation. Fentanyl can also be used in administered at a dose of 1 to 1.2 mg/kg given via rapid IV push,
patients with primary cerebral processes associated with pre- and provides intubating conditions similar to those created by
sumed elevated intracranial pressure if the blood pressure and use of succinylcholine.15 Vecuronium and pancuronium should
heart rate are normal. not be used for emergency airway management unless neither
succinylcholine nor rocuronium is available (Table 19-4).
Paralysis with Induction
Rapidly administer an intravenous (IV) bolus of an induction Positioning
agent to produce complete loss of consciousness, followed The airway can be considered to have three separate axes: oral,
immediately by rapid administration of a NMBA to induce com- pharyngeal, and laryngeal. In neutral head position, these axes
plete motor paralysis. approximate a right angle (Figure 19-13). By combining proper
Induction Agents. With few exceptions, patients should head positioning with head elevation and cervical spine exten-
receive an induction agent before neuromuscular blockade. Para- sion, these axes become more aligned and the trajectory to
lyzing a conscious patient without providing adequate sedation establish an airway is made straighter (Figure 19-14). The sniffing
can lead to detrimental physiologic and psychological sequelae. position can be accomplished by placing rolls, a daypack, or
Unless the patient has a Glasgow Coma Scale score of 3 or suffers even shoes under the posterior occiput (Figure 19-15).
from profound refractory shock (i.e., those for whom even a The sniffing position is helpful in all patients. It is crucial in
small dose of an induction agent might precipitate cardiovascular morbidly obese patients, where alignment of upper airway axes
collapse), induction is mandatory. 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
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
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 curonium [0.1 mg/kg] or vecuronium [0.1 mg/kg]) may be used
413
Epistaxis and nasal turbinate injury from blind nasotracheal tion less likely with an LMA than with a BMV device. LMAs
intubation can be reduced by pretreatment with vasoconstrictor provide ventilation equivalent to that of ETTs. LMA use may be
agents and proper technique. If sufficient topical anesthesia is preferred to ETT intubation when access to the patient is limited,
provided, patients typically tolerate this procedure well. Long- when unstable neck injury may exist, or when appropriate victim
term complications (e.g., sinusitis, turbinate destruction) are positioning for tracheal intubation is impossible. With elective
uncommon and result from multiple intubation attempts or pro- anesthesia, the LMA has an extremely high rate of successful
longed intubation. 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
ALTERNATIVE AIRWAY ADJUNCTS shown ease of insertion, high rates of successful insertion, and
successful ventilation.20
AND TECHNIQUES The LMA Fastrach is designed to facilitate blind intubation
In certain wilderness settings, tracheal intubation may be difficult through a specially designed mask employing an epiglottic eleva-
or impossible. Under such circumstances, alternative airway tor bar. Placement of the iLMA results in successful ventilation
adjuncts or techniques may be employed to provide an airway. in nearly all cases and successful subsequent intubation in 85%
Alternative airways that require blind passage of an ETT into the to 95% of cases. When augmented by flexible fiberoptic endos-
airway may be simpler to master than passing an ETT under copy, the rate of successful subsequent intubations rises to
direct vision. To achieve good outcomes with these devices approximately 100%. The LMA Fastrach has significant advan-
and techniques, providers must maintain a high level of knowl- tages when compared with a standard LMA. It provides a means
edge and skills through frequent practice (e.g., simulation) and for rescue ventilation and intubation. The LMA Fastrach comes
field use. 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
LARYNGEAL MASK AIRWAY well as standard LMAs for ventilation and oxygenation, and can
The laryngeal mask airway (LMA) is a modified ETT with an also facilitate blind intubation with standard adult ETTs. Both
inflatable oval cuff (i.e., the laryngeal mask) at its base (Figure work well for intubating a difficult airway, especially when aug-
19-16A-D). Blindly insert the LMA into the pharynx and advance mented by flexible endoscopy.11
it until resistance is felt as the distal portion of the LMA lodges
in the laryngopharynx. Inflating the collar seals the LMA around Combitube
the laryngeal inlet and facilitates tracheal ventilation. The Combitube is a double-lumen, adult-only, dual-cuffed airway.
Although LMAs do not ensure protection against aspiration, One lumen contains ventilating side holes at the hypopharyngeal
studies have shown that aspiration is uncommon and regurgita- level. The distal end is closed. The other lumen has an open
TRAUMA
PART 4
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
CHAPTER 19 Emergency Airway Management
.2
No No.1
No.1
No.1
2
2
No.
No.
A Insertion B Esophageal placement C Tracheal 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 posterior channel that accepts a nasogastric tube, allowing tube
an esophageal airway, and the other functions as a tracheal passage through the device to allow aspiration of gastric con-
airway (Figure 19-17). A Combitube is typically blindly inserted tents. The device’s airway seal may be lost after insertion and
and advanced until two guide marks printed on the tube reach requires deflation of the balloons and repositioning. The King LT
the patient’s teeth. The pharyngeal and distal balloons are airway is available in newborn through adult sizes.
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-
VIDEO LARYNGOSCOPY
gus. It will intubate the trachea in 3% to 5% of cases. Determine Video laryngoscopes consist of a video camera functionally asso-
the location (i.e., esophagus or trachea) of the distal orifice and ciated in one of many ways with a laryngoscope blade and
ventilate through the appropriate opening. handle, or other intubation device. For instance, the blade and
Advantages of a Combitube over a BVM include isolation of handle may be attached by video cable to a high-resolution color
the airway, reduced aspiration risk, and more reliable ventilation. display, or a miniaturized display may be attached directly to the
Disadvantages include large size, more difficulty with placement, handle. This technology effectively places the operator’s eye on
and competition with newer and more easily applied devices. a screen that transmits an image of the leading edge of the
Fatal complications with the Combitube may result from incorrect laryngoscopy blade. The blade may have a hypercurved (Glide-
identification of the position (trachea or esophagus) of the distal Scope) or traditional (Storz C-MAC) laryngoscope shape (Figures
lumen. An end-tidal carbon dioxide or esophageal detector 19-19 and 19-20). The video laryngoscopes with integrated moni-
device should be used in conjunction with the Combitube. 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-
KING LT tional laryngoscopes, the video scope improves glottic exposure
The King LT airway is a single-lumen, dual-cuffed airway with in both operative and emergency department populations, and
ventilation outlets between a large pharyngeal and a smaller it has higher first-pass success rates when compared with con-
esophageal balloon (Figure 19-18). The King LT airway is inserted ventional laryngoscopes.3,17,18,21 Video laryngoscopy is replacing
blindly. A single pilot balloon inflates both cuffs simultaneously. direct laryngoscopy as a first-line maneuver. Video laryngoscopes
Although it is similar to the Combitube, the King LT is shorter, tend to be expensive, but lower-cost devices (e.g., King Vision
easier to insert, and easier to inflate, and does not inadvertently video laryngoscope) are available (Figure 19-22). The King Vision
intubate the trachea.4 Newer versions of the King LT have a 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 19-18 King Laryngeal Tube (LT) inflated with the prepackaged
syringe. Figure 19-19 GlideScope titanium blades.
415
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.
416
CHAPTER 19 Emergency Airway Management
Cricoid Cricothyroid
cartilage membrane
Cricoid
cartilage
Thyroid
cartilage
Cricothyroid
space
A B C
L R
D E F
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 Improvised Cricothyrotomy
hand holding the thyroid cartilage, make a vertical midline If formal cricothyrotomy equipment is not available, a knife and
incision with a No. 11 scalpel blade from the thyroid cartilage a hollow object (i.e., substitute for the tracheostomy tube) may
caudad approximately 3 to 4 cm (1.2 to 1.6 inches) (see Figure be used. An improvised cricothyrotomy could be performed
19-23A). using a modified IV macro drip chamber or the cut barrel of a
Place a tracheal hook through the cricothyroid space. Hold 1-mL or 3-mL syringe (see Chapters 28 and 46). Any small hollow
cephalad traction with the nondominant hand (see Figure object (e.g., ballpoint pen casing, sports-bottle straw, inflation
19-23B-D). tube for white-water floatation bag) may be employed as a cri-
Make a transverse incision across the exposed cricothyroid cothyrotomy tube. Objects with an internal diameter of at least
membrane (see Figure 19-23E,F). If time permits, insert silk stay 3 mm (0.12 inch) provide the best gas exchange.
sutures in the trachea (see Figure 19-23G,H). Dilate the opening
in the cricothyroid membrane using a Trousseau dilator while NEEDLE CRICOTHYROTOMY WITH
maintaining traction with the hook (see Figure 19-23I-K). PERCUTANEOUS TRANSTRACHEAL
Place a Shiley cuffed tracheostomy tube through the opening
created in the cricothyroid membrane. Initially aim posteriorly
(TRANSLARYNGEAL) JET VENTILATION
and then redirect caudally once through the opening (see Figure An alternative surgical airway procedure is needle cricothyrotomy
19-23L). The tracheal hook may be removed before insertion of with percutaneous transtracheal jet ventilation (TTJV). With this
the tube to avoid damaging the tube. If a tracheostomy tube is technique, a transtracheal catheter is inserted through the crico-
not available, an ETT may be substituted. thyroid membrane into the trachea and connected to a jet ventila-
tion system consisting of high-pressure tubing, an oxygen source
Rapid Four-Step Cricothyrotomy at 50 psi, and an in-line one-way valve to intermittently admin-
The rapid four-step cricothyrotomy is accomplished as follows ister oxygen. One hundred percent oxygen is delivered at 12 to
and as shown in Figure 19-24: 20 bursts/min. The inspiratory phase should last 1 second. The
From a position at the head of the victim, palpate and identify expiratory phase should last 2 to 4 seconds. Advantages of this
landmarks, especially the cricoid and thyroid cartilages and cri- technique include simplicity, safety, and speed. In adults, this is
cothyroid membrane. an appropriate procedure only in the most dire circumstances;
Using a No. 20 scalpel, incise the cricothyroid membrane and even then, it should be considered a temporizing measure
overlying skin simultaneously with a single horizontal 1.5-cm because the tube’s small diameter makes oxygenation and
(0.6-inch) incision. While maintaining the blade within the removal of carbon dioxide incredibly challenging. In TTJV, there
airway, slide a tracheal hook alongside the caudal side of the is typically less bleeding than with cricothyrotomy. Age is not a
blade into the wound. contraindication. In children less than 10 years old, this is the
Orient the hook caudally. Place gentle traction on the cricoid preferred surgical airway technique. During TTJV, the upper
TRAUMA
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
Standard
endotracheal
tube connector
419
REFERENCES study of 188,064 patients registered in the Danish Anaesthesia Data-
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 a patient with facial trauma proceeds as it does with any other
time that an individual is in a remote place, far from definitive medical condition. In emergency situations, the chief complaint
hospital-based care. This occurs in disaster medicine, military and and history of the present illness are obtained as one is perform-
tactical medicine, rural medicine, and traditional wilderness med- ing the primary survey, which evaluates and treats inadequacies
icine. These fields have in common environments with con- of airway, breathing, and circulation. The patient’s baseline
strained resources, the necessity for robust prehospital patient mental status is assessed, and any neurologic disabilities are
care, and delayed access to definitive care. These conditions identified.
require integrating evacuation and rescue training, evaluating Airway assessment begins with examination of the mouth and
environmental threats, and understanding and managing re- pharynx for foreign bodies, such as blood clots, tooth or bone
sources during disasters. A more expansive definition of wilder- fragments, and dentures. If the airway is obstructed, perform a
ness medicine takes into consideration the type of injury, the chin lift or jaw thrust, or insert an oropharyngeal airway to hold
setting in which the injury occurred, and how a particular injury the tongue forward. If there is a potential cervical spine fracture,
relates to human interaction with the environment.41 In all of keep the head and neck in a neutral position without hyperex-
these environments and situations, facial injuries occur and tension. Position the patient to maintain the airway and facilitate
require urgent initial management to diminish the morbidity, respiration; in many instances, this will be the prone position.
chance of mortality, and disruption of recreational activities. Raise the head above the heart to decrease bleeding and swell-
The Joint Theater Trauma Registry is responsible for collecting ing, or position the victim seated with the head forward so that
and organizing medical treatment data about patients from blood drains from the mouth or nose. If these measures fail,
combat operations who are treated at U.S. medical facilities. perform endotracheal intubation or cricothyrotomy. Do not leave
Although the head, face, and neck account for only 12% of the the patient unattended, especially when in a supine position.
body surface area, approximately 40% of all injuries currently After the airway is secured and the patient stabilized, perform
sustained during military conflicts are to these areas. This propor- a secondary survey to obtain an abbreviated history of the
tion is higher than reported for previous military conflicts, and present injury or illness and to extract pertinent information, such
most likely results from improved body armor and relative lack as a history of allergies, any medications taken, the medical
of protective devices for the head and face.32,38,50 Soldiers are at history, the last oral intake, and the events leading up to the
high risk for sustaining oral and facial trauma during training and injury. If the patient has sustained significant head or facial
assaults.52 Traumatic facial injuries account for significant rates of trauma, determine if the patient experienced loss of conscious-
morbidity and mortality among the U.S. armed forces, so improved ness or has symptoms of nausea, vomiting, visual disturbances,
functional protection for the vulnerable facial region must be or headache. Assess the patient’s pain, and ask about its charac-
developed. Experience and data gathered during military con- ter, onset, location, radiation, duration, and exacerbating or alle-
flicts have been of tremendous value with regard to further viating factors.
education of medical providers about the emergency care of A systematic approach to examination in oral and maxillofa-
facial trauma. Military research has been instrumental in advanc- cial emergencies allows for efficient collection of relevant infor-
ing trauma care principles and guidelines used to manage trauma mation. Clean the face, mouth, head, and neck of blood and
in both civilian and military populations. debris; this unmasks soft tissue injuries and facilitates diagnosis.
In addition to military-related injuries, sports-related accidents Next, observe the head, neck, and face, and note any asymmetry.
and outdoor recreational activities are responsible for a signifi- Palpate all facial bones, temporomandibular joints, muscles, and
cant number of facial injuries. Skiing, bicycling, soccer, and areas of suspected injury for tenderness, crepitus, swelling,
mountain biking account for more than 60% of sports-related instability, dislocation, fracture, and foreign bodies. Bimanually
accidents. Traumatic injuries from falls, collisions, and self- palpate the lips, cheeks, and floor of the mouth. Observe the
inflicted injuries result in facial bone fractures, dentoalveolar patient slowly opening the mouth, and examine for the range of
trauma, and soft tissue damage. The injury pattern depends on motion and any deviation with opening. Evaluate facial soft tissue
the sporting activity, with high-speed and high-impact sports swelling for hematoma formation, especially in areas associated
causing more fractures and low-speed and low-impact sports with underlying cartilage, such as the ear and nose.
producing more dental injuries.48 Perform an intraoral examination of the lips, cheeks, mouth,
A growing number of people participate in a wide variety of tongue, hard palate, soft palate, and pharynx. Examine facial
outdoor recreational activities that take them far away from lacerations carefully to determine if they penetrate into the oral
definitive medical services.14,46 Wilderness recreation and adven- cavity or contain foreign material. Gently retract the lips with the
ture activities create many situations that place individuals at risk teeth closed to examine the soft tissues and occlusion. Examine
for facial traumatic injuries. The National Outdoor Leadership the dentition for fractures and mobility. Observe the gingiva for
School collects and publishes data about injuries, illnesses, near- bleeding, swelling, trauma, color, firmness, and recession.
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 DIAGNOSIS AND TREATMENT OF
reported injury incidents over a period of 25 years from 1984 to
2009; the majority of these were soft tissue injuries.26 FACIAL INJURIES
TEMPOROMANDIBULAR JOINT DISORDERS
HISTORY AND EXAMINATION OF Temporomandibular Joint Dislocation
Temporomandibular joint (TMJ) dislocation is more commonly
FACIAL INJURIES referred to as mandibular dislocation. Dislocation of the man-
Before evaluating and treating a patient in the wilderness, the dibular condyles causes inability to close the mouth and may
safety of the setting and situation must be evaluated. Evaluating result from external trauma or, more frequently, from mandibular
420
Articular
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.
422
maintain a soft diet for 1 week. Wrap a bandage around the head
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.
423
Septal branch of anterior
ethmoidal artery Anterior ethmoidal artery
Frontal sinus
Ethmoid bone Frontal Posterior ethmoidal artery
Watershed area sinus
(Kiesselbach’s plexus) Sphenopalatine
artery Sphenoid sinus
(septal branch)
Sella turcica
Septal
cartilage Sphenoid
sinus Sphenopalatine artery
Vomer (lateral nasal branch)
Eustachian tube
Septal branch
of superior
labial artery
Site of posterier
Palate Great palatine epistaxis
A artery B
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. If nose pinching does not stop the bleeding, apply a local
Epistaxis is normally classified as anterior or posterior, depending anesthetic and vasoconstrictor to the nasal mucosa over Little’s
on the anatomic location. A particularly rich collection of vessels area. Anesthetic preparations include topical tetracaine 1%,
and common site of anterior nosebleed is Kiesselbach’s plexus cocaine 1% to 4%, lidocaine 5%, ephedrine 5%, and aqueous
on the lower anterior part of the nasal septum (i.e., Little’s area). epinephrine 1 : 1000. Vasoconstrictive nasal sprays include phen-
TRAUMA
Ninety percent of episodes of epistaxis occur in this area. Poste- ylephrine 0.5% (Neo-Synephrine) and oxymetazoline 0.05%
rior bleeding originates primarily from a branch of the spheno- (Afrin). Apply anesthetics and vasoconstrictors by drip or spray,
palatine artery called the posterior nasal artery, which forms part on a cotton pledget, or with a cotton-tipped applicator. Objects
of Woodruff’s plexus19,49 (Figure 20-9). Anterior epistaxis may be placed in the nose should be inserted along the floor of the nose
managed definitively in the wilderness, but posterior epistaxis and have a string attached or include another method for easy
requires immediate evacuation because of continued hemorrhage removal. Avoid pushing material laterally into the turbinates or
PART 4
and the potential for airway compromise.29 superiorly toward the cribriform plate. Leave the vasoconstrictor
in place until it effectively staunches bleeding. This may take
Evaluation from 10 minutes to 24 hours.29
The initial evaluation includes determining if bleeding is unilat- Epistaxis refractory to pressure and topical vasoconstrictors
eral or bilateral and whether it is coming from an anterior or may require chemical cauterization using a silver nitrate (75%
posterior site. A nosebleed usually occurs on one side of the concentration) stick that reacts to the mucosal lining to produce
nasal cavity. However, with profuse bleeding, blood can pass local chemical damage. After applying a topical anesthetic, apply
behind the nasal septum and also appear on the unaffected side. the cautery stick to the bleeding point with firm pressure for 5
Most individuals bleed from an anterior site, which is visualized to 10 seconds. Apply cautery only to one side of the septum,
on intranasal speculum examination; with posterior epistaxis, the and be careful not to perforate the septum by applying too much
bleeding site cannot be seen on intranasal examination. pressure.13
When there is more vigorous anterior nasal bleeding, nose
Treatment pinching, topical chemical vasoconstrictors, and cautery may not
Have the patient sit upright with the head tipped slightly forward. be effective. In such an instance, inject the anterior bleeding site
This maneuver decreases blood flow through the nasopharynx with 0.5 to 1 mL of lidocaine 0.5%, 1%, or 2% that contains
and allows blood to drip passively out of the nose rather than 1 : 100,000 epinephrine. This tamponades bleeding and provides
flowing posteriorly and causing choking, aspiration, and vomiting a vasoconstrictive effect. Alternatively, insert into the nares
of swallowed blood. Have the patient blow the nose to remove directly over the bleeding site a small piece of absorbable or
clots immediately before examination. Warm saline lavage of degradable material that does not require removal. Such materi-
each nostril may accelerate activation of the clotting cascade and als include oxidized regenerated cellulose (Oxycel or Surgicel),
allow for better visualization of the bleeding areas.49 Bleeding purified bovine collagen foam or paste (Gelfoam), microfibrillar
may resume, but there will be improved access and visibility for collagen (Avitene), porcine gelatin (Surgiflo), bovine gelatin-
application of a vasoconstrictor drug or chemical cautery. Ask human thrombin (FloSeal), QuikClot, recombinant factor VIIa,
the patient if he or she has placed anything inside the nose to topical thrombin, hemostatic matrix, nosebleed gauze, and fibrin
stop the bleeding, so that it can be removed before additional glue.19,33,34,39 When bleeding has stopped, instruct the patient not
packing is placed. Examine the nasal cavity with a nasal specu- to blow the nose or probe the area for 48 hours. After the bleed-
lum to determine the site of bleeding. If anterior bleeding is ing episode is over, increasing the humidity, warming inspired
suspected, instruct the patient to pinch the fleshy alae tightly air, and moisturizing the nasal mucosa with topical gels, lotions,
against the cartilaginous septum of the nose between the thumb and ointments help to prevent recurrent bleeding.
and index finger for at least 20 minutes. Applying cold com- Treat persistent epistaxis by packing the anterior cavity or
presses to the nose and instructing the patient to suck on ice can posterior cavity, or both. If bleeding is not controlled by the
improve this.39 Pinching the bony bridge of the nose does not previous methods, insert a lubricated anterior nasal sponge or
provide direct pressure on the bleeding vessels. Alternatively, tampon. Improvise with gynecologic tampons, sponges, and
hands-free techniques that involve using commercial or impro- gauze. Current commercial options include Merocel, Medtronic,
vised (e.g., from taping together two tongue depressors) external Rapid Rhino, ArthroCare, Weimert Epistaxis Packing, and Rhino
pressure devices or clips work well.19 Rocket34 (Figure 20-10).
424
CHAPTER 20 Management of Facial Injuries
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- Detach the sutures from the catheters, and tie them over a bolster
rior packing is necessary. The basic technique involves placing placed underneath the nose. Secure the middle suture outside
a 12-mm (0.5-inch) petrolatum- or antibiotic-impregnated strip of the mouth to allow for removal 48 hours later (Figure 20-13).
gauze into the nasal cavity. An adult patient requires 90 to 120 cm Commercially available preshaped nasal balloons (e.g., Brigh-
(3 to 4 ft) of such gauze to pack the nose adequately and ton, Nasostat, Naso-Blymp, Simpson plug, and EpiStat nasal
tamponade bleeding. Layer the gauze in tiers beginning on the catheter) are manufactured specifically for treatment of posterior
nasal floor and proceeding to the roof of the nose. Leave both epistaxis. They have a postnasal balloon and mobile anterior
ends of the gauze outside of the nose and taped to the face to balloon that are inflated independently. These are contraindi-
prevent inadvertent aspiration. Improvised anterior nasal tam- cated in cases of severe head trauma, basilar skull fracture, or
ponade can be accomplished with a Foley catheter (Figures 20-11 suspected craniofacial fractures that involve cerebrospinal fluid
and 20-12). (CSF) rhinorrhea19,34 (Figure 20-14).
Nasal packing blocks sinus drainage and can predispose to A standard 14F to 16F Foley urinary catheter with a 30-mL
sinusitis. Some studies in the literature contradict the following balloon can function as a posterior pack. Trim the distal catheter
recommendation when in an emergency department setting, but tip to prevent irritation. Insert the lubricated catheter through the
we recommend that any patient who has the nose packed in the nose into the posterior pharynx until it is visualized in the oro-
field be placed on a prophylactic antistaphylococcal antibiotic, pharynx; inflate with a minimum of 3 to 5 mL of air or saline,
such as 875 mg of amoxicillin with 125 mg of clavulanic acid gently pull it forward into the nasopharynx until the balloon
(Augmentin) by mouth three times daily, 500 mg of dicloxacillin engages, and hold it in position by clamping the external end
by mouth four times daily, 150 to 450 mg of clindamycin by with a hemostat or an umbilical clamp. Balloons filled with air
mouth four times daily, or 160 mg of trimethoprim and 800 mg tend to deflate over time, and those filled with water may rupture
of sulfamethoxazole (Bactrim) by mouth twice daily until the and cause aspiration.13,49 Pack the anterior nasal cavity with a
packing is removed after 48 hours.29 nasal sponge or gauze.
If the bleeding site is posterior and cannot be visualized, insert Hot water irrigation has been documented as an alternative
a formal posterior nasal pack, commercially available nasal strategy for posterior epistaxis. Occlude the posterior pharynx
balloon device, or Foley catheter. These methods rely on direct with a balloon catheter, and irrigate the nares with heated water
pressure or blood accumulation within the nasal cavity, which (i.e., 45° C to 50° C [113° F to 122° F]). This reduces blood flow
leads to tamponade. Placing a formal posterior nasal pack is dif- by causing mucosal edema and clears blood clots from the
ficult and involves gently inserting a lubricated soft tube into nose.19,34
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,
FACIAL BONE FRACTURES
chest tubes, or improvised substitutes. Prepare a cylindrical pack Anyone suffering from head or facial injury should be closely
of 10- by 10-cm (4- by 4-inch) gauze, and hold it in shape by examined for facial fractures. Proper management includes a
tying three silk sutures around it and leaving the ends approxi- detailed examination for signs and symptoms of bony fractures,
mately 10 cm (4 inches) long. The pack should be the same stabilizing measures, and a plan for repair. The vast majority of
diameter as a circle made by the patient’s thumb and forefinger facial fractures are not surgical emergencies, and if they are
(i.e., the “OK” sign). Attach the two end sutures to the oral ends attended to within 2 weeks, can be properly treated without
of the catheters. Pull the nasal ends of the catheters carefully long-term sequelae. In the acute setting, the level of concern
back out of the nose until the pack is firmly positioned against should be higher for facial fractures that occur with visual loss,
the posterior aspect of the nasal cavity above the soft palate. 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
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
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 piece of a SAM splint large enough to fit the nasal contours. Rest
may have premature closure of sutures and uneven growth; the splint on the adjacent part of the face without placing pres-
therefore, a consultant should evaluate the injury, preferably sure on the nasal bridge. Secure the splint with strips of adhesive
within 4 days of its occurrence10,30 (Figure 20-16). tape. Do not pack the nose unless it is necessary to control
Digital manipulation of a displaced nasal bone fracture can in epistaxis or drain a septal hematoma. No antibiotics are needed
some instances quickly reduce the fracture with minimal effort. for a nasal fracture unless packing is placed. If packing is
It is important to note that due to swelling at the time of injury, required in a wilderness setting to control epistaxis or after drain-
deformity may result even with proper reduction.31,37 With any age of a septal hematoma, administer 500 mg of penicillin V
nasal fracture, make a protective splint by cutting a triangular potassium or amoxicillin by mouth four times a day for 5 days.10
427
A
B
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- as a deviation, bulging, or widening of the nasal septum. Symp-
cosal blood vessels. If the mucosa remains intact, blood will toms include nasal obstruction, pain, rhinorrhea, and fever
accumulate between the septal cartilage and mucoperichondrium (Figure 20-17).
and cause formation of a hematoma, either immediately or within Inspect the nasal septum for asymmetry, swelling, pain, and
the first 24 to 72 hours after injury. Septal hematoma appears a fluctuant area. The mucosa of the fluctuant area will usually
have a bluish or reddish hue. The bulging area of the septum,
TRAUMA
Hematoma
428
detachment, vitreous hemorrhage, lens dislocation, and hyphema,
429
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
Le Fort I Le Fort II
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
Le Fort III midline to the fractured and painful side on mouth opening.
Bilateral condylar fractures often result in an anterior open bite
TRAUMA
passes laterally and inferiorly through the lacrimal bones, inferior indicate fractures of the temporal bone with condyle retrodis-
orbital rims, and orbital floors near the zygomaticomaxillary placement. To evaluate occlusion, have the patient bite down.
suture. It continues posteriorly along the lateral walls of the Any deviation of the bite or change in level of the occlusal plane,
maxilla, and through the pterygoid plates into the pterygomaxil- especially in the mandible, should raise suspicion for a fracture.
lary fossa. The Le Fort III fracture pattern is frank craniofacial There will sometimes be a gingival tear with bleeding and ecchy-
disjunction, occurring through the frontomaxillary, zygomatico- mosis at the site of discontinuity. Sublingual hematoma is a
frontal, and orbital floors; nasofrontal sutures; cribriform plate of common sign of mandibular fracture. In edentulous areas, there
the nose; and ethmoid and sphenoid sinuses. The fracture forces will also be a discrepancy in the level of the bone, sometimes
are so great that there is a complete separation of the facial bones accompanied by a disruption in the mucosa18 (Figure 20-22).
from the cranial base47 (Figure 20-19). Definitive repair of a simple mandibular fracture is not usually
Examine a patient for a Le Fort I maxillary fracture by grasping a surgical emergency. However, it is wise to note that airway
the anterior maxillary segment by the central incisors between distress may occur with bilateral mandibular fractures or complex/
the thumb and forefinger and gently rocking the maxilla antero- comminuted mandibular fractures in which significant edema has
posteriorly. If a Le Fort I fracture is present, the entire maxilla arisen in the floor of the mouth. Delay in repair does not increase
and palate will move in relation to the upper midface. With a the risk of infectious complications, but persons who are treated
unilateral fracture, the two halves of the maxilla may move after 3 days have a higher incidence of operative technical com-
independently. plications, such as infected hardware, nonunion, or malunion.
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
Region of the
gently while grasping the nasal bridge between the thumb and
coronoid process
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. Region of
Manipulation of a Le Fort III craniofacial disjunction fracture the condylar
process
results in separation and movement of the entire midface in rela- Region of
tion to the cranium. This injury is often accompanied by intra- Region of the ramus
cranial trauma. There is usually subconjunctival hemorrhage, the alveolar
ecchymosis, and bilateral periorbital edema that causes eyelid process
closure. Fractures that involve dural tears and meningeal lacera- Region of
tion cause CSF rhinorrhea. When this is suspected, the nose Region of the Region of the angle
should not be packed, and prophylactic antibiotics (e.g., 500 mg symphysis the body
azithromycin by mouth once a day) should be initiated.
Rarely, a posteriorly displaced Le Fort fracture can cause FIGURE 20-20 Anatomic regions of the mandible. (Modified from
airway compromise. Only in this case should the maxilla be Dingman RO, Natvig P: Surgery of facial fractures, Philadelphia, 1964,
disimpacted in the field by using forward traction. Saunders.)
430
Temporarily immobilize more posteriorly located fractures
B
FIGURE 20-22 Mandibular fracture. A, Note the malocclusion before
reduction. B, Normal.
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 FIGURE 20-24 Lip laceration involving the vermilion border.
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 exits the infraorbital foramen 1 cm (0.4 inch) below the infraor-
stabilize wound margins after suture removal. bital ridge. Place the third finger of the nondominant hand on
The face has an excellent vascular supply, which allows for the infraorbital foramen, and use the second finger and thumb
wound closure with minimal risk of infection if treatment can be to lift the upper lip. Insert the needle over the canine tooth at
accomplished within 6 hours of the injury. Topical antibiotics are the level of the gingival buccal sulcus. Aspirate while advancing
useful, but prophylactic oral antibiotics should not be initiated, toward the foramen, and inject 2 mL of anesthetic (Figures 20-25
because these wounds rarely become infected. More complicated and 20-26).
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
TONGUE LACERATIONS
TRAUMA
devascularization, require prophylactic oral antibiotic treatment Tongue lacerations may be difficult to suture because of poor
against normal bacterial flora associated with the affected site visualization. Simple, small, linear lacerations less than 1 cm (0.4
and consideration for the mechanism of trauma. Inspect all facial inch) long and located centrally usually heal well without sutur-
wounds frequently for evidence of vascular compromise or infec- ing. All lacerations that are deep or gaping or that bisect the
tion, or both. Significant infections require bandage removal, tongue should be closed with absorbable 4-0 or 5-0 suture.5 Suf-
possible surgical drainage, and intravenous antibiotics. ficient local anesthesia can be provided by a combination of
PART 4
Any injury that involves the eyelids, auricular helical rims, topical lidocaine and a nerve block. Apply local anesthesia by
nasal alar rims, or vermilion border has potential significant cos- applying gauze soaked with lidocaine 4% to the tongue for 5
metic and functional implications and must be evaluated and minutes, and then locally infiltrate the wound with lidocaine 1%
managed with extreme caution. 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
INJURIES TO THE LIPS of the anterior border of the mandibular ramus with your thumb.
Lips are mobile muscular folds that have three distinct regions: Using a tongue blade, push away the buccal surface of the
oral mucosa, skin, and a noncornified layer of stratified epithe- cheek to expose the target area. Position the syringe barrel over
lium called the vermilion. The vermilion border is the junction the opposite premolar and parallel to the occlusive surface of
between the skin and the dry vermilion. Realigning the border the lower teeth. Insert the needle into the oral mucosa medial
and restoring the natural architecture of the philtrum are crucial to the ridge, 1 cm (0.4 inch) above the occlusive surface of the
to successful cosmetic repair. mandibular third molar. Aspirate while slowly advancing the
During repair of a through-and-through lip laceration, first needle 2 cm (0.8 inch), and inject 2 mL of anesthetic to block
close the muscular layer with 5-0 absorbable sutures, and then the inferior alveolar nerve. The lingual nerve runs with the infe-
realign and stabilize the vermilion border with a vertical mattress rior alveolar nerve at the mandibular foramen. It supplies the
nonabsorbable suture. Next, close the inner mucosal layer with anterior two-thirds of the tongue, floor of the mouth, and gums.
4-0 absorbable sutures, the wet and dry vermilion with 5-0 Block the lingual nerve by withdrawing the needle 1 cm (0.4
absorbable sutures, and the external skin with 6-0 nonabsorbable inch) while aspirating, and then injecting another 1 mL of anes-
sutures. Through-and-through lacerations of the lower lip that do thetic. Prescribe a liquid or soft diet after any intraoral repair.
not involve the vermilion border occur when lower incisors Advise the patient to gently swish and spit four times a day
impale tissue during facial blunt trauma. First, cleanse and close and after eating with warm saline, antiseptic mouthwash,
the mucosal layer from an intraoral approach. Irrigate to remove chlorhexidine gluconate 0.12%, or half-strength hydrogen perox-
foreign material and oral bacteria, and then rescrub the extraoral ide (Figure 20-27).
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
INJURIES TO THE EYELID
A mental nerve block anesthetizes the chin and lower lip; an It is essential that providers recognize eyelid lacerations that
infraorbital nerve block anesthetizes the cheek, upper lip, lower require referral to an ophthalmologist. Simple upper and lower
eyelid, and lateral aspect of the nose. These blocks provide lid lacerations may be managed without consultation, but
adequate anesthesia without tissue distortion and are easily per- complex lacerations that involve tissue avulsion or the tarsal
formed. The mental nerve exits the mandible through the mental plate, lid margins, orbital septum, levator palpebrae superioris,
foramen in the midpupillary line 1 cm (0.4 inch) inferior to the or lacrimal drainage system may require semiurgent ophthalmo-
apex of the second bicuspid. While retracting the lower lip with logic referral for definitive care. The presence of a penetrating
the nondominant hand, insert the needle 5 mm (2 inches) inferior globe injury must be identified.24 Upper eyelid lacerations with
to the tooth, and inject 2 mL of anesthetic. The infraorbital nerve exposure of orbital fat and ptosis in the presence of a horizontal
432
surface with a nonabsorbable monofilament suture. Repair other
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
to prevent notching (Figure 20-32). Precise realignment of the
FIGURE 20-30 Supraorbital, supratrochlear, and infratrochlear nerve INJURIES TO THE CHEEK
blocks. This is the site for local injection of the supratrochlear and
infratrochlear nerves, as well as for the lateral and medial branches of Contusions and lacerations of the cheek or parotid region may
the supraorbital nerve. (From Roberts JR, Hedges JR: Clinical proce- involve other structures, including the external auditory meatus,
dures in emergency medicine, 5th ed, St Louis, 2009, Saunders.) 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.
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- mineral oil combined with lidocaine 2% or 4%, and alcohol. If
ration may cause tinnitus, vertigo, and hearing loss. attempts are made to remove a moving insect, the insect or
Before examining the ear, it is important to ascertain if device may cause ear damage.
attempts have been made to remove the foreign body by the With appropriate tools, foreign body removal may be
patient, because this may have caused ear canal injury, tympanic attempted in the wilderness. Instill a topical anesthetic, such as
membrane perforation, or worsening foreign body impaction. lidocaine 1% to 2%, into the canal. Unfortunately, topical anes-
Ear canal irrigation may cause enlargement of some foreign thetics are poorly absorbed through the impermeable keratinized
bodies. epithelial surface of the external auditory canal. Auralgan, a
Within the external auditory ear canal, there are two areas of topical combination of benzocaine and other ingredients, does
anatomic narrowing where foreign objects usually become stuck. not provide adequate anesthesia for painful procedures. Local
These include a point of bony narrowing called the isthmus at anesthetic injection within the canal is painful and difficult to
the junction between bone and cartilage, and a point near the perform, and frequently does not provide adequate anesthesia
inner end of the cartilaginous portion of the canal lateral to the of the inner ear and tympanic membrane.
tympanic membrane.37 Examine the ear with adequate lighting, A common technique to provide local anesthesia of the canal
an otoscope, and a large-size speculum to visualize the ear canal requires insertion of a large speculum immediately inside the
and allow injection of a local anesthetic. Grasp the superior pinna auditory meatus to facilitate use of a 25- to 27-gauge needle that
and retract it in a posterosuperior direction to straighten the is 3 to 5 cm (1.2 to 2 inches) in length in order to inject 0.25 to
tortuous canal and to achieve a more complete view of the 0.5 mL of lidocaine 1% or a 1 : 10 mixture of sodium bicarbonate
external auditory canal. 8.4% with lidocaine into the subcutaneous tissue, stopping after
Anesthetize or immobilize an insect within the ear canal to a small bulge in the skin is raised. Inject all four quadrants, as
decrease patient distress and facilitate removal. Immobilizing well as deeper tissues along the anterior wall and at the posterior
agents include lidocaine 2% gel, lidocaine 10% spray or liquid, wall of the bone–cartilage junction (Figure 20-38).
438
CHAPTER 20 Management of Facial Injuries
1
C A
Lacrimal
apparatus
2
3 B
5 4
439
BOX 20-1 Wilderness Medical Kit for Facial Trauma
440.e1
CHAPTER 21
Wound Management
RAMIN JAMSHIDI
440
changed once daily or more frequently as needed for soilage or
441
A B C
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 irrigant, this has not proved to be more efficacious. Whatever the
have passed since injury, closure is generally safe. If conditions method available to generate potable water (e.g., iodine tablets,
are fitting and the provider has sufficient experience, this author mechanical filter, irradiation, boiling), it is sufficient to generate
supports closure up to 24 hours after injury. An intermediate irrigation fluid for wound care. Hydrogen peroxide is injurious
option is partial wound closure, in which the “corners” and/or to deep tissues and should not be used as an irrigant.
deeper layers of tissue are reapproximated while a portion of the The greatest impact on wound cleanliness is gained from the
wound is left open to heal by secondary intention. This helps volume of irrigant and simple mechanical debridement. Debride-
TRAUMA
minimize wound morbidity and discomfort while allowing drain- ment is achieved by removal of obvious foreign material (as with
age if infection were to develop. 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
TREATMENT “gush,” because dilution of wound contaminants is far superior
Personal protective equipment should be donned before inter- with small serial volumes. Although the matter has not been
PART 4
rogating, preparing, possibly closing, and dressing a wound. Eye systematically researched, a guideline that is often used is a
shields and gloves are considered mandatory equipment. Eye minimum of 100 mL per centimeter of wound length. Optimal
shields are particularly important in preventing exposure of stream pressure has been determined to be 5 to 10 psi, but in a
mucous membranes to bodily fluids. Gloves are essential; they remote setting, use of pressure gauges or regulators is unneces-
should be made of a material other than latex and should contain sarily cumbersome; it is sufficient to realize that excessive pres-
no talcum or other lubricant. Talcum, calcium carbonate, and sures are not required.54,60 A large (20- to 60-mL) syringe attached
cornstarch are common glove lubricants, and all have been to a 19- or 20-gauge needle or catheter is an effective instrument
shown to cause wound granulomas, foreign body reactions, for this purpose, and will approximate that pressure. Alterna-
adhesions, and chronic sinuses. Sterile gloves are less cumber- tively, holes can be punched into the cap of a squeezable water
some to work with but are not required, because they do not bottle to generate a similar effect. A splash shield at the tip of
reduce the incidence of infection in an austere setting.47 Use of the instrument decreases the risk of personal exposure. If not
a mask has also not been demonstrated to reduce rates of acute available as a specific commercial product for this purpose, one
wound infection but certainly provides a protective barrier for can easily be fashioned from a paper or plastic plate, or the base
the care provider. Hair coverings are not necessary, because of a disposable water bottle or drinking cup.
studies have failed to demonstrate reduction in wound infection Preparing for the actual wound closure, the skin edges may
rates. 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
CLEANSING TECHNIQUES because of potential toxicity. If concentrated ethyl alcohol (i.e.,
Cleansing involves removing devitalized tissue, clearing debris, liquor) is available, it may be effective in reducing wound con-
and copiously irrigating the area.25 This may involve vigorous tamination, but this has not been systematically evaluated. These
manipulation of painful and sensitive tissues, so if oral analgesics agents should be used to cleanse the skin surrounding the
are available, they should be used. Constricting jewelry and wound, using gauze soaked with the liquid to paint an overlap-
equipment should be removed from the affected area (e.g., rings, ping spiral from the wound outward to a distance of approxi-
piercings). Ideally, hair around the wound is trimmed because mately 5 cm. The cleansed skin must be allowed to dry to
the roots harbor bacteria. Hair should be trimmed to a few mil- achieve the full effect; this takes 3 to 5 minutes at 20° C (68° F).
limeters in height because shaving at the surface increases wound Honey has been used for thousands of years as an antimicro-
infection rates by causing superficial skin trauma.3 Eyebrow hair bial dressing, but only in recent years has it been scientifically
is an important exception, because trimming or shaving can result evaluated for effects on wound healing. The antibacterial effects
in permanent abnormal hair growth. If hair trimming is not pos- are believed to be due to acidity, osmolarity, and chemical factors
sible, an antiseptic ointment can be used to paste the hair down such as hydrogen peroxide and methylglyoxal. The latter is
away from the wound. present only in manuka honey (a generally edible honey), which
Water should be used to clean the wound. There is no dem- has been formulated into commercial wound care products.
onstrated benefit to use of saline solutions, and there is no Despite regulation by the Food and Drug Administration (FDA),
absolute need for the irrigant to be sterile.8,19,43 Although some purity and potency vary greatly among honey products, and
persons mention use of dilute (1%) povidone-iodine as an clinical research into their efficacy is ongoing.41 Some of the
442
commercial dressings available are lightweight, weather-resistant, agents have found widespread use in the military and are becom-
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
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
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*
Low cost
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 bility and versatility; characteristics of the most versatile sutures
suturing delicate skin, as in elderly patients or those receiving for acute traumatic wounds are listed in Table 21-5.16,20,51 When
chronic steroid therapy. Preparing the skin with adhesive and suturing deep tissue, absorbable materials of immediate durabil-
tape adds strength to the closure and decreases the likelihood ity, such as polyglactin (e.g., Vicryl) or copolymeric glycolic, and
of the suture tearing through the skin. This is performed as lactic acids (e.g., Polysorb) should be used. At 2 weeks, these
described above except that the entire tape length is applied to materials retain approximately three-quarters of their original
the skin without creation of a nonsticky edge. Full-thickness strength.13,18 Nondyed varieties are preferred within 5 mm (0.2
sutures are then passed through skin and tape as though they inch) of the skin surface to avoid wound tattooing. For mucosal
were one tissue layer. lesions (such as within the mouth), rapid-absorbing gut suture is
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
A B C
FIGURE 21-8 A, Interrupted simple sutures. B, Interrupted vertical mattress sutures. C, Interrupted hori-
zontal mattress sutures.
447
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.
strength reaches 70% of baseline.21,55 Leaving skin closure mate- chronic corticosteroid use, or other types of immunocompromise.
rial in place longer keeps tension off the wound but increases Wound factors include delay to cleansing and repair, extensive
the likelihood of visible scarring from the suture or staple itself; devitalized tissue, heavy contamination or retained debris, bites,
therefore, the timing of removal varies based on the durability oral lacerations, foot wounds, open fractures, or injury to poorly
and visibility of the affected area. On the face or neck, sutures perfused tissue (bone, joint, tendon).4,34,42
are removed at 3 to 5 days; on the fingers or hand, at 5 to 7 Tetanus is caused by Clostridium tetani, an organism found
PART 4
days; on the scalp, leg, chest, or abdomen, at 7 to 10 days; on 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
History of Immunization
(Doses of Adsorbed
Tetanus Toxoid Clean and
Previously Received) Minor Wound All Other Wounds*
448
antibiotic. The chosen antibiotic (first-generation cephalosporin
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 FIGURE 21-11 Minor puncture wound that has developed a secondary
infection is present. The treatment for cellulitis is a systemic abscess and associated cellulitis. (Courtesy Ramin Jamshidi, MD.)
449
TABLE 21-8 Wound Care First-Aid Kit
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
thickness burns that are circumferential or involve more than 5%
of the body surface area. Many wilderness-acquired wounds that Complete references used in this text are available
do not necessitate evacuation still require formal medical evalu- online at expertconsult.inkling.com.
ation upon the return to civilization.44 These include any persis-
REFERENCES 34. Lammers RL, Hudson DL, Seaman LE. Prediction of traumatic wound
450.e1
63. Waterbook AL, Germann CA, Southall JC. Is epinephrine harmful 65. Zilinsky I, Bar-Meir E, Zaslansky R, et al. Ten commandments for
when used with anesthetics for digital nerve blocks? Ann Emerg Med minimal pain during administration of local anesthetics. J Drugs Der-
2007;50:472. matol 2005;4:212.
64. Wheeler WM. Ants: Their structure and behavior. New York: Colum- 66. Zuber TJ. The mattress sutures: Vertical, horizontal, and corner stitch.
bia University Press; 1960. Am Fam Physician 2002;66:2231.
TRAUMA
PART 4
450.e2
CHAPTER 22
Wilderness Orthopedics
JULIE A. SWITZER, RALPH S. BOVARD, AND ROBERT H. QUINN
The textbook discussion of orthopedic trauma in wilderness military engagement, and forces of nature. Recent disasters,
medicine has traditionally focused on discrete musculoskeletal such as the Great Indian Ocean tsunami of 2004, Hurricane
injury to individuals or small groups in the mountain, sea, or Katrina in August 2005, and the Haiti and Chile earthquakes of
desert setting. The scope of wilderness medicine today has 2010, serve as powerful examples of situations in which ortho-
widened significantly to include injuries caused by terrorism, pedic injuries were myriad and provision of care was limited in
450
the musculoskeletal system should be undertaken in a systematic
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
FIGURE 22-1 Improvised traction following the 2010 earthquake in or uncooperative person. In the conscious person, the results of
Haiti. (Courtesy Sam Slishman.) 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
significant part by the remoteness of setting or inaccessibility of group against resistance (Figure 22-2). If possible, once the vic-
resources. tim’s condition has been stabilized, nerve function to the distal
The wilderness practitioner needs to approach trauma outside extremities is documented. Initial findings should be compared
the normal clinic or hospital setting with a sense of anticipation periodically, with repeat examinations during transport. Any
and improvisation. One needs to be prepared for a scenario change and, in particular, any deterioration in condition should
of chaos, inadequate medical supplies or support, sepsis, and be noted.
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
SKELETAL FUNCTION
with segmental loss, and severed limbs of natural or terroristic The skeletal anatomy should be carefully inspected and palpated.
disasters. Issues of triage and prioritization become paramount. Angular deformity suggests a fracture; palpable crepitus confirms
Successful organization of resources and mobilization of person- the diagnosis. The health care provider in the field should
nel often determine the outcome of the operation. Improvisation perform appropriate splinting after placing the limb in anatomic
in splinting to stabilize or immobilize shattered limbs can mini- alignment using gentle axial traction. After noting the degree and
mize neurovascular compromise and reduce morbidity and mor- orientation of the limb’s position when the victim is found, there
tality (Figure 22-1). 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
SCOPE OF THE PROBLEM pain substantially outweighs the common in-hospital routine of
Musculoskeletal injuries account for 70% to 80% of injuries that imaging before manipulation. Distinguishing intraarticular or very
occur in a wilderness setting.11,20 Presumably as a result of the proximal or distal fractures must wait for the definitive care facil-
use of flak jackets and core protective gear that shield axial and ity, where imaging studies can be done. Similarly, distinguishing
central anatomic structures, bone and soft tissue injuries have a wrist or ankle ligamentous injury from a fracture is not required
become more common, accounting for 70% of injuries in the for initial treatment.
Iraq and Afghanistan wars.17 In the initial management of a mus- Diagnosis is usually made by palpation of the limb and frac-
culoskeletal injury that occurs in a wilderness or austere setting, ture location. If a tuning fork is available, it can be used in the
the following must be considered: cause and time of injury, following manner: the tuning fork is struck and placed on one
direction of the causative force in relation to the individual or end of a limb in question. If the vibration cannot be auscultated
limb, and environment where the accident occurred. These at the other end of the bone, or if the vibration is significantly
factors may indicate the severity of the injury and help deter- diminished when compared with the other limb, a discontinuity
mine the examination and treatment priorities that can affect the (fracture) may exist. Ultrasound can also be employed if doubt
outcome. remains regarding the existence and location of a fracture.
Stabilization of a victim’s cardiovascular and pulmonary status Palpation of long bones begins distally and proceeds across
is critical. Cardiovascular stabilization includes control of massive all joints. A splint should be applied if there is palpable crepitus,
hemorrhage. Once this has been accomplished, examination of 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
In general, one can trust that an alert and cooperative patient port. If the victim can cooperate, each joint is taken through an
will not consciously participate in maneuvers that will cause active range of motion to quickly locate any injury. When this is
further harm. Unless the patient is being stoic or purposefully not possible, passive motion of each joint is evaluated after pal-
overriding pain, the patient will not attempt to stand or ambulate pation in order to detect swelling and/or crepitus.
with a potentially unstable spine, or bear weight on a fracture at Any dislocation should be promptly reduced after complet-
risk for displacement or instability. A patient who can comfort- ing the neurovascular examination. This generally considerably
ably perform a range of motion or bear weight on an injured relieves the victim’s discomfort. Once relocation has occurred,
extremity, either before or after immobilization, is generally stability is evaluated by careful controlled motion. Joints with
acting safely. The rescuer needs to be particularly cautious with associated fractures or interposed soft tissues may still be unsta-
someone who is attempting to “play through the pain.” 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,
JOINT FUNCTION including orientation of the pull, amount of force involved,
Each joint has a normal range of and limits to motion to ensure amount of sedation, and residual instability of the joint, should
stability. Making the diagnosis of a joint injury in the field allows be provided to the definitive care physician (see Reduction and
appropriate splinting and prevents further damage during trans- Relocation Maneuvers, p. 458).
452
POTENTIALLY LIFE-THREATENING
453
Wilderness Medical Society Recommendations for
Spine Clearance/Immobilization in the Austere Environment
Isolated
penetrating trauma Yes No
Significant
Yes
Immobilize spine pain or
tenderness ( 7/10)
No
No
A B
FIGURE 22-7 Calcaneus fracture.
454
CHAPTER 22 Wilderness Orthopedics
Acetabulum
Femoral head
FIGURE 22-11 Right hip dislocation with acetabular and femoral head
FIGURE 22-9 Pelvic injury after being thrown from a horse. Pubic fractures.
symphysis widening of greater than 2.5 cm (1 inch) is generally con-
sidered to be unstable. to determine whether there is injury to the posterior pelvis. Pos-
terior pelvic fractures are identified by instability of the pelvis
should not cause significant patient discomfort or respiratory associated with posterior pain, swelling, and ecchymosis. This
compromise or impede access to the airway or sites of hemor- victim should be immediately evacuated on a backboard, taking
rhage. Cervical spine immobilization that involves attainment of care to minimize leg and torso motion.
standard neutral alignment is contraindicated (and generally Hemodynamic instability may occur with pelvic fractures,
unnecessary) in the presence of certain circumstances of pene- particularly if the injury is the result of translational or shear
trating trauma, as well as in ankylosing spondylitis. In these situ- forces or if posterior pelvic structures are primarily involved.
ations, if the intent is to prevent further motion of the head and Bleeding associated with a pelvic injury is usually from fractured
neck, it is reasonable to achieve immobilization of the victim in cancellous bone, retroperitoneal lumbar venous plexus injury, or,
the position in which she or he is found. 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
PELVIC INJURIES a suspected unstable pelvic fracture may provide stability and
Pelvic fractures generally occur with a fall from a significant accomplish adequate tamponade of bleeding from the fracture25
height, high-velocity ski accident, or vehicle crash. The Young (Figure 22-12). Other similarly intended devices (e.g., T-Pod
and Burgess classification of pelvic fractures is based on the Responder Pelvic Stabilization Device, VBM Pelvic Sling) are
mechanism of injury. Pelvic fractures are categorized as antero- available or may be improvised. The applied sling belt (pelvic
posterior compression, lateral compression, or vertical shear inju- binder) or improvised contrivance should be left in place until
ries.5 These fracture patterns have been shown to correlate with definitive care is available (Figure 22-13). Degloving injuries can
blood loss, associated injuries, multisystem morbidities, and mor- also be seen in high-energy pelvic injuries (Figure 22-14).
tality.5,7,35 Anteroposterior compression injuries can result in rota- In addition to these high-energy injuries, simple nondisplaced
tional instability if there is more than 2.5 cm (1 inch) of pubic inferior or superior ramus fractures and avulsion fractures can
symphysis separation (Figure 22-9). Furthermore, if the posterior occur. On clinical examination, these pelvic fractures are gener-
pelvic ring is disrupted, there can be both rotational and vertical ally appreciated as areas of tenderness without instability. Lateral
instability. These injuries, which may include acetabular frac- compression injuries are usually stable, with impaction of the
tures, are often accompanied by hemorrhagic, neurologic, uro- posterior structures.
logic, gynecologic, and gastrointestinal injuries (Figures 22-10
and 22-11).
The posterior pelvic ring accounts for approximately 60% of GENERAL CONSIDERATIONS IN EXTREMITY
pelvic stability. With a suspected pelvic fracture, it is important 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 22-10 Highly unstable pelvic ring injury with pubic rami frac-
tures and displaced iliac wing fracture. This patient also had a severe
bladder injury. FIGURE 22-12 SAM Sling.
455
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.
roll of clothes or a water bottle can be placed as high as the applied to the already injured soft tissues.
victim’s midface on both sides of the head and secured into Upper extremity splints may be made from plaster or fiber-
position to prevent rotational movement. Tape applied from the glass, which can be applied over a soft cotton roll. Lightweight
supporting stretcher across the objects and the victim’s forehead prefabricated fiberglass splints are easy to use and effective for
adds stability. A child with a suspected spine injury should be initial management of injuries (Figure 22-17). These splints are
transported on a backboard, with the child’s body slightly ele- prepadded and can be applied with either cold or warm water,
vated relative to the head (Figure 22-15). Any victim with a or even directly out of the package if water is not readily avail-
suspected major pelvic injury is transported in a similar fashion, able. The warmer the water, the faster the fiberglass sets and the
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
456
CHAPTER 22 Wilderness Orthopedics
FIGURE 22-17 Water-activated FareTec splint for distal radial fracture,
with wrist and hand in position of function.
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
1 2
3 4
and immobilization. The ankle is held in neutral position and the • Traction: in-line or longitudinal force application
splint applied firmly. For transport, the lower extremity is posi- • Fracture fragment disengagement; included in this step is
tioned with the hip and knee extended and the ankle in neutral recreation of the forces that created the fracture
position. Victims with unstable lower extremity fractures or dis- • Reapposition of fracture ends
PART 4
locations are transported in the recumbent position with the • Counteraction of forces that led to deformity
afflicted limb elevated. Steady traction and patience are the mainstays of fracture and
For hip or femoral fracture or dislocation, properly applied dislocation reduction and relocation maneuvers.4
traction can decrease blood loss from hemorrhage into the frac- For distal radial fracture, the usual dorsiflexion deformity is
ture site and substantially decrease pain. If proper traction cannot reproduced and a flexion force is applied through the fracture.
be applied, splinting (particularly with a vacuum mattress) can Steady traction can assist with reduction (Figures 22-26 to 22-28).
provide reasonable stability and pain control. Multiple portable For ankle fracture, traction is applied. Most fractures are
traction devices are commercially available (Figures 22-23 and caused by an eversion and external rotational force. Reduction
22-24). The ischium and/or pubis are proximal structures against is undertaken and a splint applied so that the ankle can be
which the splint is set. The ankle is usually the structure through splinted in inversion and internal rotation, known as the Quigley
which traction is applied (Figure 22-25). Lightweight splints that maneuver. Care must be taken so that excessive force is not
may be of use in the wilderness setting include those known exerted on a limb that has already sustained significant vascular
either by their manufacturer or developer, such as Donway, or nerve injury (Figure 22-29).
Thomas, Kendrick, Slishman, Reel, FareTec, Sager, CT-6, and
Hare splints (see Chapter 23). It behooves a backcountry health Traction Pins
care provider to be thoroughly familiar with any splinting device Skeletal traction is applied in the setting of a fractured pelvis
being carried. If commercial splints are unavailable and effective (including the acetabulum) or femur. This mode of stabiliza-
improvised splinting is not possible, the injured leg can be tion can be used for temporary or more definitive treatment.
strapped to the noninjured leg, with a tree limb or walking stick This technique can be used in a natural disaster setting (see
placed between the legs. If possible, the victim is transported on Figure 22-1).
a backboard or similar device that limits motion of the pelvis and A distal femoral traction pin is inserted from medial to lateral.
lower extremity. The knee is flexed during insertion to facilitate access to the
medial aspect of the distal femur and to allow for flexion of the
Reduction and Relocation Maneuvers knee once the pin has been placed; if the pin is placed with
Even in the wilderness, the four principles of fracture reduction the knee in extension, the iliotibial band might be tethered and
should be followed: 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
FIGURE 22-24 Lower extremity splint. tibial crest. These pins should not be placed in children, because
458
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
proximity of the tibial tubercle apophysis puts this important adult, this likely will be between 6.8 and 13.6 kg (15 and
structure at risk during insertion of the pin (Figure 22-30). 30 pounds).
A calcaneal pin can also be used to apply lower extremity
traction. This type of traction pin may be of particular benefit in External Fixators
the setting of ipsilateral femoral and tibial injuries. It is usually External fixator application for fracture may be of benefit in the
placed medial to lateral, with care being taken to avoid the pos- setting of a natural disaster. For example, in the aftermath of the
terior tibial neurovascular bundle. The pin is driven through the earthquakes in Haiti in 2010, external fixator application for
calcaneus and exits laterally (Figure 22-31). femoral or tibial fracture was one of the most commonly employed
If possible, balanced traction should be maintained. This fracture treatment procedures. External fixators applied in the
helps to counteract deforming forces and allows relatively com- field or in the setting of limited resources are usually applied in
fortable movement in bed. There are no hard-and-fast rules for a manner consistent with the use of the fixator as a neutralization
the amount of weight to apply. If balanced traction is employed, device. The external fixator maintains the relative position of
the rule of thumb is for enough traction to be applied that the bone fragments, resists external deforming forces, and prevents
ipsilateral buttock is elevated slightly off the bed. When radiog- significant soft tissue injury (by the bone ends).
raphy is available, traction is applied until the fracture fragments Principles of external fixator application are use of sterile
are well aligned and nearly out to length. For an average-sized 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
A B
FIGURE 22-31 Calcaneal traction pin placement in the setting of sub-
FIGURE 22-28 Reduced fracture-dislocation. talar dislocation.
460
CHAPTER 22 Wilderness Orthopedics
Deep
peroneal Rectus femoris
nerve muscle
Anterior
tibial artery
and vein
Vastus
Superficial lateralis
peroneal muscle
nerve Sciatic 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 Classification of Open Fractures of the Extremities
(Figure 22-32). Familiarity with the Gustilo-Anderson open fracture classification
A few simple techniques may contribute to the longevity of system is useful. This assigns musculoskeletal trauma to one of
the fixator. The position and length of stab wound incisions in three major categories (types I to III) depending on the mecha-
the skin should not result in tension between the threaded pin nism of injury, extent of soft tissue damage, and degree of skel-
and skin interface. To prevent osteonecrosis, holes in the bone etal involvement.
for the threaded pins should be predrilled. Threaded pins should Type I Fracture
be bicortical; however, to reduce the risk of nerve or vessel • Wound is less than 1 cm (0.4 inch), with minimal soft
injury, care should be taken not to advance the pins more than tissue injury.
a few millimeters beyond the far cortex. • Wound bed is clean.
• Fracture is usually a simple transverse, short oblique frac-
ture, with minimal comminution.
OPEN FRACTURES OF THE EXTREMITIES Type II Fracture
Recognizing an open fracture is imperative; without prompt • Wound is greater than 1 cm (0.4 inch), with moderate soft
surgical treatment, the incidence of osteomyelitis in this setting tissue injury.
is high.13 With an open fracture, the fractured bone communi- • Wound bed may be moderately contaminated.
cates with a break in the skin. With subcutaneous bones (e.g., • Fracture is usually a simple transverse, short oblique frac-
tibia), open fractures are easily identified, but with other bones ture, with minimal to moderate comminution.
that have more surrounding soft tissue (e.g., humerus, femur, Type III Fracture. Type III fractures involve extensive
pelvis), recognition is more difficult because the fractured bone damage to soft tissues, including muscle, skin, and neurovascular
end usually retracts after it punctures the skin and is then covered structures. They often result from a high-velocity injury or have
by soft tissue. A laceration near a fracture may be an indication a severe crushing component. The following special patterns are
of an open fracture. Most open fractures persistently ooze blood classified as type III fractures:
or fat globules from the laceration (Figure 22-33). Clothes should • Open segmental fracture, irrespective of the size of the
be removed to allow the skin to be examined. 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.
FIGURE 22-33 Type IIIB open tibia-fibula fracture that occurred as a The Mangled Extremity Severity Score can provide prognostic
result of a fall while the individual was holding a chainsaw. considerations for limb salvage versus amputation.15
461
BOX 22-1 Antibiotic Options
Natural disasters and warfare can also result in a mangled or
crushed limb. Splinting, monitoring for compartment syndrome,
Intravenous Solutions and expeditious evacuation are imperative.
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 TOURNIQUETS FOR EXTREMITY INJURIES
Intramuscular Injections Although use of tourniquets outside of a medical facility histori-
Ceftriaxone (Rocephin) 1 g q 24 hr cally has been considered anathema, there has been a resurgence
Oral in their use in the field by the military. In the Iraq and Afghan
Ciprofloxacin 750 mg bid and cephalexin (Keflex) 500 mg qid theaters, soldiers are trained in application of tourniquets on
Water Exposure themselves and others; tourniquet use in the setting of a mangled
Ciprofloxacin 400 mg IV or 750 mg PO bid; or a sulfonamide and or badly injured extremity has saved many lives. Sacrificing a
trimethoprim combination (Bactrim DS: 800 mg sulfamethoxazole limb to save a soldier is a difficult but clear decision.21 A tourni-
and 160 mg trimethoprim) with either cefazolin (Ancef) 1 g IV q quet should only be applied in the presence of a life-threatening
8 hr or cephalexin (Keflex) 500 mg PO q 6 hr injury and should be left inflated until definitive care can be
Dirt or Barnyard Exposure instituted. Ischemia lasting for more than 2 hours risks permanent
Add penicillin 20 million units IV daily or 500 mg PO q 6 hr
limb damage and for more than 6 hours will generally lead to
amputation. The time of inflation should be conspicuously
If Penicillin Allergy marked on the patient’s limb or forehead. An improvised tour-
Use clindamycin 900 mg IV q 8 hr or 450 mg PO q 6 hr in place of niquet may be employed; it should be at least 4 cm (≈ 1.6 inches)
penicillins and cephalexin (Keflex) in width and be applied with sufficient pressure (generally using
Alternatives a windlass technique) to completely obstruct arterial flow.
Erythromycin 500 mg PO q 6 hr or amoxicillin with clavulanic acid
875 mg PO bid
AMPUTATION OF INJURED EXTREMITIES
Bid, twice a day; IV, intravenously; PO, orally; qid, 4 times a day.
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
Management of Open Fractures of the Extremities pressure points is generally ineffective. Without cooling, an
General care of an open fracture outdoors depends on evacua- amputated part remains viable for 4 to 6 hours. Cleanse the
tion time. An open fracture requires prompt operative irrigation, amputated part with saline or water, wrap it in moistened sterile
debridement, and stabilization. If evacuation can be completed gauze or a towel, place it in a plastic bag, and transport the bag
TRAUMA
within 8 hours, realign the fracture, administer a broad-spectrum in an ice water mixture. Do not use dry ice. Keep the amputated
antibiotic, and splint the extremity. If bone ends extrude through part with the victim throughout the evacuation (Figures 22-34
the skin, try to reduce the exposed bone back into the wound and 22-35).
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,
COMPARTMENT SYNDROME
PART 4
in addition to antibiotic administration and splinting, irrigation A compartment syndrome begins when locally increased tissue
and debridement may be attempted in the field. Antibiotic options pressure reduces capillary blood flow to a muscle compartment.
are listed in Box 22-1. If tetanus vaccine is available and has not When local blood flow is unable to meet metabolic demands of
been given in the past 5 years, this should also be provided. the tissue, ischemia ensues. In the wilderness, compartment
The likelihood of infection developing in the presence of an syndrome most frequently occurs in association with a fracture,
open fracture is directly related to the volume and virulence of crush injury, or severe contusion. It can also occur when the
bacteria present in the wound at the time of definitive wound victim has been lying for a period of time across an extremity
coverage or closure.19 Interventions in the field can be performed so that the body weight occludes the arterial blood flow. Elevated
in an effort to lower the eventual bacterial load and, therefore, local tissue pressure (compartment pressure within 10 to
risk of infection. Organic debris should be removed from the 20 mm Hg of diastolic arterial blood pressure) can also occur
wound. Irrigation can be performed. Ample data have shown with acute hemorrhage or after revascularization of an ischemic
that potable water is equivalent to sterile saline in reducing extremity. Because perfusion pressure is the most important vari-
wound infection, and relatively low volumes (< 1 L) can be able in development of compartment syndrome, hypotension can
effective if irrigation is promptly accomplished. High-pressure increase the risk.
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.
462
the compartmental fascia in each of the four lower leg
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.
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.
with high-energy injuries, in conjunction with thoracic injuries, plains of pain around the sternum and frequently has difficulty
such as rib fracture or pneumothorax. Palpation and auscultation taking a deep breath. When the dislocation is posterior, signifi-
for breath sounds assist in making the associated diagnoses. 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-
FIGURE 22-38 Three-dimensional computed tomography view of nohumeral) “dislocation.” Acromioclavicular separations are clas-
scapula fracture. Complete disassociation of the glenoid from the sified as grade I, II, or III (Figure 22-41). These injuries are acutely
scapular body is present. painful, but surgery rarely improves the clinical outcome. The
464
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
465
FIGURE 22-44 Traction and countertraction for dislocated shoulder
reduction.
maneuver2,8,9,22,33 (Figures 22-44 to 22-50). Self-reduction has Greater tuberosity or glenoid fracture may accompany acute
been proposed but is arguably a challenging procedure. The glenohumeral dislocation. Transient musculocutaneous and/or
technique favored by the authors uses sustained, gentle traction- axillary nerve neurapraxia occurs in approximately 20% of shoul-
countertraction to overcome muscle spasm, minimize rotational der dislocations.31
maneuvers, and avoid leveraging (Figure 22-51). Dislocation of the glenohumeral joint remains an injury of
Of interest to the wilderness caregiver might be the “Eskimo potential long-term consequence for the patient. It is especially
PART 4
technique” used by natives of Greenland, in which the patient is important for the younger individual, whose risk for recurrent
lifted from the ground by the affected arm (while lying on the dislocation may exceed 50%, to visit an orthopedic surgeon.31
unaffected side) so that the patient’s body weight serves as Arthroscopic or open repairs of the damaged anterior capsule
a countertraction.26 Mel Gibson, in his Lethal Weapon films, and labrum may be appropriate in some cases after the first
demonstrates a body-slam technique that may be performed, injury, and recurrent dislocations of the glenohumeral joint
in the absence of an assistant or physician, against any solid 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
466
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.)
467
R
69
G
HH
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
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.
A B
FIGURE 22-56 Anteroposterior (A) and lateral (B) views of intraarticu- FIGURE 22-58 Fracture of the neck of the radius, sustained in a fall.
lar distal humeral fracture-dislocation sustained in a fall from an all- Pain on palpation at the lateral aspect of the elbow, in the region of
terrain vehicle. 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 A sling is provided for comfort. If reduction is not successful after
only the forearm over the platform while applying gentle down- three attempts or if a nerve injury is suspected, a splint is applied
ward traction via the wrist and guiding reduction of the olecra- to the arm as it lies and evacuation performed.
non with the opposite hand (Figure 22-60). Reduction provides Subluxation of the radial head in children (nursemaid’s elbow)
nearly complete relief of pain and restoration of the normal occurs when a longitudinal pull is applied to the upper extremity
surface anatomy. A posterior splint is applied with the elbow in (Figure 22-61). The orbicular ligament partially tears, allowing a
PART 4
90 degrees of flexion and the forearm in neutral position. Col- portion of it to slip over the radial head. An audible snap may
lateral elbow ligament injuries and possible interposed bone or 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
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.
471
Diaphysis
(shaft of bone)
Epiphyseal Metaphysis
disk
(growth plate)
Epiphysis A
Normal Type I
B
Type II Type III
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
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.
472
CHAPTER 22 Wilderness Orthopedics
Extensor pollicis
longus
Scaphoid
Extensor pollicis
brevis Abductor pollicis
longus FIGURE 22-71 Sunken knuckle sign, fourth metacarpal.
FIGURE 22-68 The scaphoid (navicular) bone sits in the anatomic
snuffbox of the radial aspect of the wrist.
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
FIGURE 22-69 Scaphoid fracture with scapholunate widening. 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.
H Irreducible or complex dislocations occur when the volar
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
FIGURE 22-70 Hook of hamate (H) fracture. and definitive treatment obtained as soon as possible.
473
Fracture
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-
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
FIGURE 22-73 The single most important element preventing farther away from its insertion. This is the Stener lesion. Unless surgi-
reduction in a complex metacarpophalangeal dislocation is interposi- cally restored, the ulnar ligament will not heal properly and will be
tion of the volar plate within the joint space. It must be extricated unstable to lateral stress. (Redrawn from Stener B: Skeletal injuries
surgically. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: associated with rupture of the ulnar collateral ligament of the meta-
Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991, carpophalangeal joint of the thumb: a clinical and anatomical study,
JB Lippincott.) 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.
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
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-
FIGURE 22-81 Comminuted femoral shaft fracture in a 30-year-old ment. As with any reduction or relocation maneuver, adequate
TRAUMA
who rolled his all-terrain vehicle and hit a tree. Subcutaneous pieces analgesia and a slow, progressive increase in traction force are
of bone laterally suggest how close this injury was to being an open
helpful. This is not a technique that involves a sudden jerking
fracture.
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.
high-velocity injuries sustained, for example, in motorized vehicle Another technique for relocating a posteriorly dislocated hip
PART 4
accidents or snow skiing or snowboarding. These fractures occur has been described.14 The Captain Morgan technique is named
in the femoral neck or intertrochanteric or subtrochanteric regions for the similarity of the pose of the person executing this maneu-
(Figure 22-81; see also Figure 22-6). The victim complains of ver and the posture that “Captain Morgan” assumes on the
severe pain within the proximal thigh. There may be generalized eponymous bottle of rum. The caregiver maintains the patient in
swelling or deformity around the hip region. Movement of the the supine position. The caregiver flexes the patient’s hip and
affected limb, which is noticeably shortened and externally knee to 90 degrees. The caregiver places his or her thigh under
rotated, produces significant pain. After a careful sensory, motor, the calf of the flexed, dislocated hip. With one hand pressing
and circulatory examination, the limb is realigned, and a splint downward on the ipsilateral ankle of the dislocated hip and the
is applied if available. An improvised traction splint may need other hand lifting upward behind the ipsilateral knee of the
to be fabricated. If none is available, the victim is transported on dislocated hip, the caregiver plantarflexes her or his own ankle
a backboard, with the limbs strapped together or tied to a board of the leg that is under the patient’s thigh. This slow plantarflex-
with a tree limb placed between them. ion, along with the concomitant downward pressure distally and
Femoral neck fracture is associated with significant risk for upward pressure proximally, allows the caregiver’s thigh to be
posttraumatic femoral head necrosis (see Figure 22-6). Without used as a fulcrum to facilitate the hip relocation (Figure 22-84).
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 FIGURE 22-82 Right hip dislocation with femoral head fracture.
476
CHAPTER 22 Wilderness Orthopedics
A
Hand B
Hand A
477
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
FIGURE 22-87 Open patellar fracture wound with typical stellate
applied to the limb, and the victim is moved on a backboard.
appearance. 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
With a patellar fracture, the injury may be obvious on deep the tibial-femoral joint. Generalized ligamentous laxity may pre-
palpation. This is often an open injury because there is very little dispose to this problem. Patellofemoral dislocation, especially
soft tissue overlying this sesamoid bone (Figure 22-87). After an recurrent, is more common in females than males and may be
initial neurovascular examination, the limb is realigned. A pos- associated with an accentuated Q angle, the angle created
terior splint is applied to the realigned limb for transportation. between a line drawn from the anterior superior iliac spine to
As with all fractures, open wounds in the region of the fracture the center of the patella and a line drawn from the tibial tubercle
or an abnormal nerve or vascular examination should prompt to the center of the patella. Dislocation of the patella may result
immediate evacuation. from a twisting injury or asymmetric quadriceps contraction
during a fall. These mechanisms can occur with hiking, climbing,
Knee Dislocation and skiing accidents. The patella usually dislocates to a position
TRAUMA
Knee (tibial-femoral) dislocation is a high-energy injury. It is lateral to the articular surface of the distal femur. Although neu-
usually obvious because of the amount of deformity (Figure rovascular injuries rarely occur in association with a dislocated
22-88). The most common dislocation directions are anterior and patella, a screening examination should be conducted.
posterior. Knee dislocation represents a true emergency because The patella can often be reduced by simply straightening the
5% to 40% of these injuries have associated vascular injuries.1,29,34 knee. If this is not successful, gentle pressure is applied to the
A large series reported an above-knee amputation rate of 86% patella to push it back up into the distal femoral articular groove.
PART 4
for vascular injuries associated with knee dislocations that were A knee splint is applied with the joint in extension; weight
not repaired within 8 hours of injury.12 The vascular injury occurs bearing is allowed. The knee is kept in extension until definitive
because of tethering of the popliteal vessels by the soleus fascia care can be obtained. A radiograph is ultimately required to rule
along the posterior border of the tibia. When this injury is sus- out osteochondral fractures, which can be associated with this
pected, a careful screening neurovascular examination must be 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,
FIGURE 22-88 Anterior knee dislocation. Significant attention should the entire limb should be inspected for distal sensory, motor, and
be devoted to relocation, if possible, and to assessment of the neuro- vascular function before realignment. A posterior splint is applied
vascular structures that run posterior to the knee joint, such as the for transport. The limb should be serially examined for the onset
popliteal artery and the tibial and common peroneal nerves. of compartment syndrome.
478
CHAPTER 22 Wilderness Orthopedics
FIGURE 22-89 Tibial plateau fracture sustained in fall from a height.
ANKLE AND FOOT INJURIES FIGURE 22-91 Distal tibia-fibula fracture in a young Enduro rider:
Salter-Harris II fracture.
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 with the foot and ankle in neutral position. During transport, the
fracture, which is generally produced by torsional moments of limb is elevated above the level of the heart.
force around a fixed foot (Figure 22-91). With the pilon tibial
fracture, axial loading from a fall or jump may also be involved. Ankle Dislocation or Sprain
Any significant pain and swelling should be noted as the footgear Ankle dislocation is almost always accompanied by fractures of
is removed. Palpation along the medial and lateral malleoli one or more malleoli. This dislocation generally occurs with falls
confirms the clinical suspicion. After footgear is removed to onto uneven surfaces or with twisting injuries of moderate veloc-
inspect the skin for open wounds, neurovascular examination is ity. The area about the ankle is carefully examined for open
performed. injuries, and a neurovascular examination is conducted. The
If there is a rotational deformity in the ankle, it should be ankle joint is aligned by grasping the posterior heel, applying
realigned with gentle traction before applying a posterior splint 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
FIGURE 22-90 Tibia fracture sustained in a snowmobile accident. 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
Dorsal tarsometatarsal
Dorsal metatarsal ligament
ligaments 1st metatarsal bone
TRAUMA
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
480
CHAPTER 22 Wilderness Orthopedics
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 FIGURE 22-97 Subtalar fracture dislocation.
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. uneven surface. The calcaneus may be dislocated medially or,
Fracture of the lateral process of the talus, which is a fairly more commonly, laterally relative to the talus (Figure 22-97). The
common lower extremity fracture in snowboarders, may be con- position of the heel relative to the ankle is assessed. With either
fused with lateral ankle sprain, so radiographs are generally dislocation, a reduction is attempted if it will be more than 3
needed to rule out this injury.9 Inversion injuries are also infre- hours until the victim will reach a definitive care center.
quently associated with fractures at the insertion of the peroneus Medial dislocation is reduced more easily than is lateral dis-
brevis tendon. This injury can be identified by point tenderness location, in which the posterior tibial tendon frequently becomes
at the base of the fifth metatarsal, but a radiograph is required displaced onto the lateral neck of the talus, blocking the reduc-
for definitive diagnosis. Early management is the same as for an tion. The maneuver is the same for both: The heel is grasped
ankle sprain. The eponym Jones fracture is used to describe the with the knee flexed (relaxing the gastrocnemius-soleus complex),
more worrisome transverse fracture to the metaphyseal portion the deformity is accentuated, linear traction is applied, and the
of the fifth metatarsal; nonunion is a concern with this injury heel is brought over to the ankle joint. This maneuver is gener-
(Figure 22-96). ally successful for medial dislocation, but lateral dislocation,
especially when associated with open wounds, often requires
Hindfoot Dislocation open treatment. After reduction is attempted, a posterior splint
The subtalar joint may infrequently be dislocated in a significant is applied and the limb is elevated above the level of the heart.
fall or jump when an individual lands off balance or on an 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).
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 MTP joint dislocation of the toe is relatively uncommon but can
foot at subtalar joint. B, Medial aspect of lateral subtalar dislocation. 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
Tarsal Fracture prevents it. Injuries of this type at the great toe may be associated
PART 4
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
483
A joint space opening of more than 10 mm (0.4 inch) or the feels as though he or she has been struck by a baseball bat at
absence of an end point with valgus stress applied to the knee the posterior aspect of the ankle. Active plantarflexion is impos-
is consistent with a grade 3 injury. The MCL is attached to the sible. In the Thompson squeeze test, the injured person kneels
medial meniscus, so injury to the medial knee may also cause on an elevated surface without sitting on the haunches and
injury to the medial compartment cartilage. If symptoms do not allows the feet to hang over the edge of the surface. Squeezing
improve in a timely fashion, further evaluation to rule out a the calf does not result in involuntary plantarflexion on the
meniscal tear is appropriate. injured side.
MCL injury is typically treated with conservative management. Apply a short-leg splint as a temporizing measure. The affected
A hinged knee brace that stabilizes the knee from varus and individual may bear weight as tolerated. This injury may be
valgus stress is indicated. treated with or without surgery.
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.
HAMSTRING STRAIN OR TEAR
The LCL can be strained or torn. The LCL may be injured in Hamstring strain or tear can occur when there is a hyperflexion
association with a cruciate ligament injury. Complex injuries to mechanism applied to the hip simultaneously with a hyperexten-
the posterior lateral corner of the knee may also involve the sion mechanism to the leg (eccentric load). Hamstring tear or
popliteus tendon and can be disabling in terms of knee stability. strain can also occur as an overuse injury. The best way to treat
The LCL connects from the lateral femoral condyle to the head this injury is to apply ice, stretch gently, and bear weight as toler-
of the fibula but has no direct attachment to the lateral meniscus ated. Most hamstring tears heal with conservative management.
(as does the MCL with the medial meniscus). If a complete tear or significant avulsion from the ischial tuberos-
Most isolated LCL sprains, like MCL sprains, heal with conser- ity occurs, surgical repair may be indicated. There are no
vative management. The typical time frame of 6 to 12 weeks may evidence-based recommendations for repair. However, in active
be anticipated for return to full unrestricted activity. A hinged people with more than 2 cm (0.8 inch) of retraction from the
knee brace that protects the knee from valgus stress is indicated. ischium, repair can result in decreased pain and improved func-
When associated with a multiligament injury, especially a cruciate tion over time.
ligament disruption and posterior lateral instability, surgical repair
may be necessary to restore function.
Individuals and athletes who wish to return to competitive
JOINT OR BURSAL EFFUSIONS
sports typically have ACL injuries repaired; PCL tears are treated Joint or bursal effusions occur when there is excess synovial fluid
on a case-by-case basis because many individuals can compen- production. Effusions may result from trauma (e.g., hemarthrosis
sate for this injury without surgery. An ACL-deficient knee often with an ACL tear, or lipohemarthrosis with a tibial plateau frac-
results in ongoing instability (a “trick knee”), even in nonathletic ture). Because it is rarely possible to perform aspiration under
TRAUMA
individuals, and the risk for tearing the meniscus or causing other sterile conditions in the wilderness, the effusion should be treated
damage to the knee is high. Rehabilitation from this injury usually with NSAIDs, compression dressing, and application of cold. A
takes a minimum of 6 months. painful effusion without trauma in a person over the age of 40
Meniscal tears in the setting of a ligamentous injury are years is more likely gout or pseudogout than infection. If there
common (Figure 22-104). Some tears (bucket handle tears) can is strong suspicion that the effusion may be infected (e.g., accom-
become caught in the joint, and may result in a “locked knee.” panied by fever, chills, and lack of trauma), antibiotics can be
PART 4
Manipulative procedures to slightly widen the joint space wherein administered, accompanied by prompt evacuation for aspiration.
lies the lodged meniscal fragment might liberate an incarcerated
fragment. Sometimes, surgery is the sole solution for this problem.
OVERUSE SYNDROMES AND
ACHILLES TENDON RUPTURE SPECIAL CONSIDERATIONS
Achilles tendon rupture occurs most commonly in the 35- to
55-year-old age group. This injury usually happens as an indi-
PLANTAR FASCIITIS
vidual applies an eccentric (lengthening while contracting) load Plantar fasciitis is inflammation of the fascia (tough connective
to the calf and Achilles tendon. The affected individual often 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.
Medial
meniscus
tear 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
FIGURE 22-104 Medial meniscus tear. the palmar aspects of the radial digits. They also complain of
484
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
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 lateral tibia. Irritation and inflammation occur along the path of
aggravated with prolonged wrist extension or flexion. The the iliotibial band at the bony prominences over which it runs,
Phalen’s sign, which is numbness and tingling in the median proximally at the greater trochanter and distally at the lateral
nerve distribution after sustained wrist flexion, is suggestive of femoral epicondyle. Treatment for these conditions in the wilder-
CTS. Thenar muscle atrophy is seen only in severe cases. CTS ness involves NSAIDs, ice, and, insofar as it is possible, decreased
may occur during pregnancy, or it may be caused by endocrine activity. Stretching can also be of benefit for these conditions,
disorders (diabetes or hypothyroidism) or acute or chronic especially as a preventive measure or as treatment over the
trauma. Treatment consists of wrist splinting in slight extension, long term.
activity modification, and NSAIDs. 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
STRESS FRACTURES benefit.
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).
SPINAL DISORDERS
Victims complain of pain with weight bearing, swelling, tender- Back strain and pain episodes may dampen the enthusiasm of
ness to palpation, and increased warmth at the fracture site. even the most dedicated outdoor enthusiast. Most often, these
Treatment consists of activity reduction, protective weight bear- events represent low back strain with associated muscle spasm.
ing, and avoidance of activities that produce pain. As the pain These conditions often occur in the setting of heavy lifting,
subsides, the activity level can be increased. Resolution of symp- bending, or twisting activities. Treatment involves low-impact
toms may require 2 to 3 months. 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
BURSITIS, INFLAMMATION, AND IRRITATION manifests with or without focal radicular symptoms. In an indi-
The iliotibial band travels along the lateral thigh, from its origin vidual with severe, intractable pain, loss of motor strength, or
at the iliac crest to insertion at Gerdy’s tubercle on the proximal loss of bowel or bladder function, evacuation may be necessary.
485
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.
vigorously active in yoga and carries a full backpack down into If concern exists about a possible joint infection, a corticosteroid
the Grand Canyon on an annual pilgrimage (Figure 22-108). should not be injected; treatment with appropriate antibiotics and
surgical referral may be indicated.
The experienced wilderness medicine practitioner can perform
CORTICOSTEROID INJECTIONS these procedures in an emergency or disaster setting as long as
Corticosteroid injections are commonly performed in the clinic the sterile “no-touch” technique is used and the benefits of the
setting when degenerative joint disease is present or when 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-
FIGURE 22-107 Lumbar spine radiograph of active individual that etrations of the tendon, ligament, or fascia. Tendon sheath injec-
demonstrates significant scoliosis. tions require the caregiver to be able to insert the needle through
486
approach beneath the patella may also be employed. A 10-mL
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 FIGURE 22-111 Injection for lateral epicondylitis (tennis elbow): The
do not improve with conservative measures may benefit from a needle is inserted over the lateral epicondyle of the humerus at the
corticosteroid injection into the region of the trochanteric bursa origin of the extensor carpi radialis brevis (ECRB) muscle tendon. Inject
(Figure 22-110). The injection should be performed at the point using a fan-wise, peppering technique. The dosage is 10 mg of triam-
of maximal tenderness. With the patient lying on the unaffected cinolone acetonide and 0.75 mL of 1% lidocaine, for a total volume of
side, the skin over the greater trochanter is prepped using a 1 mL. (From Saunders S, Longworth S, editors: Injection techniques in
fenestrated drape and sterile procedure. Depending on the musculoskeletal medicine, 4th ed, Edinburgh, 2013, Churchill Living-
patient’s body habitus, a spinal needle may be required to pen- stone, p 131.)
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. Direct aspiration should be performed before injection to evalu-
TRAUMA
ate the fluid aspirant. For a common adult dosage, a 2-mL syringe
Olecranon Bursitis Injection and 22-gauge needle are used to inject 20 mg of triamcinolone
Olecranon bursitis may occur following a traumatic fall or injury acetonide (40 mg/mL) and 1.5 mL of 1% lidocaine.
to the elbow with fluid accumulation of a hemorrhagic nature.
Spontaneous swelling may also occur without known antecedent Medial and Lateral Epicondylitis Injection
injury. Infection of the olecranon bursa is a frequent concern. Medial (golfer’s elbow) epicondylitis and lateral (tennis elbow)
PART 4
488
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.
489
A B C
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 skills and/or significant impact loading, as categorized in Table
and won the Senior PGA Tour in 1998. 22-3. Sports and fitness regimens vary significantly with the com-
• Golfing great Jack Nicklaus had a total hip arthroplasty in petence, confidence, and risk tolerance of the individual. High-
1999 and returned to high-level play. risk and high-impact activities may cause accelerated wear and
PART 4
• Figure skater Rudy Galindo had bilateral ceramic-on- loosening of implants that lead to the need for early revision.
ceramic total hip arthroplasties in 2003 and was landing The necessity for revision arthroplasty has a markedly increased
triple jumps with Champions on Ice in 2004. cost and rate of complications relative to primary joint replace-
• A 69-year-old mountaineer, after bilateral total hip arthro- ment, and the functional result tends to deteriorate with each
plasties in 1987 and 1995, climbed two peaks over 6000 m successive revision.
in the Andes. Although dislocation of a normal hip is a rare event caused
• Floyd Landis had a hip resurfacing in 2006, was riding a by high-energy trauma, hip replacements dislocate with relative
stationary bike 5 days after surgery, and has since returned ease. If this occurs, the reduction maneuver is the same as
to competitive cycling. described above.
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
PROSTHETICS IN THE WILDERNESS
to learn a “new” sport that requires advanced proprioceptive 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
FIGURE 22-115 Bilateral total hip arthroplasties in a patient who, fol- (C.W. HOG). Many members of this organization suffer from
lowing her second surgery, climbed to the summit of Mt. Rainier. spinal cord injuries, cerebral palsy, amputations, or other
490
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.)
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
BOX 22-2 Indications for Emergency Evacuation
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 in long-term disability.32 The 5 million people each year who are
thousands of years. For instance, orthopedic splinting was placed in spine immobilization after traffic collisions account for
well documented in ancient Egypt more than 5000 years ago49 most spinal cord injuries. In one wilderness study, only 3.6% of
(Figure 23-1). mountain trauma patients who were alive when rescued had
First and foremost, splints and slings stabilize injuries by limit- spine injuries.27
ing movement (Box 23-1). Limiting movement minimizes pain Spine stabilization has traditionally been first accomplished by
and decreases potential further tissue damage. Splinting eases manual techniques and then by mechanical devices (e.g., back-
transportation from the field, minimizes blood loss, and aids in boards, collars, straps), which we review below. We will also
healing.19 In general, all fractures and dislocations should be review newer immobilization devices. In light of recent evidence
splinted before transport unless the patient’s life is at immediate and guidelines, the indications, risks, and benefits of spine immo-
risk or the rescue scene is unsafe.20 Basic splint types include bilization merit review.
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.
INDICATIONS FOR SPINE IMMOBILIZATION
Examples include newspapers, pillows, umbrellas, and other The most common scenario for prehospital spine immobilization
supportive materials (Figure 23-2).8 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-
SPINE IMMOBILIZATION force spine trauma in the wilderness setting. Falls and other
Spinal cord injuries are rare, affecting 40 to 50 individuals per high-force mechanisms are other causes. Worrisome symptoms
million annually in the United States. These injuries may result include spine pain or palpable tenderness, altered mental status,
492
neurologic complaints, or a head injury. Factors that may com-
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
evidenced by development of selective immobilization guide- recently proposed. The treatment algorithm was specifically cali-
lines. Several states and emergency medical systems (EMSs) brated so as to minimize the risk of exacerbating a potentially
across the nation are beginning to use protocols that decrease unstable spine injury weighed against the risks to rescuers and
the number of trauma patients subjected to prehospital spine victim in the austere setting.45 (Figure 23-3). Further research is
immobilization. Studies show that prehospital care providers can still warranted to better classify appropriate indications, validate
safely apply these spine injury assessment protocols and not miss guidelines, and further assess the risk-benefit ratio for spine
clinically significant spine injuries.16,40,50 immobilization in the wilderness.
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)
CERVICAL SPINE IMMOBILIZATION TECHNIQUE
low-risk criteria. Each has similar parameters, requiring that the High cervical spine (C-spine) injuries have great potential for
patient be awake, alert, and conversant, and without significant morbidity and disability. The goals of C-spine immobilization are
distracting injury or intoxication. In addition, the guidelines to minimize movement and maintain “neutral” alignment. Stan-
further state that the physical examination should reveal no pain 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
BOX 23-3 Complications of Spine Immobilization include the trapezius muscles (posterior), clavicle, and sternum
(anterior). Hard collars alone do not adequately limit cervical
Tight straps and a rigid board may cause discomfort or distress. motion. Backboards and lateral support devices are required in
Tight straps may cause vascular compromise. conjunction with a hard collar (Figures 23-4 and 23-5). Newer
An immobilized position may interfere with normal respiratory vacuum spine boards also serve this purpose (Figure 23-6). The
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.
494
CHAPTER 23 Splints and Slings
A
C D
FIGURE 23-5 A to C, Different lateral support devices. D, Complete standard cervical hard collar is not effective. Children who are
spine immobilization. (Courtesy Laerdal Medical Corporation.) 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
patient’s neck requires manual stabilization in a neutral, in-line raising the shoulders to the level of the head by placing a pad
position until he or she is fully immobilized. Standard emergency underneath the shoulders (Figure 23-11). This should be consid-
medical services equipment includes lateral support devices ered for all children who are on backboards.42,43
(foam or plastic). In the wilderness setting, these devices can be Cases of neurologic deterioration, and even death, have now
improvised by rolling clothes, sheets, or blankets and placing been reported with the use of a cervical collar in patients with
them on both sides of the head while securing everything in ankylosing spondylitis.53 In these patients, a cervical collar is
place with tape (see Figure 23-2).24 contraindicated.
SPECIAL CONSIDERATIONS
Special populations require accurately sized equipment. This
includes people with a very long or short neck for whom a
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 the suspected cervical injury of a seated patient, an intermediate
other available and malleable material rolled to the desired thick- device is required. There are many forms of this short board,
ness and placed underneath the patient’s neck. The ends are such as a Kendrick Extrication Device (see Figure 23-10). Short
crossed over the patient’s chest and secured. As with the cervical boards are applied only after manual in-line stabilization and
hard collar, the patient’s C-spine is maintained in a neutral posi- cervical collar placement have been performed. When the short
tion during application and for as long as possible afterward by board is in place, the patient can be safely transferred to full
manual in-line stabilization2,9 (see Figure 23-7). spine immobilization.9
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
FULL SPINE IMMOBILIZATION
small, lightweight, versatile, and portable. These characteristics From a supine (lying) position and after placement of a cervical
are advantageous in the wilderness setting (see Figure 23-9).38 A collar, the patient is logrolled, or the slide and transfer technique
similar device can be fashioned by wrapping sleeping mattress is used to place the patient onto a board or vacuum splint. With
padding or closed-cell foam around the support of a rolled wire the logroll technique, three people are required to transfer a
splint (Figure 23-12). 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
THORACOLUMBAR IMMOBILIZATION head, the patient is rolled onto the least-injured side. The board
A full-length immobilization device best accomplishes immobili- is slid underneath the patient while the back is evaluated for
zation of the thoracolumbar spine. In addition, a cervical collar, injuries. With the lift and slide technique, multiple attendants are
lateral neck stabilizers, and backboard straps are essential for full also required. One individual maintains manual, in-line stabiliza-
spine immobilization. If the patient is already upright, standing, tion of the head and neck while the other rescuers straddle the
or lying supine, application of full-body immobilization is victim in preparation for lifting the upper torso, hips, pelvis, and
straightforward, as described later in this chapter. However, with 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 Logrolling is not required with scoop stretchers, thereby mini-
stabilizing the head and neck directs the others to raise the mizing spine movement (see Figure 23-16). Scoop stretchers, like
patient off the ground to enable the remaining rescuer to slide other rigid devices, are otherwise compromised by the same
the spine board under the patient from the foot end. Body disadvantages listed above.
straps and lateral neck stabilizers are then placed (Figures 23-13 Vacuum splint devices offer certain advantages over rigid
and 23-14).9 hard backboards. They can be applied more quickly and are
Choices for full-body splints include hard backboards, scoop significantly more comfortable (Figure 23-19 and see also Figure
stretchers, and full-body vacuum splints (Figures 23-15 to 23-18). 23-18). They also offer a similar degree of spine immobiliza-
Full-body hard backboards have been traditionally used. Unfor- tion.30 Several studies have demonstrated that a vacuum mattress
tunately, their size and weight make them undesirable for back- provides significantly superior spine stability, increased speed
country use. Secured straps minimize spine movement during of application, and markedly improved patient comfort when
transport. These are especially important with vomiting patients, compared with a backboard. Vacuum mattress immobilization of
when the airway is potentially compromised and a quick change the potentially injured spine is the current recommendation of
of position is required to allow for removal and drainage of the International Commission for Mountain Emergency Medi-
emesis.9 Hard backboards are uncomfortable. Spine pain that is cine.19 During mountain rescue, vacuum splints are therefore
induced by a backboard may be misinterpreted, and this can the preferred device for total spine immobilization (Figure 23-20
complicate and delay therapy.23 Because rigid backboards can and see also Figures 23-18 and 23-19). In circumstances in
induce pain, patient agitation, pressure ulcers, and respiratory remote austere settings with limited resources where quick extri-
compromise, a recent position statement from EMS physicians cation is necessary, semirigid spine boards can be improvised
and trauma surgeons has advocated limiting their use.41 (Figure 23-21).
497
A
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
498
CHAPTER 23 Splints and Slings
A
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.)
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
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.
Splint Indication
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
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
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-
FIGURE 23-24 Improvising a pelvic compression device. This card- Washington, Inc.)
board splint is used to treat the lower extremity. (Courtesy Alan
Gianotti, MD.)
Soft splints allow for more laxity than do rigid splints, but can
TRAUMA
502
CHAPTER 23 Splints and Slings
A
FIGURE 23-27 Pliable metal ladder splints. (Courtesy Ferno-
Washington, Inc.)
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 FIGURE 23-32 Military antishock trouser/pneumatic antishock gar-
position paper of the National Association of EMS Physicians for ment. (Courtesy Common Cents EMS Supply.)
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 lower extremity hemorrhage).17 Postulated successful mecha-
from pelvic fractures, gynecologic bleeding, ruptured ectopic nisms for correcting hypotension include increasing peripheral
PART 4
pregnancy, severe traumatic hypotension, and uncontrolled 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
A PASG use include diaphragmatic rupture, penetrating thoracic
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.
504
Contraindications to traction splint placement are fractures constraints of the patient’s hiking boot. The time-tested alterna-