Wilderness Medicine, 5th Edition

Conversion Charts b LENGTH 1 inch = 2.54 cm 1 foot = 0.3048 m 1 yard = 0.9144 m 1 mile = 1.609 km

1 cm = 0.3937 inches 1 m = 3.2808 feet 1 m = 1.0936 yards 1 km = 0.6214 miles

b VOLUME 1 oz (U.S., liquid) = 29.5735 mL 1 oz (U.K.) = 28.4131 mL 1 CUP = 0.2366 L 1 pint (U.S., liquid) = 0.4732 L 1 pint (U.K.) = 0.5683 L 1 quart (U.S.) = 0.95 L 1 quart (U.K.) = 1.14 L 1 gallon (U.S.) = 3.7854 L 1 gallon (U.K.) = 4.55 L

1 mL = 0.0338 oz (U.S., liquid) 1 mL = 0.0352 oz (U.K.) 1 L = 4.2268 CUPS 1 L = 2.1 134 pints (U.S., liquid) 1 L = 1.7598 pints (U.K.) 1 L = 1.06 quarts (U.S.) 1 L = 0.88 quarts (U.K.) 1 L = 0.2642 gallons (U.S.) 1 L = 0.22 gallons (U.K.)

b WEIGHT 1 oz = 28.3495 g 1 Ib = 0.4536 kg

1 g = 0.0353 oz 1 kg = 2.2046 Ibs

b ENERGY 1 Joule = 0.000239 Kcal

1 Kcal = 4184 Joules

b TEMPERATURE To convert Fahrenheit to Celcius: degrees F - 32 x 5/9 To convert Celcius to Fahrenheit: degrees C x 9/5 + 32

Contributors Javier A. Adachi, MD Assistant Professor, Department of Infectious Diseases, Infection Control, and Employee Health, The University of Texas MD Anderson Cancer Center; Clinical Assistant Professor, Department of Internal Medicine, The University of Texas Health Science Center at Houston Medical School, Houston, Texas; Visiting Professor, Universidad Peruana Cayetano Heredia, Lima, Peru Martin E. Alexander, BScF, MScF, PhD, RPF Adjunct Professor, Wildland Fire Science and Management, Department of Renewable Resources, University of Alberta; Senior Fire Behavior Research Officer, Northern Forestry Centre, Canadian Forest Service, Edmonton, Alberta; Honorary Research Associate, Faculty of Forestry and Environmental Management, University of New Brunswick, Fredericton, New Brunswick, Canada Robert C. Allen, DO, FACEP Colonel, United States Air Force MC CFS; Chief, Aeromedical Evacuation Branch, USAF School of Aerospace Medicine, Brooks City-Base, Texas Bryan E. Anderson, MD Assistant Professor of Dermatology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania Susan Anderson, MD, MS Adjunct Clinical Assistant Professor, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford; Travel, Tropical, and Wilderness Medicine Consultant, Travel Medicine and Urgent Care, Palo Alto Medical Foundation, Palo Alto, California Christopher J. Andrews, BE, MBBS, MEngSc, MAppLaw, PhD, DipCSc, EDIC Consulting Medical Practitioner and Electrical Engineer, Indooroopilly Medical Centre, Brisbane, Queensland, Australia E. Wayne Askew, PhD Professor and Director, Division of Nutrition, University of Utah College of Health, Salt Lake City, Utah Dale Atkins, BA United States Representative, Avalanche Commission, International Commission for Alpine Rescue Switzerland, RECCO, AB, Lidingö, Sweden Brett D. Atwater, MD Fellow in Cardiovascular Medicine, Department of Medicine, University of Wisconsin Hospital and Clinics, Madison, Wisconsin

Paul S. Auerbach, MD, MS, FACEP Clinical Professor of Surgery, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Kira Bacal, MD, PhD, MPH Health Policy Fellow, Voinovich Center for Leadership and Public Affairs, Ohio University, Athens, Ohio; Consultant, Mauri Ora Associates, Auckland, New Zealand Howard D. Backer, MD, MPH, FACEP Lecturer, Department of Public Health, University of California, Berkeley; Chief, Immunization Branch, Medical Consultant, Emergency Preparedness, Division of Communicable Disease Control, California Department of Health Services, Richmond, California Greta J. Binford, PhD Assistant Professor, Department of Biology, Lewis & Clark College, Portland, Oregon Jolie Bookspan, MEd, PhD Instructor, Temple University; Director, Neck and Back Pain Sports Medicine; Advisory and Review Board, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Warren D. Bowman, MD, FACP Clinical Associate Professor Emeritus, Department of Internal Medicine, University of Washington School of Medicine, Seattle, Washington; Staff Physician (Retired), Department of Internal Medicine, Division of Hematology-Oncology, The Billings Clinic, Billings, Montana Leslie V. Boyer, MD, FACMT Associate Professor of Clinical Pediatrics, Department of Pediatrics, University of Arizona College of Medicine, Tucson, Arizona George H. Burgess Director, Florida Program for Shark Research, Florida Museum of Natural History, University of Florida, Gainesville, Florida Robert K. Bush, MD Professor, Department of Medicine, University of Wisconsin School of Medicine and Public Health; Professor (Courtesy), Food Research Institute, University of Wisconsin; Chief of Allergy, William S. Middleton VA Hospital, Madison, Wisconsin Sean Paul Bush, MD, FACEP Professor of Emergency Medicine, Department of Emergency Medicine, Loma Linda University School of Medicine; Director, Fellowship of Envenomation Medicine, Department of Emergency Medicine, Loma Linda University Medical Center, Loma Linda, California

v

vi

Contributors

Frank K. Butler, Jr., MD Command Surgeon, U.S. Special Operations Command, Tampa, Florida Steven C. Carleton, MD, PhD Associate Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine; Emergency Physician, Center for Emergency Care, University Hospital, Inc., Cincinnati, Ohio Betty Carlisle, MD Assistant Adjunct Professor, Division of Public Health, Center for Global Health, University of Rochester, Rochester, New York; Director, McMurdo Medical, and Base Physician, Amundsen-Scott Station and Palmer Station, Antarctica John W. Castellani, PhD Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts Monalisa Chatterjee, MPhil PhD Candidate, Department of Geography, Rutgers University, New Brunswick, New Jersey Richard F. Clark, MD Professor of Medicine, University of California, San Diego, School of Medicine; Director, Division of Medical Toxicology, Department of Emergency Medicine, UCSD Medical Center; Medical Director, California Poison Control System, San Diego Division, San Diego, California Bryan R. Collier, DO, FACS, CNSP Assistant Professor of Surgery, Vanderbilt University School of Medicine; Assistant Professor of Surgery, Department of Surgical Sciences, Division of Trauma and Surgical and Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee Donald C. Cooper, PhD, CFO, OFE, NREMT-P Deputy Fire Chief, Cuyahoga Falls Fire Department, City of Cuyahoga Falls; President, National Rescue Consultants, Inc., Cuyahoga Falls, Ohio Mary Ann Cooper, MD Professor, Departments of Emergency Medicine and Bioengineering, University of Illinois College of Medicine at Chicago, Chicago, Illinois Larry Ingram Crawshaw, PhD Professor, Department of Biology, Portland State University; Professor, Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon Gregory A. Cummins, DO, MS Assistant Clinical Instructor, Adjunct Faculty, Department of Internal Medicine, Kansas City University of Medicine and Biosciences, Kansas City; Hospitalist, Department of Internal Medicine, North Kansas City Hospital, North Kansas City, Missouri Daniel F. Danzl, MD Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky

Richard C. Dart, MD, PhD Professor of Surgery, Division of Emergency Medicine, University of Colorado School of Medicine; Director, Rocky Mountain Poison and Drug Center, Denver Health, Denver, Colorado Samhita Dasgupta, BS Department of Biology, Portland State University, Portland, Oregon Ian Davis, MBBCH, BSc (Hons) Resident Medical Officer, Department of Accident and Emergency, Cirencester Hospital, Gloucestershire; Polar Medicine, Medical Cell, Royal Geographical Society, London; Chief Medical Officer, Polar Challenge, Venture Group, Cirencester, England, United Kingdom Kathleen Mary Davis, MS Superintendent, Montezuma Castle and Tuzigoot National Monuments, National Park Service, U.S. Department of the Interior, Camp Verde, Arizona Kevin Jon Davison, ND, LAc Clinic Director, Maui East-West Clinic, Haiku, Hawaii Chad P. Dawson, PhD Professor, Faculty of Forest and Natural Resources Management, State University of New York, College of Environmental Science and Forestry, Syracuse, New York Thomas G. DeLoughery, MD, FACP Professor of Medicine and Pathology, Department of Medicine and Pathology, Divisions of Hematology and Laboratory Medicine, Oregon Health and Science University, Portland, Oregon Mark W. Donnelly, MD Attending Physician, Department of Emergency Medicine, Samaritan Lebanon Community Hospital, Lebanon, Oregon Howard J. Donner, MD Family Physician, Telluride, Colorado Eric Douglas, BA, DMT Director of Training, Divers Alert Network, Durham, North Carolina Herbert L. DuPont, MD Chief, Internal Medicine, St. Luke’s Episcopal Hospital; Director, Center for Infectious Diseases, University of Texas, Houston, School of Public Health; Mary W. Kelsey Chair, University of Texas, Houston, Medical School; H. Irving Schweppe, Jr., Chair and Vice Chairman, Department of Medicine, Baylor College of Medicine, Houston, Texas Thomas J. Ellis, MD Associate Professor, Department of Orthopaedic Surgery, Oregon Health and Science University, Portland, Oregon Blair Dillard Erb, MD, FACP Grand Junction, Colorado; Past President, Wilderness Medical Society, Lawrence, Kansas

Contributors Timothy B. Erickson, MD, FACEP, FACMT, FAACT Professor, Department of Emergency Medicine, and Director, Division of Toxicology, University of Illinois College of Medicine at Chicago, Chicago, Illinois Charles D. Ericsson, MD Professor of Medicine and Head, Clinical Infectious Diseases, Department of Medicine, University of Texas Medical School at Houston; Chief of Infectious Diseases, Hermann Hospital; Chief of Infectious Diseases and Medical Director of Infection Control, Lyndon Baines Johnson Hospital; Director, Travel Medicine Clinic, University of Texas Medical School at Houston, Houston, Texas Joanne Feldman, MD, MS Wilderness Medicine Fellow and Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Murray E. Fowler, DVM Professor Emeritus, Department of Medicine and Epidemiology, University of California, Davis, School of Veterinary Medicine, Davis, California

vii

Kimberlie A. Graeme, MD Associate Professor, Department of Emergency Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota; Consultant, Department of Emergency Medicine, Mayo Clinic Scottsdale, Scottsdale, Arizona Andrea R. Gravatt, MD, FAAP Clinical Assistant Professor, Department of Pediatric Medicine, University of Washington School of Medicine; Clinical Assistant Professor, Department of Pediatrics, Children’s Hospital and Regional Medical Center, Seattle; Attending Physician, Department of Pediatric Emergency Medicine, Mary Bridge Children’s Hospital, Tacoma, Washington Colin K. Grissom, MD Associate Professor of Medicine (Clinical), Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Utah School of Medicine; Co-Director, Shock Trauma Respiratory Intensive Care Unit, Critical Care Medicine, LDS Hospital; Assistant Medical Director, Life Flight, LDS Hospital and Intermountain Health Care, Salt Lake City, Utah

Mark S. Fradin, MD Clinical Associate Professor, Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina

Peter H. Hackett, MD Clinical Director, Altitude Research Center, University of Colorado School of Medicine, Denver; Director, Center for Altitude Medicine; Director of Emergency Services, Telluride Medical Center, Telluride, Colorado

Bryan L. Frank, MD Past President, International Council of Medical Acupuncture and Related Techniques, Brussels, Belgium; President, Global Mission Partners, Edmond, Oklahoma

Charles G. Hawley, BS Vice President of Product Development, West Marine, Watsonville, California

Luanne Freer, MD, FACEP Staff Physician, Emergency Department, Bozeman Deaconess Hospital, Bozeman, Montana; Medical Director, Yellowstone National Park, Yellowstone, Wyoming Steven P. French, MD Co-Founder, Yellowstone Wyoming

Grizzly

Foundation,

Jackson,

Stephen L. Gaffin, PhD Professor of Physiology, American University of the Caribbean, St. Maarten, Netherlands Antilles; Research PhysiologistImmunologist, Thermal and Mountain Medicine, U.S. Army Medical Corps (Retired), Framingham, Massachusetts Angela F. Gardner, MD, FACEP Assistant Professor, Division of Emergency Medicine, Department of Surgery, University of Texas Medical Branch, Galveston, Texas Daniel Garza, MD Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford; Team Physician, San Francisco 49ers, San Francisco, California Gordon G. Giesbrecht, PhD Professor, Health, Leisure and Human Performance Research Institute; Professor, Department of Anesthesia, University of Manitoba Faculty of Medicine, Winnipeg, Manitoba, Canada

Sue L. Hefle, PhD† Associate Professor, Food Allergy Research and Resource Program, University of Nebraska, Lincoln, Nebraska John P. Heggers, PhD, FAAM, CWS (AAWM) Professor of Surgery (Plastic) (Retired), University of Texas Medical Branch School of Medicine; Director of Clinical Microbiology and Director of Microbiology Research, Shriners Burns Institute, Galveston, Texas David M. Heimbach, MD Professor of Surgery, University of Washington School of Medicine, Seattle, Washington Lawrence E. Heiskell, MD, FACEP, FAAFP Department of Emergency Medicine, Marine Corps Air Ground Combat Center, Robert E. Bush Naval Hospital, Twenty Nine Palms; Director, International School of Tactical Medicine, Palm Springs, California John C. Hendee, PhD Professor Emeritus and Dean (Retired), University of Idaho College of Natural Resources, Moscow, Idaho; Vice President for Science and Education, WILD Foundation, Boulder, Colorado Henry J. Herrmann, DMD, FAGD Private Practice, Falls Church, Virginia †

Deceased.

viii

Contributors

Ronald L. Holle, MS Meteorologist, Holle Meteorology & Photography, Oro Valley, Arizona Renee Y. Hsia, MD, MSc Stanford/Kaiser Emergency Medicine Residency Program, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Franklin R. Hubbell, DO Clinical Professor, University of New England College of Osteopathic Medicine, Biddeford, Maine Steve E. Hudson Deputy Director, Walker County Emergency Management Agency; President, Pigeon Mountain Industries, Inc., LaFayette, Georgia Kenneth V. Iserson, MD, MBA Professor, Department of Emergency Medicine, University of Arizona College of Medicine; Chair, Bioethics Committee and Emergency Physician, University Medical Center; Medical Director, Southern Arizona Rescue Association (SARA); Director, Arizona Bioethics Program, University of Arizona Health Sciences Center, Tuscon, Arizona Michael E. Jacobs, MD United States Coast Guard Licensed Captain; MedSail Founder and Program Director; Medical Director, Vineyard Medical Services, Martha’s Vineyard, Massachusetts Suzanne C. Jensen, MD Emergency Physician, Department of Emergency Medicine, Mills-Peninsula Hospital, Burlingame, California Lee A. Kaplan, MD Clinical Professor (Voluntary), Division of Dermatology, Department of Medicine, University of California, San Diego, School of Medicine; Dermatologist Medical Group, La Jolla, California James W. Kazura, MD Professor of International Health, Medicine and Pathology, Center for Global Health and Diseases, Case Western Reserve University School of Medicine; Professor of Medicine, University Hospitals of Cleveland, Cleveland, Ohio Garry W. Killyon, MD, DDS, FACS Assistant Professor, Department of Surgery, Division of Plastic Surgery, University of Texas Medical Branch; Shriners Burns Hospital, Galveston, Texas Kenneth W. Kizer, MD President and CEO, Medsphere Systems Corporation, Aliso Viejo, California Judith R. Klein, MD, FACEP Assistant Clinical Professor of Medicine, Emergency Services, Department of Medicine, University of California, San Francisco, School of Medicine; San Francisco General Hospital, San Francisco, California

Karen Nolan Kuehl, MD, FACEP Adjunct Assistant Professor, Department of Emergency Medicine, Oregon Health and Science University; Attending Physician, Department of Emergency Medicine, Legacy Good Samaritan Hospital, Portland, Oregon; Attending Physician, Department of Emergency Medicine, St. John’s Hospital, Jackson, Wyoming Peter Kummerfeldt, AD (Rescue and Survival Operations) President, OutdoorSafe, Inc., Colorado Springs, Colorado Carolyn S. Langer, MD, JD, MPH Instructor, Harvard School of Massachusetts

Public

Health,

Boston,

Daniel M. Laskin, DDS, MS Professor and Chairman Emeritus, Department of Oral and Maxillofacial Surgery, Virginia Commonwealth University Schools of Dentistry and Medicine; Professor of Surgery, Department of Oral and Maxillofacial Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia Patrick H. “Rick” LaValla President, ERI International, Olympia, Washington; Director of Operations, All Hands Consulting, Columbia, Maryland; Director, International Search and Rescue Alliance Catherine Yumi Lee, MPH Research Faculty Associate, School of Public Health, New York Medical College, Valhalla, New York Jay Lemery, MD Attending Physician, Department of Emergency Medicine, Weill Medical College of Cornell University; Attending Physician, Department of Emergency Medicine, New York-Presbyterian Hospital, New York, New York Matthew R. Lewin, MD, PhD Assistant Professor of Medicine, Division of Emergency Medicine, Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, California James R. Liffrig, MD, MPH Lieutenant Colonel, U.S. Army Medical Corps; Chief, Department of Family Medicine, Womack Army Medical Center, Fort Bragg, North Carolina Grant S. Lipman, MD Clinical Instructor of Surgery, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Binh T. Ly, MD Associate Clinical Professor, Department of Medicine, University of California, San Diego, School of Medicine; Director, Medical Toxicology Fellowship, UCSD Medical Center, Division of Medical Toxicology, and California Poison Control System–San Diego Division; Associate Director, Emergency Medicine Residency, Department of Emergency Medicine, UCSD Medical Center, San Diego, California

Contributors

ix

Edgar Maeyens, Jr., MD Private Practice in Dermatology and Dermatopathology; Department of Medicine, Division of Dermatology, Bay Area Hospital, Coos Bay, Oregon; Advisory Board Member, Nicholas School of the Environment and Earth Sciences, Marine Laboratory, Duke University, Durham, North Carolina

Jude T. McNally, RPh, DABAT Managing Director, Arizona Poison and Drug Information, University of Arizona, Tucson, Arizona

Swaminatha V. Mahadevan, MD, FACEP, FAAEM Assistant Professor of Surgery/Emergency Medicine; Associate Chief, Division of Emergency Medicine, Department of Surgery; and Medical Director, Stanford University Emergency Department, Stanford University School of Medicine, Stanford, California

James Messenger Lieutenant, Cuyahoga Falls Fire Department, City of Cuyahoga Falls, Cuyahoga Falls, Ohio

Roberta Mann, MD Clinical Associate Professor, Department of Surgery, University of Southern California Keck School of Medicine, Los Angeles; Medical Director, Torrance Memorial Burn Center and Wound Healing Center, Torrance Memorial Medical Center, Torrance, California Rick Marinelli, ND, MAcOM Clinical Professor, National College of Naturopathic Medicine, Oregon College of Oriental Medicine; Clinic Director, Natural Medicine Clinic, Portland, Oregon Ariel Dan Marks, MD, MS, FACEP Director of Quality Improvement, Emergency Department, Sequoia Hospital, Redwood City, California James G. Marks, Jr., MD Professor and Chair, Department of Dermatology, Penn State Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey, Pennsylvania Denise Martinez, MS, RD Clinical Instructor, Division of Nutrition, University of Utah College of Health, Salt Lake City, Utah Michael J. Matteucci, MD Assistant Clinical Professor, Department of Medicine, University of California, San Diego, School of Medicine; Attending Physician, Division of Medical Toxicology and Department of Emergency Medicine, University of California, San Diego, Medical Center; Assistant Residency Director, Department of Emergency Medicine, Naval Medical Center San Diego, San Diego, California

Liran Mendel, MSc Researcher, Heller Institute for Medical Research, Sheba Medical Center, Tel-Hashomer, Israel

Timothy P. Mier, BA, EMT-P Lieutenant and Deputy Fire Marshal, Cuyahoga Falls Fire Department, City of Cuyahoga Falls, Cuyahoga Falls, Ohio James K. Mitchell, PhD Professor of Geography, Rutgers University, Piscataway, New Jersey David G. Mohler, MD Associate Clinical Professor, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, California Richard E. Moon, MD, FACP Professor of Anesthesiology and Associate Professor of Medicine, Duke University School of Medicine; Medical Director, Center for Hyperbaric Medicine and Environmental Physiology; Senior Medical Consultant, Divers Alert Network, Duke University Medical Center, Durham, North Carolina Daniel S. Moran, PhD Department of Physiology and Pharmacology, Tel-Aviv University Sackler School of Medicine, Tel-Aviv; Institute of Military Physiology, Heller Institute for Medical Research, Sheba Medical Center, Tel-Hashomer, Israel Barry Morenz, MD Associate Professor of Clinical Psychiatry, University of Arizona College of Medicine; Medical Staff, Department of Psychiatry, University Medical Center, Tucson, Arizona John A. Morris, Jr., MD Professor of Surgery and Biomedical Informatics, Department of Surgery, Division of Trauma, Vanderbilt University School of Medicine; Director, Division of Trauma and Surgical Critical Care, Department of Surgery, Division of Trauma, Vanderbilt University Medical Center, Nashville, Tennessee

Vicki Mazzorana, MD, FACEP Clinical Assistant Professor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Robert W. Mutch, BA, MSF Consultant, Fire Management Montana

Robert L. McCauley, MD Professor of Plastic and Reconstructive Surgery and Pediatrics, Department of Surgery, University of Texas Medical Branch; Chief, Plastic and Reconstructive Surgery, Shriners Hospital for Children, Galveston, Texas

Arian Nachat, MD Ultrasound Director, Valley Emergency Physicians, Oakland; Undersea and Hyperbaric Fellow, Department of Emergency Medicine; Attending and Clinical Instructor, Long Beach Memorial Medical Center, Long Beach, California

Loui H. (Clem) McCurley Technical Specialist, Alpine Rescue Team, Evergreen, Colorado; Vice President, Pigeon Mountain Industries, Inc., LaFayette, Georgia; Past President, Society of Professional Rope Access Technicians (SPRAT), Wayne, Pennsylvania

Roger J. Nagy, MD Assistant Director, Department of Trauma, Penrose-St. Francis Hospitals; Partner, Colorado Springs Surgical Associates, PC, Colorado Springs, Colorado

Applications,

Missoula,

x

Contributors

Andrew B. Newman, MD, FCCP Adjunct Professor of Medicine, Pulmonary and Critical Care, Stanford University School of Medicine, Stanford; Chairman and Managing Director, Ocean Medicine Foundation, Palo Alto, California

Mark Plotkin, PhD President, Amazon Conservation Team, Arlington, Virginia

Donna L. Nimec, MD Director, Pediatric Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Boston, Massachusetts

William P. Riordan, Jr., MD Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

David A. Nix, MD, PhD Academic and Administrative Follow, Stanford/Kaiser Emergency Medicine Residency Program, and Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Robert C. Roach, PhD Chief, Research Division, Altitude Research Center, University of Colorado at Denver Health Sciences Center, Denver, Colorado

Eric K. Noji, MD, MPH Senior Policy Advisor for Health and National Security, Office of Terrorism Preparedness and Emergency Response, Centers for Disease Control and Prevention, Atlanta, Georgia Donald B. Nolan, MD Clinical Associate Professor of Neurology, University of Virginia School of Medicine, Charlottesville; Attending Physician (Retired), Department of Neurology, Carilion Roanoke Memorial Hospitals, Roanoke, Virginia Robert L. Norris, MD, FACEP Associate Professor of Surgery and Chief, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Bohdan T. Olesnicky, MD, ABEM, ABIM Vice Chairman, Department of Emergency Medicine, Christ Hospital, Jersey City, New Jersey; Instructor, International School of Tactical Medicine, Palm Springs, California Sheryl K. Olson, RN, BSN, CCRN Rotor Wing Flight Nurse, Colorado Springs; Wilderness Medicine and Survival/Safety Instructor, WildernessWise, LLC, Manitou Springs, Colorado Edward J. (Mel) Otten, MD, FACMT Professor of Emergency Medicine and Pediatrics and Director, Division of Toxicology, University of Cincinnati College of Medicine, Cincinnati, Ohio Ketan H. Patel, MD Stanford/Kaiser Emergency Medicine Residency Program, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Sheila B. Reed, MS Partner, InterWorks LLC, Madison, Wisconsin

Martin C. Robson, MD Emeritus Professor, Department of Surgery, University of South Florida College of Medicine, Tampa, Florida Matthew T. Roe, MD, MHS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina Sandra M. Schneider, MD, FACEP Professor and Chair, Department of Emergency Medicine, University of Rochester School of Medicine and Dentistry; Emergency Physician-in-Chief, Department of Emergency Medicine, Strong Memorial Hospital, Rochester, New York Robert B. Schoene, MD Professor of Medicine, Division of Pulmonary, Critical Care Medicine and Physiology, University of California, San Diego, School of Medicine; Program Director, Internal Medicine Residency, Department of Medicine, University of California, San Diego, Medical Center, San Diego, California Jamie Shandro, MD, MPH Assistant Professor, Division of Emergency Medicine, Harborview Medical Center, University of Washington School of Medicine, Seattle, Washington David J. Smith, Jr., MD Juan Bolivar Chair of Surgical Oncology, Professor, and Director, Division of Plastic Surgery, Department of Surgery, University of South Florida College of Medicine; Medical Director, Tampa General Hospital Regional Burn Center, Tampa, Florida

Naresh J. Patel, DO Private Practice, Fort Wayne Allergy and Asthma Consultants, Fort Wayne, Indiana

Alan M. Steinman, MD, MPH Professional Affiliate, Health, Leisure and Human Performance Research Institute, University of Manitoba, Winnipeg, Manitoba, Canada; Rear Admiral (Retired), U.S. Public Health Service, U.S. Coast Guard

Sheral S. Patel, MD Pediatric Infectious Diseases, International Adoption, and Travel Medicine, Coventry, Connecticut

Robert C. Stoffel, BS President and CEO, Emergency Response International, Cashmere, Washington

Timothy F. Platts-Mills, MD Emergency Physician, Department of Emergency Medicine, University of California, San Francisco, Fresno, Medical Education Program, Fresno, California

Jeffrey R. Suchard, MD, FACEP, FACMT Associate Professor of Clinical Emergency Medicine and Director of Medical Toxicology, Department of Emergency Medicine, University of California, Irvine, Medical Center, Orange, California

Contributors Marc F. Swiontkowski, MD Professor and Chair, Department of Orthopaedic Surgery, University of Minnesota Medical School, Minneapolis, Minnesota Julie A. Switzer, MD Assistant Professor, Department of Orthopaedic Surgery, University of Minnesota Medical School, Minneapolis; Director of Geriatric Trauma, Department of Orthopaedic Surgery, Regions Hospital, St. Paul, Minnesota Steve L. Taylor, PhD Professor, Food Allergy Research and Resource Program, University of Nebraska, Lincoln, Nebraska Robert I. Tilling, PhD Senior Research Geologist—Volcanologist (Scientist Emeritus), Volcano Hazards Team, U.S. Geological Survey, Menlo Park, California David A. Townes, MD, MPH, FACEP Associate Professor and Associate Residency Program Director, Division of Emergency Medicine, University of Washington School of Medicine; Founder and Medical Director, AdventureMed, Seattle, Washington Stephen J. Traub, MD Assistant Professor of Medicine, Harvard Medical School; CoDirector, Division of Toxicology, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Karen B. Van Hoesen, MD, FACEP Clinical Professor of Medicine and Director, Undersea and Hyperbaric Medicine Fellowship, Department of Emergency Medicine, University of California, San Diego, School of Medicine, San Diego, California Christopher Van Tilburg, MD Editor, Wilderness Medicine; Medical Committee Member, Mountain Rescue Association John Walden, MD, DTM&H Professor and Associate Dean, Department of Family and Community Health, Marshall University Joan C. Edwards School of Medicine, Huntington, West Virginia

xi

Helen L. Wallace, BS Department of Biology, Portland State University, Portland, Oregon Andrew Wang, MD Associate Professor of Medicine, Division of Cardiovascular Medicine, Duke University School of Medicine, Durham, North Carolina David A. Warrell, MA, DM, DSc, FRCP, FRCPE, FMedSci Emeritus Professor of Tropical Medicine, Nuffield Department of Clinical Medicine, and Honorary Fellow of St. Cross College, University of Oxford; Consultant Physician (Acute General Medicine and Infectious Diseases), Oxford Radcliffe Hospitals NHS Trust, Oxford, United Kingdom Eric A. Weiss, MD, FACEP Assistant Professor, Division of Emergency Medicine, Department of Surgery; Director, Wilderness Medicine Fellowship; and Medical Director, Office of Disaster Planning and Service Continuity, Stanford University School of Medicine, Stanford; Medical Director, Emergency Medical Services, San Mateo County, California Lynn E. Welling, MD Adjunct Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda, Maryland; Assistant Clinical Professor of Medicine, Department of Emergency Medicine, University of California, San Diego, School of Medicine; Staff Emergency Physician, Naval Medical Center San Diego; Staff Emergency Physician, Scripps Mercy Hospital and Medical Center, San Diego; Staff Emergency Physician, Sharps Grossmont Hospital, La Mesa, California James A. Wilkerson III, MD Merced Pathology Medical Group, Inc. (Retired), Merced, California Knox Williams, MS Director (Retired), Colorado Avalanche Information Center, Boulder, Colorado Sarah R. Williams, MD, FACEP Director, Emergency Department Ultrasound, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Foreword More than a decade ago, I had the good fortune to be searching for new species of flowering lianas in the remote jungles of central Suriname. A tropical downpour had just ended, and we wandered through a forest still dripping from the rain shower. The air had become cool and buoyant, perfumed with a panoply of enticing floral scents. Within a few hours of collecting, however, the heat had once again set into the equatorial lowland forest. Members of our small expedition sat down underneath the shade of a large bergibita tree on granitic stones covered with a fine green moss to take a rest in the torpid jungle atmosphere. As I struggled to fish granola out of my waterproof daypack, the botanist accompanying me cursed and jumped to his feet. “Something bit me!” he exclaimed. We searched the site but never found the offending creature. Only two small pinpoints on the skin of his ankle, separated by no more than a couple of millimeters, could scarcely be discerned, nothing remotely commensurate to the pain experienced by my friend. I asked our Indian guide—a shaman of the Trio tribe and a man of few words—what had happened. He replied, “Mwe,” the Trio word for spider. In short order, the botanist became very ill. He became dizzy and dropped to his knees. Delirium set in as he begged for water and crawled into a nearby shallow stream. Nausea set in, accompanied by dry heaves. This famously stoic scientist was reduced to sobbing from the excruciating pain, which seemed to wrack every joint of his body. My first aid kit offered no remedy with which we could be hopeful of improvement. My colleague’s condition steadily deteriorated. Fighting the urge to panic, I tried to determine the best course of action. Should I attempt to move him? Leave him and seek help? We were dozens of miles of trackless jungle away from any Western-trained health care professional or even the most rudimentary pharmaceuticals or supportive care. I was terrified and powerless to help my friend. I felt a presence and looked up from my incapacitated colleague onto the stream bank. There sat the medicine man, serenely surveying the scene with calm, knowing eyes. I had hired him to teach us the indigenous names of the plants we were collecting, never anticipating that we might need his healing services as well. Working in the Amazon as an ethnobotanist for 20 years, I have developed an immense respect for the traditional knowledge of these ancient healers. I asked the shaman if my ailing colleague would die. The Indian grunted as he pointed his chin at the botanist. “Not going to die,” he said, in his language. “Going to suffer, but not die.” His words began to lift my weight of concern, but were soon contradicted by the pitiful cries and moans of my colleague. “Well,” I urgently asked, “do you know of any therapies that can help him?”

“Yes,” he nodded, standing up from his resting place on the ground and brushing coarse sand off his red breechcloth. “Give me your machete.” He took the knife and disappeared into the bush. About three minutes later, he returned with two meters of a dull brown liana stem from the Philodendron family. The medicine man walked into the stream, turned the botanist onto his back, sliced the liana into four pieces and carefully let the liana sap drip onto the bite marks on the victim’s ankles. In less than 10 minutes, our patient felt well enough to sit up. His dizziness and nausea had diminished substantially. Within a half-hour, we were able to help him back to camp, where he spent the rest of the day recuperating in his hammock. He dozed fitfully for most of the afternoon, awoke in time to eat a hearty dinner by the campfire, and then slept through the night. By the next morning, he seemed back to normal. This episode is likely how most of wilderness medicine was originally practiced and how, in more than a few remote corners of the world, it is still practiced today. For most of human history and prehistory, there was not a significant presence of doctors, validated drugs, or hospitals. There were, of course, healers (e.g., shamans, herbalists, bonesetters) and remedies (usually plants, but also other substances ranging from molds to insects to honey to soils); these evolved from trial and error to our current scientific approach. So it was a supreme irony when Paul Auerbach and his colleagues coalesced the field of Wilderness Medicine two and a half decades ago—clearly a case of back to the future! In my world of ethnobotany, work and adventure carry me far from medical security. I have the good fortune to work in remote places where much of Western medicine has never been available. This is not thrill seeking—it is my professional calling. For large portions of my life, I live in the wilderness. Thus, I regularly witness the practice of wilderness medicine. It is at once remarkable and frightening—remarkable in the sense that indigenous healers know so many things from which we could derive enormous benefit and frightening because their medicine is laden with empiricism, mysticism, and lack of what we would consider detailed scientific substantiation. Some would call it “primitive,” but that shouldn’t be taken to mean it is incorrect. In fact, time and time again, as in the case of the spider bite, I have seen it heal. In an age in which medicine becomes increasingly specialized and enhanced by technology, I like to think of practitioners of wilderness medicine as masters of “Renaissance medicine.” They must be willing to abandon urban trappings and tools to get “down and dirty.” Furthermore, they must know much more than they learned in medical school. If you are in a mountaineering accident, do you want the first healer on the scene to be a doctor whose expertise is confined to cancer? If you fall out of a tree and break your bones, do you want the first responder to be someone who has never attended a fracture?

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When my wife was bitten by a copperhead snake in Virginia several years ago, she was taken by ambulance to a major, wellequipped suburban hospital. The good news was that she had no end of doctors eager to examine her. The bad news was that none of them had ever treated or even seen a snakebite, hence their interest in having a look! I was able to track down Paul Auerbach, who talked the treating physician through the necessary treatment. I had known enough to turn to my friend from the Wilderness Medical Society. Where else in the medical world can you consistently find people adept at treating victims of snakebite, frostbite, lightning strikes, volcanic eruptions, and scorpion envenomation? This is not to argue that wilderness medicine is restricted solely to treating obscure afflictions or problems of the past. The marriage of traditional wisdom with cutting edge science offers new and important potential for better treatment of everything from high-altitude pulmonary and cerebral edema to

heat stroke. These new approaches may incorporate everything from wisdom of local peoples to biodesign of novel medical devices. Remember that doctors now place leeches on healing wounds, which is more effective than drugs designed by modeling proteins with computers. We live in an interesting epoch in which our societies are increasingly urban and technology oriented. Yet, something in our souls yearns for regular and sustained contact with the wonders of Mother Nature. The demand for ecotourism is expanding at an astounding rate. Doctors, nurses, and other health care providers simply must know what to do when confronted by the inevitable afflictions that result from our species’ collisions with the natural world. Mark J. Plotkin, PhD Amazon Conservation Team www.amazonteam.org

Preface I am very excited to present this fifth edition of Wilderness Medicine, which supports a phase of tremendous growth and excitement in the discipline. As man extends into remote reaches of the globe and large populations encounter environmental changes at an ever-increasing rate, this medicine of exploration, adventure, travel, and disaster response has become indispensable. Although much of the medicine practiced in remote areas or under environmental extremes is emergency in nature, and local conditions and considerations by necessity dominate, the field of wilderness medicine has advanced beyond the exciting rescues of extreme alpinists and survivalists. It has expanded in scope to include the practice of medicine in situations of constrained resources, during times of catastrophe, and often in impoverished countries. In noble responses to events that generate urgent and profound medical needs, practitioners skilled in wilderness medicine have become rescuers and leaders noted for their resourcefulness and rugged practicality. Because humans continually try to dominate the landscape in their disregard for the environment and fellow man, nature is the force with which we must constantly reckon. All major hazards ultimately involve the power and energy of mighty winds, harsh solar radiation, extreme cold, and the like. I am particularly gratified that wilderness medicine is a discipline on the verge of becoming a specialty, on its own and possessed of profound relevance. Wilderness medicine is advanced in basic science laboratories and by academicians who witness their efforts translated under harsh field conditions within hazardous wilderness areas above, upon, and under every natural surface on Earth, and soon, in space. We might investigate the application of protein kinase inhibition to treat reperfusion injury in the mitochondria of endothelial cells, then find willing volunteers on expeditions to investigate its application for prevention and treatment of frostbite. Curiosity about the stinging mechanism of jellyfish, combined with observation of clownfish protected with a host anemone, leads to clinical trials in which volunteers demonstrate the efficacy of a topical jellyfish sting inhibitor. Drugs designed to treat hypertension and sexual dysfunction are evaluated for potency in the prevention and treatment of high altitude pulmonary edema. Cooling devices designed for elite athletes may save the lives of firefighters. On mountaintops, within jungle canopies, and in arid canyonlands, we seek to understand the forces of pressure, temperature, and weather, so that we may enjoy better health and safer journeys. The growth of wilderness medicine as a field of study and practice is remarkable only with respect to the brief history of the term. When Ed Geehr, Ken Kizer, and I dreamed up the Wilderness Medical Society, it was not a brainstorm, but an obvious response to pent-up demand. There are innumerable physicians, allied health professionals, rescuers, and laypersons dedicated by profession and avocation to wilderness environments. The current status of wilderness medicine is characterized by increasing interest from the medical community as

structure is imposed on persons and institutions possessing expertise. Wilderness medicine is now well established, so training programs are being tailored to correspond to the educational level and certifications of trainees and practitioners. However, as we attempt to apply urban standards of hygiene and health to every environment in which man has a consistent presence, wilderness medicine must never lose sight of its origin in the medical concerns existing in true wilderness territories. Herein lies the essential nature and appeal of the specialty. Is wilderness medicine important in an age of widespread communicable disease and potential pandemics? How many people are victims of shark attacks versus how many persons suffer from diabetes? How many climbers reach the Seven Summits versus how many elders are stricken with congestive heart failure? How many children fall prey to high altitude pulmonary edema versus how many infants acquire HIV from their mothers? The inquisitive mind seeks not to partition what we learn from our test tubes and urban patients, but to constantly integrate and extrapolate. I am thoroughly convinced that wilderness medicine supports some of the most practical education and skills acquisition in the health care profession. Medicine and its science are intricate, so what is learned in one venue is commonly applicable across a wide spectrum of human disease. We owe it to our hearts and minds to pursue every aspect of medicine that challenges our imaginations and ingenuity. As an additional benefit, it is a joy to observe a healer normally bound to an urban existence lifted in spirit by recognition that medicine applies equally well to adventure, travel, and discovery. Furthermore, while wilderness medicine was not conceived solely to be medicine in the absence of customary resources, it has to a certain extent evolved that way. Wilderness medicine is not practiced in wilderness hospitals, but in the field—not on paved pathways, but in forests, at base camp, and on the beach. We will advance the science, increase the teaching, and improve the practice of wilderness medicine. Even while wilderness medicine is often practiced solo, it brings people together, bonded by their community of search and rescue, medicine, and love of the outdoors. We will reach out in public health and service related to wilderness medicine. Many global health issues are in part within the purview of wilderness medicine. In response to these, and other, scourges of mankind, practitioners of wilderness medicine will bring their expertise to bear on developing sensible solutions that can actually be implemented. Injury prevention will have its day in a more concerted effort to make the outdoors safe for those who choose or need to enter it. In this new age of medicine, when diagnostics and therapeutics in the hospital have evolved to molecular and nano methods, what is the impact of technology on wilderness medicine? At the true wilderness level, not much. Technology can mitigate risk only to a certain degree. In the field, there is not yet computed tomography or magnetic resonance imaging, and I do not foresee a wilderness intensive care unit, notwithstand-

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ing the space station. Perhaps when we have miniaturized everything, we will occasionally interpret ultrasounds and read brain waves on mountains and glaciers, but that will not change the essence of making do when all you have is your senses and courage. So, downstream wilderness medicine is very hands-on and frequently improvisational. One need only consider what was valuable in the wake of recent tidal waves, hurricanes, mudslides, and earthquakes to appreciate our increasing need for people who practice medicine with very little on short notice under extreme environmental stress. Much in this volume is new and enhanced. In deference to current political conflicts that are perpetrated in rugged environments, it has become appropriate to introduce concepts related to the military, so that medics are familiar with considerations of tactics. Because astronauts seek to expand their boundaries, unique medical concerns of this new wilderness are once again part of the discussion. Competitive athletes take their marathons, races, and survival events farther into the backcountry, so there is new emphasis on adventure sports and the medicine necessary to support them. When the first edition of this book was published, my colleagues and I dove, climbed, soared, and trekked with impunity. These days, our lungs and limbs talk back to us, and we appreciate the opportunities for contemplation as much as challenges. Who among us will not grow older or develop functional limitations? The wilderness is for everyone and should not be limited to only the hardiest and most intrepid. Therefore, I have added chapters on pre-existing conditions, chronic illnesses, and persons with disabilities. More in-depth coverage of “traditional” wilderness medicine topics, such as acclimatization, natural hazards, search and rescue, and poisonous and venomous creatures is ably provided by a very dedicated group of experts. To allow sufficient space

for all the upgrades, the references have been moved to an accompanying DVD-ROM. As in previous editions, I am greatly indebted to my remarkable wife Sherry and children, Brian, Lauren, and Dan; to all of the tireless contributors; and to the supportive and gracious Todd Hummel, Jennifer Shreiner, and Michael Goldberg at Elsevier. I practice and preach wilderness medicine with passion—for medicine, for my patients, for my colleagues, and for the wilderness. I am perpetually amazed by remarkable tales of adversity, endurance, rescue, faith, the will to live, and the indomitable human spirit. That is most fitting for the setting in which these events occur, for at most times in the wilderness, we are able to appreciate everything that is natural and wonderful upon this Earth. As you peruse this book, take a few moments to reflect upon the images of the wilderness that grace the opening of the sections. Whether you stand before a majestic mountain, descend into a vast blue ocean, walk softly through a coniferous forest, or lie in a misty moonlit meadow and count shooting stars, you are at peace. Imagine the soothing sounds of a river, the caress of a snowflake, or the penetrating warmth of a desert rock. Wilderness is our greatest blessing, for it exists to support life, yet bestows uncommon beauty. We may manipulate and seek to conquer our environment, but in the end, it is always we who must adapt to the forces of nature. Wilderness medicine, then, exists on the premise that humans will encounter forces beyond their control. As we learn to keep ourselves healthy and whole in the outdoors, we come to appreciate the essences of healing and renewal. In medicine, there is service to the living. In wilderness medicine, there is service to humankind and our precious habitat. Paul S. Auerbach, MD, MS

Photo credits for cover images and section openers Cover: Polar Touch, Manitoba, photo by Tim Floyd, MD; Thomserku Silouette, photo by Lanny Johnson; clownfish on shipwreck, Truk Lagoon, Federated States of Micronesia, photo by Ian Jones, MD; barrier reef, south of Papua New Guinea, photo by Ian Jones, MD; sandstorm, Sossusvlei Sand Dunes, Namibia, photo by Cyril Mazansky, MD; White Mountains, New Hampshire, photo by Tim Floyd, MD; Yosemite, photo by Mathias Schar, MD. Section One (page 1): Exum Ridge, photo by Lanny Johnson; Inca Trail, photo by Paul Auerbach, MD. Section Two (page 109): Sandstorm, Sossusvlei Sand Dunes, Namibia, photo by Cyril Mazansky, MD; Black and White or Not, photo by Gordon Giesbrecht, PhD. Section Three (page 285): Emerald Pool, photo by Lanny Johnson. Section Four (page 399): Helicopter rappel at Mt. Moran, photo by Lanny Johnson; moon over Ama Dablam, photo by Lanny Johnson. Section Five (page 693): View of Ama Dablam from Kunde, photo by Lanny Johnson; Salt Flats, photo by Daniel Ryan, MD. Section Six (page 891): Coastal brown bear sow and cubs enjoy a salmon meal at McNeil River, Alaska, photo by Luanne Freer, MD; tundra wolf, photo by Donna Nayduch, RN, MSN, ACNP (www.wolfsanctuary.net). Section Seven (page 1251): Flower, photo by Daniel Ryan, MD; Germany (leaves), photo by Mathias Schar, MD. Section Eight (page 1367): Havasupai, photo by Mathias Schar, MD. Section Nine (page 1567): Squid eye, photo by Paul Auerbach, MD; oceanic whitetip shark, Kona, Hawaii, photo by Marty Snyderman. Section Ten (page 1807): Crystal Crag from Mammoth Crest, photo by Mathias Schar, MD; Yosemite, photo by Mathias Schar, MD. Section Eleven (page 1893): White Mountains, New Hampshire, photo by Tim Floyd, MD; Khunde camp, photo by Lanny Johnson. Section Twelve (page 1985): Climber on Middle Grand, photo by Lanny Johnson; Aurora Borealis, Manitoba, photo by Tim Floyd, MD. Section Thirteen (page 2183): Golden eagle, Idaho, photo by Tim Floyd, MD; Death Canyon, Grand Teton National Park, photo by Tim Floyd, MD.

1

High-Altitude Medicine Peter H. Hackett and Robert C. Roach

Millions of people visit recreation areas above 2400 m in the American West each year. Hundreds of thousands visit central and south Asia, Africa, and South America, many traveling to altitudes over 4000 m.311 In addition, millions live in large cities above 3000 m in South America and Asia. The population in the Rocky Mountains of North America has doubled in the past decade. Increasingly, physicians and other health care providers are confronted with questions of prevention and treatment of high-altitude medical problems (Box 1-1) as well as the effects of altitude on preexisting medical conditions. Despite advances in high-altitude medicine, significant morbidity and mortality persist (Table 1-1). Clearly, better education of the population at risk and of those advising them is essential. This chapter reviews the basic physiology of ascent to high altitude, as well as the pathophysiology, recognition, and management of medical problems associated with high altitude. The clinical issues likely to be encountered in lowlanders visiting high-altitude locations are emphasized, and medical problems of people living at high altitude are discussed (see Box 1-1).


DEFINITIONS High Altitude (1500 to 3500 m*) The onset of physiologic effects of diminished inspiratory oxygen pressure (Pio2) includes decreased exercise performance and increased ventilation (lower arterial Pco2) (Box 1-2). Minor impairment exists in arterial oxygen transport (arterial oxygen saturation [Sao2] at least 90%), but arterial Po2 is significantly diminished. Because of the large number of people who ascend rapidly to 2500 to 3500 m, high-altitude illness is common in this range (Table 1-2, and see Table 1-1).

Very High Altitude (3500 to 5500 m) Maximum Sao2 falls below 90% as the arterial Po2 falls below 60 mm Hg (Table 1-3 and Fig. 1-1). Extreme hypoxemia may occur during exercise, during sleep, and in the presence of highaltitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.

Extreme Altitude (above 5500 m) Marked hypoxemia, hypocapnia, and alkalosis are characteristic of extreme altitudes. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no *To convert meters to feet, multiply meters × 3.2808. To convert feet to meters, multiply feet × .3048.

2

permanent human habitation occurs above 5500 m. A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude illness.


ENVIRONMENT AT HIGH ALTITUDE

Barometric pressure falls with increasing altitude in a logarithmic fashion (see Table 1-2). Therefore, the partial pressure of oxygen (21% of barometric pressure) also decreases, resulting in the primary insult of high altitude: hypoxia. At approximately 5800 m, barometric pressure is one-half that at sea level, and on the summit of Mt. Everest (8848 m), the Pio2 is approximately 28% that at sea level (see Figure 1-1 and Table 1-2). The relationship of barometric pressure to altitude changes with the distance from the equator. Thus, polar regions afford greater hypoxia at high altitude in addition to extreme cold. West467 has calculated that the barometric pressure on the summit of Mt. Everest (27° N latitude) would be about 222 mm Hg instead of 253 mm Hg if Everest were located at the latitude of Mt. McKinley (62° N). Such a difference, he claims, would be sufficient to render an ascent without supplemental oxygen impossible. In addition to the role of latitude, fluctuations related to season, weather, and temperature affect the pressure–altitude relationship. Pressure is lower in winter than in summer. A lowpressure trough can reduce pressure 10 mm Hg in one night on Mt. McKinley, making climbers awaken “physiologically higher” by 200 m. The degree of hypoxia is thus directly related to the barometric pressure, not solely to geographic altitude.467 Temperature decreases with altitude (an average of 6.5° C per 1000 m [3.6° F per 1000 ft]), and the effects of cold and hypoxia are generally additive in provoking both cold injuries and highaltitude pulmonary edema.351,462 Ultraviolet light penetration increases approximately 4% per 300-m gain in altitude, increasing the risk of sunburn, skin cancer, and snowblindness. Reflection of sunlight in glacial cirques and on flat glaciers can cause intense radiation of heat in the absence of wind. The authors have observed temperatures of 40° to 42° C (104° to 108° F) in tents on both Mt. Everest and Mt. McKinley. Heat problems, primarily heat exhaustion, are often unrecognized in this usually cold environment. Physiologists have not yet examined the consequences of heat stress or rapid, extreme changes in environmental temperature combined with the hypoxia of high altitude.

Chapter 1: High-Altitude Medicine Above the snow line is the “high-altitude desert,” where water can be obtained only by melting snow or ice. This factor, combined with increased water loss through the lungs from increased respiration and through the skin, commonly results in dehydration that may be debilitating. Thus, the high-altitude environment imposes multiple stresses, some of which may contribute to or be confused with the effects of hypoxia.

BOX 1-1. Medical Problems of High Altitude LOWLANDERS ON ASCENT TO HIGH ALTITUDE

Acute hypoxia High-altitude headache Acute mountain sickness High-altitude cerebral edema Cerebrovascular syndromes High-altitude pulmonary edema High-altitude deterioration Organic brain syndrome Peripheral edema Retinopathy Disordered sleep Sleep periodic breathing High-altitude pharyngitis and bronchitis Ultraviolet keratitis (snowblindness) Exacerbation of preexisting conditions

3


ACCLIMATIZATION TO HIGH ALTITUDE

Rapid ascent from sea level to the altitude at the summit of Mt. Everest (8848 m) causes loss of consciousness in a few minutes and death shortly thereafter. Yet climbers ascending Mt. Everest over a period of weeks, without supplemental oxygen, have experienced only minor symptoms of illness. The process by which individuals gradually adjust to hypoxia and enhance survival and performance is termed acclimatization. A complex series of physiologic adjustments increases oxygen delivery to cells and also improves their hypoxic tolerance. The severity

BOX 1-2. Glossary of Physiologic Terms PB Po2 Pio2

LIFE-LONG OR LONG-TERM RESIDENTS OF HIGH ALTITUDE

Chronic mountain sickness (chronic mountain polycythemia) High-altitude pulmonary hypertension, with or without right heart failure Problems of pregnancy: preeclampsia, hypertension, and low-birth-weight infants Exacerbation of common illnesses, such as lung disease

Barometric pressure* Partial pressure of oxygen Partial pressure of inspired oxygen (0.21 × [PB − 47 mm Hg]) (47 mm Hg = vapor pressure of H2O at 37° C) Po2 in alveolus Pco2 in alveolus Po2 in arterial blood Pco2 in arterial blood Arterial oxygen saturation (HbO2 ÷ total Hb × 100) Respiratory quotient (CO2 produced ÷ O2 consumed) PAo2 = Pio2 − (PAco2/R)

PAo2 PAco2 Pao2 Paco2 Sao2% R Alveolar gas equation

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

TABLE 1-1. Incidence of Altitude Illness in Various Groups

STUDY GROUP Western State Visitors Mt. Everest Trekkers Mt. McKinley Climbers Mt. Rainier Climbers Mt. Rosa, Swiss Alps Indian Soldiers Aconcagua Climbers

MAXIMUM ALTITUDE REACHED (m)

AVERAGE RATE OF ASCENT*

3500

1–2

15,000

~2000 ~2500 ~≥3000 3000–5200

5500

1200

3000–5300

6194

1–2 (fly in) 10–13 (walk in) 3–7

18–20 22 27–42 47 23 30–50 30

4392

1–2

2850 4559 3000–5500

2850 4559 5500

3300–5800

6962

NUMBER AT RISK PER YEAR

SLEEPING ALTITUDE (m)

30 million

10,000 †

Unknown 4200

3000

PERCENT WITH HAPE AND/OR HACE

REFERENCES

0.01

183

1.6 0.05 2–3

155 — 321 147

67

—

250

1–2 2–3 1–2

7 27

— 5 2.3–15.5

273 83, 273, 401 420, 421

2–8

39 (LLS > 4)

2.2

341

PERCENT WITH AMS

†

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

PART ONE: MOUNTAIN MEDICINE

m Sea level 1,000 1,219 1,500 1,524 1,829 2,000 2,134 2,438 2,500 2,743 3,000 3,048 3,353 3,500 3,658 3,962 4,000 4,267 4,500 4,572 4,877 5,000 5,182 5,486 5,500 5,791 6,000 6,096 6,401 6,500 6,706 7,000 7,010 7,315 7,500 7,620 7,925 8,000 8,230 8,500 8,534 8,839 8,848 9,000 9,144 9,500 10,000

ft

PB

PIO2

Sea level 3,281 4,000 4,921 5,000 6,000 6,562 7,000 8,000 8,202 9,000 9,843 10,000 11,000 11,483 12,000 13,000 13,123 14,000 14,764 15,000 16,000 16,404 17,000 18,000 18,045 19,000 19,685 20,000 21,000 21,325 22,000 22,966 23,000 24,000 24,606 25,000 26,000 26,247 27,000 27,887 28,000 29,000 29,029 29,528 30,000 31,168 32,808

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

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

FIO2 AT SL 0.209 0.185 0.180 0.174 0.174 0.167 0.164 0.161 0.155 0.154 0.149 0.144 0.143 0.137 0.135 0.132 0.126 0.126 0.121 0.117 0.116 0.111 0.109 0.107 0.102 0.102 0.098 0.095 0.093 0.089 0.088 0.085 0.081 0.081 0.077 0.075 0.074 0.070 0.069 0.067 0.064 0.064 0.060 0.060 0.059 0.057 0.054 0.049

*Barometric pressure is approximated by the equation PB = Exp(6.6328 − {0.1112 × altitude − [0.00149 × (altitude2)]}), where altitude = terrestrial altitude in meters/1000, or km. Pio2 is calculated as (PB − 47) (where 47 = water vapor pressure at body temperature) × fraction of O2 in inspired air. The equivalent Fio2 at sea level for a given altitude is calculated as Pio2 ÷ (760 − 47). Substituting ambient PB for 760 in the equation allows similar calculations for Fio2 at different altitudes. Exp, Exponent. Meters = feet × .3048. Feet = meters × 3.2808.

SaO2

160

100

140

90 PIO2

120

80

100 80

70

SaO2 (%)

TABLE 1-2. Altitude Conversions Barometric Pressure (PB), Estimated Partial Pressure Inspired Oxygen (PIO2), and the Equivalent Oxygen Concentration at Sea Level (FIO2 at SL)*

Partial pressure oxygen (mm Hg)

4

PaO2

60

60 40 20 0

2000

760

590

4000

6000

50 8000 10000

Altitude (m) 460

306

277

215

Barometric pressure (mm Hg)

Figure 1-1. Increasing altitude results in a decrease in inspired PO2 (PIO2), arterial PO2 (Pao2), and arterial oxygen saturation (SaO2). Note that the difference between PIO2 and PaO2 narrows at high altitude because of increased ventilation, and that SaO2 is well maintained while awake until over 3000 m. (Data from Morris A: Clinical pulmonary function tests: A manual of uniform lab procedures.Intermountain Thoracic Society,1984,and Sutton JR,Reeves JT,Wagner PD,et al: Operation Everest II: Oxygen transport during exercise at extreme simulated altitude. J Appl Physiol 64:1309–1321, 1988, with permission.)

of hypoxic stress, rate of onset, and individual physiology determine whether the body successfully acclimatizes or is overwhelmed. Individuals vary in their ability to acclimatize, no doubt reflecting certain genetic polymorphisms. Some adjust quickly, without discomfort, whereas acute mountain sickness (AMS) develops in others, who go on to recover. A small percentage of people fail to acclimatize even with gradual exposure over weeks. The tendency to acclimatize well or to become ill is consistent on repeated exposure if rate of ascent and altitude gained are similar, supporting the notion of important genetic factors. Successful initial acclimatization protects against altitude illness and improves sleep. Longer-term acclimatization (over weeks) primarily improves aerobic exercise ability. These adjustments disappear at a similar rate on descent to low altitude. A few days at low altitude may be sufficient to render a person susceptible to altitude illness on re-ascent, especially high-altitude pulmonary edema (HAPE). The improved ability to do physical work at high altitude, however, persists for weeks.268 People who live at high altitude during growth and development appear to realize the maximum benefit of acclimatization changes; for example, their exercise performance matches that of persons at sea level.312

Ventilation By reducing alveolar carbon dioxide, increased ventilation raises alveolar oxygen, improving oxygen delivery (Fig. 1-2, and see Figure 1-1). This response starts at an altitude as low as 1500 m (Pio2 = 124 mm Hg; see Table 1-2) and within the first few minutes to hours of high-altitude exposure. The carotid body, sensing a decrease in arterial Po2, signals the central res-

Chapter 1: High-Altitude Medicine

5

TABLE 1-3. Blood Gases and Altitude POPULATION Altitude residents* Acute exposure†

Chronic exposure during Operation Everest II‡ Acclimatized subjects studied during acute exposure to the simulated summit of Everest§

ALTITUDE (m)

ALTITUDE (ft)

PB (mm Hg)

PaO2 (mm Hg)

SaO2 (%)

1,646 2,810 3,660 4,700 5,340 6,140 6,500 7,000 8,000 8,848 8,848

5,400 9,200 12,020 15,440 17,500 20,140 21,325 22,966 26,247 29,029 29,029

630 543 489 429 401 356 346 324 284 253 253

73.0 (65.0–83.0) 60.0 (47.4–73.6) 47.6 (42.2–53.0) 44.6 (36.4–47.5) 43.1 (37.6–50.4) 35.0 (26.9–40.1) 41.1 ± 3.3 — 36.6 ± 2.2 30.3 ± 2.1 30.6 ± 1.4

95.1 (93.0–97.0) 91.0 (86.6–95.2) 84.5 (80.5–89.0) 78.0 (70.8–85.0) 76.2 (65.4–81.6) 65.6 (55.5–73.0) 75.2 ± 6 — 67.8 ± 5 58 ± 4.5 —

PaCO2 (mm Hg) 35.6 33.9 29.5 27.1 25.7 22.0

(30.7–41.8) (31.3–36.5) (23.5–34.3) (22.9–34.0) (21.7–29.7) (19.2–24.8) 20 ± 2.8 — 12.5 ± 1.1 11.2 ± 1.7 11.9 ± 1.4

Data are mean values and (range) or ±SD, where available. All values are for subjects of age 20 to 40 years who were acclimatizing well. *Data from reference 265. † Data from reference 293. ‡ Data from reference 434. § Data from reference 360.

12

10

.

VE (L/min, BTPS)

14

8 PACO2 (mm Hg)

40

35

30

25

SaO2 (%)

100

90

80

0 1 Denver

2

3

4

5

Days at 4300 m

. Figure 1-2. Change in minute ventilation (VE), alveolar carbon dioxide (PACO2), and arterial oxygen saturation (SaO2) during 5 days’ acclimatization to 4300 m. BTPS, Body temperature, ambient pressure, saturated with water vapor. (Modified from Huang SY, Alexander JK, Grover RF, et al: J Appl Physiol 56:602–606, 1984, with permission.)

piratory center in the medulla to increase ventilation. This carotid body function (hypoxic ventilatory response, or HVR) is genetically determined464 but influenced by a number of extrinsic factors. Respiratory depressants such as alcohol and soporifics, as well as fragmented sleep, depress the HVR. Agents that increase general metabolism, such as caffeine and coca, as well as specific respiratory stimulants, such as progesterone242 and almitrine,159 increase the HVR. (Acetazolamide, a respiratory stimulant, acts on the central respiratory center rather than on the carotid body.) Physical conditioning apparently has no effect on the HVR. Numerous studies have shown that a good ventilatory response enhances acclimatization and performance and that a very low HVR may contribute to illness363 (see Acute Mountain Sickness, and High-Altitude Pulmonary Edema). However, over a normal range of values, the HVR is not a reliable predictor of susceptibility to altitude illness. Other factors influence ventilation on ascent to high altitude. As ventilation increases, hypocapnia produces alkalosis, which acts as a braking mechanism on the central respiratory center and limits a further increase in ventilation. To compensate for the alkalosis, within 24 to 48 hours of ascent the kidneys excrete bicarbonate, decreasing the pH toward normal; ventilation increases as the negative effect of the alkalosis is removed. Ventilation continues to increase slowly, reaching a maximum only after 4 to 7 days at the same altitude (see Figure 1-2). The plasma bicarbonate concentration continues to drop and ventilation to increase with each successive increase in altitude. People with lower oxygen saturation at altitude have higher serum bicarbonate values; whether the kidney might be limiting acclimatization or whether this reflects poor respiratory drive is not clear.86 This process is greatly facilitated by acetazolamide (see Acetazolamide Prophylaxis). The paramount importance of hyperventilation is readily apparent from the following calculation: the alveolar Po2 on the summit of Mt. Everest (about 33 mm Hg) would be reached at only 5000 m if alveolar Pco2 stayed at 40 mm Hg, limiting an

6

PART ONE: MOUNTAIN MEDICINE

ascent without supplemental oxygen to near this altitude. Table 1-3 gives the measured arterial blood gases resulting from acclimatization to various altitudes.

Circulation The circulatory pump is the next step in the transfer of oxygen, moving oxygenated blood from the lungs to the tissues.

Systemic Circulation Increased sympathetic activity on ascent causes an initial mild increase in blood pressure, a moderate increase in heart rate and cardiac output, and an increase in venous tone. Stroke volume is low because of decreased plasma volume, which drops as much as 12% over the first 24 hours478 as a result of the bicarbonate diuresis, a fluid shift from the intravascular space, and suppression of aldosterone.30 Resting heart rate returns to near sea level values with acclimatization, except at extremely high altitude. Maximal heart rate follows the decline in maximal oxygen uptake with increasing altitude. As the limits of hypoxic acclimatization are approached, maximal and resting heart rates converge. During Operation Everest II (OEII), cardiac function was appropriate for the level of work performed and cardiac output was not a limiting factor for performance.349,431 Interestingly, myocardial ischemia at high altitude has not been reported in healthy persons, despite extreme hypoxemia. This is partly because of the reduction in myocardial oxygen demand from reduced maximal heart rate and cardiac output. Pulmonary capillary wedge pressure is low, and catheter studies have shown no evidence of left ventricular dysfunction or abnormal filling pressures in humans at rest.140,207 On echocardiography, the left ventricle is smaller than normal because of decreased stroke volume, whereas the right ventricle may become enlarged.431 The abrupt increase in pulmonary artery pressure can cause a change in left ventricular diastolic function, but because of compensatory increased atrial contraction, no overt diastolic dysfunction results.5 In trained athletes doing an ultramarathon, the strenuous exercise at high altitude did not result in left ventricular damage; however, wheezing, reversible pulmonary hypertension, and right ventricular dysfunction occurred in a third of those completing the race and resolved within 24 hours.91

Pulmonary Circulation A prompt but variable increase in pulmonary vascular resistance occurs on ascent to high altitude as a result of hypoxic pulmonary vasoconstriction, which increases pulmonary artery pressure. Mild pulmonary hypertension is greatly augmented by exercise, with pulmonary pressure reaching near-systemic values,140 especially in people with a previous history of highaltitude pulmonary edema.27,93 During OEII, Groves and colleagues140 demonstrated that even when associated with a mean pulmonary artery pressure of 60 mm Hg, cardiac output remained appropriate and right atrial pressure did not rise above sea level values. Thus, right ventricular function was intact in spite of extreme hypoxemia and pulmonary hypertension. Administration of oxygen at high altitude does not completely restore pulmonary artery pressure to sea level values, an indication that increased pulmonary vascular resistance does not result solely from hypoxic vasoconstriction.274 The explanation is likely to be vascular remodeling with medial hypertrophy. See Stenmark and colleagues for an excellent review of molecular and cellular mechanisms of the pulmonary vascular

response to hypoxia, including remodeling.427 Pulmonary vascular resistance returns to normal within days to weeks after descent to low altitude.

Cerebral Circulation Cerebral oxygen delivery is the product of arterial oxygen content and cerebral blood flow (CBF) and depends on the net balance between hypoxic vasodilation and hypocapnia-induced vasoconstriction. CBF increases, despite the hypocapnia, when Pao2 is less than 60 mm Hg (altitude greater than 2800 m). In a classic study, CBF increased 24% on abrupt ascent to 3810 m and then returned to normal over 3 to 5 days.412 More recent studies have shown considerable individual variation39,41,218 and also an impairment of cerebral autoregulation.216,260,450 The individual variation in cerebral blood flow is linked to individual variation in the ventilatory response to hypoxia.2 Regional brain tissue oxygenation assessed by near-infrared spectroscopy reveals mild tissue hypoxia.165,212,388 Overall, global cerebral metabolism is well maintained with moderate hypoxia.87,304

Blood Hematopoietic Responses to Altitude

Ever since the observation in 1890 by Viault453 that hemoglobin concentration was higher than normal in animals living in the Andes, scientists have regarded the hematopoietic response to increasing altitude as an important component of the acclimatization process. On the other hand, hemoglobin concentration apparently has no relationship to susceptibility to high-altitude illness on initial ascent, although this has not been adequately studied. In response to hypoxemia, erythropoietin is secreted and stimulates bone marrow production of red blood cells.409 The hormone is detectable within 2 hours of ascent, nucleated immature red blood cells can be found on a peripheral blood smear within days, and new red blood cells are in circulation within 4 to 5 days. Over a period of weeks to months, red blood cell mass increases in proportion to the degree of hypoxemia. Iron supplementation can be important: women who take supplemental iron at high altitude approach the hematocrit values of men at altitude169 (Fig. 1-3). The increase in hemoglobin concentration seen 1 to 2 days after ascent is due to hemoconcentration secondary to decreased plasma volume, rather than a true increase in red blood cell mass. This results in a higher hemoglobin concentration at the cost of decreased blood volume, a tradeoff that might impair exercise performance. Longer-term acclimatization leads to an increase in plasma volume as well as in red blood cell mass, thereby increasing total blood volume. Overshoot of the hematopoietic response causes excessive polycythemia, which may actually impair oxygen transport because of increased blood viscosity. Although the “ideal” hematocrit at high altitude is not established, phlebotomy is often recommended when hematocrit values exceed 60% to 65%. During the American Medical Research Expedition to Mt. Everest (AMREE), hematocrit was reduced by hemodilution from 58% ± 1.3% to 50.5% ± 1.5% at 5400 m with no decrement in maximal oxygen uptake and an increase in cerebral functioning.393

Oxyhemoglobin Dissociation Curve The oxyhemoglobin dissociation curve (ODC) plays a crucial role in oxygen transport. Because of the sigmoidal shape of the

Chapter 1: High-Altitude Medicine

50

100

Men

7

~ No change

Women (Fe)

~10% Decrease

80

46 Women (
Fe)

44 60 42 Sea level

40 1

20

40

60

SaO2 (%)

Hematocrit (%)

48

40

Days at 4300 Meters

Figure 1-3. Hematocrit changes on ascent to altitude in men and in women,with and without supplemental iron (Fe).(Modified from Hannon JP,Chinn KS,Shields JL:Fed Proc 28:1178–1184, 1969, with permission.)

B

20

A

0

curve, Sao2% is well maintained up to 3000 m, despite a significant decrease in arterial Po2 (see Figure 1-1). Above that altitude, small changes in arterial Po2 result in large changes in arterial oxygen saturation (Fig. 1-4). The oxygen saturation determines arterial oxygen transport, but the Po2 determines diffusion of oxygen from the capillary to the cell. In 1936, Ansel Keys and colleagues230 demonstrated an in vitro right shift in the position of the ODC at high altitude, a shift that favors release of oxygen from blood to the tissues. This change occurs because of the increase in 2,3-diphosphoglycerate (2,3-DPG), which is proportional to the severity of hypoxemia. In vivo, however, this is offset by alkalosis, and at moderate altitude little net change occurs in the position of the ODC. On the other hand, the marked alkalosis of extreme hyperventilation, as measured on the summit and simulated summit of Mt. Everest (Pco2 8 to 10 mm Hg, pH > 7.6), shifts the ODC to the left, which facilitates oxygen–hemoglobin binding in the lung, raises Sao2%, and is thought to be advantageous.391 This concept is further supported by observing that when people with a very left-shifted ODC, caused by an abnormal hemoglobin (Andrew-Minneapolis), were taken to moderate (3100 m) altitude, they had less tachycardia and dyspnea and remarkably had no decrease in exercise performance.175 High-altitude adapted animals also have a left-shifted ODC.

Tissue Changes The next link in the oxygen transport chain is tissue oxygen transfer, which depends on capillary perfusion, diffusion distance, and driving pressure of oxygen from the capillary to the cell. The final link, then, is use of oxygen within the cell. Banchero15 has shown that capillary density in dog skeletal muscle doubled in 3 weeks at a barometric pressure of 435 mm Hg. A recent study in humans noted neither change in capillary density, nor in gene expression thought to enhance muscle vascularity.267 Ou and Tenney334 revealed a 40% increase in mitochondrial number but no change in mitochondrial size, whereas the study of Oelz and colleagues332 showed that high-altitude climbers had normal mitochondrial density. A significant drop

0

20

40

60

80

100

120

PaO2 (mm Hg)

Figure 1-4. Oxyhemoglobin dissociation curve showing effect of 10 mm Hg decrement in PaO2 on arterial oxygen saturation at sea level (A) and near 4400 m (B). Note the much larger drop in SaO2 at high altitude. (Modified from Severinghaus JW, Chiodi H, Eger EI, et al: Circ Res 19:274–282, 1966, with permission.)

in muscle size is often noted after a high-altitude expedition due to net energy deficit,267,270 and it results in shortening of the diffusion distance for oxygen. This occurs in spite of no de novo synthesis of capillaries or mitochondria, yet results in increased capillary density and ratio of mitochondrial volume to contractile protein fraction, which are primarily a result of the atrophy.267,270

Sleep at High Altitude Disturbed sleep is common at high altitude. Its cause appears to be multifactorial. Reflecting the great interest in sleep in general, more than 140 papers have addressed sleep at altitude in the last 10 years; a complete discussion is outside our purview. The interested reader is referred to recent reviews and online databases (Medline).454,463 Nearly all subjects complain of disturbed sleep at high altitude, with severity increasing with the altitude. At moderate altitude, sleep architecture is changed, with reduction in stage 3 and 4 sleep, increase in stage 1 time, and little change in stage 2. Overall, there is a shift from deeper sleep to lighter sleep. In addition, more time is spent awake, with significantly increased arousals. Authors have reported either slightly less rapid eye movement (REM) time, or no change in REM compared to low altitude. REM sleep may improve over time at altitude.232 The subjective complaints of poor sleep are out of proportion to the small reduction (if any) in total sleep time, and appear to be due to sleep fragmentation. With more extreme hypoxia, sleep time was dramatically short-

8

PART ONE: MOUNTAIN MEDICINE

Placebo

Sleep saturation at 5360 m 100 80 SaO2 %

Respiratory Pattern 100 80 60 40

SaO2 (%)

60 40

Arrival Acclimatized

20 Acetazolamide

0

Time asleep in minutes

Respiratory Pattern 100 80 SaO2 (%) 60 40

Figure 1-5. Respiratory patterns and arterial oxygen saturation (SaO2) with placebo and acetazolamide in two sleep studies of a subject at 4200 m. Note pattern of hyperpnea followed by apnea during placebo treatment,which is changed with acetazolamide.(Modified from Hackett PH, Roach RC, Harrison GL, et al: Am Rev Respir Dis 135:896–898, 1987, with permission.)

ened and arousals increased, without a change in ratio of sleep stages but with a reduction in REM sleep.8 The mechanisms of this change in sleep architecture and fragmentation are poorly understood. Periodic breathing appears to play only a minor role in altering sleep architecture at high altitude.390 The arousals have been linked to periodic breathing in some studies but not others. Other factors might include change in circadian rhythm and perhaps body temperature.82 Problematic sleep is quite variable, with predisposing factors such as obesity explaining a degree of susceptibility to both deranged sleep and sleep-disordered breathing in some individuals.125 Recent studies of infants and children488 and athletes in simulated altitude devices used for training also revealed deranged sleep quality in these groups.233,234,337 Although deranged sleep is a frequent complaint in high-altitude visitors, it seems to have little relation to susceptibility to altitude illness or other serious problems. Symptomatic treatment that avoids respiratory depression is safe. (See Treatment under Acute Mountain Sickness section.)

Periodic Breathing Periodic breathing is most common in early and light sleep, may occur during wakefulness when drowsy, and does not occur in REM sleep. The pattern is characterized by hyperpnea followed by apnea (Fig. 1-5), and it is caused by a battle for control of breathing between the peripheral chemoreceptors (carotid body) and the central respiratory center. Respiratory alkalosis during the hyperpnea acts on the central respiratory center, causing apnea. During apnea, Sao2% decreases, carbon dioxide increases, and the carotid body is stimulated, causing a recurrent hyperpnea and apnea cycle. The apnea is central, not associated with snoring, and with absence of rib cage movement. Persons with a high hypoxic ventilatory response have more periodic breathing, with mild oscillations in Sao2%,246 whereas

50 100 150 200 250 300 350 400 450 500

Figure 1-6. Sleep oxygenation improves with acclimatization to same altitude. Top line is maximum and bottom line is minimum SaO2 in an acclimatized person. Shaded area shows maximum and minimum SaO2 values for new arrival at 5360 m (17,581 feet). (Modified from Sutton JR, Houston CS, Mansell AL, et al: N Engl J Med 301:1329–1331, 1979, with permission.)

persons with a low hypoxic ventilatory response have more regular breathing overall but may suffer periods of apnea with extreme hypoxemia distinct from periodic breathing.159 As acclimatization progresses, periodic breathing lessens but does not disappear, especially over 5000 m, and Sao2% increases (Fig. 1-6).8,432 Periodic breathing has not been implicated in the etiology of high-altitude illness, but nocturnal oxygen desaturation has been implicated.111,121 Eichenberger and colleagues have also reported greater periodic breathing in persons with HAPE, secondary to lower Sao2%.108 As with fragmented sleep, the intensity of periodic breathing is quite variable. Total sleep time with periodic breathing can vary from 1% to over 90%.494 Most studies report no association between periodic breathing and AMS. This may relate to the fact that persons with periodic breathing tend to have higher HVR, and greater average ventilation and oxygenation.463

Pharmaceutical Aids Acetazolamide, 125 mg at bedtime, diminishes periodic breathing and awakenings, improves oxygenation and sleep quality, and is a safe and superior agent to use as a sleeping aid (see Figure 1-5). It has the added benefit of diminishing symptoms of AMS. Other agents include diphenhydramine (Benadryl, 50 to 75 mg) or the short-acting benzodiazepines such as triazolam (Halcion, 0.125 to 0.25 mg) and temazepam (Restoril, 15 mg). Although caution is warranted for any agent that might reduce ventilation at high altitude, some studies have suggested that benzodiazepines in low dosages are generally safe in this situation.104,131,327 Another option is to use both acetazolamide and a benzodiazepine. Bradwell and colleagues55 showed that acetazolamide (500 mg slow-release orally) given with temazepam (10 mg orally) improved sleep and maintained Sao2%, counteracting a 20% decrease in Sao2% when temazepam was given alone. The nonbenzodiazepine hypnotic zolpidem (Ambien, 10 mg) was shown to improve sleep at 4000 m without adversely affecting ventilation.42

Exercise Maximal oxygen consumption drops dramatically on ascent to high altitude (see references 122 and 364 for recent reviews).

Chapter 1: High-Altitude Medicine

40

180

Alveolar

Endurance time · VO2max

160

Arterial 140

30

120 PO2 (torr)

Sea level performance (%)

9

100

20

Mixed venous

Assumed critical PO2

80

Loss of consciousness

. VO2max

10

60

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

40 0

2

4

6

8

10

12

Days at altitude

. Figure 1-7. On ascent to altitude, VO2max decreases and remains suppressed. In contrast, . endurance time (minutes to exhaustion at 75% of altitude-specific VO2max) increases with acclimatization.(Modified from Maher JT,Jones LG,Hartley LH:J Appl Physiol 37:895–898,1974, with permission.)

. Maximal oxygen uptake (Vo2max) falls from sea level by approximately 10% for each 1000 m of altitude gained above . 1500 m. Those with the highest sea level Vo2max values have . the largest decrement in Vo2max at high altitude, but overall performance at high altitude is not consistently related to sea . level Vo2max.332,358,469 In fact, . many of the world’s elite mountaineers have quite average Vo2max values, in contrast to other endurance athletes.332 Acclimatization at moderate altitudes . enhances submaximal endurance time but not Vo2max 122 (Fig. 1-7). Oxygen transport during exercise at high altitude becomes increasingly dependent on the ventilatory pump. The marked rise in ventilation produces a sensation of breathlessness, even at low work levels. The following quotation is from a highaltitude mountaineer: After every few steps, we huddle over our ice axes, mouths agape, struggling for sufficient breath to keep our muscles going. I have the feeling I am about to burst apart. As we get higher, it becomes necessary to lie down to recover our breath.297 In contrast to the increase in ventilation with exercise, at increasing altitudes in OEII, cardiac function and cardiac output were maintained at or near sea level values for a given oxygen consumption (workload).349 . Recent work has attributed the altitude-induced drop in Vo2max to (1) the lower Pio2, (2) impairment of pulmonary gas exchange, and (3) reduction of maximal cardiac output and peak leg . blood flow, each explaining about one third of the loss in Vo2max.65 However, mechanisms to explain impairment of gas exchange and lower blood flow remain elusive. Wagner459 proposes that the pressure gradient for diffusion of oxygen from capillaries to the working

0 0

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400

600

800

1000

1200

Oxygen uptake (mL O2/min)

Figure 1-8. Calculated changes in the PO2 of alveolar gas and arterial and mixed venous blood as oxygen uptake (mL O2/min) is increased for a climber on the summit of Mt. Everest. Unconsciousness develops at a mixed venous PO2 of 15 mm Hg. DMO2, muscle diffusing capacity for O2. (Modified from West JB: Respir Physiol 52:265–279, 1983, with permission.)

muscle cells may be inadequate. Another concept is that increased cerebral hypoxia from exercise-induced desaturation is the limiting factor.75,211 Mountaineers, for example, become lightheaded and their vision dims when they move too quickly at extreme altitude (Fig. 1-8).466

Training at High Altitude Optimal training for increased performance at high altitude depends on the altitude of residence and the athletic event. For aerobic activities (events lasting more than 3 or 4 minutes) at altitudes above 2000 m, acclimatization for 10 to 20 days is necessary to maximize performance.88 For events occurring above 4000 m, acclimatization at an intermediate altitude is recommended. Highly anaerobic events at intermediate altitudes require only arrival at the time of the event, although mountain sickness may become a problem. The benefits of training at high altitude for subsequent performance at or near sea level depend on choosing a training altitude that maximizes the benefits and minimizes the “detraining” inevitable when maximal oxygen uptake is limited (altitude greater than 1500 to 2000 m). Hence, data from training above 2400 m have shown no increase in subsequent sea level performance. Also, intermittent exposures to hypoxia seem to have no benefit.221,445 Runners returning to sea level after 10 days’ training at 2000 m had faster running times and an increase in aerobic power, plasma volume, and hemoglobin concentration.14 More recent work suggests training benefits from training at low altitude while sleeping at high altitude—the “live

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PART ONE: MOUNTAIN MEDICINE

high, train low” approach.258,429 Coaches and endurance athletes from around the world are convinced of the benefits of training and/or sleeping at moderate altitude to improve sea level performance. The benefit appears due to enhanced erythropoietin production and increased red cell mass, which requires adequate iron stores and thus usually iron supplementation.279,374,428 Some individuals do not respond to “live high, train low,” perhaps because of an inability to increase erythropoietin levels sufficient to raise red cell mass and thus increase oxygen carrying capacity.68,217


HIGH-ALTITUDE SYNDROMES High-altitude syndromes are illnesses attributed directly to hypobaric hypoxia, even if exact mechanisms are unclear. Clinically and pathophysiologically, these syndromes overlap. Rapidity of onset of hypoxia is crucial; for example, sudden exposure to extreme altitude may result in death from acute hypoxia (asphyxia), whereas more gradual ascent to the same altitude may result in AMS or no illness at all. Where symptoms of acute hypoxia end and AMS begins is vague, as reflected in the classic experiments of Bert.49 In terms of altitude illness, the general concept of a spectrum of illness with a common underlying pathogenesis is well accepted and provides a useful framework for discussion. For the neurologic syndromes, the spectrum progresses from high-altitude headache to AMS to high-altitude cerebral edema (HACE). In the lung, the spectrum includes pulmonary hypertension, interstitial edema, and HAPE. These problems all occur within the first few days of ascent to a higher altitude, have many common features, and respond to descent or oxygen. Longer-term problems of altitude exposure include high-altitude deterioration and chronic mountain sickness.

Neurologic Syndromes Neurologic syndromes at high altitude reflect both the nervous system’s sensitivity to hypoxia and the effects of compensatory mechanisms. Although brain ATP production and metabolism remain intact during hypoxia, neurotransmitter synthesis is sensitive to hypoxia, and impaired synthesis of neurotransmitters accounts for symptoms of acute cerebral hypoxia as well as cognitive defects at high altitude. The compensatory cerebral vasodilation at altitude appears to play a role in causing altitude headache, and it also contributes to development of AMS and HACE. However, much of the pathophysiology of AMS and HACE remains a mystery. Focal neurologic deficits without cerebral edema are also difficult to explain; cerebral artery spasm and watershed hypoxia have both been invoked. The understanding of the exact etiology of these neurologic syndromes due to hypoxia will parallel advances in neuroscience; the emphasis in altitude illness is finally and appropriately on the brain.368

Acute Cerebral Hypoxia Acute, profound hypoxia, although of greatest interest in aviation medicine, may also occur on terra firma when ascent is too rapid or when hypoxia abruptly worsens. Carbon monoxide poisoning, pulmonary edema, sudden overexertion, sleep apnea, or a failed oxygen delivery system may rapidly exaggerate hypoxemia. In an unacclimatized person, loss of consciousness from acute hypoxia occurs at an Sao2 of 40% to 60% or at an arterial Po2 of less than about 30 mm Hg. Tissandier, the sole

survivor of the flight of the balloon Zenith in 1875, gave a graphic description of the effects of acute hypoxia: But soon I was keeping absolutely motionless, without suspecting that perhaps I had already lost use of my movements. Towards 7,500 m, the numbness one experiences is extraordinary. The body and the mind weakens little by little, gradually, unconsciously, without one’s knowledge. One does not suffer at all; on the contrary. One experiences inner joy, as if it were an effect of the inundating flood of light. One becomes indifferent; one no longer thinks of the perilous situation or of the danger; one rises and is happy to rise. Vertigo of the lofty regions is not a vain word. But as far as I can judge by my personal impression, this vertigo appears at the last moment; it immediately precedes annihilation—sudden, unexpected, irresistible. I wanted to seize the oxygen tube, but could not raise my arm. My mind, however, was still very lucid. I was still looking at the barometer; my eyes were fixed on the needle which soon reached the pressure number of 280, beyond which it passed. I wanted to cry out “We are at 8,000 meters.” But my tongue was paralyzed. Suddenly I closed my eyes and fell inert, completely losing consciousness.49 The ascent to over 8000 m took 3 hours, and the descent less than 1 hour. When the balloon landed, Tissandier’s two companions were dead. The prodigious work that Paul Bert conducted in an altitude chamber during the 1870s showed that lack of oxygen, ratherthan an effect of isolated hypobaria, explained the symptoms experienced during rapid ascent to extreme altitude. There exists a parallelism to the smallest details between two animals, one of which is subjected in normal air to a progressive diminution of pressure to the point of death, while the other breathes, also to the point of death, under normal pressure, an air that grows weaker and weaker in oxygen. Both will die after having presented the same symptoms.49 Bert goes on to describe the symptoms of acute exposure to hypoxia: It is the nervous system which reacts first. The sensation of fatigue, the weakening of the sense perceptions, the cerebral symptoms, vertigo, sleepiness, hallucinations, buzzing in the ears, dizziness, pricklings . . . are the signs of insufficient oxygenation of central and peripheral nervous organs. . . . The symptoms . . . disappear very quickly when the balloon descends from the higher altitudes, very quickly also . . . the normal proportion of oxygen reappears in the blood. There is an unfailing connection here.49 Bert was also able to both prevent and immediately resolve symptoms by breathing oxygen. Modern studies of acute hypoxic exposure in simulated altitude chambers use the measurement of time of useful consciousness; that is, the time until a subject can no longer take corrective measures, such as putting on an oxygen mask. With exposure to 8500 m (28,000 feet), that time is 60 seconds during moderate activity and 90 seconds at rest. Acute hypoxia can be quickly reversed by immediate administration of oxygen, rapid pressurization or descent, or correc-

Chapter 1: High-Altitude Medicine tion of an underlying cause, such as relief of apnea, removal of a carbon monoxide source, repair of an oxygen delivery system, or cessation of overexertion. Hyperventilation increases time of useful consciousness during severe hypoxia.

High-Altitude Headache Headache is generally the first unpleasant symptom consequent to altitude exposure and is sometimes the only symptom.183 It may or may not be the harbinger of AMS, which is defined as the presence of headache plus at least one of four other symptoms, in the setting of an acute altitude gain.365 One could even argue that it is the headache itself that causes other symptoms such as anorexia, nausea, lassitude, and insomnia, as is commonly seen in migraine or tension headaches, and that mild AMS is essentially due to headache. The International Headache Society (IHS) has defined high-altitude headache as “a headache that develops within 24 hours after sudden ascent to altitudes above 3,000m” and that is “associated with at least one other symptom typical of high altitude, including (a) Cheyne-Stokes respiration at night, (b) a desire to overbreathe and (c) exertional dyspnea.” This definition is problematic in that many experience altitude headache between 2000 and 3000 m, and the other symptoms have no demonstrated association with headache. Recent studies have attempted to characterize the clinical features and incidence of headache at altitude. Silber and colleagues found that 50 of 60 trekkers (83%) in Nepal up to 5100 m developed at least one headache when over 3000 m.416 Older persons were less susceptible; women and those with headaches in daily life had more severe headaches but not more headaches than others. Of those with headache, 52% did not have AMS by the Lake Louise criteria; 44% did not have one of the symptoms in the IHS definition, indicating its ineffectiveness. Various medications alleviated the headache 70% of the time, especially when it was mild. The clinical features were widely variable. In general, the headaches were bilateral, generalized, dull, and exacerbated by exertion or movement, and they often occurred at night and resolved within 24 hours. Thus,

11

the headaches had some features of increased intracranial pressure. Persons with history of migraine did not have a higher incidence of headache. The term high altitude headache (HAH) has been used in the literature for decades, and studies directed toward the pathophysiology and treatment of HAH have been reported. Obviously, these are, to an extent, studies of AMS as well. Headache lends itself to investigation better than some other symptoms do, as headache scores have been well validated.214 In general, the literature suggests that HAH can be prevented by the use of nonsteroidal anti-inflammatory drugs57,61 and acetaminophen172 as well as the drugs commonly used for prophylaxis of AMS, acetazolamide and dexamethasone. Some agents appear more effective than others, with ibuprofen and aspirin apparently superior to naproxen.57,58,62 A serotonin agonist (sumatriptan, a 5-HT1 [serotonin type 1] receptor agonist) was reported to be effective for HAH prevention or treatment in some studies59,448 but not in others.23 Flunarizine, a specific calcium antagonist used for treatment of migraine, was not effective in one study.40 Interestingly, oxygen is often immediately effective for HAH (within 10 minutes) in subjects with and without AMS, indicating a rapidly reversible mechanism of the headache.21,158 The response to many different agents might reflect multiple components of the pathophysiology or merely the nonspecific nature of analgesics. As Sanchez del Rio and Moskowitz have pointed out, different inciting factors for headache may result in a final common pathway, such that the response to different therapies is not necessarily related to the initial cause of the headache.392 They recently provided a useful multifactorial concept of the pathogenesis of HAH, based on current understanding of headaches in general.392 They suggest that the trigeminovascular system is activated at altitude by both mechanical and chemical stimuli (vasodilation, nitric oxide, and other noxious agents), and in addition, the threshold for pain is quite likely altered at high altitude (Fig. 1-9).392 If AMS and especially HACE ensue, altered intracranial dynamics may also play a role, via compression or distention of pain-sensitive

Hypothalamus Brainstem

Autonomic response

CNS processing

High-altitude headache

Lower threshold for pain

Hypoxia

Trigeminovascular system activation

eNOS upregulation

↑ NO

Figure 1-9. 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 [eds]: Hypoxia: Into the Next Millennium. New York, Plenum/Kluwer Academic, 1999, pp 145–153, with permission.)

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structures. The near future may bring a better understanding of the pathophysiology of these often debilitating headaches and new treatments as well.

Acute Mountain Sickness Epidemiology and Risk Factors Although the syndrome of AMS has been recognized for centuries, modern rapid transport and proliferation of participants in mountain sports have increased the number of victims and therefore public awareness (see Table 1-1). The incidence and severity of AMS depend on the rate of ascent and the altitude attained (especially the sleeping altitude), duration of altitude exposure, level of exertion, recent altitude exposure, and inherent physiologic (genetic) susceptibility.155,370,401 For example, AMS is more common on Mt. Rainier because of the rapid ascent, whereas high-altitude pulmonary or cerebral edema is uncommon because of the short stay (less than 36 hours). People with a demonstrated susceptibility to AMS had twice the incidence of AMS compared to nonsusceptible people, and this was independent of rate of ascent.401 The basis for inherent susceptibility is still unknown; clearly it depends on genetic factors. Recent altitude exposure can be protective; 5 days or more in the previous 2 months above 3000 m reduced susceptibility to AMS on ascent to 4559 m by one half, which was as effective as slow ascent401 (Fig. 1-10). Compared with persons living at a lower altitude, residence at 900 m or above reduced the incidence of AMS from 27% to 8% when ascending to between 2000 and 3000 m in Colorado.183 Age has an influence on incidence,155 with those older than 50 years somewhat less vulner-

able.369,416 In a large study in Colorado, those older than 60 years had an incidence of AMS that was half that seen in those younger than 60. In contrast, a study of 827 mountaineers in Europe showed no influence of age on susceptibility.401 Perhaps the different populations and physical activity explain the different results. No study has ever shown the older ages to be more susceptible. Children from 3 months to puberty studied in Colorado had the same incidence as young adults.440,489 A small study of tourists in Chile, however, found lower oxygen saturation and higher AMS in the 6- to 48-month age group at 4440 m. The largest study of children to date, of Han Chinese after ascent to Tibet, showed essentially the same incidence of AMS in 464 children as in 5335 adults, 34% and 38%, respectively.481 Women apparently have the same371,401 or a slightly greater incidence of AMS155,183,451 but may be less susceptible to pulmonary edema.83,424 There appears to be no relationship between AMS and the menstrual cycle.355 Most studies show no relationship between physical fitness and susceptibility to AMS. However, obesity seems to increase the odds of developing AMS.124,183 Smoking does not increase risk of AMS,183,225 and neither does use of oral contraceptives.225,330 In summary, the most important variables related to AMS susceptibility are genetic predisposition, altitude of residence, rate of ascent, and prior recent altitude exposure.

Diagnosis The diagnosis of AMS is based on the setting, symptoms, physical findings, and exclusion of other illnesses. The setting is generally rapid ascent of unacclimatized persons to 2500 m or

70%

60%

Nonsusceptible Susceptible

Prevalence of AMS

50%

40%

30%

20%

10%

0% Ascent 3 days and pre-exposure 5 days

Either ascent 3 days or pre-exposure 5 days

Ascent 4 days and pre-exposure 5 days

Rate of ascent and pre-exposure

Figure 1-10. The prevalence of acute mountain sickness (AMS) and 95% confidence intervals in nonsusceptible (blue bars) and susceptible (red bars) mountaineers in relationship to the state of acclimatization defined as slow ascent (more than 3 days), fast ascent (3 days or less), pre-exposed (5 days or more above 3000 m in the preceding 2 months), and not pre-exposed (4 days or less above 3000 m in the preceding 2 months). From Schneider M, Bernasch D,Weymann J, et al: Med Sci Sports Exerc 34:1886–1891, 2002, with permission.)

Chapter 1: High-Altitude Medicine higher from altitudes below 1500 m. For partially acclimatized persons, abrupt ascent to a higher altitude, overexertion, use of respiratory depressants, and perhaps onset of infectious illness321 are common contributing factors. The cardinal symptom of early AMS is headache, followed in incidence by fatigue, dizziness, and anorexia.155,183,421 The headache is usually throbbing, bitemporal, worse during the night and on awakening, and made worse by Valsalva’s maneuver or stooping over (see High-Altitude Headache). A good appetite is distinctly uncommon; nausea is common. These initial symptoms are strikingly similar to an alcohol hangover. Frequent awakening may fragment sleep, and periodic breathing often produces a feeling of suffocation. Although sleep disorder is nearly universal at high altitude, also affecting those without AMS, these symptoms may be exaggerated during AMS. Affected persons commonly complain of a deep inner chill, unlike mere exposure to cold temperature, accompanied by facial pallor. Other symptoms may include vomiting, dyspnea on exertion, and irritability. Lassitude can be disabling, with the victim too apathetic to contribute to his or her own basic needs. Pulmonary symptoms vary considerably. Everyone experiences dyspnea on exertion at high altitude; it may be difficult to distinguish normal from abnormal. Dyspnea at rest is distinctly abnormal, however, and presages HAPE rather than AMS. Cough is also extremely common at high altitude, and not particularly associated with AMS. Recent work suggests that altitude hypoxia actually lowers the cough threshold, as measured with an inhaled citric acid stimulus.283 However, any pulmonary symptom mandates careful examination for pulmonary edema. Specific physical findings are lacking in mild AMS. A higher heart rate has been noted in those with AMS,29,330 but Singh

13

and associates421 noted bradycardia (heart rate less than 66 beats/min) in two thirds of 1975 soldiers with AMS. Blood pressure is normal, but postural hypotension may be present. Occasionally, localized rales are present,273 but this has also been observed in those without AMS.153 A slightly increased body temperature with AMS may be present but is not diagnostic.271 Peripheral oxygen saturation as measured by pulse oximetry correlated poorly with presence of AMS during rapid ascent330,369,380 but was related to AMS during trekking.34 Sao2 at altitude on Denali was predictive of developing AMS on further ascent.366 Overall, pulse oximetry is of limited usefulness in diagnosis of AMS. Funduscopic examination reveals venous tortuosity and dilation. Retinal hemorrhages may or may not be present and are not diagnostic; they are more common in AMS than non-AMS individuals at 4243 m.153 Absence of the normal altitude diuresis, evidenced by lack of increased urine output and retention of fluid, is an early finding in AMS, although not always present.30,154,373,421,435 More obvious physical findings develop if AMS progresses to HACE. Typically, with onset of HACE, the victim wants to be left alone, lassitude progresses to inability to perform perfunctory activities such as eating and dressing, ataxia develops, and, finally, changes in consciousness appear, with confusion, disorientation, and impaired judgment. Coma may ensue within 24 hours of the onset of ataxia. Ataxia and confusion are the most useful signs for recognizing the progression from AMS to HACE; all persons proceeding to high altitudes should be aware of this fact. It is clinically useful to classify AMS as mild or as moderate to severe on the basis of symptoms (Table 1-4). Importantly, AMS can herald the beginning of life-threatening cerebral edema.

TABLE 1-4. Clinical Classifications of Acute Mountain Sickness (AMS) HIGH-ALTITUDE HEADACHE (HAH)

MILD AMS

Symptoms

Headache only

Headache, plus one more symptom (nausea/vomiting; fatigue/lassitude; dizziness or difficulty sleeping) All symptoms of mild intensity

LL-AMS score* Physical signs

1–3, headache only None

2–4 None

Findings

None

None

Pathophysiology

Unknown; cerebral vasodilatation, trigeminovascular system†?

Unknown; same as HAH?

MODERATE TO SEVERE AMS Headache, plus one or more symptoms (nausea/vomiting; fatigue/lassitude; dizziness or difficulty sleeping) Symptoms of moderate to severe intensity 5–15 None Antidiuresis Slightly increased body temperature Slight desaturation Widened A-a gradient Elevated ICP White matter edema (CT, MRI) Vasogenic edema

*The self-report Lake Louise AMS score. † See Figure 1-11. CT, computed tomography; HAPE, high-altitude pulmonary edema; ICP, intracranial pressure; MRI, magnetic resonance imaging.

HIGH-ALTITUDE CEREBRAL EDEMA (HACE) ±Headache Worsening of symptoms seen in moderate to severe AMS — Ataxia Altered mental status HAPE common: positive chest film, rales, dyspnea at rest Elevated ICP White matter edema (CT, MRI) Advanced vasogenic cerebral edema

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Box 1-3. Differential Diagnosis of High-Altitude Illnesses Acute mountain sickness and high-altitude cerebral edema

High-altitude pulmonary edema

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

Differential Diagnosis Given the nonspecific nature of the symptoms, AMS is commonly confused with other conditions. Box 1-3 lists conditions that the authors have seen confused with AMS and HACE. AMS is most commonly misdiagnosed as a viral flulike illness, hangover, exhaustion, dehydration, or medication or drug effect. Unlike an infectious illness, uncomplicated AMS is not associated with fever and myalgia. Hangover is excluded by the history. Exhaustion may cause lassitude, weakness, irritability, and headache and may therefore be difficult to distinguish from AMS. Dehydration, which causes weakness, decreased urine output, headache, and nausea, is commonly confused with AMS. Response to fluids helps to differentiate the two. AMS is not improved by fluid administration alone, and body hydration does not influence susceptibility to AMS (contrary to conventional wisdom).9 Hypothermia may manifest as ataxia and mental changes. Sleeping medication can cause ataxia and mental changes, but soporifics may also precipitate high-altitude illness because of increased hypoxemia during sleep. Migraine may be very difficult to distinguish from AMS. A trial of oxygen breathing or descent can be helpful to discriminate these other conditions from AMS.

Carbon Monoxide Carbon monoxide poisoning is a danger at high altitude, where field shelters are designed to be small and windproof. Cooking inside closed tents and snow shelters during storms is a particular hazard.116,228,255,441,447 The effects of carbon monoxide and high-altitude hypoxia are additive. A reduction in oxyhemoglobin caused by carbon monoxide increases hypoxic stress, rendering a person at a physiologically higher altitude, which may precipitate AMS. Because of preexisting hypoxemia, smaller amounts of carboxyhemoglobin produce symptoms of carbon monoxide poisoning. These two problems may coexist. Immediate removal of the victim from the source of carbon monoxide and forced hyperventilation, preferably with supplemental oxygen, rapidly reverse carbon monoxide poisoning.

Pathophysiology The basic cause of AMS is hypoxemia (Fig. 1-11), but the syndrome is different from acute hypoxia. Because symptoms are somewhat worse with hypobaric hypoxia than with normobaric hypoxia, hypobaria apparently also plays a minor role, most likely through its effect on fluid retention.266,372 Because of a time lag in onset of symptoms after ascent and lack of immediate or complete reversal of all symptoms with oxygen, AMS is thought to be secondary to the body’s responses to modest hypoxia. In addition, even though an altitude of 2500 to 2700 m presents only a minor decrement in arterial oxygen transport (Sao2 is still above 90%), AMS is common and some individuals may become desperately ill. An acceptable explanation of pathophysiology must therefore address lag time, individual susceptibility to even modest hypoxia, and how acclimatization prevents the illness. Findings documented in mild to moderate AMS include relative hypoventilation,288,313 impaired gas exchange (interstitial edema),138,250 fluid retention and redistribution,30,373,435 and increased sympathetic drive.26,29 In mild to moderate AMS, limited data show that neither intracranial pressure (ICP) nor cerebrospinal fluid (CSF) pressure is elevated.13,173,480 In contrast, increased ICP and cerebral edema are documented in moderate to severe AMS, reflecting the continuum from advanced AMS to HACE.190,241,287,421,474 Relative hypoventilation may be due primarily to decreased drive to breathe (low hypoxic ventilatory response) or may be secondary to ventilatory depression associated with AMS.313,363 Persons with quite low hypoxic ventilatory response are more likely to suffer AMS than are those with a high ventilatory drive.180,288,313 For persons with intermediate hypoxic ventilatory response values (the majority of people), ventilatory drive has no predictive value.300,363 The protective role of a high hypoxic ventilatory response most likely results from overall increased oxygen transport, especially during sleep and exercise. Pulmonary dysfunction in AMS includes decreased vital capacity and peak expiratory flow rate,421 increased alveolar–arterial oxygen difference,138,181 decreased transthoracic impedance,213 and occasionally rales.273 These findings are compatible with interstitial edema—that is, increased extravascular lung water, most likely related to fluid retention and an increased interstitial water compartment. That exercise can contribute to interstitial edema at altitude was recently confirmed.7 Whether this can be considered a mild form of HAPE is unclear. The fact that nifedipine effectively prevents HAPE but does not prevent AMS or the increased alveolar–arterial oxygen gradient observed in AMS181 speaks against the increased lung water of AMS being related to HAPE. In addition, in contrast to the results in HAPE, alveolar lavage analysis in persons with AMS was normal. The mechanism of fluid retention may be multifactorial. Renal responses to hypoxia are variable and depend on plasma arginine vasopressin (AVP) concentration and sympathetic tone.176,435 Persons with AMS had elevated plasma or urine AVP levels in some studies,26,421 but cause and effect could not be established. Other studies showed no AVP elevation.30 The usual decrease in aldosterone on ascent to altitude does not occur in persons with AMS, and this may contribute to the antidiuresis.30 The renin-angiotensin system, although suppressed compared with its activity at sea level in both AMS and non-AMS groups, was more active in persons with AMS.29 Atrial natriuretic peptide (ANP) is elevated in AMS. Although this is most

Chapter 1: High-Altitude Medicine

15

Altitude hypoxia Leukocytes

↓ HVR, sleep, and exercise ↓ PaO2

↑ Sympathetic activity

Endothelial activation ↑ CBF ↑ CBV

↑ Cytokines, VEGF ↑ iNOS

Kidney

↑ Pcap ↑ Sodium and/or water retention

↑ BBB permeability Vasogenic edema

Peripheral edema Brain swelling

Adequate cerebrospinal compliance?

Yes

No AMS

No

AMS/HACE

Figure 1-11. Proposed pathophysiology of acute mountain sickness (AMS). BBB, blood–brain barrier; CBF, cerebral blood flow; CBV, cerebral blood volume; HACE, high-altitude cerebral edema; HVR, hypoxic ventilatory response; iNOS, inducible nitric oxide synthase; Pcap, capillary pressure;VEGF, vascular endothelial growth factor.

likely compensatory, elevated plasma ANP levels may contribute to vasodilation and increased microvascular permeability.29,472 One factor that can explain many of these changes is increased sympathetic activity, which reduces renal blood flow, glomerular filtration rate, and urine output, and suppresses renin.435 Increased sympathetic nervous system activity is also consistent with the greater rise in norepinephrine noted in subjects with AMS.26 See Krasney237 for a discussion of the critical role of central sympathetic activation on the kidney and its role in the pathophysiology of AMS. Whatever the exact mechanism, it seems that renal water handling switches from net loss or no change to net gain of water as persons become ill with AMS. The effectiveness of diuretics in treating AMS also supports a pivotal role for fluid retention and fluid shifts in the pathology of AMS.138,421 Persons with moderate to severe AMS or HACE display white matter edema on brain imaging and elevated intracranial pressure, whereas those with mild AMS do not.13,164,190,241,259,287,421 Possible mechanisms include cytotoxic edema with a shift of

fluid into the cells, or vasogenic edema from increased permeability of the blood–brain barrier (BBB), or both. The classic view that hypoxia causes failure of the ATP-dependent sodium pump and subsequent intracellular edema188 is untenable, given the newer understanding of brain energetics; ATP levels are maintained even in severe hypoxemia.415 The evidence now favors vasogenic brain edema as the cause of advanced AMS or HACE.164 The fact that dexamethasone is so effective for AMS also suggests vasogenic edema, as this is the only steroidresponsive brain edema. In addition, a model of AMS in conscious sheep exposed to 10% oxygen for several days supports the vasogenic brain-swelling hypothesis.239 The pathophysiology may be similar to that of hypertensive encephalopathy, another type of hyperperfusion encephalopathy407 in which loss of vascular autoregulation results in increased pressures transmitted to the capillaries with resultant white matter edema.251,252 Supporting this notion, Van Osta and colleagues showed that cerebral autoregulation was impaired the most in those with more severe AMS.450 Because prolonged cerebral vasodilation

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by itself, however, is not sufficient to induce vasogenic edema, Hackett148 and Krasney238 have proposed the additional factor of increased BBB permeability in the pathophysiology of AMS. Possible mechanisms of altered BBB permeability in AMS/HACE include vascular endothelial growth factor (VEGF), inflammatory cytokines, products of lipid peroxidation, reactive oxygen species, endothelium-derived products such as nitric oxide, and direct neural and humoral factors known to affect the BBB. The study by Schoch and colleagues provided impressive evidence for a role for VEGF.402 Mice on hypoxic exposure developed brain edema associated with elevated brain levels of VEGF; when given an antibody to VEGF, mice developed no cerebral edema.402 A recent study testing the hypothesis of a leaky BBB due to reactive oxygen species found evidence of free radical generation in subjects with AMS, but no evidence of altered BBB permeability despite the presence of mild brain swelling.13 Although the free radicals were not associated with BBB leak, their role in causing symptoms of AMS by another mechanism could not be excluded. The question of whether mild AMS, especially headache alone, is due to vasogenic cerebral edema is not yet answered (see High-Altitude Headache). Magnetic resonance imaging (MRI) studies demonstrated brain swelling in all subjects ascending rapidly to moderate altitude, regardless of the presence of AMS.114,210,322 The change in brain volume was greater than that expected from increased cerebral blood volume alone (due to vasodilation), but the individual components of blood and brain parenchyma could not be determined with MRI. Therefore, whether edema was present was not established. Regardless, the changes in the ill and the well groups were similar. Interestingly, Kilgore and colleagues did show a small but significant increase in T2 signal of the corpus callosum, hinting that vasogenic edema was starting, and the increase in the AMS group was twice that of the non-AMS group, though not quite statistically significant.231 Although it is still very much an open question, the literature to date does not confirm that mild AMS or headache alone is related to brain edema. To summarize, moderate to severe AMS and HACE represent a continuum from mild to severe vasogenic cerebral edema. Headache alone, or the earliest stages of AMS, might be related to edema or could be related to other factors, such as cerebral vasodilation or a migraine mechanism; further research is needed to clarify this issue.

Individual Susceptibility and Intracranial Dynamics. What might explain individual susceptibility to AMS? Correlation of AMS with HVR, ventilation, fluid status, lung function, and physical fitness has been weak at best. Ross hypothesized in 1985 that the apparently random nature of susceptibility might be explained by random anatomic differences.386 Specifically, he suggested that persons with smaller intracranial and intraspinal CSF capacity would be disposed to develop AMS, because they would not tolerate brain swelling as well as those with more “room” in the craniospinal axis. It is the displacement of CSF through the foramen magnum into the spinal canal that is the first compensatory response to increased brain volume, followed by increased CSF absorption and decreased CSF formation. Studies have shown that the increase in ICP for a given increase in brain volume is directly related to the tightness of the brain in the cranium (the brain volume–to–intracranial volume ratio) and to the volume of the spinal canal.413 Thus, the greater the initial CSF volume, the more accommodation

that can take place in response to brain edema. Increases in volume are buffered by CSF dynamics. In light of our present understanding of increased brain volume on ascent to altitude, Ross’s hypothesis is very attractive. Preliminary data that showed a relationship of pre-ascent ventricular size or brain volume–to–cranial vault ratios and susceptibility to AMS support this hypothesis, and the idea deserves further study.148,490 Figure 1-11 incorporates this concept into the pathophysiology.

Natural Course of Acute Mountain Sickness The natural history of AMS varies with initial altitude, rate of ascent, and clinical severity. Symptoms can start within as little as 2 hours after arrival, and rarely if ever start after 36 hours at a given altitude. AMS usually resolves over the next 24 to 48 hours. The more rapid the ascent, and the higher the altitude, the more likely it is that the symptoms will appear sooner and be worse. Singh and associates421 followed the illness in soldiers airlifted to altitudes of 3300 to 5500 m. Incapacitating illness lasted 2 to 5 days, but 40% still had symptoms after 1 week and 13% after 1 month. Nine soldiers failed to acclimatize in 6 months and were considered unfit for duty at high altitude.421 Chinese investigators report that a percentage of lowland Han Chinese stationed on the Tibet Plateau cannot tolerate the altitude because of persistent symptoms and must be relocated to the plains.483 Persistent anorexia, nausea, and headache may afflict climbers at extreme altitude for weeks and can be considered a form of persistent AMS. The natural history of AMS in tourists who sleep at more moderate altitudes is much more benign. Duration of symptoms at 2700 m was 15 hours, with a range of 6 to 94 hours.309 Most individuals treat or tolerate their symptoms, as the illness resolves over 1 to 3 days while acclimatization improves, but some people with AMS seek medical treatment or are forced to descend if symptoms persist. A small percentage of those with AMS (8% at 4243 m)155 go on to develop cerebral edema, especially if ascent continues in spite of illness.

Treatment The proper management of AMS is based on the severity of illness at presentation, and often depends on logistics, terrain, and experience of the caregiver. Early diagnosis is the key, as treatment in the early stages of illness is easier and more successful (Box 1-4). Proceeding to a higher sleeping altitude in the presence of symptoms is contraindicated. The victim must be carefully monitored for progression of illness. If symptoms worsen despite an extra 24 hours of acclimatization or treatment, descent is indicated. The two indications for immediate descent are neurologic findings (ataxia or change in consciousness) and pulmonary edema. Mild AMS can be treated by halting the ascent and waiting for acclimatization to improve, which can take from 12 hours to 3 or 4 days. Acetazolamide (250 mg twice a day orally, or as a single dose) speeds acclimatization and thus terminates the illness if given early.138,276 Symptomatic therapy includes analgesics such as aspirin (500 mg or 650 mg), acetaminophen (650 to 1000 mg), ibuprofen57 or other nonsteroidal antiinflammatory drugs, or codeine (30 mg) for headache. Promethazine (Phenergan, 25 to 50 mg by suppository or ingestion) is useful for nausea and vomiting. Persons with AMS should avoid alcohol and other respiratory depressants because of the danger of exaggerated hypoxemia during sleep.

Chapter 1: High-Altitude Medicine

17

BOX 1-4. Field Treatment of High-Altitude Illness HIGH-ALTITUDE HEADACHE AND MILD ACUTE MOUNTAIN SICKNESS

Stop ascent, rest, and acclimatize at same altitude Acetazolamide, 125 to 250 mg bid, to speed acclimatization Symptomatic treatment as necessary with analgesics and antiemetics OR descend 500 m or more MODERATE TO SEVERE ACUTE MOUNTAIN SICKNESS

Low-flow oxygen, if available Acetazolamide, 125 to 250 mg bid, with or without dexamethasone, 4 mg PO, IM, or IV q6h Hyperbaric therapy OR immediate descent HIGH-ALTITUDE CEREBRAL EDEMA

Immediate descent or evacuation Oxygen, 2 to 4 L/min Dexamethasone, 4 mg PO, IM, or IV q6h Hyperbaric therapy HIGH-ALTITUDE PULMONARY EDEMA

Minimize exertion and keep warm Oxygen, 4 to 6 L/min until improving, then 2 to 4 L/min If oxygen is not available: Nifedipine, 10 mg PO q4h by titration to response, or 10 mg PO once, followed by 30 mg extended release q12 to 24h Inhaled beta-agonist Consider sildenafil 50 mg every 8 hrs Hyperbaric therapy OR immediate descent PERIODIC BREATHING

Acetazolamide, 62.5 to 125 mg at bedtime as needed

Descent to an altitude lower than where symptoms began effectively reverses AMS. Although the person should descend as far as necessary for improvement, descending 500 to 1000 m is usually sufficient. Exertion should be minimized. Oxygen, if available, is particularly effective (and supply is conserved) if given in low flow (0.5 to 1 L/min by mask or cannula) during the night. Hyperbaric chambers, which simulate descent, have been used to treat AMS and aid acclimatization. They are effective and require no supplemental oxygen. Lightweight (less than 7 kg) fabric pressure bags inflated by manual air pumps are now being used on mountaineering expeditions and in mountain clinics (Fig. 1-12). An inflation of 2 pounds per square inch (PSI) is roughly equivalent to a drop in altitude of 1600 m; the exact equivalent depends on the initial altitude.223,361 A few hours of pressurization results in symptomatic improvement and can be an effective temporizing measure while awaiting descent or the benefit of medical therapy.223,320,336,375,439 Long-term (12 hours or more) use of these portable devices is necessary to resolve AMS completely. Acetazolamide is of unquestionable prophylactic value and is now commonly and successfully used to treat AMS as well,

Figure 1-12. Gamow bag used to treat a patient with high altitude pulmonary edema at Everest Base Camp Medical Clinic (5350 m). (Photo courtesy Luanne Freer, MD.)

although data supporting this are minimal.138,276 Singh and colleagues successfully used furosemide (80 mg twice a day for 2 days) to treat 446 soldiers with all degrees of AMS; it has not since been studied for treatment.421 Furosemide induced brisk diuresis, relieved pulmonary congestion, and improved headache and other neurologic symptoms. Spironolactone, hydrochlorothiazide, and other diuretics have not yet been evaluated for treatment. The steroid betamethasone was initially reported by Singh and colleagues421 to improve symptoms of soldiers with severe AMS. Subsequently, studies have found dexamethasone to be effective for treatment of all degrees of AMS.113,163,227 Hackett and colleagues163 used 4 mg orally or intramuscularly every 6 hours, and Ferrazinni and associates113 gave 8 mg initially, followed by 4 mg every 6 hours. Both studies reported marked improvement within 12 hours, with no significant side effects. Symptoms increased when dexamethasone was discontinued after 24 hours.163 Clinicians debate whether the use of dexamethasone should also require descent. Is it safe to continue on after treatment with dexamethasone, or while taking the medication? In reality, people do, and problems seem to be few. In the authors’ opinion, dexamethasone use should be limited to less than 48 hours, to minimize side effects. This is generally sufficient time to descend, or to better acclimatize, with or without acetazolamide. The mechanism of action of dexamethasone is unknown; it does not affect oxygen saturation, fluid balance, or periodic breathing.259 The drug blocks the action of VEGF,402 diminishes the interaction of endothelium and leukocytes (thus reducing inflammation),134 and may also reduce cerebral blood flow.220 Dexamethasone seems to not improve acclimatization, as symptoms recur when the drug is withdrawn. Therefore, an argument could be made for using dexamethasone to relieve symptoms and acetazolamide to speed acclimatization.48

Prevention Graded ascent is the surest and safest method of prevention, although particularly susceptible individuals may still become ill. Current recommendations for people without altitude

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experience are to avoid abrupt ascent to sleeping altitudes greater than 3000 m and to spend 2 to 3 nights at 2500 to 3000 m before going higher, with an extra night for acclimatization every 600 to 900 m if continuing ascent. Abrupt increases of more than 600 m in sleeping altitude should be avoided when over 2500 m. However, a recent study on Aconcagua reinforced the notion that individual susceptibility is a key factor; those who are resistant to AMS can safely proceed much more quickly on the mountain.341 Day trips to higher altitude, with a return to lower altitude for sleep, aid acclimatization. Alcohol and sedative-hypnotics are best avoided on the first 2 nights at high altitude. Whether a diet high in carbohydrates reduces AMS symptoms is controversial.80,171,437 Exertion early in altitude exposure contributes to altitude illness,370 whereas limited exercise seems to aid acclimatization. Because altitude exposure in the previous weeks is protective, a faster rate of ascent may then be possible.

Acetazolamide Prophylaxis. Acetazolamide is the drug of choice for prophylaxis of AMS. A carbonic anhydrase (CA) inhibitor, acetazolamide slows the hydration of carbon dioxide: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3− CA CA The effects are protean, involving particularly the red blood cells, brain, lungs, and kidneys. By inhibiting renal CA, acetazolamide reduces reabsorption of bicarbonate and sodium and thus causes bicarbonate diuresis and metabolic acidosis starting within 1 hour after ingestion. This rapidly enhances ventilatory acclimatization, increasing oxygenation. Importantly, the drug maintains oxygenation during sleep and prevents periods of extreme hypoxemia (see Figure 1-5).159,433,436 Because of acetazolamide’s diuretic action, it counteracts the fluid retention of AMS. It also diminishes nocturnal antidiuretic hormone (ADH) secretion72 and decreases CSF production and volume and possibly CSF pressure.410 Which of these effects is most important in preventing AMS is unclear. Numerous studies taken together indicate that acetazolamide is approximately 75% effective in preventing AMS in persons rapidly transported to altitudes of 3000 to 4500 m.110 Indications for acetazolamide prophylaxis include rapid ascent (in 1 day or less) to altitudes over 3000 m; a rapid gain in sleeping altitude, for example, moving camp from 4000 to 5000 m in a day; and a past history of AMS or HAPE. The ideal dosage of acetazolamide for prevention is debated. Many studies have shown that 250 mg twice a day or three times a day was effective, as well as 500 mg in sustained action capsule taken every 24 hours.70,126,137,152,250,353,476 To reduce the side effects, especially paresthesias, clinicians have more recently been using smaller dosages (125 mg twice a day)298; two studies so far support this,32,254 whereas one does not.66 Renal carbonic anhydrase is blocked at a dosage of 5 mg/kg/day. As this seems to be the important effect for preventing AMS, this is probably the ideal dosage, both in children and adults. Thus, adjusting the dosage for body weight might provide the best effect with the fewest side effects. Duration of medication use varies; the standard advice is to start 24 hours before ascent. Most authors recommend continuing for at least the first 2 days at high altitude, and longer if there is a continuing gain in altitude. Acetazolamide can also be taken episodically, to speed

acclimatization at any point while gaining altitude, or to treat mild AMS. There is no rebound when discontinued. Although the danger of altitude illness passes after a few days of acclimatization, acetazolamide may still be useful for sleep. Acetazolamide has side effects, most notably peripheral paresthesias and polyuria, and less commonly nausea, drowsiness, impotence, and myopia. Because it inhibits the instant hydration of carbon dioxide on the tongue, acetazolamide allows carbon dioxide to be tasted and can ruin the flavor of carbonated beverages, including beer. As a nonantibiotic sulfonamide drug, acetazolamide is usually tolerated well by people with a history of sulfa antibiotic allergy; approximately 10% may have an allergic reaction.430 In those without a history of allergy to sulfa antibiotic, the incidence of hypersensitivity reaction to a sulfonamide nonantibiotic was 1.6%.430 The same analysis concluded that people who are penicillin allergic are in fact more likely to react to drugs such as acetazolamide than are people who are sulfa allergic. Nonetheless, it is wise to be cautious for those with a history of allergy, especially anaphylaxis to either sulfa or penicillin. Many experts recommend a trial dose of the medication well before the altitude sojourn, to determine if the drug is tolerated well. Although the usual allergic reaction is a rash starting a few days after ingestion, anaphylaxis to acetazolamide does rarely happen.

Dexamethasone Prophylaxis. Dexamethasone effectively prevents AMS. A dosage of 2 mg every 6 hours or 4 mg every 12 hours was sufficient for sedentary subjects,220 but for exercising subjects at or above 4000 m, this was insufficient,47,163,377 and 4 mg every 6 hours was necessary to prevent AMS.378 The initial chamber study in 1984 was with sedentary subjects.220 The drug reduced the incidence of AMS from 78% to 20%, comparable to previous studies with acetazolamide. Dexamethasone was not as effective in exercising subjects on Pike’s Peak,377 but subsequent work has shown effectiveness comparable to that of acetazolamide.37,110,259,308,491 The combination of acetazolamide and dexamethasone proved superior to dexamethasone alone.491 Because of potential serious side effects and the rebound phenomenon, dexamethasone is best reserved for treatment rather than for prevention of AMS, or used for prophylaxis when necessary in persons intolerant of or allergic to acetazolamide. Other Agents for AMS Prevention. Studies with Ginkgo biloba have had inconsistent results. Four studies had positive results, ranging from 100% to 50% reduction in AMS when given either 5 days or 1 day before ascent.127,269,315,381 Three studies were negative, two of which were follow-up studies by investigators with positive results previously.70,126,254 Conflicting results can possibly be explained by differences in dosing, duration of pretreatment, and varying rates of ascent, but most likely they result from differences in preparations of ginkgo. Ginkgo biloba is a complicated plant extract whose active ingredient in terms of preventing AMS is unknown. Even in the “standardized” preparations (24% flavonoids and 6% terpene ginkolides), the amounts of specific chemicals can vary considerably. Until the active ingredient is discovered and standardized, results with ginkgo will continue to be mixed. Meanwhile, as the product is very safe and inexpensive, does not require a prescription, and can be helpful, it is reasonable to

Chapter 1: High-Altitude Medicine consider its use. Acetazolamide, however, is probably the superior agent. Spironolactone,215,249 naproxen, calcium channel blockers, antacids, and medroxyprogesterone acetate have shown ineffectiveness for AMS prevention. Bailey and Davies tested an antioxidant cocktail for prevention of AMS.12 They reasoned that free-radical–mediated damage to the BBB might play a role in the pathophysiology. They preloaded nine subjects with daily l-ascorbic acid, dl-α-tocopherol acetate, and α-lipoic acid, and nine subjects with placebo for 3 weeks, and then maintained dosing during a 10-day trek to Everest base camp. Those on antioxidants had a slightly lower AMS score, higher arterial oxygen saturation, and better appetite.12 Although these results were of marginal clinical value, the use of antioxidants certainly deserves further study. See Bärtsch and colleagues for a detailed discussion of the antioxidant hypothesis.20

High-Altitude Cerebral Edema High-altitude cerebral edema is an uncommon but deadly condition, usually occurring in those with AMS or HAPE. Although HACE is most common over 3000 m, it has been reported as low as 2100 m.96 Reliable estimates of incidence range from 0.5% to 1% in unselected high-altitude visitors,28,152 but it was 3.4% in those who had developed AMS.152 HACE occurs in 13% to 20% of persons with HAPE,123,179,203 and in up to 50% of those who die from HAPE. In addition, HAPE is very common in those diagnosed with HACE; one series from Colorado reported that 11 of 13 with a primary diagnosis of HACE also had HAPE. Pure cerebral edema, without pulmonary edema, appears to be uncommon. The mean altitude of onset was 4730 m in one survey but was lower (3920 m) when there was an association with HAPE.204 Data are insufficient to draw any conclusions regarding effects of sex, age, preexisting illness, or genetics on susceptibility to HACE. Clinically and pathophysiologically, advanced AMS and HACE are similar, so a distinction between them is inherently blurred. See a recent review for a more complete discussion.156 HACE is an encephalopathy, whereas AMS is not. The hallmarks of HACE are ataxic gait, severe lassitude, and altered consciousness, including confusion, impaired mentation, drowsiness, stupor, and coma. Headache, nausea, and vomiting are frequent but not always present. Hallucinations, cranial nerve palsy, hemiparesis, hemiplegia, seizures, and focal neurologic signs have also been reported.99,167,190,421 Seizures are distinctly uncommon. Retinal hemorrhages are common but not diagnostic. The progression from mild AMS to unconsciousness may be as fast as 12 hours but usually requires 1 to 3 days; HACE can develop more quickly in those with HAPE. An arterial blood gas study or pulse oximetry often reveals exaggerated hypoxemia. Clinical examination and chest radiography may reveal pulmonary edema. Laboratory studies and lumbar puncture are useful only to rule out other conditions. Computerized tomography (CT) may show compression of sulci and flattening of gyri, and attenuation of signal more in the white matter than gray matter. MRI is more revealing, with a characteristic high T2 signal in the white matter, especially the splenium of the corpus callosum, and most evident on diffusion-weighted images.164,479 The following case report from Mt. McKinley illustrates a typical clinical course of HACE in conjunction with HAPE.

19

Clinical Presentation H.E. was a 26-year-old German lumberjack with extensive mountaineering experience. He ascended to 5200 m from 2000 m in 4 days and attempted the summit (6194 m) on the fifth day. At 5800 m he turned back because of severe fatigue, headache, and malaise. He returned alone to 5200 m, stumbling on the way because of loss of coordination. He had no appetite and crawled into his sleeping bag too weak, tired, and disoriented to undress. He recalled no pulmonary symptoms. In the morning H.E. was unarousable, slightly cyanotic, and noted to have CheyneStokes respirations. After 10 minutes on high-flow oxygen, H.E. began to regain consciousness, although he was completely disoriented and unable to move. A rescue team lowered him down a steep slope, and on arrival at 4400 m 4 hours later he was conscious but still disoriented, able to move extremities but unable to stand. Respiratory rate was 60 breaths/min and heart rate was 112 beats/min. Papilledema and a few rales were present. Sao2% was 54% on room air (normal is 85% to 90%). On a nonrebreathing oxygen mask with 14 L/min oxygen, the Sao2% increased to 88% and the respiratory rate decreased to 40 breaths/min. Eight milligrams of dexamethasone were administered intramuscularly at 4:20 pm and continued orally, 4 mg every 6 hours. At 5:20 pm, H.E. began to respond to commands. The next morning he was still ataxic but was able to stand, take fluids, and eat heartily. He was evacuated by air to Anchorage (sea level) at 12:00 pm. On admission to the hospital at 3:30 pm, roughly 36 hours after regaining consciousness, H.E. was somewhat confused and mildly ataxic. Arterial blood gas studies on room air showed a Po2 of 58 mm Hg, pH of 7.5, and Pco2 of 27 mm Hg. Bilateral pulmonary infiltrates were present on the chest radiograph. Magnetic resonance imaging of the brain revealed white matter edema, primarily of the corpus callosum (Fig. 1-13). On discharge the next morning H.E. was oriented, bright, and cheerful and had very minor ataxia and clear lung fields.

Pathophysiology The pathophysiology of HACE is a progression of the same mechanism seen in advanced AMS (see Acute Mountain Sickness, Pathophysiology; also see Figure 1-11), and appears to be vasogenic edema. In cases similar to this, lumbar punctures have revealed elevated CSF pressures, often more than 300 mm H2O,190,474 evidence of cerebral edema on CT scans and MR images,164,236 and gross cerebral edema on necropsy.98,99 Small petechial hemorrhages were also consistently found on autopsy, and venous sinus thromboses were occasionally seen.98,99 Welldocumented cases have often included pulmonary edema that was not clinically apparent. Whereas the brain edema of reversible HACE is most likely vasogenic, as the spectrum shifts to severe, end-stage HACE, then gray matter (presumably cytotoxic) edema develops as well, culminating in brain herniation and death. As Klatzo235 has pointed out, as vasogenic edema progresses, the distance between brain cells and their capillaries increases, so that nutrients and oxygen eventually fail to diffuse and the cells are rendered ischemic, leading to intracellular (cytotoxic) edema. Raised intracranial pressure produces many of its effects by decreasing cerebral blood flow, and brain tissue becomes

20

PART ONE: MOUNTAIN MEDICINE response to steroids and oxygen seems excellent if they are given early in the course of the illness and disappointing if they are not started until the victim is unconscious. Coma may persist for days, even after evacuation to low altitude, but other causes of coma must be considered and ruled out by appropriate evaluation.190 The average duration of hospital stay in one series of patients with severe HACE was 5.6 days, and average time to full recovery was 2.4 weeks, with a range of 1 day to 6 weeks.164 Two patients of the 44 in the series by Dickinson remained in coma for 3 weeks.99 Sequelae lasting weeks are common164,190; longer-term follow-up has been limited, but presumed permanent impairment has been reported.156,190 Prevention of HACE is the same as for AMS and HAPE.

Focal Neurologic Conditions without AMS or Cerebral Edema

Figure 1-13. Magnetic resonance image of a patient with high-altitude cerebral edema. Increased T2 signal in splenium of corpus callosum (arrow) indicates edema.

ischemic on this basis also.294 Focal neurologic signs caused by brainstem distortion and by extra-axial compression, as in third and sixth cranial nerve palsies, may develop,382 making cerebral edema difficult to differentiate from primary cerebrovascular events. The most common clinical presentation, however, is change in consciousness associated with ataxia, without focal signs.487

Treatment Given the sporadic nature and generally remote location of this disorder, it is not surprising there are no controlled trials regarding treatment of HACE. All experts agree that successful treatment requires early recognition. At the first sign of ataxia or change in consciousness, descent should be started, dexamethasone (4 to 8 mg intravenously, intramuscularly, or orally initially, followed by 4 mg every 6 hours) administered, and oxygen (2 to 4 L/min by vented mask or nasal cannula) applied if available (see Box 1-4). Oxygen can be titrated to maintain Sao2 at greater than 90% if oximetry is available. Comatose patients require additional airway management and bladder drainage. Attempting to decrease intracranial pressure by intubation and hyperventilation is a reasonable approach, although these patients are already alkalotic, and over-hyperventilation could result in disastrous cerebral ischemia. Loop diuretics such as furosemide (40 to 80 mg) or bumetanide (1 to 2 mg) may reduce brain hydration, and have been used successfully,97,421 but an adequate intravascular volume to maintain perfusion pressure is critical. Hypertonic solutions of saline, mannitol, or oral glycerol have been suggested but are rarely used in the field. Controlled studies are lacking, but empirically the

Various localizing neurologic signs, transient in nature and not necessarily occurring in the setting of AMS, suggest migraine, cerebrovascular spasm, transient ischemic attack, local hypoxia without loss of perfusion (watershed effect), or focal edema. Cortical blindness is one such condition. Hackett and colleagues161 reported six cases of transient blindness in climbers or trekkers with intact pupillary reflexes, which indicated that the condition was due to a cortical process. Treatment with breathing of either carbon dioxide (a potent cerebral vasodilator) or oxygen resulted in prompt relief, suggesting that the blindness was due to inadequate regional circulation or oxygenation. Descent effected relief more slowly. Other conditions that could be attributed to spasm or transient ischemic attack (TIA) have included transient hemiplegia or hemiparesis, transient global amnesia, unilateral paresthesias, aphasia, and scotoma.31,36,52,67,262,477,493 The true mechanism of these focal findings is unknown, and it may be multifactorial. Young, healthy altitude sojourners are unlikely to have TIA syndrome from cerebrovascular disease. The occurrence of stroke in a young, fit person at high altitude is uncommon but tragic. A number of case reports have described climbers with resultant permanent dysfunction.71,189,423 Indian soldiers at extreme altitude have a high incidence of stroke.219 Cerebral venous thrombosis presents more insidiously, and diagnosis is often delayed.143,222,389,423,443,493 Factors contributing to stroke may include polycythemia, dehydration, patent foramen ovale, and increased intracranial pressure if AMS is present, increased cerebrovenous pressure, cerebrovascular spasm, and, in certain episodes, coagulation abnormalities.33 Stroke may be confused with HACE. Neurologic symptoms, especially focal abnormalities without AMS or HAPE that persist despite treatment with oxygen, steroids, and descent, suggest a cerebrovascular event and mandate careful evaluation with a complete neurologic workup.

Clinical Presentation E.H., a 42-year-old male climber on a Mt. Everest expedition, awoke at 8000 m with dense paralysis of the right arm and weakness of the right leg. On descent the paresis cleared, but at base camp (5000 m) severe vertigo developed, along with extreme ataxia and weakness. Neurologic consultation on return to the United States resulted in a diagnosis of multiple small cerebral infarcts, but none was visible on CT scan of the brain. The hematocrit value 3

Chapter 1: High-Altitude Medicine weeks after descent from the mountain was 70%. Over the next 4 years, signs gradually improved, but mild ataxia, nystagmus, and dyslexia persist. The focal and persistent nature of the cerebral symptoms and signs, although multiple, indicates an etiology related to cerebrovascular effects rather than intracranial pressure. The hematocrit value on the mountain was greater than 70%, high enough for increased viscosity and microcirculatory sludging to contribute to ischemia and infarction. No familial thrombophilia was detected. Treatment of stroke is supportive. Oxygen and steroids may be worthwhile to treat any AMS or HACE component. Immediate evacuation to a hospital is indicated. Persons with transient ischemic attacks at high altitude should probably be started on aspirin therapy and proceed to a lower altitude. Oxygen may quickly abort cerebrovascular spasms and will improve watershed hypoxic events. When oxygen is not available, rebreathing to raise alveolar Pco2 may be helpful through increasing cerebral blood flow.

Cognitive Changes at High Altitude If cerebral oxygen consumption is constant, what causes the well-documented, albeit mild, cognitive changes at high altitude? The cognitive changes may be related to specific neurotransmitters that are affected by mild hypoxia. For example, tryptophan hydroxylase in the serotonin synthesis pathway has a high requirement for oxygen (Km = 37 mm Hg).79,129 Tyrosine hydroxylase, in the dopamine pathway, is also oxygen sensitive. Gibson and Blass suggested that a decrease in acetylcholine activity during hypoxia might explain the lassitude.129 In a fascinating study, Banderet and Lieberman showed that increased dietary tyrosine reduced mood changes and symptoms of environmental stress in subjects at simulated altitude.16 Further work with neurotransmitter agonists and antagonists will help shed light on their role in cognitive dysfunction at altitude and could lead to new pharmacologic approaches to improve neurologic function.

High-Altitude Pulmonary Edema The most common cause of death related to high altitude, HAPE is completely and easily reversed if recognized early and treated properly. Undoubtedly, HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of “pneumonia” within days of arriving at high altitude. The death of Dr. Jacottet, “a robust, broadshouldered young man,” on Mt. Blanc in 1891 (he refused descent so that he could “observe the acclimatization process” in himself) may have provided the first autopsy of HAPE. Angelo Mosso wrote, From Dr. Wizard’s post-mortem examination . . . the more immediate cause of death was therefore probably a suffocative catarrh accompanied by acute edema of the lungs. . . . I have gone into the particulars of this sorrowful incident because a case of inflammation of the lungs also occurred during our expedition, on the summit of Monte Rosa, from which, however, the sufferer fortunately recovered.319 On an expedition to K2 (Karakoram Range, Pakistan) in 1902, Alistair Crowley85 described a climber “suffering from edema of both lungs and his mind was gone.” In the Andes, physicians were familiar with pulmonary edema peculiar to high

21

altitude,209,264 but it was not until Houston187 and Hultgren and Spickard197 that the English-speaking world became aware of high altitude pulmonary edema (see Rennie354 for a review). Hultgren and colleagues208 then published hemodynamic measurements in persons with HAPE, demonstrating that it was a noncardiogenic edema. Since that time, many studies and reviews have been published, and HAPE is still the subject of intense investigation. The reader is referred to recent reviews.19,27,145,403,468 Individual susceptibility, rate of ascent, altitude reached, degree of cold,351 physical exertion and certain underlying medical conditions are all factors determining the prevalence of HAPE. The incidence varies from less than 1 in 10,000 skiers at moderate altitude in Colorado to 1 in 50 climbers on Mt. McKinley (6194 m) and up to 6% of mountaineers in the Alps ascending rapidly to 4559 m.24 Hultgren and colleagues reported 150 cases of HAPE over 39 months at a Colorado ski resort at 2928 m.206 Some regiments in the Indian Army had a much higher incidence of HAPE (15%) because of very rapid deployment to the extreme altitude of 5500 m422 (see Table 1-1). Persons who had a previous episode of HAPE had a 60% attack rate when they went to 4559 m in 36 hours; however, with a slower ascent, some of the same individuals were able to climb over 7000 m without developing HAPE.19,25 Although HAPE occurs in both sexes, it is perhaps less common in women.83,203,424 Whether all persons are capable of developing HAPE (with a very rapid ascent to a sufficiently high altitude and with heavy exercise) is arguable.27 With a sudden push to a higher altitude, even well-acclimatized individuals can succumb to HAPE, and some studies suggest that HAPE is a spectrum, with many persons contracting subclinical extravascular lung water.84 Nonetheless, a population of HAPEsusceptible persons with unique physiologic characteristics has been described (see HAPE Susceptibility). These individuals represent the small percentage of people who develop HAPE when others in the same circumstances do not.

Clinical Presentation D.L., a 34-year-old man, was in excellent physical condition and had been on numerous high-altitude backpacking trips, occasionally suffering mild symptoms of AMS. He drove from sea level to the trailhead and hiked to a 3050 m sleeping altitude the first night of his trip in the Sierra Nevada. He proceeded to 3700 m the next day, noticing more dyspnea on exertion when walking uphill, a longer time than usual to recover when he rested, and a dry cough. He complained of headache, shivering, dyspnea, and insomnia the second night. The third day the group descended to 3500 m and rested, primarily for D.L.’s benefit. That night D.L. was unable to eat, noted severe dyspnea, and suffered coughing spasms and headache. On the fourth morning, D.L. was too exhausted and weak to get out of his sleeping bag. His companions noted that he was breathless, cyanotic, and ataxic but had clear mental status. A few hours later he was transported by helicopter to a hospital at 1200 m. On admission he was cyanotic, oral temperature was 37.8° C (100° F), blood pressure 130/76 mm Hg, heart rate 96 beats/min, and respiratory frequency 20 breaths/min. Bilateral basilar rales were noted up to the scapulae. Findings of the cardiac examination

22

PART ONE: MOUNTAIN MEDICINE

TABLE 1-5. Severity Classification of High-Altitude Pulmonary Edema GRADE 1 Mild 2 Moderate 3 Severe

SYMPTOMS

SIGNS

CHEST FILM

Dyspnea on exertion, dry cough, fatigue while moving uphill (if any) Dyspnea, weakness, fatigue on level walking; raspy cough; headache; anorexia Dyspnea at rest, productive cough, orthopnea, extreme weakness

HR (rest) < 90–100; RR (rest) < 20; dusky nail beds; localized rales HR 90–100; RR 16–30; cyanotic nail beds; rales present; ataxia may be present Bilateral rales; HR > 110; RR > 30; facial and nail-bed cyanosis; ataxia; stupor; coma; blood-tinged sputum

Minor exudate involving less than 25% of one lung field Some infiltrates involving 50% of one lung or smaller area of both lungs Bilateral infiltrates > 50% of each lung

HR, heart rate; RR, respiratory rate. Modified from Hultgren HN: In Staub NC (ed): New York, Dekker, 1978, pp 437–469.

were reported as normal. Romberg and finger-to-nose tests revealed 1+ ataxia. Arterial blood gas studies on room air revealed Po2 24 mm Hg, Pco2 28 mm Hg, and pH 7.45. The chest radiograph showed extensive bilateral patchy infiltrates (Fig. 1-14C). D.L. was treated with bed rest and supplemental oxygen. On discharge to his sea level home 3 days later, his pulmonary infiltrates and rales had cleared, although his blood gas values were still abnormal: Po2 76 mm Hg, Pco2 30 mm Hg, and pH 7.45. He had an uneventful, complete recovery at home. D.L. was advised to ascend more slowly in the future, staging his ascent with nights spent at 1500 m and at 2500 m. He was taught the early signs and symptoms of HAPE and was advised about pharmacologic prophylaxis. This case illustrates a number of typical aspects of HAPE. Victims are frequently young, fit men who ascend rapidly from sea level and may not have previously suffered HAPE even with repeated altitude exposures; this ascent may have been faster than previous ascents. HAPE usually occurs within the first 2 to 4 days of ascent to higher altitudes (above 2500 m), most commonly on the second night.146 Decreased exercise performance and increased recovery time from exercise are the earliest indications of HAPE. The victim usually notices fatigue, weakness, and dyspnea on exertion, especially when trying to walk uphill; he or she often ascribes these nonspecific symptoms to various other causes. Signs of AMS, such as headache, anorexia, and lassitude, are present about 50% of the time.203 A persistent dry cough develops. Nail beds and lips become cyanotic. The condition typically worsens at night, and tachycardia and tachypnea develop at rest. Dyspnea at rest and audible congestion in the chest herald the development of a serious condition. In contrast to the usual 1- to 3-day gradual onset, HAPE may strike abruptly, especially in a sedentary person who may not notice the early stages.455 Orthopnea is uncommon (7%). Pink or blood-tinged, frothy sputum is a very late finding. Hemoptysis was present in 6% in one series.206 Severe hypoxemia may produce cerebral edema with mental changes, ataxia, decreased level of consciousness, and coma. Hultgren and colleagues reported an incidence of HACE of 14% in those with HAPE at ski resorts.206 On admission to the hospital, the victim does not generally appear as ill as would be expected on the basis of arterial blood gas and radiographic findings. Elevated temperature of up to

38.5° C (101.3° F) is common. Tachycardia correlates with respiratory rate and severity of illness (Table 1-5).208 Rales may be unilateral or bilateral and usually originate from the right middle lobe. Concomitant respiratory infection is sometimes present. Patients with pulmonary edema sometimes present with predominantly neurologic manifestations and minimal pulmonary symptoms and findings. Cerebral edema, especially with coma, may obscure the diagnosis of HAPE.157 Pulse oximetry or chest radiography confirms the diagnosis. The differential diagnosis includes pneumonia, bronchitis, mucus plugging, pulmonary embolism or infarct, heart failure, acute myocardial infarction, and sometimes asthma (see Box 1-3). Complications include infection, cerebral edema, pulmonary embolism or thrombosis, and such injuries as frostbite or trauma secondary to incapacitation.19,157,204

Hemodynamics Hemodynamic measurements show elevated pulmonary artery pressure and pulmonary vascular resistance, low to normal pulmonary wedge pressure, and low to normal cardiac output and systemic arterial blood pressure (Table 1-6).205,339 Echocardiography demonstrates high pulmonary artery pressure, tricuspid regurgitation, normal left ventricular systolic function, somewhat abnormal diastolic function,5 and variable rightsided heart findings of increased atrial and ventricular size.160,333 The electrocardiogram usually reveals sinus tachycardia. Changes consistent with acute pulmonary hypertension have been described, such as right axis deviation, right bundle branch block, voltage for right ventricular hypertrophy, and P wave abnormalities.19,203 Atrial flutter has been reported, but ventricular arrhythmias have not.

Laboratory Studies

Kobayashi and colleagues236 reported clinical laboratory values in 27 patients with HAPE that showed mild elevations of hematocrit and hemoglobin, probably secondary to intravascular volume depletion and perhaps plasma leakage into the lung. Elevation of the peripheral white blood cell count is common, but rarely is it greater than 14,000 cells/mL3. The serum concentration of creatine phosphokinase (CPK) is increased. Most of the rise in CPK has been attributed to skeletal muscle damage, although in two patients, CPK isoenzymes showed brain fraction levels of 1% of the total, which may have indicated brain

Chapter 1: High-Altitude Medicine

TABLE 1-6. Hemodynamic Measurements during High-Altitude Pulmonary Edema (HAPE) and after Recovery in Two Subjects and in a Group of 31 Control Subjects MEASUREMENT Sao2% Mean pulmonary artery pressure (mm Hg) Wedge pressure (mm Hg) Cardiac index (L/m2) Pulmonary vascular resistance (dyne/cm−5) Mean arterial blood pressure (mm Hg)

RECOVERY*

CONTROLS†

58.0 63.0

84.0 18.0

89.0 21.3

1.5

3.5

7.1

2.5 1210.0

4.4 169.0

4.1 169.0

—

96.0

HAPE*

82.0

*HAPE and recovery values from Penaloza D, Sime F: Am J Cardiol 23:369–378, 1969. † Mean values from 31 normal subjects studied at 3700 m; from Hultgren HN, Grover RF: Ann Rev Med 19:119–152, 1968.

damage.236 BNP values in patients with HAPE may be normal or elevated. Arterial blood gas studies consistently reveal respiratory alkalosis and marked hypoxemia more severe than expected for the patient’s clinical condition. Because respiratory or metabolic acidosis has not been reported, arterial blood gas studies are unnecessary if noninvasive pulse oximetry is available to measure arterial oxygenation. At 4200 m on Mt. McKinley, the mean value of arterial Po2 in HAPE was 28 ± 4 mm Hg. Values as low as 24 mm Hg in HAPE are not unusual. Arterial oxygen saturation values in HAPE subjects at 4300 m ranged from 40% to 70%, with a mean of 56% ± 8%,406 and at 2928 m, mean Sao2 was 74%.206 Arterial acid–base values may be misleading in patients taking acetazolamide, because this drug produces significant metabolic acidosis.

Radiographic Findings The radiographic findings in HAPE have been described in original reports.208,281,457,458 Findings are consistent with noncardiogenic pulmonary edema, with generally normal heart size and left atrial size and no evidence of pulmonary venous prominence, such as Kerley lines. The pulmonary arteries increase in diameter.458 Infiltrates are commonly described as fluffy and patchy with areas of aeration between them and in a peripheral location rather than central. Infiltrates may be unilateral or bilateral, with a predilection for the right middle lung field, which corresponds to the usual area of rales. Pleural effusion is rare. The radiographic findings generally correlate with the severity of the illness and degree of hypoxemia. A small right hemithorax, absence of pulmonary vascular markings on the right, and edema confined to the left lung are criteria for diagnosis of unilateral absent pulmonary artery.151 Radiographic findings of HAPE are presented in Figure 1-14. Clearing of infiltrates is generally rapid once treatment is initiated. Depending on severity, complete clearing may take from 1 day to several days. Infiltrates are likely to persist longer if

23

the patient remains at high altitude, even if confined to bed and receiving oxygen therapy. Radiographs taken within 24 to 48 hours of return to low altitude may still be able to confirm the diagnosis of HAPE.

Pathologic Findings More than 20 autopsy reports of persons who died of HAPE have been published.10,98,324,421,422,474 Of those whose cranium was opened, more than half had cerebral edema. All lungs showed extensive and severe edema, with bloody, foamy fluid in the airways. Lung weights were 2 to 4 times normal. The left side of the heart was normal. The right atrium and main pulmonary artery were often distended. Proteinaceous exudate with hyaline membranes was characteristic. All lungs had areas of inflammation with neutrophil accumulation. The diagnosis of bronchopneumonia was common, although bacteria were not noted. Pulmonary veins, the left ventricle, and the left atrium were generally not dilated, in contrast to the right ventricle and atrium. Most reports mention capillary and arteriolar thrombi and alveolar fibrin deposits, as well as microvascular and gross pulmonary hemorrhage and infarcts. The autopsy findings thus suggest a protein-rich, permeability-type edema, with thrombi or emboli. Confirmation of HAPE as a permeability edema was obtained by analysis of alveolar lavage fluid by Schoene and associates.404,406 These authors found a 100-fold increase in lavage fluid protein levels in patients with HAPE compared with well control subjects and patients with AMS.406 The lavage fluid also had a low percentage of neutrophils, in contrast to findings in adult respiratory distress syndrome. Further evidence for a permeability edema was a 1 : 1 ratio of aspirated edema fluid protein to plasma protein level found by Hackett and colleagues.150 In addition, the lavage fluid contained vasoactive eicosanoids and complement proteins, indicative of endothelium–leukocyte interactions. More recent research using repeated bronchoalveolar lavage as HAPE was developing found that inflammation was absent early on, suggesting that inflammation is a response to the alveolar damage rather than an initiating event.438

Mechanisms of High-Altitude Pulmonary Edema An acceptable explanation for HAPE must take into account three well-established facts: excessive pulmonary hypertension, high-protein permeability leak, and normal function of the left side of the heart. A mechanism consistent with these facts is failure of capillaries secondary to overperfusion and capillary hypertension (Fig. 1-15).

Role of Pulmonary Hypertension. Excessive pulmonary artery pressure (PAP) is the sine qua non of HAPE; no cases of HAPE have been reported without pulmonary hypertension. All persons ascending to high altitudes or otherwise enduring hypoxia, however, have some elevation of PAP. The hypoxic pulmonary vasoconstrictor response (HPVR) is thought to be useful in humans at sea level because it helps match perfusion with ventilation. When local areas of the lung are poorly ventilated because of infection or atelectasis, for example, the HPVR directs blood away from those areas to well-ventilated regions. In the setting of global hypoxia, as occurs with ascent to high altitude, HPVR is presumably diffuse and all areas of the lung constrict, causing a restricted vascular bed and an increase in PAP, which is of little if any value for ventilation–

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A

B

C

D

Figure 1-14. A, Typical radiograph of high-altitude pulmonary edema (HAPE) in 29-year-old female skier at 2450 m. B, Same patient 1 day after descent and oxygen administration, showing rapid clearing. C, Bilateral pulmonary infiltrates on radiograph of a patient with severe HAPE after descent (case presented in text). D, Ventilation and perfusion scans in person with congenital absence of right pulmonary artery after recovery from HAPE.

Chapter 1: High-Altitude Medicine

25

Altitude hypoxia HVR, sleep, and exercise ↓ PaO2

↑ Sympathetic activity

Uneven HPV Pulmonary and peripheral venous constriction

Exercise PHTN

Overperfusion

↑ Pulmonary blood volume

↑ Pcap

Capillary stress failure ↓ Alveolar Na and H2O clearance Capillary leak

High-altitude pulmonary edema

Figure 1-15. Proposed pathophysiology of high-altitude pulmonary edema. HPV, hypoxic pulmonary vasoconstriction; HVR, hypoxic ventilatory response; Pcap, capillary pressure; PHTN, pulmonary hypertension.

perfusion matching at high altitude. The degree of HPVR varies widely among individuals (as well as among species) and is most likely an inherent trait. Persons who are HAPE susceptible have a greater increase in PAP than those who are not (see HAPE Susceptibility). Although other factors, such as the vigor of the ventilatory response and the subsequent alveolar Po2 value, may help determine the ultimate degree of pulmonary hypertension, HPVR appears to be the dominant factor. Because all persons with HAPE have excessive pulmonary hypertension, but not all those with excessive pulmonary hypertension have HAPE, it appears that pulmonary hypertension is a necessary factor but in itself is not the cause of HAPE.

Overperfusion and Capillary Leak. To explain how pulmonary hypertension might lead to edema, Hultgren suggested that in those who develop HAPE, the hypoxic pulmonary vasoconstriction is uneven and the delicate microcirculation in an unconstricted (relatively dilated) area is subjected to high pressure and flow, leading to leakage (edema). The unevenness could be due to anatomic characteristics, such as distribution of muscularized arterioles, or to functional factors, such as loss of HPVR in severely hypoxic regions.198 Uneven perfusion is suggested clinically by the typical patchy radiographic appearance and is supported by lung scans and MRI during acute hypox-

ia that show uneven perfusion in persons with a history of HAPE.184,456 Persons born without a right pulmonary artery are highly susceptible to HAPE (see Figure 1-14D),151 supporting the concept of overperfusion of a restricted vascular bed as a cause of edema, since the entire cardiac output flows into one lung. Other causes of overperfusion of the pulmonary circulation include left-to-right shunts, such as atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). The rapid reversibility of the illness and the response to vasodilators are also consistent with this mechanism. When the hydrostatic pressure is reduced, the alveolar fluid is quickly reabsorbed. Other factors contributing to increased hydrostatic pressure, such as exercise or a high salt load with subsequent hypervolemia, also may play a role in HAPE. In fact, the authors have several times observed onset of HAPE after a large salt intake. Some studies have also suggested a role for pulmonary venous constriction, which would contribute to increased capillary hydrostatic pressure.160,275 The end result of overperfusion and increased capillary pressure275 is distention, increased filtration of fluid, and even rupture of the capillary–alveolar membrane, termed “stress failure,”470,471 with subsequent leakage of cells and proteins.

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Alveolar Fluid Balance. Fluid filtration into the interstitial and alveolar space, reabsorption back across the epithelial membrane, and clearance of interstitial fluid by lymph result in a dynamic balance that generally prevents alveolar flooding. On ascent to altitude, the hydrostatic pressure gradient for filtration is increased. As might be expected, multiple lines of evidence suggest that extravascular lung water is increased at altitude.84,136,460 Despite this, very few people develop frank alveolar flooding. This may well be because of differences in hydrostatic pressure in those resistant and susceptible to HAPE. However, persons who contract HAPE appear to also have an impaired ability to clear alveolar fluid. On a constitutive (genetic) basis, HAPE subjects have lower activity of the epithelial sodium channel (ENaC) and therefore reduced ability to transport sodium across the epithelium back into the interstitial space.280,394,395 (It is the sodium gradient across the epithelium that determines movement of water from the alveolus.) In addition, epithelial sodium transport is diminished by hypoxia per se, so that those with already impaired function become more impaired at altitude. To what extent HAPE may be due to failure of reabsorption of alveolar fluid will require more research185 (see Figure 1-15). Control of Ventilation. As in AMS, control of ventilation may play a role in the pathophysiology of HAPE. Those with HAPE had a lower HVR than persons who acclimatized well,162,285 but not all persons with a low HVR become ill. Thus, low HVR appears to play a permissive, rather than causative, role in the development of HAPE. A brisk HVR, and therefore a large increase in ventilation, appears to be protective. Persons who tend to hypoventilate are more hypoxemic and presumably suffer greater pulmonary hypertension. Possibly more important, a low HVR may permit episodes of extreme hypoxemia during sleep (see Figure 1-6). Supporting this concept is the frequency with which the onset of HAPE occurs during sleep, especially in persons who have ingested sleep medications.146,162 In addition, a HAPE victim with a low HVR does not mount an adequate ventilatory response to the severe hypoxemia of the illness and may suffer further ventilatory depression through central nervous system (CNS) suppression (hypoxic ventilatory depression). Such persons, when given oxygen, show a paradoxical increase in ventilation.162 Despite the correlation of HAPE with low HVR, its value as a sea-level predictor is poor.93

HAPE Susceptibility Persons susceptible to HAPE (HAPE-s) show at sea level an abnormal rise of pulmonary artery pressure and pulmonary vascular resistance during a hypoxic challenge at rest and during exercise, and even during exercise in normoxia, suggesting overreactivity of the pulmonary circulation to both hypoxia and exercise.109,141,224 Part of this reactivity may be related to greater alveolar hypoxemia secondary to lower HVR,162,182,286 but other factors have been uncovered. Microneurographic recordings from the peroneal nerve during hypoxia established a direct link in HAPE-s between the rise in PAP and greater sympathetic activation,106 indicating that sympathetic overactivation might contribute to HAPE. Smaller and less distensible lungs have been noted in HAPE-s, which might limit the ability to accommodate increased flow by vascular recruitment and thus result in higher vascular resistance.109,182,426 Another characteristic of HAPE-s is abnormal endothelial function, as evidenced by reduced nitric oxide (NO) synthesis during hypoxia46,63,400 and during

Nitric oxide - overview

Hypoxia

eNOS

NO

cGMP

L-arginine

Vascular muscle relaxation

Degradation by PDE-5

Figure 1-16. The nitric oxide pathway and action of PDE-5 inhibitors.In the presence of a PDE5 inhibitor, cGMP, the second messenger of NO, is not degraded and vasodilation is therefore enhanced. eNOS, endothelial nitric oxide synthase; NO, nitric oxide; cGMP, cyclic guanosine monophosphate; PDE-5, phosphodiesterase 5.

HAPE,105 and higher levels of endothelin, a potent pulmonary vasoconstrictor.397,427 The importance of reduced NO is reinforced by studies showing improvement in pulmonary hemodynamics when either NO or a phosphodiesterase (PDE)-5 inhibitor, sildenafil or tadalafil, was given to HAPE subjects6,128,272,400 (Fig. 1-16). As mentioned previously, HAPE-s subjects are also characterized by impairment of respiratory transepithelial sodium and water transport, making it harder to reabsorb alveolar fluid396,399 (see Figure 1-15).

Genetics of HAPE The first major genetic studies in lowlanders visiting high altitudes have focused on HAPE because it is the most fully understood pathophysiologic process occurring in lowlanders visiting high altitudes. Although many of the characteristics of HAPEsusceptible persons are apparently genetically determined, actual genetic studies are conflicting and difficult to interpret. Good evidence for a genetic component to HAPE susceptibility comes from study of major human leukocyte antigen (HLA) alleles in 28 male and 2 female subjects with a history of HAPE compared with HLA alleles in 100 healthy volunteers.168 The HLA-DR6 and HLA-DQ4 antigens were associated with HAPE, and HLA-DR6 with pulmonary hypertension. These findings suggest that immunogenetic susceptibility may underlie the development of HAPE, at least in some cases. Given the importance of endothelial function in HAPE, investigators have looked at gene polymorphisms for endothelial nitric oxide synthase (eNOS). Two recent studies have established a link between HAPE-s and the Glu298Asp alleles of the eNOS gene in Japanese and Indian subjects.1,103 An additional study of NOS3-related gene polymorphisms that could explain decreased NO synthesis found no relation to HAPE-s.465 This may be explained by racial differences, or by the specific processes encoded by the different gene fragments. The insertion-deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has also garnered attention, because the renin-aldosterone-angiotensin system (RAAS) is known to be activated in HAPE,29 and the ACE gene has also been linked to performance at altitude.310 The I/D polymorphism was not associated with HAPE susceptibility in populations of Indians, Japanese, and whites.94,186,245 However, one variant of the angiotensin receptor gene was correlated with HAPE susceptibility in Japanese people.186

Chapter 1: High-Altitude Medicine

27

In summary, gene polymorphisms coding for the angiotensin receptor and endothelial nitric oxide distinguish HAPE-sensitive from HAPE-resistant subjects. In the near future, single nucleotide polymorphism scanning techniques, as well as RNA gene expression techniques, will be used to explore genetic contributions to high-altitude physiology and pathophysiology. The search for a genetic basis of HAPE susceptibility continues.102,318

Treatment Treatment choices for HAPE depend on severity of illness and logistics. Early recognition is the key to successful outcome, as with all high-altitude illnesses (see Box 1-4). In the wilderness, where oxygen and medical expertise may be unavailable, persons with HAPE need to be urgently evacuated to lower altitude. However, because of augmented pulmonary hypertension and greater hypoxemia with exercise, exertion must be minimized. If HAPE is diagnosed early, recovery is rapid with a descent of only 500 to 1000 m and the victim may be able to re-ascend slowly 2 or 3 days later. In high-altitude locations with oxygen supplies, bed rest with supplemental oxygen may suffice, but severe HAPE may require high-flow oxygen (4 L/min or greater) for more than 24 hours. Hyperbaric therapy with the fabric pressure bag is equivalent to low-flow oxygen and can help conserve oxygen supplies.361 Oxygen immediately increases arterial oxygenation and reduces pulmonary artery pressure, heart rate, respiratory rate, and symptoms. When descent is not possible, oxygen (or a hyperbaric bag) can be lifesaving. Rescue groups should make delivery of oxygen to the victim, by airdrop if necessary, the highest priority if descent is slow or delayed. If oxygen is not available, immediate descent is lifesaving. Waiting for a helicopter or rescue team has too often proved fatal. Since cold stress elevates PAP, the victim should be kept warm.69 The use of a mask providing pressure (resistance) on expiration (EPAP) was shown to improve gas exchange in HAPE, and this may be useful as a temporizing measure.405 The same is accomplished with pursed-lip breathing. An unusual case report suggested that a climber may have saved his partner’s life by postural drainage to expel airway fluid.50 Drugs are of limited necessity in HAPE, because oxygen and descent are so effective. Medications that reduce pulmonary blood volume, PAP, and pulmonary vascular resistance are physiologically rational to use when oxygen is not available or descent is delayed. Singh and associates421 reported good results with furosemide (80 mg every 12 hours), and greater diuresis and clinical improvement occurred when 15 mg parenteral morphine was given with the first dose of furosemide. Their use, however, has been eclipsed by recent results with vasodilators. The calcium channel blocker nifedipine (30 mg slow release every 12 to 24 hours or 10 mg orally repeated as necessary) was effective in reducing pulmonary vascular resistance and PAP during HAPE, and it slightly improved arterial oxygenation.25 Clinical improvement, however, was not dramatic. Nifedipine is well tolerated and unlikely to cause significant hypotension in healthy persons, and it avoids the danger of CNS depression from morphine and possible hypovolemia from diuretics. Clinical improvement is much better, however, with oxygen and descent than with any medication. Nitric oxide is a potent pulmonary vasodilator and improves hemodynamics in HAPE, but it is rarely available, and in any event it is usually given with oxygen. The PDE-5 inhibitors, which increase cyclic guanosine

Figure 1-17. Chest radiograph of severe HAPE in a 4-year-old girl with a small, previously undiagnosed patent ductus arteriosus that predisposed her to HAPE.

monophosphate (cGMP) to produce pulmonary vasodilation during hypoxia128,356,357 (see Figure 1-16), have shown value for prevention of HAPE272 but have not yet been studied for treatment. Whether these agents will prove to be more effective than nifedipine for treatment is unknown. A theoretical advantage is that the PDE-5 inhibitors produce less systemic vasodilation. Nifedipine, and perhaps other vasodilators, might be useful as adjunctive therapy but are no substitute for definitive treatment (see Box 1-4).144 After evacuation of the victim to a lower altitude, hospitalization may be warranted for severe cases. Treatment consists of bed rest and oxygen (sufficient to maintain Sao2% greater than 90%). Rapid recovery is the rule. A rare instance of progression to adult respiratory distress syndrome has been reported, but it was impossible to exclude other diagnoses completely.495 Antibiotics are indicated for infection when present. Occasionally, pulmonary artery catheterization or Doppler echocardiography is necessary to differentiate cardiogenic from high-altitude pulmonary edema. Endotracheal intubation and mechanical ventilation are rarely needed. A HAPE victim demonstrating unusual susceptibility, such as onset of HAPE despite adequate acclimatization, or onset below 2750 m, might require further investigation, such as echocardiography, to rule out an intracardiac shunt. In children, undiagnosed congenital heart disease is worth considering (Fig. 1-17). Hospitalization until blood gases are completely normal is not warranted; all persons returning from high altitude are at least partially acclimatized to hypoxemia, and hypocapnic alkalosis persists for days after descent. Distinct clinical improvement, radiographic improvement over 24 to 48 hours, and an arterial Po2 of 60 mm Hg or a Sao2% greater than 90% are adequate discharge criteria. Patients are advised to resume normal activities gradually and are warned that they may require up to 2 weeks to recover complete strength. Physicians should recommend preventive measures, including graded ascent with adequate time for acclimatization, and should provide instruction on the use of acetazolamide, nifedipine, or PDE-5 inhibitors for future

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ascents. An episode of HAPE is not a contraindication to subsequent high-altitude exposure, but education to ensure proper preventive measures and recognition of early symptoms is critical.

Prevention The preventive measures previously described for AMS also apply to HAPE: graded ascent, time for acclimatization, low sleeping altitudes, and avoidance of alcohol and sleeping pills (see Box 1-4). Exertion may contribute to onset of HAPE, especially at moderate altitude. Reports from North America at 2500 to 3800 m have included hikers, climbers, and skiers, all of whom were exercising vigorously. Menon296 clearly showed that sedentary men taken abruptly to higher altitude were just as likely to become victims of HAPE. Prudence dictates not overexerting for the first 2 days at altitude. Considerable clinical experience suggests that acetazolamide prevents HAPE in persons with a history of recurrent episodes. Recent work showing that acetazolamide blocks hypoxic pulmonary hypertension supports this practice.45,240 Nifedipine (20 mg slow release every 8 hours) prevented HAPE in subjects with a history of repeated episodes.25 The drug should be carried by such individuals and started at the first signs of HAPE or, for an abrupt ascent, started when leaving low altitude. The PDE-5 inhibitors sildenafil and tadalafil effectively block hypoxic pulmonary hypertension and will also prevent HAPE.272 The optimal dosage has not been established; regimens for sildenafil have varied from a single dose of 50 or 100 mg just prior to exposure for acute studies,128,356 to 40 mg three times a day for 2 to 6 days at altitude,340,357 and for tadalafil, 10 mg every 12 to 24 hours.115,272 Most recently, and rather surprisingly, dexamethasone was found effective in preventing HAPE in susceptible subjects. Maggiorini and colleagues gave 8 mg dexamethasone every 12 hours, starting 2 days prior to exposure, and found it as effective as tadalafil in reducing PAP and preventing HAPE.272 Dexamethasone has many actions in the lung, and which action might be responsible for this observed effect is unknown.27 As evidenced by this list of therapies, any agent that blocks hypoxic pulmonary hypertension will block onset of HAPE, reinforcing the concept of pulmonary hypertension as the sine qua non of high-altitude pulmonary edema.

Reentry Pulmonary Edema In some persons who have lived for years at high altitude, HAPE develops on re-ascent from a trip to low altitude.107 Authors have suggested that the incidence of HAPE on re-ascent may be higher than that during initial ascent by flatlanders,29,200 but data on true incidence are difficult to obtain. Children and adolescents are more susceptible than adults.107 Hultgren199 found a prevalence of HAPE in Peruvian natives of 6.4 per 100 exposures in the 1- to 20-year age group, and 0.4 per 100 exposures in persons over 21 years. The phenomenon has been observed most often in Peru, where high-altitude residents can return from sea level to high altitude quite rapidly. Cases have also been reported in Leadville, Colorado,408 but reports are conspicuously rare from Nepal and Tibet,482 perhaps because such rapid return back to high altitude is not readily available.485 Severinghaus411 has postulated that the increased muscularization of pulmonary arterioles that develops with chronic highaltitude exposure generates an inordinately high pulmonary artery pressure on re-ascent, causing the edema.


OTHER MEDICAL CONCERNS AT HIGH ALTITUDE

High-Altitude Deterioration The world’s highest human habitation is at approximately 5500 m, and above this altitude, deterioration outstrips the ability to acclimatize.229 The deterioration is more rapid the higher one goes above the maximum point of acclimatization. Above 8000 m, deterioration is so rapid that without supplemental oxygen, death can occur in a matter of days.461 Lifepreserving tasks such as melting snow for water may become too difficult, and death may result from dehydration, starvation, hypothermia, and especially neurologic and psychiatric dysfunction.387 Loss of body weight is a prominent feature of high-altitude deterioration. Body weight is progressively lost because of anorexia and malabsorption during expeditions to extreme high altitude. Pugh345 reported a 14 to 20 kg body weight loss in climbers on the 1953 British Mt. Everest Expedition. Nearly 30 years later, with improvement in food and cooking techniques, climbers on the American Medical Research Expedition to Mt. Everest still lost an average of 6 kg.54 This was due in part to a 49% decrease in fat absorption and a 24% decrease in carbohydrate absorption. During OEII, in which the “climbers” were allowed to eat foods of their choosing ad libitum, they still suffered large weight losses: 8 kg overall, including 3 kg of fat and 5 kg of lean body weight (muscle).191,384 At 4300 m, weight loss was attenuated by adjusting caloric intake to match caloric expenditure.64 Thus, significant weight loss with prolonged exposure to high altitude may be overcome with adequate caloric intake, but decreased appetite is a problem.226,446 At very high altitudes, an increase in caloric intake may not be sufficient to completely counteract the severe anorexia and weight loss, as other mechanisms may come into play. At extreme altitude, Ryn387 reported an incidence of acute organic brain syndrome in 35% of climbers going above 7000 m, in association with high altitude deterioration. This syndrome, with its features of frank psychosis and impaired judgment, could directly threaten survival.

Children at High Altitude Children born at high altitude in North America appear to have a higher incidence of complications in the neonatal period than do their lower altitude counterparts.329 In populations better adapted to high altitude over many generations, neonatal transition has not been as well scrutinized, but there does appear to be some morbidity.473 High-altitude residence does not clearly impact eventual stature, but growth and development are slowed.92,314 In the developing world, confounding factors such as nutrition and socioeconomic status make these issues difficult to assess.195 Children residing at high altitude are more likely to develop pulmonary edema on return to their homes from a low-altitude sojourn than are lowland children on induction to high altitude. Some of these children may have preexisting pulmonary hypertension of various causes.90 Lowland children traveling to high altitude are just as likely to suffer AMS as are adults.344 No data indicate that children are more susceptible to altitude illness, although diagnosis can be more difficult in preverbal children.489 Despite this somewhat reassuring fact, very conservative recommendations are made regarding taking children to high altitude; it should be made

Chapter 1: High-Altitude Medicine clear that these opinions are not based on science.35,343 Durmowicz and colleagues showed that children with respiratory infections were more susceptible to HAPE.107 Children can be given acetazolamide or dexamethasone as necessary for AMS or HACE. The dosage of acetazolamide for prevention or treatment of AMS in children is 5 mg/kg/day in divided doses. See Pollard and colleagues for an excellent consensus document on children at altitude.344

High-Altitude Syncope Syncope within the first 24 hours of arrival occurs occasionally at moderate altitude325,326 but is not observed in mountaineers at higher altitudes; it is a problem of acute induction to altitude. The mechanism is an unstable cardiovascular control system, and it is considered a form of neurohumoral (or neurocardiogenic) syncope.119 An unstable state of cerebral autoregulation may also play a role.492 These events appear to be random and seldom occur a second time. Preexisting cardiovascular disease is not a factor in most cases. Postprandial state and alcohol ingestion seem to be contributing factors. Altitude syncope has no direct relationship to high-altitude illness.36

Alcohol at High Altitude Two questions regarding alcohol are frequently asked: (1) does alcohol affect acclimatization, and (2) does altitude potentiate the effects of alcohol? Epidemiologic research indicated that 64% of tourists ingested alcohol during the first few days at 2800 m.183 The effect of alcohol on altitude tolerance and acclimatization might therefore be of considerable relevance. Roeggla and colleagues determined blood gases 1 hour after ingestion of 50 g of alcohol (equivalent to 1 L of beer) at 171 m and again after 4 hours at 3000 m. A placebo-controlled, double-blinded, paired design was used. For the 10 subjects, alcohol had no effect on ventilation at the low altitude, but at the high altitude it depressed ventilation, as gauged by a decreased arterial Po2 (from 69 to 64 mm Hg) and increased Pco2 (from 32.5 to 34 mm Hg).379 Whether this degree of ventilatory depression would contribute to AMS and whether repeated doses would have greater effect were not tested. Nonetheless, the authors argue that alcohol might impede ventilatory acclimatization and should be used with caution at high altitude. Conventional wisdom proffers an additive effect of altitude and alcohol on brain function. McFarland, who was concerned about the interaction in aviators, wrote, “The alcohol in two or three cocktails would have the physiological action of four or five drinks at altitudes of approximately 10,000 to 12,000 feet.”291 Also, “Airmen should be informed that the effects of alcohol are similar to those of oxygen want and that the combined effects on the brain and the CNS are significant at altitudes even as low as 8,000 to 10,000 feet.”291 His original observations were made on two subjects in the Andes in 1936. He found that blood alcohol levels rose more rapidly and reached higher values at altitude, but he noted no interactive effect of alcohol and altitudes of 3810 and 5335 m.292 Most subsequent studies refuted the increased blood alcohol concentration data except at the highest altitudes, over 5450 m. Higgins and colleagues, in a series of chamber studies,177,178 found blood alcohol levels were similar at 392 m and at 3660 m, and they noted no synergistic effects of alcohol and altitude. Lategola and colleagues253 found that blood alcohol uptake curves were the

29

same at sea level and at 3660 m, and performance on math tests showed no interaction between alcohol and altitude. In another study of 25 men, performance scores were similar at sea level and at a simulated 3810-m altitude, with a blood alcohol level of 88 mg%.77 Performance was not affected by hypoxia, only by alcohol, and older subjects were more affected. When more demanding tasks were tested, Collins found that a blood alcohol level of 91 mg% affected performance, as did an altitude of 3660 m during night sessions when the subjects were sleep deprived, but there was no significant interaction between altitude and alcohol.76 In the one study in which Collins and colleagues were able to discern some altitude effect, there was a simple additive interaction of altitude (hypoxic gas breathing) and alcohol.78 He concluded that performance decrements due to alcohol might be increased by altitudes of 3660 m (12,000 feet) if subjects are negatively affected by that altitude without alcohol. All of these aviation-oriented studies used acute hypoxia equivalent to no more than 3500 m. Perhaps the highest altitude (without supplemental oxygen) at which alcohol was studied was 4350 m, on the summit of Mt. Evans in Colorado. Freedman and colleagues found that alcohol affected auditory evoked potentials to the same extent as that seen in Denver—that is, no influence of altitude was detectable.118 In summary, the limited data on blood gases at altitude after alcohol ingestion support the popular notion that alcohol could slow ventilatory acclimatization and therefore might contribute to AMS. Considerable data at least up to 3660 m, however, refute the belief that altitude potentiates the effect of alcohol. How altitude and alcohol might interact during various stages of acclimatization in individuals at higher altitudes is still unknown.

Thrombosis: Coagulation and Platelet Changes After deaths due to altitude illness, autopsy findings of widespread thrombi in the brain and lungs, as well as the impression that thrombosis is greater at altitude,219 have led to many investigations of the clotting mechanism at high altitude. For a review, see Grover and Bärtsch.139 Although changes in platelets and coagulation have been observed in rabbits, mice, rats, calves, and humans on ascent to high altitude,174 these generally occur with very rapid ascent. In vivo studies using more realistic ascent profiles up to 4500 m in the mountains, and higher in chambers, have generally not found changes in coagulation and fibrinolysis.139 Although the increased incidence of thrombosis in soldiers and others at extreme altitude can be attributed to dehydration, polycythemia, and forced inactivity, there is some evidence of enhanced fibrin formation with a stay of a few weeks above 5000 m.379 As for thrombosis in HAPE, Singh and colleagues419 reported increased fibrinogen levels and prolonged clot lysis times during HAPE, attributed to a breakdown of fibrinolysis. These authors also reported thrombotic, occlusive hypertensive pulmonary vascular disease in soldiers who had recently arrived at extreme altitude.418 A series of experiments by Bärtsch and colleagues, however, carefully examined this issue in well subjects and in those with AMS and HAPE.22,139 They concluded that HAPE is not preceded by a prothrombotic state and that only in “advanced HAPE” is there fibrin generation, which abates rapidly with oxygen treatment. They considered the coagulation and platelet activation as an epiphenomenon rather than as an inciting pathophysiologic factor, and most likely due to

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inflammation from the structural damage to the capillaries or the extreme hypoxemia. A difficult clinical question is whether ascent to altitude might result in thrombosis in persons with familial thrombophilia, such as factor V Leiden, a common anomaly, or protein C deficiency, antiphospholipid syndrome, or others. Such cases have been reported,33,53 but cause and effect cannot be established. In addition, persons with a past history of deep vein thrombosis or pulmonary embolism wonder if they are at increased risk at high altitude, as do women on hormonal contraceptives. Unfortunately, the literature does not help provide guidance for these individuals. Some experts empirically recommend an aspirin a day during altitude exposure for such patients, and this seems to be a safe suggestion. Others have raised the possibility that aspirin therapy might cause or exacerbate retinal hemorrhages at high altitude. Although no study has investigated this at altitude, research from patients with diabetic retinopathy has shown no danger of increased hemorrhages from aspirin.17 In addition, a retinal hemorrhage in a climber was treated with aspirin, and the hemorrhage resolved.248

Peripheral Edema Edema of the face, hands, and ankles at high altitude is common, especially in females. Incidence of edema in at least one area of the body in trekkers at 4200 m was 18% overall, 28% in women, 14% in men, 7% in asymptomatic trekkers, and 27% in those with AMS.153 Although not a serious clinical problem, edema can be bothersome. The presence of peripheral edema demands an examination for pulmonary and cerebral edema. In the absence of AMS, peripheral edema is effectively treated with a diuretic. Treatment of accompanying AMS by descent or medical therapy also results in diuresis and resolution of peripheral edema. The mechanism is presumably similar to fluid retention in AMS, but it may also be merely due to exercise.299

Immunosuppression Mountaineers have observed that infections are common at high altitude, slow to resolve, and often resistant to antibiotics.321 On the American Medical Research Expedition to Mt. Everest in 1981, serious skin and soft tissue infections developed. “Nearly every accidental wound, no matter how small, suppurated for a period of time and subsequently healed slowly.”393 A suppurative hand wound and septic olecranon bursitis did not respond to antibiotics but did respond to descent to 4300 m from the 5300-m base camp. Nine of 21 persons had significant infections not related to the respiratory tract. Most highaltitude expeditions report similar problems. Data from OEII indicated that healthy individuals are more susceptible to infections at high altitude because of impaired Tlymphocyte function; this is consistent with previous Russian studies in humans and animals.295 In contrast, B cells and active immunity are not impaired. Therefore, resistance to viruses may not be impaired, whereas susceptibility to bacterial infection is increased. The degree of immunosuppression is similar to that seen with trauma, burns, emotional depression, and space flight. The mechanism may be related, at least in part, to release of adrenocorticotropic hormone, cortisone, and beta-endorphins, all of which modulate the immune response. Intense ultraviolet exposure has also been shown to impair immunity. Persons with serious infections at high altitude may need oxygen or descent for effective treatment. Impaired immunity because of altitude

should be anticipated in situations where infection could be a complication, such as trauma, burns, and surgical and invasive procedures.

High-Altitude Pharyngitis and Bronchitis Sore throat, chronic cough, and bronchitis are nearly universal in persons who spend more than 2 weeks at an extreme altitude (over 5500 m).263,283 All 21 members of the 1981 American Medical Research Expedition to Mt. Everest suffered these problems.393 Only two of eight subjects in OEII (where the temperature was greater than 21° C [70° F] and relative humidity was greater than 80%) developed cough, and only above 6500 m. Only four had sore throat. Acute hypoxia directly lowers the cough threshold, thus exacerbating high-altitude cough.283 But other factors are at play. In the field, these problems usually appear without fever or chills, myalgia, lymphadenopathy, exudate, or other signs of infection. The increase in ventilation, especially with exercise, forces obligate mouth breathing at altitude, bypassing the warming and moisturizing action of the nasal mucous membranes and sinuses. Movement of large volumes of dry, cold air across the pharyngeal mucosa can cause marked dehydration, irritation, and pain, similar to pharyngitis. Vasomotor rhinitis, quite common in cold temperatures, aggravates this condition by necessitating mouth breathing during sleep. For this reason, decongestant nasal spray is one of the most coveted items in an expedition medical kit. Other countermeasures include forced hydration, hard candies, lozenges, and steam inhalation. High-altitude bronchitis can be disabling because of severe coughing spasms. Cough fractures of one or more ribs are not rare.263 Purulent sputum is common. Response to antibiotics is poor; most victims resign themselves to taking medications such as codeine and do not expect a cure until descent. Bronchitis developed in 13 of 19 climbers above 4300 m on Aconcagua.347 Mean sputum production was 6 teaspoons per day. All reported that onset was after a period of excessive hyperventilation associated with strenuous activity. Although an infectious etiology is possible, experimental evidence suggests that respiratory heat loss results in purulent sputum and in sufficient airway irritation to cause persistent cough.290 This is supported by the beneficial effect of steam inhalation and lack of response to antibiotics. Many climbers find that a thin balaclava, porous enough for breathing, traps some moisture and heat and effectively prevents or ameliorates the problem.

Chronic Mountain Sickness In 1928 Carlos Monge307 described a syndrome in Andean highaltitude natives that was characterized by headaches, insomnia, lethargy, plethoric appearance, and polycythemia greater than expected for the altitude. Known variously as Monge’s disease, chronic mountain polycythemia, and chronic mountain sickness (CMS), the condition has now been recognized in all highaltitude areas of the world.244,306,338 Both lowlanders who relocate to high altitude and native residents are susceptible. Chinese investigators reported that 13% of lowland Chinese males and 1.6% of females who had relocated to Tibet developed excessive polycythemia (hemoglobin level greater than 20 g/dL blood).486 The incidence in Leadville, Colorado, is also high in men over age 40 and distinctly low in women.243 The increased hematopoiesis is apparently related to greater hypoxic stress, which may have a number of causes, such as lung disease, sleep apnea syndromes, and idiopathic hypoventilation. A diag-

Chapter 1: High-Altitude Medicine nosis of “pure” chronic mountain polycythemia excludes lung disease and is characterized by relative alveolar hypoventilation, excessive nocturnal hypoxemia, and respiratory insensitivity to hypoxia.257,306 Some studies suggest that even for the degree of hypoxemia, the red blood cell mass is excessive, implying excessive amounts or overactivity of erythropoietin.475 The new international guidelines propose a hemoglobin value greater than 21 g/dL for men and 19 g/dL for women as essential for the diagnosis, as well as residence above 2500 m and absence of lung disease.257 The reader is referred to recent reviews for in-depth information.305,350,352,484 In addition, an international consensus group has recently published their papers on definition and scoring of CMS.256,257 Therapy of CMS is routinely successful. Descent to a lower altitude is the definitive treatment. The syndrome reappears after returning to high altitude. Supplemental oxygen during sleep is valuable. Phlebotomy is a common practice and provides subjective improvement, although without significant objective changes.475 The respiratory stimulants medroxyprogesterone acetate (20 to 60 mg/day)242 and acetazolamide (250 or 500 mg/day)359 have also been shown to reduce the hematocrit value by improving oxygenation. Acetazolamide (250 mg) increased nocturnal Sao2 by 5%, decreased mean nocturnal heart rate by 11% and the number of apnea/hypopnea episodes during sleep by 74%, and decreased hematocrit by 7%.359 The response to acetazolamide emphasizes the contribution of hypoventilation and nocturnal desaturation to CMS. Another approach was based on the knowledge that ACE inhibitors blunt hypoxia-mediated erythropoietin release. Plata and colleagues showed that 5 mg/day of enalapril for 2 years reduced hemoglobin concentration, packed cell volume, and proteinuria, and reduced the need for phlebotomy.342 Pulmonary hypertension and right heart failure may also occur in those with CMS.

High-Altitude Pulmonary Hypertension High-altitude pulmonary hypertension (HAPH) is a syndrome occurring in children and adults living over 2500 m. It is characterized by a mean pulmonary artery pressure greater than 30 mm Hg or a systolic pressure greater than 50 mm Hg, measured at the altitude of residence; it is associated with right ventricular hypertrophy and heart failure, and the absence of CMS.257 Historical terms for this condition include subacute adult and subacute infantile mountain sickness, and highaltitude heart disease. Symptoms include cough, cyanosis, dyspnea, and signs of right heart failure. Treatment is similar to that for CMS, with relocation to a low altitude the best solution. Other but inferior therapies include supplemental oxygen, and pulmonary vasodilators such as calcium channel blockers, PDE5 inhibitors, and nitric oxide and prostaglandin inhibitors.257

High-Altitude Retinopathy and Ultraviolet Keratitis

Box 1-5. Advisability of Exposure to High and Very High Altitude for Common Conditions (without Supplemental Oxygen) PROBABLY NO EXTRA RISK

Young and old Fit and unfit Mild obesity Diabetes Previous coronary artery bypass grafting (without angina) Mild chronic obstructive pulmonary disease (COPD) Asthma Low-risk pregnancy Controlled hypertension Controlled seizure disorder Psychiatric disorders Neoplastic diseases Inflammatory conditions CAUTION

Moderate COPD Asymptomatic pulmonary hypertension Compensated congestive heart failure (CHF) Morbid obesity Sleep apnea syndromes Troublesome arrhythmias Stable angina or coronary artery disease High-risk pregnancy Sickle cell trait Cerebrovascular diseases Any cause of restricted pulmonary circulation Seizure disorder (not on medication) Radial keratotomy CONTRAINDICATED

Sickle cell anemia (with history of crises) Severe COPD Symptomatic pulmonary hypertension Uncompensated CHF

populations also require special consideration, such as the very young, the pregnant, and older adults. This section presents an overview of current knowledge regarding these issues. Despite the importance of the interaction of altitude and common medical conditions, research has so far been limited. See the review by Hackett for a more complete discussion.149 Conditions that can be aggravated by high-altitude exposure are listed in Box 1-5.

See Chapter 25.

Respiratory Diseases


COMMON MEDICAL CONDITIONS

Chronic Lung Disease

AND HIGH ALTITUDE

Persons with certain preexisting illnesses might be at risk for adverse effects on ascent to high altitude, either because of exacerbation of their illnesses or because these illnesses might impact acclimatization and susceptibility to altitude illness. Certain

31

While oxygen saturation remains above 90% in a normally acclimatizing, healthy, awake person until over 3000 m (see Figure 1-1), persons with hypoxemic lung disease reach this threshold at a lower altitude that depends on the baseline blood oxygen values. As a result, these persons might have altituderelated problems at lower altitudes than would healthy individuals. In terms of their lung disease, improved airflow will

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result from decreased air density at high altitude, but hypoxemia, pulmonary hypertension, disordered control of ventilation, and sleep-disordered breathing could all become worse. Unfortunately, few data are available to guide the clinician advising such a person undertaking a trip to altitude.74 Hypoxic gas breathing at sea level can predict oxygenation at high altitude, but this does not always correlate with symptoms, and it is not convenient. Sea level Po2 values of 68 and 72 mm Hg successfully classified more than 90% of the subjects with a Pao2 greater than 55 mm Hg at simulated altitudes of 1525 m and 2440 m, respectively.132,133 Such predictions have been further refined with the addition of spirometry.101 A Pao2 of 55 mm Hg results in a saturation of 90% at high altitude, where there is slight alkalosis. These data suggested that persons with Pao2 values lower than these at sea level might require supplemental oxygen at modest altitudes. However, in the only clinical studies to date, patients with moderate chronic obstructive pulmonary disease (COPD) did quite well at altitude.135,289 Graham and Houston found that eight subjects with COPD taken to 1920 m had only minor symptoms on ascent, despite the fact that mean Pao2 declined from 66 mm Hg at sea level to 51 mm Hg while at rest, and from 63 to 47 mm Hg with exercise. The patients did acclimatize, with a drop in Pco2 and a corresponding increase in Pao2 over 4 days, the same response as seen in healthy persons. Matthys and colleagues studied 10 patients at a simulated altitude of 2500 m. Mean PAP increased from 21 to 25 mm Hg, Pao2 decreased from 68 to 51 mm Hg at rest, and the only symptom was an increase in fatigue.289 The authors concluded that travel to this moderate altitude is safe for such patients. They speculated that these persons might have been partially acclimatized because of their hypoxic lung disease, and they were therefore less likely to develop AMS. Unfortunately, no further investigations with sicker patients or at higher altitudes have yet been reported. Persons with COPD who become uncomfortable at altitude should be treated with oxygen therapy. Oxygen should also be considered for those predicted to become severely hypoxemic.43 To adjust oxygen therapy at altitude for persons already on supplemental oxygen, the fractional concentration of O2 in inspired gas (Fio2) is increased by the ratio of higher to lower barometric pressure (see Table 1-2). Oxygen also improved hemodynamics (lowered blood pressure) and decreased pulsus paradoxus and pulse pressure in patients with COPD at a simulated altitude of 2438 m.44 With the advent of simple and inexpensive pulse oximetry, patients can be counseled to monitor their oxygen saturation, determine the need for oxygen, and titrate their own oxygen use. Interestingly, reports of patients with COPD developing altitude illness are absent from the literature. On the other hand, the issue has not been specifically addressed. Any degree of pulmonary hypertension might be expected to increase the likelihood of HAPE, and although this has been clearly demonstrated in other conditions (see High-Altitude Pulmonary Edema), it has not yet been reported with pulmonary hypertension associated with COPD. No research has yet addressed the use of medications such as acetazolamide or medroxyprogesterone in these patients, to determine if respiratory stimulants might improve altitude tolerance.

Cystic Fibrosis Children with cystic fibrosis have been reported to do poorly at high altitude,425 and hypoxic testing has also tried to predict the

need for supplemental oxygen on ascent in this condition.331,383 As with COPD, such tests are not particularly useful and tend to underestimate the oxygen requirements, as they are done only during rest and while awake. Supplemental oxygen should be available for these children, and oxygen saturation monitoring might be desirable in certain circumstances. The physician should be liberal with the use of antibiotics and adjunctive therapy for exacerbations at high altitude, given the likely danger of greater hypoxemia and the greater difficulty of treating infections at high altitude. Cystic fibrosis encompasses a wide range of pulmonary impairment; one patient with mild disease was able to hike to 5600 m.74

Asthma The available literature suggests that people with asthma, both residents and sojourners, do well at moderate altitude, primarily because of decreased allergens and pollution.51,417,452 Indeed, high altitude as a treatment for asthma has been popular in Europe for many decades. The effect is comparable to that seen with high dosages of inhaled steroids.74 However, because altitude exposure often includes exercise (and cold), people with asthma who have exercise-induced bronchospasm, rather than allergic asthma, might have problems at altitude. Matsuda and colleagues284 investigated the effect of altitude on 20 asthmatic children with exercise-induced bronchospasm in a hypobaric chamber simulating 1500 m, but with the temperature and humidity held constant. Except for the increased respiratory rate during exercise, as expected, all other physiologic variables were unchanged compared with those at sea level. The authors concluded that the modest altitude of 1500 m does not exacerbate exercise-induced asthma. Golan and colleagues screened travelers and found 147 people with asthma who trekked to high altitude. Risk factors for an asthma attack at altitude were use of inhaled bronchodilators more than three times a week prior to travel, and intensive physical exertion during the trek.130 A small but careful study was done with 11 people with asthma who were in stable condition with normal respiratory function at sea level. Cogo and her colleagues tested both methacholine challenge and hyperosmolar aerosol at sea level and multiple altitudes up to 5050 m. At no altitude was there an increase in bronchial responsiveness, and at the highest altitude there was a decrease.73 They concluded that the positive aspects of high altitude prevailed over potential negative factors for people with asthma, and they attributed the benefit to the increase in circulating catecholamines found in their subjects. In the presence of bronchoconstriction at high altitude, however, hypoxemia is likely to be greater than at low altitude, and for this reason there could be an association between asthma and HAPE or AMS. Reassuringly, no such relationship has yet been reported. Mirrakhimov and colleagues investigated the effect of acetazolamide in 16 asthmatic patients taken to 3200 m. Taking acetazolamide resulted in these patients’ having the same benefits as people without asthma, with higher oxygen saturation and fewer AMS symptoms compared with the placebo control group.303 Seven of the eight asthmatic patients in the control group developed symptoms of AMS, a rather high incidence, but there was no nonasthmatic control group for comparison. Whether this incidence was abnormal is unknown. Persons with asthma ascending to high altitude should be advised to be at maximal function before ascent, to continue on their usual medications, including steroids, and to have steroids

Chapter 1: High-Altitude Medicine and bronchodilators with them in the event of an exacerbation. Because airway heat loss can be a trigger for bronchospasm, the use of an airway warming mask might be helpful, but this is unproven.385 In summary, the available data, although limited, suggest that high altitude does not exacerbate asthma, and that it actually improves allergic asthma. Further work needs to determine if asthma might have any influence on susceptibility to AMS and HAPE; anecdotally, this does not seem to be the case. Although it seems likely that a severe asthma attack at high altitude would be more dangerous than at low altitude, no data are available to answer this question. Although caution and adequate preparation are necessary, asthma is not a contraindication to high-altitude travel.

Pulmonary Vascular Disorders Because of the danger of HAPE, pulmonary hypertension (of any etiology) is at least a relative contraindication to highaltitude exposure. In addition, hypoxic pulmonary vasoconstriction will most likely exaggerate preexisting pulmonary hypertension and could lead to more significant symptoms in those with congenital cardiac defects, primary pulmonary hypertension (PPH), and related disorders. This caution also applies to unilateral absent pulmonary artery, granulomatous mediastinitis, and restrictive lung diseases, all of which have been associated with HAPE.151,361,444 As Hultgren has observed, however, some patients with PPH are able to tolerate high altitude, and hypoxic gas breathing can be used to identify an individual’s response to hypoxia if clinically indicated. Persons with PPH who must travel to high altitude might benefit from calcium channel blockers, isoproterenol, and/or low flow oxygen.202 A report by Naeije and colleagues highlighted the increased susceptibility to HAPE in those with pulmonary hypertension: a lowland woman with pulmonary hypertension secondary to fenfluramine developed two episodes of HAPE.323 The first episode was at 2300 m, and the second one at only 1850 m, with skiing up to 2350 m. Other conditions warranting caution include bronchopulmonary dysplasia, recurrent pulmonary emboli, mitral stenosis, kyphoscoliosis, and scleroderma. Whether pulmonary hypertension is primary or secondary, patients should be made aware of the potential hazards of high altitude, including right heart failure and HAPE. A mean PAP of greater than 30 mm Hg is a useful threshold for caution (or oxygen) on ascent to altitude.74

Sleep Apnea, Sleep-Disordered Breathing Persons with snoring, sleep apnea syndrome, and sleepdisordered breathing (SDB) who become mildly hypoxemic at sea level may become severely hypoxemic at high altitude. This could contribute to high-altitude illness and aggravate attendant problems such as polycythemia, pulmonary hypertension, cardiac arrhythmia, or insomnia. On the other hand, changes in ventilatory control and breathing secondary to altitude hypoxia might conceivably improve certain apnea syndromes. In general, the scant research available has shown that obstructive sleep apnea tends to improve at altitude, whereas central apnea can become worse.57a Patients with SDB being treated with continuous positive airway pressure (CPAP) should be aware that the hypobaria of high altitude decreases the delivered pressure of CPAP machines that do not have pressurecompensating features. They therefore might need to adjust their machines. The error is greater at higher altitude and higher initial pressure setting.120 For those not being treated with CPAP

33

but who exhibit hypoxemia during sleep at low altitude, the physician might want to consider supplemental nocturnal oxygen during an altitude sojourn.

Cardiovascular Conditions Hypertension In healthy persons rapidly ascending to high altitude, the change in blood pressure, if any, is variable, depending on the magnitude of hypoxic stress, cold, diet, exercise, and genetic factors. Most studies report a slight increase in blood pressure, associated with increased catecholamine activity and increased sympathetic activity.348 One well-controlled study showed an increase in blood pressure at 3500 m from a mean of 105/66 mm Hg at sea level to 119/77 mm Hg at 3 days, 111/75 mm Hg at 3 weeks, and back to 102/65 mm Hg on return to sea level.282 Pugh reported transient increases in blood pressure in athletes at the Olympics in Mexico City.346 Certain individuals, however, appear to have a pathologic response on induction to high altitude. For example, arterial hypertension develops in 10% of lowland Chinese who move to Tibet.414 The authors consider this a form of altitude maladaptation and treat the condition by returning the affected individuals to low altitude. After a period of at least 2 months, however, downregulation of adrenergic receptors results in attenuation of the initial blood pressure response. This mechanism is thought to be the reason that longterm residents of high altitude have lower blood pressure than do their sea level counterparts.201,376 Apparently for the same reason, chronic altitude exposure has also been shown to inhibit progression of hypertension.302 As for the effect of short-term altitude exposure on preexisting hypertension, studies have generated mixed results. In general, the response in patients with hypertension is similar to that in those without hypertension—that is, a small increase in blood pressure, with an exaggerated response in some individuals. The greater the hypoxic stress (the higher the altitude), the greater is the change in blood pressure. Altitudes less than 3000 m seem to result in little if any change.369 Palatini and colleagues studied 12 normotensive patients and 12 untreated mild hypertensive patients with 24-hour ambulatory blood pressure monitoring at sea level, after 12 hours at 1210 m and after 1.5 to 3 hours at 3000 m.335 The authors concluded that the increase of blood pressure in both normotensive and hypertensive patients was not important at 1200 m but could become so at 3000 m. However, individual variability was great; the maximal change was 17.4 mm Hg for systolic and 16.3 for diastolic blood pressure. Two other studies were able to demonstrate a slightly greater blood pressure response in hypertensive compared with normotensive patients on ascent to 2572 and 3460 m.89,398 Again, these authors also noted important individual variation, with some subjects increasing their systolic blood pressure by as much as 25 mm Hg at rest and 40 mm Hg during exercise, compared with sea level measurements. The important question of whether the blood pressure would continue to increase over the first 2 weeks at high altitude, as it does in normotensive patients, has not yet been addressed. At a more modest altitude, Halhuber and coworkers claimed a significant reduction in the blood pressure of 593 persons with hypertension after 14 days at 1700 to 2000 m in the Alps.166 A similar study of hypertensive patients at higher altitude is needed. Patients receiving antihypertensive treatment should continue their medications while at high altitude. Because some persons

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may unpredictably become markedly hypertensive acutely,202 blood pressure monitoring should be considered, especially in those with labile hypertension or those who become symptomatic at altitude. Hypertension in short-term high-altitude sojourners for the most part should be considered transient and should not be treated, as it rarely reaches dangerously high levels and will resolve on descent. Given the large number of hypertensive patients visiting ski resorts and trekking at high altitude, however, the occasional person with an exaggerated response will require treatment.202 Because the mechanism appears to be increased alpha-adrenergic activity, an alphablocker might be the best choice of therapy for these individuals. A preliminary report also suggested that nifedipine might be useful, and superior to atenolol.95 The best medication, dosage, and duration still need to be determined. There is no evidence to date to suggest that hypertensive patients are more likely to develop high-altitude illnesses. Although it requires some caution, hypertension does not seem to be a contraindication to high-altitude exposure.

Arteriosclerotic Heart Disease Life-long residence at high altitude appears to offer some protection from coronary artery disease and the attendant acute coronary artery events,301 perhaps in part because of increased myocardial vascularity. Other factors that might explain this finding, such as genetics, fitness, and diet, have not been adequately evaluated. The effect on the healthy heart of acute, transient exposure to high altitude also appears to be benign. Various avenues of research have indicated that the healthy heart tolerates even extreme hypoxia quite well, all the way to the summit of Mt. Everest (Pao2 less than 30 mm Hg). Numerous electrocardiograms (ECGs), echocardiograms, heart catheterizations, and exercise tests have failed to demonstrate any evidence of cardiac ischemia or cardiac dysfunction in healthy persons at high altitudes. This could partly result from the marked reduction in maximal exercise with increasing altitude, which reduces maximal heart rate and myocardial oxygen demand, and also from the increased coronary blood flow. A person with coronary artery disease (CAD), however, may not have the same adaptive capacities. For example, diseased coronary arteries might have limited ability to vasodilate and might actually constrict, because of unopposed sympathetic activation.261 What, then, are the risks, and what should be the advice to those with CAD considering a visit to high altitude? Surprisingly little literature is available to help the physician advise such persons. Does high altitude provoke acute coronary events or sudden death? In the United States, no evidence from state or county mortality statistics suggests an increased prevalence of acute coronary events in visitors to high-altitude locations. In Europe, Halhuber and colleagues reported an incidence of only 0.2% for myocardial infarction in 434 patients with CAD taken to altitudes between 1700 and 3200 m for 4 weeks in the Alps.166 He also reported a very low incidence of sudden death in 151,000 vacationers in the Alps, 69,000 of who were over age 40. In contrast are data from Austria claiming a higher rate of sudden cardiac death in the mountains, compared with the overall risk of sudden cardiac death.60 However, the altitudes were rather low (1000 to 2100 m), and no increased risk was evident in men who participated regularly in sports. The authors suggested that abrupt onset of exercise in sedentary men combined with altitude stress might induce cardiac sudden death, but whether altitude contributed at all is unclear.

In summary, limited data suggest no increased risk for sudden cardiac death or myocardial infarction at altitudes up to 2500 m. Another important question is whether altitude will exacerbate stable ischemia. The slight increase in heart rate and blood pressure on initial ascent to altitude might exacerbate angina in those with coronary artery disease, as described by Hultgren.202 One study evaluated nine men with stable exercise-induced angina by exercise treadmill test at 1600 m (Denver), and within the first hour of arrival at 3100 m.316 Cardiac work was slightly higher for a given workload at high altitude compared with low altitude, and as a result, the onset of angina was at a slightly lower workload. The authors found that a heart rate of 70% to 85% of the rate that produced ischemia at low altitude was associated with angina-free exercise at 3100 m, and they suggested that angina patients at altitude adjust their activity level on the basis of heart rate, at least on the day of arrival.316 Brammel and colleagues reported similar results and suggested that those with angina need to reduce their activity at high altitude to avoid angina episodes.56 In a more recent study, Levine and colleagues investigated 20 men who were much older than those in the previous investigations (mean age, 68 ± 3 years), and they performed symptom-limited exercise tests.261 With acute exposure to 2500 m, the double product (heart rate times systolic blood pressure) required to induce 1 mm ST depression was decreased about 5%, but after 5 days of acclimatization at 2500 m, this value was unchanged from sea level. The degree of ischemia (maximal ST-segment depression) was the same at sea level, with acute altitude exposure, and after 5 days at 2500 m. Also, no new wall motion abnormalities on echocardiography were seen at high altitude. Only one subject exhibited increased angina at altitude, and one person with severe coronary artery disease developed a myocardial infarction after maximal exercise at 2500 m. The authors concluded that patients with CAD who are well compensated at sea level do well at a moderate altitude after a few days of acclimatization, but that acutely, the angina threshold may be lower and activity should be reduced.261 Finally, a study of 97 older adults visiting 2500 m, many with CAD and abnormal ECGs, found no new ECG changes and no events suggestive of ischemia. In contrast to the Levine study, these subjects did not do exhaustive exercise tests but merely their usual activities, which included walking in the mountains.369 Taken altogether, these various investigations indicate that those with CAD, including older adults, generally do well at the modest altitude of 2500 m, but that reducing their activities the first few days at altitude is wise. To address the question of whether altitude might provoke cardiac arrhythmia, Levine and colleagues, in their study mentioned previously,261 found that premature ventricular contractions (PVCs) increased 63% on acute ascent but returned to baseline after 5 days of acclimatization. A simultaneous rise in urine norepinephrine in these subjects indicated that sympathetic activation was the cause of the increased ectopy. They observed no increase in higher-grade ectopy, however, and no changes in signal-averaged ECG suggestive of a change in fibrillation threshold; in other words, the PVCs appeared benign. Halhuber and coworkers also found increased ectopy in their subjects, and also no serious adverse events.166 In addition, Alexander described asymptomatic PVCs and ventricular bigeminy in himself while trekking to 5900 m. Subsequent evaluation found no evidence of heart disease, and the event prompted him to thoroughly review the subject of altitude, age,

Chapter 1: High-Altitude Medicine and arrhythmia.4 Although no dangerous arrhythmias have ever been reported in high-altitude studies, persons with troublesome or high-grade arrhythmia have not been evaluated on ascent to high altitude. The available evidence suggests that patients whose arrhythmias are well controlled on medication should continue the medication at altitude, whereas those with poorly controlled arrhythmias might do better to avoid visiting high altitude. In terms of advising persons with CAD or high likelihood of CAD about altitude exposure, the stress of high altitude on the coronary circulation appears to be minimal at rest but significant in conjunction with exercise. Ideally, no one with known CAD or even risk factors for CAD should undertake unaccustomed exercise at any altitude, and especially at high altitude. Therefore, advising an exercise program at sea level prior to exercising at altitude is prudent. The same technique of risk stratification that is commonly used at sea level can be applied for providing advice for high altitude.196 Using the standard recommendations, asymptomatic men over age 50 with no risk factors require no testing. For asymptomatic men over age 50 with risk factors, an exercise test is recommended to determine risk status prior to exercising at high altitude, and then further evaluation as indicated. Patients with previous myocardial infarction, bypass surgery, or angioplasty are considered at high risk only if they have a strongly positive exercise treadmill test. Patients with multiple-vessel bypass grafts who were asymptomatic, and who had normal exercise test results at sea level, have successfully visited altitudes over 5000 m. High-risk patients may require coronary angiography to establish appropriate management. Alexander has proposed different criteria for those with CAD at high risk at altitude: an ejection fraction less than 35% at rest, a fall in exercise systolic blood pressure, ST-segment depression greater than 2 mm at peak heart rate, and high-grade ventricular ectopy.3 For these persons, he recommends ascent to no more than 2500 m, and proximity to medical care. Both sets of recommendations, while reasonable, need to be validated with outcome studies.

Heart Failure Although information on the effect of high altitude on heart failure is scant, physicians in resort areas have noted a tendency toward acute decompensation within 24 hours of arrival in those with a history of heart failure. Those with CAD and low ejection fractions (less than 45%), but without active heart failure, actually did quite well, as gauged by exercise tests during acute exposure to 2500 m.112 Compared with 23 control subjects, the decrement in exercise performance was similar, and no complications or signs of ischemia developed. Although these results are encouraging for such patients, observations were not made past the first few hours at altitude. One concern is that those with heart failure might be more likely to retain fluid at altitude, especially if AMS were to develop, and that this could aggravate failure. Supporting this notion, Alexander found that ejection fraction declined at altitude during an exercise study in patients with angina, with an increase in enddiastolic and systolic volume as measured by two-dimensional echocardiogram.3 Ventricular contractility was not depressed, however, and these changes were attributed to fluid overload. Patients with heart failure need to be informed about possible consequences of high-altitude exposure. In particular, they need to avoid AMS (which is associated with fluid retention), continue their regular medications, and be prepared to increase

35

their diuretic should symptoms of failure exacerbate. Acetazolamide prophylaxis may be useful to consider for speeding acclimatization, inducing diuresis, and preventing AMS, but its efficacy in these patients remains untested.

Obesity The interaction of obesity and altitude has not received much attention. A small study suggested a slight increased susceptibility to AMS in mildly obese men,124 possibly due to lower nocturnal oxygen saturation that was present despite greater than normal hypoxic and hypercapnic chemosensitivity.125 Another, larger study examined men with metabolic syndrome (obesity, hypertension, diabetes, and hyperlipidemia) with a 3-week stay at 1700 m and found normal altitude responses and a loss of body fat.142 In fact, altitude has been suggested as a treatment for obesity. Obese men and women (mean body mass index, 47.1) who were permanent residents at a mean altitude of 2448 m, however, had a 96% incidence of systolic pulmonary artery hypertension (>30 mm Hg), which was related to alveolar hypoventilation.449

Sickle Cell Disease Sickle cell (SC) crisis is a well-recognized complication of highaltitude exposure.117 Even the modest altitude of a pressurized aircraft (1500 to 2000 m) causes 20% of persons with hemoglobin SC and sickle-thalassemia genetic configuration to have a vaso-occlusive crisis.278 High-altitude exposure may precipitate the first vaso-occlusive crisis in persons previously unaware of their condition. Persons with sickle cell anemia and a history of vaso-occlusive crises are advised to avoid altitudes over 1800 m unless they are taking supplemental oxygen. Persons with sickle cell disease who live at high altitude in Saudi Arabia have twice the incidence of crises, hospitalizations, and complications as do Saudis at low altitude. Splenic infarction syndrome has been reported more commonly in those with sickle cell trait than in those with sickle cell anemia, probably because sickle cell disease produces autosplenectomy early in life. Frequent reports in the literature emphasize the need to consider splenic syndrome caused by sickle cell trait in any person with left upper quadrant pain, even at an altitude of only 1500 m.247,278 A number of authors have suggested that nonblack persons with the trait may be at greater risk for splenic syndrome at high altitude than are black persons.247 Treatment of splenic syndrome consists of intravenous hydration, oxygen, and removal to a lower altitude.442 The overall incidence of problems in persons with the trait is low, however, and no special precaution other than recognition of the splenic syndrome is recommended. The U.S. Army, for example, does not consider soldiers with the trait unfit for duty at high altitude.100

Pregnancy In high-altitude natives, pregnancy-associated hypertension is 4 times more common than in low-altitude pregnancies, preeclampsia is more common, and full-term infants are small for gestational age.311,314 These problems raise the issue of whether short-term altitude exposure may also pose a risk. So far, there is no evidence that these problems, or others such as spontaneous abortion, abruptio placentae, or placenta previa, can result from a sojourn at high altitude.328 Unfortunately, however, few data exist on the influence of a high-altitude visit during pregnancy on the mother and the fetus. For moderate

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altitude, the research to date has been reassuring.193,194 Artal and colleagues studied seven sedentary women at 34 weeks gestation. Maximal and submaximal exercise tests were completed at sea level and 6000 feet (1830 m) after 2 to 4 days of acclimatization.11 They reported the expected decrease in maximal aerobic work but found no difference from sea level in fetal heart rate responses, or in maternal lactate, epinephrine, and norepinephrine levels. In a small number of subjects, the authors considered it safe for third-trimester women to engage in brief bouts of exercise at moderate altitude. A similar conclusion was reached in a study of 12 pregnant women who exercised after ascent to 2225 m. The authors found no abnormal fetal heart rate responses and considered the exercise at altitude benign for both mother and fetus.38 Huch also concluded that short-term exposure, with exercise, was safe during pregnancy.193 In summary, the available data, though limited, indicate that shortterm exposure to altitudes up to 2500 m, with exercise, is safe for a lowland woman with a normal pregnancy. Another avenue of research has been alteration of blood gases during pregnancy. Human and animal studies with acute hypoxic challenge, as well as oxygen-breathing studies, have drawn two conclusions: (1) that a compromised placental–fetal circulation could be unmasked at high altitude, and (2) that a fetus with a normal placental–fetal circulation seems to tolerate a level of acute hypoxia far exceeding a moderate altitude exposure.18,81,362 On the basis of the available research, it seems prudent to recommend that only women with normal, low risk pregnancy

2

undertake a sojourn at high altitude. For these women, exposure to an altitude at which Sao2 will remain above 85% most of the time (up to 3000 m altitude) appears to pose no risk of harm, but further study is needed to place these recommendations on a more solid scientific footing. An ultrasound or other assessment may be useful to rule out the more common complications prior to travel. Of course, it is not the altitude per se that determines whether the fetus becomes stressed but rather the maternal (and fetal) arterial oxygen transport. A woman with high-altitude pulmonary edema at 2500 m, for example, is much more hypoxemic than a healthy woman at 5000 m. Therefore, a strategy for preventing altitude illness, especially pulmonary edema, must be explained and implemented. Similarly, elevated carboxyhemoglobin from smoking, lung disease, and other problems of oxygen transport will render the pregnant patient at altitude more hypoxemic, and physiologically comparable to a higher altitude. Consideration of a high-altitude sojourn in the developing world, or in a wilderness setting, raises other issues that may be more important than the modest hypoxia. These include remoteness from medical care should a problem arise, quality of available medical care, use of medications for such important things as malaria and traveler’s diarrhea (many of which are contraindicated in pregnancy), and risks for trauma.

The references for this chapter can be found on the accompanying DVD-ROM.

Avalanches Knox Williams, Dale Atkins, and Colin K. Grissom

An avalanche is a mass of snow that slides down a mountainside. In the United States, approximately 100,000 avalanches occur annually, of which about 100 cause injury, death, or destruction of property. Based on a database of reported incidents, about 200 people a year are caught in avalanches (that is, they are bodily involved in the moving snow or its effects). Of these, 84 are partly or wholly buried, 30 sustain injury, and 30 are killed. Average annual property damage varies tremendously depending on the winter. In the last 10 years, damages have ranged from as low as $30,000 to a high of $13.5 million; the median is $298,000. This chapter describes the properties of the mountain snowpack that contribute to avalanche formation and describes avalanche safety techniques.


PROPERTIES OF SNOW Physical Properties Although snow cover appears to be nothing more than a thick, homogeneous blanket covering the ground, it is in fact one of the most complex materials found in nature. It is highly variable and goes through significant changes in relatively short periods. In nature, snow cover is variable on both the broad geographic scale (Antarctic snow is quite different from snow found in the Cascade Mountains of North America) and on the microscale (where snow conditions may vary greatly from one side of a rock or tree to the other). All snow crystals are made

36

PART ONE: MOUNTAIN MEDICINE

altitude, the research to date has been reassuring.193,194 Artal and colleagues studied seven sedentary women at 34 weeks gestation. Maximal and submaximal exercise tests were completed at sea level and 6000 feet (1830 m) after 2 to 4 days of acclimatization.11 They reported the expected decrease in maximal aerobic work but found no difference from sea level in fetal heart rate responses, or in maternal lactate, epinephrine, and norepinephrine levels. In a small number of subjects, the authors considered it safe for third-trimester women to engage in brief bouts of exercise at moderate altitude. A similar conclusion was reached in a study of 12 pregnant women who exercised after ascent to 2225 m. The authors found no abnormal fetal heart rate responses and considered the exercise at altitude benign for both mother and fetus.38 Huch also concluded that short-term exposure, with exercise, was safe during pregnancy.193 In summary, the available data, though limited, indicate that shortterm exposure to altitudes up to 2500 m, with exercise, is safe for a lowland woman with a normal pregnancy. Another avenue of research has been alteration of blood gases during pregnancy. Human and animal studies with acute hypoxic challenge, as well as oxygen-breathing studies, have drawn two conclusions: (1) that a compromised placental–fetal circulation could be unmasked at high altitude, and (2) that a fetus with a normal placental–fetal circulation seems to tolerate a level of acute hypoxia far exceeding a moderate altitude exposure.18,81,362 On the basis of the available research, it seems prudent to recommend that only women with normal, low risk pregnancy

2

undertake a sojourn at high altitude. For these women, exposure to an altitude at which Sao2 will remain above 85% most of the time (up to 3000 m altitude) appears to pose no risk of harm, but further study is needed to place these recommendations on a more solid scientific footing. An ultrasound or other assessment may be useful to rule out the more common complications prior to travel. Of course, it is not the altitude per se that determines whether the fetus becomes stressed but rather the maternal (and fetal) arterial oxygen transport. A woman with high-altitude pulmonary edema at 2500 m, for example, is much more hypoxemic than a healthy woman at 5000 m. Therefore, a strategy for preventing altitude illness, especially pulmonary edema, must be explained and implemented. Similarly, elevated carboxyhemoglobin from smoking, lung disease, and other problems of oxygen transport will render the pregnant patient at altitude more hypoxemic, and physiologically comparable to a higher altitude. Consideration of a high-altitude sojourn in the developing world, or in a wilderness setting, raises other issues that may be more important than the modest hypoxia. These include remoteness from medical care should a problem arise, quality of available medical care, use of medications for such important things as malaria and traveler’s diarrhea (many of which are contraindicated in pregnancy), and risks for trauma.

The references for this chapter can be found on the accompanying DVD-ROM.

Avalanches Knox Williams, Dale Atkins, and Colin K. Grissom

An avalanche is a mass of snow that slides down a mountainside. In the United States, approximately 100,000 avalanches occur annually, of which about 100 cause injury, death, or destruction of property. Based on a database of reported incidents, about 200 people a year are caught in avalanches (that is, they are bodily involved in the moving snow or its effects). Of these, 84 are partly or wholly buried, 30 sustain injury, and 30 are killed. Average annual property damage varies tremendously depending on the winter. In the last 10 years, damages have ranged from as low as $30,000 to a high of $13.5 million; the median is $298,000. This chapter describes the properties of the mountain snowpack that contribute to avalanche formation and describes avalanche safety techniques.


PROPERTIES OF SNOW Physical Properties Although snow cover appears to be nothing more than a thick, homogeneous blanket covering the ground, it is in fact one of the most complex materials found in nature. It is highly variable and goes through significant changes in relatively short periods. In nature, snow cover is variable on both the broad geographic scale (Antarctic snow is quite different from snow found in the Cascade Mountains of North America) and on the microscale (where snow conditions may vary greatly from one side of a rock or tree to the other). All snow crystals are made

Chapter 2: Avalanches of the same substance, the water molecule, but local environmental conditions control the type and character of snow found at a given location. At a single site, the snow cover varies from top to bottom, resulting in a complex, layered structure. Individual layers may be quite thick or very thin. In general, thicker layers represent consistent conditions during one storm, when new snow crystals falling are of the same type, wind speed and direction vary little, and temperature and precipitation are fairly constant. Thinner layers, perhaps only millimeters in thickness, often reflect conditions between storms, such as the formation during fair weather of a melt–freeze crust, a period of strong winds creating a wind crust, or the occurrence of surface hoar, the winter equivalent of dew. Delicate feathershaped crystals of surface hoar deposited from the moist atmosphere onto the cold snow surface overnight offer a beautiful glistening sight as they reflect the sun of the following day. However, they are very fragile and weak, and once buried by subsequent snowfalls, they may be major contributors to avalanche formation. One property of snow is strength, or hardness, which is of great importance in terms of avalanche formation. Snow can vary from light and fluffy, easy to shovel, and especially delightful to ski through, to heavy and dense, impossible to penetrate with a shovel, and hard enough to make it very difficult for a skier to carve a turn, even with sharp metal edges. The arrangement of the ice skeleton and the changing density (mass per unit volume) produce this wide range of conditions. In the case of snow, density is determined by the volume mixture of ice crystals and air. The denser the snow layer, the harder and stronger it becomes, as long as it is not melting. The density of new snow can have a wide range of values. This depends on how closely the new snow crystals pack together, which is controlled by the shape of the crystals. The initial crystals have a variety of shapes, and some pack more closely together than others (Fig. 2-1). For example, needles pack more closely than stellars and as a consequence may possess a density 3 to 4 times that of stellars. Wind can alter the shape of new snow crystals, breaking them into much smaller pieces that pack very closely together to form wind slabs. These in turn may possess a density 5 to 10 times that of new stellars falling in the absence of wind. Because these processes occur at different times and locations at the surface of the snow cover and are buried by subsequent snowfalls, a varied, nonhomogeneous layered structure results. Therefore, what may seem to the casual observer to be minor variations in atmospheric conditions can have an important influence on the properties of snow. After snow has been deposited on the ground, the density increases as the snow layer settles vertically or shrinks in thickness. Because an increase in density equals an increase in strength, the rate at which this change occurs is important with respect to avalanche potential. Snow can settle simply because of its own weight. It is highly compressible because it is composed mostly of empty air pockets within an ice skeleton of snow crystals. In a typical layer of new snow, 85% to 95% of the volume is empty air pockets. Individual ice crystals can move and slide past each other, and because the force of gravity causes them to move slowly downward, the layer shrinks. The heavier the snow above is and the warmer the temperature, the faster this settlement proceeds. At the same time, the complex, intricate shapes that characterize the new snow crystals begin to change. They become

37

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

rounded and suitable for closer packing. Intricate crystals change because they possess a shape that is naturally unstable. New snow crystals have a large surface area-to-volume ratio and are composed of crystalline solid close to its melting point. In this aspect, snow crystals are almost unique among materials found in nature. Surface energy physics dictates that this unstable condition will change; the warmer the temperature is, the faster the change. Under very cold conditions, the original shapes of the snow crystals are recognizable after they have been in the snow cover for several days or even a week or two. As temperatures warm and approach the melting point, such shapes disappear within a few hours to a day. Changes in the shape or texture of snow crystals are examples of initial metamorphism. The geologic term metamorphism defines changes that result from the effects of temperature and pressure. As the crystal shapes simplify, they can pack more closely together, enhancing further settlement (Fig. 2-2). The changes generally occur within hours to a few days. The structure of snow cover changes over a period of weeks to months via other processes. Settlement, which may initially have been rapid, continues at a much slower rate. Other factors begin to exert dominant influences on metamorphism. These factors include the difference in temperature measured upward or downward in the snow layer, called the temperature gradient.

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PART ONE: MOUNTAIN MEDICINE

Kinetic metamorphism

Ice grain

Densification and strengthening of snowpack

Figure 2-2. Settlement. As the crystal shapes become more rounded, the crystals can pack more closely together, and the layer settles or shrinks in thickness.

Water vapor Ice grain

Low temperature

Heat flow High temperature

Temperature gradient Temperature °C 0° –5° –10° 150

Energy exchange with atmosphere

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

100 Snow height cm 50

Temperature profile

0 Heat supply from earth

Figure 2-3. When an insulating layer of snow separates the warm ground from the cold air, a temperature gradient develops across the snow layer.

Averaged over 24 hours, snow temperatures generally are coldest near the surface and warmest near the ground at the base of the snow cover, creating a temperature gradient across a snow layer sandwiched between cold winter air and relatively warm ground (Fig. 2-3). The temperature gradient crosses both ice and large void spaces filled with air. Within the ice skeleton, the temperature adjacent to the ground is warmer than that of the snow layer just above, and this pattern continues through the snow cover in the direction of the colder surface. Warm air contains more water vapor than cold air; this holds true for the air trapped within the snow cover. The greater the amount of water vapor, the greater the pressure. Therefore, both a pressure gradient and a temperature gradient exist through the snow cover. When a pressure difference exists, the difference naturally tends to equalize, just as adjacent high and low atmospheric pressure centers cause movement of air masses. Pressure differences within snow cause vapor to move upward through the snow layers. The air within the layers of the snow cover is saturated with water vapor, with a relative humidity of 100%. When air moves upward to a colder layer, the amount of water vapor that can be supported in the air pocket diminishes. Some vapor changes to ice and is deposited on the surrounding ice grains. We witness a similar process when warm, moist air in a heated room comes in contact with a cold win-

dowpane. The invisible water vapor is cooled to its ice point, and some of the vapor changes state and is deposited as frost on the window. Figure 2-4 shows how the texture of the snow layer changes during this temperature-gradient process. Water molecules sublimate from the upper surfaces of a grain. The vapor moves upward along the temperature (and vapor) gradient and is deposited as a solid ice molecule on the underside of a colder grain above. If this process continues long enough (it continues as long as a strong temperature gradient exists), all grains in the snow layer are transformed from solid to vapor and back to solid again; that is, they recrystallize. New crystals are completely different in texture from their initial form. They become large, coarse grains with facets and sharp angles and may eventually evolve into a hollow cup form. Examples of these crystals are shown in Figure 2-5. The process is called temperature-gradient metamorphism, or kinetic metamorphism, and well-developed crystals are commonly known as depth hoar. Depth hoar is of particular importance to avalanche formation. It is very weak because there is little or no cohesion or bonding at the grain contacts. Depth hoar or temperaturegradient snow layers can be compared to dry sand. Each grain may possess significant strength, but a layer composed of grains is very weak and friable because the grains lack connections. Thus depth hoar is commonly called “sugar snow.” Depth hoar usually develops whenever the temperature gradient is equal to or greater than about 10º C (18° F) per meter. In the cold, shallow snow covers of a continental climate, such as that of the Rocky Mountains, a gradient of this magnitude is common within the first snow layers of the season. Therefore, a layer of depth hoar is frequently found at the bottom of the snow cover, and the resulting low strength becomes a significant factor for future avalanches. In the absence of a strong temperature gradient, a totally different type of snow texture develops. When the gradient is less

Chapter 2: Avalanches

39

Equilibrium metamorphism Convex high vapor pressure H2O transfer

H2O transfer

Concave low vapor pressure

A Figure 2-6. In the equilibrium metamorphism process, ice molecules sublimate from crystal points (convexities) and redeposit on flat or concave areas of the crystal.

Equilibrium metamorphism

B Figure 2-5. A, Mature depth hoar grains. Facets and angles are visible. Grain size, 3 to 5 mm. B, Advanced temperature-gradient grains attain a hollow cup-shaped form. Size, 4 mm. (Polarized-light photos by Doug Driskell.)

Sharp concave regions

Necks form—sintering

Figure 2-7. Equitemperature grain growth. In the presence of weak temperature gradients, bonds grow at the grain contacts.

than about 10º C (18° F) per meter, there is still a vapor pressure difference, but upward movement of vapor through the snow layers is at a much slower rate. As a result, water vapor deposited on a colder grain tends to cover the total grain in a more homogeneous manner, rather than showing the preferential deposition characteristic of depth hoar. This process produces a grain with a smooth surface of 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 (convexity) (Fig. 2-6). Connecting bonds formed at the grain contacts give the snow layer strength over time (Fig. 2-7). Bond growth, called sintering, yields a cohesive texture, in complete contrast to the cohesionless texture of depth hoar. This type of grain has been referred to by various terms (destructive metamorphism, equitemperature metamorphism, and equilibrium metamorphism) but can generally be described as fine-grained or well-sintered (bonded) snow. Bonded and interconnected grains are shown in Figure 2-8. The preceding paragraphs describe the big picture in terms of what happens to snow layers after they have been buried by

Figure 2-8. Bonded or sintered grains resulting from equitemperature metamorphism. Grain size, 0.5 to 1 mm. (Polarized-light photo by Doug Driskell.)

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subsequent snowfalls. If the layer is subfreezing (i.e., if no melt is taking place), one of the two processes described previously is occurring, or perhaps a transition exists between the two. Within the total snow cover, these processes may occur simultaneously, but only one can take place within a given layer at a given time. Both processes accelerate with warmer snow temperature because more water vapor is involved. The temperature gradient across the layer determines whether the process involves the growth of weak depth hoar crystals or the development of a stronger snow layer with a sintered, interconnected texture.

Slab Avalanche Formation There are two basic types of avalanche release. The first is a point-release, or loose snow, avalanche (Fig. 2-9). A loose snow avalanche involves cohesionless snow and is initiated at a point, spreading 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. This type of avalanche usually involves only small amounts of nearsurface snow. The second type of avalanche, the slab avalanche, requires a cohesive snow layer poorly anchored to the snow below because of the presence of a weak layer. The cohesive blanket of snow breaks away simultaneously over a broad area (Fig. 2-10). A slab release can involve a range of snow thicknesses, from the near-surface layers to the entire snow cover down to the ground. In contrast to a loose snow avalanche, a slab avalanche has the potential to involve very large amounts of snow. To understand the conditions in snow cover that contribute to slab avalanche formation, it is essential to reemphasize that snow cover develops layer by layer. Although a layered structure can develop by metamorphic processes, distinct layers develop in numerous other ways, most of which have some influence on avalanche formation. The layered structure is directly tied to the two ingredients essential to the formation of slab avalanches: the cohesive layer of snow and the weak layer beneath. If the snow cover is homogeneous from the ground to the surface, there is no danger of slab avalanches, regardless of the snow type. If the entire snow layer is sintered, dense, and strong, stability is very high. Even if the entire snow cover is composed of a very weak layer of depth hoar, there is still no hazard from slab avalanches because the cohesionless character does not allow propagation of the cracks necessary for slab avalanches to form. However, the combination of a basal layer of depth hoar with a cohesive layer above, for example, provides exactly the ingredients for slab avalanche danger. For successful evaluation of slab avalanche potential, information is needed about the entire snowpack, not just the surface. A hard wind slab at the surface may seem strong and safe to the uninitiated, but when it rests on a weaker layer, which may be well below the surface, it may fail under the weight of a skier and be released as a slab avalanche. Many snow structure combinations can contribute to slab formation. One scenario involves thick layers of weak snow, which result from the development of depth hoar early in the season. The typical combination of climatic factors that produce these layers is early winter snowfalls followed by several weeks of clear, cold weather. Even at higher elevations in the moun-

Figure 2-9. Loose snow or point-release avalanche. (Photo courtesy USDA Forest Service.)

tains, snow cover on the slopes with a southerly aspect may melt off during a period of fair weather. However, in October and early November, the sun angle is low enough that steep slopes with a northerly aspect receive little or no direct heating from the sun. Snow remains on the ground but not without change. Snow on north-facing slopes experiences optimal conditions for depth hoar formation: a thin, low-density snow cover (maximum opportunity for vapor flow) is sandwiched between

Chapter 2: Avalanches

41

Figure 2-10. Slab avalanche. (From USDA Forest Service:Williams K, Armstrong B:The Snowy Torrents. Jackson,WY,Teton Bookshop, 1984, with permission. Photo by Alexis Kelner.)

Figure 2-11. Snow layer combinations that often contribute to avalanche formation.

the warm ground, still retaining much of its summer heat, and the cold air above. This snow layer recrystallizes over a period of weeks. When the first large storm of winter arrives in November, cohesive layers of wind-deposited snow accumulate on a very weak base, setting the scene for a widespread avalanche cycle. Figure 2-11 describes other combinations that result in brittle or cohesive layers of snow on a weak layer.

Mechanical Properties: How Snow Deforms on a Slope Almost all physical properties of snow can be easily seen or measured. A snowpit provides a wealth of information regarding these properties, layer by layer, throughout the thickness 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 has a tendency to settle simply from its own weight. When this occurs on level ground, the settlement is perpendicular to the ground and the snow layer increases in density and gains in strength. The situation is not so simple when snow rests on a slope. The force of gravity is divided into two components, one

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PART ONE: MOUNTAIN MEDICINE

Figure 2-12. Depending on prevailing conditions, snow may deform and stretch in a viscous or flowing manner, or it may respond more like a solid, and fracture.

tending to cause the snow layer to shrink in thickness, and a new component acting parallel to the slope, which tends to pull the snow down the slope. Down-slope movement within the snow cover occurs at all times, even on gentle slopes. The speed of movement is slow, generally on the order of a few millimeters per day up to millimeters per hour within new snow on steep slopes. The evidence of these forces is often clearly visible in the bending of trees and damage to structures built on snow-covered slopes. Although the movement is slow, when deep snow pushes against a rigid structure, the forces are significant, and even large buildings can be pushed off their foundations. Snow deforms in a highly variable fashion. It is generally described as a viscoelastic material. Sometimes it deforms as if it were a liquid (viscous) and at other times it responds more like a solid (elastic). Viscous deformation implies continuous and irreversible flow. Elastic deformation implies that once the force causing the deformation is removed, some small part of the initial deformation is recovered. The elasticity of snow is not so obvious, primarily because the amount of rebound is very small compared with that of more familiar materials. In regard to avalanche formation, it is important to know when snow acts primarily as an elastic material and when it responds more like a viscous substance. These conditions are shown in Figure 2-12. Laboratory experiments have shown that conditions of warm temperatures and slow application of force favor viscous deformation. We see 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. In contrast, when temperatures are very cold or when force is applied rapidly, snow reacts like an elastic material. If enough force is applied, it fractures. We think of such a substance as brittle; the release of stored elastic energy causes fractures to move through the material. In the case of snow cover on a steep slope, forces associated with accumulating snow or the weight of a skier may increase until the snow fails. At that point, stored elastic energy is released and is available to drive brittle fractures over great distances through the snow slab.

Figure 2-13. The consistent 90-degree angle between crown face and bed surface of the avalanche shows that slab avalanches result from an elastic fracture. (Photo by A. Judson.)

The slab avalanche provides the best example of elastic deformation in snow cover. Although the deformation cannot actually be seen, evidence of the resultant brittle failure is clearly present in the form of the sharp, linear fracture line and crown face of the slab release (Fig. 2-13). The crown face is almost always perpendicular to the bed surface, evidence that snow has failed in a brittle manner. To fully understand the slab avalanche condition or the stability of the snow cover, its mechanical state must be considered. Snow is always deforming down-slope, but throughout most of the winter the strength of the snow is sufficient to prevent an avalanche. The snow cover is layered, and some layers are weaker than others. During periods of snowfall, blowing snow, or both, an additional load, or weight, is being applied to the snow in the starting zone, the snow is creeping faster, and these new stresses are beginning to approach the strength of the weakest layers. The weakest layer has a weakest point somewhere within its continuous structure. If the stresses caused by the load of the new snow or the weight of a skier reach the level at which they equal the strength of the weakest point, the snow fails completely at that point (Fig. 2-14). This means that the strength at that point immediately goes to zero. This is analogous to what would happen if someone on a tugof-war team were to let go of the rope. If the remainder of the team was strong enough to make up for the lost member, not much would change immediately. The same situation exists with the snow cover. If the surrounding snow has sufficient strength to make up for the fact that the strength at the weakest point has now gone to zero, nothing happens beyond perhaps a local movement or settlement in the snow. If, however, the surrounding snow is not capable of doing this, the area of snow next to the initial weak point fails, and then the area next to it, and the chain reaction begins. As the initial crack forms in the now unstable snow, the elastic energy is released, which in turn drives the crack further, releasing more elastic energy, and so forth. 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

A

B Figure 2-14. Slab avalanche released by a skier. (Photo by R. Ludwig.)

C

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PART ONE: MOUNTAIN MEDICINE

propagate, allowing entire basins, many acres in area, to be set in motion within a few seconds.


AVALANCHE DYNAMICS The topic of avalanche dynamics includes how avalanches move, how fast they move, and how far and with how much destructive power they travel. The science of avalanche dynamics is not well advanced, although much has been learned in the past few decades. Measured data for avalanche velocity and impact pressure are still lacking. Although any environmental measurement presents its own set of problems, it is clear that opportunities for making measurements inside a moving avalanche are extremely limited. Although avalanche paths exist in a variety of sizes and shapes, they all have three distinct parts

with respect to dynamics (Fig. 2-15). In the starting zone, usually the steepest part of the path, the avalanche breaks away, accelerates down the slope, and picks up additional snow. From the starting zone, the avalanche proceeds to the track, where it remains essentially constant and picks up little or no additional snow as it moves; the average slope angle has become less steep and frequently the snow cover is more stable than in the starting zone. (However, a study by Sovilla and colleagues19a from Switzerland in 2000 showed that a significant amount of snow could be entrained into the avalanche from the track.) Small avalanches often stop in the track. After traveling down the track, the avalanche reaches the runout zone. Here the avalanche motion ends, either slowly as it decelerates across a gradual slope, such as an alluvial fan, or abruptly as it crashes into the bottom of a gorge or ravine. As a general rule, the slope angle of starting zones is 30 to 45 degrees, of the track it

Starting zone

Track

Runout zone

Figure 2-15. The three parts of an avalanche path: starting zone, track, and runout zone. (Photo by B. Armstrong.)

Chapter 2: Avalanches

45

is 20 to 30 degrees, and of the runout zone it is less than 20 degrees. Few actual measurements of avalanche velocities have been made, but enough data have been obtained to provide some typical values for the various avalanche types. For the highly turbulent dry-powder avalanches, the velocities are commonly in the range of 75 to 100 mph (34 to 45 m/s), with rare examples in the range of 150 to 200 mph (67 to 89 m/s). Such speeds are possible for powder avalanches because large amounts of air in the moving snow greatly reduce the forces resulting from internal friction. As snow in the starting zone becomes dense, wetter, or both, movement becomes less turbulent and a more flowing type of motion reduces typical velocities to the range of 50 to 75 mph (22 to 34 m/s). During spring conditions when the snow contains large amounts of liquid water, speeds may reach only about 25 mph (11 m/s) (Fig. 2-16). 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, such as the side walls of a gully, which would normally direct the flow of the avalanche around a bend, may be overridden by a high-velocity powder avalanche (Fig. 2-17). The slower-moving avalanches, which travel near the ground, tend to follow terrain features, giving them somewhat predictable courses. Because avalanches can travel at very high speeds, the resultant impact pressures can be significant. Smaller and mediumsize events (impact pressures of 1 to 15 kilopascals [kPa]) have the potential to heavily damage wood-frame structures. Extremely large avalanches (impact pressures of more than 150 kPa) possess the force to uproot mature forests and even destroy structures built of concrete. Some reports of avalanche damage describe circumstances that cannot be easily explained simply by the impact of large amounts of fast-moving dense snow. Some observers have noted that as an avalanche passed, some buildings actually exploded, perhaps from some form of vacuum created by the fast-moving snow. Other reports indicate that a structure was destroyed by the “air blast” preceding the avalanche because there was no evidence of large amounts of avalanche debris in the area. However, this is more likely to be damage resulting from the powder cloud, which may be composed of only a few inches of settled snow yet it contributes significantly to the total impact force. The presence of snow crystals can increase the air density by a factor of 3 or more. A powder cloud traveling at a moderate dry-avalanche speed of 60 mph (27 m/s) could have the impact force of a 180-mph (80 m/s) wind, well beyond the destructive capacity of a hurricane.


IDENTIFYING AVALANCHE PATH CHARACTERISTICS

Characteristics such as elevation, slope profiles, and weather determine whether a mountain can produce avalanches. The ingredients of an avalanche, snow and a steep-enough slope, are such that any mountain can produce an avalanche if conditions are exactly right. To be a consistent producer of avalanches, a mountain and its weather must work in harmony.

Elevation Mountains must be at high-enough latitudes or must be high enough in elevation to build and sustain a winter snow cover

Figure 2-16. A dry-snow avalanche may have a slowing motion and travel near the surface or, with lower density snow and higher velocities,the turbulent dust cloud of the powder avalanche develops.

before their slopes can become avalanche threats. Temperature drops steadily with elevation. This has the obvious effect of allowing snow to build up deeper and remain longer at higher elevations before melting depletes the snow cover. A less obvious effect of the temperature and elevation relationship on avalanche formation is the demarcation called the treeline.

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PART ONE: MOUNTAIN MEDICINE only 10 degrees, but the avalanche was big enough to kill seven skiers. This extreme applies only to a water-saturated snowpack, which behaves more like a liquid than a solid. A more realistic slope is 22 degrees, the “angle of repose” for granular substances, such as sand and dry, unbonded snow. Round grains will not stack up in a pile having sides much steeper than 22 degrees before gravity rearranges the pile. Drysnow avalanches have occurred on slopes of 22 to 25 degrees; these are rare because snow grains are seldom round and seldom touch without forming bonds. A useful minimum steepness for producing avalanches is 30 degrees. Avalanches occur with the greatest frequency on slopes of 30 to 45 degrees. These are the angles in which the balance between strength (the bonding of the snow trying to hold it in place) and stress (the force of gravity trying to pull it loose) is most critical. On even steeper slopes, the force of gravity wins; snow continually rolls or sloughs off, preventing buildup of deep snowpacks. Exceptions exist, such as damp snow plastered to a steep slope by strong winds.

Orientation

Figure 2-17. The large powder cloud associated with a fast-moving dry-snow avalanche. (Photo by R. Armstrong.)

This is the level above which the combined effects of low temperature, strong winds, and heavy snowfall prevent tree growth. The treeline can be quite variable in any mountain range, depending on the microclimates. On a single mountain, treeline is generally higher on south slopes than on north slopes (in the northern hemisphere), because more sunshine leads to warmer average temperatures on southern exposures. Latitudinal variation in the elevation of treeline ranges from sea level in northern Alaska to almost 3658 m (12,000 feet) in the Sierras of southern California and the Rockies of New Mexico. Mountains that rise above treeline are more likely to produce avalanches. Dense timber anchors the snowpack, so avalanches can seldom start. Below treeline, avalanches can start on slopes having no trees or only scattered trees, a circumstance arising either from natural conditions, such as a streambed or rockslide area, or from human-made conditions, such as clearcuts. Above treeline, avalanches are free to start, and once set in motion, they can easily cut a swath through the trees below. The classic avalanche path is one having a steep bowl above treeline to catch the snow and a track extending below treeline. Avalanches run repeatedly down the track and ravage whatever vegetation grows there, leaving a scar of small or stunted trees that cuts through larger trees on either side.

Slope Angle In snow that is thoroughly saturated with water, so that a slush mixture is formed, the slope needs only to have a slight tilt to produce an avalanche. For example, a wet-snow avalanche in Japan occurred on a beginner slope at a ski area. The slope was

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

Avalanche Terrain The frequency with which a path produces avalanches depends on a number of factors, with slope steepness a major one. The easiest way to create high stress is to increase the slope angle; gravity works that much harder to stretch the snow out and rip it from its underpinnings. A slope of 45 degrees produces many more avalanches than one of 30 degrees. However, specific terrain features are also important. Broad slopes that are curved into a bowl shape and narrow slopes that are confined to a gully efficiently collect snow. Those having a curved horizontal profile, such as a bowl or gully, trap blowing snow coming from several directions; the snow drifts over the top and settles as a deep pillow. On the other hand,

Chapter 2: Avalanches the plane-surfaced slope collects snow efficiently only if it is being blown directly from behind. A side wind scours the slope more than loads it. The surface conditions of a starting zone often dictate the size and type of avalanche. A particularly rough ground surface, such as a boulder field, does not usually produce avalanches early in the winter, as it takes considerable snowfall to cover the ground anchors. Once most of the rocks are covered, avalanches pull out in sections, the area between two exposed rocks running one time, and the area between two other rocks running another. A smooth rock face or grassy slope provides a surface that is too slick for snow to grip. Therefore, full-depth avalanches are distinctly possible; if the avalanche does not run during the winter, it is likely to run to ground in the spring, once melt water percolates through the snow and lubricates the ground surface. Vegetation has a mixed effect on avalanche releases. Bushes provide anchoring support until they become totally covered; at that point they may provide weak points in the snow cover, because air circulates well around the bush, providing an ideal habitat for the growth of depth hoar. It is common to see that the fracture line of an avalanche has run from a rock to a tree to a bush, all places of healthy depth hoar growth. A dense stand of trees can easily provide enough anchors to prevent avalanches. Reforestation of slopes devoid of trees because of logging, fire, or avalanche is an effective means of avalanche control. Scattered trees on a gladed slope offer little if any support to hold snow in place. Isolated trees may do more harm than good by providing concentrated weak points on the slope.


FACTORS CONTRIBUTING TO AVALANCHE FORMATION

The factors that contribute to avalanche release are terrain, weather, and snowpack. Terrain factors are fixed; however, the states of the weather and of the snowpack change daily, even hourly. Precipitation, wind, temperature, snow depth, snow surface, weak layers, and settlement are all factors determining whether an avalanche will occur.

Snowfall New snowfall is the event that leads to most avalanches: more than 80% of all avalanches fall during or just after a storm. Fresh snowfall adds weight to existing snow cover. If the snow cover is not strong enough to absorb this extra weight, avalanche releases occur. The size of the avalanche is usually related to the amount of new snow. Snowfalls of less than 6 inches (15 cm) seldom produce avalanches. Snows of 6 to 12 inches (15 to 30 cm) usually produce a few small slides, and some of these harm skiers who release them. Snows of 1 to 2 feet (30 to 60 cm) produce avalanches of larger size that present a considerable threat to skiers and pose closure problems for highways and railways. Snows of 2 to 4 feet (60 to 120 cm) are much more dangerous, and snowfalls greater than 4 feet produce major avalanches capable of large-scale destruction. These figures are guidelines based on data and experience and must be considered with other factors to arrive at the true hazard. For example, a snowfall of 10 inches (25 cm) whipped by strong winds may be serious; a fall of 2 feet of feather-light snow in the absence of wind may produce no avalanches.

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

Rain Light rain falling on a cold snowpack invariably freezes into an ice crust, which adds strength to the snow cover. At a later time, the smooth crust could become a sliding layer beneath the new fall of snow. Heavy rain (usually an inch or more) greatly weakens the snow cover. First, it adds weight. An inch of rain is the equivalent in weight to 10 to 12 inches (25 to 30 cm) of snow. Second, it adds no internal strength of its own (in the form of a skeleton of ice, as new snow would), while it dissolves bonds between snow grains as it percolates through the top snow layers, reducing strength even further.

New Snow Density and Crystal Type A layer of fresh snow contains only a small amount of solid material (ice); the large majority of the volume is occupied by air. It is convenient to refer to snow density as a percentage of the volume occupied by ice. New snow densities usually range from 7% to 12%. In the high elevations of Colorado, 7% is an average value; in the more maritime climates of the Sierras and Cascades, 12% is a typical value. Density becomes an important factor in avalanche formation when it varies from average values. Wet snowfalls or falls of heavily rimed crystals, such as graupel, may have densities of 20% or greater. (Graupel is a snowflake that has been transformed into a pellet of soft ice because of riming inside a cloud.) A layer of heavier-thannormal snow presents a danger because of excess weight. Snowfall that is much lighter than normal, 2% to 4% for example, can also present a dangerous situation. If the low-density layer quickly becomes buried by snowfall of normal or high density, a weak layer has been introduced into the snowpack. By virtue of low density, the weak layer has marginal ability to withstand the weight of layers above, making it susceptible to collapse. Storms that begin with low temperatures but then warm up produce a layer of weak snow beneath a stronger, heavier layer. Density is closely linked to crystal type. Snowfalls consisting of graupel, fine needles, and columns can accumulate at high densities. Snowfalls of plates, stellars, and dendritic forms account for most of the lower densities.

Wind Speed and Direction Wind drives fallen snow into drifts and cornices from which avalanches begin. Winds pick up snow from exposed, windward slopes and drive it onto adjacent, leeward slopes, where it is deposited into sheltered hollows and gullies. A speed of 15 mph (7 m/s) is sufficient to pick up freshly fallen snow. Higher speeds are required to dislodge older snow. Speeds of 20 to 50 mph (9 to 22 m/s) are the most efficient in transporting snow into avalanche starting zones. Speeds greater than 50 mph can create spectacular banners of snow streaming from high peaks, but much of this snow is lost to evaporation in the

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air or is deposited far down the slope away from the avalanche starting zone. Winds play a dual role in increasing avalanche potential. First, wind scours snow from a large area (of a windward slope) and deposits it in a smaller area (of a starting zone). Wind can thus turn a 1-foot snowfall into a 3-foot drift in a starting zone. The rate at which blowing snow collects in bowls and gullies can be impressive. In one test at Berthoud Pass, Colorado, the wind deposited snow in a gully at a rate of 18 inches (45 cm) per hour. Another wind effect is that blowing snow is denser after deposit than before. This is because snow grains are subjected to harsh treatment in their travels; each collision with another grain knocks off arms and sharp angles, reducing size and allowing the pieces to settle into a denser layer. The net result of wind is to fill avalanche starting zones with more and heavier snow than if the wind had not blown.

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

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

Depth of Snow Cover Of the snowpack factors contributing to avalanche formation, depth of snow cover is the most basic. When the early-winter snowpack covers natural anchors, such as rocks and bushes, the start of the avalanche season is at hand. North-facing slopes are usually covered before other slopes. A scan of the terrain usually suffices to weigh this clue, but another method can be used to determine the time of the first significant avalanches. Long-term studies show a relationship between snow depth at a study site and avalanche activity. For example, along Red Mountain Pass, Colorado, it is unlikely that an avalanche large enough to reach the highway will run until close to 3 feet (90 cm) of snow covers the ground at the University of Colorado’s snow study site. At Alta, Utah, once 52 inches (130 cm) of snowpack has built up, the first avalanche to cover the road leading from Salt Lake City can be expected.

Nature of the Snow Surface How well new snow bonds to the old snow surface is a key factor in determining whether an avalanche will release within the layer of new snow or deeper in the snowpack. A poor bond, usually new snow resting on a smooth, cold surface with snowfalls of 1 foot (30 cm) or more, almost always produces a new-snow avalanche. A strong bond, usually onto a warm, soft, or rough surface, may produce nothing at all, or if weaknesses lie at deeper layers of the snow cover, a large snowfall will cause avalanches to pull out older layers of snow in addition to the new snow layer. These avalanches have more potential for destruction. A cold, hard snow surface offers little grip to fresh, cold snow. Ice crusts are commonly observed to be avalanche-sliding surfaces. The crust could be a sun crust, a rain crust, or a hardened layer of firm snow that has survived the summer. Firm layers are especially dangerous in early winter when first snows fall.

Weak Layers Any layer susceptible to collapse or failure because of the weight of the overburden is a weak link. Of the snowpack contributory factors, this is the most important, because a weak layer is essential to every avalanche. The weak layer releases along what is called the failure plane, sliding surface, or bed surface. One common weak layer is an old snow surface that offers a poor bond for new snow. Another weak layer that forms on

Chapter 2: Avalanches the snow surface is hoar frost, or surface hoar (see Physical Properties, earlier). On clear, calm nights, it forms a layer of feathery, sparkling flakes that grow on the snow surface. The layer can be a major contributor to avalanche formation when buried by a snowfall. Many avalanches have been known to release on a buried layer of surface hoar, sometimes a layer more than 1 month old and 6 feet (180 cm) or more below the surface. A weak layer that is almost always found in the snowpacks that blanket the Rocky Mountains and occasionally the Cascades and Sierra Nevadas is temperature-gradient snow, or depth hoar. The way to decide whether a temperature-gradient layer is near its collapse point is to test the strength of the overlying layers and the support provided around the edges of the slope. This is no easy task. One method is to try jumping on your skis while standing on a shallow slope. Collapse is a good indication that similar snow cover on a steeper slope will produce an avalanche. Often, skiers and climbers cause inadvertent collapses while skiing or walking on a depth hoar–riddled snowpack. The resulting “whoomf” sound is a warning of weak snow below. Finally, a weak layer can be created within the snow cover when surface melting or rain causes water to percolate into the snow and then fan out on an impermeable layer, thereby lubricating that layer and destroying its shear strength. Combining the contributory factors on a day-by-day basis is the avalanche forecaster’s art. Every avalanche must have a weak layer to release on, so knowledge of snow stratigraphy, or layering, and what sort of applied load will cause a layer to fail is the essence of forecasting.


SAFE TRAVEL IN

AVALANCHE TERRAIN

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

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

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bowls and gullies are almost always capable of producing avalanches.

Route Finding Good route-finding techniques are necessary for safe travel in avalanche terrain (Fig. 2-18). The object of a good route in avalanche country is more than avoiding avalanches. It should also be efficient and take into account the abilities and desires of the group to choose a route that is not overly technical, tiresome, or time consuming. The safest way to avoid avalanches is to travel above or below and well away from them. When taking the high route, the traveler should choose a ridgeline that is above the avalanche starting zones. It is safest to travel the windward side of the ridge. The snow cover is usually thinner and windpacked, with rocks sticking through—not the most pleasant skiing, but safe. Cornice collapses present a very real hazard; they should be avoided by staying on the roughened snow more to windward. Skiers taking the low route in the valley should not linger in the runouts of avalanche paths. Even though it is unlikely that a skier traveling along the valley could trigger an avalanche high up on the slope, the skier should not boost the odds of getting caught in an avalanche released by natural forces far above. Slopes of 30 degrees or more should be avoided. By climbing, descending, and traversing only in gentle terrain, avalanche terrain can be avoided.

Stability Evaluation Tests Skiers can perform several tests of stability. On a small slope that is not too steep (and therefore will not avalanche), the skier can try a ski test by skiing along a shallow traverse and then setting the ski edges in a hard check. Any cracks or settlement noises indicate that the same slope, if steeper, would have probably avalanched, and on the steeper slope it would have taken less weight or jolt to cause the avalanche. Another test is to push a ski pole into the snow, handle end first. This helps to feel the major layering of the snowpack. For example, the skier may feel the layer of new snow, midpack stronger layers, and depth hoar layers, if the pole is long enough. Hard-snow layers and ice lenses resist penetration altogether. This test reveals only the gross layers; thin weak layers, such as buried surface hoar or a poor bond between any two layers, cannot be detected. Thus, the ski pole test has limited value. A much better way to directly observe and test snowpack layers is to dig a hasty snowpit. (This is an excellent use of the shovel that, in the next section, we recommend the skier carry.) In a spot as near as possible to a suspected avalanche slope without putting the traveler at risk, a pit 4 to 5 feet (120 to 150 cm) deep and 3 feet (90 cm) wide should be dug. With the shovel, the uphill wall is shaved until it is smooth and vertical. Now the layers of snow can be observed and felt. The tester can see where the new snow touches the layer beneath, poke the pit wall with a finger to test hardness, and brush the pit wall with a paintbrush to see which layers are soft and fall away and which are hard and stay in place after being brushed. By grabbing a handful of depth hoar, the skier can see how large the grains are and how poorly they stick together. The shovel shear test gauges the shear strength between layers and thus locates weak layers. First a column of snow is isolated from the vertical pit wall. Both sides and the back of the column are cut with the shovel or a ski, so that the column is free

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Poor route

Poor route

Good route

Good route

Gentle slopes te

d oo

rou

G

Poor route Poor route

Steep slopes

Good route

Figure 2-18. Four ski-touring areas showing the safer routes (green dashed lines) and the more hazardous routes (red dotted lines). Arrows indicate areas of wind loading. (From USDA Forest Service: Avalanche Handbook, Agricultural Handbook 489, with permission. Photo by Alexis Kelner.)

Chapter 2: Avalanches

A

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B

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

standing. The dimensions are a shovel’s width on all sides. The tester inserts the shovel blade at the back of the column and gently pulls forward on the handle. An unstable slab will shear loose on the weak layer, making a clean break; the poorer the bond, the easier the shear. A five-point scale is used to rate the shear: “very easy” if it breaks as the column is being cut or the shovel is being inserted; “easy” if a gentle pull on the shovel does the job; “moderate” if a slightly stronger shovel-pry is required; “hard” if a solid tug is required; “very hard” if a major effort is needed to break the snow. Generally, “very easy” and “easy” shears indicate unconditionally unstable snow, “moderate” means conditionally unstable, and “hard” and “very hard” mean stable. The value of the shovel shear test is that it can find thin weak layers undetectable by any other method. Its shortcoming is that it is not a true test of stability, as it does not indicate the amount of weight required to cause shear failure. A test that does a better job of indicating actual stability is the Rutschblock, or shear block, test. This test is calibrated to the skier’s weight and the stress he or she would put on the snow. Again, a snowpit is dug with a vertical uphill wall, but the pit must be about 8 feet (240 cm) wide. By cutting into the pit wall, the skier isolates a block of snow that is about 7 feet (210 cm) wide (a ski length) and goes back 4 feet (120 cm) (a ski pole length) into the pit wall. Both sides and the back are cut with a shovel or ski so that the block is free standing. Wearing skis, the skier climbs around and well uphill from the isolated block and carefully approaches it from above. With skis across the fall line, the skier gently steps onto the block, first with the downhill ski and then the uphill ski, so that he or she is standing on the isolated block of snow. If the slab of snow has not yet failed, gently flexing the knees applies a little more pressure. Next some gentle jumps are tried. The stress should be increased by jumping harder until the block eventually shears loose or crumbles apart. The results are interpreted as “extremely unstable” if the block fails while the skier is cutting it, approaching it from

above, or merely standing on it; “unstable” if it fails with a knee flex or one gentle jump; “moderately stable” if it fails after repeated jumps; and “very stable” if it never fails but merely crumbles. These are objective results that help answer the bigger question—will it slide?—and help the mountain traveler decide how much risk to take.

Avalanche Rescue Equipment Shovel The first piece of safety equipment the skier or climber should own is a shovel. It can be used to dig snowpits for stability evaluation, and snow caves for overnight shelter. A shovel is also needed for digging in avalanche debris, as such snow is far too hard for digging with the hands or skis. The shovel should be sturdy and strong enough to dig in avalanche debris, yet light and small enough to fit into a pack. There is no excuse for not carrying a shovel. Shovels are made of aluminum or high-strength plastic and can be collapsible. Many good types are available in mountaineering stores.

Probe Several pieces of equipment are designed specifically for finding buried avalanche victims. The first is a collapsible probe pole. Organized rescue teams keep rigid poles in 10- or 12-foot (3 to 4 m) lengths as part of their rescue caches. The recreationist can buy probe poles of tubular aluminum or carbon fiber that come in 18-inch (45-cm) sections that fit together to make a fulllength probe. Ski poles with removable grips and baskets can be screwed together to make an avalanche probe. Survivors of an accident use probes to search for buried victims.

Avalanche Rescue Beacon Avalanche rescue beacons, or transceivers, have become the most-used personal rescue device worldwide. When used properly, they are a fast and effective way to locate buried avalanche victims. In the United States, these have become standard issue

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for ski area patrollers involved in avalanche work and for helicopter-skiing guides and clients. They are also commonly used by highway departments, search and rescue teams, and an increasing number of winter recreationists. Since beacons were introduced in the United States, they have saved at least 55 lives. Beacons save at least three or four lives per winter. All transceivers act as transmitters that emit a signal on a world-standard frequency of 457 kHz. A buried victim’s unit emits this signal, and the rescuers’ units receive the signal. The signal carries 30 to 46 m (100 to 150 feet) and, once picked up, guides searchers specifically to the buried unit. Beacon technology is evolving rapidly and the beacons on the market are improving. Two types of beacon have emerged: analog, which processes the signal in the traditional way to allow for a stronger (louder) signal as the receiving beacon approaches the sending beacon, and digital, which uses a computer chip to process the signal, displaying a digital readout of the distance and the general direction to the buried unit. Transceivers are not radio devices but are audio-magnetic-induction devices, so the directional arrows point only along a flux line of the sending unit’s magnetic field. Likewise, the displayed distance is the distance along a flux line rather than a direct distance to the sending unit. Both the analog and the digital types operate on the same frequency and therefore are compatible with one another. However, slightly different search techniques may be necessary to use each type most efficiently, and special training and practice are required before the user attains proficiency. The main brands available in the United States are ARVA, Barryvox, Ortovox, Pieps, Tracker, and SOS. Merely possessing a beacon does not ensure its lifesaving capability. Frequent practice is required to master a beaconguided search, which may not be straightforward. Skilled practitioners can find a buried unit in less than 5 minutes once they pick up the signal. Because speed is of the essence in avalanche rescue, beacons are certainly lifesavers. The best-proven rescue equipment is a beacon for a quick find, a collapsible probe pole to confirm and pinpoint the spot, and a shovel for a quick recovery (Box 2-1).

Avalanche Airbag In 1995, a new rescue device made in Germany was introduced in Europe. The ABS Avalanche Airbag System (Fig. 2-19) was originally designed specifically for guides and ski patrollers but today can be used by anyone venturing into avalanche terrain. Since 1995, the system has undergone continued and significant improvements. The airbag works because of inverse segregation. An avalanche in motion is composed of many different-sized particles of snow. Because of gravity, granular flows segregate, with smaller particles sinking to the lower portion of the flow and larger particles rising to the surface. The process of inverse segregation depends primarily on the relative sizes of the particles in a granular flow. A person is already a large particle and the airbag makes the user an even larger particle, making the separation effect even greater. The airbag is integrated into a special backpack, and the user deploys it by pulling a ripcord-like handle. This releases a cartridge of nitrogen gas that escapes at high velocity and draws in outside air through jets that inflate two 75-L airbags in 2 seconds. By 2004, there had been about 70 documented uses of the ABS Avalanche Airbag System, with three deaths. In one case

the airbag failed to work, and in the second case the user did not or could not deploy the airbag. The third incident involved a user who successfully deployed the airbag, only to be completely buried by a second avalanche moments later. Despite these failures, Brugger and Falk in an expanded study found that the ABS reduces the likelihood of burial from 39% to 16.2%.5 The ABS system is the most effective piece of equipment for saving lives in avalanche terrain. Brugger and Falk showed that it reduces mortality significantly, from 23% to 2.5% compared with the 75.9% to 66.2% reduction for avalanche rescue transceivers.5 This dramatic reduction in mortality occurs because the ABS system prevents burial, and very few partly buried or not buried victims (about 4% to 5%) die in avalanches. Commercial sales of ABS system in the United States have been delayed because of problems obtaining certification for the nitrogen-gas cartridges. The German company hopes to have U.S. Department of Transportation approval in 2007.

AvaLung In 1996, Dr. Thomas Crowley received a patent for an emergency breathing device to extract air from the snow surrounding a buried avalanche victim. The AvaLung functions as an artificial air pocket whose goal is to prolong survival time for the buried victim. Black Diamond Equipment, Ltd. (Salt Lake City, Utah) secured distribution rights in 2000 and redesigned the device in 2002. Called the AvaLung 2, it is worn outside the clothing like a bandoleer. If buried, the victim can breathe through a mouthpiece and inhale air from the surrounding snow. The carbon dioxide (CO2)-rich exhaled air is redirected into another area of the snow, reducing re-inhalation of CO2 (see Avalanche Victim Physiology and Medical Treatment after Rescue, later). The AvaLung system has been proven in numerous simulated burials, allowing subjects to breathe for 1 hour in tightly packed snow, including dense, wet snow. As of 2004, there were three known uses in avalanches. In two cases, the burials were very short, but in a third case a helicopter skier survived a 4-foot (120-cm) burial of 35 to 45 minutes. The ABS Avalanche Airbag and the AvaLung are designed to help avalanche victims and are an adjunct to the basic companion rescue equipment of transceiver, probe, and shovel. These devices should never be used to justify taking additional risks. Because surviving any avalanche is uncertain, this equipment should never replace good judgment.

Crossing Avalanche Slopes Travel through avalanche country always involves risk, but certain travel techniques can minimize that risk. Proper travel techniques might not prevent an avalanche release but can improve the odds of surviving. The timing of a trip has a lot to do with safety. Most avalanches occur during and just after storms. Waiting a full day after a storm has ended can allow the snowpack to react to the new snow load and gain strength. Before crossing a potential avalanche slope, the skier or hiker should get personal gear in order by tightening up clothing, zipping up zippers, and putting on hat, gloves, and goggles. Clothing should be padded and insulating. If a heavy mountaineering pack is carried, the straps should be loosened or slung over one shoulder only, so that the pack can be easily discarded if the person is knocked down. A heavy pack makes a person

Chapter 2: Avalanches

53

Box 2-1. Avalanche Transceiver Search INITIAL SEARCH

Grid Search

1. Have everyone switch their transceivers to “receive” and turn the volume to “high.” 2. If enough people are available, post a lookout to warn others of further slides. 3. Should a second slide occur, have rescuers immediately switch their transceivers to “transmit.” 4. Have rescuers space themselves no more than 30 m (100 feet) apart and walk abreast along the slope. 5. For a single rescuer searching within a wide path, zigzag across the rescue zone. Limit the distance between crossings to 30 m (100 feet). 6. For multiple victims, when a signal is picked up, have one or two rescuers continue to focus on that victim while the remainder of the group carries out the search for additional victims. 7. For a single victim, when a signal is picked up, have one or two rescuers continue to locate the victim while the remainder of the group prepares shovels, probes, and medical supplies for the rescue.

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

LOCATING THE VICTIM

With practice, the induction line search is more efficient than the conventional grid search for getting close to the sending beacon, but the conventional grid search is still necessary to pinpoint the buried victim. The induction line search is very similar to the flux line search used by digital transceivers. Users should always study the owner’s manual to learn the best techniques for the specific brand of avalanche rescue beacon. Induction Line Search (Preferred Method)

When an induction line search is used, the rescuer may initially follow a line that leads away from the victim (Fig. 2-30). Remember to lower transceiver volume if it is too loud, because the ear detects signal strength variations better at lower volume settings. 1. After picking up a signal during the initial search, hold the transceiver horizontally (parallel with the ground), with the front of the transceiver pointing forward (see Figure 2-30A). 2. Holding the transceiver in this position, turn until the signal is maximal (maximum volume), then walk five to seven steps (about 5 m), stop, and turn again to locate the maximum signal (see Figure 2-30B). When locating the maximum signal, do not turn yourself (or the transceiver) more than 90 degrees in either direction. If you rotate more than 90 degrees to locate the maximum signal, you will become turned around and follow the induction line in the reverse direction. 3. Walk another five steps, as just described, and then stop and orient the transceiver toward the maximum signal. Reduce the volume. 4. Continue repeating these steps. You should be walking in a curved path along the “induction line” toward the victim (see Figure 2-30C). 5. When the signal is loud at minimum volume setting, you should be very close to the victim and can begin the pinpoint search (see next).

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PART ONE: MOUNTAIN MEDICINE

top-heavy, making it difficult to swim with the avalanche. The skier should remove pole wrist straps and ski runaway straps, because poles and skis attached to the victim hinder swimming motions and only serve to drag the victim under. Finally, a person wearing a rescue beacon should be certain it is transmitting. If possible, the person should cross low on the slope, near the bottom or in the runout zone. Crossing rarely causes a release in the starting zone far above. The greater risk is getting hit by an untimely natural release from above. If crossing high without reaching the safety of the ridge is necessary, the starting zone should be traversed as high as possible and close to rocks, cliff, or cornice. Should the slope fracture, most of the sliding snow will be below and the chance of staying on the surface of the moving avalanche will be better. Invariably, the person highest on the slope runs the least risk of being buried. A person who must climb or descend an avalanche path should keep close to its sides. Should the slope fracture, escaping to the side improves the chance of surviving. Only one person at a time should cross, climb, or descend an avalanche slope; all other members should watch from a safe location. Two commonsense principles lie behind this advice. First, only one group member is exposed to the hazard, leaving the others available as rescuers. Second, less weight is put on the snow. All persons should traverse in the same track. This not only reduces the amount of work required but also disturbs less snow, which lowers the chance of avalanche release. Skiers and climbers should never drop their guard on an avalanche slope. They should not stop in the middle of a slope, but only at the edge or beneath a point of protection, such as a rock outcropping. It is possible for the second, third, or even tenth person traversing or skiing down a slope to trigger the avalanche. Trouble should always be anticipated, and an escape route, such as getting to the side or grabbing a tree, should be kept in mind.

Avalanche Rescue Self Rescue Escaping to the Side. The moment the snow begins to move around the person, there is a split second in which to make a decision or make a move. The person should shout to alert companions and then close the mouth and breathe through the nose to prevent inhalation of a mouthful of snow. Whether on foot, skis, or snowmobile, the person should first try to escape to the side of the avalanche or try to grab onto a tree. Staying on one’s feet or snow machine gives some control and keeps the head up. Escaping to the side gets the person out altogether or to a place where the forces and speeds are less. Turning skis or the snow machine downhill in an effort to outrun the avalanche is a bad move: the avalanche invariably overtakes its victims. Swimming. For years, the command to swim if caught in an avalanche was dogma. However, in recent years the effectiveness of swimming is being called into question. It is the process of inverse segregation (see Avalanche Airbag, earlier) rather than swimming that keeps the victim on or near the surface. The most important thing to do when caught and being tumbled is to get a hand or both hands in front of the face to create an air pocket. Cumbersome or heavy gear should be discarded. Ski poles should be tossed away; with luck, the avalanche will strip

away the skis. Skiers should try to discard gear, but snowmobile riders should try to stay on their snow machine. Once off their machine, riders are twice as likely to be buried as are their machines. Human-triggered avalanches tend to stop abruptly and almost instantly lock the person in place. There is no further chance to move hands to the face to create an air pocket, and without an air pocket, very few buried victims survive.

Reaching the Surface. Anyone caught in an avalanche should fight for his or her life. Creating an air pocket is the key to survival, but some victims, sensing themselves to be near the surface, have thrust out a hand or a foot. Any clue on the surface that gives the rescuers something to see greatly improves the odds of survival.

Companion Rescue Marking the Last-Seen Area. A companion or eyewitness to an accident needs to act quickly and positively. The rescuer’s actions over the next several minutes may mean the difference between life and death for the victim. First, the victim’s lastseen spot should be fixed and marked with a piece of equipment, clothing, a tree branch, or anything that can be seen from a distance down-slope. It is usually safe to move out onto the bed surface of an avalanche that has recently run. It is dangerous when the fracture line has broken at midslope, leaving a large mass of snow still hanging above the fracture. Searching for Clues. The fall line should be searched below the last-seen area for any clues of the victim. The snow should be scuffed by kicking and turning over loose chunks to look for anything that might be attached to the victim or that will reveal the victim’s trajectory and thus narrow the search area. Shallow probes should be made into likely burial spots with an avalanche probe, ski, ski pole, or tree limb. Likely spots are the uphill sides of trees and rocks, and benches or bends in the slope where snow avalanche debris piles up. The toe of the debris should be searched thoroughly; many victims are found in this area. Rescue Beacons. If the group was using beacons, all companions must immediately switch their units to receive mode. While making the fast scuff-search for visual clues, companions should at the same time search the debris, listening for the beeping sound from the buried beacon. When they detect a signal, companions must narrow the search area quickly. If skilled with a transceiver, companions can pinpoint the burial site in a few minutes. Going for Help. A difficult question in rescues is when to seek outside help. If the accident occurs in or near a ski area and there are several companions, one person can be sent to notify the ski patrol immediately. If only one companion is present, the correct choice is harder. The best advice is to search the surface quickly but thoroughly for clues before leaving to notify the patrol. If a patrol phone is close, the companion should notify the patrol and wait to accompany the patroller back to the avalanche. If the avalanche occurs in the backcountry far from any organized rescue team, all companions should remain at the site. The guiding principle in backcountry rescues is that companions search until they cannot or should not continue. When

Chapter 2: Avalanches

55

Organized Rescue Three-Stage Rescue. A full-scale avalanche search-and-rescue operation is divided into three stages. The goal of stage I is to find and extricate the buried victim or victims. Teams of rescuers dispatched to the avalanche are known as columns. The first team—known as the hasty search team—should consist of skilled and swift-traveling rescuers competent in not only avalanche rescue but also route finding and hazard evaluation. Basic rescue tools for stage I are probes, shovels, avalanche rescue dogs, the RECCO system (see later), and basic first-aid equipment. The hasty team performs the initial search, looking for clues with hopes of making a quick find. If unlucky, the team determines the most likely burial areas. The person reporting the avalanche should meet rescuers at the accident site, or the reporting person should be returned to the same vantage point from where they witnessed the accident to best guide rescuers to locate last-seen areas. Arriving rescuers continue the hasty search until sufficient clues can steer rescuers to positioning probe lines. The goal of stage II is to provide emergency medical care and evacuation. This stage consists of one or two small teams to transport resuscitation and medical equipment along with sleeping bags and rescue sleds to the site. Ideally, stage II should begin 10 to 15 minutes after the start of stage I to ensure that necessary medical and evacuation equipment reach the site. Stage I often continues long after stage II has been deployed. Stage III provides support for stages I and II when the rescue is prolonged. This support may include additional rescuers to take over for cold and tired searchers, hot food and drink, tents, warm clothing, and perhaps lights for nighttime searching. Probing. Probing avalanche debris is a simple but slow method of searching for buried victims. For more than 40 years, the traditional probe line used by rescue teams was composed of about a dozen rescuers standing elbow to elbow with a probe pole 3 to 3.5 m (about 10 to 12 ft) long. The rescuers would probe once between their feet—each probe entering the snow about 75 cm (30 inches) from the neighbors on either side—and then advance 70 cm (about 30 inches) and probe again. The probability of detection (POD) was thought to be about 70% to 76%. If the probe line missed on the first pass—which tended to happen—the area was probed again and again. Behind the probe line, shovelers stood ready to check out any possible strike. The line did not stop in such an event but continued to march forward with a methodical “down, up, step” cadence. Canadian avalanche workers modified this traditional probe line method in the late 1990s when they found it more efficient to probe three times per step rather than one time per step and slightly tightened the probe-grid spacing. However, experience showed that for all probe lines, the PODs were much less than described in the literature. In 2004, Ballard and colleagues developed a computer program that simulated a human body in an avalanche and compared the probabilities of detection for any probe-grid spacing.1 The results showed the POD for the traditional probe line to be 59% rather than the 70% believed earlier. As probe-grid spacings were reduced, the POD increased, but the search times also increased. Rescuers must balance the speed of the search with the length of time of the

50cm

deciding when to stop searching, the safety of the companions must be weighed against the decreasing survival chances of the buried victim.

50cm

50cm

Figure 2-20. Three-probe spacing for 50 × 50-cm three-hole-per-step probe method.

search. At a grid spacing of less than 50 cm, the search time increased faster than the POD. Thus, a grid spacing of 50 by 50 cm (20 by 20 inches) was optimal, yielding the best combination of POD and search time. For a three-hole-per-step (3HPS) probe, probers stand with arms out, wrist to wrist. Probers first probe between their feet and then probe 50 cm to the right and then 50 cm to the left (Fig. 2-20). At a command from the leader, the line advances 50 cm (one step). This method gives an 88% chance of finding the victim on the first pass with an estimated time to discovery that is nearly identical to the traditional spacing. Ski patrols and mountain rescue teams that have adopted the 3HPS with a 50 × 50-cm grid have been pleased with the improved efficiency and effectiveness of the probe line. Because rescuers insert more probes per rescuer, it is possible to have fewer rescuers on a probe line, and short probe lines are easier to manage and faster than long probe lines. Five rescuers doing 3HPS at 50-cm intervals form a slightly longer probe line than nine rescuers using the traditional method. To ensure proper spacing, it is most helpful to use a guidon cord with marked 50-cm intervals. Suspended between two rescuers, the lightweight guidon cord positions rescuers and probes to the right spots, allowing the line to move smoothly and efficiently without interruption. When a guidon cord is not used, the probe line must be frequently stopped and reassessed to ensure proper spacing. Rescuers managing the guidon cord should also place red flags every 3 to 5 m to mark the edge of the searched area. If the victim is missed on the first pass, the second pass can be offset by 25 cm (10 inches) in each direction and the area researched. The second pass increases the POD to 99%. Rescue teams use probe lines to find most avalanche victims not equipped with transceivers, RECCO reflectors, or when an avalanche rescue dog fails to locate the victim. However, these search methods should all be used concurrently. Because probe lines are time intensive, few victims are found alive by this technique alone (see Table 2-2).

RECCO. RECCO (RECCO AB, Sweden, www.recco.com) is an electronic rescue system that enables organized rescue teams to find victims who are equipped with a reflector (Fig. 2-21). The system consists of two parts: a detector used by the rescue teams (either on the ground or from helicopters) and the reflector worn by the recreationist. About the size and weight of a notebook computer, the detector is easily transported to the accident site. The detector transmits a directional radar signal. When it hits the reflector, the signal’s frequency is doubled and reflected back to the detector, and the rescuer can follow the

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PART ONE: MOUNTAIN MEDICINE

A

B

Figure 2-21. 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 helicopter. (Courtesy RECCO AB, Sweden.)

25 20 15 10 5

2000-01 to 2003-04

1995-96 to 1999-00

1990-91 to 1994-95

1985-86 to 1989-90

1980-81 to 1984-85

1975-76 to 1979-80

1970-71 to 1974-75

1965-66 to 1969-70

0 1960-61 to 1964-65

Avalanche deaths have increased in the United States each decade since 1950. Figure 2-22 shows annual deaths averaged over 5-year periods. From 1950 to 2004, 716 people have died in avalanches. Of these, 566 (79%) were men and 63 (9%) were women. (Interestingly, not all accident reports list the sex of the victim.) The average age of all victims is 30 years. The youngest was 6; the oldest, 67. Figure 2-23 shows the activity groups for the victims. Most victims (86%) were pursuing some form of recreation at the time of the accident, with climbers, backcountry skiers, and snowmobilers heading the list. The backcountry-skiers category also includes ski mountaineers, helicopter skiers, and snowcat skiers. The distinction between backcountry skiers and lift skiers is that lift skiers pursue their sport in and around devel-

30

1955-56 to 1959-60


THE MODERN AVALANCHE VICTIM

35

1950-51 to 1954-55

Avalanche Guard. If the threat of a second avalanche exists, one person should stand in a safe location to shout out a warning. This gives the searchers a few seconds to flee to safety. Rescues are often carried out under dangerous conditions, and self-preservation should be a major consideration.

U.S. Avalanche Fatalities 1950-2004

Average fatalities

signal to the buried person. The reflectors are small, passive (no batteries) electronic transponders that are fitted into outerwear, ski and snowboard boots, and helmets. The system will detect some electronic equipment (with diminished range) such as cell phones, electronic cameras, radios, and even turned-off avalanche rescue beacons, so RECCO should be used by rescue teams together with avalanche rescue dogs, rescue beacons, and probers in the first response to any avalanche rescue. In North America, more than 120 ski areas, mountain rescue teams, and National Parks have detectors. Worldwide, more than 500 ski resorts and helicopter rescue teams have them.

5-year period

Figure 2-22. Avalanche fatalities in the United States averaged by five-winter periods, 1950–51 to 2003–04.

oped ski areas and rely on lifts to get them up the hill. Outof-bounds lift skiers are skiers who leave the ski area boundary or ski into “closed” areas within the ski area. In-area skiers are those caught and killed on open terrain within the ski area boundary; it should be noted that only three deaths have occurred on open runs in the last 30 years. Miscellaneous recreation includes sledders and persons playing in the snow,

Chapter 2: Avalanches

U.S. Avalanche Fatalities by Activity 1950-2004

57

220 200 Number of Fatalities 1950-2004

Climber Ski tourers Snowmobilers Snowboarders Out-of-bounds skiers In-area skiers Snowshoers and hikers Miscellaneous

180 160 140 120 100 80 60 40

Motorists and highway workers

20

Residents

0 CO AK WA UT MT WY ID CA NH NV OR NM NY ME AZ

Others at work Ski patrolers

State

Miners

Figure 2-24. Avalanche fatalities in the United States from 1950–51 to 2003–04 by state.

Rescuers 0

50

100

150

200

Number of fatalities TOTAL = 716

Figure 2-23. Avalanche fatalities in the United States from 1950–51 to 2003–04 by activity categories.

campers, and even a most unlucky ski kayaker. Among nonrecreation groups, avalanches strike houses (residents), highways (motorists and plow drivers), and the workplace (ski patrollers and others whose job puts them at risk). Since 1950, 15 states have registered avalanche fatalities (Fig. 2-24).

Statistics of Avalanche Burials Numerous factors affect a buried victim’s chances for survival: time buried, depth buried, clues on the surface, rescue equipment, injury, ability to fight the avalanche, body position, snow density, presence and size of air pocket, and luck. A victim who is uninjured and able to fight on the downhill ride usually has a better chance of being only partly buried, or, if completely buried, a better chance of creating an air pocket for breathing. A victim who is severely injured or knocked unconscious is like a rag doll being rolled, flipped, and twisted. Being trapped in an avalanche is a life-and-death struggle, with the upper hand going to those who fight the hardest. Avalanches kill in two ways. First, serious injury is always possible in a tumble down an avalanche path. Trees, rocks, cliffs, and the wrenching action of snow in motion can do horrible things to the human body. About one quarter of all avalanche deaths are caused by trauma, especially to the head and neck. Second, snow burial causes asphyxiation (either obstructed airway or hypercapnia) in three quarters of avalanche deaths, and a very small percentage of avalanche victims succumb to hypothermia (see Avalanche Victim Physiology and Medical Treatment after Rescue, later). The problem of breathing in an avalanche does not start with being buried. A victim

swept down in the churning maelstrom of snow has an extraordinarily hard time breathing. Inhaled snow clogs the mouth and nose; asphyxiation occurs quickly if the victim is buried with the airway already blocked. Snow that was light and airy when a skier carved turns in it becomes viselike in its new form. Where the snow might have been 80% air to begin with, it might be less than 50% air after an avalanche, and it is much less permeable to airflow, making it harder for the victim to breathe (but see AvaLung, earlier.) Snow sets up hard and solid after an avalanche. It is almost impossible for victims to dig themselves out, even if buried less than a foot deep. Hard debris also makes recovery very difficult in the absence of a sturdy shovel. The pressure of the snow in a burial of several feet is sometimes so great that the victim is unable to expand the chest to draw a breath. Warm exhaled breath freezes on the snow around the face, eventually forming an ice lens that cuts off all airflow. This takes longer than snowclogged airways, but the result is still death by asphyxiation. Another factor that affects survival is the position of the victim’s head—that is, whether the person is buried face up or face down. Data from a limited number of burials show the victim is twice as likely to survive if buried face up. In the faceup position, an air pocket forms around the face as the back of the head melts into the snow; in the face-down position, an air pocket cannot form as the face melts into the snow. The statistics on survival are derived from a large number of avalanche burials (Figs. 2-25 and 2-26). In compiling these figures, the authors have included only persons who were totally buried in direct contact with the snow. Victims buried in the wreckage of buildings or vehicles are not included, as they can be shielded from the snow and can find sizable air pockets. Under such favorable circumstances, some victims have been able to live for days. In 1982, Anna Conrad lived for 5 days at Alpine Meadows, California, in the rubble of a demolished building, the longest survival on record in the United States. A completely buried victim has a poor chance of survival, which is related to both time and depth of burial, as shown in

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PART ONE: MOUNTAIN MEDICINE

100

Alive Dead % Survival

90 80 70

TABLE 2-1. Rescue Results as a Function of Rescuer, 1950–2004

Found alive Found dead

60 50

SELFRESCUE

COMPANIONS

RESCUE TEAMS

TOTAL

48 (14%) —

198 (60%) 116 (23%)

87 (26%) 383 (77%)

333 499

Type of rescue for buried avalanche victims in direct contact with snow, based on a sample of 832 burials in the United States from 1950–51 to 2003–04.

40 30 20

TABLE 2-2. Rescue Results as a Function of Locating Method, 1950–2004

10

7. 0 

6. 9

5. 9

6. 0-

5. 0-

4. 9 4. 0-

3. 9

2. 9

3. 0-

2. 0-

1. 9 1. 0-

0. 1-

0. 9

0

Feet

Figure 2-25. Percent survival versus depth of burial for U.S. avalanche fatalities and survivors in direct contact with the snow (not in a structure or vehicle) from 1950–51 through 2003–04.

Survival probability (%)

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

80

Attached object or body part visible Hasty search or spot probe Coarse or fine probe Transceiver Avalanche dog Voice Other (e.g., digging, bulldozer) Found after a long time Not found, not recovered Not known Inside vehicle Inside structure Totals

ALIVE

DEAD

TOTAL

140 26 23 55 6 30 20 0 0 19 30 23 372

54 46 163 83 60 1 14 42 35* 34 10 30 572

194 72 186 138 66 31 34 42 35 53 40 53 944

60 Method of locating (first contact) buried avalanche victims, based on a sample of 944 avalanche burials in the United States from 1950–51 to 2003–04. *Eleven climbers died in an ice avalanche on Mt. Rainier (June, 1981); bodies not recovered.

40 20 0 0

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

Figure 2-26. The solid blue line indicates data from Switzerland for survival probability for completely buried avalanche victims in open areas from 1981 to 1998 (N = 638) in relation to time (minutes) buried under the snow.Median extrication time was 37 minutes.The dashed red line represents survival probability for completely buried avalanche victims in open areas (N = 422) based on the Swiss data for 1981 to 1991 as calculated by Falk and colleagues.9 (From Brugger H, Durrer B, Adler-Kastner L, et al: Resuscitation 51:7–15, 2001, with permission.)

Figure 2-25. Survival probabilities diminish with increasing burial depth, partly because it takes longer to uncover the more deeply buried victim. To date, no one in the United States who has been buried deeper than 2.1 m (7 feet) has been recovered alive; however, in Europe, two victims survived burials of 6 to 7 m (20 to 23 ft).7,23 As important as burial depth may be in survival, time is the true enemy of the buried victim. Survival statistics in the United States are very similar to those in Europe. Figure 2-26 presents the European survival probability function, showing decreasing survival with increasing burial time. In the first 15 minutes, more persons are found alive (>90%) than dead. At 30 minutes, an equal number are found

dead and alive. After 30 minutes, more are found dead than alive, and the survival rate continues to diminish with increasing time. Speed is essential in the search. Because under favorable circumstances, buried victims can live for several hours beneath the snow, rescuers should never abandon a search prematurely. A miner in Colorado buried by an avalanche near a mine portal was able to dig himself free from nearly 1.8 m (6 feet) of debris after approximately 22 hours. In 2003, two snowshoe hikers caught near Washington’s Mt. Baker survived burials of 22 and 24 hours. Such long survival times are a reminder that no rescue should be abandoned prematurely on the assumption that the victim is dead.

Rescue Statistics A buried victim’s chance of survival directly relates not only to depth and length of time of burial but also to the type of rescue. Table 2-1 shows the statistics on survival as a function of the rescuer. Buried victims rescued by companions or groups nearby have a much better chance of survival than those rescued by organized rescue teams, time being the major influencing factor. Of those found alive, 60% were rescued by companions and 26% by an organized rescue team. Table 2-2 compares the results of rescue by different techniques. Seventy-two percent of victims (140 of 194) who were

Chapter 2: Avalanches buried with a body part (such as a hand) or an attached object (such as a ski tip) protruding from the snow were found alive. In most cases, this was simply good luck, but in some cases it was the result of actively fighting with the avalanche or of thrusting a hand upward when the avalanche stopped. Either way, this statistic shows the advantages of a shallow burial: less time required to search, shorter digging time, and the possibility of attached objects or body parts being visible on the debris. Of the fatalities in this category, many were skiing or snowboarding alone with no companion to spot the hand or ski tip and provide rescue. Organized probe lines have found more victims than any other method, but because of the time required, most victims (88%) are recovered dead. Only 23 people were found alive by this method, with 163 recovered dead. Rescue transceivers are an efficient technique for locating victims, but two problems have limited the number of survivors even among those wearing them. First, few beacon wearers are well practiced in using the beacon instantly and efficiently, and second, even after a quick pinpointing of the burial location, extricating the victim from deep burials may take too long to save the life. To recover a victim buried 1 m (3 ft) deep, companions have to remove at least 1.5 tons of snow. Since the first transceiver rescue in 1974, only 40% (55 of 138) of buried victims found with transceivers have been recovered alive. As dismal as this statistic is, there is a bright spot within the data. Prior to 2000, only 30% of transceiver users survived, but since 2000, 57% have survived burials (P = .003). The year 2000 marks the beginning of widespread use of digital avalanche rescue transceivers, which most people find easier to use. However, transceivers still do not guarantee a live rescue, which requires regular practice and training along with a dose of good luck. Despite the sound-insulating properties of snow, 31 victims who were shallowly buried were able to yell and be heard by rescuers (voice contact). An unfortunate case was the man whose moans were heard but who was dead when uncovered 20 minutes later. Trained search dogs are capable of locating buried victims very quickly, but because they are often brought to the scene only after extended periods of burial, there have been few live rescues. In the March 1982 avalanche disaster at Alpine Meadows, California, a dog made the first live recovery of an avalanche victim in the United States. Since then, dogs have made five additional live recoveries. Search and rescue teams and law enforcement agencies work closely with search dog handlers, and trained avalanche dogs are becoming common fixtures at ski areas in the western United States. A trained avalanche dog can search more effectively than 30 searchers. It moves rapidly over avalanche debris using its sensitive nose to scan for human scent diffusing up through the snowpack. Dogs are not 100% effective, however: they have found bodies buried 10 m deep but have also passed over some buried only 2 m (6 ft) deep. These statistics point out the extreme importance of rescue skills. Organized rescue teams, such as ski patrollers and mountain rescuers, must be highly practiced. They must have adequate training, manpower, and equipment to perform a hasty search and probe the likely burial areas in a minimal time. For backcountry rescues, a buried victim’s best hope for survival is to be found by the companions. The need to seek outside rescue units practically ensures a body recovery mission.

59

Avalanche Victim Physiology and Medical Treatment after Rescue Avalanche Victim Morbidity and Mortality Asphyxiation is the most common cause of death during avalanche burial. About 75% of avalanche deaths result from asphyxiation, about 25% from trauma, and very few from hypothermia.13,16,22,24 Because asphyxiation is the major cause of death during avalanche burial, time to extrication is a major determinant of survival. Fully buried avalanche victims have a greater than 90% chance of survival if extricated within 15 minutes, but only 30% after about 35 minutes (see Figure 2-26),4,9 emphasizing the need for companion rescue at the avalanche site. Survival beyond 30 minutes of burial requires an air pocket for breathing, and if the air pocket is large enough, avalanche victims may survive for hours and develop severe hypothermia. Traumatic injury to avalanche victims depends on the terrain where the avalanche occurred. If the victim is carried through trees or over rock bands, then traumatic injury is more likely and may result in death. Grossman and colleagues, using data that included both partial and complete burials in Utah and Europe, reported that traumatic injuries occurred in 25% of survivors of avalanche accidents13 (Table 2-3). The most common traumatic injuries were major orthopedic, soft tissue, and craniofacial injuries. Johnson and colleagues reviewed autopsy reports from 28 avalanche deaths in Utah over a 7-year period. Among 22 avalanche victims who died from asphyxiation, half had mild or moderate traumatic brain injury, which the authors argued could cause a depressed level of consciousness and contribute to death from asphyxiation.14 All six of the avalanche deaths that were due to trauma had severe traumatic brain injury.

Respiratory Physiology of Avalanche Burial Asphyxiation occurs during avalanche burial because inhaled snow occludes the upper airway or because expired air is rebreathed. Acute upper airway obstruction resulting in asphyxiation is one of the causes of early asphyxiation—that is, during the first 15 to 30 minutes of avalanche burial. Asphyxiation due to rebreathing expired air may also occur during this time if

TABLE 2-3. Injuries in Survivors of Avalanche Burial (Partial and Total)

Total Injuries Major orthopedic Hypothermia requiring treatment at hospital arrival Skin/soft tissue Craniofacial Chest Abdominal

UTAH

EUROPE

9 (Total, 91 avalanche accidents) 3 (33%) 2 (22%)

351 (Total, 1447 avalanche accidents) 95 (27%) 74 (21%)

1 (11%) — 3 (33%) —

84 (25%) 83 (24%) 7 (2%) 4 (1%)

From Grossman MD, Saffle JR, Thomas F, Tremper B: J Trauma 29:1705–1709, 1989.

PART ONE: MOUNTAIN MEDICINE

100

SpO2 (%)

25

20 80

60 10

FIO2 (%)

15 A

8

6

4

10

B

5

0

FICO2 (%)

there is no air pocket for breathing, or it may be delayed if an air pocket is present. Inspired air contains 21% oxygen (O2) and less than 0.03% CO2, whereas expired air contains about 16% O2 and 5% CO2. Rebreathing expired air in an enclosed space results in progressive hypoxia and hypercapnia that will eventually result in death from asphyxiation. The larger the air pocket, the greater is the surface area for diffusion of expired air into the snowpack and for diffusion of ambient air from the snowpack into the air pocket, and thus the longer is the survival time before death occurs from asphyxiation. An ice mask is formed when water in the warm, humid expired air freezes on the snow surface in front of the face. Because this barrier is impermeable to air, it accelerates asphyxiation by preventing diffusion of expired air away from the air pocket in front of the mouth. The physiology of asphyxiation from breathing with an air pocket in the snow was demonstrated in a study by Brugger and colleagues.6 Subjects sat outside a snow mound and breathed through an air-tight mask connected by respiratory tubing to 1or 2-L (0.9- to 1.8-quart) air pockets in snow. The snow had a density similar to that of avalanche debris (i.e., 150 to 600 kg/m3, or 15% to 60% water). The initial fraction of inspired oxygen (Fio2) in the air pocket was 21%, and the initial fraction of inspired CO2 (Fico2) was near 0%. As expired air was rebreathed in the air pocket, Fio2 decreased to about 10% and Fico2 increased to about 6% over 30 minutes (Fig. 2-27). These changes in O2 and CO2 in the air pocket resulted in a decreased arterial O2 saturation as measured by a pulse oximeter (Spo2%) and an increased end-tidal CO2 (ETco2) partial pressure. Most subjects were not able to complete the entire 30 minutes of the study and had to stop secondary to dyspnea, hypercapnia, and hypoxia. Hypoxemia and hypercapnia occur as expired air is rebreathed. A smaller air pocket or denser snow causes a more rapid development of hypoxia and hypercapnia. Larger air pockets and less-dense snow allow more mixing of expired air with ambient air in the snowpack and result in longer survival before hypoxia and hypercapnia become severe enough to cause death from asphyxiation. Brugger and colleagues suggest that an equilibrium may occur where the Fio2 and Fico2 in an air pocket reach a plateau within a physiologically tolerable range, and the avalanche victim may survive prolonged burial. This may occur even with small air pockets, as has been observed in the extrication of survivors of avalanche burials of up to 2 hours in duration.4 Radwin and colleagues18 demonstrated that there is sufficient ambient air in densely packed snow to permit normal oxygenation and ventilation as long as all expired air is diverted out of the snowpack. They studied subjects totally buried in dense snow who inhaled air directly from the snowpack (density, 300 to 680 kg/m3, or 30% to 68% water) through a two-way nonrebreathing valve attached to respiratory tubing that diverted all expired air to the snow surface. Subjects maintained normal oxygenation and ventilation for up to 90 minutes. This study demonstrated that there is sufficient air for breathing in snow with a density similar to that of avalanche debris, as long as expired air is not rebreathed. This is the principle behind the AvaLung (see Avalanche Rescue Equipment, earlier), designed to prolong survival during avalanche burial. Figure 2-28 describes its operation. Although the device prevents ice mask formation, the expired air permeates around the buried person’s body and through the snow and eventually contaminates inspired air. Grissom and colleagues11 compared

ETCO2 (kPa)

60

0 0

5

10

15 20 Time (min)

25

30

Figure 2-27. Curves of individual respiratory parameters in subjects breathing with a tightfitting face mask connected to respiratory tubing running into 1- or 2-L air pockets in dense snow (N = 28).The x-axis represents time in minutes. Some subjects did not complete the 30minute study because of dyspnea or hypoxia. A, Arterial oxygen saturation (SpO2%) as measured by a digital pulse oximeter on the left y-axis (red lines), and fraction of inspired oxygen (FIO2%) on the right y-axis (blue lines). B, Partial pressure of end-tidal CO2 (ETCO2) (kPa) on the left y-axis (red lines) and fraction of inspired CO2 (FICO2%) on the right y-axis (blue lines). (From Brugger H, Sumann G, Meister R, et al: Resuscitation 58:81–88, 2003, with permission.)

breathing with this device while buried in dense snow, and breathing without the device but with a 500-cc (0.45-quart) air pocket in the snow. Mean burial time was 58 minutes when breathing with the device, and 10 minutes when breathing with a 500-cc air pocket in the snow. Development of hypoxia and hypercapnia were significantly delayed by breathing with the device. The AvaLung has resulted in survival from actual avalanche burials.17

Medical Treatment and Resuscitation of Avalanche Burial Victims The key points regarding assessment and treatment of an extricated avalanche burial victim are presented in an algorithm in Figure 2-29. An initial impression of the level of consciousness is made as the head is exposed and cleared of snow. Opening the airway and ensuring adequate breathing are the primary medical interventions. Every effort should be made to clear the

Chapter 2: Avalanches

61

A

B

C d

on iam

c Bla

kD

Figure 2-28. The AvaLung 2 (Black Diamond Equipment,Ltd.,Salt Lake City,UT),a breathing device intended to prolong survival during avalanche burial by diverting expired air away from inspired air drawn from the snowpack, is worn over all other clothing. White arrows show flow of inspiratory air, and red arrows show flow of expiratory air. The subject breathes in and out through the mouthpiece (A). Inhaled air enters from the snowpack through the one-way inspiratory valve on the side of the housing inside the mesh-protected harness on the chest (B). Expired air leaves the lungs via the mouthpiece and travels down the respiratory tubing to the housing and then passes through an expiratory one-way valve located at the bottom of the housing (B) and travels via respiratory tubing inside the harness around to the back (C). (AvaLung photo courtesy Black Diamond Equipment, Ltd.)

airway of snow as soon as possible and to provide assisted ventilation if the breathing is absent or ineffective. These measures should not wait until the entire body is extricated. If traumatic injury to the spinal column is suspected, or if there is evidence of head or facial trauma, then the spinal column is immobilized as the airway is opened, adequate breathing ensured, and oxygen provided. When the avalanche burial victim is unconscious, maintenance of the airway may be challenging because of the space limitations of the snow hole. If endotracheal intubation is required for the unconscious apneic patient not yet fully extricated from snow burial, then the inverse intubation technique19 may be required. In this technique, the laryngoscope is held in the right hand while straddling the patient’s body and facing the head and face. While facing the patient, insert the laryngoscope blade into the oropharynx with the right hand so that the larynx and cords can be visualized by leaning over and looking into the patient’s mouth; the endotracheal tube is then passed through the cords with the left hand. After an adequate airway and breathing are established and supplemental oxygen is provided, the circulation is assessed. The conscious patient is assumed to have a perfusing rhythm, and further treatment is directed at treating mild hypothermia and traumatic injuries. A patient found unconscious but with a pulse may have moderate or severe hypothermia and should be handled gently to avoid precipitating ventricular fibrillation (VF). Medical treatment of this patient is focused on ensuring adequate oxygenation and ventilation, either noninvasively

with a bag-valve-mask device or by endotracheal intubation if clinically indicated, and on immobilizing the spinal column for transport and treating any obvious signs of trauma. Intravenous access may be obtained and warmed isotonic fluids infused. The treatment of hypothermia is described later. If a pulse is not present after opening the airway and ventilating the patient, cardiopulmonary resuscitation (CPR) is begun. Before CPR is initiated, however, careful evaluation for the presence of a pulse should occur. Avalanche burial victims are hypothermic, which causes peripheral vasoconstriction and makes the pulse difficult to palpate. In addition, moderate to severe hypothermia causes depression of respiration and bradycardia. Before initiating CPR, palpation for a pulse should be done for a period of 30 to 45 seconds after the airway is opened and assisted ventilations are begun. CPR initiated on a severely hypothermic patient who actually has a perfusing rhythm may cause VF. If electrocardiographic monitoring is available, the cardiac rhythm is assessed, or alternatively an automatic external defibrillator may be applied. If the patient has VF, up to three defibrillations are attempted in the moderate or severely hypothermic patient with a core body temperature less than 30° C (86° F).8 If these are unsuccessful, further attempts at defibrillation are done only after rewarming. Drugs usually administered as part of advanced cardiac life support (ACLS) are not effective below a core body temperature of about 30° C, and they may accumulate to toxic levels with a rebound effect as rewarming occurs.8 If the patient is hypothermic but

62

PART ONE: MOUNTAIN MEDICINE

Extrication from avalanche burial

Conscious?

Treat for Hypothermia I (core temperature 32° C or 90° F) or Hypothermia II (28° to 32° C or 82° to 90° F): Clear the airway; provide oxygen, dry warm insulation, hot drink containing sugar if awake, and medical transport to closest appropriate facility.

Yes

No Breathing?

Treat for Hypothermia II (core temperature 28° to 32° C or 82° to 90° F) or Hypothermia III (24° to 28° C or 75° to 82° F): Clear the airway; provide oxygen, assist ventilations, consider intubation and ventilation with heated and humidified oxygen, provide dry warm insulation, infuse heated IV fluid, and provide medical transport to tertiary care facility.

Yes

No Obvious fatal injuries? No

Yes

Cease efforts

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

Heart monitor asystole?

No

If rhythm is VF, defibrillate a maximum of 3 times if core temperature 30° C or 86° F and hold ACLS drugs until rewarmed. Treat for hypothermia III or IV as below.

No

Death from asphyxiation likely; cease efforts when clinically indicated. May continue resuscitation and transport to the nearest appropriate medical facility. A K of greater than 12 mEq/liter suggests that resuscitation may be futile and that death has occurred from asphyxiation.

Yes Burial 1 hour Yes Core temperature 30° C or 86° F?

No

Yes Air pocket and free airway?

No

Yes Treat for hypothermia III or IV (core temperature 28° C or 82° F): Endotracheal intubation, assisted ventilation with warmed humidified oxygen, monitor ECG, begin CPR, infuse warmed IV fluids, provide dry insulation, provide medical transport to a facility capable of extracorporeal rewarming.

Figure 2-29. Assessment and medical care of extricated avalanche burial victims.

has a core body temperature greater than 30° C, the standard ACLS protocol is followed with longer intervals between administrations of drugs. The likelihood of successful resuscitation of an avalanche burial victim who is in cardiac arrest at the time of extrication depends on whether cardiac arrest occurred from asphyxiation or from hypothermia. In burials of less than 1 or 2 hours with a core body temperature of greater than 30° C, resuscitation is unlikely to be successful because death has most likely occurred from asphyxiation. Avalanche victims extricated from burials of greater than 1 or 2 hours who have no signs of life but who are severely hypothermic (core temperature kidney, quadriceps muscle > brain.163 In rat brain, lung, and skin, HSP-70 concentration peaked at 1 hour and returned to baseline at 3 hours after the stress. In liver, however, HSP-70 peaked 6 hours after the stress.48 The

Chapter 10: Pathophysiology of Heat-Related Illnesses

255

determination of HSP-72 may be useful as a diagnostic probe of recent heat injury, as an enzyme-linked immunosorbent assay (ELISA) for HSP-72 determination has become commercially available (Stress-Gen, Vancouver).65 Most studies on HSPs have been carried out in isolated cells and in rodent models. In humans, the minimal conditions of threshold Tc and duration for a single heat shock to induce HSPs is not certain. Some cells can survive very brief exposures (1 second) to temperatures as high as 60° C (140° F), because they induce HSPs that render them thermotolerant.62 After a single heat shock in human peripheral blood mononuclear cells, HSP72 concentration is unchanged for 1 to 2 hours, then rises rapidly to plateau at 4 hours. It gradually falls after 12 to 18 hours but remains above baseline at 24 hours.184 Overall, however, on a single supra-threshold stress, HSPs in many or most tissues rise within an hour or two of the stress and remain elevated for 12 to 48 hours and possibly for as long as a week.224 During sports activities or exercise in summer, however, Tc can become elevated several times over a few hours. Such stimuli may have profound effects on the time course of HSP elevation and protection, but this has not been well studied.247,313 This temporary thermoprotection by HSPs to heat and exercise is not long-term acclimatization. Long-term acclimatization is a different process, although it may in part involve HSPs. It develops over a period of several days in response to several periods of moderate heat and may persist for weeks. In the work of Horowitz,247 acclimatization involves alterations in autonomic, cellular, and molecular responses to heat, varying in their intensities and interrelationships over time. Some studies suggest that increased HSP-72 during rigorous exercise is one of the adaptive mechanisms to cope with 249,328 increased stress. Rats run on a treadmill for 30 minutes per . day at 75% Vo2max showed increases in HSP-72 within 10 weeks.123 Endurance exercise–trained rats had higher levels of HSP-72, as well as lower levels of lipid peroxidation, in their ventricles and could develop higher systolic pressures.122,414 During exercise of an unacclimatized individual in moderate and warm temperatures or at rest in tropical or desert heat, Tc may rise to levels that severely decrement performance or may lead to heatstroke, collapse, and even death. Therefore, the presence of HSPs is extremely important. A better understanding of the role of HSPs may ultimately lead to methods for faster acclimatization to heat. The ability to produce HSPs may depend on diet, because vitamin D–deficient animals showed reduced HSP production.281

swine and improved the course of hemodynamic variables; it decreased peak pulmonary arterial pressure and pulmonary vascular resistance index values, increased systemic arterial pressure and systemic vascular resistance index values, and favorably altered hypodynamic/hyperdynamic CO.296 Elevated HSP-70 (by heat shock) protected rat intestine against toxin (ricin)-induced acute intestinal inflammation, with reduced generation of leukotriene B4 and neutrophilic infiltrate in their ileums.493 Monocytes and granulocytes constitutively express more HSP-70 and are more heat resistant than lymphocytes. LPS raises HSP-70 content even more and may be the reason that those cells can survive and function in hostile inflammatory microenvironments.161 Not only does raising HSP levels protect against heat, but reducing them is damaging during stress. For example, reducing HSP-72 induction by 40% (by a specific toxin) rendered cardiac myocytes more susceptible to hypoxic injury.377 In principle, it may be possible in humans and experimental models to elevate HSPs by one stress (e.g., temporary hypoxia) to render athletes more tolerant to heat, cold, or toxins. This would be expected to benefit not only athletes but also soldiers deployed to hot climates and patients soon to undergo surgery.

Protection. In a number of different systems, HSP levels elevated by a variety of stresses (heat shock, brief cyanide exposure, arsenite, peroxide, hypoxia, and toxins) were beneficial to membranes, cells, tissue, and organs. HSP-70 protected cells and their ultrastructure against these or other stressors.7,51,291,523 They protected against membrane damage caused by toxins (ionomycin) and cytokines.211,316 Well-healing wounds show high levels of hsp70mRNA, whereas poorly healing wounds have lower levels.392 Overexpression of HSP-70 in transgenic mice rendered their hearts more resistant to ischemic injury.344 Human cell types (proximal tubular epithelia) that normally exhibit great resistance to hypoxia also contain high basal levels of HSP-70.512 Elevated HSP-72 (by heat shock or arsenite) protected rats against heatstroke morbidity and mortality.551 Elevated HSP-72 blunted liberation of inflammatory mediators (interleukin-6 and thromboxane B2) in LPS-challenged

Training. Long-term exercise training in the heat induced HSPs. In one study of rat brains, HSP-70 content rose only if the exercising rats became hyperthermic, whereas exercise alone did not induce central HSP-70 expression.523 On the other hand, in another study in rats, in spleen cells, peripheral lymphocytes, and soleus muscles, exercise alone induced HSP-60, HSP-70, HSP-90, and HSP-100.336 In male rowers in training, the HSP70 content in an active muscle rose each week (181%, 405%, 456%, and 363%) with maximal HSP production at the end of the second training week.536 In humans walking 30 minutes on a treadmill at their individual anaerobic thresholds, mRNA for HSP-70 rose but not the HSP-70 protein itself. That is, a single bout of exercise in humans may not be sufficient to induce HSP70 protein.416 Combined stressors may be additive or synergistic in their effects. Exposure of cells to either a moderately elevated tem-

Age. In normal adult rats, heat and exercise can each induce HSP-72. However, in aged rats, only exercise could induce HSP72.314 That is, aging caused them to lose their ability to induce HSPs by heat. Among humans, older adults have lower levels of HSP-70 in their peripheral blood mononuclear cells (PBMCs) than do the young.116 This loss of HSP protection may in part account for increased susceptibility of the aged to classic heatstroke, as is seen in heat waves. Race. HSP production may be race related. In one study, heatinduced HSP levels were very intense in cells isolated from native Turkmen men living in Turkmenistan, the hot desert of middle Asia, but very weak in Russians living in moderate climatic regions of European Russia. At the same time, cells isolated from Turkmen men better survived heat stress.264 Not surprisingly, organisms living many generations in hot climates become better adapted to it over time. No large-scale systematic study of racial influences on HSPs has been reported. However, one report indicates a difference in basal and heat induced levels of HSP-70 between Europeans and nonEuropeans in South Africa, and it suggests that there may be different susceptibilities to stress and disease.55

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PART TWO: COLD AND HEAT

perature or to a low level of ethanol does not induce HSPs. However, when the two stresses were applied at the same time, the cells induced large amounts of HSPs. Thus hyperthermia and ethanol acted synergistically to increase HSP gene expression.431 Practically, this implies that HSPs may be induced by overlapping periods of exercise, heat, hypoxia, and sleep deprivation.

Consequences of Elevated HSP-70. There is a downside to the production of HSPs during stress injury. While HSPs are being synthesized, the cell ceases or slows production of many other proteins. As a result, in cells at normal temperatures, synthesis of HSPs (induced by a short heat stress) retards cell growth,157 even as it protects against subsequent heat injury. Not only is growth retarded but heat-shocked immune cells secreted reduced amounts of cytokines in response to LPS.422 Therefore, persons with elevated HSPs may have reduced or inappropriately altered immune function. This was clear in immune gene activities shown in a recent genomics study.486 Clearly, the potential benefits of deliberately inducing HSPs, with presumed improved resistance to heat, hypoxia, and certain chemicals and toxins, must be weighed against a potentially decreased ability to resist infections.

Thyroid Hormone and Protein Isoforms Thyroid gland function is an important component of heat acclimation. IL-1 inhibits release of thyroid hormone from the thyroid gland.113,138 Because IL-1 becomes elevated in response to heat and many other stresses (see Figure 10-5),182 its ability to inhibit thyroid hormone release may be part of the overall protective mechanisms and responses to stress.278 A reduction in thyroid hormone concentration has a number of biochemical and physiologic consequences. Deficiency of thyroid hormone has a negative cardiac chronotropic effect, reducing cardiac contractility and increasing systemic vascular resistance.66 Basal metabolic rate (BMR) falls with thyroxine deficiency, and because its secretion rate is lower in summer and higher in winter, there is corresponding seasonal alteration in BMR and all other processes influenced by thyroxine concentrations.245 One component of heat acclimatization is reduction in BMR.245 Chronic heat stress decreases blood flow to the thyroid gland217 and reduces the rate of thyroid hormone production, leading to decreased food intake, growth rate, oxygen consumption, and BMR.435 Deficiency in thyroid hormone during acute stress may be fatal. A young woman was discovered unconscious in a sauna and later died with a diagnosis of heatstroke. On autopsy, she was found to have preexisting Hashimoto’s thyroiditis.473 Muscle contains characteristic isoforms of myosin, each with different intrinsic metabolic activities, such as the rate of its actin-activated ATPases. Myosin molecules are composed of heavy and light subunits that associate in a specific manner, each of which is specific to muscle type during development and maturation; that is, ventricular myosin in a fetal heart is different from that of an adult heart.89 In some muscles, acclimation leads to a higher proportion of “slow” myosin ATPase isoforms, such as the replacement of myosin heavy chain type IIb (MHCIIb) with type Iix.133,250 The hearts of heat-acclimated rats become more efficient (amount of oxygen required per unit force time per gram of tissue)246 as a result of the presence of altered isoforms of contractile proteins. Thirty to 90 minutes of daily exercise for 10 weeks reduced the percentage of MHCIIb fibers in

rat hind-limb muscles and increased the slower, but more efficient, MHCIIa fibers. That is, increasing the training duration increases the fast-to-slow shift in myosin isoforms.121 Excess thyroid hormone increases the amount of myosin isozyme VI, with its high rate of ATPase and contractile speed, at the expense of the normal V3 isozyme, leading to greater speed and strength but reduced efficiency. In the case of sweat secretion, on acclimation there is an intrinsically higher rate of sweat secretion because of isoform alterations along the secretory tubules. Administration of thyroid hormone to neonatal rats rapidly replaces fetal cardiac ventricular myosin with its adult isoform. On the other hand, if the synthesis of thyroid hormone is suppressed, then the slower, fetal isoform predominates.66 Thyroid hormone concentration regulates protein isoforms, activities, and therefore the output of metabolic heat.253 The speed and extent of contractility of heart muscle depend on the number of Ca release channels in the sarcoplasmic reticulum (SR) (more channels permit faster Ca2+ entry into the cytoplasm and faster contraction) and on the rate of Ca uptake by the SR (faster Ca2+ uptake means faster relaxation). In ventricles, low thyroid hormone levels reduce the number of Ca release channels, which depresses contractility. In the atria, low thyroid hormone also increases the density of muscarinic receptors, rendering them more sensitive to negative chronotropic agents. In summary, low thyroid hormone levels depress cardiac function and render the heart more sensitive to agents that decrease atrial contraction, and less sensitive to agents that increase HR and contraction.15,295,312,432 Acclimation occurs under conditions of relative or actual hypothyroidism. As a result, the acclimated heart shows altered myosin isoforms and increased phospholamban content but lowered contractile velocity, rate of Ca uptake by the SR, and relative oxygen consumption. These changes increase overall efficiency of the heart at the expense of contractile velocity.79,360 Thyroid hormone increases the number of Na+,K+-ATPase pumps97 and decreases the density of voltage-dependent calcium channels on plasma membranes (leading to reduced intracellular Ca2+ content).159 Thyroid hormone and sustained aldosterone, such as from excess sweat loss and elevated plasma Na+, also alter metabolic processes and electrical activity of cells by regulating intracellular Na+ and K+ concentrations. In the short term, they increase the number of functional Na+,K+-ATPase pumps by recruiting preformed but inactive pumps and their subunits to the plasma membrane. In the long term, they induce synthesis of new pump subunits.97,155 Therefore, the prolonged and reduced levels of thyroid hormone seen during acclimatization decrease the number of those pumps, hence reducing metabolic activity.463 Almost any traumatic insult to the body alters hormonal level by elevating corticotropin releasing hormone, in turn decreasing thyroid hormone, growth hormone (GH), gonadotropinreleasing hormone, luteinizing hormone, follicle-stimulating hormone, and gonadal steroid concentrations, while increasing ACTH, cortisol, and prolactin levels (see Figure 10-5).46 Reduction in thyroid hormone concentration commences within a few hours, may be maximal after 1 to 4 days, and persists for the duration of the illness.338 Among heatstroke victims, decreases in serum thyroid hormone correlated with severity of heatstroke, according to peak Tc.91 That is, severity of heatstroke was related to depression of thyroid function. After the patients

Chapter 10: Pathophysiology of Heat-Related Illnesses completely recovered, thyroid function tests returned to normal. The hypothyroid state may protect by preventing undesirable catabolic effects. Therefore, thyroid replacement therapy is not currently recommended.91 In summary, long-term acclimatization to heat and exercise involves changes on a molecular level, involving alterations in intracellular HSP concentrations, increased IL-1, reduced thyroid hormone, increased aldosterone, increased number of Na+,K+-ATPase membrane pumps, and alterations in protein isoforms, altogether contributing to the physiologic adaptations in organ function.246


IMMUNE SYSTEM In the processes of digestion and absorption of ingested food, chyme remains in the intestines for hours to days. Although we absorb a large share of the nutrients, bacteria present in the gut lumen also utilize nutrients from the chyme and reproduce rapidly, reaching concentrations of 109 to 1012 organisms per gram.168 Dead gram-negative bacteria slough off into their milieu large amounts of the highly toxic cell wall component LPS, which may reach concentrations of 1 mg/g in the feces, a million times the lethal concentration if it were in plasma. As long as LPS remains within the intestines, it is not harmful. Small amounts that leak into the circulation are rapidly inactivated by several mechanisms. Some LPS is phagocytosed by bound Kupffer cells within the liver reticuloendothelial system (RES), where it is partly detoxified and then bound by hepatocytes for further degrading509; some LPS binds to circulating antilipopolysaccharide antibodies176; some binds to high-density lipoprotein (HDL)513; and some binds to LPS-binding protein (LBP).544 If large amounts of LPS rapidly enter the circulation, it could overwhelm the protective systems, allowing LPS to express its toxic effects rapidly. At plasma concentrations between approximately 10 and 100 pg/mL, LPS initiates a cascade of molecular events, leading to nausea, vomiting, diarrhea, fever, and headache.44 Higher concentrations can lead to conditions identical to those of gram-negative bacteremia, including vascular collapse, shock, and death.80 In fact, during gram-negative bacteremia, normal immune mechanisms may destroy all viable circulating bacteria so that at the time of death there may be zero live bacteria in the plasma. The circulating LPS appears to be the immediate cause of septic shock.534

Intestinal Ischemia and Lipopolysaccharide Release During exercise, blood flow to muscle may rise from a resting value of 1 to 2 mL/100 g/min to as high as 300 mL/100 g/min to deliver oxygen and nutrients. As Tc rises, blood flow to the skin also rises to provide cooling. This strains the cardiovascular system’s ability to maintain blood flow to the heart, brain, and liver.304,350 During heavy exercise, it is important that blood flow to the liver be substantially maintained to remove lactate and other metabolites from the blood and to provide glucose for energy.304 To maintain blood pressure under still more intense exercise and thermal stress, blood flow is reduced to those organs less immediately critical—that is, the intestines and kidneys. If splanchnic blood flow drops sufficiently, reduced delivery of oxygen leads to regions of local ischemia and transitory damage

257

to the barrier function of the gut wall. If this is prolonged, there may be permanent ischemic injury to the gut wall.415,418 Occurrence of several transitory bouts of local hypoxia and metabolic stress in splanchnic tissues may, during reperfusion, generate free radicals, exacerbating the ischemic injury.221 Exercise at . 80% Vo2max for 30 minutes at 22° C (71° F) increased permeability of human intestines to small molecules.401 Ischemic injury of the intestines causes the diarrhea or water intoxication occasionally encountered during a marathon run as a consequence of the inability to reabsorb water ingested during the race.304 For example, in one extreme case, after winning a marathon in 1979, Derek Clayton stated that “two hours later . . . I was urinating quite large clots of blood, and I was vomiting black mucus and had a lot of black diarrhea.”166 Another athlete, Dr. Peter Rogers, stated that during training for two Olympiads (gymnastics, 1972, 1976) and one world championship, many of the athletes developed bloody diarrhea after long periods of intense training (personal communication, 2005). Intense and prolonged running is a common cause of gastrointestinal bleeding; up to 85% of ultramarathoners demonstrate guaiacpositive stools from a 100-km (62.1-mile) race.29 Endotoxemia, the ultimate consequences of reduced intestinal blood flow, may be severe. Because of the high LPS gradient across the gut wall, almost any insult to the integrity of the gut wall leads to a rise in plasma LPS. Severe hemorrhage reduces splanchnic blood flow and oxygen delivery to the walls of the stomach, small intestine, and sigmoid colon.128 This has led to local elevations in the permeability barrier of the gut wall and caused endotoxemia.181 In a swine model, blood flow through the superior mesenteric artery was progressively occluded, leading to progressive tissue hypoxia and a local shift to anaerobic metabolism, producing lactate and a fall in the pH of the gut wall.162 At about the same time, LPS entered the circulation. This may lead to an ominous positive-feedback loop, because infusing LPS itself causes hypotension, reduced splanchnic blood flow, and an increase in gut permeability so severe that whole bacteria can be translocated into the circulation.162,529 The size of putative holes in the gut wall accounting for the rise in LPS permeability depends on the duration of the ischemia. When the superior mesenteric artery of canines was occluded, LPS (molecular or micellar) leaked out into the circulation within 20 minutes, but whole live bacteria (several orders of magnitude larger) required 6 hours of occlusion.406 In other species, these times may be much shorter.117 In a different model, nonhuman primates breathed a hypoxic gas mixture for an hour.17 The resultant hypoxemia rapidly initiated a reflex response designed to maintain oxygenation of the heart and brain at the expense of the rest of the body. This reflex caused intestinal blood flow to fall and was so intense that it resulted in transient ischemic injury to the gut wall and translocation of LPS into the circulation within only 5 to 10 minutes of breathing the hypoxic gas mixture. When the immune system was suppressed by whole-body ionizing radiation, the same hypoxic stress caused LPS to rise to higher levels and persist in the blood for a longer period. On the other hand, when the gut flora had been reduced three to four orders of magnitude by administration of nonabsorbable antibiotics for a week, there was no detectable translocation of LPS and bacteria by hypoxia.117,168 There is a fitness component to alterations in splanchnic blood flow. When experimental animals (as compared with

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30 Anti-LPS 20 LPS (ng/mL)

0.3

Hep. portal v. 10

Femoral a. 0.2 Hep. portal v.

0

LPS

0.1

Femoral a. 0 37

38

39

40

41

42

43

44

Rectal temperature (°C)

Figure 10-13. Effect of heating on villus structure. Representative light micrographs of rat small intestinal tissue over a 60-minute course at 41.5° to 42° C. Note the generally normal appearing villi at 15 minutes (slight subepithelial space at villous tips), compared with initial sloughing of epithelia from villous tips at 30 minutes, massive lifting of epithelial lining at top and sides of villi at 45 minutes, and completely denuded villi at 60 minutes. Bars represent 100 µM. (From Lambert GP, Gisolfi CV, Berg DJ, et al: J Appl Physiol 92:1750–1761, 2002, with permission.)

sedentary animals) were heat stressed, the fit ones with their greater cardiovascular capacity better maintained BFspl, they had reduced amounts of ischemic damage to the gut wall, and reduced quantities of LPS translocated into the circulation.444 That is, fitness may reduce the LPS load during intense exercise. Such studies show that the permeability barrier in the gut wall is rapidly damaged by hypotension, reduced blood flow, and hypoxia, thus permitting LPS to enter the portal and systemic circulations at a high rate. It has been reported that after heatstroke patients are cooled, they may develop secondary fever and infection carrying a high death rate.470 The susceptibility of such patients to infections470 may result from a combination of changes in lymphocyte subpopulations, together with the increase in gut wall permeability to LPS and bacteria caused by hyperthermia and associated hypotension.117

Role of Lipopolysaccharide in Heatstroke Pathophysiology Heatstroke temperatures greater than 43° C (109.4° F) cause a large increase in permeability of isolated rat intestinal walls to LPS that persists even after the temperature is reduced to 37° C (98.6° F).384 This suggests that heat causes major direct thermal injury of the gut wall at approximately 42° to 43° C (107.6° to 109.4° F) (Fig. 10-13).318 The time course of the movement of LPS through the intestinal wall into the circulation resulting from hypoxia, ischemia, and ionizing radiation was determined in nonhuman primates125 and compared with hyperthermia (Tamb = 41° C [105.8° F], RH = 100%, 3 to 4 hours).327 As Tc rose, plasma LPS concentration remained low until 42° to 43° C (107.6° to 109.4° F) (Fig. 10-14). At this temperature, there was a sudden rise in LPS concentration, first in the portal

Figure 10-14. Endotoxemia caused by heatstroke in anesthetized nonhuman primates. At Tre of 42° to 43° C (107.6° to 109.4° F), plasma lipopolysaccharide (LPS) concentration rose first in the hepatic portal vein,and 10 to 15 minutes later in the systemic circulation.However,a decline in consumed anti-LPS antibodies occurred at temperatures as low as 39° to 40° C (102.2° to 104° F). (Modified from Gathiram P, Wells MT, Brock-Utne JG, Gaffin SL: Circ Shock 25:223–230, 1988, with permission.)

vein, and 10 to 15 minutes later in the systemic circulation. This sequence appears to be the main route of LPS: out of the lumen of the intestines, through the portal vein to the liver, and into the vena cava and systemic circulation as a result of heatstroke and intestinal ischemia.192 In a previous study of infection by injecting live gramnegative bacteria, Gaffin and coworkers534 noted that when the concentration of live gram-negative bacteria or LPS rose, the concentration of measurable circulating LPS-specific antibodies fell because they became bound to circulating LPS and thus were no longer detectable by an immunoassay.534 It had been expected therefore that in the heatstroke experiments, the concentration of natural (i.e., background) anti-LPS antibodies would also immediately fall at 42° to 43° C (107.6° to 109.4° F). Contrary to expectations, natural anti-LPS began to decline at temperatures as low as 39° to 40° C (102.2° to 104° F) (see Figure 10-14).192 This suggests that as Tc rose to only 39° to 40° C, LPS actually began to leak into the circulation at a slow rate, gradually consuming the anti-LPS antibodies. As Tc continued to rise, at a certain point massive damage to the gut wall occurred, leading to rapid leakage of LPS into the portal vein. It is not clear how much of this damage is caused by reduced oxygen delivery from reduced intestinal blood flow, how much by direct thermal damage of the gut wall, and how much by other causes. Anti-LPS antibodies were protective against heatstroke in vervet monkeys up to a Tc of 43.5° C (110.3° F), but no higher.191 This suggests that LPS-induced toxicity is important in the pathophysiology of heatstroke death only up to 43.5° C (108.5° F). Above this temperature, other mechanisms are more important, such as direct thermal damage to nervous tissue. LPS had previously been implicated as a factor in heatstroke death by indirect observations. Injection of very low doses of LPS leads to rapid tolerance to ordinarily lethal doses of LPS.136,208 Administration of low doses of LPS protected rats against subsequent heatstroke. When activity of the reticuloen-

Chapter 10: Pathophysiology of Heat-Related Illnesses dothelial system (the main mechanism for removal of LPS from the circulation) was reduced, the mortality of heatstroke increased.137 Ryan and colleagues441 found the inverse effect. Rats were heated to a Tc of 42.5° C (108.5° F) and then were passively cooled. The next day they were challenged with a lethal dose of LPS, and mortality rate dropped from 71% in the control rats to zero in the previously heat-stressed rats. The importance of LPS in fatal heatstroke death was confirmed in a canine model of heatstroke.232 Tc was raised to 42° C (107.6° F) for 3 hours and then cooled to 38° C (100.4° F). Deaths occurred only in the animals with rises in plasma LPS concentration.

Exertional Heatstroke Several studies support the idea that the immune system and LPS are involved in the pathophysiology of heatstroke. Leukocytosis is a general response to most forms of stress, including muscular activity,190 administration of epinephrine or glucocorticoid, and excitement. Prolonged or severe exercise initiates mobilization and activation of neutrophils and causes proteolysis of skeletal muscle and production of acute phase proteins by the liver.76 Exercise leads to local disruption of tissues and sloughing of tissue fragments that circulate and activate the complement system. This activation primes monocytes for further activation by LPS or by fragments of tissue subsequently damaged.78 Severe exercise causes reduction in splanchnic blood flow and impaired renal function, with an increase in urinary excretion of proteins so profound (>100-fold) that it led to an actual depletion of circulating proteins.33,415 To understand the relationship between splanchnic shutdown and heatstroke pathophysiology, it is necessary to consider the contents of the intestinal lumen and the likely results of their leakage into the systemic circulation. Many of the clinical signs in a heatstroke victim, including blood-clotting disturbances, are similar to those seen in septic shock cases.202 LPS activates a blood factor leading to disseminated intravascular coagulation,39,555 a common complication of septic shock. It was suggested that LPS participates in the pathophysiology of heatstroke. Similarities between heatstroke and septic shock are described in Box 10-5. Because core temperatures of long-distance runners may rise above 40° C (104° F), a study of runners who collapsed during an ultramarathon (89.5 km [55.6 mi]) run on a warm day was conducted.68 Those runners reached or were carried into the medical tent at the finish line, where blood samples were taken from 98 of them before initiating volume therapy (Fig. 10-15). Eighty of 98 runners had plasma LPS levels above normal values, including two in the lethal range. It should be noted that the body can tolerate short periods of high LPS concentrations.534 Although hypovolemia and hemoconcentration resulting from sweating may have caused a few high normals to cross into the elevated range, this was not the case for the majority. Of those who finished the race, the smaller group with normal, low LPS levels finished faster. Furthermore, this normal group had higher levels of natural anti-LPS in their plasma. That is, the presence of high levels of anti-LPS antibodies correlated with low levels of LPS and better performance. This high antiLPS antibody and low LPS group also had reduced indexes of nausea, vomiting, and headache and recovered faster (within 2 hours) than did the larger high-LPS and low-anti-LPS group (up to 2 days).

259

Box 10-5. Common Factors in Heat Illnesses and Sepsis CLINICAL

Neurologic symptoms Fatigue, weakness, confusion, delirium, stupor, coma, dizziness, paralysis, amnesia Tachycardia Nausea, vomiting, diarrhea Headache Myalgia Hypotension Spasm, rigors Oliguria, renal failure Hyperventilation Organ failure Shock LABORATORY

Metabolic acidosis Hematocrit elevated Urea elevated Lactate elevated Disseminated intravascular coagulation Cytokines elevated Hepatic dysfunction Lipopolysaccharides elevated

In triathlon participants, concentrations of LPS rose and of anti-LPS antibodies fell at the end of the third race.54 Some athletes were found to have higher levels of natural anti-LPS antibodies than others. When individuals were questioned about their training regimen, it became clear that those who trained the hardest (miles swum, bicycled, and run the 3 weeks before the triathlon) had the highest levels of anti-LPS antibodies. It may be that one component of the benefit of physical training is increased levels of natural anti-LPS antibodies. We proposed that as a result of severe training, temporary periods of intestinal ischemia occurred, leading to entry of low to moderate levels of LPS into the circulation, which was enough to stimulate the immune system and induce anti-LPS antibodies. When a marathon was run on a cold day, no elevations in plasma LPS were seen (T. Noakes and S. Gaffin, 1988, unpublished observations). It is not clear what combinations of heat load and exertional factors are required to decrease BFspl sufficiently to damage the gut wall for translocation of LPS into the circulation.

Classic Heatstroke Survival of hospitalized heatstroke patients depends in large part on the rapidity of cooling on entry to a hospital intensive care unit. This time factor may be important because of the time required for the production of cytokines, which is in the range of minutes to hours. Seventeen Hadj patients with classic (nonexertional) heatstroke were admitted to a hospital an average of 2 hours after the onset of heatstroke.59 Each victim’s Tc was greater than 40.1° C (104.2° F). They suffered from delirium, convulsions, and coma. Plasma LPS concentrations ranged from 8 to 12 ng/mL, extremely high and in the potentially lethal range.524 Furthermore, TNF and IL-1 concentrations were also

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0.4

TABLE 10-3. Elevated Cytokines Due to Heatstroke in 17 Military Recruits Who Developed Exertional Heatstroke*

Plasma LPS (ng/mL)

P⬍0.025

EXERTIONAL HEAT STROKED

0.3 Rectal temperature‡ IL-1β‡ TNF-α‡ IL-6‡ IFN-γ‡ IL-2r‡ IL-4 IL-10 IL-8‡ Monocyte chemoattractant protein 1‡ RANTES‡

0.2

0.1

0 ⬍8

⬎8

Time to completion of race (h) Plasma LPS Nausea, vomiting, diarrhea 100 80

0.3

60 0.2 40

N, V, D (%)

Plasma LPS (ng/mL)

0.4

0.1 20 0

0 0.1 ng/mL normal

⬎0.1 ng/mL high

Plasma LPS (ng/mL)

Figure 10-15. Role of lipopolysaccharide (LPS) and anti-LPS IgG in long-distance races. The Comrades’ Marathon is an 89.5-km race between Pietermaritzburg and Durban, Republic of South Africa, run on a warm day. Blood samples were obtained from collapsed runners prior to treatment. On examination, they all looked the same. However, of 89 samples analyzed, 80% had elevated levels (>0.1 ng/mL) of LPS, and 20% had normal low levels. Top: Those with low levels of circulating LPS ran the double marathon significantly faster before they collapsed. Bottom: Those with low levels of circulating LPS had higher morbidity indexes of nausea,vomiting, and diarrhea and all recovered within 2 hours.Those with elevated levels of LPS had more serious symptoms and required up to two days to recover.(Redrawn from Brock-Utne JG, Gaffin SL,Wells MT, et al: S Afr Med J 73:533–536, 1988.)

41.2 (99.7 3.1 4.9 15.8 7.3 1568 2.5 12.9 84.2 959

± ± ± ± ± ± ± ± ± ± ±

1.2° C 1.4° F) 1.5 pg/mL 4.1 pg/mL 3.2 pg/mL 4.9 pg/mL 643 pg/mL 1.2 pg/mL 9.4 pg/mL 79.9 pg/mL 589 pg/mL

12,464 ± 10,505 pg/mL

CONTROLS† 37.6 (106.2 1.2 1.2 1.2 2.4 610 1.2 2.5 10.4 158

± ± ± ± ± ± ± ± ± ± ±

0.8° C 2.1° F) 0.8 pg/mL 2.4 pg/mL 1.2 pg/mL 4.1 pg/mL 214 pg/mL 0.8 pg/mL 4.9 pg/mL 3.2 pg/mL 217 pg/mL

5570 ± 2894 pg/mL

*The severity of exertional heatstroke was evaluated using a simplified acute physiology (SAP) score. Interleukin (IL)-6, interferon-gamma (IFN)-γ, and IL-2 receptor positively correlated with the SAP score. Among chemokines, only serum monocyte chemoattractant protein 1 was positively correlated with the SAP score (r = .78, P < .001). There was no correlation between either cytokines or chemokines and body temperature. † Controls were 17 military recruits undergoing exercise who did not develop heatstroke. ‡ Conclusions: Proinflammatory cytokines IL-1β, tumor necrosis factor (TNF)-α, IL-6; Th1 cytokines INF-γ and IL-2 receptor; and chemokines IL-8, monocyte chemoattractant protein 1, and RANTES (regulated on activation, normal T cell expressed and secreted) are increased in patients with exertional heatstroke. Helper T-2 cytokines may play a role as anti-inflammatory cytokines. From Lu KC, Wang JY, Lin SH, et al: Crit Care Med 32:399–403, 2004.

cytosis increased with increasing Tc. There were also substantial decreases in helper T cells (CD4) and B cells (CD19) as a result of heatstroke. Heatstroke is known to elevate catecholamine levels.84 Because epinephrine causes leukocytosis with an increase in NK and T suppressor/cytotoxic cells, these authors suggested that heatstroke raised catecholamines, which in turn altered lymphocyte subpopulations. On the other hand, hyperthermia causes elevated cortisol,276 which causes the opposite effect, lymphocytopenia.58 In the preceding study, two of the 11 heatstroke patients had a decreased number of lymphocytes. To account for the reduction in lymphocytes, the authors suggested that in those two patients the effects of cortisol, rather than of catecholamines, were dominant. That is, changes in subpopulations of lymphocytes in heatstroke may depend (on an individual basis) on the relative rises in concentration of catecholamines and cortisol, as well as on individual sensitivities to them. However, this is not yet clearly established.

Adaptation and the Immune System Cytokines and Shock

very high. The authors suggested that these cytokines exacerbated the hyperthermia of heatstroke through induction of prostaglandins. Nine of 11 heatstroke patients showed marked leukocytosis resulting from a large increase in the number of T suppressor cytotoxic cells (CD8) and NK cells (CD16/CD56).58 This leuko-

Cytokines are a class of protein cell regulators produced by a wide variety of cell types throughout the body. They control timing, amplitude, and duration of the immune response.99 They are relatively low molecular weight proteins (40° C [104° F]) that it should be considered a subgroup of EHS. Neuroleptic seizures and overdose of recreational drugs share with EHS the features of massive muscle contractions (with consequent overuse of high-energy compounds) and rhabdomyolysis.303 Because the use of recreational drugs is not expected to decline and the number of persons using neuroleptic drugs is probably on the increase, the involvement of heatstroke pathophysiology should be considered in treating those cases. In an unusual situation during mountaineering in summer, two persons died of heatstroke and acute rhabdomyolysis. Both patients had received treatment with antipsychotic drugs, including a phenothiazine.306 Ergogenic aids are also a problem. A highly trained, heat-acclimatized infantry soldier suffered from exertional heatstroke during a 12-mile road march shortly after taking an ephedra-based supplement. Because there are no clear ergogenic benefits in using ephedra alone, clinicians and military commanders should strongly discourage the use of ephedra-containing substances in active duty soldiers undergoing strenuous exercise.395 In summary, heatstroke in a summertime vacation area might be complicated by the use of therapeutic or recreational drugs or ergogenic aids.

Malignant Hyperthermia Malignant hyperthermia is a rare life-threatening disorder involving hypermetabolism, rapid rise in body temperature, and rigidity of skeletal muscle. It is induced by exposure to volatile anesthetics during surgical procedures in affected patients. In about half these patients, mutations were seen in the gene for the Ca2+ release channel (RyR).107,213,323 The anesthetic binds to RyR and activates the Ca2+ release channel, causing massive calcium entry into the cytoplasm. This activates contractile proteins, calmodulin, and a variety of calcium-sensitive enzymes, which leads to muscle rigidity, hypercatabolism, fulminating hyperthermia, and metabolic acidosis.107 Rhabdomyolysis, hyperkalemia, and myoglobinemia458 are commonly associated with malignant hyperthermia, with plasma K+ rising as high as 10 mmol/L.357 Underlying illnesses in five cases of rhabdomyolysis included heatstroke, high fever, and grand mal seizures with associated hyperthermia. Nevertheless, there were multiple factors responsible for rhabdomyolysis in each case, such as hypokalemia, hypophosphatemia, shock, and arteriosclerosis.378 A 41-year-old man susceptible to malignant hyperthermia developed an infection and selfmedicated with a cold medicine. He presented with high fever, dysarthria, dysphagia, and progressive weakness of his muscles and developed massive rhabdomyolysis with acute renal failure.279

Neuroleptic Seizure Treatment of psychiatric patients with neuroleptic drugs, as well as with antidepressants, antiemetics, and others,141 may lead to

Chapter 10: Pathophysiology of Heat-Related Illnesses the uncommon but often fatal neuroleptic malignant syndrome, characterized by hyperthermia as high as 42° C (107.6° F), “lead pipe” (skeletal muscle) rigidity, dyspnea, coma, extrapyramidal syndrome, rhabdomyolysis, severe metabolic acidosis, leukocytosis, and elevated creatine kinase.104,234,270 A number of factors predispose to neuroleptic seizure, including dehydration, exhaustion, aggression, and restraints265; high environmental temperature; high doses of neuroleptics; abrupt discontinuation of antiparkinsonism agents; and administration of lithium.141 Successful treatment of these cases includes immediate withdrawal of the drug, administration of dantrolene, and either oral bromocriptine or the combination of levodopa and carbidopa.141

Drug Overdose Although the toxicity of drug overdose is well recognized, it is not often appreciated that the hyperthermia attained can be in the range reported for heatstroke. Such hyperthermia has been induced with cocaine130 and amphetamine derivatives, such as 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) and 3,4-methylenedioxyethamphetamine (MDEA, Eve).504 Other components of this syndrome include hyperkalemia, rhabdomyolysis,475 sympathetic hyperactivity, convulsions, rectorrhagia, psychosis, disseminated intravascular coagulation in the absence of positive blood cultures, and acute renal failure.237

Susceptibility to Heatstroke There may be an inherited susceptibility to EHS. Muscle biopsy specimens taken from two men in military service who had recovered from EHS had abnormal responses to halothane, a well-known cause of malignant hyperthermia.213 Furthermore, muscles from members of their families had abnormal responses to halothane or ryanodine, a drug that binds to the Ca2+ release channels of the sarcoplasmic reticulum.8 A ryanodine contracture test has been proposed as an in vitro diagnostic test to screen for surgical patients susceptible to malignant hyperthermia.8 This test might be useful in identifying, retrospectively, a possible subgroup of patients with EHS.

Changes in Cognitive Function Changes in cognitive function appear to occur before development of physical symptoms associated with heat stress.82 Typically, heat stress causes distortion of the sense of time,36,37,112 memory impairment,540 deterioration in attention, and decreased ability to calculate mathematical problems.92,209,539 Health care personnel should be trained to recognize that confusion, changes in affect, and impaired ability to function in the work environment can be early signs of heat injury under heat stress conditions.82

Vasovagal Syncope Syncope is the cause of about 3% of emergency department visits and 6% of hospital admissions.193 Vasovagal syncope is responsible for 28% to 38% of syncopal episodes in patients 35 to 39 years old.115,274,348 Benign presyncope or syncope may result from diminished venous return to the heart because of blood pooling in the peripheral circulation. Syncope encompasses psychological disturbances activating an autonomic vasodilation response; reflex syncope caused by heavy coughing, micturition, or pressure on an irritable carotid sinus; and reduced vasomotor tone caused by hypotensive drugs or alcohol.144

263

The frequency of vasovagal syncope is greater in the young than in older adults, whereas orthostatic hypotension is more common in older persons.334 Propranolol does not prevent the vasovagal reaction in response to head-up tilt.334 Therefore, after the age of 40, presyncope may suggest a more serious condition, such as gastrointestinal bleeding, myocardial or valvular heart disease, or severe anemia. Cardiovascular syncope resulting from arrhythmia carries a 1-year mortality rate of about 30%.275

Hyperventilation Dizziness A slight but prolonged increase in respiratory rate or tidal volume may accompany an increase in anxiety.144 This can lead to increased blood oxygen content and decreased Pco2, with accompanying alkalosis. Altogether, these lead to generalized cerebrovascular vasoconstriction with ischemia and dizziness.

Heat-Induced Syncope The associated clinical syndromes vary in severity depending on the cause of hyperthermia and, therefore, so does the duration of central nervous system (CNS) dysfunction. Transient or temporary loss of consciousness associated with a mild form of heat syncope has its origins primarily in the cardiovascular system. It is a consequence of a reduced effective blood volume rather than an actual loss of volume. In an upright and stationary person, blood volume is displaced into the dependent limbs by gravity. If that person is also heat stressed, more blood is displaced into the peripheral circulation to support heat transfer at the body surface. These combined reductions in effective blood volume can temporarily compromise venous return, cardiac output, and cerebral perfusion. Patients are usually erect at the outset and sometimes report prodromal symptoms of restlessness, nausea, sighing, yawning, and dysphoria.293 Hypotension results predominantly from vasodilation and bradycardia. This systemic disorder is self-limited because when the person faints and assumes a horizontal position, central blood volume is restored, cardiac filling rises, blood pressure is restored, and the problem is remedied. Transient loss of consciousness in syncope has a metabolic basis within ischemic cells of the brain. Despite this, the effects, although startling to onlookers and frightening to the patient, appear to be readily reversible. There is no risk of direct thermal injury to brain cells complicating the circulatory origin of this sudden decline in effective arterial volume. The incidence of syncopal attacks falls rapidly with increasing days of work in the heat (see Figure 10-10), suggesting the importance of salt and water retention in preventing this disorder (Table 10-4). Individuals medicated with diuretics would be at high risk. Furthermore, potassium depletion and hypokalemia may lower blood pressure and blunt cardiovascular responsiveness.305 In stark contrast to simple syncope is the profound CNS dysfunction dominating the early course of heatstroke. Thus, if a person faints in a setting where hyperthermia is possible and does not rapidly return to consciousness, heatstroke should be suspected, cooling measures instituted, and body temperature monitored.

Exertion-Induced Syncope, Cramps, and Respiratory Alkalosis During basic military training, a cluster of 17 syncopal episodes was associated with a seldom-described form of heat exhaus-

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TABLE 10-4. Signs and Symptoms of Salt and Water Depletion Heat Exhaustion SIGNS AND SYMPTOMS Recent weight gain Thirst Muscle cramps Nausea Vomiting Muscle fatigue or weakness Loss of skin turgor Mental dullness, apathy Orthostatic rise in pulse rate Tachycardia Dry mucous membranes Increased rectal temperature Urine Na+/Cl− Plasma Na+/Cl−

SALT DEPLETION HEAT EXHAUSTION

WATER DEPLETION HEAT EXHAUSTION

DILUTIONAL HYPONATREMIA

No Not prominent In most cases Yes In most cases Yes Yes Yes Yes Yes Yes Yes Negligible Below average

No Yes No Yes No Yes Yes Yes Yes Yes Yes In most cases Normal Above average

Yes Sometimes Sometimes Usually Usually No No Yes No No No No Low Below average

*Data from Armstrong LE, Curtis WC, Hubbard RW, et al: Med Sci Sports Exerc 25:543–549, 1993; Shopes E: Water intoxication: Experience from the Grand Canyon (abstract). Presented at the 10th Annual Meeting of the Wilderness Medical Society, August 1994, Squaw Valley, Idaho, p 265.

TABLE 10-5. Clinical Data for 17 Patients with Heat Exhaustion CASE NO. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

AGE

Activity

SYNCOPE

CRAMPS

Tre (°F)

RR (bpm)

Na+ (mEq/L)

pH

Pco2 (mmHg)

19 20 20 21 21 22 20 20 20 18 19 18 20 19 23 18 17

Marching Running mile Rifle range Marching/running Marching Marching Rifle range Marching Marching Marching Marching Marching Marching Marching Rifle range Marching Marching

Yes Yes No Yes No No No Yes No Yes Yes Yes No Yes Yes Yes Yes

Abd Legs/abd No Hands Severe abd/legs Legs Mild Abd/legs Abd Chest Tetany Severe Mild Abd/legs Abd/legs Chest/legs Abd

99.6 98.4 99.4 100.4 102.4 100.0 100.0 100.8 101.4 100.8 101.5 100.6 98.6 100.7 101.0 101.2 101.6

24 30 24 22 35 22 22 30 24 18 30 30 26 30 32 28 22

142 145 143 162 141 152 140 145 — 140 160 130 141 145 148 148 146

— — — 7.47 7.50 7.70 — 7.52 7.69 7.56 7.44 7.71 7.77 7.76 7.66 7.78 7.53

— — — 34.0 32.4 14.8 — 28.8 19.8 29.4 34.2 17.2 15.2 16.3 19.7 14.7 28.4

Abd, abdomen; RR, respiratory rate; Tre, rectal temperature. From Boyd AE, Beller GA: Acid-base changes in heat exhaustion during basic training. Proc Army Sci Conf 1:114, 1972.

tion (Table 10-5).260 This heat exhaustion, in contrast to hypovolemic salt depletion, was characterized by hyperventilation, respiratory alkalosis, syncope, and tetany. Most victims also experienced abdominal cramps, yet this was independent of lactic acidosis and hyponatremia. These descriptions were unique in that the heat syncope episodes were not those classically described as the venous pooling or postural hypotension variety.32,387 The incapacitated trainees arrived at a heat ward within 10 to 30 minutes of the onset of symptoms, and blood samples were drawn immediately on admission. They exhibited moderate to marked respiratory alkalosis, but only two appeared to be severely dehydrated; nearly all (16 of 17 patients) had severe cramps of the abdominal or extremity muscles.

Clinical data recorded on admission are shown in Table 10-5. Almost all the casualties occurred in the afternoon during July, 1971, at Fort Polk, Louisiana. All were diagnosed with heat exhaustion resulting from training in the field (12 of 17 while speed marching). Rectal temperatures on admission were elevated, even though most of the victims had been doused with water before evacuation from the field. Serum electrolytes were in the normal range in the majority of victims. However, hemoconcentration with elevated serum sodium level was observed in four patients. One of 17 patients had a low serum sodium level and also experienced severe muscle cramps. The majority of these patients were not water or salt depleted, and 15 of the 16 remaining patients with cramps had normal to elevated serum sodium and chloride levels. The mean arte-

Chapter 10: Pathophysiology of Heat-Related Illnesses

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TABLE 10-6. Protective Effect of Hypertonic 10% Albumin versus Saline on Experimental Heatstroke-Induced Cerebral Ischemia-Hypoxia Injury in Amelioration of Rises in Glutamate, Glycerol, Lactate, and Free Radicals in Brain

Mean arterial pressure Intracranial pressure Cerebral perfusion pressure Cerebral blood flow Brain Po2 Striatal glutamate Striatal glycerol Striatal lactate/pyruvate ratio Striatal hydroxyl radicals Striatal neuronal damage score

SALINE

10% ALBUMIN

42 ± 3 mm Hg 33 ± 3 mm Hg 9 ± 3 mm Hg 109 ± 20 blood perfusion units 6 ± 1 mm Hg 51 ± 7 nM 24 ± 3 nM 124 ± 32 694 ± 22% rise 2.25 ± 0.05

64 ± 6 mm Hg 10 ± 2 mm Hg 54 ± 5 mm Hg 452 ± 75 blood perfusion units 15 ± 2 mm Hg 3 ± 2 nM 4 ± 2 nM 7±3 119 ± 7% rise 0.38 ± 0.05

Adapted from Chang CK, Chiu WT, Chang CP, Lin MT: Clin Sci (Lond) 106:501–509, 2004.

rial pH for this group of patients was 7.62 ± 0.03 (SEM), and five had a pH of 7.67 or greater. Arterial Pco2 was reduced to a mean value of 23.5 ± 2 mm Hg. Thus, all patients had moderate to marked respiratory alkalosis, and nine had obvious tetany with carpopedal spasm.64 The presence of carpopedal spasm and paresthesias in the distal extremities and perioral area helps distinguish this form of cramps from the classic variety. These data associate exertion-induced heat exhaustion with a form of respiratory alkalosis characterized by syncope, tetany, and muscle cramps and may possibly be the result of “an exaggeration of the normal physiologic ventilatory response to thermal extremes.”64 Hyperventilation with its resulting decrease in cerebral blood flow288,471,525 could account for a significant number of cases of exercise-induced heat syncope. Recumbency, rest, and oral replacement of fluid and electrolyte deficits are usual recommendations. Rebreathing of expired air is directed at alleviating carpopedal spasm, but it should be done with extreme caution because of its hypoxemic effect. Classic syncope is usually associated with postural hypotension, whereas heat exhaustion and heat cramps are usually associated with water and electrolyte imbalance. Most literature suggests that unacclimated workers have higher salt losses in the heat than those who are acclimated.317,325 Thus this series is a good example of the real world with a mixed bag of heat illness symptoms. To explain these clinical results, one should recall that acclimated individuals have higher sweat rates (2.5 L/hr versus 1.5 L/hr) than unacclimated persons, but they also have increased tolerance to exercise. If both groups voluntarily work at maximal sweat rates for any given task, those who are heat acclimated could produce higher salt losses despite their reduced sweat sodium concentrations. In such a scenario, the acclimated individuals would be predicted to be the more prone to heat cramps.10 However, Table 10-6 indicates that there are higher salt losses for unacclimated individuals at any given sweat rate or volume of sweat lost. The differential diagnosis of heat cramps should also include exercise-induced peritonitis.500

Heat-Induced Tetany In excessively hot environments, men at rest hyperventilate.216 Adolph and Fulton2 described dyspnea and tingling in the hands

and feet of men being dehydrated in the heat. In 1941, during a voyage through the intense heat of the Persian Gulf, a ship’s engineer was reported to experience spontaneous hyperventilation and attacks of tetany.541 He could reproduce these symptoms simply by deliberately overbreathing. This appeared to be the first clinical description of heat-induced hyperventilation tetany. The exposure of male test subjects to hot, wet conditions led to physiologic changes and the onset of symptoms ranging from slight tingling of the hands and feet to more severe carpopedal spasm.260,261 The frequency and severity of symptoms were apparently not related to the absolute change in the four measured parameters (Pco2, CO2, pH, and Tre) but rather to the rate of change. When the subject’s tolerance time was short, changes occurred rapidly and the incidence of symptoms was high; conversely, when the tolerance time was long, the same degree of change occurred but the incidence of symptoms was low. It was suggested that rapid changes of the four parameters lead to imbalance between intracellular and extracellular compartments and that this imbalance may be one of the factors inducing symptoms. Again, treatment consists of rest, cooling, and rebreathing expired air.

Heat Cramps Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated.147 Heat cramps are brief, intermittent, and often excruciating; muscle contractions are a frequent complication of heat exhaustion and occurred in about 60% of 969 cases of heat exhaustion.102,325,495 The term heat cramps is a misnomer because heat itself does not cause them; rather, they occur in muscles subjected to intense activity and fatigue. The victim with salt depletion at the time of heat exhaustion is clearly ill and has numerous symptoms other than cramps. Furthermore, fatigue, giddiness, nausea, and vomiting are common and may occur before and more prominently than cramps. Sometimes, heat cramps occur as the only complaint, with minimal systemic symptoms. Furthermore, there is a difficulty in distinguishing abdominal heat cramps from gastrointestinal upset.

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During the 1930s, steel workers, coal miners, sugar cane cutters, and boiler operators were among the most common victims of classic heat cramps.502 Three factors common to most reports are that cramps are preceded by several hours of sustained effort, they are accompanied by heavy sweating in hot surroundings, and they are combined with ingestion of large volumes of water. A fourth factor (see later discussion) may be cooling of the muscles. Serum Na+ levels ranged from 121 to 140 mEq/L (normal, 135 to 145 mEq/L).502 In an industrial setting, heat cramps occur most commonly late in the day, after physical activity has ceased; they sometimes occur while a person is showering and occasionally occur in the evening.325 Hyponatremia and hypochloremia are diagnostic of heat cramps that might be due to salt deficit or some degree of water intoxication.305 If overdrinking causes gastric distention, nausea420 could trigger vasopressin release and contribute to renal water retention. Classic heat cramps are distinguished from hyperventilationinduced tetany in that they are not generalized but are limited to contractions of voluntary skeletal muscles subjected to prior exertion, and they usually affect only a few muscle bundles at a time. Nevertheless, the pain can be excruciating in severe cases. As one bundle relaxes, an adjacent bundle contracts for 1 to 3 minutes. The cramp thus appears to wander over the affected muscle. Three precipitating conditions (exhaustive work, hemodilution, and cooling the muscle) can each depolarize muscle cells.305 This could explain the association of cramps with showering in cool water, because cooling slows the Na+,K+-ATPase pumps and depolarizes the cell, which may thus reach excitation threshold.477 Heat cramps do not occur at the same frequency in all populations. For example, the Indian Armed Forces has a very low incidence340 and Shibolet observed no cases within Israeli Defense Forces.472 These data suggest that heat-acclimated individuals are less likely to experience them. This is consistent with the observation that the incidence was greatest during the first few days of a heat wave.502 Heat cramps generally respond rapidly to sodium chloride solutions. Mild cases may be treated orally with 0.1% to 0.2% NaCl solutions (two to four 10-grain salt tablets [56 to 112 mEq] or 1/4 to 1/2 teaspoon of table salt dissolved in a quart of water). Cooling and flavoring enhance palatability. Oral salt tablets are gastric irritants and not recommended. In severe cases, IV isotonic saline (0.9% NaCl) or small amounts of hypertonic saline (3% NaCl) are administered by physicians for rapid relief.

Heat Exhaustion Classic heat exhaustion is a manifestation of cardiovascular strain resulting from maintaining normothermia in the heat. Symptoms of heat exhaustion include various combinations of headache, dizziness, fatigue, hyperirritability, anxiety, piloerection, chills, nausea, vomiting, heat cramps, and heat sensations in the head and upper torso.20,21,256 Clinical descriptions include tachycardia, hyperventilation, hypotension, and syncope. Although the boundary between heat exhaustion and heatstroke is usually defined as 39.4° to 40° C (102.9° to 104° F), the differential diagnosis is often tenuous229 or even considered artificial.472 The victim may collapse with either a normal or an elevated temperature (severe cases, around 40° C), usually with profuse sweating. Spontaneous body cooling can occur, which is not prominent in severe heatstroke. The clinical determination of heat exhaustion is primarily a diagnosis of exclusion.

Classic heat exhaustion, like classic heatstroke, tends to develop over several days or longer and presents ample opportunity for development of imbalances in electrolytes and water. The hyponatremia and hypochloremia of patients with either heat cramps or salt-depletion heat exhaustion often develops over 3 to 5 days324 and usually in the unacclimatized individual who has not fully developed salt-conserving mechanisms.482,483 In salt-depletion heat exhaustion, muscle cramps, nausea, and vomiting may be intense, but victims do not feel very thirsty.14,256 The major cause of fluid and electrolyte imbalance (salt depletion, water depletion, water intoxication) involved in a particular case of heat exhaustion can be discovered from the history of events surrounding collapse.75,305,325,516 Other forms of heat exhaustion are characterized by the type of fluid or electrolyte deficit (primarily pure water or salt deficiency), their underlying causes (prolonged heat exposure versus intense, short-term exertion), the intensity of hyperthermia, and the absence or form of CNS disturbance. If external cooling does not rapidly lower Tc to normal or, in fact, precipitates severe shivering, intercurrent illness is suspected. Anecdotal experience in the field suggests that approximately 20% of persons with suspected heat exhaustion have some form of viral or bacterial gastroenteritis. This is especially likely if nondisinfected water or ice has been consumed. At any given loss of body weight, the decrement in plasma volume increases with the salt content of sweat. This would be the case for relatively unacclimated individuals. On the other hand, the more dilute the sweat (approaching a pure water deficit) and therefore the greater the retention of salt, the greater the increase in osmolality, plasma sodium, and thirst. Table 10-4 compares and contrasts the signs and symptoms of salt and water depletion heat exhaustion with dilutional hyponatremia. It is clear that at some point both syndromes share many symptoms. Vomiting and cramps appear to signal a significant sodium deficit, in addition to some degree of water deficit.

Heat Illness and Coexistent Disease Coexistent illness or infection predisposes an individual to heatstroke.195 In one study of heat illnesses, 11.2% of patients537 also had gastrointestinal (choleraic) illness.537 The reverse is also true: heat waves produce excess deaths of people with all categories of disease. For example, in one heat wave week in New York in the late summer of 1948, deaths from cardiovascular diseases and diabetes more than doubled (1364 versus 585), and pneumonia deaths tripled.151 Infection predisposes to heat illness, and heat stress exacerbates infections, leading to greater morbidity and mortality.329 Relatively few studies have been reported on the susceptibility to infection during heat exposure, or the influence of infection on heat tolerance; there is need for further research into the effects of diseases on thermoregulation.286


POSSIBLE NEW THERAPIES IL-1 Receptor Antagonist Heatstroke of rats causes hypotension that may be related to the production of inflammatory cytokines such as IL-1. Therefore, interference with the IL-1 pathways by blocking the IL-1 receptor appeared to be a promising means of improving heatstroke symptoms and survival. A single injection of IL-1 recep-

Chapter 10: Pathophysiology of Heat-Related Illnesses tor antagonist (IL-1ra) immediately after the onset of heatstroke in rats blunted the hypotension response to heat, and the rats survived much longer (91 minutes versus 17 minutes) than controls.94 With continuous perfusion of IL-1ra, the survival time increased to 10 hours from the onset of heatstroke. Because heatstroke may lead to a time-dependent shift of Th1 to Th2 cytokine production, timing of such a therapy would be critical, and difficult to perform safely in the field. Currently, the beneficial effects of IL-1ra have not been proven in humans, and the authors do not recommend such therapy. However, if clinical trials should prove its effectiveness, then after initiating cooling procedures and volume therapy, and after transportation to a hospital, administration of IL-1ra may be become part of heatstroke therapy.94

Insulin Rats were rendered diabetic (by streptozotocin) and then heatstroked by exposure to a Tamb of 43° C (109.4° F) for 60 min. Administration of insulin to the diabetic rats attenuated the high core temperature and heart rate, and improved cerebral blood flow and hypotension.388

Free Radical Scavengers Part of the pathophysiology of heatstroke involves production of highly toxic free radicals, or reactive oxygen species. Therefore, administration of scavengers of free radicals seems an obvious choice for therapy.550 Magnolol, obtained from the plant Magnolia officinalis, is a potent free radical scavenger that is 1000-fold more active than α-tocopherol in inhibiting lipid peroxidation in rat mitochondria. In rats heatstroked by exposure to a Tamb of 42° C (107.6° F), magnolol (20 mg/kg, IV) attenuated the pathophysiology associated with heatstroke.87 This pharmaceutical is not recommended for therapy until it undergoes clinical trials and has been proven successful in humans.

Hypertonic Albumin Heatstroked rats were treated with either 10% albumin or an equal volume of saline, and cooled by exposure to a Tamb of 24° C (75.2° F) for 12 min. As seen in Table 10-6, hypertonic albumin had a neuroprotective effect compared with saline controls in reducing elevations of glutamate, glycerol, lactate, and free radicals in the brain.86 The mechanism for this is not understood. It is somewhat counterintuitive, as a rat would normally be expected to be rendered hyperosmotic by heatstroke.

w-3 Fatty Acids At the biochemical level, binding of IL-1 to its specific membrane receptor activates G proteins, which increase intracellular concentration of cyclic adenosine monophosphate (cAMP), which in turn activates membrane phospholipases. Activation of the phospholipases produces arachidonic acid, leukotrienes, prostaglandins, and thromboxanes, ultimately leading to cell damage and organism pathophysiology.88,199 The phospholipases hydrolyze phospholipid esters of fatty acids, which in western diets are largely ω-6 fatty acids.263,321 The ω-6 fatty acids are hydrolyzed into the key metabolite, arachidonic acid. Cells contain two major enzyme classes that can act on arachidonic acid: lipoxygenases and cyclooxygenases. Lipoxygenase acts on arachidonic acid to enter a pathway that results in the formation of 5-hydroperoxyeicosatetraenoic acid (5HPETE) and a series of toxic leukotrienes. Of these, LTB4,

267

LTC4, and LTD4 are the most important. LTB4 induces inflammation, increases capillary leakage, and causes leukocytes to aggregate. LTC4 and LTD4 are potent bronchoconstrictors involved in asthma.105,223 Cyclooxygenase converts arachidonic acid into prostaglandin G2 (PGG2), which is converted into PGH2 with the formation of toxic free radicals. PGH2 is a central metabolite on which a variety of enzymes act to form mainly toxic products, such as thromboxane A2 (TxA2) and many different prostaglandins, including the toxic PGD2. TxA2 causes platelets to aggregate, is a strong vasoconstrictor, and increases capillary leakage. To a person in shock or with another circulatory disorder, such agents could convert a severe but treatable condition into a lethal one. In summary, eating a normal Western diet results in the presence of large amounts of ω-6 fatty acids in phospholipid cell membranes, predisposing to the formation of arachidonic acid and a large number of its toxic metabolites. For a review of prostaglandin and thromboxane biochemistry, see references.57,371,391 In fish-enriched diets laden with ω-3 fatty acids, a high proportion of the ω-6 fatty acids in plasma membranes are replaced by the ω-3 fatty acids, phospholipases hydrolyze the phospholipids into eicosapentaenoic acid, and no arachidonic acid is produced. Therefore, no strongly toxic thromboxanes, prostaglandins, and leukotrienes are produced. Instead, only slightly toxic leukotriene B5 is formed. A diet enriched in fish oil (rich in ω-3 fatty acids) dramatically downregulates key immunoregulatory cytokines involved in autoimmune disease.267 Mice fed fish oil for 6 weeks showed reduced fever and weight loss caused by LPS injection and did not have the rise in PGE2 that normally results from LPS activity. These changes suggest that the pathophysiology induced by toxic arachidonic acid metabolites can be reduced or prevented by dietary replacement of ω-6 fatty acids with ω-3 fatty acids.310 However, there was an exaggerated rise in TNFα, a toxin in itself, possibly because of the lack of the negative feedback from PGE2. Therefore, although these studies appear promising, they must be interpreted with extreme caution and are not recommended to guide prophylaxis for heatstroke. There has not yet appeared a clinical study showing that injection or ingestion of ω-3 fatty acids protects humans against heat illnesses. However, supplementing a normal Western diet with fish oil capsules replaces a significant proportion of ω-6 fatty acids by ω-3 fatty acids in human cell membranes within 6 weeks, and possibly much sooner.153

Cyclooxygenase Inhibitors Fever, in contrast to exercise hyperthermia, represents a physiologic state in which the hypothalamic thermostat has been reset above 37° C (98.6° F) by exogenous pyrogens released from bacteria or viruses131 or by IL-1,150,270,372 IL-2, or interferon-α and interferon-β.50 Cytokines may be responsible in part for other clinical symptoms of fever, including fatigue, malaise, and edema. αMelanocyte-stimulating hormone inhibits IL-1-induced fever and the acute phase response.335 Neutralizing antibodies to IL1 and TNF have been found in the sera of both normal and sick individuals and may play a role in their regulation.501 Current evidence suggests that aspirin-like cyclooxygenase inhibitors interfere with IL-1-induced fever or shock responses by inhibiting prostaglandin synthesis.397 Nevertheless, in an experimental model of heatstroke, rats were pretreated with aspirin and survived longer than did controls.254

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Defervation Circulating LPS reaches the thermoregulatory control center in the anterior hypothalamus, activates cyclooxygenase, and induces prostaglandins.244,358 LPS is also bound by the liver, where it stimulates the vagus nerve to signal the hypothalamus to produce prostaglandins.433 At the onset of fever, a patient often feels chilled and shivers to elevate Tc by additional metabolic heat. A new, higher, preferred ambient temperature is behaviorally established.393 The physiologic change is even more important. Once this new set point temperature is established, the thermoregulatory center uses all available thermoregulatory mechanisms to maintain it. As a result, attempts at whole-body cooling are met with sensations of extreme discomfort and violent shivering. When unsuccessful attempts to cool patients who have suspected heat illness result in chills and violent shivering, coexistent infection or disease is suggested. This prostaglandin-mediated pathway may be responsible for fever, normal circadian temperature variation, pathologic temperature elevations, and temperature elevations related to stress.41,298 Although there may be pyrogens that do not act via prostaglandins,113,262 treatment, if necessary, should be directed at agents that block the action of the pyrogen at the hypothalamic receptor sites. External application of cold to reduce true fever may be counterproductive497 and is often ineffective, even after antipyretic therapy.27,385 The body defends the higher temperature set point against environmental cooling. Therapy for fever that uses agents to block the causative molecular interaction is the most rational and clinically effective approach. Aspirin and other antipyretic agents, such as acetaminophen, indomethacin, ibuprofen, and other newer nonsteroidal anti-inflammatory compounds, are effective and act either directly or indirectly

11

through inhibition of the prostaglandin mechanism.114,372 The normal febrile response is generally self-limited in both magnitude and duration.533 Vasopressin521 and melanotropin382 appear to act centrally to suppress temperature elevation and may be important in preventing extreme hyperthermia.

Should Antipyretic Therapy Be Routine? High temperatures enhance resistance to viral and bacterial infections in experimental animals.38,81,174 For example, replication of DNA viruses is inhibited by mild hyperthermia,194,242,337 and measles virus membrane protein is selectively blocked by heating cultures to 39° C (102.2° F).394 Some host defense functions438,518 that become more effective at 40° C (104° F) than at 37° C (98.6° F) level off or diminish at 42° or 43° C (107.6° or 109.4° F).497 Although fever has long been recognized as a manifestation of disease24 and may be identified as a debilitating problem even in the absence of other signs or symptoms,527 antipyretic therapy should not be instituted routinely for every febrile episode.165,206 Furthermore, although administration of aspirin lowers fever by altering the thermoregulatory set point in the hypothalamus, it also leads to a greater rise in Tc in response to a standardized heat stress and therefore is not a universal temperature-lowering agent.156 In summary, at Tc up to approximately 40° C (104° F), the febrile process has a role in host defense, and routine antipyretic therapy for fever is generally unnecessary and may be harmful,497 especially because of the link between aspirin and Reye’s syndrome.497 Instead, treatment should be based on evaluation of relative risks.49,139,297 The references for this chapter can be found on the accompanying DVD-ROM.

Clinical Management of Heat-Related Illnesses Daniel S. Moran and Stephen L. Gaffin

This chapter discusses clinical observations of heatstroke victims and management of heat-related illnesses. In heatstroke, the most severe heat illness associated with excess body heat, early clinical signs are nonspecific. A common picture of heatstroke is sudden collapse of an individual during physical activity in a warm environment. This is usually followed by loss of consciousness with elevated core temperature (Tc) greater than 40° C (104° F), rapid heart rate (HR), tachypnea, hypotension, and, possibly, shock. Severity of heat illness depends on the

degree of elevation in Tc and its duration. Heatstroke is an extreme medical emergency that can be fatal if not diagnosed and treated promptly. Therefore, to prevent and minimize complications and save lives, proper management and clinical care are essential. This chapter focuses on the three different phases of heatstroke (acute, hematologic and enzymatic, and late), problems with recognition of heat illnesses, diagnosis and complications of heatstroke, treatment, and awareness of risk factors.

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Defervation Circulating LPS reaches the thermoregulatory control center in the anterior hypothalamus, activates cyclooxygenase, and induces prostaglandins.244,358 LPS is also bound by the liver, where it stimulates the vagus nerve to signal the hypothalamus to produce prostaglandins.433 At the onset of fever, a patient often feels chilled and shivers to elevate Tc by additional metabolic heat. A new, higher, preferred ambient temperature is behaviorally established.393 The physiologic change is even more important. Once this new set point temperature is established, the thermoregulatory center uses all available thermoregulatory mechanisms to maintain it. As a result, attempts at whole-body cooling are met with sensations of extreme discomfort and violent shivering. When unsuccessful attempts to cool patients who have suspected heat illness result in chills and violent shivering, coexistent infection or disease is suggested. This prostaglandin-mediated pathway may be responsible for fever, normal circadian temperature variation, pathologic temperature elevations, and temperature elevations related to stress.41,298 Although there may be pyrogens that do not act via prostaglandins,113,262 treatment, if necessary, should be directed at agents that block the action of the pyrogen at the hypothalamic receptor sites. External application of cold to reduce true fever may be counterproductive497 and is often ineffective, even after antipyretic therapy.27,385 The body defends the higher temperature set point against environmental cooling. Therapy for fever that uses agents to block the causative molecular interaction is the most rational and clinically effective approach. Aspirin and other antipyretic agents, such as acetaminophen, indomethacin, ibuprofen, and other newer nonsteroidal anti-inflammatory compounds, are effective and act either directly or indirectly

11

through inhibition of the prostaglandin mechanism.114,372 The normal febrile response is generally self-limited in both magnitude and duration.533 Vasopressin521 and melanotropin382 appear to act centrally to suppress temperature elevation and may be important in preventing extreme hyperthermia.

Should Antipyretic Therapy Be Routine? High temperatures enhance resistance to viral and bacterial infections in experimental animals.38,81,174 For example, replication of DNA viruses is inhibited by mild hyperthermia,194,242,337 and measles virus membrane protein is selectively blocked by heating cultures to 39° C (102.2° F).394 Some host defense functions438,518 that become more effective at 40° C (104° F) than at 37° C (98.6° F) level off or diminish at 42° or 43° C (107.6° or 109.4° F).497 Although fever has long been recognized as a manifestation of disease24 and may be identified as a debilitating problem even in the absence of other signs or symptoms,527 antipyretic therapy should not be instituted routinely for every febrile episode.165,206 Furthermore, although administration of aspirin lowers fever by altering the thermoregulatory set point in the hypothalamus, it also leads to a greater rise in Tc in response to a standardized heat stress and therefore is not a universal temperature-lowering agent.156 In summary, at Tc up to approximately 40° C (104° F), the febrile process has a role in host defense, and routine antipyretic therapy for fever is generally unnecessary and may be harmful,497 especially because of the link between aspirin and Reye’s syndrome.497 Instead, treatment should be based on evaluation of relative risks.49,139,297 The references for this chapter can be found on the accompanying DVD-ROM.

Clinical Management of Heat-Related Illnesses Daniel S. Moran and Stephen L. Gaffin

This chapter discusses clinical observations of heatstroke victims and management of heat-related illnesses. In heatstroke, the most severe heat illness associated with excess body heat, early clinical signs are nonspecific. A common picture of heatstroke is sudden collapse of an individual during physical activity in a warm environment. This is usually followed by loss of consciousness with elevated core temperature (Tc) greater than 40° C (104° F), rapid heart rate (HR), tachypnea, hypotension, and, possibly, shock. Severity of heat illness depends on the

degree of elevation in Tc and its duration. Heatstroke is an extreme medical emergency that can be fatal if not diagnosed and treated promptly. Therefore, to prevent and minimize complications and save lives, proper management and clinical care are essential. This chapter focuses on the three different phases of heatstroke (acute, hematologic and enzymatic, and late), problems with recognition of heat illnesses, diagnosis and complications of heatstroke, treatment, and awareness of risk factors.

Chapter 11: Clinical Management of Heat-Related Illnesses

269

TABLE 11-1. Comparison of Classic and Exertional Heatstroke CHARACTERISTICS

CLASSIC

EXERTIONAL

Age group Health status Concurrent activity Drug use

Older adults Chronically ill Sedentary Diuretics, antidepressants, antihypertensives, anticholinergics, antipsychotics May be absent Usually absent; poor prognosis if present Usually absent Uncommon Uncommon Mildly elevated Unusual Mild 39° C

no

Flushed skin HR >120 bpm

yes no DD

yes

Known cause

yes

yes

no yes

Heat exhaustion, suspected heatstroke

Tre > 40° C

• Cooling • IV fluids

• Cooling • IV fluids

Evacuation

Not heatstroke/ heat exhaustion

yes

Tre > 40° C

Exertional heatstroke

no

no Suspected heatstroke

Recovery

yes

Hospitalization

Follow up 24 hr

Figure 11-3. Flow chart for on-site emergency medical treatment of exertional heat illnesses. CPR, cardiopulmonary resuscitation; DD, differential diagnosis; HR, heart rate; IV, intravenous; Tre , rectal temperature. (Modified from Shapiro Y, Seidman DS: Med Sci Sports Exerc 22:6, 1990.)

tance that these measures only barely delay evacuation of the victim to a hospital or the closest medical facility. In a comatose victim, airway control should be established by insertion of a cuffed endotracheal tube. When available, administration of supplemental oxygen may help meet increased metabolic demands and treat the hypoxia commonly associated with aspiration, pulmonary hemorrhage, pulmonary infarction, pneumonitis, or pulmonary edema.56,122 Positive-pressure ventilation is indicated if hypoxia persists despite supplemental oxygen administration (Fig. 11-3).

As discussed previously, resuscitative measures may rapidly lower body temperature. Monitoring and recording Tre on site may be important for the correct diagnosis of heatstroke. Vital signs should be monitored, with attention to blood pressure and pulse. Although normotension should not be taken as a reassuring sign, hypotension should be recognized for the ominous sign it always represents. If possible, urine and blood samples should be obtained for electrolyte evaluation, especially Na+ to avoid hyponatremia, before fluid infusion.

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Vascular access should be established without delay by insertion of a large-gauge IV catheter. Administration of normal saline or lactated Ringer’s solution should be started. Recommendations regarding the rate of administration of fluids vary. Some authors advise a rate of 1200 mL (1.26 qt) over 4 hours,136 but we consider this to be too conservative. Others encourage a 2-L (2.11-qt) bolus over the first hour and an additional liter of fluid per hour for the next 3 hours.160 Vigorous fluid resuscitation may precipitate development of pulmonary edema, so careful monitoring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid should be administered during the first hour after collapse and additional fluids administered according to the level of hydration.61 Cooling measures should be initiated immediately. However, cooling techniques are ineffective when the victim suffers seizures that increase storage of body heat. Therefore, convulsions should be controlled by IV administration of 5 to 10 mg of diazepam, as necessary. As a result of drastic cooling, Tsk may decrease enough to cause shivering. IV administration of chlorpromazine (50 mg)97 or diazepam (5 mg) is effective to suppress shivering and prevent an additional rise in body temperature from metabolic heat production.

Heat-Induced Syncope In an upright and stationary person, blood volume is displaced into the dependent limbs by gravity. If that person is also heat stressed, more blood is displaced into the peripheral circulation to support heat transfer at the body surface. These combined reductions in effective blood volume can temporarily compromise venous return, cardiac output, and cerebral perfusion. Fainting is usually brief and responds to horizontal positioning and improved venous return. The patient should be allowed to rest in cooler, shadier surroundings (as the solar heat load can be >200 kcal/hr) and should be offered cool water. The patient should be cautioned against protracted standing in hot environments, advised to flex leg muscles repeatedly while standing to enhance venous return, and warned to assume a sitting or horizontal position at the onset of warning signs or symptoms, such as vertigo, nausea, or weakness. Normally, muscles in the legs act as a “second heart” and, in concert with venous valves, promote venous return, thereby counteracting orthostatic pooling and the predisposition to syncope. Consistent with this, nonfainters have higher intramuscular pressure than do fainters. In stark contrast to simple syncope is the profound CNS dysfunction dominating the early course of heatstroke. Thus, if a person faints in a setting where hyperthermia is possible and does not rapidly return to consciousness, heatstroke should be suspected, cooling measures instituted, and body temperature monitored.

Cooling Methods Much debate exists in the literature regarding the best approach to cooling heatstroke victims.37,45,75,165,180,181 Morbidity and mortality are directly related to duration and intensity of elevated Tc. Therefore, the rate at which any given method lowers body temperature is extremely important. Another consideration in choosing a cooling modality is the need for access to the victim for continuous monitoring. Proulx and colleagues142 used cooling water immersion at 2° C (35.6° F) to achieve a cooling body rate of 0.35° C/min. At water temperatures of 8, 14, and 20° C (46.4°, 57.2°, and

68° F), cooling rate was 0.19°, 0.15°, and 0.19° C/min, respectively. Shivering was seldom observed during the 20° C water immersion. In contrast, Clements and coworkers35 found no significant differences between the cooling rates of water immersion at 5.2° C and at 14° C (41.4° and 57.2° F). According to these two studies and others,78 a clear recommendation regarding optimal water temperature for cooling cannot be stated. Khogali and coworkers180 developed a body cooling unit designed to maximize evaporative cooling by maintaining cutaneous vasodilation and minimizing shivering. The patient is suspended on a net and sprayed from all sides with water at 15° C (59° F). Warm (45° to 48° C [113° to 118.4° F]) air is blown over the victim. Cooling rates of 0.06° C/min (0.11° F/min) have been obtained. Although this method is widely recommended as the treatment of choice, the rate of cooling is actually much less than that accomplished by icewater immersion. Although not always available, ice-water or cold-water immersion is an effective and easily available method of rapidly lowering core body temperature. However, its use is one of the more hotly debated topics in the heatstroke literature. In most cases, increased thermal conductivity of water results in reduction of Tc to less than 39° C (102.2° F) in 10 to 40 minutes.46 This reflects a mean rate of cooling of 0.13° C/min (0.23° F/ min)—that is, twice the rate of the body cooling unit. Use of cold water rather than ice water resulted in the same rate of cooling—0.13° C/min.136 Cold-water immersion is less uncomfortable for the victim than is immersion in ice water. In several hundred EHS victims in a military population, there were no fatalities or permanent sequelae after treatment with ice-water immersion and massage.46,136 Although other cooling methods reduce the rate of mortality, none has been as successful as ice water–soaked sheets or immersion.67 Poulton and Walker141 treated heatstroke patients by using a light helicopter as a large powerful fan to provide surface cooling and enhance evaporation of water sprayed over the patients. These authors found the method to be an efficient cooling concept. However, the helicopter rotary blade downdraft carries potential risks for the patient and medical staff attendants. In discussing an alternative cooling method, Khogali101,180 summarizes the most commonly offered criticisms of ice-water immersion: • Exposure to severely cold temperatures may cause peripheral vasoconstriction with shunting of blood away from the skin, resulting in a paradoxical rise in core temperature. • Induction of shivering (in response to the cold) may cause additional elevation in temperature. • Exposure to ice water causes marked patient discomfort. • Working in ice water is uncomfortable for medical attendants. • Accessing the patient to monitor vital signs or administer cardiopulmonary resuscitation is more difficult. • It is difficult to maintain sanitary conditions if vomiting or diarrhea develops. Although the first two criticisms may appear physiologically appropriate, review of the medical literature fails to provide documentation that a rise in body temperature after ice-water immersion or shivering is a problem.46 In fact, vascular resistance decreased during ice bath cooling and persisted until normothermia was achieved.136 This is an expected observation. The hypothalamic set point for temperature regulation is not

Chapter 11: Clinical Management of Heat-Related Illnesses raised during heatstroke (unlike during febrile illness), and brain temperature accounts for approximately 90% of the thermoregulatory response, compared with the skin’s 10%.152 The shivering response should occur only if body temperature is allowed to fall below normal. When shivering occurred, IV chlorpromazine treatment (25 to 50 mg) was effective.90 Heatstroke victims rarely require cardiopulmonary resuscitation, so this concern should not preclude use of ice baths to treat heatstroke. The documented efficacy of ice-water immersion in rapidly reducing body temperature, and therefore morbidity and mortality, overrides any consideration of transient personal discomfort for the patient or medical attendants. If other methods are used initially, any victim whose Tc does not reach 38.9° C (102.2° F) within 30 minutes after beginning treatment should be placed in a tub containing ice water or on a stretcher above the tub and covered with ice water–drenched sheets and massaged.67 The tub should be deep enough for submersion of the neck and torso. Rapidly falling Tc may not be accurately reflected by measured Tre,36 so, with any cooling technique, active cooling should be discontinued when core body temperature falls to 39° C (102.2° F) to prevent inducing hypothermia. Ducharme and colleagues,143 however, suggested that to avoid hypothermia, the cooling of body core temperatures of hyperthermic individuals should not go below 38.5° C (101.3° F)—that is, it is not necessary to eliminate all of the heat gained. In summary, ice-water treatment cools EHS patients fastest, can be easily set up with little training, is available in most hospitals without purchasing capital equipment, and may also be used on classic heatstroke victims. However, when treating older adults with classic heatstroke, a case-by-case decision should be made that balances the risk of a theoretical, but never shown, harmful stress by ice-water treatment, against the clear benefit of rapid cooling. Otherwise, cold-water or ice-water cooling is the method of choice. Various ancillary modalities have been proposed to facilitate cooling, including administration of cold IV fluids, gastric lavage with cold fluids, and inhaling cooled air. Although these therapies lower body temperature, their effects are minimal compared with ice-water immersion. Cooling blankets are ineffective for inducing the rapid lowering of body temperature required in treatment of heatstroke. Use of antipyretics is inappropriate and potentially harmful in heatstroke victims. Aspirin and acetaminophen lower temperature by normalizing the elevated hypothalamic set point caused by pyrogens; in heatstroke, the set point is normal, with temperature elevation reflecting failure of normal cooling mechanisms. Furthermore, acetaminophen may induce additional hepatic damage, and administration of aspirin may aggravate bleeding tendencies. Alcohol sponge baths are inappropriate under any circumstances, because absorption of alcohol may lead to poisoning and coma.


HOSPITAL EMERGENCY MEDICAL TREATMENT

If airway control was not previously established, a cuffed endotracheal tube should be inserted to protect against aspiration of oral secretions (Fig. 11-4). Supplemental oxygen and, when necessary, positive-pressure ventilation should be provided. Temperature should be monitored at 5-minute intervals by

279

means of an esophageal or rectal probe. Cooling measures should be maintained for Tc greater than 38° C (100.4° F). IV access should be obtained as quickly as possible. In the emergency department, IV fluid should be administered to EHS victims as a bolus of 1 L (1.05 qt). Administration of additional fluid should be based on the clinical situation after laboratory results are obtained; the object is to support the circulatory system without risk of inducing pulmonary or cerebral edema. Most heatstroke victims arrive with high cardiac index, low peripheral vascular resistance, and mild right-sided heart failure with elevated central venous pressure. Only moderate fluid replacement is indicated if effective cooling results in vasoconstriction and increased blood pressure. A Swan-Ganz pulmonary artery catheter may be necessary to assess appropriate fluid supplementation. Some victims have low cardiac index, hypotension, and elevated central venous pressure. These persons have been successfully treated with an isoproterenol drip (1 mg/min).136 Patients with low cardiac index, low central venous pressure, hypotension, and low pulmonary capillary wedge pressure should receive fluid. Cardiac monitoring should be maintained during at least the first 24 hours of hospitalization. Use of norepinephrine and other α-adrenergic drugs should be avoided because they cause vasoconstriction, thereby reducing heat exchange through the skin. Anticholinergic drugs that inhibit sweating, such as atropine, should also be avoided. As previously discussed, chlorpromazine may be used to treat uncontrollable shivering that might lead to rising body temperature. However, chlorpromazine should be used advisedly because it may cause hypotension or seizures, and its anticholinergic effects may interfere with sweating. For these reasons, some physicians prefer to use diazepam to control shivering. A Foley catheter should be placed to monitor urine output. Myoglobinuria and hyperuricemia can be prevented by promoting renal blood flow by administering IV mannitol (0.25 mg/kg) or furosemide (1 mg/kg).160 Early dialysis should be reconsidered if anuria, uremia, or hyperkalemia develops. Cooling and hydration usually correct any acid–base abnormality; however, serum electrolytes should be monitored and appropriate modifications of IV fluids made. Glucose should be monitored repeatedly because either hypoglycemia or hyperglycemia may occur after heatstroke.156 Oral and gastric secretions are evacuated via a nasogastric tube connected to continuous low suction. Although antacids and histamine-2 blockers have been used to prevent gastrointestinal bleeding, no studies to date demonstrate their efficacy in heatstroke victims. As previously discussed, clotting disturbances peak 18 to 36 hours after onset of heat injury.164 Coagulation tests (platelet count, prothrombin time, fibrinogen levels, fibrin split products) should be obtained on admission and after 24 hours. DIC may develop 24 to 72 hours after admission and is marked by acute onset of bleeding from venipuncture sites, gingivae, nasal mucosae, lungs, or the gastrointestinal tract. DIC is best prevented by rapid cooling of initial hyperthermia and replacement of clotting factors and platelets by transfusion of fresh frozen plasma and platelets. Acute hepatic dysfunction is exhibited by elevated levels of aminotransferases and bilirubin. Peak levels are seen 36 to 72 hours after collapse. These high levels may last for several days.61,125,162 Muscle damage is displayed primarily by marked elevation of serum CPK activity levels, which peak 24 to 48

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PART TWO: COLD AND HEAT

Hospitalization

CPR if required

IV Diazepam 5-10 mg

yes Seizures? no

no

Seizures controlled?

Tre > 38.5° C ?

no

yes

yes

Heatstroke

CONTROL Fluid/electrolytes balance Acid-base balance Coagulation disturbances Renal insufficiency Other disturbances

Figure 11-4. Flow chart for hospital medical treatment of exertional heat illnesses;CPR,cardiopulmonary resuscitation;IV, intravenous; Tre, rectal temperature. (Modified from Shapiro Y, Seidman DS: Med Sci Sports Exerc 22:6, 1990.)

Cooling rehydration (IV)

yes

Impaired biochemistry?

no

Follow up 48 hr

On admission and periodically CHECK Acid-base balance Electrolytes Glucose Serum enzymes Liver function tests Renal function tests Coagulation factors

hours after collapse and usually return to normal spontaneously within 5 days. Muscle and liver enzymes and bilirubin values should be carefully followed, but drastic intervention (e.g., liver transplant) is rarely necessary.

Prognosis The combination of rapid reduction of body temperature, control of seizures, proper rehydration, and prompt evacuation to an emergency medical facility results in a 90% to 95% survival rate in heatstroke victims, with morbidity directly related to duration of hyperthermia.159 A poor prognosis is associated with a Tc of greater than 41° C (105.8° F), prolonged duration of hyperthermia, hyperkalemia, acute renal failure, and elevated serum levels of liver enzymes. Therefore, misdiagnosis, early inefficient treatment, and delay in evacuation are the major

causes of deterioration in the patient’s condition. Full recovery without evidence of neurologic impairment has been achieved even after coma of 24 hours’ duration and subsequent seizures.162 Persistence of coma after return to normothermia is a poor prognostic sign.164 Neurologic deficits may persist, but usually for a limited period of 12 to 24 months, and only rarely for longer. One recent study of classic heatstroke reported that 33% of patients left the hospital with some neurologic impairment.48

Dantrolene No drug has been found to have a significant effect in reducing body temperature. Antipyretics are ineffective because the thermoregulatory set point is not affected in heatstroke. Furthermore, antipyretics might be harmful, as they cannot be readily

Chapter 11: Clinical Management of Heat-Related Illnesses metabolized in the heat-affected liver. However, dantrolene has been used quite successfully in the treatment of several hypercatabolic syndromes, such as malignant hyperthermia, neuroleptic malignant syndrome, and other conditions characterized by muscular rigidity or spasticity.171,179 Dantrolene stabilizes the Ca2+ release channel in muscle cells, reducing the amount of Ca2+ released from cellular calcium stores. This lowers intracellular Ca2+ concentrations, muscle metabolic activity, and muscle tone, and thus heat production.32,134 In some studies, dantrolene was claimed to be effective in treating heatstroke, but in others it improved neither the rate of cooling nor survival.30,49,121,173 In six rhabdomyolysis patients, intramuscular Ca2+ concentrations were 11 times higher than in controls, and dantrolene successfully lowered this elevated Ca2+.118 Collectively, the limited data available are at best inconsistent. In spite of growing evidence for a possible benefit of dantrolene treatment in heatstroke, justification for its routine use in such cases is not proved, although future clinical trials may change this assessment.9,22,116,144 Moran and colleagues126 studied dantrolene in a hyperthermic rat model. They found it effective as a prophylactic agent in sedentary animals only. Dantrolene induced more rapid cooling by depressing Ca2+ entry into the sarcoplasm. This led to relaxation of peripheral blood vessels with attenuated production of metabolic heat. Dantrolene also may be effective in treating heatstroke by increasing the cooling rate. However, in other animal models, dantrolene was not superior to conventional cooling methods.185

Neuroleptic Seizure Psychiatric patients treated with high doses of neuroleptic drugs, antidepressants, antiemetics, and other drugs52 may develop fatal neuroleptic malignant syndrome, characterized by hyperthermia as high as 42° C (107.6° F), “lead pipe” (skeletal muscle) rigidity, dyspnea, coma, extrapyramidal syndrome, rhabdomyolysis, severe metabolic acidosis, leukocytosis, and elevated creatine kinase.39,84,91 Successful treatment of these cases includes immediate withdrawal of the offending drug, administration of dantrolene, and either oral bromocriptine or the combination of levodopa and carbidopa.52


PREVENTION Prevention of heat illness relies on awareness of host risk factors, altering behavior and physical activity to match these risk factors and environmental conditions, and a requirement for appropriate hydration during physical exercise in the heat. More aggressive educational activity of the media explaining heat illness and its prevention to the public is to be strongly promoted. Primary care physicians should incorporate this information in the anticipatory guidance of routine health assessment. Despite a wealth of medical literature on heat injury, some athletic coaches continue to use physical or psychological methods to force athletes to compete or run under intolerably hot conditions. This practice should be viewed as irresponsible, dangerous, and possibly criminally negligent.

Awareness of Host Risk Factors Any underlying condition that causes dehydration or increased heat production, or that causes decreased dissipation of heat, interferes with normal thermoregulatory mechanisms and predisposes an individual to heat injury. Older individuals are less

281

heat tolerant than are younger persons to EHI, and are more susceptible to classic heatstroke because of decreased secretory ability of sweat glands and decreased ability of the cardiovascular system to increase blood flow to the skin. When healthy young adults exercise strenuously in the heat, EHS may occur despite the absence of host risk factors. In particular, persons with type II muscle fiber predominance are more susceptible to EHS because these fibers are “faster” but less efficient than are other fiber types.89 In principle, because women have a thicker subcutaneous fat layer and a Tc that is 0.4° to 0.5° C (0.7° to 0.9° F) higher during the luteal phase than in the follicular phase, they may be at greater risk for heat injury during the luteal phase, but this has not been documented in controlled studies.169 Elite and professional athletes, the general public, and the military have widely used ergogenic aids, such as the herb ephedra (ma huang) containing ephedrine, to improve performance and lose weight. Because ephedra increases metabolic rate, it has caused numerous cases of heat illnesses and deaths worldwide and is banned. Because there are no clear ergogenic benefits in using ephedra alone, use of ephedra-containing substances should be discouraged.137 In children, the ratio of basal metabolic rate to surface area is higher than it is in adults. As a result, the child’s Tsk is higher. Although the secretory rates of sweat glands are lower in children, they have greater numbers of active sweat glands per area of skin than do adults and overall greater sweat rates per unit area.88 Any reduction in sweat rates would therefore put children especially at risk. Endocrine abnormalities, such as hyperthyroidism and pheochromocytoma, cause a marked increase in heat production. Acute febrile illness, by virtue of the elevated hypothalamic set point caused by pyrogens, also leads to increased heat production. Muscular activity associated with uncontrolled gross motor seizures or delirium tremens also releases significant metabolic heat. The primary means of heat dissipation is production and evaporation of sweat. Any condition that reduces this process places the individual at risk for thermal injury. Poor physical conditioning, fatigue, sleep deprivation, cardiovascular disease, and lack of acclimation all limit the cardiovascular response to heat stress. Obesity places an individual at risk from reduced cardiac output, increased energy cost of moving extra mass, increased thermal insulation, and altered distribution of heatactivated sweat glands.128 Older adults and the young show decreased efficiency of thermoregulatory functions and increased risk of heat injury. Several congenital or acquired abnormalities affect sweat production and evaporation. Ectodermal dysplasia is the most common form of congenital anhidrosis. Widespread psoriasis, scleroderma, miliaria rubra (“prickly heat,” caused by plugging of the sweat ducts with keratin), or deep burns may also limit sweat production. Dehydration affects both central thermoregulation and sweating. A mere 2% decrease in body mass through fluid loss produces an increase in HR, an increase in Tc, and a decrease in PV. In an otherwise healthy adult, gastrointestinal infection with vomiting and diarrhea may cause sufficient dehydration to place the individual at risk for EHS. Chronic conditions that may contribute to dehydration include diabetes mellitus, diabetes insipidus, eating disorders (especially bulimia), and mental retardation. Alcoholism and illicit drug use are among the 10

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PART TWO: COLD AND HEAT

Box 11-3. Drugs That Interfere with Thermoregulation DRUGS THAT INCREASE HEAT PRODUCTION

• • • •

Thyroid hormone Amphetamines Tricyclic antidepressants Lysergic acid diethylamide (LSD)

DRUGS THAT DECREASE THIRST

• Haloperidol

Clothing Different regions of the body are not equivalent in their sweat production.87 The face and scalp account for 50% of total sweat production, whereas the lower extremities contribute only 25%. When exercising under conditions of high heat load, maximal evaporation of sweat is facilitated by maximal exposure of skin. Clothing should be lightweight and absorbent. Although significant improvement has been made in the fabrication of athletic uniforms, the uniforms and protective gear required by certain branches of the military and public safety officers continue to add to the risk of heat injury. Development of protective clothing that permits more effective heat dissipation is indicated.

DRUGS THAT DECREASE SWEATING

• • • •

Antihistamines (diphenhydramine) Anticholinergics Phenothiazines Benztropine mesylate

From references 16, 46, 81, 108, 162, 164.

major risk factors for heatstroke in the general population.104 An important effect of alcohol consumption is inhibition of ADH secretion, leading to relative dehydration. Despite evidence that hypohydration limits physical performance, voluntary dehydration continues to be routine in certain athletic arenas.9,13,28,174 Wrestlers, jockeys, boxers, and bodybuilders commonly lose 3% to 5% of their body mass 1 to 2 days before competition. In addition to restricting fluid and food, they use other pathogenic weight control measures, such as self-induced vomiting, laxatives and diuretics, and exposure to heat (saunas, hot tubs, and “sauna suits”). Athletes undergoing rapid dehydration are at risk not only for heat injury but also for other serious medical conditions, such as pulmonary embolism.47 Box 11-3 highlights common medications that interfere with thermoregulation. Special attention should be paid to the role of antihistamines in reducing sweating. This class of medications is commonly obtained over the counter, and the general population should be warned of the dangers of exercising in the heat when taking antihistamines. Although it has been widely believed that sustaining an episode of heatstroke predisposes the individual to future heat injury, this has been refuted in a recent study of heatstroke victims.14 Ten heatstroke patients were tested for their ability to acclimate to heat; by definition, the ability to acclimate to heat indicates heat tolerance. Nine of these patients demonstrated heat tolerance within 3 months after the heatstroke episode; the remaining patient acclimated to heat a year after his heat injury. In no case was heat intolerance permanent. Although individuals may show transient heat intolerance after thermal injury, evidence for permanent susceptibility to thermal injury is lacking.

Adaptation to Environmental Conditions Appropriate adaptation to hot environmental conditions encompasses many forms of behavior, including modification of clothing, degree of physical activity, searching for shade, anticipatory enhancement of physical conditioning, acclimation to heat stress, and attention to hydration.

Activity Behavioral actions can effectively minimize the occurrence of classic heatstroke. Lack of residential air conditioning places indigent persons at risk during heat waves. By sitting in a cool or tepid bath periodically throughout the day, the individual can decrease the heat stress and thereby prevent heat injury. The more than 10,000 deaths in the 2003 heat wave in Europe could have been reduced by simple announcements by public health officials of exactly this preventive measure. Modification of physical activity should not be based solely on any individual parameter of Tamb, wet bulb temperature or relative humidity, or solar radiation, as all of these contribute to heat load. The wet bulb globe temperature (WBGT) is an index of heat stress that incorporates all three factors. This value may be calculated (see Table 11-2) or obtained directly from portable heat stress monitors that measure all three parameters simultaneously to compute the WBGT. Alternatively, the heat index may be obtained from national weather stations. Current recommendations from the American College of Sports Medicine (ACSM) for prevention of thermal injuries during distance running are based on the WBGT.8 It is stated that “distance races (≥16 km or 10 miles) should not be conducted when the WBGT exceeds 28° C (82.4° F). During periods of the year when the daylight Tamb often exceeds 27° C (80° F), distance races should be conducted in the early morning or in the evening to minimize the heat load from Tamb and solar radiation.”8 In the British Army, the strenuous Combat Fitness Test (CFT) occasionally leads to heat casualties. To prevent a mean rise in Tc of 0.7° C (1.26° F) and to minimize heat illnesses, calculations indicate that the CFT should not be undertaken when the end WBGT is expected to be greater than 25° C (77° F).26 Table 11-3 presents a suggested modification of sports activity that is also based on the WBGT. Although ACSM guidelines for summer indicate that vigorous physical activity should be scheduled in the mornings or in the evenings, it should be cautioned that the highest humidity of the day is usually during early morning. In 1999, Montain and coworkers124 updated the replacement guidelines for warm weather training (see Chapter 64, Table 64-7). It is important to note that compliance with these recommendations does not remove all risk of heat injury. Developing another index of heat stress that provides a better basis for prevention of EHS is indicated. Recently, a new, userfriendly, miniaturized 5.1 × 2.5 × 1.3 cm (2- × 1- × 0.5-inch) device based on measuring Tamb and RH with microsensors was developed for assessment of heat stress.129 However, further miniaturization and evaluations of this device are required.3

Chapter 11: Clinical Management of Heat-Related Illnesses

TABLE 11-3. Modification of Sports Activity on the Basis of Wet Bulb Globe Temperature (WBGT) INDEX (°F) 2,000 —

— >25,000

— —

— —

— —

>65,200

>53,840

53,090 289,470

28,000

89,340

VOLCANO Merapi Kelut Vesuvius Etna Merapi Awu Oshima Cotopaxi Makian Papadajan Laki Asama Unzen Mayon Tambora Galunggung Nevado del Ruiz Awu Cotopaxi Krakatau Awu La Soufriere Montagne Pelée Santa María Taal Kelut Merapi Lamington Hibok-Hibok Agung Mount St. Helens El Chichón Nevado del Ruiz

Totals: GRAND TOTAL From Tilling RI: Rev Geophys 27:239, 1989.

TABLE 15-3. Fatalities from Volcanic Eruptions, 1783–2000 FATALITIES VOLCANIC HAZARD Post-eruption famine and disease epidemics Pyroclastic flows Lahars Volcanogenic tsunamis Debris avalanches Air fall Volcanic gases Lava flows TOTAL

No.

%

75,000 67,500 42,500 42,500 10,000 10,000 1,750 750 250,000

30 27 17 17 4 4 400 mg/24 hr; reduce dosage in older adults; patients with cirrhosis, 50 mg every 12 hr

COX-2, cyclooxygenase-2. From Burnham T, et al (eds): Drug Facts and Comparisons. St. Louis, Facts and Comparisons, 1999; Emermann CL, Spenetta J: Pain management in the emergency department. Emerg Med Rep 23:53–67, 2002; and Lawrence R, Rosch P, Plowden J: Magnet Therapy: The Pain Cure Alternative. Rocklin, CA, Prima, 1998.


PHARMACOLOGIC TREATMENT OF PAIN

Analgesics See Tables 17-1 and 17-2 for oral and parenteral dosage recommendations.

Opioid Analgesics Opium emerged as the first widely used narcotic analgesic by the time of the Renaissance, generally in the form of a powder or sticky gum. It was often combined with alcohol to form laudanum. Prussian pharmacist Frederich Sertürner isolated morphine from opium in the 19th century. Development of the hypodermic needle and syringe by Rynd in Ireland and Pravaz in France greatly enhanced morphine’s clinical utility in pain management.38 Narcotic agonists affect the mu (µ), kappa (κ), and delta (δ) opiate receptors in the central nervous system (CNS) and

periphery.44 Morphine and other opioids are administered orally, intranasally,48 sublingually, transdermally, subcutaneously, intramuscularly, intravenously, and rectally. Morphine is metabolized primarily in the liver; approximately 10% is excreted through the kidneys. Hepatic and renal damage impact the recipient’s response, so tolerance for a given dosage must not be presumed with these conditions. Bioavailability depends on tissue perfusion. Morphine is a potent analgesic with sedative and euphoric effects that also depresses the CNS and respiratory drive. Critical patient assessment is always required when using narcotic analgesics to detect respiratory depression and hypotension. This is particularly true in situations of hypoxia, such as occur at high altitude. Other opioid agonists include codeine, which is a controlled substance in the United States but available over the counter in many other countries, and meperidine, methadone, propoxyphene, and hydromorphone. Semisynthetic narcotics that exhibit much shorter durations of action include fentanyl and sufentanyl.

Chapter 17: Principles of Pain Management

417

TABLE 17-2. Common Parenteral Analgesics: Dosage Recommendations in 70-kg Adults DRUG

DOSAGE (mg)

INTERVAL (hr)

RISKS, PRECAUTIONS

Narcotic Agonists Codeine Fentanyl Hydromorphone Levorphanol Morphine Meperidine

15–75 IM 50–100 µg 1–2 IM 4 10–20 IM, 2.5 IV 50–100 IM, 25–50 IV

4–6 0.5–1 3–4 6–8 3–5 2–4

Oxymorphone

1

3–4

Narcotic side effects Narcotic side effects, wide range of dosages Narcotic side effects, choice over morphine in hepatic impairment Narcotic side effects Narcotic side effects Narcotic side effects, active metabolite accumulates in renal impairment and may cause seizures Narcotic side effects

Narcotic Agonists/Antagonists Buprenorphine 0.3–0.6 IM Butorphanol 2–4 IM Dezocine 5–20 IM, 5–10 IV Nalbuphine 10–20 IM, 1–5 IV

6–8 3–4 2–4 3–6

May May May May

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Ketorolac 15–30 IM, 2–5 IV

4–6

Similar to aspirin

Dissociative Analgesic/Anesthetic Ketamine 50–75 IM, 15–30 IV

2–4

Increased intracranial pressure

precipitate precipitate precipitate precipitate

narcotic narcotic narcotic narcotic

withdrawal withdrawal withdrawal withdrawal

IM, intramuscularly; IV, intravenously. From Burnham T, et al (eds): Drug Facts and Comparisons. St. Louis, Facts and Comparisons, 1999; Emermann CL, Spenetta J: Pain management in the emergency department. Emerg Med Rep 23:53–67, 2002; and Lawrence R, Rosch P, Plowden J: Magnet Therapy: The Pain Cure Alternative. Rocklin, CA, Prima, 1998.

Potential adverse side effects may include obtundation, sedation, anaphylaxis, nausea, vomiting, rash, respiratory depression, and hypotension. Narcotic antagonists such as naloxone and other emergency resuscitative medications should be available when using opioids in the wilderness, just as in the contemporary clinical setting. Potent opioid analgesics should be given with care to victims with suspected head injury or neurologic illness.57 Narcan (Naloxone) is an opioid antagonist that may reverse narcotic effects. Doses of 0.2 mg intravenously (IV), or 0.4 mg IV, intramuscularly (IM), or subcutaneously, may be given and repeated every 2 to 5 minutes until CNS, respiratory, or hypotensive narcotic symptoms are reversed, to a maximum dosage of 10 mg. Nalmefene is a similar narcotic antagonist but with a longer duration of action. Intravenous dosages of 0.25 µg every 2 to 5 minutes to a total dosage of 1 mg (four doses) may be given.6 Continuous monitoring of blood pressure, mental status, and respiratory status is critical, with possible repeat doses necessary in 1 to 2 hours. Pain may return with narcotic reversal; a balance between pain alleviation and physiologic stability is desired. Additionally, narcotic antagonists may lead to acute narcotic withdrawal symptoms in persons with a tolerance to and dependence on narcotics. Narcotic agonist-antagonist combinations first became popular with pentazocine, which causes less euphoria, but it is abused and so has addictive potential. These agents in general cause less addiction but may depress the brain and respiration,39 which may have special significance in a high-altitude setting where impaired cerebral and pulmonary function may occur. These medications do not provide the narcotic agonist effects needed in narcotic-dependent persons, so they may experience withdrawal symptoms without narcotic agonists. Familiar drugs in this class include buprenorphine, butorphanol, and nalbuphine.

Non-narcotic Analgesics Salicylates. Non-narcotic analgesics provide mild to moderate pain relief and are generally safer than narcotics. Acetylsalicylic acid (aspirin) is a mild analgesic that reduces fever, inhibits platelet function, and diminishes inflammation. It has significant GI effects including gastric irritability, erosion, and bleeding ulcers, so it is often better tolerated in an enteric-coated formulation. Persons who have a history of GI ulcers or severe indigestion should avoid aspirin. Dosage should not exceed 650 mg orally every 4 hours. Other salicylate analgesics include diflunisal, choline magnesium trisalicylate, and salsalate. The latter two have minimal GI toxicity and antiplatelet effects. Salicylates are contraindicated in persons with known allergy to the class of drugs, and in children (less than age 15 years) with viral respiratory illnesses, because their use has been linked to Reye’s syndrome.1 Para-Aminophenols. Acetaminophen is a para-aminophenol that is a mild analgesic and antipyretic.11 It has no antiplatelet, anti-inflammatory, or antiprostaglandin effect, and it is less likely than aspirin to cause serious gastric irritation. The dosage should not exceed 650 mg every 4 hours. Ingestion of more than 10 g over 24 hours may lead to severe hepatic damage; the drug should be used with extreme caution in anyone with preexisting liver disease. Many over-the-counter medications contain acetaminophen, so these should not be used in combination with pure acetaminophen or in persons with liver disease.

Nonsteroidal Anti-inflammatory Drugs Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for mild to moderate pain and may provide ample clinical benefit without concern for the respiratory depression seen with narcotic analgesics. The mechanism of action is most likely a result of inhibition of prostaglandin-mediated amplification of

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chemical and mechanical irritant effects on the sensory pathways.37 NSAIDs undergo rapid absorption after oral or rectal administration, followed by hepatic metabolism and renal excretion of their conjugated metabolites. Injectable forms of various NSAIDs, such as ketorolac, have also been developed in recent years. This nonsteroidal class of medications includes chemically unrelated compounds that are grouped together because of their therapeutic actions. These include acetic acid, propionic acid, oxicam, and pyrazolone derivatives. Adverse effects of NSAIDs include GI distress and bleeding, CNS disturbances (vertigo, drowsiness), renal dysfunction, and prolonged bleeding from platelet function inhibition. In certain circumstances, NSAID-induced immunosuppression increases propensity to bacterial infection. Indomethacin is an indoleacetic acid derivative with analgesic, antipyretic, and anti-inflammatory (antiprostaglandin) effects. Both rectal and oral administrations lead to rapid absorption. Reasonable caution should be used in persons with hepatic or renal dysfunction. Gastrointestinal toxicity has been reported with its use, including gastric ulceration and perforation, as well as bone marrow suppression. Other acetic acid derivatives include sulindac, tolmetin, ketorolac, and diclofenac. Ibuprofen is a nonsteroidal propionic acid derivative antiinflammatory agent with prostaglandin antagonist activities. It has analgesic and antipyretic properties similar to those of aspirin and acetaminophen, but it may be better for women with dysmenorrhea because its antiprostaglandin effects somewhat relax the uterus. Its anti-inflammatory properties may be very useful for arthritis and acute injuries. Like aspirin, ibuprofen can be a gastric irritant and should be avoided in persons with a history of GI ulcer, indigestion, or hiatal hernia. Oral and rectal administrations lead to rapid absorption. Ibuprofen has been reported to cause nonspecific fluid retention. Although not studied in wilderness medicine research to this point, its potential to aggravate high-altitude illnesses, from acute mountain sickness to high-altitude pulmonary or cerebral edema, should be considered. The usual dosage is 400 to 600 mg every 4 to 6 hours. Other propionic acid derivatives include naproxen, fenoprofen, ketoprofen, and flurbiprofen.11 A newer class of NSAID medications available in the United States is the cyclooxygenase-2 (COX-2) inhibitor group, consisting of celecoxib (Celebrex) and valdecoxib (Bextra), as well as the recently withdrawn medication rofecoxib (Vioxx). Rofecoxib was withdrawn in 2004 as a result of studies showing significant increases in adverse cardiovascular events in patients taking the medication continuously for 18 months.69 These medications inhibit inflammation and also demonstrate analgesic and antipyretic properties. The analgesia offered by COX2 inhibitors is similar to that of other NSAID medications, but the COX-2 inhibitors have less GI toxicity.47 The mechanism of action is believed to be through inhibition of prostaglandin synthesis via inhibition of cyclooxygenase-2. These medications may be taken orally once per day, but they are not cleared for patients younger than 18 years or for patients with advanced renal disease. Elimination is primarily via hepatic metabolism, with little of the drug recovered in the urine. Side effects primarily include GI distress, hypertension, skin rashes, and peripheral edema. The recommended dosage for rofecoxib is 12.5 to 25 mg once daily. Celecoxib may be given either 100 mg twice a day or 200 mg daily (neither method has a clinical advantage over the other). The recent demonstration of adverse

cardiac events shown in patients who are given high dosages of COX-2 may become extended to naproxen and other classes of pain medications as more data are evaluated. Dexketoprofen (Keral) is a recently developed stereoisomer of the NSAID ketoprofen. It is currently available in most of Europe and Central America, and it is being considered for inclusion in the pharmacopoeia of Africa and Asian countries, although it was removed from the market in the United Kingdom in March 2004.7,66 It is a rapidly acting analgesic with fewer GI distress symptoms than most NSAID medications. The eutomer has been separated and the inactive isomer (distomer) has been discarded to potentially reduce unwanted side effects. These changes have resulted in halving the dosage relative to ketoprofen, with similar clinical effects. The usual dosage is 25 mg three times a day, which has been tolerated on an empty stomach. Taking the medication 30 minutes prior to eating may further speed its onset of action.50,65

Dissociative Analgesia Ketamine is a dissociative anesthetic agent that has been demonstrated to provide significant analgesia. Its mechanism of action is probably related to its agonist effects on the glutamate receptor of the N-methyl-d-aspartate (NMDA) subtype.45 NMDA is thought to affect central or peripheral neuropathic pain transmission more than it does nociceptive transmission in tactile or thermal modalities.3,28 Ketamine is believed to activate µ-opioid receptors responsible for analgesia and δ-opioid receptors for dysphoria.21 As a consideration in wilderness settings where respiratory depression may be a significant concern, ketamine may provide significant analgesia, and its dissociative state, with less respiratory depression or loss of glossopharyngeal reflexes. Ketamine possesses sympathomimetic activity that may prove useful in injured persons with depressed cardiac function or shock, and it may also provide bronchodilation for victims with reactive airway disease. It is contraindicated with head injury because it increases intracranial pressure,27 which is caused by increased cerebral blood flow and direct cerebral vasodilation. Cerebral metabolic oxygen requirements increase as well.4 Ketamine is ideally administered by a trained physician with adequate monitoring capability. An intravenous dose of 0.2 to 0.4 mg/kg of ketamine provides analgesia, and 1 to 2 mg/kg IV or 2 to 4 mg/kg IM leads to profound analgesia and a dissociative state. A quiet and calm setting will diminish unpleasant dissociative experiences for the recipient.

Novel Nonopioid, Noncyclooxygenase Inhibitor Analgesics Capsaicin, the crystalline alkaloid in chili peppers (Capsicum species) that causes the heat sensation, has been used increasingly in recent decades for pain management. This odorless, colorless, tasteless alkaloid retains its potency despite time, cooking, or freezing. Capsaicin was discovered by Bucholtz in 1816 and was first synthesized by Spath and Darling in 1930.64 In fact, capsaicin refers to a complex of one synthetic and six naturally occurring and related compounds known as capsaicinoids. These compounds range in potency from mild to extremely hot to the taste or with stimulation of the mucous membranes, potentially producing severe irritation and a numbing sensation. One milligram of pure capsaicin can blister the skin and can give the feeling that a burning hot metal probe has been placed on the skin. On ingestion, the alkaloids are

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Chapter 17: Principles of Pain Management quickly metabolized in the liver and are excreted in the urine within a few hours.64 Sensory neuron depolarization occurs following topical application of capsaicin to the skin, with binding to the vanilloid receptor subtype 1 (VR-1) and a deluge of calcium ions entering the neuron. With continuous application, substance P is depleted at the nerve ending. Thus, although the first topical application of capsaicin usually produces a burning sensation, repeated applications become better tolerated, and analgesia ensues. This commonly requires a day or two of being applied four times per day until the burning sensation ceases. Some find using lower concentrations of the commercial applications allows a more tolerable process until the analgesia is established. Once established, it is important that the patient continue the daily use of capsaicin preparations to maintain the analgesia. If the application is not tolerable, a true detergent or rubbing alcohol is generally needed to remove the cream or gel preparation from the skin.61 Clinical research and practice have shown usefulness of capsaicin product creams and gels for many painful conditions including postherpetic neuralgia, trigeminal neuralgia, atypical facial pain, diabetic neuropathy, arthritis pain, postmastectomy pain, psoriasis, and epicondylitis. Wilderness medical practitioners may encounter travelers using the product on an ongoing basis for these or other conditions or may consider its use for various painful conditions experienced on an expedition. Commercial preparations are commonly found in concentrations of 0.025%, 0.05%, and 0.075%. Contact of these products with mucous membranes should be avoided. Neurotropin is an oral nonopioid, noncyclooxygenase inhibitor analgesic developed in Japan. The preparation contains an extract that is isolated from the inflamed cutaneous tissue of rabbits injected with vaccinia virus. Each tablet contains four neurotropin units of extract; the recommended dosage is one tablet twice daily.29,32 The parenteral preparation has been available in Japan for 50 years, and the oral tablets have been available for 15 years. Although it is not currently available in the United States, it is increasingly marketed and available in other countries and is a viable option for analgesia in patients engaged in wilderness and travel activities in these countries. Neurotropin is indicated in chronic and acute pain, including low back pain, neck-shoulder-arm syndrome, and postherpetic neuralgia. The most common side effects include rash and GI distress, nausea, vomiting, and anorexia. Studies have shown this medication to compare favorably in analgesic quality to ketoprofen. Its mechanism of action is thought to be inhibition of bradykinin release, as well as through the descending pain inhibitory system with effects on serotonergic 5-HT3 and noradrenergic a2 receptors in the spinal dorsal horn. It has demonstrated an increased skin temperature effect in peripheral tissues, but the mechanism of action of this effect is as yet unknown.32

Local Anesthetics Local Anesthetic Pharmacology For centuries, indigenous healers have used coca shrub leaves native to the mountains of the Andes to create a mouthnumbing effect. Gaedicke extracted the alkaloid erythroxylin in 1855, from which Niemann isolated cocaine in 1860.9 Carl Koller first reported using ophthalmic cocaine anesthesia in 1884. Subsequent enthusiasm led to the use of cocaine for anes-

TABLE 17-3. Comparable Anesthetic Dosages* for Peripheral Blocks and Local Infiltration DOSAGE (mg/kg) Amide Anesthetics Lidocaine Prilocaine Etidocaine Mepivicaine Bupivacaine Ester Anesthetics Procaine Tetracaine 2-Chloroprocaine

5 5 4 5 2 5 1–2 5

*No epinephrine included.

thesia of the nasopharynx and oropharynx for surgery of the ear, nose, and throat. Erdtman of Sweden synthesized lidocaine in 1943.9 Local anesthetics (Table 17-3) bind to sodium channels on sensory, motor, and sympathetic fibers and block nerve conduction through sodium-blocking properties in free nerve endings, peripheral nerves, spinal roots, and autonomic ganglia. Normally, the cell’s sodium-potassium pump constantly pumps sodium out of and potassium into the cell to restore membrane ionic gradients. The anesthetic renders the membrane impermeable to the influx of sodium during depolarization, and the nerve cell thus remains polarized. Anesthetic drug binding occurs within the sodium channel after the drug enters the channel from the intracellular side of the nerve membrane.12 Variables such as nerve length, rate of nerve impulse transmission, myelination, and the concentration and volume of local anesthetic determine the rate of onset and extent of therapeutic effect. Anesthetic potency and onset and duration of action depend on factors that include volume, perfusion, edema, lipid solubility, protein binding, and ionization. In general, the S stereoisomer has less toxicity and greater duration than does the R stereoisomer. Anesthetic metabolism and elimination are functions of the specific anesthetic’s chemical structure.12 Lidocaine was the first of the amino amide class of local anesthetics. It is metabolized by hepatic microsomal enzymes. Since its metabolites do not include para-aminobenzoic acid (PABA), allergic reactions are rare. Procaine is a synthetic amino ester local anesthetic. This class of anesthetic is hydrolyzed by cholinesterase to form PABA, which is responsible for the allergic reactions seen with ester anesthetics. Because the esters are relatively unstable, they do not tolerate repeated autoclaving for sterilization.8 Although no studies have specifically addressed the effects of temperature extremes on supplies in wilderness settings, it is prudent to protect these medications from heat as much as is reasonably possible. A local anesthetic may provide relief in a topical application prior to more invasive cleansing and debridement. TAC, a mixture of tetracaine (0.5%), adrenaline (1:2000), and cocaine (11.8%) in saline, may be soaked into a sterile bandage and placed directly over a wound. This combination may provide good analgesia and moderate vasoconstriction.42 However, pediatric deaths and morbidity resulting from cocaine absorption from the aqueous mixture of the original 11.8% cocaine

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solution have been reported, especially when there was mucosal absorption of the mixture. Subsequent studies demonstrated that a 5.9% cocaine mixture was also effective, and further, that a viscous preparation may decrease the likelihood of inadvertent mucosal contact. Vinci and colleagues demonstrated that the 5.9% viscous preparation was safe in 25 pediatric emergency patients when contact with mucosal surfaces was avoided .53 EMLA (the acronym for eutectic mixture of local anesthetics) is a mixture of 2.5% lidocaine and 2.5% prilocaine. After this cream is applied to intact skin under a nonabsorbent dressing for at least 45 minutes, an invasive procedure such as intravenous needle insertion or suturing of a small laceration may be more easily tolerated. EMLA is now available in 5- and 30-g tubes and as a 1-g anesthetic disc for single application.63

Anesthetic Toxicity The blood level of anesthetic after tissue injection depends on absorption, dosage, metabolism, and elimination. Increased tissue vascularity and vasoactivity of the anesthetic greatly affects blood concentration after injection. Infiltration into a highly vascular site, such as around an intercostal nerve and pleura, leads to a more rapid escalation of the blood level than injection into the less vascular subcutaneous tissues. A mixture of anesthetic and epinephrine leads to slower absorption, but this must be avoided when injecting distal extremities and digits, where epinephrine-induced vasoconstriction may lead to acute ischemic injury. Because of the possibility of unintentional direct intravascular injection, all local and regional anesthetic infiltrations should be made after negative aspiration for blood and in small aliquots between aspiration attempts. As anesthetic toxicity levels are approached, common early symptoms include circumoral numbness, tinnitus, and cephalgia. CNS toxicity in the form of seizures occurs at lower anesthetic blood levels than does cardiotoxicity in the form of ventricular arrhythmias and cardiovascular collapse. The CNS effects of lidocaine on the brain are paradoxical. At blood concentrations of 3 to 5 µg/mL, lidocaine is an anticonvulsant, whereas blood concentrations of 10 to 12 µg/mL are associated with seizures. Generally, cardiotoxicity is achieved at approximately 150% of the blood level concentration required for anesthetic CNS toxicity. Bupivacaine has demonstrated increased cardiotoxicity, out of proportion to its increased potency relative to lidocaine.12 Anesthetic allergy per se is uncommon. It is estimated that perhaps 99% of all adverse anesthetic reactions are related to pharmacologic toxicity of the anesthetic or to epinephrine mixed with the agent.12 Ester anesthetic allergies are related to PABA metabolites; therefore, intolerance to PABA-containing sunscreens may indicate allergic tendency to ester anesthetics, although this is somewhat controversial. Allergies to amide anesthetics in preservative-free vials are rare. There is no known evidence of cross-sensitivity between amide and ester anesthetic classes.

Anesthetic Infiltration Techniques and Nerve Blocks Soft tissue analgesia may be accomplished with local injection of 1% lidocaine. Generally, the maximal injectable dosage for lidocaine is 4 mg/kg. Care should be taken to inject from the wound periphery toward the center of the wound to decrease the chance of spreading bacteria or foreign matter to adjacent

tissue.42 In larger wounds, injections should proceed from an area that is previously anesthetized to lessen the discomfort of subsequent injections. Local anesthetic injection typically causes temporary pain because of the pH of the solution. Buffered solutions are available or may be created by the addition of sodium bicarbonate. Sodium bicarbonate (1 mEq/mL) is added to lidocaine or other anesthetic in a bicarbonate to anesthetic ratio of 1:10. Tolerance to the injection will also be improved by gentle and slow injection, which also allows the physician to be prudent with the total dosage of anesthetic. The addition of epinephrine is not generally recommended for soft tissue, although it may provide useful hemostasis, especially in lacerations of the head and scalp. Epinephrine should be avoided on nose tips, ear lobes, distal extremities, and digits to avoid ischemic injury and even subsequent necrosis. Many central and regional nerve blocks require special training, including a thorough knowledge of anatomy and management of potential complications. However, several blocks may be appropriate in a wilderness setting if the physician is cautious and limits the amount of anesthetic injected. All infiltrations should be made after aseptic preparation of the skin whenever possible.

Digital Nerve Block Anesthesia to the digits is easily accomplished with a lowvolume field block to the medial and lateral aspects of the digit at the base of the respective phalanx (Fig. 17-1). The digital nerves should be approached from the dorsum of the hand or foot rather than from the palm or sole. The dorsal digital nerves and proper digital nerves course along the medial and lateral aspects of the digits roughly at the 10 and 2, and at the 4 and 8 o’clock positions, respectively, in a sagittal section of the finger. A volume of 3 to 5 mL lidocaine (0.5% to1.0%) injected as a field block with a 25-gauge (or 27-gauge) needle to the medial and lateral aspects of the proximal digit will give a satisfactory digital block. An epinephrine-containing anesthetic should not be used, as this could lead to circulatory compromise and possible necrosis of the digit.

Wrist Block The entire hand may be anesthetized by blocking the three main nerves at the wrist (Fig. 17-2). The radial nerve at the wrist supplies the cutaneous branches of the dorsum of the hand, the dorsal and palmar aspects of the thumb, and distally to the dorsal aspects of the distal interphalangeal joint of the index finger, the long finger, and the radial aspect of the ring finger. Median nerve sensory distribution includes the palmar surface of the hand, the ulnar aspect of the thumb, and the palmar aspects of the index finger, the long finger, and the radial portion of the ring finger. Median nerve innervation extends dorsally over the index, long, and ring fingers to the distal interphalangeal joint. The ulnar nerve gives sensation to the palmar and dorsal surfaces of the lateral hand, the fifth finger, and the ulnar half of the ring finger.5 To perform this block, a 25-gauge needle is used to inject 2 to 4 mL of 1% lidocaine into the subcutaneous tissue overlying the radial artery. A superficial subcutaneous injection from this point and over the radial styloid will anesthetize cutaneous branches that have emerged from the proximal forearm and that extend into the hand. The median nerve is blocked with 2 to 4 mL of 1% lidocaine just proximal to the palmar wrist crease

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Site of median nerve block

Fourth digital block; Ulnar aspect

Site of radial nerve block

Radial aspect

Flexor carpi radialis tendon

A Flexor carpi ulnaris tendon

Site of ulnar nerve ring block

Figure 17-2. Landmarks for wrist block. (Photo by Bryan L. Frank, MD.) Needle entry sites

to the ulnar artery, which is radial to the flexor carpi ulnaris tendon at the level of the ulnar styloid. Again, a superficial subcutaneous injection from this site and over the ulnar styloid will block cutaneous branches that have emerged more proximal in the forearm and that extend to the hand.46

Ankle Block

Dorsal digital nerve Palmar digital nerve

B Figure 17-1. A, Site of digital nerve block. B, Digital nerve anatomy. (A, photo by Bryan L. Frank, MD.)

between the tendons of the palmaris longus and the flexor carpi radialis muscles. Injection is made deep to the volar fascia. If a paresthesia is elicited (as a result of contact with the nerve), the needle is withdrawn slightly prior to injection. The ulnar nerve is blocked with 2 to 4 mL of 1% lidocaine injected just lateral

Anesthesia of the foot is easily accomplished with blocks of the sensory nerves at the ankle (Fig. 17-3). Using a 25-gauge needle, the deep peroneal nerve, providing sensation between the great and second toes, is blocked with 5 mL of 1% lidocaine between the tendons of the tibialis anterior and the extensor hallucis longus at the level of the medial and lateral malleoli. The needle may be passed to the bone just lateral to the dorsalis pedis artery. The superficial peroneal nerve is injected with 5 mL of 1% lidocaine with a superficial ring block between the injection of the deep peroneal nerve and the medial malleolus. This will block sensation to the medial and dorsal aspects of the foot. The posterior tibial nerve is injected with 5 mL of 1% lidocaine just posterior to the medial malleolus, adjacent to the posterior tibial artery. As the needle is slowly advanced toward the nerve, eliciting a paresthesia by slightly contacting the nerve with the needle will increase the likelihood of success of the block.31 Posterior tibial nerve distribution includes the heel and plantar foot surface. Paresthesias are followed with a slight withdrawal of the needle prior to injection. The sural nerve, providing sensation to the posterolateral foot, is blocked with 5 mL of 1% lidocaine between the lateral malleolus and the Achilles tendon, followed by a subcutaneous infiltration originating from this site and over the lateral malleolus.46

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Site for sural nerve block

Site for superficial peroneal nerve block

A Site for superficial peroneal nerve block

Site for saphenous nerve block

trigger point deactivation may be accomplished with a 27-gauge needle. Injection of a trigger zone is typically performed directly into the painful myofascial point and in a four-quadrant zone from the center of the trigger point. As the needle is advanced in the central point, 0.5 mL of anesthetic is injected and then the needle is withdrawn to where the needle tip is just subcutaneous, and it is then advanced 1 to 2 cm into the adjacent tissue at a 45° to 60° angle from the skin surface in each quadrant from the center point, with 0.5 mL of anesthetic injected at each quadrant. Muscle twitches or fasciculations may accompany the injections, but they need not be sought. A volume of 2 to 3 mL of 1% lidocaine is usually ample for each trigger zone. There is no benefit to adding corticosteroids to the anesthetic. Using an acupuncture needle (or a 27- or 30-gauge needle) may deactivate the trigger zones nicely using a similar four-quadrant pecking of the myofascial zone, without injection of anesthetic. In this technique, the acupuncture needle is simply advanced centrally into the trigger zone and then briskly advanced and retracted several times. Then, as with the injection technique, the needle is partially withdrawn so that the needle tip is just subcutaneous, and then it is redirected to each of the four quadrants around the central point, briskly pecking in each quadrant as at the central point. A 1- to 11/2-inch needle may be used to peck briskly several times in each direction, and also at a 45° to 60° angle from the center of the trigger zone. Depth of insertion is typically 1 to 2 cm. Soiled skin should be prepared as for an intramuscular injection.

Intravenous Regional Anesthesia by Bier Block

B Figure 17-3. Landmarks for ankle block. (Photo by Bryan L. Frank, MD.)

Trigger Point Injections Persons who suffer from neck and shoulder or lower back strain may benefit greatly from deactivation of myofascial trigger zones (Fig. 17-4). The pain relief may be profound and may enable an adventure to continue without disruption. Travell and Simons have extensively described primary and secondary painful points and their referral patterns. Myofascial pain may be intense and may be referred to a large zone of the body.51 Successful deactivation of trigger zones may be accomplished with either dry needling (acupuncture) or injection of 1% lidocaine. In the absence of anesthetic or acupuncture needles,

The Bier block may provide sufficient anesthesia for a physician unfamiliar with the anatomy and technique of a more sophisticated proximal nerve block to stabilize an arm or a leg fracture (Fig. 17-5). Because a tourniquet is necessary, a Bier block should not be used for longer than 60 minutes. A vein of the hand or foot on the extremity to be blocked is cannulated with a 20- to 22-gauge intravenous or butterfly catheter, which is then capped and taped in place. The extremity is then raised above the level of the heart for 1 to 2 minutes to diminish the volume of blood in the distal limb. If tolerated, an Esmarch (rubber) or elastic bandage is wrapped from the hand or foot toward the proximal arm or leg to exsanguinate the limb. If a compression bandage is not tolerated, adequate exsanguination may occur by elevating the extremity for 5 to 10 minutes, or by applying an inflatable splint. A tourniquet is applied and the pressure is held at 50 to 100 mm Hg above systolic blood pressure. In the wilderness, a blood pressure cuff would be an effective tourniquet, or a strap, rope, or tubing may be used. The limb is then placed horizontally for the injection, using 25 mL of 1% lidocaine for the upper extremity and 35 mL for the lower extremity. The anesthetic is slowly infused through the previously inserted intravenous or butterfly catheter at a rate of approximately 0.5 mL/sec. Caution should be taken to avoid extravasation of the anesthetic into the surrounding tissues. Anesthesia will ensue over the first 10 to 15 minutes as the lidocaine diffuses from the intravascular space and binds to the soft tissue. It is important to discontinue the injection if the tourniquet pressure is not maintained during the injection to prevent anesthetic toxicity from an unrestricted intravenous bolus injection. The tourniquet should remain inflated for 60

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4-Quadrant injection technique

Syringe/needle

Figure 17-4. Trigger point injections. Trigger point surface location

Trigger point

Skin

Skin surface view

Subcutaneous tissue Muscle Lateral view

ary amine tricyclic drugs, such as amitriptyline, imipramine, doxepin, and clomipramine, are commonly used for pain problems. Antidepressant medications are presumably effective for treating chronic pain problems because they block presynaptic reuptake of serotonin and/or norepinephrine by the amine pump.2 The drugs are rapidly absorbed after oral administration, although this may be decreased by antimuscarinic effects. They are highly protein bound and have half-lives of 1 to 4 days. They are generally oxidized by the hepatic microsomal system and conjugated with glucuronic acid. Elimination occurs via urine and feces.25 Side effects may include dry mouth, urinary retention, constipation, and hyperactivity.20 Photosensitivity may place wilderness travelers at risk for sunburn, and orthostatic hypotension may lead to falls. Patients with overdoses present with excessive sedation, anticholinergic effects on the cardiac conduction system, significant hypotension, respiratory depression, arrhythmias, and coma. Figure 17-5. Preparation for intravenous regional block using field supplies. (Photo by Bryan L. Frank, MD.)

minutes maximum, at which time most of the anesthetic should be protein bound in the soft tissues. The tourniquet may then be released on a single occasion, whereupon the anesthetic effect will diminish within 5 to 10 minutes.

Adjuvant Pharmaceuticals Pharmaceutical agents other than analgesics and local anesthetics may offer significant relief and may avoid or decrease the potential adverse effects of analgesics and anesthetics.

Antidepressants Wilderness travelers may be taking antidepressant medications for chronic pain or psycho-emotional dysfunction. Continuation of these medications is important to avoid intensification of pain or psycho-emotional lability. Chronic pain conditions that may benefit from antidepressants include migraine cephalgia, postherpetic neuralgia, and diabetic neuropathy. The terti-

Anticonvulsants Of the heterogeneous group of drugs classified as anticonvulsants, nine have been useful as adjuvant medications in pain management: phenytoin, valproic acid, topiramate, levetiracetam, lamotrigene, neurontin, pregabalin, carbamazepine, and clonazepam. Their chemical structures bear little relationship to each other. Serum levels have not been clearly established as useful parameters in pain management. The mechanism of action of each of these drugs is unique and varies from altering sodium, calcium, and potassium flux, to enhancing GABA activity or binding.25 Side effects vary but may include nausea, vomiting, and CNS effects such as drowsiness, ataxia, and confusion. It is important to rule out drug effects as a factor in wilderness-related illnesses. It is not recommended that these drugs be used for acute management of pain in the wilderness.

Antihistamines Antihistamines may be useful as adjuvants in a wilderness travel setting. Specifically, hydroxyzine seems to provide an additive

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TABLE 17-4. Skeletal Muscle Relaxants DRUG Baclofen

DOSAGE (mg)

INTERVAL (hr)

Carisoprodol

3–5 start, increase 8 5 mg every 3 days 350 4–6

Chlorphenesin

400

6–8

Chlorzoxazone Cyclobenzaprine

250–750 10

4–6 12–24

Diazepam

2–10

6–8, variable

Metaxalone Methocarbamol Orphenadrine

800 1000–1500 100

6–8 4–6 8–12

RISKS, PRECAUTIONS Dizziness, ataxia, confusion, severe abrupt withdrawal Dizziness, ataxia, headache, tremor, syncope, severe abrupt withdrawal, contraindicated with acute intermittent porphyria Confusion, headache, dizziness (8 weeks or less); avoid in patients with hepatic disease Dizziness, paradoxical stimulation, rare severe hepatotoxicity Anticholinergic; may cause hypotension, arrhythmias; avoid with MAOI use and in patients with hypertension, CHF, arrhythmia, glaucoma, urinary retention, severe depression, or suicide attempts Dizziness, paradoxical stimulation, cardiopulmonary depression; use only in patients with severe anxiety Hepatic impairment, rash, dizziness, headache; avoid with drug-induced anemia Dizziness, headache, rash Anticholinergic; headache, dizziness

CHF, congestive heart failure; MAOI, monoamine oxidase inhibitors.

analgesic effect in combination with narcotic analgesics, while also lending antiemetic and sedative properties. Hydroxyzine may cause ataxia and disinhibition, and it has, rarely, been associated with convulsions in high dosages.25 A dosage of 50 to 100 mg IM may improve clinical pain management. Similarly, oral antihistamines, such as diphenhydramine 25 to 50 mg, may provide useful adjuvant effects.

Muscle Relaxants Muscle relaxants (Table 17-4) are a diverse group of drugs with similar clinical effects but different pharmacologic properties. They are not true skeletal muscle relaxants in the sense of blocking neuromuscular transmission. Rather, they act by depressing reflexes in a general fashion in the CNS. They are indicated for the relief of muscle spasm related to acute, painful, musculoskeletal injuries. Side effects of these centrally acting muscle relaxants include decreased alertness, motor coordination, and physical dexterity, as well as nausea, vomiting, and abdominal pain. Recent studies have shown muscle relaxants to be effective in the management of low back pain. Efficacy is probably increased when muscle relaxants and NSAID analgesics are used in combination.17 Common centrally acting muscle relaxants include carisoprodol (Soma, 350 mg PO three times a day to four times a day), metaxalone (Skelaxin, 800 mg per os [PO] three times a day to four times a day), and methocarbamol (Robaxin, 1.5 g PO four times a day for the first 48 to 72 hours, then 1 g PO four times a day). The specific mechanism of action of these agents in humans is unknown, but it appears to be related to centrally acting sedation. Cyclobenzaprine (Flexeril, 10 to 20 mg PO three times a day) is structurally related to the tricyclic antidepressant medications. Diazepam (Valium, 2 to 10 mg PO, IM, or IV) is a benzodiazepine that induces calm and anxiolysis via effects on the thalamus and hypothalamus.6 Tizanidine (Zanaflex, 8 mg three times a day) is an α-2 agonist with musclerelaxing properties.

Intra-articular Injections of Hyaluronan Substances Travelers with degenerative osteoarthritis (OA) of the knees may find hiking, trekking, and other wilderness activities very

painful, reducing their ability to participate in these activities. However, some may engage in these activities and experience exacerbation of their symptoms while in a remote or wilderness setting. These exacerbated symptoms may impact the pleasure and safety of the travelers and their companions. OA is felt to be related to decrease in the amount or quality of hyaluronan. Synvisc is a gel-like mixture of hylan A and hylan B polymers (derived from the hyaluronan of chicken combs) and saline. Injection of this “drug-free” hylan complex has proved to be useful to many sufferers of OA, with significant reductions in oral analgesic use. Studies have not demonstrated efficacy in less than a series of three weekly injections; thus, immediate response to injection in the wilderness setting should not be expected.66


HIV/AIDS—SPECIAL WILDERNESS CLINICAL CONSIDERATIONS

With advances in treatment of patients with acquired immunodeficiency syndrome (AIDS) and human immunodeficiency virus (HIV) infection, many are pursuing more activities and living healthier lives than a decade ago. These activities include travel into wilderness and remote locations. For many of these travelers, HIV/AIDS is undertreated and misdiagnosed. An estimated 85% of HIV/AIDS patients receive inadequate therapy, which can significantly reduce their quality of life and options for wilderness travel.68 Patients with HIV/AIDS commonly experience pain, which may include headaches, oropharyngeal pain and odynophagia, earaches, abdominal and chest pain, myalgias, and arthralgias. New or unexplained pains should initiate a medical investigation so that pain therapeutic agents do not mask emerging associated illnesses. Associated diseases that may lead to pain in these patients include neuropathies, postherpetic neuralgia, avascular necrosis of the hip, osteopenia, myopathies, renal calculi, herpes simplex, candida esophagitis, and pancreatitis. Additionally, various diagnostic and therapeutic procedures may initiate or increase pain for these patients. As seen in the peripheral neuropathies of patients with HIV/AIDS, the virus may attack the nerve endings in the extremities, with resulting

Chapter 17: Principles of Pain Management burning, numbness, and dysesthesias. This is often referred to as distal symmetrical polyneuropathy (DSP), and it may prevent or complicate these patients’ wilderness endeavors. Additionally, therapeutic medications may also lead to pain in patients with HIV/AIDS, as is seen with didanosine, dicalcitabine, isoniazid, Videx (ddI), and Zerit (d4T).67,68 Treatment of pain in patients with HIV/AIDS commonly includes oral non-narcotic and narcotic medications. Aspirin, acetaminophen, and NSAIDs are commonly utilized for mild to moderate pain, whereas opioids are the primary therapeutics for severe pain. Many physicians are reluctant to prescribe narcotics to patients because of potential addiction, studies show the risk for addiction in patients with HIV/AIDS to be small. Longer-acting medications, including methadone and timerelease morphine, may offer greater pain management and allow increased wilderness activities. The fentanyl patch transdermal system providing medication release over three days may significantly help those who poorly tolerate oral administration. Adjuvant medications, including caffeine, antihistamines, anticonvulsants, and antidepressants, should be considered so that significant pain relief can be obtained with lower narcotic dosages and thus lower opioid side effects. Persons with a narcotic addiction either prior to or subsequent to narcotic pain management will need to have very strict limits and guidelines set by a specialist in addiction medicine. Drug interactions are of concern, as various anti-HIV medications may interfere with narcotic medications. Ritonavir (Norvin) increases levels of meperidine, propoxyphene, and fentanyl, and efavirenz and nevirapine lower the methadone level. Phenytoin lowers the methadone level and NSAIDs increase the lithium level. These medication interactions are also important to consider for over-the-counter medications, for botanical and herbal remedies, and for illicit drugs as well. Tobacco smoking shortens the half-life of NSAIDs and increases the metabolism of meperidine, morphine, and propoxyphene. Cannabis is known to increase the effect of morphine, ritonavir increases the level of MDMA (methylenedioxymethamphetamine; Ecstasy) and alcohol increases the abacavir (Ziagen) level.67




COMPLEMENTARY AND ALTERNATIVE MEDICINE THERAPIES

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Figure 17-6. Typical acupuncture needle placement for lateral ankle strain.(Photo by Bryan L. Frank, MD)

Figure 17-7. Typical acupuncture needle placement around injured knee. (Photo by Bryan L. Frank, MD.)

Complementary and alternative are terms used to denote therapies and modalities that may not be supported by Westerndesigned prospective, randomized studies, that are not commonly taught in U.S. medical colleges, or that are not generally covered by traditional health insurance plans.55 Some of these therapies can provide a significant contribution to the management of pain in the wilderness.

Acupuncture Acupuncture developed over the past 3 to 5 millennia in Asia, and it has been practiced over the past several hundred years in the Western world. In many cases, acupuncture developed in geographic areas and under social conditions very similar to the primitive or undeveloped conditions familiar to wilderness travelers. The use of acupuncture by physicians to treat trauma and illness in wilderness settings has been described recently in medical literature.22,24 Properly administered, acupuncture should have a very low risk of morbidity and may be extremely

Figure 17-8. Patient with auricular needles in place. (Photo by Bryan L. Frank, MD.)

effective in alleviating pain and even restoring function to an injured wilderness traveler (Fig. 17-6 through Fig. 17-9). Stux and Pomeranz, and others, have demonstrated endorphin, enkephalin, monamine, and adrenocorticotropic hormone (ACTH) release with acupuncture stimulation.49 Furthermore,

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Tendinomuscular meridian treatment lateral ankle sprain

Box 17-3. Pain Management First Aid Kit* BASICS

Esmarch bandage, 3 × 36 inches Tourniquet Hot and cold gel packs SI 18 Gathering point

ORAL MEDICATIONS

Acetylsalicylic acid (ASA), 500 mg Acetaminophen, 500 mg Carisoprodol (Soma), 350 mg, or metaxalone (Skelaxin), 500 mg Diazepam (Valium), 5-mg tabs Hydrocodone, 5-mg tabs INJECTABLE MEDICATIONS

Local points

Naloxone, two ampules, 0.4 mg each Ketamine, 50 mg/mL, 5 to 10 mL Lidocaine 1%, 30 mL Procaine 1%, 30 mL Midazolam (Versed), 5 mg/mL, 5-mL vial Morphine, 5 mg/mL, 5 mL Meperidine (Demerol), 50 mg/mL, 5 mL TOPICAL THERAPIES

Jing-well (opening) points BL 67, GB 44 (rt)

Figure 17-9. Tendinomuscular meridian treatment for lateral ankle sprain. (From Frank BL: Medical acupuncture in wilderness and Third World settings.Wilderness Med Lett 14:1, 1997.)

the gate theory of pain modulation and altered sympathetic activity33 may apply as well. Clinically, improved microvascular circulation may lead to decreases in tissue edema, which in turn may diminish pain and aid in restoring function. Release of ACTH leads to increased circulating corticosteroids; decreased inflammation may contribute to decreased pain and improved healing.30 Contemporary medical acupuncturists are typically trained in a variety of styles or traditions. Many physicians utilize a combined approach of acupuncture point selections based on neuroanatomy and those that are felt to have energetic effects in the body. Additionally, acupuncture microsystems are often employed, in which the entire body is represented in a small area such as the ear, scalp, or hand. These microsystems are often quite beneficial for acute pain relief (see Figure 17-8).24 Sterile acupuncture needles are compact, lightweight, and easy to include in a daypack or first-aid kit (Box 17-3). Integration of acupuncture into the biomedical care of wilderness trauma, pain, and illness may dramatically enhance patient comfort and facilitate extrication from a remote setting. For example, a common clinical case that often responds to acupuncture is a sprained ankle. An energetic style of acupuncture that is especially useful for common trauma utilizes the tendinomuscular meridians (TMMs) of the acupuncture energetic subsystems. The indications for activation of the TMMs treatment include acute strains, sprains, abrasions, and hematomas. The method of activation for this style of treatment is to place a needle in the “Jing-well” or “Ting” point of one

Arnica cream, 5-mL tube Capsaicin ointment, 2-g tube TAC (mixture of tetracaine [0.5%], adrenaline [1 : 2000], and cocaine [11.8%] in saline), 10 mL† Biomagnets (200 to 800 gauss), two to four small ADDITIONAL SUPPLIES

Intravenous (IV) cannula, 20-gauge, three IV cannula, 18-gauge, three IV tubing, two Normal saline, 500 mL IV D5LR (5% dextrose in lactated Ringer’s), 500 mL Acupuncture needles, 50 *Items subject to training and scope of practice. This pain kit is in addition to regular first-aid kit. † EMLA (2.5% lidocaine and 2.5% prilocaine) should be used if there is a concern for cocaine toxicity.

to three of the meridians involved in the lesion. This is followed by placing a needle in the “gathering point” for the meridians, then by placement of needles around the area of induration, swelling, or bruising, approximately 1 cm out from the edge. All needles in this treatment are placed only 2 to 3 mm deep and are left in place for 20 to 45 minutes. Commonly, a lateral ankle sprain involves both the gallbladder and bladder TMM zones. The Ting (Jing-well) points for these meridians are at GB 44 and BL 67 on the lateral angles of the fourth and fifth toes, respectively. The gathering point for these meridians is at SI 18, just below the zygoma in line with the lateral canthus. Locally, four to six needles are typically placed around the swelling or ecchymosis of the ankle sprain (see Figure 17-9). Recovery from the sprain may proceed much more rapidly with this acupuncture input than with the conventional therapies of rest, ice, compression, and elevation (RICE) alone. Failure to achieve 70% to 85% or greater decrease in pain over 24 to 48 hours may alert the medical

Chapter 17: Principles of Pain Management acupuncturist that an injury is more serious than initially appreciated. Most acupuncture treatment requires substantial training to be responsibly integrated with conventional Western therapies. National and international standards of training have been established for Western-trained physicians who desire to incorporate acupuncture into their traditional medical practices. The American Academy of Medical Acupuncture (AAMA) is the professional organization representing U.S. physician acupuncturists whose training meets or exceeds standards established by the World Health Organization’s affiliate, the World Federation of Acupuncture and Moxibustion Societies. Physicians interested in learning acupuncture may contact the AAMA (www.medicalacupuncture.org) for information on training programs designed specifically for physicians. The National Commission for Certification of Acupuncture and Oriental Medicine provides testing and resources primarily for U.S. nonphysician acupuncturists.23 The International Council of Medical Acupuncture and Related Techniques (ICMART) is composed of approximately 84 physician acupuncture organizations from around the world and provides international educational congresses and symposia.

Herbal and Botanical Remedies The term herb is broadly defined as a nonwoody plant that dies down to the ground after flowering. The term botanical is a more general description of flora, although common interpretation describes any plant used for medicinal therapy (see Chapter 60), nutritional value, or food seasoning or dyeing (coloring).14 The use of botanicals, like the use of acupuncture, may be encountered in wilderness travels as a part of the indigenous culture and medical care. Botanicals are often prepared as infusions, with the plant’s soft portions placed in a pot and covered by boiling water to create a supernate. Herbal decoctions are traditionally prepared in special earthen crocks or in containers of stainless steel, ceramic, or enamel by contemporary practitioners, specifically avoiding aluminum and alloyed metal pots. The herb is placed in the container and covered with cold water that is then boiled, covered, and simmered. Travelers may encounter an herbal remedy intended to be applied to the skin, dispensed as a poultice, a botanical liniment, an ointment, or an oil. Alternatively, many modern herbalists utilize capsule forms of herbs for ease of administration. Combinations of several herbs are often more effective than a single herb, and common formulas have been recorded worldwide for centuries.33 Appropriate application or prescription of botanical products rarely leads to toxicity or adverse reactions, although such are possible if botanicals are used excessively or carelessly. Botanical products that have been used for pain include morphine, isolated from the opium poppy, and cocaine, from coca leaves (Erythroxylum coca). Often used as a seasoning or food, oregano (Origanum vulgare) has been reported to be beneficial for rheumatic pain.33 Sunflower (Helianthus annuus) is a source of phenylalanine, useful for general pain. Turmeric (Curcuma longa) contains curcumin, an anti-inflammatory substance that is beneficial for rheumatoid arthritis, and ginger (Zingiber officinale) is beneficial for rheumatoid arthritis, osteoarthritis, and fibromyalgia. Clove (Syzygium aromaticum) is endorsed by the German botanical resource, Commission E, topically for dental pain, and red peppers (Capsicum species) contain substance P–depleting capsaicin and also salicylates. Often taken as an infusion or decoction, kava kava (Piper methysticum) contains

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both dihydrokavain and dihydromethysticin, which have analgesic effectiveness similar to that of aspirin. Evening primrose (Oenothera biennis) is a great source of tryptophan and has been demonstrated to relieve pain associated with diabetic neuropathy. Lavender (Lavandula species) contains linalool and linalyl aldehyde, which appear to be useful, in topical and aromatherapy form, for pain of burns and other injuries.14 Willow (Salix species), which has been used to treat pain since 500 bc, contains salicin and other salicylate compounds. Commission E has recognized willow as an effective pain reliever for headaches, arthritis, and many other pains. Other salicylate-containing plants include wintergreen and birch bark. All botanicals containing salicylates should be avoided in persons who are sensitive or allergic to aspirin products. Furthermore, children who have viral infections such as a cold or influenza should avoid these products, as salicylates have been implicated in the development of Reye’s syndrome.14 Chamomile (Matricaria chamomilla) contains chamazulene, which is reportedly beneficial for abdominal pain related to GI spasm or colic. As an antihistaminic, it has mild calming or sedative properties. It is used in Europe to treat leg ulcers and may be beneficial for painful, irritated bites and stings.14 Plantain major (Plantago major) is also commonly useful for bites and stings, poison ivy discomfort, and toothache, and it has been used traditionally by Native Americans as a wound dressing. Aloe gel (Aloe vera) has been used since ancient times to treat burns and sunburn and to promote wound healing. Especially useful for sprains and strains is the mountain daisy or arnica (Arnica montana), which is also endorsed by the German Commission E. Arnica was in the U.S. Pharmacopoeia from the early 1800s to the 1960s, and it has long been used by Native Americans and others for relieving back pain and other myofascial pains and bruising. It is used topically or internally, often in homeopathic form. Comfrey (Symphytum officinale) has been used since ancient Grecian times for skin problems.15 It contains alloin, which is anti-inflammatory, and is endorsed by Commission E to topically treat bruises, dislocations, and sprains. Comfrey has experienced a controversial safety record because oral ingestion of its pyrrolizidine alkaloids has been associated with hepatotoxicity and carcinogenicity.14 For this reason, only topical use of comfrey is recommended.

Magnet Therapy Magnet therapy has been described for approximately 4000 years in the Hindu Vedas and the Chinese acupuncture classic, Huang Te Nei Ching. The application of magnetic stones, or lodestones, is said in ancient legends of Cleopatra and others to have decreased pain and preserved youth. Early Romans used the discharge of the electric eel to treat arthritis and gout.35 Danish physicist Oerstad proved in 1820 that an electric current flowing through a wire had its own magnetic field. (In modern medicine, the most familiar use of magnetic energy is in magnetic resonance imaging.) There are various theories about the effectiveness of permanent magnets for use in pain and healing. Lawrence and coworkers reported increased blood circulation and increased macrophage activity,35 and others have hypothesized effects on peripheral nerves, including blockage or modification of sensory neuron action potentials and enhanced regeneration of peripheral nerves.36,40,43,54 Most permanent magnets marketed at this time for management of pain are approximately 200 to 1200 gauss in strength. At this level, there is little, if any, risk in trying a magnet for

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pain reduction, assuming the patient is properly evaluated to provide other care when appropriate. This author has seen the benefits of magnets in his pain medicine practice over many years. Many patients report significant pain reduction within hours; others report relief after wearing the magnets for a week or more. In wilderness travel, it is reasonable to carry a few therapeutic magnets, as they are usually lightweight, compact, and unbreakable. Magnets marketed for pain therapy range in size from a 2-inch (5 cm) circle to a 6- by 12-inch (15–30 cm) rectangular pad. Most are only a few millimeters thick, and they

18

are often flexible. These are becoming more readily available through multilevel marketing, television infomercials, health food stores, and the internet. Some people have also experienced pain relief with simple, small magnets such as those used to place notes and photographs on a refrigerator. The magnet should be placed directly over the area of pain, and it can be held in place with tape, clothing, or straps. The references for this chapter can be found on the accompanying DVD-ROM.

Bandaging and Taping Daniel Garza

Taping and bandaging are both useful skills in wilderness medicine. Taping can be used to support injured joints and soft tissues; bandaging is most often used to secure a wound dressing (Fig. 18-1). Bandaging with an elastic wrap is an alternative to taping and, over larger joints, such as the knee, is often preferable. In general, taping requires practice, but some simple techniques can be easily mastered. It is most often utilized in mild to moderate sprains and strains, where some functional capacity such as weightbearing and lifting are maintained. Although taping offers dynamic support, it is in no way comparable to splinting, which can immobilize an extremity. The most common tape applied is white athletic (or adhesive) tape, often used by trainers in organized sports. Athletic tape may be applied to skin, although it may lose adhesion if the body part is not shaved and tape adhesive not applied. Some keys to successful taping include the following: • Avoid leaving any gaps in the tape because these will lead to blisters. • Avoid excessive tension on tape strips that serve to fill these gaps. • Apply tape in a manner that follows the skin contour to avoid wrinkles. • Try to overlap a half-width on successive strips. Bandaging is accomplished by either elastic wraps or gauze rolls of various widths. Once a dressing is applied to a wound, appropriate bandaging allows the patient to feel confident that it will remain secure throughout reasonable amounts of activity. Regardless of the method used, it is important to remember that taping and bandaging, especially when circumferential, should not be so tight as to limit circulation. Signs and symptoms of overly tight application are similar to a mild compartment syndrome, classically characterized by the five P’s:

Pain Pallor Paralysis Pulselessness Paresthesias


TAPING Types of Tape Athletic tape is composed of fibers woven into strips that are coated with zinc oxide, an adhesive compound. Although most commonly colored white, athletic tape is available in a variety of colors. This is the most commonly used tape in athletics and first aid for support and prevention of injury. It is available in a variety of widths. Although the major advantage of athletic tape is versatility, its major disadvantage is the tendency of zinc oxide to lose adhesive properties with heat and moisture, thus resulting in loss of support when the patient sweats. There are a variety of techniques used to increase the durability of athletic tape under these conditions, described later in this section. Elastic tape (e.g., Elastikon by Johnson & Johnson) is cotton elastic cloth tape with a rubber-based adhesive. The elasticity of the tape allows for greater flexibility and is particularly useful for large joints such as the knees or shoulders.

Skin Preparation Skin preparation involves measures meant to increase longevity of tape adhesion and patient comfort. If tape is to be applied directly to the skin, the area is usually shaved to remove hair that may interfere with direct contact. Care must be taken to avoid small abrasions in the skin when shaving because these can serve as sites of infection. If the area cannot be shaved in a clean and deliberate manner, it may be advisable to avoid. Any

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pain reduction, assuming the patient is properly evaluated to provide other care when appropriate. This author has seen the benefits of magnets in his pain medicine practice over many years. Many patients report significant pain reduction within hours; others report relief after wearing the magnets for a week or more. In wilderness travel, it is reasonable to carry a few therapeutic magnets, as they are usually lightweight, compact, and unbreakable. Magnets marketed for pain therapy range in size from a 2-inch (5 cm) circle to a 6- by 12-inch (15–30 cm) rectangular pad. Most are only a few millimeters thick, and they

18

are often flexible. These are becoming more readily available through multilevel marketing, television infomercials, health food stores, and the internet. Some people have also experienced pain relief with simple, small magnets such as those used to place notes and photographs on a refrigerator. The magnet should be placed directly over the area of pain, and it can be held in place with tape, clothing, or straps. The references for this chapter can be found on the accompanying DVD-ROM.

Bandaging and Taping Daniel Garza

Taping and bandaging are both useful skills in wilderness medicine. Taping can be used to support injured joints and soft tissues; bandaging is most often used to secure a wound dressing (Fig. 18-1). Bandaging with an elastic wrap is an alternative to taping and, over larger joints, such as the knee, is often preferable. In general, taping requires practice, but some simple techniques can be easily mastered. It is most often utilized in mild to moderate sprains and strains, where some functional capacity such as weightbearing and lifting are maintained. Although taping offers dynamic support, it is in no way comparable to splinting, which can immobilize an extremity. The most common tape applied is white athletic (or adhesive) tape, often used by trainers in organized sports. Athletic tape may be applied to skin, although it may lose adhesion if the body part is not shaved and tape adhesive not applied. Some keys to successful taping include the following: • Avoid leaving any gaps in the tape because these will lead to blisters. • Avoid excessive tension on tape strips that serve to fill these gaps. • Apply tape in a manner that follows the skin contour to avoid wrinkles. • Try to overlap a half-width on successive strips. Bandaging is accomplished by either elastic wraps or gauze rolls of various widths. Once a dressing is applied to a wound, appropriate bandaging allows the patient to feel confident that it will remain secure throughout reasonable amounts of activity. Regardless of the method used, it is important to remember that taping and bandaging, especially when circumferential, should not be so tight as to limit circulation. Signs and symptoms of overly tight application are similar to a mild compartment syndrome, classically characterized by the five P’s:

Pain Pallor Paralysis Pulselessness Paresthesias


TAPING Types of Tape Athletic tape is composed of fibers woven into strips that are coated with zinc oxide, an adhesive compound. Although most commonly colored white, athletic tape is available in a variety of colors. This is the most commonly used tape in athletics and first aid for support and prevention of injury. It is available in a variety of widths. Although the major advantage of athletic tape is versatility, its major disadvantage is the tendency of zinc oxide to lose adhesive properties with heat and moisture, thus resulting in loss of support when the patient sweats. There are a variety of techniques used to increase the durability of athletic tape under these conditions, described later in this section. Elastic tape (e.g., Elastikon by Johnson & Johnson) is cotton elastic cloth tape with a rubber-based adhesive. The elasticity of the tape allows for greater flexibility and is particularly useful for large joints such as the knees or shoulders.

Skin Preparation Skin preparation involves measures meant to increase longevity of tape adhesion and patient comfort. If tape is to be applied directly to the skin, the area is usually shaved to remove hair that may interfere with direct contact. Care must be taken to avoid small abrasions in the skin when shaving because these can serve as sites of infection. If the area cannot be shaved in a clean and deliberate manner, it may be advisable to avoid. Any

Chapter 18: Bandaging and Taping obvious abrasion should be covered with a thin layer of gauze or small adhesive strip before taping. There are a variety of commercially available skin adhesives in aerosolized form. These preparations use benzoin as the adhesive. One example is Cramer’s Tuf-Skin. Skin adhesives are applied after the skin has been shaved and abrasions dressed. If the area is not shaved, a foam underwrap or prewrap is used to protect body hair. Prewrap is generally supplied in 3-inch rolls in a variety of colors. After applying a topical skin adherent, such as Tuf-Skin, prewrap is applied over the part to be taped in a simple, continuous circular wrap. The prewrap is sufficiently self-adherent that it does not need to be taped down. Heel-and-lace pads and foam pads are used to provide greater comfort by relieving potential pressure points. When tape is

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applied over bony prominences, it can create tension on the skin surface that leads to blistering. Heel-and-lace pads are prefabricated pieces of white foam that are stuck together with petroleum jelly and then applied to the anterior and posterior aspects of the talus when the ankle is taped. Pads of foam can be cut to size to fit over painful areas that need to be taped, as in medial tibial stress syndrome, or to be used for support in special cases, such as taping for patellar subluxation.

Ankle Taping The most common injury to the lower extremity while hiking is a sprained ankle. It is usually the result of inverting the ankle on an unstable surface. Pain and swelling linger for several days, and taping can help offer support if the patient is able to bear weight. Because most injuries occur to the lateral ligaments, taping supports the lateral surface by restricting inversion. In general, taping of the ankle consists of anchor strips on the lower leg and foot, stirrups that run in a medial to lateral direction underneath the calcaneus, and support from either a figure8 or heel-lock technique (Fig. 18-2). The heel lock requires some expertise to perform, so most operators are more comfortable with the figure-8 initially.

Toe Taping Taping toes that are sprained or fractured is simple and effective. This treatment involves “buddy-taping” to the adjacent toe with one or two pieces of tape to provide support. A piece of gauze, cotton, or cloth can be placed between the toes to avoid skin breakdown. A sprain of the first metatarsophalangeal joint, also known as “turf toe,” can be a chronic and painful condition. Taping for turf toe attempts to support and stabilize the joint and is described in Figure 18-3.

Lower Leg Taping Figure 18-1. Athletic tape (front row) and elastic bandages (back row) come in various sizes.

A

Medial tibial stress syndrome, commonly referred to as “shin splints,” can be taped for support and comfort. Tape is brought

B

Figure 18-2. Ankle taping. A, (1) Ankle at 90 degrees;(2) apply anchors of 1.5-inch tape at the lower leg and distal foot. B, (3) Apply 3 stirrups from medial to lateral in a slight fan-like projection.

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C

D

E

F

G

H

Figure 18-2, cont’d. C, (4) Fill in gaps with horizontal strips. D, (5) Begin figure 8. Apply tape across front of ankle in left-to-right direction. E, (6) Continue under the foot to the opposite side and cross back over the top of the foot.F, (7) Complete by wrapping around the leg and end at the anterior aspect of ankle.G, (8) Apply heel locks for both feet (omit if not familiar with this technique). Start in left-to-right direction and apply tape across front of joint. H, (9) Wrap around the heel (bottom margin of tape should be above the superior edge of the calcaneus) to form the first heel lock.

Chapter 18: Bandaging and Taping

I

431

J

Figure 18-2, cont’d. I, (10) Continue under the foot to the opposite side and cross back over the top of the foot.J, (11) The tape is then brought back around the superior margin of the calcaneus and down and around the heel. K, (12) Finish by wrapping around the ankle. Repeat figure 8 or heel lock as desired.

K

from a lateral to medial direction, and a small foam pad can be cut to cover the area of tenderness. Underwrap should be used over a foam pad to secure it in place (Fig. 18-4).

piece of foam into taping the knee can help relieve symptoms. As with all taping around the knee, underwrap should not be used (Fig. 18-6).

Knee Taping

Finger Taping

Because it is a large joint, taping the knee requires expertise and special consideration. Underwrap should not be used because adequate traction to support the joint can only be achieved by taping directly to the skin. The patient’s knee should be shaved 6 inches above and below the joint line. In addition, standard athletic tape should not be used because it cannot provide enough support. Three-inch elastic tape provides the foundation. Taping for injuries to the medial aspect of the knee is described in Figure 18-5.

Patella Taping Subluxation of the patella is exacerbated by the stress of walking long distances across uneven terrain. Incorporating a

Injuries to the fingers are common in a variety of outdoor settings. Both simple fractures and sprains can be initially treated by taping. The most common scenarios involve fingers that are hyperextended or that are “jammed.” Injuries in this scenario are often to the palmar ligaments and tendons. Patients may find it difficult to flex the finger against the resistance of an examiner’s finger or may demonstrate tenderness over the palmar aspect of the finger. Swelling is almost always present and may be difficult to localize. This presentation is also seen after reduction of a dorsal dislocation of the proximal interphalangeal joint. In all these cases, it is always best to splint or tape the finger in slight flexion to avoid further injury to the flexor apparatus.

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1. Apply two anchors: First anchor around IP joint of first toe with 1-inch tape. Second anchor around midfoot with 11/2-inch tape. 2. Apply strip of 1-inch tape from distal to proximal anchor along medial aspect.

3. Continue with a strip of 1-inch tape from lateral edge of distal anchor along plantar aspect of first MTP joint to medial aspect of proximal anchor.

4. Cross with a strip of 1-inch tape extending from the medial aspect of the toe to the plantar aspect of the proximal anchor.

5. Begin dorsal strips by applying 1-inch tape from medial aspect of distal anchor across the dorsal aspect of the MTP joint to the proximal anchor.

6. Cross over the previous strip by applying 1-inch tape from lateral aspect of distal anchor to medial aspect of proximal anchor.

7. Close with 1-inch strips around the toe and 11/2-inch tape around the forefoot.

Figure 18-3. Toe taping.

Chapter 18: Bandaging and Taping

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1. (Optional) Underwrap is applied over a foam pad.

Figure 18-4. Lower leg taping. 2. With the patient placing his or her heel on a rock or roll of tape, begin applying 11/2-inch tape from the superior margin of the malleoli to the calf.

Fingers are buddy-taped to the adjacent finger as a natural splint (Fig. 18-7). The second and third fingers and fourth and fifth fingers are always paired. If the third and fourth fingers are paired, this makes injury to the second and fifth fingers more likely with subsequent activity. A small piece of gauze, cotton, or cloth should be placed between the fingers to avoid blistering or pressure on a tender joint. Strips of tape should be applied around fingers but not over the joints. Although not as common, injuries to the extensor tendons can occur. Typically these occur with hyperflexion, but they can also occur with hyperextension and axial loading.1 A mallet finger results from fracture of the base of the distal phalange, the site of attachment for the extensor tendon. The resulting inability of the distal phalange to extend fully results in a partially flexed “mallet” finger. Injuries in which the extensor mechanism is clearly disrupted should be treated with the finger taped in full extension. Often a straight splint, such as a tongue blade or smooth stick, can be placed on the dorsal surface and the finger taped to it for additional extensor support (Fig. 18-8). Any injury to the fingers or hands should always be evaluated by a physician, who can determine whether radiographs are necessary. Given the importance of maintaining optimal function of the hands for one’s personal and professional activities, this point cannot be overemphasized.

Thumb Taping The thumb is frequently injured when placed in extreme extension or abduction, such as occurs when it is caught in the strap of a ski pole when falling. Taping can prevent reproducing the mechanism of injury, particularly when grasping an object (Fig. 18-9).

Wrist Taping Wrist sprains generally occur during falls and initially can be difficult to distinguish from fractures. Although splinting is initially the most desirable treatment, there are two basic taping approaches that can be used, depending on the nature of the injury. As with the finger, the most important factor is whether the injury occurred in hyperextension or hyperflexion. Anchors are placed around the palm and distal wrist, whereas support strips to prevent undesirable movements are placed on the palmar aspect for hyperextension injuries or dorsal aspect for hyperflexion injuries (Fig. 18-10).

Elbow Taping The two most common soft tissue injuries to the elbow result from hyperextension and from excessive valgus force. Each of these injuries can result in significant ligament and tendon injury. Taping techniques are meant to prevent reproducing painful movements while maintaining function. Because these techniques allow for substantial joint movement, underwrap

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1. The patient maintains the knee in slight flexion (10 –15 degrees) by placing the heel on a small stone or cap of a spray can.

2. Apply two anchor strips of 3-inch elastic tape 6 inches above and below the joint line.

3. Apply a strip of 3-inch elastic tape from the anterolateral aspect of the lower leg, across the knee joint and up to the posteromedial aspect of the thigh.

4. Apply a second strip from posterior calf to anterior thigh, forming an X.

Figure 18-5. Knee taping.

5. Repeat steps 3 and 4 twice.

6. Apply two additional anchor strips of 3-inch elastic tape 6 inches above and below the joint for closure.

7. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the tape and provide additional support.

Chapter 18: Bandaging and Taping

1. Cut a piece of foam into a C shape, measured to encircle half of the patient’s patella.

2. The patient maintains the knee in slight flexion (10–15 degrees) by placing the heel on a small stone or cap of a spray can.

3. Apply two anchor strips of 3-inch elastic tape 4 inches above and below the patella.

Figure 18-6. Patella taping. 4. Apply the foam pad cut to fit the patient’s patella. Elastic tape (3-inch) is applied in a manner that reproduces the curvature of the foam pad.

5. Starting from the medial aspect of the lower leg anchors, bring the elastic tape around the lateral aspect of the patella and back to the medial aspect of the upper leg anchors.

6. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the taping and provide additional support.

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Figure 18-7. Buddy-taping of fingers.

A

B A

C B Figure 18-8. A and B, Extension taping of finger with small splint.

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Figure 18-9. Thumb taping. A, (1) Using 1.5-inch athletic tape, wrap an anchor strip around the wrist.B, (2) Using 0.75-inch tape,start at volar aspect and continue along the dorsal aspect of the thumb towards the first web space.C, (3) Allow the patient to crimp the tape as it comes across the web space and continue around base of thumb.

Chapter 18: Bandaging and Taping

D

E

F

G

H

I

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Figure 18-9, cont’d. D, (4) Bring the tape around to the volar aspect of the wrist and tape at that point.To complete a thumb spica, apply several more strips in succession.To reinforce, rather than repeating a series of strips, continue as follows. E, (5) Apply an anchor strip from volar to dorsal aspects of wrist through the first web space (note crimping). F, (6) Apply strip from dorsal to volar aspect of anchor strip. G, (7) Apply successive strips until at wrist. H, (8) Add a finishing anchor strip through first web space. I, (9) Complete with anchor strip at wrist.

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A

B

C

D

Figure 18-10. Wrist taping. A, (1) With the hand wide-open, apply one anchor across the palm of the hand and two to three anchors across the distal forearm. B, (2) Measure out the distance between the two anchors and construct a fan of three strips at varying angles on a smooth surface. C, (3) For hyperextension injuries, apply these support strips to the palmar aspect. For hyperflexion injuries, apply them to the dorsal aspect. D, (4) Apply another set of anchors over the support strips.

should not be used, and tape should be applied directly to skin to allow for maximal adhesion. Taping for a hyperextension injury employs a fan of elastic or tape, similar to that used in the wrist, to prevent excessive extension (Fig. 18-11). Individuals who have suffered a valgus stress injury require reinforcement from elastic tape placed on the medial aspect of the elbow (Fig. 18-12).

Injuries to the acromioclavicular joint most commonly occur when a patient falls on the lateral aspect of the shoulder. Enough force is transmitted through the acromioclavicular ligament to stretch or tear it, resulting in a sprain, or “separated shoulder.” Tape must be applied directly to the skin (Fig. 18-13).

Shoulder Taping


BANDAGING

Taping the glenohumeral joint is rarely done, primarily because it results in so significant a restriction of movement that the patient cannot function effectively. As such, taping offers little advantage over a sling. Taping of the acromioclavicular joint, however, can be effective in reducing pain and maintaining adequate function at the glenohumeral joint.

Bandaging may be used to wrap and support an injury or to help dress a wound. Many of the techniques described in the section on taping, such as figure-8 patterns, are used in bandaging.

Chapter 18: Bandaging and Taping

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1. The arm is supinated and extended just short of where pain is experienced. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.

2. Apply 3-inch elastic tape from distal to proximal anchors that form an X over the antecubital fossa. A total of four strips should be applied.

Figure 18-11. Elbow taping. 3. Apply closure strips above and below the elbow over the original anchors.

4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.

Types of Bandages The type of bandage used depends on its purpose. Elastic bandages (e.g., Ace wrap) come in a variety of widths and are used to wrap injuries such as sprains and strains. These bandages generally come with separate clips or clips built into the bandage to secure it. Of note is the double-length 6-inch elastic bandage that is useful for wrapping large joints such as the knee and shoulder. Bandaging wounds generally involves rolled gauze or cottonbased wraps that secure a dressing in place. These wraps are more desirable than elastic bandages in wound care because they do not place as much tension on the wound dressing. A triangular bandage, which is often used to create a sling, can be folded two to three times into a strap, called a cravat (Fig. 18-14). Cravat dressings are useful for applying pressure to a wound that is bleeding to promote hemostasis.

In the discussion of bandaging different parts of the body later in this chapter, the method for using an elastic bandage is described. When securing a wound dressing, the same methods may be used, except that rolled gauze or cotton bandages should be substituted. If there is a special technique for wound care, it will be described separately.

Securing Bandages Because bandages are not adhesive, they must be secured with tape or clips, or by tying them to the body. Two techniques for tying off a bandage are as follows: 1. As you are finishing wrapping with a bandage, bend the free end backward over your fingers, creating a loop. Now double back around the body part and tie the remaining free end to the loop to secure the bandage2 (Fig. 18-15).

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1. The arm is supinated and flexed to approximately 30 degrees. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.

2. Apply 3-inch elastic tape that forms an X over the medial joint line. The first strip begins at the posterior aspect of the proximal anchor and crosses to the anterior aspect of the distal anchor. The second strip begins at the anterior aspect of the proximal anchor and crosses to the posterior aspect of the distal anchor.

Figure 18-12. Elbow taping (valgus stretch injury).

Apply a total of four strips. 3. Apply closure strips above and below the elbow over the original anchors.

4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.

2. As you are finishing wrapping, tear or cut the remaining portion of bandage lengthwise down the middle. Double back with one of the resulting strips and tie off.

Ankle and Foot Bandaging Ankle bandaging with a 2- to 3-inch elastic wrap can be used to support a sprain. The bandage can be applied over a sock or directly to the skin. It is usually simplest to use a series of figure8 wraps, or, if preferable, a series of heel locks as described in the section on ankle taping. Anchors and stirrups are not used. When bandaging the foot, the same technique should be carried out to the metatarsophalangeal (MTP) joint. Circumferentially bandaging the foot by itself will result in the bandage slipping, as opposed to bandaging the ankle as well.

Knee Bandaging A double-length 6-inch elastic bandage can provide support to the knee. Ask the patient to hold the knee in slight flexion by placing his heel on a small stone or piece of wood (Fig. 18-16A). The elastic wrap is then applied circumferentially from midquadriceps to mid-calf (see Fig. 18-16B). If using gauze to secure a dressing or a smaller elastic wrap, then a series of figure-8 wraps can be applied, leaving the patella exposed.

Thigh and Groin Bandaging Quadriceps, hamstring, and hip adductor (“groin”) strains can all be treated with an elastic bandage in a hip spica. The bandage is modified slightly for the groin strain (Fig. 18-17).

Chapter 18: Bandaging and Taping

1. Apply three anchor strips with 3-inch elastic tape. Place the first anchor around the midhumerus. Place the second anchor beginning inferior to the nipple anteriorly and around to the inferior tip of the scapula in the posterior. Apply the third anchor from the anterior portion of the second anchor, over the trapezius and extending to the posterior portion of the second anchor. Note that a 3-inch gauze pad is incorporated into this anchor to protect the nipple. 2. Apply a longitudinal strip of 3-inch elastic tape from the anterior aspect of the first anchor, over the acromioclavicular joint and ending on the posterior aspect of the third anchor.

Figure 18-13. Shoulder taping.

3. Apply the next strip overlapping two thirds of the third anchor laterally. It should extend from posterior to anterior portions of the second anchor and cross over the acromioclavicular joint.

4. Apply the next strip from the posterior aspect of the first anchor, over the acromioclavicular joint and ending at the anterior aspect of the third anchor.

5. Repeat steps 2 through 4 two more times. (Optional) Wrap a 6-inch elastic bandage in a shoulder spica for additional support. (See Bandaging section.)

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A Figure 18-14. Making a cravat from a triangular bandage. (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT, Lyons Press, 2003. p 262.)

A

B

Figure 18-15. A and B, Securing a bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy. Ski Patrol Magazine 2005;Winter: 63.)

Although the quadriceps and hamstring can be supported by wrapping only the leg with a 6-inch elastic bandage, the hip spica helps prevent slipping and provides additional support.

Wrist and Hand Bandaging Support to the wrist can be supplied by a 2- to 3-inch elastic wrap using a continuous technique (Fig. 18-18). This same technique can be used with gauze to secure a dressing to a wound that can occur when falling on an outstretched hand. A hand cravat bandage can be used for wounds that continue to bleed despite manual pressure2 (Fig. 18-19).

Finger Bandaging Finger wounds are generally easily treated with adhesive bandages. However, if size or degree of bleeding necessitates a larger dressing, then the following method may be used: Fold a 1-inch rolled gauze back and forth over the tip of the finger to cover and cushion the wound (Fig. 18-20). Then wrap

B Figure 18-16. A, Knee positioned in slight flexion with heel-lift while bandage is applied. B, Completed knee bandage.

the gauze around the finger until the gauze is snug. On the last turn around the finger, pull the gauze over the top of the hand so that it extends beyond the wrist. Split this lengthwise; tie the ends around the wrist to secure the bandage.

Thumb Bandaging Application of a bandage or dressing to the thumb usually involves a thumb spica, as described in the taping section. Rather than apply individual strips, the gauze or elastic bandage is looped continuously.

Shoulder Bandaging A shoulder spica is used to support shoulder sprains, strains, and subluxations (Fig. 18-21). A triangular bandage can be used to dress a shoulder wound (Fig. 18-22).

Chapter 18: Bandaging and Taping

1. Wrap a double-length 6-inch elastic bandage around the mid-thigh in a medial to lateral direction and continue proximally.

2. At the groin crease, continue up and around the waist once to help anchor the bandage.

Figure 18-17. Thigh and groin bandaging. 3. Return to the thigh to complete the figure-ofeight. For quadriceps and hamstring strains, concentrate on wrapping the leg, using an additional figure-of-eight to anchor the wrap. For groin strains, concentrate on supporting the hip adductors by alternating wrapping the leg with figure-of-eight wraps.

4. Finish wrap on the leg.

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A

B

C

D

Figure 18-18. Wrist bandaging. A, (1) Begin by encircling the wrist 2 to 3 times. B, (2) Continue across the dorsum of the hand, through the first web space and around the base of the proximal phalanges. C, (3) Continue down and across the dorsum of the hand. D, (4) Circle the wrist and bring across the dorsum of the hand to form a figure-8. E, (5) Repeat, alternating figure-8 patterns on the dorsum of the hand and secure at the wrist.

E

Chapter 18: Bandaging and Taping

1. After dressing the wound, the patient closes his fist around rolled gauze.

2. Starting from the anterior aspect of the wrist, wrap one end around the dorsum of the hand, over the fingers and back to the wrist.

3. With tension, wrap the other end around the dorsum of the hand, over the fingers and back to the wrist, creating an X.

Figure 18-19. Hand cravat bandage. (Redrawn from Donelan S:That’s a wrap:Wound bandaging made easy. Ski Patrol Magazine 2005;Winter: 66.) 4. Cross both ends around the wrist.

5. Tie the ends to secure the dressing.

Figure 18-20. To begin a finger bandage, place layers of gauze over the fingertip. (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT: Lyons Press, 2003, p 263.)

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1. Begin by encircling the mid-humerus with a double-length 6-inch elastic bandage and continue proximally while wrapping. Once near the axilla, wrap over the acromioclavicular joint and around the posterior thorax.

2. Continue under the opposite axilla, across the chest and bring down over the acromioclavicular joint and onto the upper arm.

Figure 18-21. Shoulder bandaging.

3. Repeat the figure-of-eight pattern as the length of the bandage allows and finish on the upper arm.

1. Lay the base of the bandage over the shoulder with the apex pointed toward the arm. Tie the two free ends just anterior to the axilla.

Figure 18-22. Shoulder bandaging (triangular bandage). (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT: Lyons Press, 2003, p 264.)

2. Roll the apex up the arm to the desired point of coverage and tie off.

Scalp Bandaging

Ear Bandaging

Wounds to the scalp often require a dressing placed over hair, making adhesion very difficult. The dressing can be secured with a triangular bandage in a method that allows for considerable tension should pressure be necessary to stop bleeding (Fig. 18-23).

A wound to the pinna may require a compression dressing. If so, gauze should be placed both anterior and posterior to the ear to allow it to maintain its natural curvature. A cravat is used to secure the dressing (Fig. 18-24). This method may be used for wounds anywhere along the side of the head or under the chin.

Chapter 18: Bandaging and Taping

1. Drape a triangular bandage just over the eyes and fold the edge 1 inch under to form a hem. Allow the apex to drop over the back of the neck.

2. Cross the free ends over the back of the head and tie in a half-knot.

Figure 18-23. Scalp bandaging. (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT: Lyons Press, 2003, p 265.)

3. Bring the free ends to the front of the head and tie a complete knot. At the posterior aspect of the head, tuck the apex into the half-knot.

1. Place the cravat over the wound at the cravat’s midpoint. Wrap one end over the head and the other under the chin.

2. Cross the cravat just above ear level and wrap ends in opposite directions.

Figure 18-24. Ear bandaging. (Redrawn from Auerbach PS:Medicine for the Outdoors,4th ed. Guilford, CT: Lyons Press, 2003, p 266.)

3. Tie off the ends.

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Figure 18-25. Bandage for the injured eye. A cravat or cloth is rolled and wrapped to make a doughnut-shaped shield, which is fixed in place over the eye. (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT: Lyons Press, 2003, p 175.) Figure 18-26. Holding an eye patch in place with a cravat. Hang a cloth strip over the uninjured eye. Hold the patch in place with the cravat. Tie the cloth strip to lift the cravat off the uninjured eye (Redrawn from Auerbach PS:Medicine for the Outdoors,4th ed.Guilford,CT:Lyons Press, 2003, p 262.)

Eye Bandaging When bandaging an eye, a shield is placed over the eye socket to protect the globe, followed by application of a bandage over the shield. The shield may be commercially available sterile pads, cut foam or felt, stacked gauze, or a shirt or cravat fashioned into a doughnut shape (Fig. 18-25). The bandage is fashioned from a cravat and a spare piece of 15-inch cloth or shirt. The spare cloth is placed over the top of the head from posterior to anterior such that the anterior portion lies over the

19

unaffected eye. A cravat is then applied horizontally to hold the shield over the injured eye. To expose the uninjured eye, pull up both ends of the spare cloth and tie at the top of the head (Fig. 18-26). The references for this chapter can be found on the accompanying DVD-ROM.

Emergency Airway Management Swaminatha V. Mahadevan

Emergency airway management encompasses the assessment, establishment, and protection of the airway in combination with effective oxygenation and ventilation. Timely, effective airway management can literally mean the difference between life and death, taking precedence over all other clinical considerations. Airway management in the wilderness must often be provided in austere or unusual environments under less than ideal circumstances. Many of the resources and equipment readily available in a hospital or emergency department setting are not accessible in the wilderness. As with other aspects of wilderness medicine, improvisation may prove invaluable.


AIRWAY ANATOMY A full understanding of airway anatomy is essential for airway evaluation and management. Internally, the airway is made up of

many structures and well-defined spaces, and originates at the nasal and oral cavities (Fig. 19-1). The nasal cavity extends from the nostrils to the posterior nares or choanae. Resistance to airflow through the nose is almost twice that of the mouth, explaining why patients mouth-breathe when they require high flow rates (e.g., with exercise). The nasopharynx extends from the end of the nasal cavity to the level of the soft palate. The tonsillar lymphoid structures are the principal impediments to airflow through the nasopharynx. The oral cavity is bounded by the teeth anteriorly, hard and soft palate above, and tongue below. The oropharynx, which communicates with the oral cavity and nasopharynx, extends from the soft palate to the tip of the epiglottis. The tongue is the principal source of obstruction in the oropharynx. This obstruction results in part from decreased muscle tone of the genioglossus muscle, which contracts to move the tongue forward during inspiration and dilate the pharynx. The oropharynx continues as the laryngopharynx (hypopharynx), which extends from the epiglottis to the upper border of

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Figure 18-25. Bandage for the injured eye. A cravat or cloth is rolled and wrapped to make a doughnut-shaped shield, which is fixed in place over the eye. (Redrawn from Auerbach PS: Medicine for the Outdoors, 4th ed. Guilford, CT: Lyons Press, 2003, p 175.) Figure 18-26. Holding an eye patch in place with a cravat. Hang a cloth strip over the uninjured eye. Hold the patch in place with the cravat. Tie the cloth strip to lift the cravat off the uninjured eye (Redrawn from Auerbach PS:Medicine for the Outdoors,4th ed.Guilford,CT:Lyons Press, 2003, p 262.)

Eye Bandaging When bandaging an eye, a shield is placed over the eye socket to protect the globe, followed by application of a bandage over the shield. The shield may be commercially available sterile pads, cut foam or felt, stacked gauze, or a shirt or cravat fashioned into a doughnut shape (Fig. 18-25). The bandage is fashioned from a cravat and a spare piece of 15-inch cloth or shirt. The spare cloth is placed over the top of the head from posterior to anterior such that the anterior portion lies over the

19

unaffected eye. A cravat is then applied horizontally to hold the shield over the injured eye. To expose the uninjured eye, pull up both ends of the spare cloth and tie at the top of the head (Fig. 18-26). The references for this chapter can be found on the accompanying DVD-ROM.

Emergency Airway Management Swaminatha V. Mahadevan

Emergency airway management encompasses the assessment, establishment, and protection of the airway in combination with effective oxygenation and ventilation. Timely, effective airway management can literally mean the difference between life and death, taking precedence over all other clinical considerations. Airway management in the wilderness must often be provided in austere or unusual environments under less than ideal circumstances. Many of the resources and equipment readily available in a hospital or emergency department setting are not accessible in the wilderness. As with other aspects of wilderness medicine, improvisation may prove invaluable.


AIRWAY ANATOMY A full understanding of airway anatomy is essential for airway evaluation and management. Internally, the airway is made up of

many structures and well-defined spaces, and originates at the nasal and oral cavities (Fig. 19-1). The nasal cavity extends from the nostrils to the posterior nares or choanae. Resistance to airflow through the nose is almost twice that of the mouth, explaining why patients mouth-breathe when they require high flow rates (e.g., with exercise). The nasopharynx extends from the end of the nasal cavity to the level of the soft palate. The tonsillar lymphoid structures are the principal impediments to airflow through the nasopharynx. The oral cavity is bounded by the teeth anteriorly, hard and soft palate above, and tongue below. The oropharynx, which communicates with the oral cavity and nasopharynx, extends from the soft palate to the tip of the epiglottis. The tongue is the principal source of obstruction in the oropharynx. This obstruction results in part from decreased muscle tone of the genioglossus muscle, which contracts to move the tongue forward during inspiration and dilate the pharynx. The oropharynx continues as the laryngopharynx (hypopharynx), which extends from the epiglottis to the upper border of

Chapter 19: Emergency Airway Management

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Nasal cavity Nasopharynx

Figure 19-1. Lateral airway anatomy. (Redrawn from Mahadevan SV, Garmel GM [eds]: An Introduction to Clinical Emergency Medicine: Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina.com.)

Oral cavity

Oropharynx Vallecula

Epiglottis

Laryngeal inlet Laryngopharynx Larynx Glottis

the cricoid cartilage (at the level of the C6 vertebral body). The larynx, which lies between the laryngopharynx and trachea, serves as an organ of phonation and a valve to protect the lower airway from aspiration. The larynx is made up of muscles, ligaments, and cartilages, including the thyroid, cricoid, arytenoids, corniculates, and epiglottis. The flexible epiglottis, which originates from the hyoid bone and base of the tongue, covers the glottis during swallowing and provides protection from aspiration. During laryngoscopy, the epiglottis is as an important landmark for airway identification and laryngoscopic positioning. The vallecula is the space at the base of the tongue formed posteriorly by the epiglottis and anteriorly by the anterior pharyngeal wall. The laryngeal inlet is the opening to the larynx bounded by the epiglottis, aryepiglottic folds, and arytenoid cartilages. The glottis is the vocal apparatus including the true and false vocal cords and the glottic opening. The triangular fissure between these vocal cords is the glottic opening, the narrowest segment of the larynx in adults. Externally identifiable landmarks are also important to airway assessment and management (Fig. 19-2). The mentum is the anterior aspect of the mandible, forming the tip of the chin. The hyoid bone forms the base of the floor of the mouth. The thyroid cartilage forms the laryngeal prominence (“Adam’s apple”) and thyroid notch. The cricoid cartilage, lying inferior to the thyroid cartilage, forms a complete ring that provides structural support to the lower airway. The cricothyroid membrane lies between the thyroid and cricoid cartilage and serves as an important site for surgical airway management.

Knowledge of the anatomic differences between adults and children is integral to effective pediatric airway management. These important differences are summarized in Table 19-1 and Figure 19-3.


ASSESSMENT OF THE AIRWAY

AND RECOGNITION OF AIRWAY COMPROMISE

Assessment of the airway begins with evaluation of airway patency and respiratory function. The goal of this assessment is to determine whether the airway is patent and protected, and whether breathing is present and adequate. This is accomplished by inspection, auscultation, and palpation, commonly known as the “look, listen, and feel” approach. Visual signs of airway compromise include agitation, obtundation, and cyanosis. Blue, gray, or ashen skin, especially around the eyes, lips, and nail beds, is a worrisome finding. Significant airway compromise may present without cyanosis, such as an allergic reaction with upper airway edema and vasodilation (causing flushed red skin), or unconsciousness resulting from carbon monoxide poisoning. Bradypnea, tachypnea, or irregular respirations may be a sign of impending respiratory compromise. Breathing that is shallow, deep, or labored may indicate respiratory insufficiency. Respiratory muscle fatigue may result in recruitment of the accessory muscles of respiration, clinically manifested

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Hyoid bone Thyroid membrane Thyroid notch Laryngeal prominence Thyroid cartilage Cricothyroid membrane

Figure 19-2. External airway anatomy. (Redrawn from Mahadevan SV, Garmel GM [eds]: An Introduction to Clinical Emergency Medicine: Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina. com.)

Cricoid cartilage Tracheal rings Thyroid gland

TABLE 19-1. Anatomic Airway Differences between Children and Adults ANATOMY Large intraoral tongue occupying relatively large portion of the oral cavity High tracheal opening: C1 in infancy versus C3–4 at age 7, C4–5 in adults Large occiput that may cause flexion of the airway; large tongue that easily collapses against the posterior pharynx Cricoid ring narrowest portion of the trachea as compared with the vocal cords in adults Consistent anatomic variations with age, with fewer abnormal variations related to body habitus, arthritis, chronic disease Large tonsils and adenoids may bleed. More acute angle between epiglottis and laryngeal opening results in nasotracheal intubation attempt failures. Small cricothyroid membrane

CLINICAL SIGNIFICANCE 1. High anterior airway position of the glottic opening compared with that in adults 2. Straight blade preferred over curved to push distensible anatomy out of the way to visualize the larynx Sniffing position is preferred. The large occiput actually elevates the head into the sniffing position in most infants and children. A towel may be required under shoulders to elevate torso relative to head in small infants. 1. Uncuffed tubes provide adequate seal as they fit snugly at the level of the cricoid ring. 2. Correct tube size is essential because variable expansion cuffed tubes are not used. 8 years, small adult Blind nasotracheal intubation not indicated in children Nasotracheal intubation failure

Needle cricothyroidotomy difficult and surgical cricothyroidotomy impossible in infants and small children

From Walls RM, Murphy MF, Luten RC, Schneider RE (eds): Manual of Emergency Airway Management, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.

as suprasternal, supraclavicular, or intercostal retractions. Traumatic injury to the chest (e.g., flail chest) or an aspirated foreign body may result in paradoxical or discordant chest wall movement. In children, visual signs of airway compromise and respiratory distress include tachypnea, cyanosis, drooling, nasal

flaring, and intercostal retractions. A child with severe upper airway obstruction may sit upright with the head tilted back (“sniffing” position) to straighten the airway and reduce occlusion. A child with severe lower airway obstruction may sit up and lean forward on outstretched arms (“tripod” position) to augment accessory muscle function.

Chapter 19: Emergency Airway Management

Figure 19-3. Anatomic airway differences between children and adults.The anatomic differences particular to children include:1.Higher, more anterior position for the glottic opening. (Note the relationship of the vocal cords to the chin–neck junction.) 2.Relatively larger tongue in the infant, lying between the mouth and the glottic opening. 3. Relatively larger and more floppy epiglottis in the child.4.Cricoid ring is the narrowest portion of the pediatric airway; in adults, the narrowest portion is the vocal cords. 5. Position and size of the cricothyroid membrane in the infant. 6. Sharper, more difficult angle for blind nasotracheal intubation. 7. Larger relative size of the occiput in the infant. (Redrawn from Walls RM, Murphy MF, Luten RC, Schneider RE [eds]: Manual of Emergency Airway Management, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.)

Tongue

Vocal cords

Epiglottis

Cricoid membrane

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Cricoid ring

Junction of chin and neck Infant

Tongue

Vocal cords

Epiglottis

Cricoid membrane Cricoid ring

Junction of chin and neck

Adult

Under most circumstances, hearing the victim speak with a normal voice suggests that the airway is adequate for the moment. Unusual sounds or noisy respirations may be present with partial airway obstruction. Snoring indicates partial airway obstruction at the pharyngeal level; gurgling may be heard with blood or secretions in the airway; stridor may be associated with partial airway obstruction at the level of the larynx (inspiratory stridor) or the level of the trachea (expiratory stridor); hoarseness suggests a laryngeal process. The central face and mandible should be assessed for structural integrity because injuries to these structures may lead to airway distortion and compromise. The anterior neck should be carefully inspected for penetrating wounds, asymmetry, or swelling that may herald impending airway compromise. Palpation of subcutaneous air suggests direct airway injury. In the unconscious victim, feel for air movement at the mouth and nose. Open the mouth to inspect the upper airway, taking care not to extend or rotate the neck. Identify and remove any vomitus, blood, or other foreign bodies. Look for swelling, bleeding, or other abnormalities of the oropharynx. The gentle use of a tongue blade may facilitate this task. The victim’s ability to spontaneously swallow and handle secretions is an important indicator of intact airway protective mechanisms. In the unconscious victim, absence of a gag reflex has traditionally been linked to loss of protective airway reflexes. Auscultation of the lung fields should demonstrate clear and equal breath sounds. Diminished breath sounds may result from a pneumothorax, hemothorax, or pleural effusion. Wheezing and dyspnea are often associated with lower airway obstruction.


OPENING THE AIRWAY Opening the airway and ensuring airway patency are essential for adequate oxygenation and ventilation. These are the first priorities in airway management. The conscious victim uses the musculature of the upper airway and protective reflexes to maintain a patent airway and protect against aspiration of foreign substances, gastric contents, or secretions. In the severely ill, compromised, or unconscious victim, these protective airway mechanisms may be impaired or absent. Upper airway obstruction in the unconscious victim is most commonly the result of posterior displacement of the tongue and epiglottis at the level of the pharynx and larynx. This occlusion results directly from the loss of tonicity of the submandibular muscles, which provide direct support to the tongue and indirect support to the epiglottis. Upper airway obstruction may be alleviated by head positioning, manual airway techniques, and mechanical airway adjuncts.

Head Positioning If the mechanism of injury or physical examination suggest possible of cervical spine injury, the head should be placed in the neutral position, and efforts to stabilize the neck and head should be initiated. Care should be taken not to flex, extend, or rotate the victim’s head. After cervical spine immobilization, the airway should be reevaluated for obstruction. The optimal head position for airway alignment and patency varies with age. For an infant in the supine position, the large

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS victim’s head. Then, grasp the angles of the mandible with both hands and lift, displacing the jaw forward while tilting the head back.

Jaw Thrust without Head Tilt A

Infant

Small child

Older child/adult

If a cervical spine injury is suspected or cannot be excluded, the jaw thrust without head tilt (Fig. 19-6) can be performed while maintaining neutral cervical spine alignment. In this maneuver, the jaw thrust is performed without extending or rotating the neck.

Tongue Traction If the patient is unconscious or in extremis, the airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins (Fig. 19-7). An alternative to piercing the lower lip is to pass a string through the safety pins and exert traction on the tongue by securing the end of the string to the victim’s shirt button or jacket zipper (Fig. 19-8).

B Figure 19-4. A, Clinical determination of optimal airway alignment using a line passing through the external auditory canal and anterior to the shoulder (see text for details).B, Application of the line to determine optimal position.In this small child the occiput obviates the need for head support,yet the occiput is not so large as to require support of the shoulders.Note that the line traversing the external auditory canal passes anterior to the shoulders.With only slight extension of the head on the atlanto-occipital joint, the sniffing position is achieved. (Redrawn from Walls RM, Murphy MF, Luten RC, Schneider RE [eds]: Manual of Emergency Airway Management, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.)

occiput contributes to flexion of the head and neck and resultant airway obstruction. This may be alleviated by elevating the shoulders with a small towel (Fig. 19-4). In children, slightly extending the head into the sniffing position helps relieve airway obstruction. In adults, placing a folded towel or article of clothing under the occiput, which flexes the neck at the torso, followed by gentle hyperextension of the head at the atlanto-occipital joint, provides optimal alignment of the air-way axes.

Manual Airway Techniques Although the following manual airway techniques are effective, they often require continuous involvement by a single provider to maintain airway patency.

Head Tilt with Chin Lift The head tilt with chin lift (Fig. 19-5) is a simple, effective technique for opening the airway. This maneuver is accomplished by placing the palm of one hand on the victim’s forehead and then applying firm backward pressure to tilt the head back. Simultaneously, the fingers of the other hand are then placed under the bony part of the chin and lifted, bringing the chin forward. These fingers support the jaw and maintain the headtilt position. This maneuver extends the neck; therefore, it should not be used if there is concern about a cervical spine injury.

Jaw Thrust with Head Tilt If a cervical spine injury is not suspected, the jaw thrust with head tilt maneuver may be used to gain additional forward displacement of the mandible. Position yourself at the top of the

Mechanical Airway Adjuncts Several airway adjuncts are available to maintain airway patency while freeing up the health care provider to perform other duties.

Oropharyngeal Airway The oropharyngeal airway (OPA) is an S-shaped device designed to hold the tongue off the posterior pharyngeal wall (Fig. 19-9). When properly placed, it prevents the tongue from obstructing the glottis. It also provides an air channel and suction conduit through the mouth. These devices are most effective in unconscious and semiconscious victims who lack a gag reflex or cough. The use of an OPA in a victim with a gag reflex or cough is contraindicated because it may stimulate retching, vomiting, or laryngospasm. The OPA is made of disposable plastic and comes in various sizes to accommodate children and adults. The size is based on the distance (in millimeters) from the flange to the distal tip. The proper OPA size is estimated by placing the OPA’s flange at the corner of the mouth so that the bite block segment is parallel to the victim’s hard palate; the distal tip of the airway should reach the angle of the jaw. Two types of OPAs are commonly employed. The Guedel uses a tubular design, whereas the Berman is distinguished by airway channels on each side. Technique for Insertion: 1. First, open the mouth and clear the pharynx of any secretions, blood, or vomitus. Remove dentures or partial plates if present. 2. In an adult or older child, insert the OPA upside down or at a 90-degree angle to avoid pushing the tongue posteriorly during insertion. Slide it gently along the roof of the mouth. As the oral airway is inserted past the uvula or crest of the tongue, rotate it so that the tip points down the victim’s throat. 3. In a child, grasp the tongue and gently pull it forward or use a tongue blade to displace the tongue inferiorly and anteriorly. Then, insert the OPA with the tip pointing toward the tongue and throat (i.e., the intended position following placement). 4. The flange should rest against the victim’s lips, and the distal portion should rest on the posterior pharyngeal wall. If the OPA is too short, it may displace the tongue

Chapter 19: Emergency Airway Management

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Figure 19-5. Head tilt with chin lift. (Redrawn from Mahadevan SV, Garmel GM [eds]: An Introduction to Clinical Emergency Medicine: Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina.com.)

into the hypopharynx and occlude the airway. If the OPA is too long, it may displace the epiglottis and result in an airway obstruction.

Nasopharyngeal Airway The nasopharyngeal airway (NPA) is an uncuffed trumpet-like tube that provides a conduit for airflow between the nares and pharynx (Fig. 19-10). The NPA is inserted through the nose rather than the mouth. It has a flange at the outer end to prevent displacement or slippage beyond the nostril. These devices are better tolerated than OPAs and are commonly used in intoxicated or semiconscious victims. They are also effective when trauma, trismus (“clenched teeth”), or other obstacles (e.g., wiring of the teeth) preclude placement of an oropharyngeal airway. NPAs are contraindicated in victims with basilar skull or facial fractures because inadvertent intracranial placement may occur. The NPA is made of soft, pliable rubber or plastic and comes in various sizes to accommodate children and adults. Sizes (internal diameter) vary from 12 to 36 French. Proper NPA length is determined by measuring the distance from the tip of the nose to the tragus of the ear. Technique for Insertion: 1. Lubricate the nasopharyngeal airway with a watersoluble lubricant to minimize resistance in the nasal cavity.

Do not use petroleum jelly or a non–water-based lubricant. 2. If the NPA has a beveled (angled) edge, place the airway in the nostril with the bevel directed toward the nasal septum. 3. Gently insert the NPA straight back along the floor of the nasal passage (perpendicular to the coronal plane of the face). 4. If you meet resistance, rotate the tube slightly, reattempt insertion through the other nostril, or try a smallerdiameter tube. Do not force the tube because injury to the nasal mucosa can result in bleeding. 5. Following insertion, the flange should rest on the victim’s nostril, and the distal portion of the airway should rest in the posterior pharynx, behind the tongue. Any flexible tube of appropriate diameter and length can be used as an improvisational substitute for the NPA. Examples include a Foley catheter, radiator hose, solar shower hose, siphon tubing, or inflation hose from a kayak flotation bag or sport pouch. An endotracheal tube (ETT) can be shortened and softened in warm water to substitute for a commercial nasal trumpet. The flange can be improvised using a safety pin through the nostril end of the tube (Fig. 19-11). Although OPAs and NPAs help to establish artificial airways, they do not provide definitive airway protection from aspiration.

Figure 19-6. Jaw thrust without head tilt.(Redrawn from Mahadevan SV,Garmel GM [eds]:An Introduction to Clinical Emergency Medicine:Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina.com.)

Figure 19-7. Tongue traction.The airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins. Figure 19-8. Tongue traction.An alternative to piercing the lower lip is to pass a string through the safety pins and exert traction on the tongue by securing the end of the string to the victim’s shirt button or jacket zipper.

Chapter 19: Emergency Airway Management

Figure 19-9. Oropharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM [eds]: An Introduction to Clinical Emergency Medicine: Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina.com.)

Figure 19-10. Nasopharyngeal airway. (Redrawn from Mahadevan SV,Garmel GM [eds]:An Introduction to Clinical Emergency Medicine: Guide for Practitioners in the Emergency Department. Cambridge, UK, Cambridge University Press, 2005. © Chris Gralapp, www.biolumina. com.)

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Recovery Position In the spontaneously breathing, unconscious victim who is not at risk for cervical spine injury, placement in the recovery position (Fig. 19-12) assists with maintaining a clear airway and reduces the risk for aspiration. In the recovery position, the tongue is less likely to fall back and occlude the airway, and vomitus is more likely to be expelled than inhaled. Even a diminutive rescuer can place a large person in the recovery position if the proper technique is employed.


FOREIGN-BODY AIRWAY OBSTRUCTION

Figure 19-11. Improvised nasal trumpet.

Foreign bodies, most commonly meat, may cause partial or complete airway obstruction. A victim with partial airway obstruction can usually phonate or produce a forceful cough in an attempt to expel the foreign body. When encountering a victim with a partially-obstructed airway, if air exchange is adequate, do not interfere with the person’s attempts to clear the airway. Encourage forceful coughing and closely monitor the victim’s condition. If the obstruction persists or air exchange worsens or becomes inadequate, the victim should be managed as though a complete airway obstruction exists. Worrisome findings that should prompt immediate management include a weak or ineffective cough, increased respiratory difficulty, decreased air movement, and cyanosis.

Figure 19-12. Recovery position.

Chapter 19: Emergency Airway Management

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TABLE 19-2. Relief of Choking ADULTS AND CHILDREN 2000 >40% >140 Decreased Decreased >35 Negligible Confused, lethargic Crystalloid and blood

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management

1 finger width 45°-60°

Figure 20-1. Intraosseous resuscitation performed by introducing a needle through the periosteum of the tibia inferior to the tibial tuberosity.

Vascular Access Vascular access must be obtained promptly. The standard method of obtaining access is by insertion of two large-bore (16gauge or larger) catheters, preferably into peripheral veins of the upper extremity. Alternatives include using lower extremity veins and obtaining central venous access. If peripheral access cannot be secured, the femoral vein should be the next site attempted. Advantages of femoral vein access include ease of cannulation relative to jugular and subclavian access, and fewer complications.96 Depending on expertise, the internal jugular and subclavian veins may be accessed. Despite a higher incidence of complications compared with peripheral access, central access complication rates in trauma centers have been demonstrated to be less than 5% in most studies.96 If peripheral access is inadequate or unobtainable, it is clear that the next site attempted should be determined by the provider’s level of confidence and expertise. As a last resort, venous cutdown may be considered. Despite fewer complications than central access, cutdowns are experience and equipment dependent and not recommended in the wilderness environment. Children in the wilderness younger than 6 years of age in whom venous access cannot be obtained should undergo intraosseous resuscitation. This is accomplished by introducing a needle through the periosteum of the tibia just inferior to the tibial tuberosity (Fig. 20-1). Needles that are 18- to 20-gauge are preferable, but any needle strong enough to penetrate the periosteum without bending can be used. Of the resuscitative therapies that potentially may be initiated in a well-prepared expedition, volume resuscitation deserves considerable attention. Fluid resuscitation in trauma has been a contentious topic, perhaps overly so, relative to fluid type and amounts used. A number of recent studies focusing on the prehospital administration of fluids in trauma victims not only rehashed the fluid composition debate but called into question the efficacy of prehospital resuscitation.75 Although further

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prospective trials are needed relative to fluid type and prehospital use, an impressive compilation of data has been amassed looking at resuscitative fluids in the trauma victim. Past studies have not only compared colloids with crystalloids91 but explored the use of blood and plasma substitutes, and hypertonic saline. An analysis of the details of such studies is beyond the scope of this chapter, but a summary of fluid recommendations is in order. In small volumes, hypertonic saline has been shown to be an effective resuscitative fluid, and its efficacy in closed head injury is under evaluation. Currently, no improvement in survival has been demonstrated using hypertonic saline compared with crystalloid, and its use has been associated with hypokalemia, pulmonary edema, and dramatic increases in serum sodium and osmolarity.6 The significance of these reported complications in trained hands is questionable, and hypertonic fluids may have a future role in resuscitation. Further study is warranted on the use of hypertonic saline, but its use in the wilderness setting is not recommended at this time. Artificial blood products, such as perfluorocarbons and diaspirin cross-linked hemoglobin, have been shown to be efficient resuscitative fluids in animal studies.20,80,89 However, they are expensive and not yet available for humans. Based on the current literature, it is clear that both colloids (including hetastarches and albumin) and crystalloids are efficient volume expanders.82 Larger volumes of crystalloids than colloids are needed to achieve similar resuscitative end points, usually in a ratio of 3 to 1. However, no benefit in survival using colloids has been demonstrated, and recent studies indicate that their use in critically ill patients may increase mortality.19,72 In addition, no proven detriment, including increased extravascular lung water, impaired wound healing, or decreased tissue oxygen diffusion, has been demonstrated with the use of large volumes of crystalloids. Crystalloids are safe, nonantigenic, easily stored and transported, effective, and inexpensive. Most experts in trauma care agree that crystalloid is preferable to colloid infusion in the prehospital, early resuscitative phase of trauma care. Accordingly, the resuscitative fluid recommended by ATLS protocol is normal saline. Several animal studies and recent human clinical trials in trauma victims have found that treatment with IV fluids before control of hemorrhage resulted in increased mortality rates.9,59 Although these data are compelling, they have been accumulated in victims with penetrating injuries and short prehospital times, and the definition of prehospital resuscitation in these studies comprised widely varying volumes. Prehospital resuscitative protocols remain in evolution. However, application of these data to the wilderness setting at the current time is dangerous for a number of reasons. First, the leading cause of death in wilderness trauma is head injury. Many multiple trauma victims have a head injury, and it may be impossible to discern whether an intracranial lesion is present. Although under continued study, the current approach to management of head injury is aggressive maintenance of cerebral perfusion pressure to control intracranial pressure (ICP). Under-resuscitation in the context of an intracranial injury could be catastrophic. Second, the multisystem-injured victim frequently presents with associated orthopedic injuries. A victim with closed extremity fractures with significant contained hemorrhage benefits from fluid resuscitation. Third, a victim with significant external hemorrhage that can be controlled before evacuation benefits from intravascular repletion.

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In summary, resuscitation with IV fluids should be initiated in the field, particularly in victims with head injury and unquantified multiple trauma. Victims should have vascular access secured and resuscitative fluids given in the form of normal saline as dictated by severity of injuries and hemodynamics.

Secondary Survey The secondary survey is an extension of the primary survey and should not be undertaken until the primary survey is complete and the victim has been stabilized. In addition, resuscitative regimens, if available, should have been initiated. The secondary survey is a head-to-toe assessment of the victim, including history and physical examination. The face, neck, chest, abdomen, pelvis, extremities, and skin should be examined in sequence. A more detailed neurologic examination should be completed, including reassessment of the GCS. The neck should be examined independently of the thoracolumbar spinal cord. Examination of the pelvis should not include the traditional “rocking” to determine stability because in the presence of pelvic fractures, this action may exacerbate existing comminution. The detailed secondary survey should not delay evacuation packaging. As in the nonwilderness setting, it is imperative to repeat the primary survey as the victim’s condition warrants. Specific examinations are discussed in the sections covering regional injuries.

History The victim’s history should be assessed during the secondary survey. Knowledge of the mechanism of injury and any comorbid medical conditions or allergies may enhance understanding the victim’s physiologic state. The ATLS “AMPLE” history is a useful and rapid mnemonic for this purpose: Allergies Medications currently used Past medical history/Pregnancy Last meal Event or Environment related to the injury

Adjuncts Resuscitation should be initiated simultaneously with the primary survey. The degree of resuscitation depends on available resources, experience of the rescuer(s), and environmental conditions. Under the best circumstances, initial management of the wilderness trauma victim provides for airway control, adequate oxygenation and ventilation, appropriate fluid resuscitation, and stabilization of cardiac function while continuing to monitor and reassess the patient’s vital signs. As adjuncts to the secondary survey, it also includes placement of a urinary catheter and nasogastric (NG) tube. This degree of resuscitation will be almost universally unavailable in the wilderness setting. Here, resuscitation may be limited to oral administration of warm, high-calorie fluids and maintenance of victim comfort and body temperature. An NG tube and indwelling urinary (Foley) catheter should be placed if available and appropriate. Aspiration of gastric contents can be catastrophic in terms of patient survival after trauma. Gastric decompression with an NG tube may help prevent this type of adverse event in patients with a depressed level of consciousness. It should be remembered that children can exhibit significant hemodynamic consequences secondary

to massive gastric distention. In this setting, decompression becomes critical. If possible, NG tubes should be placed in persons who are endotracheally intubated in the field. The tube can be aspirated sequentially with a syringe or left open to gravity drainage. Any suspicion of facial fracture should deter attempts to place an NG tube, and orogastric decompression should be chosen instead. A Foley catheter can assist in volume assessment and hemodynamic status determination in a critically injured victim. Hourly urine output typically does not decrease until the onset of class III hemorrhagic shock, with loss of 30% to 40% of blood volume. Contraindications to urinary catheter placement in the field are blood at the urethral meatus, high-riding prostate, scrotal hematoma, and personnel not experienced in placement.

Pneumatic Antishock Garment. The pneumatic antishock garment (PASG) is a noninvasive device inflated around the lower extremities and abdomen to augment peripheral vascular resistance and increase blood pressure. It was widely instituted as a treatment for shock in the 1980s, largely based on anecdotal data. Prospective data relevant to penetrating chest and abdominal trauma44,60 and retrospective data in blunt trauma7 indicate an increase in mortality with its use. Hemodynamically unstable pelvic fractures can be stabilized using a simple sheet wrap. Use of the PASG is not indicated in the wilderness setting.75 A new device for stabilization of a pelvic fracture in a wilderness setting is the SAM Sling (SAM Products, Newport, OR).

Injuries to the Head, Face, and Neck The secondary survey begins with examination of the entire head and scalp for evidence of skull or facial fractures, ocular trauma, lacerations, and contusions. The scalp is thoroughly palpated for tenderness, depressions, and lacerations. The bones of the face, including the zygomatic arch, maxilla, and mandible, are palpated for fractures. Detailed discussion of orofacial and eye injuries is presented in Chapters 25 and 26). Elements of the GCS are repeated. The wilderness eye is discussed in detail in Chapter 25, but general examination principles are simple. Significant periorbital edema may preclude examination of the globe, so assessment should be carried out early. The globe should be evaluated for visual acuity, pupillary size, conjunctival hemorrhage, lens dislocation, and entrapment. Persons with significant facial trauma have a high incidence of associated ocular or orbital injuries.78 Recent studies of ocular injuries in trauma victims have emphasized underappreciation by many disciplines involved in the victim’s care of ocular and periocular signs indicative of significant underlying injury.74

Head Injuries Approximately 500,000 to 2 million cases of head injury occur in the United States yearly.35 Of these, approximately 10% result in the patient’s death before reaching a hospital.5 Longterm disability associated with head injury is significant, with more than 100,000 persons suffering varying degrees of permanent impairment. Because of the high-risk nature of traumatic brain injury (TBI) and the impact of initial management on disability and survival, clinical management objectives must address both immediate survival and long-term outcome. Management guidelines for head injuries in a wilderness do not exist,

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management

Anatomy The scalp comprises five layers of tissue that cover the calvaria: skin, connective tissue, galea aponeurotica, loose areolar tissue, and periosteum of the skull. The galea is a fibrous tissue layer with important ramifications in closure of scalp wounds, discussed later in this chapter. Loose areolar tissue beneath the galea represents the site of accumulation of blood in scalp hematomas. A rich vascular network located between the dermis and the galea supplies the scalp. When lacerated, these vessels can be a significant source of hemorrhage, which may be important if evacuation is impossible or delayed. The skull is composed of two groups of bones that form the face and cranium. Cranial bones are divided into the calvaria and skull base. The calvaria is composed of frontal, ethmoid, sphenoid, parietal, and occipital bones. Within the skull, the brain is covered by three membranous layers that may be of pathophysiologic importance after injury. However, in the wilderness environment, these layers have little clinical relevance (except in terms of defining an open versus closed brain injury).

Pathophysiology of Traumatic Brain Injury Traumatic brain injury can be divided into primary and secondary brain injury. Primary injury consists of the physical or mechanical insult at the moment of impact, and the immediate and permanent damage to brain tissue. Little can be done in the wilderness setting relative to primary brain injury. Secondary brain injury is the biochemical and cellular response to the initial mechanical trauma and includes physiologic derangements that may exacerbate effects of the primary trauma. Such pathophysiologic alterations include hypoxia, hypotension, and hypothermia. Compounding these pathophysiologic alterations is elevation of ICP after TBI. Increased ICP increases cerebral ischemia and exacerbates secondary brain injury.

Volume-Pressure Curve Herniation

60 55 50 45 ICP (mm Hg)

and a wide range of clinical approaches are used in hospital settings.35 However, the literature suggests that morbidity and mortality can be reduced by means of a protocol that includes early airway control with optimization of ventilation,40 prompt cardiopulmonary resuscitation, and rapid evacuation to a trauma care facility. Initial management of head injury in the wilderness should follow established ATLS protocols. Prompt attention must then be given to victim triage, evacuation strategies, and ongoing resuscitative needs to prevent or minimize secondary brain injury. Expeditious evacuation to a neurosurgery-capable trauma center is essential. Multiple clinical and experimental studies have demonstrated the detrimental effects of hypoxia on the injured brain. A definitive airway should be established if any degree of neurologic or respiratory compromise exists. Cervical spine injuries are common in patients with TBI. Therefore, cervical spine immobilization is paramount in prevention of further devastating neurologic injury. After immobilization, attention is directed to prevention of secondary brain injury. The purpose of the wilderness head injury protocol is to allow individuals with widely varying levels of experience and expertise to identify signs of significant head injury, begin proper resuscitation in the context of prevention of secondary brain injury through airway maintenance and hemodynamic support, and evacuate appropriately.

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40 35 30 25 20 15 10

Point of hemodynamic decompensation

5 Volume of mass

Figure 20-2. Critical time period between decompensation and brainstem herniation after traumatic brain injury.

Many forms of head injury result in elevated ICP, the duration of which is significantly correlated with poor outcome. The Monro-Kellie doctrine states that the volume of intracranial contents must remain constant because the cranium is a rigid container. The normal compensatory response to increased intracranial volume is to decrease venous blood and cerebrospinal fluid (CSF) volume within the brain. If this normal response is overwhelmed, small increases in intracranial volume result in exponential increases in ICP. A rigid bony cranium cannot expand to accommodate increases in brain volume and the resultant increase in ICP. Brain parenchyma becomes compressed and eventually displaced from its anatomic location. In the most devastating circumstances, the brain parenchyma herniates toward the brainstem through the largest cranial opening (the foramen magnum) and death rapidly follows. The volume–pressure curve in Figure 20-2 relates the small, but critical, time period between neurologic symptoms, hemodynamic decompensation, and brainstem herniation. Elevation in ICP directly correlates with secondary brain injury. Therefore, the field provider must attempt to minimize ICP of head-injured patients to the greatest extent possible. The most important priority in minimizing secondary brain injury in the field is optimizing cerebral perfusion pressure (CPP). CPP is related to ICP and mean arterial pressure (MAP) as follows: CPP = MAP − ICP A CPP less than 70 mm Hg after head injury correlates with increased morbidity and mortality.5,39 Cerebral blood flow (CBF) should be maintained at approximately 50 mL/100 g brain tissue per minute.57 At 5 mL/100 g per minute, irreversible damage and potential cell death occur.5 Study data have shown a correlation between low CBF and poor outcome.57 At a MAP between 50 and 160 mm Hg, cerebral autoregulation maintains

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CBF at relatively constant levels. Not only is autoregulation disturbed in injured regions of the brain, but a precipitous fall in MAP can further impair autoregulatory function, decreasing CBF and exacerbating ischemia-induced secondary injury. The field provider is able to combat a rise in ICP by simply optimizing MAP through aggressive IV fluid resuscitation.

Diagnosis The three useful descriptions of head injury that may be applied to field recognition are history, severity, and morphology. History includes mechanism of injury, timing of the event, and related circumstances. This knowledge assists in the decisionmaking process with regard to resuscitation and evacuation.5 Mechanism of injury is identified as blunt or penetrating trauma. The anatomic demarcation between blunt and penetrating injury is traditionally defined by violation of the outer covering of the brain (dura mater). Blunt injuries in the wilderness setting most often result from falls, falling objects, or assaults. Penetrating injuries are most commonly gunshot, or other projectile, wounds. Severity of injury can be estimated by quantifying the GCS and pupillary response. The generally accepted definition of coma is a GCS score of less than or equal to 8; these patients often require endotracheal intubation. Although GCS score does not directly correlate with a need for intubation, it is essential that all head-injured patients be provided a stable, secure airway by the most appropriate means available. It is important to note the TBI victim’s best initial motor response because this is most predictive of long-term neurologic outcome. Any victim with a GCS score less than 15 who has sustained a head injury should be evacuated, if possible. A low or declining GCS score suggests increasing ICP. Abnormal pupil size or asymmetric pupillary responses suggest increased ICP. These clinical deteriorations demand the rapid attention of rescue or evacuation personnel to optimize MAP and CCP, minimize secondary brain injury, and prevent brainstem herniation. Injury morphology may be difficult to assess in the wilderness setting and relies on level of suspicion and clinical signs and symptoms. After attention to the primary survey, including airway provision and spinal immobilization, the physical examination of the secondary survey is imperative and can provide information about the presence of a TBI.

Injury Classification Intracranial injuries range from concussion to massive subdural hematoma. Subdural hematomas are more common than epidural hematomas, comprising 20% to 30% of mass lesions. “Subdurals” result from torn bridging veins between the cerebral cortex and draining venous sinuses. Their prognosis is worse than that of “epidurals,” although prompt recognition and drainage improves patient outcome. Epidermal hematomas

are most commonly located in the temporal region and result from injury to the middle meningeal artery, often associated with a fracture. These patients may present with loss of consciousness followed by a lucid interval and subsequent rapid neurologic deterioration. This sequence, however, is not frequently observed. Hemorrhagic contusion is also quite frequent, constituting 35% of traumatic injuries, and has the propensity to increase ICP significantly. Diffuse axonal injury (DAI) is the term used to describe prolonged post-traumatic coma not resulting from a mass lesion or ischemic insult. Similar to hemorrhagic contusion, DAI may result in elevated ICP.

Physical Examination After the primary survey and initial attempts to resuscitate the victim, a more complete physical examination should be done. However, this examination should not delay patient evacuation. A hallmark of TBI is altered level of consciousness. Determination of the GCS score aids in recognition of TBI and should be regularly reassessed to provide a mechanism for quantifying neurologic deterioration. Physical signs that may denote underlying brain injury include significant scalp lacerations or hematomas, contusions, facial trauma, and signs of skull fracture. Findings specific for basilar skull fracture include ecchymosis behind the ears (Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood behind the tympanic membrane on otoscopic examination (hemotympanum), frank bleeding from the ears, and CSF rhinorrhea/otorrhea also suggest skull fracture and underlying TBI. The pupillary examination may provide valuable data in assessment of underlying TBI. Herniation of the temporal lobe of the brain may be heralded by mild dilation of the ipsilateral pupil with sluggish response to light. Further dilation of the pupil followed by ptosis (drooping of the upper eyelid below its normal level), or paresis of the medial rectus or other ocular muscle, may indicate third cranial nerve compression by a mass lesion or herniation. Table 20-2 relates pupillary examinations to possible underlying brain lesions. Most dilated pupils (mydriasis) are on the ipsilateral side to the mass lesion. With direct globe injury, traumatic mydriasis may result, making evaluation of TBI more difficult. In addition, 5% to 10% of the population has congenital anisocoria (a normal difference in pupillary size between the eyes). Casual inspection may overlook a prosthetic eye, which is mistaken for a fixed pupil. Neither direct trauma nor congenital anisocoria should be assumed in a headinjured victim exhibiting mental status change in the wilderness. After quantification of GCS score, pupillary examination, and examination of the head and face for signs of external trauma, a concise neurologic examination should be performed. The goal of the field neurologic examination is to identify motor or sensory focal deficits suggestive of intracranial injury. Sensory

TABLE 20-2. Interpretation of Pupillary Findings in Head-Injured Victims PUPIL SIZE Unilaterally dilated Bilaterally dilated Unilaterally dilated or equal Bilaterally constricted Bilaterally constricted

LIGHT RESPONSE Sluggish or fixed Sluggish or fixed Cross-reactive (Marcus-Gunn) Difficult to determine; pontine lesion Preserved

INTERPRETATION Third nerve compression secondary to tentorial herniation Inadequate brain perfusion; bilateral third nerve palsy Optic nerve injury Opiates Injured sympathetic pathway

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management deficits follow general dermatome patterns shown in Figure 20-3. Unilateral hemiplegia may signify uncal herniation resulting from mass effect in the contralateral cortex because of compression of the corticospinal tract in the midbrain. Ipsilateral pupillary dilation associated with contralateral hemiplegia is a classic and ominous sign of tentorial herniation. Reflex changes in the absence of altered mental status are not indicative of TBI. Detailed evaluation of brainstem function cannot be undertaken in the wilderness setting. Performance of gag and corneal reflex evaluations may provide some information helpful in

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triage and evacuation planning, but their presence would not automatically obviate the need for prompt evacuation.

Resuscitation Resources and circumstances permitting, resuscitation should be initiated as an adjunct to the primary survey. The primary focus for the head-injured victim, similar to any traumatized victim, is the airway. During the primary survey and performance of the ABCDE sequence, IV access should be established. If IV resuscitation is impossible, it is not advisable to adminis-

Figure 20-3. Dermatome pattern, showing the skin area stimulated by spinal cord elements. Sensory deficits follow general dermatome patterns.

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ter fluids orally to the victim with head injury because of the likelihood of vomiting, airway compromise, and aspiration. Individuals sustaining head trauma have a high incidence of concomitant injuries. Up to 32% of persons with severe head injury have a long bone or pelvic fracture, 20% to 25% a chest injury, and 10% an abdominal injury. A victim who does not have a palpable femoral pulse or manifests other signs of hypotension in the context of suspected head injury must not be assumed to have a neurogenic etiology of shock, so other etiologies must be thoroughly and aggressively investigated. Resuscitation is critical in the setting of head injury for multiple reasons. Management of a head injury should be secondary to other life-threatening injuries, which, if not addressed, may preclude survival. As previously discussed, maintenance of MAP (and thus CPP) is critical in preventing secondary brain injury. The type of resuscitative fluid administered to trauma victims continues to be controversial. Previously, recommendations warned of the dangers of overhydration in head injury leading to recommendations restricting fluids. Restriction of fluid has not been shown to reduce ICP or edema formation in laboratory models of TBI. Theories of limiting cortical free water content in TBI by using hypotonic IV solutions have not been borne out in animal studies.90 The need for resuscitation and intravascular volume support has been well established. Possible resuscitative fluids include isotonic crystalloids, hypertonic crystalloids, or colloid solutions. There is convincing evidence that hypotonic fluids are not appropriate in TBI secondary to an increase in whole-brain water content and subsequent elevation in ICP. Recent data from animal studies of TBI suggest that colloid solutions offer no advantage over isotonic crystalloids, such as lactated Ringer’s solution, in terms of augmenting CBF or preventing cerebral edema.101 As previously noted, no clear prospective trial has documented any advantage of colloid over crystalloid administration in the victim with multiple systemic injuries. Evidence is accumulating that hypertonic solutions, particularly hypertonic saline, may be beneficial in TBI.92,97 However, an advantage has not been demonstrated in trauma victims overall, and expertise is necessary for their use. The recommended resuscitative fluid for the head-injured victim in the wilderness setting is isotonic crystalloid, with a target MAP of 85 to 95 mm Hg based on cuff blood pressure determinations or extrapolation from distal pulses evaluation.

Further Management Numerous adjuncts exist in the management of the head-injured victim, few of which are applicable in the wilderness setting. Once the primary and secondary surveys are complete, the airway is secured, resuscitation has been initiated, and spine immobilization has been achieved, the victim should be placed in a 30-degree head-up position. This position assists in control of ICP, and thus CPP, through augmentation of venous outflow. This maneuver should not be attempted if the spine cannot be adequately immobilized. If endotracheal intubation is possible, ventilation should be optimized without hyperventilating the victim. Hyperventilation has been used aggressively in the past to promote hypocarbia-induced cerebral vasoconstriction, theoretically to decrease brain swelling. However, if the Paco2 falls below 25 mm Hg, severe vasoconstriction ensues, effectively reducing CBF, promoting ischemia, and possibly augmenting secondary brain injury. Studies have demonstrated worse outcomes in victims with severe head injury who were hyperventilated.68 The

inability to measure or titrate Paco2 in the wilderness mandates that respiration be controlled to approximate near-normal minute ventilation. All bleeding from the scalp or face should be controlled with direct pressure. Scalp hematomas, regardless of size, should not be decompressed. Open wounds, particularly skull fractures, should be irrigated and covered with the most sterile dressing available. Fragments of displaced cranium overlying exposed brain tissue should not be replaced. If signs of skull fracture are present, immunization against tetanus and broad-spectrum antibiotic prophylaxis are recommended as soon as possible. Although diuretics have been widely used in the intensive care management of intracranial hypertension, no rationale exists for their use in the field. The wilderness trauma victim may have many injuries that are impossible to evaluate fully in the field. In this setting, particularly in the presence of hemorrhagic shock, attempts to induce osmotic diuresis to decrease ICP may be life-threatening. Diuretics such as furosemide or mannitol may exacerbate hypotension, cause metabolic alkalosis, and induce renal complications in the absence of physiologic monitoring.4 Steroids have no role in head injury in the field or intensive care unit. Studies have documented no beneficial impact on ICP or survival. Attempts at brain preservation by slowing metabolic rate and oxygen consumption have no role in the wilderness setting. Barbiturates have been used for elevated ICP refractory to other measures, but may induce hypotension, depress myocardial function, and confound the neurologic examination.4 Compared with minimizing ICP, these interventions offer no significant benefit.39 Approximately 15% of persons with severe head injury experience post-traumatic seizures. Phenytoin, if available, can be safely administered in the field, but only after a witnessed seizure. Prophylactic administration has not been shown to decrease long-term seizure activity.

Skull Fracture Skull fracture in the wilderness mandates evacuation. Therapeutic options in the field are few, with intervention limited to identifying the injury and arranging rapid transport. Skull fractures may be open or closed, linear or stellate, and may occur in the vault or skull base. These fractures are associated with a high incidence of underlying intracranial injury. In an awake and alert victim with a skull fracture, the chance of brain injury is increased 400-fold.5 Skull fractures with depression greater than the thickness of the skull may require elevation. No attempt at elevation should be made in the field. Any exposed brain surface should quickly be covered with the most sterile covering available, preferably moistened with crystalloid solution. Loose bone or brain fragments should not be manipulated. If a broad-spectrum antibiotic is available, it should be administered. After attention to the wound and stabilization of associated injuries, the victim should be rapidly evacuated.

Penetrating Head Injuries The majority of penetrating head injuries in the wilderness are gunshot wounds, although knives and arrows may penetrate the cranium. Such penetrating injuries are usually catastrophic. However, examples of survival exist with small-caliber, lowvelocity injuries and tangential wounds.58 As with closed head injury, management priorities consist of maintenance of airway, prevention of secondary brain injury, and rapid evacuation. If the cranium has been violated, the victim should receive antibi-

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management otics and tetanus immunization in the same manner as for open skull fracture. In the rare instance that the projectile is embedded in the skull, no attempt at removal should be undertaken. If the length of the projectile makes immobilization or transport cumbersome, excess length may be removed, but only if this can be done easily and without displacement of the intracranial segment.

Evacuation Survival and outcome of head injury in the wilderness correlate directly with rapidity of evacuation. Certain situations dictate immediate evacuation. Any person with evidence of an open or closed skull fracture should be evacuated. The incidence of TBI associated with skull fracture is variable but significant throughout the literature. Recent data predict that 30% to 90% of persons with raccoon eyes or Battle’s sign will show abnormalities on computed tomography (CT) scan.11,18 Similarly, any person who sustains a penetrating injury should be evacuated. Decisions concerning evacuation of victims who have sustained closed head injuries can be simplified by dividing the victims into three groups based on probability of injury. A high-risk group, defined as patients with GCS score of 13 or less, focal neurologic signs, or evidence of decreasing level of consciousness, requires evacuation. The low-risk group includes persons who have suffered a blow to the head but are asymptomatic, did not lose consciousness, and complain only of mild headache or dizziness. Data from recent studies suggest that persons who meet low-risk criteria (including GCS of 15, no loss of consciousness, minimal symptomatology, and unlikely mechanism) have a minimal chance of having significant TBI and may be closely observed.11,18 The group for which the evacuation decision is most difficult is the moderate-risk group. These persons have a history of brief loss of consciousness or change in consciousness at the time of injury, or a history of progressive headache, vomiting, or posttraumatic amnesia. If any of these signs is present in the face of concurrent systemic injury, the victim should be evacuated immediately. Studies associating clinical variables and abnormal results on CT scan have demonstrated the significance of decreased GCS score, symptoms, and loss of consciousness. If these signs are present in isolation and the evacuation can be completed in less than 12 hours, the evacuation should proceed. If the evacuation is impossible or will require longer than 12 hours, the victim should be closely observed for 4 to 6 hours. If the examination improves to normality during the observation period, it is reasonable to continue observation.

Neck Injuries Blunt Neck Injuries Injuries to the neck may be classified as blunt or penetrating. Significant blunt injuries include cervical spine injuries and laryngotracheal injuries. Seventy-five percent of injuries to the trachea are confined to the cervical region.73 Fracture of the larynx and disruption of the trachea usually require surgical intervention unavailable in the wilderness. The sooner laryngeal repair is accomplished, the better the outcome with respect to phonation.21 Victims present with a history of a significant blow to the anterior neck. Physical examination findings include difficulty with phonation, subcutaneous emphysema that may extend as far inferiorly as the abdominal wall, stridor, odynophagia, and, often, acute respiratory distress.

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Treatment is focused on establishing and maintaining an airway until evacuation can occur. Frequently, the airway is in jeopardy. Because of the propensity for injuries of this type to result in significant and progressive edema, endotracheal or nasotracheal intubation is often necessary. If these options are unavailable, airway maintenance techniques as described in the Primary Survey section should be used. In the event of intubation failure or lack of availability with impending hypoxic death, a surgical cricothyrotomy may be necessitated. A recent study of prehospital cricothyrotomy demonstrated that success rates were high regardless of medical specialty as long as previous training had been instituted.54 For further descriptions of airway management, refer to Chapter 19.

Background. Vertebral column injury, with or without neurologic deficits, must be identified in any wilderness multiple trauma victim. Approximately 2.6% of victims of major trauma suffer acute injury of the spinal cord.16 Fifteen percent of victims sustaining an injury above the clavicles and 5% to 10% of persons with a significant head injury have a cervical spine injury. In addition, 55% of spinal injuries occur in the cervical region.58 In the wilderness setting, fractures or dislocations of the cervical spine are a result of falls from significant heights, or of high-velocity ski or vehicular injuries. Twenty-eight percent of persons with cervical spine fractures have fractures elsewhere in the spine.10 Anatomy. The cervical spine consists of seven vertebrae. The anteriorly placed vertebral bodies form the weight-bearing structure of the column. The bodies are separated by intervertebral discs and held in place anteriorly and posteriorly by longitudinal ligaments. The paraspinal muscles, facet joints, and interspinous ligaments contribute as a whole to the stability of the spine. The cervical spine, based on its anatomy, is more susceptible to injury than are the thoracic and lumbar spine. The cervical canal is wide from the foramen magnum to C2, with only 33% of the canal comprised by the spinal cord itself. The clinically relevant tracts in the spinal cord include the corticospinal tract, spinothalamic tract, and posterior columns. Classification and Recognition. Fractures of the cervical spine may result in neurologic deficit, with total loss of function below the level of injury.52 Resultant spinal cord injuries should be classified according to level, severity of neurologic deficit, and spinal cord syndrome. Fractures of the C1-C2 complex generally result from axial loading (a C1 ring fracture, or Jefferson’s fracture) or an acute flexion injury (a C2 posterior element fracture, or hangman’s fracture). Approximately 40% of atlas fractures have an associated fracture of the axis. The atlas fracture, if survived, is rarely associated with cord injury but is unstable and requires strict immobilization. Usually, a complete neurologic injury at this level is unsurvivable owing to paralysis of respiratory muscle function. One third of victims sustaining an upper cervical spine injury die at the scene. The most common mechanism of injury is flexion, and the most common level of injury is C5-C6.10 Fractures and dislocations may result in partial or complete neurologic injury distal to the fracture or in no neurologic injury at all. Partial injuries to the spinal cord result from typical patterns of injury. Because flexion injuries are the most common type of injury to the cervical spine, the anterior cord syndrome (see later) is the most commonly seen serious neurologic picture.

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A careful neurologic examination in the field to grade motor strength and document sensory response to light touch and pinprick yields important information that should be documented and reported to the treating physician at the definitive care facility. The presence or absence of Babinski’s reflex should be noted, as well. When appropriate resources are available, a rectal examination should be performed. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicate the presence of spinal cord injury. When individuals with cervical spine fractures or dislocations are transported, the neck must be stabilized to prevent further injury to the spinal cord or nerve roots at the level of the fracture or dislocation. Approximately 28% of persons with cervical spine fractures have fractures elsewhere in the spine10; therefore, the entire spine must be protected during transport. Occasionally, a pure flexion event can result in dislocation of one or both of the posterior facets without fracture or neurologic injury. The victim may complain only of neck pain and limitation of motion. If so, the victim should be transported with the neck rigidly immobilized. With this injury, posterior instability is present (because the interspinous ligament is ruptured), and any further flexion stress could produce a spinal cord injury.

Physical Examination. A thorough neurologic examination should be performed. Initial documentation of deficits and frequent repeat examinations are critical to follow-up care. The classification of injury in the field begins with determination of the level of injury. Knowledge of sensory dermatomes (see Fig. 20-3) and motor myotomes is invaluable. The sensory level is the lowest dermatome with normal sensation and may differ on each side of the body. C1 to C4 are variable in their cutaneous distribution, so assessment should begin at C5. The examiner should not be confused by the occasional innervation of the pectoral skin by C1 to C4, known as the “cervical cape.” Light touch and pinprick should be assessed. Motor function should be assessed by the myotomal distribution listed in Box 20-2. Each muscle should be graded on a six-point scale: 0—Total paralysis 1—Palpable or visible contraction 2—Full range of motion without gravity 3—Full range of motion against gravity 4—Full range of motion with decreased strength 5—Normal strength Each muscle must be tested bilaterally and documented. The reflexes alluded to in the classification section must be tested, as well as anal sphincter tone.

Syndromes. There are three clinically useful spinal cord syndromes: Central cord syndrome is characterized by a disproportionate loss of motor power between the upper and lower extremities, with greater strength retained in the lower extremities. Sensory loss is variable. The mechanism of injury usually involves a forward fall with facial impact and hyperextension of the spine. Anterior cord syndrome is characterized by paraplegia and loss of pain and temperature sensation. It is the most

Box 20-2. Sensory and Motor Deficit Assessment SENSORY

C5: Area over deltoid C6: Thumb C7: Middle finger C8: Little finger T4: Nipple T8: Xiphisternum T10: Umbilicus T12: Symphysis L3: Medial aspect of thigh L4: Medial aspect of leg L5: First toe web space S1: Lateral foot S4 and S5: Perianal skin MOTOR

C5: Deltoid C6: Wrist extensors C7: Elbow extensors C8: Finger flexors, middle finger T1: Small finger abductors L2: Hip flexors L3: Knee extensors L4: Ankle dorsiflexors L5: Great toe extensors S1: Plantar flexors

common presenting syndrome caused by cervical spine injury and carries a poor prognosis. Brown-Séquard syndrome results from hemisection of the cord. It consists of ipsilateral motor loss and position sense with contralateral sensory loss two levels below the level of injury. It is usually secondary to penetrating injury.

Immobilization. After identification of injury, the caregiver faces a critical decision with important ramifications—whether to immobilize.32 Victims who would as a matter of course be immobilized in an urban setting might not be appropriate candidates for immobilization in the wilderness. The decision to immobilize converts an otherwise ambulatory victim who can actively participate in his or her own evacuation to one requiring more involved evacuation procedures. The subsequent evacuation can be dangerous to the victim and rescuers and demands significant expense and resource utilization. Risk criteria for cervical spine injury and the need for immobilization have been defined.42,56 All criteria for the exclusion of immobilization must be satisfied. These include normal mental status without chemical influence; lack of distracting injury; normal neurologic examination; and a reliable neck examination without midline neck pain, deformity, or tenderness. Figure 20-4 presents an evidence-based algorithm for determining need for immobilization. Although the need for immobilization poses hazards for the evacuation process, if criteria are met, immobilization takes precedence over ease of evacuation.62 A difficult balance must be struck in the wilderness between the likelihood of true injury and the danger to the expedition members and rescuers that may ensue when the victim is immobilized.

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Mechanism of injury suggestive of cervical spine injury? Yes/unknown Alert and oriented, no distracting injury, not intoxicated? Yes Tenderness, pain spontaneously or with movement? No Normal neurologic exam? Yes Immobilization unnecessary?

Figure 20-4. Clinical assessment of cervical spine stability. Failure of any criterion suggests need for immobilization.

If a rigid litter is not available, the victim should be maintained on the flattest surface possible. A rigid cervical collar should be placed. All collars allow some degree of movement, particularly rotation. Soft collars offer the least immobilization.30 The Philadelphia collar has been shown to allow 44% of normal rotation and 66% of normal lateral bending.58 To achieve 95% immobilization, a halo and vest are necessary. Any number of materials may be used to improvise an immobilizing device (see Chapter 21). Restriction of flexion, extension, and rotation must be achieved to the greatest degree possible. Optimal immobilization consists of a long spine board or litter, rigid collar, bolsters to the sides of the head, and tape or straps restricting movement (Fig. 20-5).

Treatment. The issue of pharmacotherapy for spinal cord injury is under continuous study. Currently, based on data accumulated by the National Acute Spinal Cord Injury Study Group, documented blunt spinal cord injury should be treated with a bolus of 30 mg/kg of methylprednisolone within 8 hours of injury followed by a continuous infusion of 5.4 mg/kg/hr over the next 23 hours.14 Steroids are not recommended in the field unless a victim clearly manifests a spinal cord injury in the absence of head injury. Because little definitive treatment for cervical spine injury can be accomplished in the field, survival and outcome depend on speed of transport and maintenance of airway. This is particularly true considering the association of cervical spine injury with head injury and major systemic trauma. Transport all victims with proven or suspected cervical spine injury to a definitive care facility.

Penetrating Neck Injuries Similar to penetrating head injury, penetrating neck injury is usually due to gun or knife wounds. Most penetrating injuries do not confer bony instability; however, stability should not be assumed. Neurologic deficits, if present, can progress with further movement of an unstable spine. Projectiles should not be removed if embedded in the neck. Penetrating injuries to the neck may not directly injure the spine, but neurologic sequelae

Figure 20-5. Proper spine immobilization.

III

II I

Figure 20-6. Zones in penetrating neck trauma (see text).

may result from blast effect. The same immobilization criteria should be implemented as when dealing with blunt injuries. Penetrating injuries to the neck are classified according to anatomic zones of injury (Fig. 20-6). Zone I injuries extend from the clavicles to the cricoid cartilage. Zone II injuries occur between the cricoid and the angle of the mandible. Zone III injuries occur superior to the angle of the mandible. Historically, treatment has been based on penetration of the platysma muscle. In the wilderness setting, if the examiner is

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confident that platysmal penetration has not occurred, the victim may be observed and the wound considered a laceration. Much debate has occurred over management of platysmal penetration within respective topographic zones, with treatment arms consisting of surgical exploration versus radiographic evaluation. In the wilderness setting, such considerations remain relevant. A penetrating injury violating the platysma muscle indicates the possibility of significant neurovascular, esophageal, or tracheal injuries, so the victim should be evacuated with close attention to the airway.

Injuries to the Thorax Background The mortality rate from thoracic trauma is approximately 10%. Approximately 25% of all trauma deaths in the United States are attributable to chest injury.5 However, only 15% of persons with penetrating thoracic trauma require thoracotomy. In the wilderness environment, blunt thoracic injuries usually result from falls or direct blows to the chest. Penetrating injuries result from gun, knife, or arrow wounds, or from impalement after a fall. Immediate, life-threatening thoracic injuries include airway obstruction, tension pneumothorax, flail chest, and cardiac tamponade.

Pathophysiology Chest injuries often result in hypoxia, hypercarbia, and acidosis. The tissue hypoxia of thoracic trauma can be multifactorial. Inadequate delivery of oxygen can be from hemorrhagic shock, direct lung injury with ventilation–perfusion mismatch (pulmonary contusion, atelectasis, hematoma), or changes in normal intrathoracic pressure dynamics (tension or open pneumothorax). Hemodynamic instability and inadequate oxygen delivery may also result from cardiac tamponade or contusion.

Physical Examination Thorough physical examination begins with visualization and inspection of the chest. Exposure of the chest should be completed in the primary survey. The airway is assessed for patency and air exchange, and the pattern of breathing is noted. In the immediate postinjury period, most trauma victims are tachypneic, partly from pain and anxiety. Dyspnea, cyanosis, the use of accessory muscles of respiration, and intercostal muscular retraction are abnormal and may give clues to the underlying injury. Chest wall movement during respiration should be symmetrical. Paradoxical chest wall movement is associated with flail chest. The chest wall should be inspected for contusions and abrasions, which may herald underlying bony or visceral injury. Distention of the external veins in a person who has just suffered thoracic trauma and is hypotensive or tachycardic (heart rate greater than 130 beats per minute) suggests impaired venous return to the heart. This finding may be seen in situations of increased intrathoracic or intrapericardial pressure and is associated with tension pneumothorax and pericardial tamponade. In tension pneumothorax, deviation of the trachea is in a direction opposite the lesion. Significant sternal bruising may herald fracture or cardiac contusion. The thorax should be palpated systematically for bony tenderness, starting at the distal clavicles and working medially toward the sternum. The sternum is divided into the manubrium, gladiolus (body), and xiphoid cartilage. The

manubrium is joined to the gladiolus by fibrocartilage, but mobility at this joint is minimal. Each rib should be palpated individually. Ribs 1 to 7 are vertebrosternal; their costal cartilages join the sternum. Ribs 8 through 10 are vertebrochondral, with each costal cartilage commonly joining the cartilage of the rib above. Ribs 11 and 12 are vertebral ribs without attachment to the sternum. Point tenderness over a rib can be associated with contusion or fracture. Displaced fractures can be palpated; occasionally, bone grating can be palpated during respiration. Subcutaneous emphysema may extend up into the neck and down to the level of the inguinal ligaments. In the trauma situation, subcutaneous emphysema is invariably associated with pneumothorax. Vocal fremitus describes palpation of vibrations transmitted through the chest wall. During speech, the victim’s vocal cords emit vibrations in the bronchial air column that are conducted to the chest wall. Diminished vocal fremitus is associated with pneumothorax or hemothorax. To test for vocal fremitus, the examiner applies the palmar arch of the examining hand against the person’s anterior chest wall. The person is asked to repeat “one, two, three” using the same pitch and intensity of voice with each repetition. If the vibrations are not well perceived, the patient is asked to lower the pitch of the voice. The chest should be symmetrical, left to right. Percussion is used to detect changes in the normal density of an organ. Percussion of the chest is performed by placing the examining fingertips on the chest wall and sequentially striking the fingertips with the tip of the index or middle finger of the other hand. In the trauma victim, dullness replacing resonance in the lower lung suggests hemothorax. Hyperresonance or tympani replacing resonance occurs only with a large pneumothorax or tension pneumothorax. If a stethoscope is not available, primitive chest auscultation can be performed using a rolled piece of cardboard or paper. Any cylinder that can transmit sound through a column of air accentuates breath sounds when placed against the chest wall. The absence of sounds normally produced by the tracheobronchial air column indicates blockage in the airways or abnormal filtering of sound by fluid in the pleural cavity. In the trauma victim, this is invariably associated with pneumothorax or hemothorax.

Blunt Chest Trauma Blunt chest trauma in the wilderness is most often associated with either a direct blow or a deceleration injury. The mechanism usually relates to a fall from a height. Compression of the chest wall by moving or falling debris may also contribute to intrathoracic injuries, as may be seen in traumatic asphyxia associated with burial in an avalanche or earthquake.

Rib Fractures. Rib fractures range in severity from an isolated nondisplaced single fracture, which causes only minor discomfort, to a major flail segment, which can be associated with an underlying hemopneumothorax and pulmonary contusion. Rib fractures are characterized by painful respiration, most severe on inspiration. Victims often breathe in a characteristically rapid, shallow pattern. Point tenderness is palpated over the fracture, and displacement can occasionally be detected. Rib fractures are detected with a compression test, in which pressure is exerted on the sternum while the victim lies supine. This will elicit pain over the fracture site.

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management Most patients with rib fractures can be managed with oral analgesics and rest. Thoracic taping and splinting are contraindicated. Multiple rib fractures are significant because of the potential seriousness of associated injuries and increased pain. However, if extreme and compromising respirations, this pain responds well to an intercostal nerve block. Victims with multiple rib fractures need to be evacuated as conditions permit. After administration of an intercostal block, a person may regain the ability to hike out of the wilderness. The morbidity of rib fractures relates to decreased inspiratory tidal volume secondary to pain and splinting. In the wilderness setting, management must focus on pain control and pulmonary toilet. If oral analgesia is insufficient to control pain, an intercostal block is ideal. Depending on the anesthetic used, varying durations of analgesia can be attained, perhaps allowing transient ambulation for evacuation. Deep breathing should be encouraged 10 times hourly to help prevent atelectasis.

Costochondral Separation. It is difficult to distinguish between a rib fracture and costochondral separation. With the latter, pain is more likely to be predominantly anterior over the costochondral junction. Pain increases with inspiration and worsens with direct palpation. Costochondral separation also responds to intercostal nerve block and oral and IV analgesics. Sternal Fracture. A sternal fracture is usually associated with a direct blow to the anterior chest wall. The injury is characterized by severe, constant chest pain that worsens with direct palpation. Sternal instability is unusual and can be associated with a significant underlying visceral injury, including pulmonary or myocardial contusion. If the sternum is unstable, the victim should immediately be evacuated by litter or helicopter. Pneumothorax. Simple pneumothorax can occur from an injury that allows air to enter through the thoracic wall or, more frequently, from an injury to the lung that permits air to escape into the pleural space. Symptoms include tachypnea, dyspnea, resonant hemithorax, absence of breath sounds, and tactile fremitus. A person with chest pain after a blunt blow to the chest, particularly with accompanying rib fracture, should be suspected of having a pneumothorax. Treatment of pneumothorax involves decompression of the pleural space. In the wilderness environment, tube thoracostomy is rarely possible. Fortunately, although victims with isolated pneumothorax may complain of chest pain or dyspnea, they are not completely disabled. With analgesia to control pain, ambulation facilitates evacuation. It may be easier and more prudent to set a slow pace with frequent rest periods than to perform an unnecessary litter evacuation. If resources and expertise allow placement of a thoracostomy tube, it should be performed only when clinically indicated. Considering possible morbidity in a remote area, prophylactic decompression should never be undertaken. Suspicion of a pneumothorax alone on physical examination does not warrant a catheter or chest tube. When a high index of clinical suspicion is accompanied by incapacitating symptoms, such as shortness of breath, decompression should be considered. The key to saving a victim’s life is understanding that a condition exists that can rapidly progress from a nondisabling condition to a life-threatening condition. Once the diagnosis of pneumothorax is entertained, vigilant observation and a high index of clinical

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suspicion are necessary in the event of progression to a tension pneumothorax. Symptoms should be closely monitored and frequent repeat examinations should be performed.

Tension Pneumothorax. A tension pneumothorax develops when a one-way air leak follows lung rupture or chest wall penetration. Air is forced into the thoracic cavity with no means of escape, and pressure mounts within the hemithorax. With sufficient increases in intrathoracic pressure, the mediastinum is shifted to the contralateral side, which impedes venous return from both the superior and inferior venae cavae. Cardiac output is diminished and the victim soon exhibits signs and symptoms of shock. Victims with tension pneumothorax manifest distended neck veins and tracheal deviation away from the side of the lesion. There is unilateral absence of breath sounds, and the hemithorax is hyperresonant or tympanitic. Respiratory distress, cyanosis, and frank cardiovascular collapse may occur. Tension pneumothorax is life-threatening and frequently associated with additional serious injuries. It mandates rapid chest decompression, followed by evacuation to a medical facility. Decompression is performed by inserting a needle or catheter into the chest and converting the tension into an open pneumothorax. Ideally, a 14-gauge catheter is inserted percutaneously over the second rib in the midclavicular or anterior axillary line (Fig. 20-7). Once the rib is identified with the tip of the needle, the needle is marched over the anterior superior surface of the rib and inserted through the intercostal muscles and pleura into the thoracic cavity. As the pressure within the hemithorax is released, a distinct rush of air is heard. The plastic catheter is advanced over the tip of the needle, the needle withdrawn, and the catheter left in place to ensure continued decompression. The needle should not be reintroduced into the catheter because it may damage or sever the catheter. Because tension pneumothorax is commonly associated with severe injury, the victim should be evacuated to a medical facility as rapidly as possible. A rubber glove or a finger cot can be attached to the external catheter opening to create a unidirectional flutter valve that allows egress of air from the pleural space. If resources are limited and treatment is needed, any number of devices can be used to decompress the chest. A sharp instrument and hollow tube sterilized as well as possible are all that is needed. Rapid cleansing of the skin surface is accomplished with antiseptic, alcohol, or water. A Heimlich valve kit is ideal for decompression and represents a valuable addition to the expedition first aid arsenal. If resources permit placement of a thoracostomy tube, adequate anesthesia and expertise are required. The skin should be sterilized if possible, and local anesthesia should be infiltrated into the skin and periosteum of the rib. Insertion is most effectively accomplished through the fifth intercostal space at the anterior axillary line. A small incision is made and the subcutaneous tissue bluntly separated with a finger or clamp. A blunt instrument, preferably a clamp, is forcefully inserted into the pleural space closely adhering to the superior surface of the rib to avoid the inferiorly located intercostal neurovascular bundle. Once the pleural space is entered, a tube (36 fr or greater in size) is inserted apically and posteriorly. The tube should then be secured with suture or tape and 10 to 20 cm H2O suction or underwater seal applied. A tube open

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Figure 20-7. Needle decompression of tension pneumothorax. This procedure is performed only for tension pneumothorax in patients with hemodynamic instability.

to the atmosphere can accomplish decompression. The end of the tube can be covered with a rubber glove, finger cot, or plastic bag. One-way flow evacuating the chest is the goal. This procedure is not without morbidity and should be used only by trained personnel under optimal conditions. Antibiotics with gram-positive coverage should be initiated if the pleural space is penetrated with an indwelling catheter or tube.

Hemothorax. Hemothorax is usually associated with multiple rib fractures resulting from a direct blow to the chest. The primary cause of a hemothorax is laceration of the lung, intercostal vessel, or internal mammary artery. The victim complains of chest pain, tenderness associated with rib fractures, inspiratory pain, and dyspnea. Vocal fremitus is absent, percussion may be flat or dull, and breath sounds are diminished or absent. A chest tube for hemothorax is rarely required in the wilderness setting, but may be placed if proper equipment is available, the patient is symptomatic, and evacuation will be prolonged. Needle aspiration of a hemothorax is unnecessary in the immediate postinjury period and may precipitate a pneumothorax. Flail Chest. When a series of three or more ribs is fractured in both the anterior and posterior plane, a portion of the chest

wall may be mechanically unstable. As negative intrathoracic pressure develops during inspiration, the unstable segment paradoxically moves inward and inhibits ventilation. A flail segment indicates a severe direct blow to the chest wall with associated multiple rib fractures and decreased tidal volumes, often with associated underlying pulmonary contusion. The contusion can be expected progressively to impair ventilation and oxygenation over the succeeding 48 hours. Victims often tolerate a flail segment for the first 24 to 48 hours, after which they require mechanical ventilation. Any victim with a flail segment should be rapidly evacuated. Because the victim is usually incapable of participating in evacuation, a litter should be prepared or aeromedical evacuation considered. Intercostal nerve block may assist in short-term management of pain and pulmonary toilet. Restrictive (to chest wall expansion during inhalation) external chest wall supports, including taping or extensive stabilization with sandbags, are contraindicated. These measures hinder chest wall movement, decrease vital capacity, and are less effective than intercostal nerve block in pain control. However, focal stabilization or cushioning of the flail segment only to control unnecessary motion and pain may provide minimal relief from the discomfort.

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management Blunt Cardiac Injuries. Blunt cardiac injuries leading to pericardial tamponade or cardiac contusion are rare. Pericardial tamponade is life-threatening. The pericardial sac is fibrous and expands little. A small amount of intrapericardial blood can severely restrict diastolic function. Blunt injury resulting in tamponade is usually from chamber rupture and rarely survivable, particularly in a remote setting. The diagnosis of tamponade can be difficult, particularly in the wilderness. Beck’s triad, which consists of distended neck veins, hypotension, and muffled heart sounds, is present in less than 33% of cases of tamponade and is particularly difficult to ascertain under nonoptimal conditions. Pulsus paradoxus, an increase in the normal physiologic decrease in blood pressure with inspiration, may be indicative of tamponade. Kussmaul’s sign, or a rise in venous pressure with spontaneous inspiration, is possible to assess outdoors. Once pericardial tamponade is diagnosed, immediate evacuation is required. Treatment consists of median sternotomy in a hospital operating room. The only temporizing measure pending evacuation is pericardiocentesis. This procedure can be lifesaving, particularly if a cardiac injury with a slow leak exists. However, its application in the wilderness setting should occur only if there is a high index of suspicion, coupled with shock and impending death unresponsive to resuscitative efforts. A long (approximately 15 cm [6 in]), 16- to 18-gauge needle with an overlying catheter is introduced through the skin 1 to 2 cm (0.5 to 0.75 in) below and to the left of the xiphoid. The needle is advanced at a 45-degree angle with the tip directed at the tip of the left scapula. When the pericardial sac is entered, aspiration with a syringe follows. The catheter is left in place and secured for possible repeat aspirations as the victim’s condition warrants. Immediate evacuation should follow. Cardiac contusion is a rare condition resulting from a severe blow to the precordium. An overlying sternal contusion or fracture may be present. The diagnosis should be suspected in an isolated high-velocity blow to the precordium with unexplained evidence of increased venous pressure, arrhythmias, and hemodynamic instability. Chest pain is invariably present, usually resulting from musculoskeletal contusion. Morbidity results from ensuing arrhythmias. Diagnosis can be definitively made only at autopsy. Electrocardiographic abnormalities after injury have correlated with subsequent arrhythmias.55 In the wilderness setting, any person who is unstable or symptomatic from an arrhythmia should be evacuated. If evacuation is not possible, it is noteworthy that fatal arrhythmia potential decreases significantly after 24 hours. Traumatic Asphyxia. Traumatic asphyxia is a rare syndrome of craniocervical cyanosis, facial edema, petechiae, subconjunctival hemorrhage, and occasional hypoxemia-related neurologic symptoms that results from severe thoracic crush injury. In the wilderness environment, it is associated with land or mudslides, avalanches, or falling debris. Any significant blunt compressive force to the thorax can result in the syndrome. Children are particularly susceptible because of high compliance of the chest wall.16 Traumatic asphyxia is not a benign condition, as a result of a high incidence of serious associated injuries,71 and the mortality rate in natural disasters is consequently high.33 A number of studies have documented the severity of associated injuries, with the syndrome useful as an indicator of potentially lethal injury.24 As documented in natural disasters, a significant crush injury component may accompany traumatic asphyxia.33 Crush

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Figure 20-8. Typical clinical facial appearance of traumatic asphyxia.

injuries and rhabdomyolysis are discussed later in the Extremity Trauma section of this chapter. The pathophysiology of traumatic asphyxia involves two elements. The crush injury results in acute increases in intrathoracic pressure and thus inferior and superior vena caval pressures. Venous flow is reversed in the veins of the head, which contain no valves. Venous hypertension leads to capillary rupture and the characteristic facial edema and petechiae. Recognition of the physical findings is imperative in diagnosing the syndrome and identifying concomitant injuries (Fig. 20-8). Treatment consists of carefully extracting and, if necessary, immobilizing the victim. Rapid extrication is the single most important factor in improving survival. Establishment and maintenance of an airway is critical because significant facial and laryngeal edema may rapidly develop. Associated injuries should then be addressed in the primary survey. Subsequent care is supportive, consisting of airway control, administration of oxygen, head elevation of 30 degrees, treatment of associated injuries, and possible evacuation. The mortality rate is low in civilian environments but higher in wilderness disaster settings. Mortality is due to pulmonary dysfunction and associated injuries. Morbidity is secondary to neurologic damage; however, the majority of neurologic sequelae clear within 24 to 48 hours. If the victim survives, long-term sequelae are rare.

Penetrating Chest Trauma Penetrating chest trauma above the nipple line is associated with hemopneumothorax and may also be associated with significant visceral injury. A victim with penetrating chest trauma below the nipple line often has intra-abdominal penetration in addition to possible thoracic injury. Such a victim requires immediate rapid evacuation. The open (“sucking”) chest wound produces profound intrathoracic physiologic alterations. Normal chest expansion creates negative intrathoracic pressure, which pulls air into the trachea and allows the lungs to expand. When the diaphragm and chest wall relax, positive pressure creates expiration. If the chest wall sustains an injury approximately two thirds the tracheal diameter, negative intrathoracic pressure for inspiration is lost, the ipsilateral lung collapses, and loss of negative

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS evaluate by physical examination. Life-threatening hemorrhage can occur into the true abdomen or retroperitoneal space.

Diagnosis. Although much progress has been made in the last decade to evaluate for the presence of blunt intra-abdominal injury, modalities such as CT, ultrasonography, and diagnostic peritoneal lavage are irrelevant in the wilderness setting. The wilderness physician must have a high index of suspicion and perform a superlative history and physical examination.

Figure 20-9. Treatment of a sucking chest wound. Sealing the wound with a gel defibrillator pad works best because this pad adheres to wet or dry skin. Petrolatum gauze or Saran Wrap also works well. Note that one side is not sealed to allow egress of air.

intrathoracic pressure affects the good lung. Consequently, it is important rapidly to reconstruct chest wall integrity. Initially, this is most easily done by placing a hand over the sucking chest wound. Field treatment includes placing petrolatum gauze on top of the wound, covering it with a 4 × 4 gauze pad, and taping it on three sides (Fig. 20-9). The untaped fourth side serves as a relief mechanism to prevent tension pneumothorax. Persons with sucking chest wounds should be rapidly evacuated to sophisticated medical care.

Injuries to the Abdomen Intra-abdominal injuries in the wilderness setting are difficult to recognize. However, if recognized, all intra-abdominal injuries require rapid resuscitation and immediate evacuation. The abdomen represents the most frequent site of life-threatening hemorrhagic shock; however, in the wilderness setting, few diagnostic and treatment options exist.

Blunt Abdominal Trauma Blunt intra-abdominal injury is commonly associated with falls. Abdominal injuries are often associated with fractures or closed head injuries. Often, the decision for evacuation is made on the basis of other injuries; however, the wilderness physician must be attuned to the potential for intra-abdominal hemorrhage as an occult injury.

Anatomy. For descriptive purposes, the abdomen may be divided into thoracic, true, and retroperitoneal compartments. The thoracic abdomen contains the liver, spleen, stomach, and diaphragm. The liver, spleen, and, more rarely, stomach may be injured by direct blows to the ribs or sternum. Twenty percent of persons with multiple left lower rib fractures have a ruptured spleen. A direct blow to the epigastrium may result in increased intra-abdominal pressure with subsequent rupture of the liver or diaphragm. The true abdomen contains the small bowel, large bowel, and bladder. Isolated bowel injuries are rare in the wilderness setting. Blunt bladder or rectal injury usually occurs in conjunction with severe pelvic fracture and carries high mortality. The retroperitoneal abdomen contains the kidneys, ureters, pancreas, and great vessels. It is notoriously difficult to

Physical Examination. The physician should look for signs of early shock: tachycardia, tachypnea, delayed capillary refill, weak or thready pulse, and cool or clammy skin. Physical examination of the abdomen begins with visualization and inspection. Contusions and abrasions may be the only harbingers of occult visceral injury. Periumbilical ecchymosis associated with abdominal hemorrhage (Cullen’s sign) is virtually never present in a victim with acute abdominal trauma. Abdominal distention secondary to hemorrhage is a very late sign and never present before shock and cardiovascular collapse. Abdominal inspection should survey the flanks, lower chest, and back. Inspection of the back should follow palpation of the spine while the victim is supine. The victim should be very carefully logrolled if there is any suspicion of spinal injury. Looking for muscle guarding, the examiner gently palpates the abdomen in all four quadrants. Any persistent guarding or tenderness after wilderness trauma mandates rapid evacuation. Percussion tenderness is an indicator of peritoneal irritation, also mandating evacuation. The presence or absence of bowel sounds has little prognostic significance. Bowel sounds may be present in the face of significant intra-abdominal hemorrhage or, conversely, absent in victims when extra-abdominal injuries induce ileus. Referred pain to the left shoulder (Kerr’s sign) strongly suggests the presence of a ruptured spleen. This pain is often exaggerated by placing the victim in Trendelenburg’s position, increasing the amount of left upper quadrant blood irritating the diaphragm. Pain from the retroperitoneal abdomen associated with injuries to the kidney or pancreas may be referred to the back. However, referred pain is usually a late finding and not helpful in the evaluation of acute trauma. Gross hematuria that does not clear immediately or is coupled with an associated injury, such as pelvic fracture or abdominal or back pain, requires immediate evacuation. To minimize blood loss, the victim should be kept stationary and the evacuation team brought as close to the victim as possible. In a wilderness setting, rectal and vaginal examination adds little to the evacuation decision when evaluating for abdominal trauma. The unstable pelvic fracture associated with rectal and vaginal injuries is usually the determinant for evacuation.

Penetrating Abdominal Trauma Penetrating intra-abdominal injuries may result from gunshot, stab, or arrow wounds. The social context in which these injuries occur (accidental, intentional, or self-inflicted) makes little difference in the wilderness setting. Recrimination, guilt, and blame only interfere with the paramount goal of immediate evacuation.

Gunshot Wounds. Low-caliber gunshot injuries often present with small entrance and no exit wounds. High-caliber, high-

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management velocity gunshot injuries may have relatively innocuous entrance wounds but may be associated with large, disfiguring exit wounds and extensive internal injuries. No matter what the caliber or trajectory and no matter where the entrance and exit, all gunshot wounds from the nipple line to the inguinal ligament should be presumed to have penetrated the abdominal cavity and created an intra-abdominal injury. These injuries mandate immediate surgical intervention. A victim of gunshot wounds to the head, neck, chest, abdomen, or groin should undergo immediate evacuation accompanied by the administration of a single-agent broad-spectrum antibiotic, such as an oral fluoroquinolone (e.g., ciprofloxacin, 750 mg PO bid). Hunting injuries are discussed in Chapter 22.

Shotgun Injuries. Shotgun injuries to the torso are managed in the same manner as gunshot wounds. Shotgun injuries have a potentially lower incidence of underlying visceral injury than gunshot wounds, but there is often extensive soft tissue damage requiring surgical debridement. The potential exists for delayed development of peritonitis from a single penetrating pellet to the viscera. Consequently, shotgun injuries should also be treated with emergency evacuation and a broad-spectrum antibiotic, as recommended previously for gunshot wounds. Occasionally, a close-range shotgun blast results in a soft tissue defect large enough for the injured bowel to extrude through the wound. The injured bowel should not be placed back into the abdomen. Injured bowel displaced from the abdominal cavity conceptually should be treated as though it were an enterocutaneous fistula. Because evacuation is often delayed in the wilderness, it is better to have fecal contents outside, rather than inside, the peritoneal cavity. The exteriorized bowel should be kept moist and covered at all times. Uncovered bowel outside the peritoneal cavity rapidly desiccates and becomes nonviable, mandating later surgical resection. Exposed bowel should be covered with an abdominal pack or cloth moistened with sterile saline at best, or at worst with potable water. The dressing should be checked and remoistened at least every 2 hours. Stab Wounds. The penetrating object is usually a knife but may be as varied as a piton, ski pole, or tree limb. Any deep skin laceration from the nipple line to the groin should be considered to have damaged an intra-abdominal organ. Whereas the odds of an abdominal gunshot wound injuring a visceral organ exceed 85%, the odds of a stab wound injuring a visceral organ are less than 50%. In certain urban hospitals, the high incidence of negative surgical explorations for stab wounds had led to a more selective approach toward patients with abdominal stab wounds.69 This approach uses local wound exploration and frequent physical examination. Although there are no data addressing the management of stab wounds in the wilderness environment, the following approach is practical and reasonable. If the wound extends into the subcutaneous tissue, the evacuation decision depends on local wound exploration. This procedure is simple to perform, even in the wilderness environment. The skin and subcutaneous tissue are infiltrated with local anesthetic, and the laceration is extended several centimeters to clearly visualize the underlying anterior fascia. It is helpful to use lidocaine (Xylocaine) 1% with epinephrine to minimize slight but annoying bleeding that

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can impair visualization. The wound should never be probed with any instruments, particularly if overlying the ribs. Wound exploration is confined to the area from the costal margin to the inguinal ligament. Local wound exploration is contraindicated in wounds that extend above the costal margin, because it is possible for such exploration to communicate with a small pneumothorax, potentially exacerbating respiratory distress. If thorough exploration of the wound shows no evidence of anterior fascial penetration, and if the victim demonstrates no evidence of peritoneal irritation, the wound can be closed with tape (Steri-Strips) or adhesive bandages, dressed, and the evacuation process delayed. Physical examination should be performed every few hours for the next 24 hours. If no peritoneal signs develop and the victim feels constitutionally strong, a remote expedition may resume with caution and an eye to evacuation should the victim become ill. In the wilderness environment, it is prudent to have a low threshold for evacuation because of technical difficulties in performing wound exploration, such as insufficient light and inadequate instruments. Persons who have been impaled by long objects, such as tree limbs or ski poles, should have the object left in place and carefully shortened, if possible, to facilitate transport.

Pelvic Trauma In the wilderness setting, fractures of the pelvis are generally associated with falls from significant heights, high-velocity ski accidents, or vehicular trauma. Pelvic fractures can be lethal. With opening of the pelvic ring, there may be hemorrhage from the posterior pelvic venous complex and occasionally from branches of the internal iliac artery. For hemodynamically unstable victims with severe pelvic fracture, resuscitative efforts should be instituted. In addition, simple techniques to reduce any increased pelvic volume through the application of sheets or slings may slow bleeding. The key factor in initial management of pelvic fractures is identification of posterior injury to the pelvic ring. Posterior ring fractures or dislocations are associated with a greater incidence of significant hemorrhage, neurologic injury, and mortality than are other pelvic fractures. The diagnosis of a posterior ring fracture is based on instability of the pelvis associated with posterior pain, swelling, ecchymosis, and motion. Persons with posterior ring fractures must be immediately evacuated on backboards, with care taken to minimize leg and torso motion. The flank, scrotum, and perianal area should be inspected for blood at the urethral meatus, swelling or bruising, or a laceration in the perineum, vagina, rectum, or buttocks suggestive of an open pelvic fracture. The pelvis should be examined carefully once, without any aggressive rocking motion. The first indication of mechanical disruption is leg length discrepancy or rotational deformity in the absence of an obvious leg fracture or hip location. For more information on pelvic fracture, see Chapter 24.

Extremity Trauma The majority of wilderness-related extremity injuries involve fractures and sprains, which are discussed in Chapter 24. This section focuses on the general field management of significant extremity vascular injury, traumatic amputation, and recognition and treatment of rhabdomyolysis.

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Vascular Injuries Injury to the major vessels supplying the limbs can occur with penetrating or blunt trauma. Fractures can produce injury to the vessels by direct laceration (rarely) or by stretching, which produces intimal flaps. Penetrating injuries can be devastating if transection of a vessel occurs. Significant vascular injuries, from both penetrating and blunt causes, can result in multiple vessel injury subtypes, each of which may be limb-threatening. Injury subtypes include laceration, transection, contusion with spasm, thrombosis, or aneurysm formation (true and false), external compression, and arteriovenous fistula. An accurate history, expeditious physical examination, and swift evacuation are the keys to life and limb salvage.

History. A complete history of the time and mechanism of injury is invaluable in planning further management. Although no absolute ischemia time has been established, a goal of less than 6 hours to reperfusion is prudent.30 The amount of blood present at the scene should be quantified. A history of bright pulsatile blood that abates is suggestive of arterial injury. Thirty-three percent of victims with arterial injuries have intact distal pulses. Physical Examination. Vascular examination in the field can be highly variable. Hypovolemia, hypothermia, and hostile conditions make an accurate examination challenging. Skin color and extremity warmth should be assessed first. Distal pallor and asymmetric hypothermia are suggestive of a vascular injury. Pulses should be palpated. In the upper extremity, the axillary, brachial, radial, and ulnar arteries should be assessed. In the lower extremity, the femoral, popliteal, posterior tibial, and dorsalis pedis pulses should be assessed. Location and direction of the wound should be determined, hemorrhage quantified, and the presence of hematomas or a palpable thrill noted. A good neurologic examination that quantifies motor and sensory deficits is critical. Because of the high metabolic demands of peripheral nerves, disruption of oxygen delivery makes neuronal cells highly susceptible to ischemic death. Conversely, skeletal muscle is relatively resistant to ischemia. Loss of sensation or limb paralysis is an alarming sign of impending anoxic necrosis. Treatment of Vascular Injuries. Significant hemorrhage should be identified and controlled in the primary survey. All hemorrhage should be controlled with direct pressure at the site of injury. Tourniquets should be applied only when direct pressure fails to control bleeding. Tourniquets should be released every 5 to 10 minutes to prevent further ischemia. Hematomas should never be explored or manually expressed. Attempts to clamp or ligate vessels are not recommended. Frequent repeat neurovascular examinations are mandatory. Once bleeding is controlled and the wound is covered with a sterile but noncompressive dressing, completion of the primary survey, identification and stabilization of associated injuries, and appropriate resuscitation with normal saline should follow. The extremity should be splinted to prevent further movement. The need for evacuation depends directly on the results of the physical examination. Examination results can be grouped into “hard signs,” indicative of ischemia or continued hemorrhage, and “soft signs” that are suggestive but not indicative of ischemia (Boxes 20-3 and 20-4).

Box 20-3. Vascular “Hard Signs” Pulsatile bleeding Palpable thrill Audible bruit Expanding hematoma Six “P’s” of regional ischemia Pain Pulselessness Pallor Paralysis Paresthesia Poikilothermia

Box 20-4. Vascular “Soft Signs” Injury in proximity to major vessel Diminished but palpable pulses Isolated peripheral nerve deficit History of minimal hemorrhage All victims with hard signs should be evacuated emergently. Based on current data, an isolated soft sign may warrant observation alone, depending on the remoteness of the expedition and the risks of evacuation. The data for observation of soft signs have emerged from hospital settings and must be applied with great caution in the wilderness. If soft signs are present, clinical suspicion is high, and evacuation can be accomplished safely, the victim should be transported and observed in a medical facility.

Traumatic Amputation In the wilderness environment, amputation victims require immediate evacuation. Hemorrhage is controlled during the primary survey with direct pressure, and resuscitation is instituted. Tourniquets are rarely required. The victim should be kept warm and calm. Reassurance and analgesics should be administered. Amputations should be completed only if minimal tissue bridges exist and it is clear that the neurovascular supply has been interrupted. Amputation of a mangled extremity, defined as an extremity with high-grade open fracture and soft tissue injury, should not be carried out in the wilderness except to free a trapped victim in order to avoid further severe injury or even death, or in the case of uncontrollable hemorrhage threatening the life of the victim, and then only by experienced surgical personnel. All other severely injured extremities should be wrapped in available sterile materials, splinted, and kept moist. Amputated extremities should be cooled if possible, optimally in a plastic bag in ice or ice water. Avoid placing the extremity in direct contact with ice. Without cooling, the amputated extremity remains viable for only 4 to 6 hours; with cooling, viability may extend to 18 hours. The amputated extremity should accompany the victim throughout the course of the evacuation.

Crush Injuries and Rhabdomyolysis Rhabdomyolysis is a potentially fatal syndrome that results from lysis of skeletal muscle cells. In its fulminant form, rhabdomyolysis can affect multiple organ systems. Compartment

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management syndrome, renal failure, and cardiac arrest represent the major complications. Any condition resulting in significant acute or subacute striated muscle damage can precipitate rhabdomyolysis. Crush injuries of the extremities and pelvis, revascularization of ischemic tissue, ischemic extremities, animal bite and snakebite,17,23 frostbite, and traumatic asphyxia33 can all result in rhabdomyolysis in a wilderness setting. Crush injuries are frequently a result of avalanches, falls from heights, or rock slides. The pathophysiology of rhabdomyolysis remains controversial. The exact mechanism of muscle injury appears not to be simple direct force or isolated ischemia and is probably multifactorial.33 The common cellular derangement is interference of the normal function of muscle cell membrane sodium-potassium adenosine triphosphatase (ATPase) with intracellular calcium influx and cell death.77 After cell death, multiple intracellular constituents, including myoglobin, creatine kinase, potassium, calcium, and phosphate, are released into the systemic circulation. The metabolic derangements of rhabdomyolysis depend directly on release of intracellular muscle constituents. Myoglobinemia, hypercalcemia, hyperphosphatemia, hyperkalemia, hyperuricemia, metabolic acidosis, coagulation defects, and contracted intravascular volume result. The clinical presentation of rhabdomyolysis may include muscle weakness, malaise, fever, tachycardia, abdominal pain, nausea and vomiting, or encephalopathy. Symptoms may mimic those of persons with spinal cord injury.8 The danger of the syndrome lies in the cardiovascular effects of electrolyte disturbances and renal failure70 secondary to changes in renal perfusion and direct toxicity of myoglobin to tubular cells. Successful treatment relies on prompt diagnosis based on clinical signs and urinalysis, aggressive hydration, and forced diuresis. Myoglobin turns urine tea-colored, which is an important indicator of significant muscle death and need for aggressive treatment. Normal saline should be administered IV at 1 to 2 L/hr to achieve a urine output of 100 to 300 mL/hr. Victims who are trapped in rubble should have resuscitation initiated before extrication, if possible. The addition of agents to alkalinize the urine and promote diuresis has been shown to improve clearance of myoglobin but not to alter survival. In addition, diuretics may be detrimental in multisystem trauma victims who are hypovolemic. All victims demonstrating myoglobinuria should be evacuated.

Injuries to the Skin and Wilderness Wound Management The goals of wilderness wound management are to minimize wound complications and promote healing. Treatment should begin with an approach to the victim as a trauma patient. Within the context of the primary survey, hemorrhage should be controlled. Then, the victim should be examined and the wound inspected. Steps to minimize infection should be undertaken, incorporating anesthesia, assessment of need for tetanus immunization and antibiotics, irrigation, and debridement. After attempts to minimize infection, a definitive plan should be established, including the need for evacuation (Box 20-5).

Wound Morphology Major lacerations are often the most obvious sign of trauma; however, injuries to the integument are rarely life-threatening.

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Box 20-5. Guidelines for Wilderness Wound Management 1. 2. 3. 4.

Identify and stabilize associated traumatic injuries Control hemorrhage Examine wound Minimize infection a. Tetanus immunization as indicated b. Antibiotics for high-risk wounds c. Irrigation d. Debridement 5. Implement definitive care

Contusions, abrasions, and lacerations should force the examiner to focus on areas of potential occult injury. Contusions often overlie extremity fractures or, when present on the torso, suggest the potential for underlying visceral injury. Extremity lacerations may be associated with fractures or may extend into the joint space. The four basic types of skin injuries are lacerations, crush injuries, stretch injuries, and puncture wounds. Lacerations rarely require closure in the wilderness environment. Commonly, multiple wound morphologies are present in the same injury, and an array of wound presentations is possible. Crush injuries may be associated with significant tissue necrosis, impaired healing, increased rates of infection, and underlying muscle damage with subsequent rhabdomyolysis. Fortunately, they are rare in the wilderness. Stretch injuries produce a split in the skin but, more important, may be associated with underlying nerve or tendon damage. Puncture wounds often appear innocuous but have a high propensity for infection. Animal bite wounds, discussed in detail in Chapters 51 and 52, can manifest any of these wound morphologies alone or in combination.

Primary Survey Many skin and soft tissue wounds encountered in the wilderness setting accompany significant injuries. Therefore, the wound must never distract the physician from associated lifethreatening injuries. The ATLS primary survey should be performed in the usual fashion.

Control of Hemorrhage The vast majority of bleeding is controlled with direct pressure, applying the most sterile covering available. Applying pressure over major arterial pressure points is discouraged, as is the use of tourniquets. In the event of bleeding not controlled by direct pressure, tourniquets may be applied with the knowledge that limb sacrifice is possible. If applied, tourniquets should be released every 5 to 10 minutes if possible to restore perfusion transiently and to assess if they are still necessary. Clamping bleeding vessels is not advised because this may cause unnecessary neurovascular injury.

Physical Examination Wound inspection and physical examination are critical in any setting. This phase of treatment may need to be abbreviated and should not delay packaging and evacuation. Although it is important to assess the extent of injury, including tissue loss and

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underlying musculoskeletal and neurovascular injury, aggressive wound exploration may worsen existing injuries. Detailed knowledge of regional anatomy is useful. The detailed neurovascular examination should be documented before anesthesia and definitive care, including assessment of pulses and regional perfusion. The neurologic examination should quantify sensory and motor function, with particular attention to functional assessment of muscle groups traversing the injured region. Two-point discrimination should be assessed in wounds involving the hands or fingers. Wounds over joints and tendons should be put through full range of motion.

Anesthesia Pain management in the wilderness is discussed in Chapter 17. Administration of anesthesia occurs before mechanical wound cleansing and definitive care. The three methods of anesthetic administration briefly discussed here are topical, local, and regional. Topical anesthesia was originally introduced for mucosal lacerations but has been shown to be effective for skin wounds. TAC (sterile tetracaine 0.5%, adrenalin [epinephrine] 1 : 2000, and cocaine 11.8% in saline) has been used with success as a topical anesthetic. Complications have included seizures and death.93 An alternative preparation consisting of lidocaine, adrenalin, and tetracaine (LAT) has been shown to be as effective as TAC without the associated complications.29 Topical anesthetics may be soaked into a sterile gauze and placed on the wound surface for 7 to 10 minutes. Disadvantages of topical anesthetics include potential for a slightly increased risk of infection and less versatility than locally injected lidocaine. Local anesthesia is the standard method for achieving soft tissue analgesia. Typically, 1% lidocaine without epinephrine is used. In adults, the maximum injectable dose of lidocaine is 4 mg/kg. Lidocaine should not be injected directly from within the wound to the periphery because this increases the chance of introducing bacteria deeper into the soft tissue.64 The injection should proceed from the periphery of the wound, with each successive needle stick entering the skin through a previously anesthetized area. Local anesthesia can be administered with relatively little discomfort using a 25-gauge needle and a 1-mL tuberculin syringe. Although using a small syringe increases the time to anesthetize a larger wound, this method minimizes both the anesthetic dose and distortion of soft tissue planes, facilitating tissue repair. Pain associated with administration of local anesthesia is due to the acidity and stretching of nerve endings within the dermis and subcutaneous tissue. Burning sensation associated with lidocaine injection is directly proportional to the rate of administration. Warming the local anesthetic,46 buffering the solution with sodium bicarbonate to a concentration of 1%, and administering anesthetic slowly in small doses all minimize pain. Regional anesthesia, defined as sensory nerve blockade proximal to the wound, is an excellent mode of anesthetizing wounds of the upper and lower extremities. Two types are regional nerve block and Bier block. Regional nerve blocks require skill and a detailed knowledge of regional anatomy. They are not suitable for the first-time user in the wilderness environment. The Bier block is reasonable to administer and is possible in the wilderness setting. It involves injection of local anesthetic

into a cannulated hand or foot vein, with concurrent control of venous outflow using a tourniquet.

Irrigation Once the wound is anesthetized, irrigation, debridement, and closure can proceed. Irrigation removes dirt, debris, foreign bodies, and bacteria from the wound. Irrigation has been extensively studied in traumatic wounds and clearly results in a decreased incidence of infection, reducing infection rates as much as 20-fold when proper technique is used. The type of irrigation fluid and the technique used are resource dependent in the wilderness setting. The cleanest fluid available should be used. Wilderness fresh water sources that are not grossly contaminated can be boiled or filtered.32 Any concentration of sterile crystalloid solution can be used, although normal saline remains the most readily available, economical, and cost-effective irrigation solution. Recent data suggest that tap water may be as effective as normal saline.66 The amount of irrigation necessary is difficult to quantify. Some authors use 60 mL (2 ounces) of irrigation solution per centimeter wound length as a guide,46 but in the wilderness setting where precision is more difficult to attain, irrigation should be continued in amounts and time intervals sufficient to remove visible debris from the wound. Many bactericidal and bacteriostatic irrigation solutions, including commercial soaps, ethyl alcohol, iodine solutions, and hydrogen peroxide, are available in wilderness first-aid kits. Many of these agents have been shown to result in significant microcellular destruction of tissues15 and, when used in high concentrations, may impair wound healing. They offer no advantage over copious irrigation with sterile water or crystalloid. Although addition of antibiotics to irrigation solutions is an attractive concept, they are costly, difficult to store, and offer no advantage over irrigation with sterile water alone. The method of wound irrigation, as well as the pressures used, have been studied extensively. The goals of irrigation are to remove bacteria, assist in the mechanical debridement of necrotic tissue, and remove foreign bodies that can impair subsequent wound healing. Optimal irrigation pressures are 5 to 8 psi, delivered through a syringe with a 16- to 20-gauge needle. A splash shield attached to the syringe should be used if available. In summary, irrigation consisting of normal saline or sterilized potable water should be delivered in a continuous fashion by the most sterile implement available at a pressure sufficient to dislodge debris but not overtly damage tissue.

Debridement Like irrigation, debridement has been shown to decrease the incidence of wound infection. In addition, debridement has the potential to improve long-term cosmesis. Debridement should be carried out sharply. Scrubbing the wound with abrasive materials does not improve infection rates and may cause damage to healthy tissue. Similarly, soaking the wound has never been shown to improve outcome. Hair removal should be undertaken only if it impairs visualization and inspection of the wound,93 or if tape is to be used as a method of temporary closure. The goal of debridement in the wilderness should be to remove grossly contaminated or devitalized tissue and to remove foreign bodies and bacteria embedded in such tissue.

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TABLE 20-3. Tetanus Prophylaxis CLEAN MINOR WOUNDS HISTORY OF IMMUNIZATION (DOSES) Unknown None to one Two Three or more Last booster within 5 years Last booster within 10 years Last booster more than 10 years ago

DIRTY MAJOR WOUNDS

TOXOID*

TIG†

TOXOID

TIG

Yes Yes Yes

No No No

Yes Yes Yes

Yes Yes No (unless wound older than 25 hr)

No No Yes

No No No

No Yes Yes

No Yes Yes

*Toxoid: Adult: 0.5 mL dT intramuscularly (IM). Child less than 5 years old: 0.5 mL DPT IM. Child older than 5 years: 0.5 mL DT IM. † Tetanus immune globulin (TIG): 250–500 units IM in limb contralateral to toxoid.

The extent of tissue removal should be based on the experience and training of the caregiver.

Tetanus Prophylaxis Spores of Clostridium tetani are ubiquitous in the environment in such places as soil, animal teeth, and saliva. Any animal bite that penetrates the skin can be responsible for a tetanus infection. The majority of cases of tetanus infection in the United States follow failure to attain adequate immunization.79 This fact accentuates the preventable nature of tetanus infections and essential role of proper immunization. If available in the wilderness setting, tetanus prophylaxis should be administered as outlined in Table 20-3.

Definitive Care of Lacerations “Definitive” care may have many definitions, depending on the setting. The planned approach to management of wounds in the wilderness is determined by a combination of morphology of the wound, infection risk factors, available resources, level of expertise, and type of expedition. Major lacerations or those associated with significant injury should be evacuated. If wound management cannot acceptably minimize infection risk factors, the victim should be evacuated. In general, wounds that can be closed or managed open and that do not impose excessive infection risk factors and do not immobilize the expedition member or group can be treated definitively in the wilderness. The wound must not impair physical ability in a way that the victim risks further injury or jeopardizes group safety.

Wound Closure. Lacerations can be closed if they are small to intermediate in size; have minimal infection risk factors; are on well-vascularized regions, such as the scalp and face; are less than 6 hours old; and have no anatomic contraindications. Closure may be accomplished with suture, staples, tape and similar bandages, or adhesives. Tape and, less frequently, adhesives are viable alternatives to sutures. Healing and cosmetic outcome depend directly on dermal apposition, which is the goal of any closure method. Advantages of sutures include meticulous closure and high wound tensile strength. The primary disadvantage is the skill

necessary to place them. The suture selected is dictated by morphology of the wound. To simplify selection in the wilderness environment, absorbable sutures, such as chromic gut and polyglactin (Vicryl), should be used to close deep layers and for subcuticular closures. Nonabsorbable sutures, such as nylon (Ethilon) and polypropylene (Prolene), should be used on the skin. Silk is reactive, has poor tensile strength, and should be avoided. No wound should be sutured by an individual who is inexperienced in basic surgical technique. In addition, no wound incurred in the wilderness is truly risk-free regarding infection. In general, the safest management strategy for lacerations in the wilderness setting is open management or closure with nonsuture alternatives. Surgical staples are easily placed, are nonreactive, have lower infection rates than sutures, and minimize time of closure.93 They should be avoided on areas of cosmetic importance, such as the face. Tapes and adhesives offer a preferable alternative to sutures. Tape and adhesive strips (e.g., Steri-Strips) are easily applied and require little technical ability. If a wound is appropriate for closure, tape offers a rapid, safe, painless, and inexpensive alternative to sutures and staples.27 The only requirement of tape use is conformity to principles of dermal apposition. Disadvantages of tape include need for adhesive solutions, such as benzoin; low tensile strength; and lack of applicability over any region of tension.93 A critical limiting factor in wilderness use of tape closure is the need for the wound to remain dry. Tissue adhesives in wound closure have been studied for 20 years.26 Recently, octylcyanoacrylate and similar synthetic agents have been shown to be equal in strength and cosmesis to sutures at 1 year.81 Advantages of adhesives include ease of application, safety, patient comfort, and low cost.94 Similar to tape, immediate tensile strength is poor and dehiscence is more likely compared with sutures.93 If closure is possible and other means are unavailable or impractical, adhesives may be used.

Scalp Lacerations. The extent and severity of scalp lacerations are often initially obscured by surrounding hair that is matted with blood. Hydrogen peroxide and water effectively remove blood from hair, although hydrogen peroxide should not be

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used to irrigate the wound. Interestingly, and most likely owing to the vascularity of the scalp, irrigation did not alter outcome in clean lacerations in one study.43 Hair surrounding the laceration is removed using a safety razor only if absolutely necessary to clean the wound. Hair removal should be limited to the immediate area of the laceration because the surrounding hair can later be twisted into strands and used to approximate the wound edges if necessary. Once wound margins have been identified, anesthetic should be applied. The key to examination of the scalp is determining the integrity of the galea. Significant degloving injury or galeal laceration may mandate evacuation. The scalp is highly vascularized. An extensive scalp laceration bleeds freely, and if it follows a fall or direct blow to the head, may be associated with an underlying skull fracture. Superficial scalp lacerations often bleed freely and may require pressure dressings to achieve hemostasis. Minor scalp lacerations can be effectively treated in the wilderness setting, after following the aforementioned infectionminimizing steps. Of note, debridement of scalp wounds should be kept to a minimum because it may be difficult to mobilize wound edges to cover the resulting soft tissue defect. In addition, cosmesis is not a significant concern on the hair-covered scalp. Acceptable closure of a minor scalp laceration can be performed using strands of hair to approximate wound edges. The hair on either side of the wound can be twisted into a thick bundle. The opposing bundles are then pulled together and crossed. They can be secured with a drop of tissue glue or tied together if glue is not available (see Figure 21-45). This method minimizes shaving.

Facial Lacerations. Facial lacerations are relatively simple to manage because they rarely damage underlying structures and are well vascularized. If suspicion exists regarding damage to cranial nerves or the parotid duct, the wound should be managed in an open fashion. Debridement should be limited to obviously necrotic tissue. Because of vascularity of the face, infection is rare, and most wounds can be closed. For small wounds, tape is a useful closure technique. Torso Lacerations. Torso lacerations require evaluation for fascial penetration. Anterior fascial penetration in the torso converts the wound from a skin wound to one requiring management of underlying chest or abdominal structures. Tissue debridement may be more aggressive over the torso because surrounding tissue planes can be mobilized for closure. Adipose tissue should not be approximated with sutures, and subdermal dead space should be obliterated with deep, nonadipose approximating sutures.

Hand Injuries Severe contusions to the hand commonly occur with crush or rope injuries. The hand should be carefully protected if marked swelling and pain with motion are present. If no joint instability or fracture is identified, a bulky hand dressing should be applied with the wrist dorsiflexed 10 degrees, the thumb abducted, and the metacarpophalangeal joints flexed 90 degrees, known as the position of function. Cotton wadding or bandages can be placed in the palm and between the fingers, and an elastic bandage can be used as an overwrap. A volar

splint allows this position to be maintained until definitive care is reached. Lacerations of the finger flexor or extensor tendons occur with accidents involving knives or other sharp objects. A flexor tendon laceration, partial or complete, can be a serious problem if not repaired early. The open wound should be cleansed and loosely taped closed if no infection risk factors are present, and the finger should be splinted in slight flexion at the interphalangeal joints and in 90 degrees of flexion at the metacarpophalangeal joint. To achieve optimal results, this injury should be managed by a hand surgeon within the first 3 to 5 days. For an extensor tendon, the open wound should be cleansed and taped closed, and a splint should be applied with the metacarpophalangeal joint in slight flexion and the interphalangeal joint extended. The victim should be seen by an orthopedic surgeon within 7 days. The nerves most commonly injured by laceration include the superficial radial nerve at the wrist, ulnar nerve at the elbow or wrist, and median nerve at the wrist. Digital nerves are commonly lacerated in accidents with knives. In general, the wound should be cleansed and taped loosely and a splint should be applied to the wrist and hand. The victim should see a hand surgeon within 7 days.

Puncture Wounds Puncture wounds carry significant infection risk where organic contamination is frequent. Significant puncture wounds to the torso should be treated according to the guidelines outlined in the section on penetrating trauma to the chest and abdomen. Puncture wounds to the extremities should be unroofed if they are proximal to the wrist or ankle. The unroofed wound should be irrigated as previously described and then packed open with sterile gauze. Delayed primary closure with tape can occur at 48 to 96 hours. Puncture wounds to the hands and feet should not be explored in the absence of detailed knowledge of anatomy. If this expertise is not available, the wound should be cleaned and the victim started on antibiotics, such as cephalexin (Keflex) 500 mg PO q6h. If the skin is punctured with a fishhook, the skin surrounding the entry point should be cleansed with soap and water. Fishhook removal techniques are discussed in Chapter 22.

Antibiotic Use and Infectious Complications The use of prophylactic antibiotics for wounds incurred in the wilderness is not recommended. Antibiotic treatment usually begins after the injury has occurred and therefore is never truly “prophylactic.” The use of antibiotics in lacerations and bite wounds should be confined to victims with significant infection risk factors, such as animal bites, heavily contaminated wounds, or comorbid medical conditions. This includes high-risk wounds, such as puncture wounds and those occurring on the hands. Debridement and irrigation are far more important than antibiotics in eliminating infection and remain the mainstay of risk reduction in any wound incurred in the wilderness. If antibiotics are indicated, selection should be tailored by available resources and coverage of likely contaminating organisms. Many single-agent broad-spectrum oral antibiotics are available. If any sign of infection develops in a wound, closed or open, including pain, discharge, erythema, edema, or fever, antibiotics should be administered. In an infected closed wound, the adhesive or sutures should be removed and the wound

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management

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TABLE 20-4. Differential Diagnostic Features of Abdominal Pain LOCATION OF PAIN AND PRIOR ATTACKS

DISEASE Acute appendicitis

MODE OF ONSET AND TYPE OF PAIN

ASSOCIATED GASTROINTESTINAL PROBLEMS

Periumbilical or localized generally to right lower abdominal quadrant Diffuse

Insidious to acute and persistent

Anorexia common; nausea and vomiting in some

Sudden; crampy

Vomiting common

Epigastric; history of ulcer in many Left lower quadrant; history of previous attacks

Abrupt; steady

Anorexia; nausea and vomiting Diarrhea common

Insidious to acute

Anorexia; nausea and vomiting

Acute pancreatitis Acute salpingitis

Epigastric or right upper quadrant; may be referred to right shoulder Costovertebral or along course of ureter Epigastric penetrating to back Bilateral adnexal; later, may be generalized

Sudden; severe and sharp Acute; persistent, dull, severe Gradually becomes worse

Frequently nausea and vomiting Anorexia; nausea and vomiting common Nausea and vomiting may be present

Ectopic pregnancy

Unilateral early; may have shoulder pain after rupture

Sudden or intermittently vague to sharp

Frequently none

Intestinal obstruction Perforated duodenal ulcer Diverticulitis Acute cholecystitis Renal colic

Gradual; steady or crampy

irrigated. Wet-to-dry dressings with normal saline should be started and the wound closely observed. Elevation and splinting may assist in relieving pain.

Management of Animal Attacks and Bite Wounds See Chapters 51 to 53.


WILDERNESS SURGICAL EMERGENCIES

The Acute Abdomen In the wilderness, the critical distinction between the surgical and nonsurgical abdomen determines whether the victim should be evacuated. A myriad of nonsurgical conditions mimic a surgical abdomen. It has been extensively reported that the bite of the black widow spider Latrodectus mactans can induce abdominal pain indistinguishable from a surgical acute abdomen,51 and mushroom ingestion can cause severe gastroenteritis.85 Pain, anorexia, nausea, vomiting, and fever are characteristic manifestations of an acute abdominal disorder. Tenderness and guarding are the hallmarks of peritoneal irritation and suggest that operation is indicated. The approach to someone with abdominal pain begins with a detailed history that includes age, sex, systemic symptoms, and past medical history. This information provides a framework for more detailed questioning about the character of the pain, its mode and time of onset, severity, and precipitating and palliating factors. In persons 15 to 40 years of age, women are more likely to have abdominal pain, but men have a higher incidence of

PHYSICAL EXAMINATION Low-grade fever; epigastric tenderness initially; later, right lower quadrant Abdominal distention; highpitched rushes Epigastric tenderness; involuntary guarding Fever common; mass and tenderness in left lower quadrant Right upper quadrant pain Flank tenderness Epigastric tenderness Cervical motion elicits tenderness; mass if tuboovarian abscess is present Adnexal mass; tenderness

surgical disease. Common genitourinary causes for abdominal pain in men include epididymitis, renal colic, urinary retention, and testicular torsion. Common causes in women include pelvic inflammatory disease (PID), urinary tract infection, dysmenorrhea, ruptured ovarian cyst, and ectopic pregnancy. Pain is the hallmark of a surgical abdomen (Table 20-4). It can be characterized by nature of onset, severity, location, and precipitating factors. The onset of abdominal pain can be explosive, rapid, or gradual. The person who is suddenly seized with explosive, agonizing pain is most likely to have rupture of a hollow viscus into the free peritoneal cavity. Colic of renal or biliary origin may also be sudden in onset, but seldom causes pain severe enough to prostrate the victim. If someone has rapid onset of pain that quickly worsens, acute pancreatitis, mesenteric thrombosis, or small bowel strangulation should be suspected. The person with gradual onset of pain is likely to have peritoneal inflammation, such as that accompanying appendicitis or diverticulitis. Severity of the pain may be characterized as excruciating, severe, dull, or colicky. Excruciating pain unresponsive to narcotics suggests an acute vascular lesion, such as rupture of an abdominal aneurysm or intestinal infarction. Both conditions are unusual in the wilderness environment. Severe pain readily controlled by medication is characteristic of peritonitis from a ruptured viscus or acute pancreatitis. Dull, vague, and poorly localized pain suggests an inflammatory process and is a common initial presentation of appendicitis. Colicky pain characterized as cramps and rushes is suggestive of gastroenteritis. The pain from mechanical small bowel obstruction is also colicky but has a rhythmic pattern, with pain-free intervals alternating with severe colic. The peristaltic rushes associated with gastroenteritis are not necessarily coordinated with colicky pain.

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Physical examination of the abdomen is initiated by inspection. Valuable clues to the underlying condition that may be obtained in this manner include stigmata of cirrhosis, distention, hyperperistalsis, or incarcerated hernia. The victim may not be able lie still, which is indicative of renal or biliary colic. Persons lying perfectly still frequently have peritoneal inflammation. Auscultation is helpful if the classic “rushes and tinkles” of small bowel obstruction are present. Palpation in the wilderness setting is most helpful in documenting the presence or absence of peritoneal signs. Shake or percussive tenderness, particularly in the context of fever, nausea, and or vomiting, indicates a need for evacuation. Rectal and vaginal examinations should be performed as dictated by the clinical presentation and setting.

General Field Treatment Principles When evaluating someone with a possible emergent surgical condition in the wilderness, correctly identifying the etiology of a given condition is less important than identifying peritoneal inflammation and the need for operation. When dealing with a surgical abdomen or other condition requiring evacuation, adjuncts to definitive hospital treatment can be initiated in the field. Dehydration and intravascular volume depletion accompany many surgical conditions, particularly when the disease process has progressed and evacuation is delayed. Crystalloid resuscitation in the field is beneficial for patients who have developed or have the potential to develop septic or hypovolemic shock. Dehydration is common in the wilderness, and frank hypovolemia can result from vomiting associated with gastroenteritis, appendicitis, renal colic, and small bowel obstruction. Perforated viscus, pancreatitis, cholecystitis, small bowel obstruction, PID, and necrotizing soft tissue infections all may feature volume depletion. The goal in the wilderness setting is to recognize the signs of hypovolemia and initiate resuscitation to decrease perioperative morbidity. Nasogastric tube decompression of the stomach may help alleviate emesis secondary to abdominal pain or obstruction. Large-bore (i.e., 18-fr) catheters are best and can be easily aspirated with a syringe. Placement should be confirmed by aspiration of gastric contents or auscultation of gastric air upon insufflation of the stomach. Foley catheters are becoming increasingly more available in wilderness first-aid kits. Recording urine output provides an effective estimate of intravascular volume status. Foley catheter placement should never hinder the possibility of ambulatory evacuation.

Appendicitis Acute appendicitis is the most common cause of a surgical abdomen in persons younger than 30 years of age. Acute appendicitis is really more than a single disease entity. In terms of physical signs and symptoms, appendicitis proceeds from inflammation to obstruction to ischemia to perforation, all within approximately 36 hours. Symptoms reflect the stage of the disease. Unfortunately, the time frame for the progression of clinical events is highly variable. Differential diagnosis of appendicitis includes gastroenteritis and mesenteric adenitis, the most common inflammatory disorders in adults. The first symptom of gastroenteritis is typically vomiting, which precedes the onset of pain and is often associated with diarrhea; it is rarely associated with localizing signs

or muscular spasm. Bowel sounds are usually hyperactive. A rectal examination rarely shows abnormalities in gastroenteritis but frequently does in adults with appendicitis. Mesenteric adenitis is often preceded by an upper respiratory infection and is associated with vague abdominal discomfort that often begins in the right lower quadrant. Abdominal examination reveals only mild right lower quadrant tenderness that is often poorly localized. The incidence of PID in young women with abdominal pain confounds the diagnosis of appendicitis. Some clinicians have documented a relationship between menses and onset of pain. If abdominal pain occurs within 7 days of menses, the incidence of PID is twice that of appendicitis. If onset of pain occurs greater than 8 days from menses, appendicitis is twice as likely as PID. This history with a pelvic examination may enable the examiner to differentiate between the two entities. Acute appendicitis mandates evacuation because untreated perforation is associated with significant mortality. Broadspectrum antibiotics (if IV capability, cefotetan [Cefotan] 2 g IV q12h, or as an alternative, piperacillin/tazobactam [Zosyn] 3.375 g IV q6h; if only oral antibiotic capabilities, a fluoroquinolone, such as ciprofloxacin [Cipro] 750 mg PO bid) should be initiated, attempting coverage against gram-negative and anaerobic organisms. IV crystalloid resuscitation should be initiated, particularly if the victim is older or perforation is suspected, and the victim should be placed at bowel rest.

Acute Cholecystitis and Biliary Colic Biliary colic refers to pain induced by obstruction of the cystic duct, usually by gallstones. The label of this condition as “colic” is a misnomer because the pain is usually constant. The condition is rarely seen before adulthood and is several times more common in women than in men. A sufferer often relates a past history of gallstones and previous episodes of similar pain, which is described as constant right upper quadrant or epigastric pain, radiating to the right scapula and back. Onset ranges from insidious to acute and frequently follows a meal. The episode usually lasts 15 minutes to 1 hour and then abates.67 If pain is severe, nausea and vomiting may be present (60% to 70%). Acute cholecystitis is an infection of the gallbladder secondary to cystic duct obstruction, usually from gallstones. In the wilderness setting, it is useful to think of these interrelated conditions as a continuum of one unified disease process. Both biliary colic and cholecystitis present with right upper quadrant pain; however, biliary colic has the potential to be self-limiting and may not require evacuation. Not all persons with biliary colic develop cholecystitis, and signs of infection should be excluded. Cholecystitis symptoms typically escalate in severity. Pain that persists more than 1 to 2 hours is suspect for cholecystitis, particularly when accompanied by fever, more significant nausea and vomiting, and right upper quadrant tenderness. Studies have shown that fever may be an unreliable predictor of severity of infection.38 Acute cholecystitis mandates hospitalization, and evacuation plans should be instituted. The disease can progress to gangrenous changes in the gallbladder wall, leading to perforation and death if untreated. The definitive treatment of cholecystitis is cholecystectomy. In the field, IV antibiotics (ampicillin/sulbactam [Unasyn] 3 g IV q6h) or an oral alternative (ciprofloxacin [Cipro] 750 mg PO

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management bid) should be given, directed at common biliary organisms, including Escherichia coli and Klebsiella, Bacteroides, Enterobacter, Streptococcus, and Proteus species. Oral antibiotics with optimal bioavailability should be initiated in the absence of parenteral forms, ensuring the broadest spectrum of coverage available. As with most abdominal infections, IV hydration should be started in the field. If significant nausea and vomiting are present, NG decompression may improve comfort and prevent aspiration.

Peptic Ulcer Disease The incidence of peptic ulcer disease (PUD) is decreasing in the United States. With the advent of treatment of Helicobacter pylori infections and the variety of acid-reducing agents available, PUD is now rarely seen by surgeons. The exception is perforation of a gastric or duodenal ulcer, which should be considered in the differential diagnosis of acute abdomen in the wilderness. Victims frequently relate a history of PUD and need for medication. This history, in combination with acute onset of unrelenting epigastric pain radiating to the back, is suspect for perforation of an ulcer. The physical examination greatly assists in differentiation between simple ulcer disease symptoms and perforation. Pain may be severe. Gastric secretions are caustic to the peritoneum and, as a result, the abdomen frequently displays a rigid, boardlike character with associated diffuse peritoneal signs. History and examination consistent with gastric or duodenal perforation mandate evacuation. Dehydration may be significant. IV resuscitation should be started and the victim placed on bowel rest.

Diverticulitis Diverticulitis is localized infection of a colonic diverticulum. Impacted material in the diverticulum, usually feces, leads to a localized inflammatory process that can lead to abscess formation and perforation. Diverticulitis presents over a wide range of severity, from mild, localized infection to intra-abdominal catastrophe. It is more common in middle age; one third of the population older than 45 years of age has diverticula, 20% of whom will develop diverticulitis.89 Victims often relate a history of previous attacks. Pain is typically described as gradual in onset and localized in the left lower quadrant of the abdomen, although right-sided diverticulitis can occur. Diarrhea and fever are frequently associated complaints. Examination findings range from mild left lower quadrant abdominal tenderness to frank peritonitis, depending on the severity of the underlying infection. Treatment in the wilderness setting consists of hydration, bowel rest, antibiotics, and evacuation. If evacuation is impossible or significantly delayed, oral broad-spectrum antibiotics may be effective. Mild cases of diverticulitis are frequently treated on an outpatient basis with broad-spectrum oral antibiotics,83 such as ciprofloxacin 750 mg PO bid. Antibiotic therapy is directed primarily at gram-negative aerobic and anaerobic bacteria, and single-agent therapy covering these organisms has been demonstrated to be as effective as multiple-agent regimens.50 Because of unpredictability of response to antibiotic treatment, evacuation is indicated.

Mechanical Small Bowel Obstruction Small bowel obstruction is a true emergency in the wilderness. When the obstruction is complete, expedient surgery is the only

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treatment. Small bowel obstruction in the United States is almost invariably the result of adhesions from previous laparotomy or incarceration of abdominal hernias, and the history often makes the diagnosis. Victims complain of sudden onset of diffuse, crampy abdominal pain associated with vomiting and obstipation. With progression of the process to strangulation and infarction of bowel, fever and tachycardia develop. Late physical examination findings reveal a distended, tympanitic abdomen. Although variable, high-pitched tinkling bowel sounds suggest obstruction. A thorough inspection for hernias should be performed. Progression of examination findings to frank peritonitis is alarming and suggests ischemic bowel. The adage, “Don’t let the sun set on a small bowel obstruction,” is sound advice in the wilderness setting. All persons suspected of having a small bowel obstruction should be evacuated immediately. In the interim, the stomach should be decompressed with an NG tube to relieve vomiting and abdominal distention, and aggressive IV hydration should be started.

Incarcerated Abdominal Wall Hernias Abdominal wall hernias are common; groin herniorrhaphy is the most common major general surgical operation performed in the United States.63 Hernias can become incarcerated or strangulated, which constitutes a surgical emergency. Seventyfive percent of hernias occur in the groin86; the majority of incarcerated hernias presenting in the wilderness setting are inguinal hernias. Other common hernias with the capacity for incarceration are incisional and umbilical hernias. Many people live with bulging asymptomatic hernias. Others manually reduce symptomatic hernias. New painful hernias or known hernias that can no longer be reduced are concerning. The pain of inguinal hernias is usually intermittent. A description of constant pain is suspect for incarceration. Associated symptoms of fever, tachycardia, nausea, and vomiting are indicative of possible incarceration or strangulation. On physical examination, a mass should be sought along the course of the spermatic cord. Masses may present from the external inguinal ring to the scrotum. The differential diagnosis for painful inguinal or scrotal masses includes lymphadenopathy, testicular torsion, and epididymitis. Associated tenderness of the spermatic cord may be present. A painful mass at the umbilicus, a previous incision site, or below the inguinal ring could represent an incarcerated umbilical, incisional, or femoral hernia, respectively. Bowel within an incarcerated hernia sac can become gangrenous in as little as 4 to 5 hours63; therefore, it is important to determine the time of incarceration. The decision to evacuate is influenced by the presence of contraindications to manual reduction (see later), which are essentially physical signs that suggest progression to strangulation. Femoral hernias should not be reduced. The danger is en masse reduction of compromised or gangrenous bowel. Contraindications to reduction include associated signs of toxicity, such as fever, tachycardia, or evidence of bowel obstruction in association with a painful, irreducible mass. If the hernia itself is exquisitely tender to palpation and the overlying skin is erythematous and warm, the hernia should not be reduced. Victims with incarcerated hernias with signs of systemic or local toxicity should be evacuated. Similarly, victims with irreducible hernias—which require emergent surgery—should be evacuated.

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A newly incarcerated hernia without contraindications to reduction may be reduced by personnel experienced in such techniques. Gentle pressure is exerted on the hernia mass toward the inguinal ring, optimally with the victim flat and hips elevated. Analgesia and sedation may aid in reduction. Gangrenous bowel can rarely be reduced by this method.93 If successful, the victim should be closely observed for signs of recurrence or abdominal pain.

Urologic Emergencies Renal colic describes a symptom complex resulting from acute obstruction of the urinary tract secondary to calculus formation. The goal of the wilderness physician is to recognize the symptom complex and institute treatment. After obstruction of the urinary tract, the pain crescendo of renal colic begins in the flank. The pain progresses anteriorly over the abdomen and radiates to the groin and testes in men and the labia in women. Because the autonomic nervous system transmits visceral pain, many abdominal complaints may manifest. Nausea and vomiting are common. With severe colic, the victim writhes in pain and is unable to find a comfortable position. Physical findings are less revealing than is the review of systems. Tenderness to deep palpation of the region of obstruction or to percussion of the flank is present. Diagnosis in the wilderness is assisted by the presence of gross hematuria. Management of ureteral colic is pain control. Although almost universally deployed, forced diuresis may reduce ureteral peristalsis. Thus, forced oral fluids or aggressive IV hydration are of questionable benefit.100 The majority of calculi pass spontaneously in 4 to 6 hours. The goal of management is to control pain until passage of the stone has occurred. A number of pharmacologic approaches may be used. Nonsteroidal antiinflammatory drugs, such as ibuprofen and ketorolac, have been shown to be effective in the management of renal colic.100 For symptoms uncontrolled by anti-inflammatory agents, narcotics may be added. Narcotic analgesics are most effective given parenterally; however, agents such as meperidine (Demerol), codeine, and hydromorphone (Dilaudid) may be given orally. Anti-inflammatory agents and analgesics can be combined. An antiemetic may be added to relieve nausea. When administering pain medication in the field, particular attention should be given to airway maintenance and induced nausea and vomiting. Any person whose symptom complex cannot be controlled must be evacuated. Additional indications for evacuation include calculus anuria and evidence of obstruction-induced infection.

Urinary Retention Urinary retention is a painful experience that requires immediate medical, and often surgical, intervention.13 The etiology of urinary retention ranges from prostatism48 in men to atonic bladder in women. In general, causes have been broadly divided into four groups: obstructive, neurologic, pharmacologic, and psychogenic.99 Twenty-five percent of men reaching 80 years of age will experience acute retention,13 which has been shown to increase prostate surgery perioperative mortality rates.76 Acute urinary retention can lead to incapacitating symptoms in the wilderness; prompt recognition and intervention are necessary. Principal symptoms are bladder distention and pain that may mimic acute abdomen, overflow incontinence, dribbling, and hesitancy. Physical examination findings include prostatic enlargement in men and lower midline abdominal tenderness and distention. If painful distention of the bladder is present, decompression should be undertaken.

A

B Figure 20-10. A, OPTION-vf (female) catheter. B, OPTION-vm (male) catheter. (Courtesy Opticon Medical, Dublin, OH)

Bladder decompression should be initially attempted with a standard Foley catheter. In men with prostatic hypertrophy, passage of the catheter may be challenging, and a large catheter or coudé catheter should be used if a standard Foley catheter cannot be passed. Instrumentation of the urethra with hemostats or dilators is dangerous and should not be attempted in the field. Recently introduced are the OPTION-vf (female; Fig. 20-10A) and OPTION-vm (male; see Fig. 20-10B) (Option Medical, Dublin, Ohio), which are valved urinary catheters that eliminate the need for urine drainage bags and connecting tubes normally required with Foley catheters. These catheters incorporate a manually activated valve at the end of the catheter that allows the patient to store urine in the bladder and to mimic normal voiding behavior. The catheters may be used with a continuous drainage adapter when appropriate, so that a bag may be placed and urination rate and volume assessed. If multiple attempts are unsuccessful and symptoms are severe, needle decompression is indicated. The skin of the suprapubic region should be anesthetized, if possible. The distended bladder is palpated to guide aspiration. A 22-gauge needle attached to a syringe is introduced through the skin of the lower abdomen two finger breadths above the pubic symphysis and directed at the anus. The needle is advanced with simultaneous aspiration of the syringe until free-flowing urine is visualized. Palpation of the bladder in combination with adherence to this technique should lead to successful decompression. Complications related to decompression can occur.84 Drainage of greater than 300 mL/hr can induce mucosal hemorrhage. In addition, 10% of victims develop postobstructive

Chapter 20: Wilderness Trauma, Surgical Emergencies, and Wound Management diuresis that may lead to dehydration, in which case aggressive oral hydration or crystalloid repletion should be undertaken. Finally, it must be recognized that surgical decompression is temporizing and retention will recur. Treatment may need to be continued or repeated. Drainage of the bladder acutely relieves symptoms and may allow ambulatory evacuation, but the underlying etiology must be addressed in a medical facility.

The Acute Scrotum Acute onset of scrotal pain and swelling requires immediate attention. Etiologies are multiple, but incarcerated hernia and testicular torsion are the most clinically significant in the field. Although any one aspect of the history and physical examination may not be diagnostic, when taken as a whole, they frequently suggest the etiology of the scrotal pathology.49 Testicular torsion can occur at any age, but it is more likely near puberty. The likelihood of testicular salvage is inversely proportional to elapsed time from torsion; this is a true surgical emergency. Acute onset of severe testicular pain is the hallmark. Mild to moderate pain is more suggestive of torsion of a testicular appendage or epididymitis. It has been stated that victims who can ambulate with minimal pain are less likely to have testicular torsion. In addition, nausea and vomiting may accompany torsion, whereas fever, dysuria, and frequency are associated with epididymitis. Physical examination reveals a patient in extreme discomfort with a swollen scrotum and a tender testicle; the affected testicle may be higher than normal and have a horizontal lie.49 Scrotal skin may be edematous and discolored. Unilateral scrotal swelling without skin changes is more indicative of a hernia or hydrocele. In testicular torsion, the affected testis is often larger than the unaffected side. Testicular torsion can be somewhat differentiated from acute epididymitis by Prehn’s sign,88 which is relief of pain accomplished by elevation of the testicle. Because torsion twists the spermatic cord and elevates the testicle, pain is not relieved by elevation (negative Prehn’s sign). Conversely, pain is relieved in epididymitis with elevation (positive Prehn’s sign). This maneuver has low sensitivity in distinguishing the two conditions, but may be helpful in conjunction with other findings.88 Treatment consists of surgical detorsion, which should be accomplished within 12 hours of torsion.49 Manual detorsion is not the treatment of choice; however, remoteness of the wilderness environment may mandate manual attempts. Studies of manual detorsion are scant and the cohorts small.41 If manual detorsion is necessitated, the victim should be placed supine. Because testicular torsion typically occurs in the medial direction, detorsion is initially attempted with outward rotation of the testis (toward the ipsilateral thigh). Simultaneous rotation in the caudal to cranial direction may be necessary to release the cremasteric muscle.31 The surgical treatment of testicular torsion includes pexis of the testis to prevent recurrent torsion. Thus, although detorsion may temporize an acute situation in the field, all victims must be evacuated for definitive treatment.

Prostatitis Fifty percent of men experience prostatic symptoms in their adult life.77 A number of forms of prostatitis have been defined, including viral, bacterial (5%), nonbacterial (65%), and chronic forms, as well as prostatodynia.79 The acute bacterial form may potentially lead to severe infection.

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Bacterial prostatitis is an infection of the prostate caused primarily by gram-negative bacteria, with 80% attributable to E. coli. It is an acute, febrile illness characterized by perineal pain radiating to the low back, chills, malaise, and voiding symptoms, such as urgency, frequency, and dysuria. Urinary retention is common, and cystitis frequently accompanies the infection. On rectal examination, the prostate gland is usually boggy, warm, and tender and enlargement is variable. In an ideal situation, treatment is individualized to the cause, which may be difficult to discern in the wilderness. The infection may respond to an oral antibiotic such as ciprofloxacin (750 mg PO bid), ampicillin (500 mg PO qid), or trimethoprim (80 mg with sulfamethoxazole 400 mg PO bid). Penetration of prostatic secretions has been shown to be best achieved by trimethoprim/sulfamethoxazole (TMP/SMX). The chosen antibiotic should be administered for 30 days. If retention is present, catheterization or suprapubic aspiration should be undertaken. Acute bacterial prostatitis can escalate in severity to systemic toxicity. Persons with evidence of systemic toxicity unresponsive to a trial of oral or parenteral antibiotic therapy should be evacuated.

Urinary Tract Infection Urinary tract infections (UTIs) are extremely common and include episodes of acute cystitis and pyelonephritis occurring in otherwise healthy individuals. These infections predominate in women; approximately 25% to 35% of women 20 to 40 years of age report having had a UTI.45 Conversely, men between the ages of 15 and 50 years rarely develop a UTI. Despite the striking difference in prevalence, symptoms are similar between men and women. The symptoms may represent urethritis, cystitis, or an upper UTI; the distinction is often difficult. Common symptoms include frequency, urgency, dysuria, suprapubic pain, flank pain, and hematuria. Flank pain with tenderness to percussion suggests pyelonephritis. On urinalysis, pyuria is nearly invariably present and hematuria may assist in the diagnosis. Definitive diagnosis is based on significant bacteriuria. The leukocyte esterase test has a screening sensitivity of 75% to 96% and a specificity of 94% to 98% in detecting greater than 10 leukocytes per high-power field.45 Treatment in the wilderness setting for both men and women should be directed at the most common causative agents, although 50% to 70% of cases resolve spontaneously if untreated. Causative bacteria include E. coli (70% to 95%); Staphylococcus species (5% to 20%); and, less frequently, Klebsiella, Proteus, and Enterococcus. Fortunately, oral antibiotics are highly effective. Although resistant E. coli strains are being reported, TMP/SMX (Bactrim DS) is an excellent first-line drug. Alternative regimens include nitrofurantoin, a fluoroquinolone, or a third-generation cephalosporin. A 3-day course of therapy has been shown to be more effective than single-dose therapy.45 For pyelonephritis, a similar antibiotic in a 10- to 14-day course is acceptable initial treatment. Evacuation should be reserved for systemic toxicity unresponsive to oral antibiotics.

Gynecologic Emergencies See Chapter 88.

Skin and Soft Tissue Infections Poor hygiene, superficial skin wounds, blisters, dermatologically significant plants, and insect bites contribute to disruption of the skin barrier. Most often seen are superficial pyodermas

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that do not extend beyond the level of the skin. These include erysipelas, impetigo, folliculitis, furunculosis, and carbunculosis. The majority of superficial skin infections are self-limited. However, with less than optimal hygiene and limited resources, skin infections may progress to deep soft tissue infections.

Cellulitis Cellulitis is acute infection of the skin involving subcutaneous tissue. The superficial form of cellulitis, erysipelas, is identified by well-demarcated, warm, and erythematous plaques with raised borders. The face, scalp, hands, and lower extremities are most often affected. Cellulitis is frequently preceded by a superficial wound. In the wilderness setting, there are ongoing infection risk factors. Members of expeditions may be physically stressed and nutritionally depleted. High altitude is associated with immunosuppression. Clostridium species and other pathogens are ubiquitous in the soil, and proper initial wound care may be suboptimal. Under such conditions, cellulitis can progress to abscess formation and tissue necrosis, leading to septicemia. Wounds that develop erythematous, warm, and boggy margins should be treated with antibiotics and closely observed. The margins of erythema should be marked to gauge progression. Treatment consists of proper wound hygiene and antibiotic therapy. Local wound measures include elevation, application of moist heat every 4 to 6 hours, and immobilization. Antibiotic therapy is directed at common causative pathogens. Group A streptococci and Staphylococcus aureus are most commonly implicated. If complications occur and the cellulitis appears to be progressing, a mixed infection is likely. Because Gram’s stain and culture-directed therapy are not possible, the most broad-spectrum antibiotic available should be administered. Parenteral antibiotics are indicated for serious or mixed infections. Penicillin G (1 to 2 million units q2–3h) is recommended, with first-generation cephalosporins as an alternative. Because oral antibiotics may be the only available therapy, they should be initiated early in the field. Suggested agents include erythromycin (for the penicillin-allergic victim); cephalexin; a macrolide, such as clarithromycin; or a fluoroquinolone, such as ciprofloxacin or levofloxacin.

purulent fluid has amassed below the dermis and rupture is impending. Warm soaks and observation are recommended by some clinicians, particularly if the presence of drainable pus is uncertain. However, the definitive treatment is drainage. Antibiotics are recommended if significant associated cellulitis is present, but penetration may be poor. Local anesthesia should be administered before incision. The lesion should be incised in line with tissue planes over the point of maximum fluctuance. The value of cruciate incisions over linear incisions is debatable; the important feature is assurance of adequate drainage to prevent recurrence. If drainage is undertaken, the incision must be large enough to adequately drain the cavity. All purulent material should be evacuated and the cavity copiously irrigated with saline or water. Packing is unnecessary if continued drainage is ensured. The wound should be covered with a sterile dressing, changed two to three times per day with concurrent irrigation, and closely observed for reaccumulation of purulence.

Necrotizing Infections

Abscess Formation

Necrotizing skin and soft tissue infections are life-threatening conditions caused by virulent, toxin-producing bacteria. Depth of tissue involvement is variable and may involve skin, fascia, or muscle. The etiology of necrotizing infections is related to breaks in normal cutaneous defenses associated with some form of injury. Although rare, such infections are of importance to the wilderness physician because of the array of documented inciting injuries and the reduction in mortality possible if diagnosis and treatment are rapid.28 Necrotizing infections have developed after innocuous-appearing injuries, including simple scratches, insect bites, ankle sprains, and sore throats.37 The incidence of necrotizing soft tissue infections is unknown, and there is no age or sex predilection. They most commonly occur on the extremities, abdominal wall, and perineum, within 1 week of the inciting event. Common pathogens include Streptococcus species, Staphylococcus, Vibrio species, Clostridium, Pseudomonas, Aeromonas, Enterobacter, and fungi. Many infections become polymicrobial. The clinical manifestations can be subtle. An area of cellulitis is commonly the first indication of infection. Pain is often excruciating, and fever is usually present. The infection then progresses to spreading erythema, induration, blue-black discoloration, and blister formation. Necrosis of skin, subcutaneous fat, muscle, or fascia follows, depending on the organism involved. Necrotic tissue exudes a foul-smelling, watery “dishwater” fluid. Subcutaneous emphysema may be present, particularly with clostridial infections, although enteric organisms may also produce air in tissues. Unfortunately, treatment is limited in the wilderness environment. Debridement of infected tissue should be carried out to the greatest degree humanely possible, but further debridement in a hospital setting is invariably necessary. The extent of debridement necessary is often striking. After debridement, parenteral antibiotics are necessary. Vancomycin and gentamicin are appropriate first-line agents. The most broad-spectrum oral antibiotic available should be initiated, and the victim expeditiously evacuated. Time is of the essence because the infection can be halted only by aggressive surgical intervention.

When untreated, many superficial skin infections convert to abscesses. Development of a raised, fluctuant mass with overlying warmth and erythema should raise suspicion that surgical drainage is necessary. Frequently, the lesion will “point” when

The references for this chapter can be found on the accompanying DVD-ROM.

Lymphangitis Acute lymphangitis is an infectious process involving subcutaneous lymphatic channels. Its recognition in the wilderness setting is important relative to its propensity to follow puncture wounds, hand wounds, infected blisters, and animal bite wounds. Clinical presentation involves linear erythematous streaks that originate in the lymphatic drainage basin of the wound and “point” to the draining nodal group. Causative agents are similar to those common for cellulitis, with the addition of Pasteurella multocida from animal bite wounds. Treatment consists of antibiotics, warm, moist soaks every 4 to 6 hours, and immobilization and elevation of the extremity. Optimal treatment consists of parenteral antibiotics, but as with cellulitis, oral agents should be initiated if parenteral drugs are not available. Broad-spectrum agents with good oral bioavailability and gram-positive coverage are recommended.87

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Eric A. Weiss and Howard J. Donner

At the heart of wilderness medicine is improvisation, a creative amalgam of formal medical science and common sense problem solving. Defined as “to fabricate out of what is conveniently at hand,” improvisation encompasses many variations, is governed by few absolute rights and wrongs, and is limited more often by imagination than by personnel or equipment.


GENERAL GUIDELINES When working with an improvised system, test the creation on a noninjured person (“work out the bugs”) before applying it to a victim. Include materials that lend themselves to improvisation in the wilderness survival kit to enhance efficiency. Creativity is needed when searching for improvisational materials. The victim’s gear can provide needed items (e.g., backpacks can be dismantled to obtain foam pads and straps). When possible, practice constructing improvised systems before they are required in an actual rescue.


IMPROVISED AIRWAY MANAGEMENT

Airway obstruction in the semiconscious or unconscious victim is usually caused by relaxation of the oropharyngeal muscles, which allows the tongue to slide back and obstruct the airway. If only one rescuer is present, maintaining a patent airway with the jaw-thrust or chin-lift technique precludes further first-aid management. You can improvise a nasal trumpet type of airway from a Foley catheter, radiator hose, solar shower hose, siphon tubing, or inflation hose from a kayak flotation bag or sport pouch. Establish a temporary airway by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins (Fig. 21-1). An alternative to puncturing the lower lip is to pass a string through the safety pins and hold traction on the tongue by securing the other end to the victim’s shirt button or jacket zipper.

Surgical Airway (Cricothyrotomy) Cricothyrotomy—establishment of an opening in the cricothyroid membrane—is indicated to relieve life-threatening upper airway obstruction when a victim cannot be ventilated effectively from the mouth or nose and endotracheal intubation is

not feasible. This may occur in a victim with severe laryngeal edema or with trauma to the face and upper larynx. Cricothyrotomy may also be useful when the person’s upper airway is obstructed by a foreign body that cannot be extracted by a Heimlich maneuver or direct laryngoscopy. In the wilderness, you can perform cricothyrotomy by cutting a hole in the thin cricothyroid membrane and placing a hollow object into the trachea to allow ventilation (Box 21-1). Locate the cricothyroid membrane by palpating the victim’s neck, beginning at the top. The first and largest prominence felt is the thyroid cartilage (“Adam’s apple”); the second prominence (below the thyroid cartilage) is the cricoid cartilage. The small space between these two, noted by a small depression, is the cricothyroid membrane (see Figure 21-4). With the victim lying on his or her back, cleanse the neck around the cricothyroid membrane with an antiseptic if one is readily available. Put on protective gloves. Make a vertical 1-inch (2.54 cm) incision through the skin with a knife over the membrane (go a little bit above and below the membrane) while using the fingers of your other hand to pry the skin edges apart. Anticipate bleeding from the wound. After the skin is cut apart, puncture the membrane by stabbing it with your knife or other sharp, penetrating object (see Figure 21-5A). Stabilize the larynx between the fingers of one hand, and insert the improvised cricothyrotomy tube through the membrane with your other hand (see Figure 215B). Secure the object in place with tape. Complications associated with this procedure include hemorrhage at the insertion site, subcutaneous or mediastinal emphysema resulting from faulty placement of the tube into the subcutaneous tissues rather than into the trachea, and perforation through the posterior wall of the trachea with placement of the tube in the esophagus.

Improvised Barrier for Mouth-to-Mouth Rescue Breathing A glove can be modified and used as a barrier shield for performing rescue breathing. Cut the middle finger of the glove at its halfway point and insert it into the victim’s mouth. Stretch the glove across the victim’s mouth and nose and blow into the glove as you would to inflate a balloon. After each breath, remove the part of the glove covering the nose to allow the victim to exhale. The slit creates a one-way valve, preventing backflow of the victim’s saliva (see Figure 21-6).

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Figure 21-1. Safety pins on tongue to open airway.

Box 21-1. Improvised Cricothyrotomy Tubes 1. IV administration set drip chamber: Cut the plastic drip chamber of a macro drip (15 drops/mL) IV administration set at its halfway point with a knife or scissors. Remove the end protector from the piercing spike and insert the spike through the cricothyroid membrane. The plastic drip chamber is nearly the same size as a 15-mm endotracheal tube adapter and fits snugly in the valve fitting of a bag-valve device (Fig. 21-2). 2. Syringe barrel: Cut the barrel of a 1- or 3-mL syringe with the plunger removed at a 45-degree angle at its midpoint to create an improvised cricothyroid airway device. The proximal phalange of the syringe barrel helps secure the device to the neck and prevents it from being aspirated (Fig. 21-3). 3. Any small hollow object: Examples include a small flashlight or penlight casing, pen casing, small pill bottle, and large-bore needle or IV catheter. Several commercial devices are small and lightweight enough to be included in the first-aid kit.

of the gauze remain outside the nasal cavity (Fig. 21-7). This prevents the victim from inadvertently aspirating the nasal packing.42 Complete packing of the nasal cavity of an adult victim requires a minimum of 1 m (3 feet) of packing to fill the nasal cavity and tamponade the bleeding site.7 Expandable packing material, such as Weimert Epistaxis Packing, Rapid Rhino (ArthroCare Corporation, Sunnyvale, CA), or the Rhino Rocket (Shippert Medical Technologies, Centennial, CO), is available commercially. A tampon or balloon tip from a Foley catheter can also be used as improvised packing.42 Anterior nasal packing blocks sinus drainage and predisposes to sinusitis. Prophylactic antibiotics are usually recommended until the pack is removed in 48 hours.42 If the bleeding site is located posteriorly, use a 14- to 16-Fr Foley catheter with a 30-mL balloon to tamponade the site.14 Prelubricate the catheter with either petroleum jelly (Vaseline) or a water-based lubricant, then insert it through the nasal cavity into the posterior pharynx. Inflate the balloon with 10 to 15 mL of water and gently withdraw it back into the posterior nasopharynx until resistance is met. Secure the catheter firmly to the victim’s forehead with several strips of tape. Pack the anterior nose in front of the catheter balloon as described earlier.

Esophageal Foreign Bodies


EAR, NOSE, AND THROAT EMERGENCIES

Epistaxis Epistaxis is a common problem in travelers. Reduced humidity in airplanes, cold climates, and high-altitude environments can produce drying and erosion of the nasal mucosa. Other etiologic factors include facial trauma, infections, and inflammatory rhinitis. Although most cases of epistaxis are minor, some present life-threatening emergencies (see Chapter 26).42 Anterior epistaxis from one side of the nasal cavity occurs in 90% of cases.11 If pinching the nostrils against the septum for a full 10 minutes does not control the bleeding, nasal packing may be needed. Soak a piece of cotton or gauze with a vasoconstrictor, such as oxymetazoline (Afrin) nasal spray, and insert it into the nose, leaving it in place for 5 to 10 minutes. Petroleum jelly–impregnated gauze or strips of a nonadherent dressing can then be packed into the nose so that both ends

Esophageal foreign bodies may cause significant morbidity. Respiratory compromise caused by tracheal compression or by aspiration of secretions can occur. Mediastinitis, pleural effusion, pneumothorax, and abscess may be seen with perforations of the esophagus from sharp objects or pressure necrosis caused by large objects.28 The use of a Foley balloon-tipped catheter can be a safe method for removing blunt esophageal foreign bodies.5,6,17 Success rates of 98% have been cited.5 Associated complications include laryngospasm, epistaxis, pain, esophageal perforation, and tracheal aspiration of the dislodged foreign body.28 Sharp, ragged foreign bodies or an uncooperative victim precludes use of this technique (Fig. 21-8).37 Lubricate a 12- to 16-Fr Foley catheter and place it orally into the esophagus while the victim is seated. After placing the victim in Trendelenburg’s position, pass the catheter beyond the foreign body and inflate the balloon with water. Withdraw the catheter with steady traction until the foreign body can be removed from the hypopharynx or is expelled by coughing.

Chapter 21: Improvisation in the Wilderness

A

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B

C Figure 21-2. Improvised cricothyrotomy tube. A, Cut plastic drip chamber at halfway point. B, Insert spike from drip chamber into the cricothyroid membrane. C, Bag-valve device will fit over the chamber for ventilation.

Adam’s apple

Cricothyroid membrane

Figure 21-3. Improvised cricothyroid airway device can be created by cutting barrel of syringe at a 45-degree angle at its midway point.

Figure 21-4. Cricothyroid membrane is found in the depression between the Adam’s apple (thyroid cartilage) and the cricoid cartilage.

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Adam’s apple (thyroid cartilage)

Cricothyroid membrane

A

B Figure 21-5. Cricothyrotomy.A, Locate cricothyroid membrane and make a vertical 1-inch incision through the skin. B, Insert pointed end of improvised cricothyrotomy tube through the membrane.

Take care to avoid lodging the foreign body in the nasopharynx. Any significant impedance to withdrawal should terminate the attempt.37 Use of this technique is recommended only in extreme wilderness settings or when endoscopy is not available.


TENSION PNEUMOTHORAX Overview Signs and symptoms of a tension pneumothorax include distended neck veins, tracheal deviation away from the side of the pneumothorax, unilateral absent breath sounds, hyperresonant hemithorax to percussion, subcutaneous emphysema, respiratory distress, cyanosis, and cardiovascular collapse. Tension pneumothorax mandates rapid pleural decompression if the victim appears to be dying. Possible complications of pleural decompression include infection; profound bleeding from puncture of the heart, lung, or a major blood vessel; or even laceration of the liver or spleen.

Figure 21-6. Improvised cardiopulmonary resuscitation (CPR) barrier is created using a latex or nitrile glove. Make a slit in the middle finger of the glove.

Improvised Pleural Decompression Technique Swab the entire chest with povidone-iodine or another antiseptic. If sterile gloves are available, put them on after washing your hands. If local anesthesia is available, infiltrate the puncture site down to the rib and over its upper border. Insert a large-bore intravenous (IV) catheter, needle, or any pointed, sharp object that is available into the chest just above

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Figure 21-7. Anterior epistaxis from one side of the nasal cavity can be treated using nasal packing soaked in a vasoconstrictor. Petroleum jelly–impregnated gauze or strips of nonadherent dressing can be packed in the nose so that both ends of the gauze remain outside the nasal cavity.

Box 21-2. Improvised Pleural Decompression Devices 1. Large-bore (12- or 14-gauge) IV catheter or needle 2. Endotracheal tube 3. Foley catheter with a rigid support (“stylet”), such as a clothes hanger, placed into the lumen 4. Section of a tent pole 5. Hose from a hydration pouch

the third rib in the midclavicular line (midway between the top of the shoulder and the nipple in a line with the nipple approximates this location) (Box 21-2). If you hit the rib, move the needle or knife upward slightly until it passes over the top of the rib, thus avoiding the intercostal blood vessels that course along the lower edge of every rib. The chest wall is 11/2 to 21/2 inches (4–6 cm) thick, depending on the individual’s muscularity and amount of fat present. A gush of air signals that you have entered the pleural space; do not push in the penetrating object further. Releasing the tension converts the tension pneumothorax into an open pneumothorax. Leave the needle or catheter in place, and use a rubber glove to make a flutter valve. Cut out a finger portion from a rubber glove, making a tiny slit cut at the tip. Place this over the external opening to create a unidirectional flutter valve that allows continuous egress of air from the pleural space (Fig. 21-9). To create a one-way flutter valve, cut a finger portion of a latex glove off at the proximal end of the finger and insert the needle

Figure 21-8. Packing the back of the nose.Insert a Foley catheter into the nose and gently pass it back until it enters the back of the throat.After the tip of the catheter is in the victim’s throat, carefully inflate the balloon with 10 to 12 mL of air or water from a syringe. Inflation should be done slowly and should be stopped if painful. After the balloon is inflated, gently pull the catheter back out until resistance is met.

or catheter into the open end of the glove finger and through the tip as shown (see Figure 21-9A). The cut-out finger portion of the glove creates a unidirectional flutter valve that allows egress of air from the pleural space during expiration, but collapses to prevent air entry on inspiration (see Figure 21-9B, C).

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Glove finger

A

with both a rigid or semirigid cervical collar and long-board immobilization. Historically, dogma about cervical spine injuries has specified a “splint ’em as they lie” approach. Transporting a victim who is not in anatomic position is arduous in the backcountry. It is uncomfortable for the victim, difficult for the rescuers, and increases the risk of further injury. In general, gentle axial traction back to anatomic position is indicated unless (1) return to anatomic position significantly increases pain or focal neurologic deficit or (2) movement of the head and neck results in any noticeable mechanical resistance.24 All cervical spine injuries (or suspected injuries) warrant full long-board immobilization. Movement of the pelvis and hips laterally is potentially more dangerous than anterior–posterior movement; therefore it is appropriate during extended transport to allow gentle flexion at the hip with immobilization in that position if the victim is more comfortable. Soft pads behind the knees and small of the back also add to the victim’s comfort during a long transport.9

Improvised Cervical Collars

B

C

Figure 21-9. A, Finger of glove is attached to needle or catheter to create flutter valve. B, Flutter valve allows air to escape. C, Flutter valve collapses to prevent air entry.


OPEN (“SUCKING”) CHEST WOUND

Penetrating trauma to the chest can produce a chest wound that allows air to be sucked into the pleura on inspiration. Place a piece of plastic food wrap, aluminum foil, or one side of a plastic sandwich bag on top of the wound and tape it on three sides. The untaped fourth side serves as a relief valve to prevent formation of a tension pneumothorax.


SPLINTING AND TRACTION*

Cervical collars are always adjuncts to full spinal immobilization; they should never be used alone. The improvised cervical collar is used in conjunction with manual cervical spine stabilization followed by complete immobilization of the victim on a spine board. A properly applied and fitted collar is a primary defense against axial loading of the cervical spine, particularly in an evacuation that involves tilting the victim’s body uphill or downhill. Improvised cervical collars have had a bad reputation, and textbooks continue to depict them made from a simple cravat wrapped around the neck. This type of system is no more effective than are the soft cervical collars often used by urban plaintiffs trying to impress a jury (i.e., not effective at all). An improvised cervical collar works effectively only if it has the following features: 1. It is rigid or semirigid. 2. It fits properly (many improvised designs are too small). 3. It does not choke the victim. 4. It allows the victim’s mouth to open if vomiting occurs. Improvisational approaches to cervical collars are outlined below.

Closed-Cell Foam System. The best closed-cell foam systems incorporate a full-size or three-quarter-length pad folded longitudinally into thirds and applied centered over the back of the victim’s neck and wrapped forward. The pad is crossed under the chin, contoured underneath opposite axillae, and secured. If the pad is not long enough, you can tape or tie on extensions. This system also works well with blankets, beach towels, or even a rolled plastic tarp. Avoid small flexible cervical collars that do not optimally extend the chin-to-chest distance.

Because of its mobility, the cervical spine is the spinal column area most commonly injured in trauma. Any obvious or suspected cervical spine injury demands full spinal immobilization

Padded Hip Belt. A padded hip belt or fanny pack removed from a large internal or external frame backpack can sometimes be modified to work perfectly. Wider is usually better. Take up excess circumference by overlapping the belt, and secure the excess material with duct tape (Fig. 21-10).

*Specific aspects of fracture care are covered in detail in other chapters. This chapter focuses on improvised systems, not on definitive orthopedic management. Improvised systems rarely provide the same degree of protection as commercial systems. Good judgment is needed.

Clothing. Bulky clothing, such as a fiber pile or fleece jacket, can be rolled and then wrapped around the victim’s neck to make a cervical collar. The extended sleeves can be used to secure the collar. Prewrapping a wide elasticized (Ace) wrap

Cervical Spine Injuries

Chapter 21: Improvisation in the Wilderness

Hip belt of inverted backpack

Cervical stabilizer Fanny pack as cervical collar

Figure 21-10. Inverted pack used as spine board.

around the jacket compresses the material to make it more rigid and supportive.

Malleable Aluminum Splint. A well-padded, aluminum splint (e.g., SAM Splint) can be adjusted to fit almost any size neck (Fig. 21-11).

Improvised Spinal Immobilization As noted, the improvised cervical collar is only an adjunct to full spinal immobilization. Two immobilization systems are (1) short-board immobilization, which is useful for short-duration transport (that is, getting the victim out of immediate danger) or when used in conjunction with a long board; and (2) longboard immobilization, used for definitive immobilization during extensive transport. Use either of these systems in conjunction with a rigid or semirigid cervical collar, as described previously. Improvised lateral “towel rolls” are often added to these systems for additional head and neck support. These rolls can be improvised from small sections of closed-cell foam (e.g., Ensolite [Armacell LLC, Mebane, NC]) sleeping pads. Alternatively, a U-shaped head support, or “horse collar,” can be made from any rolled garment, blanket, tarp, or tent fly; this is placed over the victim’s head in an inverted U and used with the improvised cervical collar and spine board. Hiking socks or stuff bags filled with dirt, sand, or gravel also work well for this purpose. Stuff bags filled with snow for support should never be used because the snow can melt during transport, which will cause excessive head and neck motion. However, snow-filled stuff bags can act as temporary support while more definitive systems are being constructed.

Improvised Short-Board Immobilization Internal Frame Pack and Snow Shovel System. Some internal frame backpacks can be easily modified by inserting a snow shovel through the centerline attachment points (the shovel handgrip may need to be removed first). The victim’s head is taped to the lightly padded shovel (Fig. 21-12); in this context, the shovel blade serves as a head bed. This system incorporates

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the remainder of the pack suspension as designed (i.e., shoulder and sternum straps with hip belt) and works well with other long-board designs, such as the continuous loop system (see Continuous Loop System section). Always assess the amount of flexion or extension the system will create on the cervical spine; if it is unacceptable, the system must be modified appropriately.

Inverted Pack System. An efficient short board can be made using an inverted internal or external frame backpack. The padded hip belt provides a head bed, and the frame is used as a short board in conjunction with a rigid or semirigid cervical collar (Fig. 21-13). Turn the pack upside down, and lash the victim’s shoulders and torso to the pack. Fasten the waist belt around the victim’s head, as in the top section of a Kendrick extrication device. The hip belt is typically too large, but excess circumference can be eliminated with bilateral Ensolite rolls. Unlike the snow shovel system, this system requires that the victim be lashed to the splint. Snowshoe System. A snowshoe can be made into a fairly reliable short spine board (Fig. 21-14). Pad the snowshoe and rig it for attachment to the victim as shown.19

Improvised Long-Board Immobilization Continuous Loop System (also known as the daisy chain, cocoon wrap, or mummy litter). In the authors’ opinion, this is the only improvised system that is adequate for immobilizing and transporting a patient with potential spine injuries. To construct the continuous loop system, the following items are needed: 1. Long climbing or rescue rope 2. Large tarp (or tent fly) 3. Sleeping pads (Ensolite or Therm-a-Rest [Cascade Designs, Inc., Seattle]) 4. Stiffeners (such as skis, poles, snowshoes, canoe paddles, or tree branches) Lay the rope out with even U-shaped loops as shown in Figure 21-15A. The midsection should be slightly wider to conform to the victim’s width. Tie a small loop at the foot end of the rope and place a tarp on the rope loops. On top of the tarp, lay foam pads the full length of the system (the pads can be overlapped to add length). Then, lay stiffeners on top of the pads in the same axis as the victim (see Fig. 21-15B). Add multiple foam pads on top of the stiffeners, followed optionally with a sleeping bag (see Fig. 21-15C). Place the victim on the pads. To form the daisy chain, bring a single loop through the pre-tied loop, pulling loops toward the center, and feeding through the loops brought up from the opposite side. It is important to take up rope slack continuously. When the victim’s armpits are reached, bring a loop over each shoulder and tie it off (or clip it off with a carabiner) (see Fig. 21-15D). One excellent modification involves adding an inverted internal frame backpack. This can be incorporated with the padding and secured with the head end of the rope. The pack adds rigidity and padding, and the padded hip belt serves as a very efficient head and neck immobilizer (see Figures 21-10 and 21-13). If the victim vomits during transport, the entire unit can be turned on its side or even partially inverted. Backpack Frame Litters. Functional litters can be constructed from external frame backpacks. Traditionally, two frames are

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A

C

B D Figure 21-11. Padded aluminum splint cervical collar. A, Place a vertical bend in the malleable aluminum splint approximately 6 inches from one end to form a vertical pillar.Then, add bilateral flares to make the splint comfortable for the victim where it rides against the lower mandible. B, Place the anterior pillar securely beneath the victim’s chin and wrap the remaining length of the splint around the victim’s neck. C, Side view of cervical collar fashioned from a SAM Splint. Note the formation of lateral, and if possible, posterior pillars. D, Frontal view.The end is angled inferiorly to provide an adequate chin-to-chest distance. Note the formation of the anterior pillar.

used, but three or four frames (Fig. 21-16) make for a larger, more stable litter. Cable ties or fiberglass strapping tape simplifies this fabrication. These litters can be reinforced with ice axes or ski poles.

Kayak System. Properly modified, the kayak makes an ideal rigid long-board improvised litter. First, remove the seat along with sections of the upper deck if necessary. A serrated river knife (or camp saw) makes this improvisation much easier. Open deck canoes can be used almost as is once the flotation material has been removed. Canoe System. Many rivers have railroad tracks that run parallel to the river canyon. The tracks can be used to slide a canoe

by placing the boat perpendicular to the tracks and pulling on both bow and stern lines.

Improvised Head Bed. A padded aluminum splint can be formed as shown to create a head bed to assist in securing the immobilized head of an injured victim. Tape this head bed to a commercial or improvised backboard (Fig. 21-17).

Pelvic Fractures Overview Unstable pelvic fractures are associated with a high incidence of morbidity and mortality.10,16,25 In one study, pelvic ring disruption in the trauma patient was associated with a mortality

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Figure 21-12. Head immobilized on a padded shovel.

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Figure 21-13. Short board using an inverted pack system.The backpack waist belt can be seen encircling the head.

Figure 21-14. Improvised snowshoe short board.A well-padded snowshoe is prerigged with webbing and attached to the victim as shown.This system can also be used in conjunction with longboard systems, such as the continuous loop system.

rate of 25%.1 Acute and uncontrolled hemorrhage and its complications are the leading causes of death in these patients.22 Hemorrhage after pelvic injury results from fracture surfaces, venous plexuses, and major arteries, usually branches of the internal iliac artery. Pelvic reduction and stabilization in the

early post-traumatic phase are reported to provide the most effective means of controlling venous hemorrhage.9 Pelvic reduction realigns bleeding fracture surfaces and reduces pelvic volume, and pelvic stabilization facilitates clot formation by reducing fracture site motion.23

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A

B

C

D Figure 21-15. Continuous loop, or “mummy,”litter made with a climbing rope.A, Rope is laid out with even U-shaped loops. B, Stiffeners such as skis and poles are placed underneath the victim to add structural rigidity. It is important to pad between the stiffeners and the victim. C, A sleeping bag may be used in addition to the foam pads. D, Loop of rope is brought over each shoulder and tied off (see text).

Circumferential wrapping and compression of the pelvic region with a sheet or strap has been studied as a means to stabilize and reduce open-book pelvic fractures.8,10 In a pair of studies from Oregon, circumferential pelvic compression was evaluated with the use of cadaveric models. Circumferential compression was found to result in significant stabilization of open-book pelvic injuries. Optimal placement of compression was at the level of the greater trochanters and the symphysis pubis, while the desired tension was found to be around 180 N (40 lb).8,10 Vermeulen and colleagues reported application of pelvic straps to 19 patients in Switzerland.40 Each strap was applied at the accident scene by emergency medical technicians (EMTs) upon suspicion of an unstable pelvic fracture. It took only 30

seconds to apply each strap. Application was subsequently found to produce significant reduction in both symphysis diastasis and pelvic inlet area. Routt and coworkers used a large circumferential sheet pulled tightly around the pelvis.33 The sheet remained in place until further stabilization could be achieved with an external fixator. Application of the sheet achieved reduction and stabilization in a safe and time-effective manner and did not interfere with resuscitation efforts. The American College of Surgeons Advanced Trauma Life Support (ATLS) course now includes a protocol for emergent management of pelvic ring disruptions, advising circumferential application of a pelvic sheet. Circumferential compression with a noninvasive pelvic sling should be considered for any patient with a suspected pelvic

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Figure 21-16. Backpack frame litter.

Figure 21-17. Improvised head bed.

Figure 21-18. Pelvic sling improvised with jacket.

fracture in the wilderness. The SAM Sling (SAM Medical Products, Newport, OR), is a commercial device that provides 150 N (33 lb) of pressure to the pelvis when applied according to the manufacturer’s instructions. It is equipped with an “autostop” buckle, which comprises spring-loaded prongs that lock the buckle in place when the correct amount of force is applied. Clothes, sheets, a sleeping bag, pads, air mattress, tent, or tent fly can be used to improvise a very effective pelvic sling in the backcountry. The object should be wide enough so that it does not cut into the victim when tightened.

2. Very gently slide the improvised sling under the victim’s buttocks and center it under the bony prominences at the outer part of the upper thigh or hips (greater trochanters/symphysis pubis) (Fig. 21-18). Cross the object over the front of the pelvis and tighten the sling by pulling both ends and securing with a knot, clamp, or duct tape. Another tightening technique is to wrap the sling snugly around the pelvis and tie an overhand knot. Place tent poles, a stick, or similar object on the knot and tie another overhand knot. Twist the poles or stick until the sling becomes tight. The sling should be tightened so that it is snug and the pelvis is returned to its normal anatomic position. 3. If a Therm-a-Rest pad or other inflatable sleeping pad is available, fold it in half so that it approximates the size of the pelvis. Gently slide the pad under the victim’s buttocks and center it under the greater trochanters and symphysis pubis. Secure the pad with duct tape, and then inflate the

Applying an Improvised Pelvic Sling 1. Ensure that objects have been removed from the patient’s pockets and that any belt has been removed so that the pressure of the sheet or object doesn’t cause additional pain by pressing items against the pelvis.

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS nical rescue, or helicopter evacuation is impossible. For example, a full-length ski splint is not compatible with evacuation in a small helicopter.

Femoral Traction Systems Every femoral traction system has six components: 1. Ankle hitch 2. Rigid support that is longer than the leg 3. Traction mechanism 4. Proximal anchor 5. Method for securing the splint to the leg 6. Additional padding

Ankle Hitch. Various techniques are used to anchor the distal extremity to the splint. Many work well, but some are impossible to recall in an emergency. Choose an easy-to-remember technique and practice it. It is best to leave the shoe on the victim’s foot and apply the hitch over it. Cut out the toe section of the shoe to periodically check circulation. Figure 21-19. Pelvic sling improvised with inflatable sleeping pad and duct tape.

pad as you would normally until it produces a snug fit and the pelvis is reduced (Fig. 21-19). 4. Place padding between the legs and gently tie the legs together to further stabilize the fracture in a position that is most comfortable for the victim.

Traction In the backcountry environment, traction is essential for two fundamental reasons: (1) the general inability to provide IV volume expansion and (2) prolonged transport time to definitive care. The primary purpose of backcountry femoral traction is to limit blood loss into the thigh. For a constant surface area, the volume of a sphere is greater than the volume of a cylinder. Pulling (via traction) the thigh compartment back into its natural cylindrical shape limits blood loss into the soft tissue. Although the main objective is to control hemorrhage and prevent shock, enhanced comfort for the victim and decreased potential for neurovascular damage are important secondary benefits. Properly applied improvised femoral traction can save lives in the backcountry, particularly on extended transports where IV fluids are not available.6

General Principles of Traction The potential variety of traction designs is unlimited, but five key design principles should be considered when evaluating any femoral traction system: 1. Does the splint provide inline traction or does it incorrectly pull the leg off to the side or needlessly plantar flex the ankle? 2. Is the splint comfortable? Be sure to ask the victim. 3. Does the splint compromise neurologic or vascular function? Constantly check distal neurovascular function. 4. Is the splint durable, or will it break when subjected to backcountry stresses? As stated earlier, it might help to try the traction design on an uninjured person and then knock the device around a bit to determine its strength. 5. Is the splint cumbersome? Many reasonable splint designs become so bulky and awkward that litter transport, tech-

Single Runner System. Loop a long piece of webbing, shoelace, belt, or rope over itself, bringing one end through the middle to create a stirrup. After rotating it away from the person by 180 degrees, slip the hitch over the shoe and ankle. Double Runner System. In this very straightforward technique, lay two short webbing loops (“runners”) over and under the ankle as shown (Fig. 21-20A). Pass the long loop sides through the short loop on both sides (see Fig. 21-20B) and adjust as needed (see Fig. 21-20C). One advantage of this system is that it is infinitely adjustable, enabling the rescuer to center the pull from any direction. As always, proper padding is essential, especially for long transports. The victim’s boot can distribute pressure over the foot and ankle but will obscure visualization and palpation of the foot. A reasonable compromise is to leave the boot on and cut out the toe section for observation. S-Configuration Hitch. This type of hitch is preferred if the victim also has a foot or ankle injury because traction is pulled from the victim’s calf instead of the ankle. Lay a long piece of webbing or similar material over the upper part of the ankle (lower calf) in an S-shaped configuration. Wrap both ends of the webbing behind the ankle and up through the loop on the other side. Pull the ends down on either side of the arch of the foot to tighten the hitch and tie an overhand knot (Fig. 21-21). Victim’s Boot System. Another efficient system uses the victim’s own boot as the hitch. Cut two holes into the side walls of the boot just above the midsole and in line with the ankle joint. Thread a piece of nylon webbing or cravat through to complete the ankle hitch (Fig. 21-22). Cutting away the toe may be necessary for neurovascular assessment. Buck’s Traction. For extended transport, Buck’s traction can be improvised using a closed-cell foam pad (Fig. 21-23). Wrap the pad around the lower leg as shown and loop a stirrup below the foot from medial calf to lateral calf. Fasten this assembly with a second cravat wrapped circumferentially around the calf over the closed-cell foam (duct tape or nylon webbing can be used instead of cravats). This system greatly increases the surface area over which the stirrup is applied and decreases the

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Figure 21-20. Double runner ankle hitch. A and B, Two webbing loops (runners) are laid over and under the ankle. C, Completed double runner ankle hitch. The beauty of this system is its infinite adjustability. The traction can be easily centered from any angle, ensuring in-line traction.

C

potential for neurovascular complications and dermal ischemia. In addition, improvised Buck’s traction has been used to manage backcountry hip fractures. However, it has been suggested that this technique may have little benefit.1 If Buck’s traction is used for a hip injury, use smaller amounts of traction (roughly ≤5 lb [2.5 kg]).

Rigid Support. The rigid support can be fabricated as a unilateral support (similar to the Sager traction splint or Kendrick traction device) or as a bilateral support, such as the Thomas half ring or Hare traction splint. Unilateral supports tend to be easier to apply than bilateral supports. The following are some ideas for rigid support. Double Ski Pole or Canoe Paddle System. This is fashioned like a Thomas half ring, with the interlocked pole straps slipped under the proximal thigh to form the ischial support. Some

mountain guides carry a prefabricated drilled ski pole section or aluminum bar that can be used to stabilize the distal end of this system (Fig. 21-24).

Single Ski Pole or Canoe-Kayak Paddle. Use a single ski pole or paddle either between the legs, which is ideal for bilateral femur fractures, or lateral to the injured leg. The ultimate rigid support is an adjustable telescoping ski pole used laterally. Adjust the pole to the appropriate length for each victim, making the splint compact for litter work or helicopter evacuation (Fig. 21-25). Tent Poles. This system uses conventional sectioned tent poles. Fit the poles together to create the ideal length rigid support. Because of their flexibility, tent poles must be well secured to the leg to prevent them from flexing out of position. Place a blanket pin or bent tent stake (Fig. 21-26) in the end of the pole

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Figure 21-21. S-configuration hitch for traction splinting.The system should be configured distally over the boot to distribute the forces.

Figure 21-23. Buck’s traction.Duct tape stirrups are added to a small foam pad that is wrapped around the leg. The entire unit is wrapped with an Ace bandage. This system helps distribute the force of the traction over a large surface area.

Figure 21-22. Traction using cut boot and cravat.

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Figure 21-24. A, Double ski pole system with prefabricated cross-bar and webbing belt traction. A prefabricated drilled ski section is used to attach the ends of two ski poles. Traction is applied with a webbing belt and sliding buckle.B, A Fastex-type or cam-lock utility strap makes a very efficient traction device and can be adapted for most systems.

B

A

Figure 21-25. Single ski pole system. An adjustable telescoping ski pole is used as the rigid support. A stirrup is attached to a carabiner placed over the end of the pole.Traction is applied by elongating the ski pole while another rescuer provides manual traction on the victim’s leg. Additional padding and securing follow (not shown).

Figure 21-26. Prefabricated drilled tent pole section and bent tent stake.The ski pole section is used to stabilize the end of a double ski pole traction system.This can be improvised on site if necessary. The bent tent stake serves as a distal traction anchor if a tent pole is used as the rigid support.

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2

3

Figure 21-27. A Prusik knot made from a small-diameter cord is used as an adjustable distal traction anchor. Although two wraps are shown in the illustration, an additional wrap adds further security when applied to a smooth surface, such as a kayak paddle.

Figure 21-29. Tent pole traction with trucker’s hitch. A bent tent stake is placed into the end of the tent pole as the distal traction anchor.A simple trucker’s hitch is used to provide traction.

windlass. Although these systems work and look good in the movies, they can be awkward to apply and are often not durable. The windlass can unspin if it is inadvertently jarred and can apply rotational forces to the leg. The amount of traction required may be difficult to estimate. A general rule is to use 10% of body weight or about 10 to 15 lb (4.5–7 kg) for the average victim. Consider practicing with a commercial system, such as a Sager Traction Device (Minto Research & Development, Inc., Redding, CA), ahead of time to get a feeling for what these forces look and feel like. Check the opposite extremity to compare length. After the traction is applied, always recheck distal neurovascular function (circulation, sensation, and movement). Figure 21-28. Two Prusik wraps are shown.Three or four wraps provide additional friction and security. If the Prusik knot slips, it can be easily taped in place.

to provide an anchor for the traction system. Alternately, use a Prusik knot (Fig. 21-27) to secure the system to the end of the tent pole (Fig. 21-28).

Cam Lock or Fastex-Like Slider. This simple, effective system uses straps that have a Fastex-like slider (ITW Fastex, Des Plaines, IL). Such straps are often used as waist belts or to hold items to packs. Alternately, a cam lock with nylon webbing can be used. Attach the belt to the distal portion of the rigid support and then to the ankle hitch. Traction is easily applied by cinching the nylon webbing (see Figure 21-24). Trucker’s Hitch. A windlass can be easily fashioned using smalldiameter line (parachute cord) and a standard trucker’s hitch for additional mechanical advantage (Fig. 21-29).

Miscellaneous. Any suitable object, such as a canoe or kayak paddle (see Figure 21-28), two ice axes taped together at the handles, or a straight branch, can be used to make a rigid support. Although skis immediately come to mind as suitable rigid components, they are too cumbersome to work effectively. Because of their length, skis may extend far beyond the victim’s feet or require placement into the axillae, which is unnecessary and inhibits mobility (e.g., sitting up during transport). Premanufactured canvas pockets, available from the National Ski Patrol System, provide a ski tip and tail attachment grommet for use with the ski system.

Prusik Knot. Almost any system can be rigged with a Prusik knot (see Figure 21-27). Prusiks are ideal for providing traction from rigid supports with few tie-on points (such as a canoe paddle shaft or a tent pole). The Prusik knot can be used to apply the traction (by sliding the knot distally) or simply as an attachment point for one of the traction mechanisms already mentioned.

Traction Mechanism. The first popularized modern improvised traction mechanism was the Boy Scout–style Spanish

Litter Traction. If no rigid support is available and a rigid litter such as a Stokes is being used, apply traction from the rigid bar

Chapter 21: Improvisation in the Wilderness at the foot end of the litter. If this system is used, ensure that the victim is immobilized on the litter with adequate countertraction, such as inguinal straps.

Proximal Anchor. The simplest proximal anchor uses a single proximal thigh strap, which can be made from a piece of climbing webbing or a prefabricated strap, belt, or cam lock (Figs. 21-30 and 21-31). A cloth cravat can be used in a pinch. On the river, a life jacket can be used (Fig. 21-32). When climbing, a climbing harness is ideal. Securing and Padding. Check all potential pressure points to ensure that they are adequately padded. An excellent padding system can be made by first covering the upper and lower leg with a folded length of Ensolite (Fig. 21-33). This is preferred over a circumferential wrap because the folded system allows you to see the extremity. The victim is more comfortable if femoral traction is applied with the knee in slight flexion (padding placed beneath the knee during transport). Secure the splint firmly to the leg. Almost any straplike object will work, but a 4- to 6-inch (10–15 cm) Ace bandage wrapped circumferentially provides a comfortable and secure union. Finally, strap or tie the ankles or feet together (with adequate padding between the legs) to give the system additional stability. Tying the ankles together also prevents the injured leg from excessive external rotation during transport, which might otherwise greatly add to the victim’s discomfort.

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incorporates the joints above and below the fracture. If possible, the splint should be fashioned on the uninjured extremity and then transferred to the injured one. On ski trips, skis and poles can be used as improvised splints. On white-water trips, canoe and kayak paddles can be used in a similar manner. Airbags used as flotation for kayaks and canoes can be converted into pneumatic splints for arm and ankle injuries. The minicell or Ethafoam (Dow, Midland, MI) pillars found in most kayaks can be removed and carved into pieces to provide upper and lower extremity splints. A life jacket can be molded into a cylinder splint for knee immobilization or into a pillow splint for the ankle. The flexible aluminum stays found in internal frame packs can be molded into upper extremity splints. Other improvised

Extremity Splints Splint all fractures before the victim is moved unless his or her life is in immediate danger. In general, make sure the splint

A

Figure 21-30. Proximal anchor using cam lock belt.The belt is applied as shown.The strap is adjusted loosely to allow the belt to ride up to the point of the hip. If the strap is improperly tightened, it can create pressure over the fracture, and it moves the traction point to a less optimal distal position. Padding is helpful, but not always necessary if the victim is wearing pants and the strap is properly adjusted.

B Figure 21-31. A, River dry bag used to create a simple proximal support with a kayak paddle. B, Here a paddle is pushed up against the proximal support strap.It is taped for security but the forces are pushing against the strap, not the tape.

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C Figure 21-31, cont’d. C, A similar technique could be used with a ski pole or other suitable object.

A

Figure 21-32. Life jacket proximal anchor. An inverted life jacket worn like a diaper forms a well-padded proximal anchor.A kayak paddle is rigged to the life jacket’s side adjustment strap.

B splinting material includes sticks or tree limbs, rolled-up magazines, books or newspapers, ice axes, tent poles, and dirt-filled garbage bags or fanny packs. Ideally, a splint should immobilize the fractured bone in a functional position. In general, “functional position” means that the legs should be straight or slightly bent at the knee, the ankle and elbow bent at 90 degrees, the wrists straight, and the fingers flexed in a curve as if the person were attempting to hold a can of soda or a baseball. Splints can be secured in place with strips of clothing, belts, pieces of rope or webbing, pack straps, gauze bandages, or elastic bandage wraps. Padded aluminum can be molded into various configurations to splint extremity injuries. Padded aluminum splints (e.g., SAM

Figure 21-33. Folded Ensolite padding often provides better visualization of the extremity than does a circumferential wrap.

Splint) are built from a thin core of aluminum, sandwiched between two layers of closed-cell foam. When molded into any of several “structural curves,” padded aluminum splints become much more rigid and can be used to immobilize most fractured or injured extremities. If prolonged use (more than a few hours) is anticipated, place absorbent material, such as cotton cloth, between the splint and the skin to prevent skin irritation. Also, to prevent uncomfortable pressure points during prolonged use, place soft padding (such as

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A

B Figure 21-34. Tripod splint for unreduced anterior shoulder dislocation. This splint holds the arm in abduction when adduction is not possible. Additional padding should be added where necessary and the splint secured to the arm with an elastic wrap or other bandaging material.

Figure 21-36. Forearm splint. These splints are used for treatment of wrist or forearm fractures. The sugar-tong splint (A) prevents pronation and supination and has the advantage of greater security and protection than the volar splint (B) because of its anterior-posterior construction.

gauze pads) around all bony prominences (Figs. 21-34 to 21-41).

Functional Splints Although most splints are designed to immobilize an injured extremity completely, in the backcountry a splint may need to allow for a limited range of motion so the victim can facilitate his or her own rescue. Many functional splints can be improvised quickly using nothing more than a closed-cell foam sleeping pad and some tape or elastic wrap. With the advent of inflatable sleeping pads (e.g., Therm-a-Rest), foam pads are not as ubiquitous as they once were in the backcountry. However, many of these splints can be made using a partially inflated Therm-a-Rest. Once applied, these pads can be inflated to provide the necessary support, fit, and comfort (Fig. 21-42).

Other Wraps and Bandages Functional Shoulder Immobilizer (Shoulder Spica Wrap)

Figure 21-35. Humerus splint. Used in conjunction with a sling and swath, this splint adds extra support and protection for a fractured humerus.

After a dislocated shoulder is reduced, standard treatment is to completely immobilize the arm with a sling and swath. This, however, prevents the victim from using the extremity to facilitate his or her own evacuation. A more functional system can be made using a 6-inch (15 cm) elastic wrap. This method allows the victim limited function (e.g., ski poling or kayak

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A

Figure 21-37. Lower leg or ankle splint. A sugar-tong splint can be used to immobilize fractures of the tibia, fibula, or ankle. When used on an adult, two splints should be used. A third splint may be placed posteriorly for additional support.

paddling) while still preventing complete abduction of the arm (Fig. 21-43).

Triangular Bandage One of the most ubiquitous components of first-aid kits and one of the easiest to replace through improvisation is the triangular bandage. The need to carry this bulky item, which is commonly used to construct a sling and swath bandage for shoulder and arm immobilization, can be eliminated by carrying two or three safety pins. Pinning the shirt sleeve of the injured arm to the chest portion of the shirt effectively immobilizes the extremity against the body (Fig. 21-44A). If the victim is wearing a short-sleeved shirt, the bottom of the shirt can be folded up and over the arm to create a pouch. This can be pinned to the sleeve and chest section of the shirt to secure the arm (see Fig. 21-44B).

B Figure 21-38. A and B, Padded aluminum thumb spica.

Triangular bandages are also used for securing splints and constructing pressure wraps. Common items, such as socks, shirts, belts, pack straps, webbing, shoe laces, fanny packs, and underwear, can easily be substituted.


WOUND MANAGEMENT The same principles that govern wound management in the emergency department apply in the wilderness. The main problem faced in the wilderness is access to adequate supplies. In deciding to close a wound primarily or pack it open, take into account the mechanism of injury, age of the wound, site of the wound, degree of contamination, and ability to effectively clean the wound.

A C

B

D

Figure 21-39. Knee immobilizer using two padded aluminum splints.The splints are folded in half, then fanned out (wider at the top for the thigh) and taped.Tape is applied to maintain the fan shape.The splint is then applied bilaterally and secured.

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Cut here

Figure 21-40. Posterior arm splint. This splint is cut from a 5- to 9-gallon (1.3–2.4 L) plastic fuel or water can.When used with appropriate padding,this forms an excellent splint for injured or fractured elbows.

Figure 21-42. Functional knee and lower leg immobilizer. Wrap a sleeping pad around the lower leg from the mid thigh to the foot. Fold the pad so that the top of the leg is not included in the splint.This provides better visualization of the extremity and leaves room for swelling. A full-length pad forms a very bulky splint and may need to be trimmed before rolling. Because of the conical shape of the lower extremity and the effects of gravity, foam-pad lower extremity splints tend to work their way inferiorly when the victim ambulates. A simple solution is to use duct tape “suspenders” to keep the splint from migrating downward.

Wound Irrigation

Figure 21-41. Webbing sling. An 8-foot (2.5 m) length of 1-inch (2.5 cm) tubular or flat webbing is used to form a functional arm sling. A Crazy Creek Chair can be used to improvise both upper and lower extremity splints. Its inherent integral strapping system precludes the need for additional straps or tape.

The primary determinants of infection are bacterial counts and amount of devitalized tissue remaining in the wound.20 Ridding a wound of bacteria and other particulate matter requires more than soaking and gentle washing with a disinfectant.26 Irrigating the wound with a forceful stream is the most effective method of reducing bacterial counts and removing debris and contaminants.29,36 The cleansing capacity of the stream depends on the hydraulic pressure under which the fluid is delivered.19,35 Irrigation is best accomplished by attaching an 18- or 19-gauge catheter to a 35-mL syringe, or a 22-gauge needle to a 12-mL syringe. This creates hydraulic pressure in the range of 7 to 8 lb/in2 and 13 lb/in2 (3 to 3.5 and 6 kg/cm2), respectively.19,31,35 The solution is directed into the wound from a distance of 1 to 2 inches (2.5–5 cm) at an angle perpendicular to the wound surface and as close to the wound as possible. The amount of irrigation fluid varies with the size and contamination of the wound, but should average no less than 250 mL.19 Remember: “the solution to pollution is dilution.” Which irrigation solution is best for open wounds? Those who subscribe to the theory that nothing should enter a wound that could not be instilled safely into the eye believe that normal saline is the best solution.12,21 In a study of 531 patients with traumatic wounds, there was no significant variation in infection rates among sutured wounds irrigated with normal saline, 1% povidone-iodine, or pluronic F68 (Shur-Clens).15

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D Figure 21-43. A–D, Shoulder spica wrap.

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Box 21-3. Recommended Technique for Wound Irrigation 1. Fill a sandwich or garbage bag with disinfected water. 2. Disinfect the water with iodine tablets, iodine solution, or povidone-iodine or by boiling it. 3. Normal saline can be made by adding 2 teaspoons (9 g) of salt per liter of water. 4. Seal the bag. 5. Puncture the bottom of the bag with an 18-gauge needle, safety pin, fork prong, or knife tip. 6. Squeeze the top of the bag forcefully while holding it just above the wound, directing the stream into the wound. 7. Use caution to ensure that none of the irrigation fluid splashes into your eyes.

A

Box 21-4. Wound Taping Technique

B Figure 21-44. Techniques for pinning the arm to the shirt as an improvised sling. A, With a long-sleeved shirt or jacket, the sleeved arm is simply pinned to the chest portion of the garment.B, With a short-sleeved shirt,the bottom of the shirt is folded up over the injured arm and secured to the sleeve and upper shirt.

Tap water has been found to be as effective for irrigating wounds as sterile saline. In fact, the infection rate was significantly lower after irrigation with tap water, and no infections resulted from the bacteria cultured from the tap water.3 Improvised wound irrigation requires only a container that can be punctured to hold the water, such as a sandwich or garbage bag, and a safety pin or 18-gauge needle (Box 21-3).

Wound Closure Before a wound is closed, remove all foreign material and grossly devitalized tissue. Debridement can be accomplished using scissors, knife, or any other sharp object, and wounds can be closed with sutures, staples, tape, pins, or glue. Although suturing is still the most widely used technique, stapling and gluing are ideal methods for closing wounds in the wilderness.

1. Obtain hemostasis, and dry the wound edges. 2. Apply benzoin or cyanoacrylate glue to the skin adjacent to the wound. Benzoin should be allowed to dry long enough for it to become tacky, but tape should be applied to the glue while the glue is still wet. 3. Tape should be cut to 1/4-inch or 1/2-inch widths (6– 13 mm), depending on the size of the laceration, and to a length that allows for 3/4 to 1 inch (2 to 3 cm) of overlap on each side of the wound. 4. Secure one half of the tape to one side of the wound. Oppose the opposite wound edge with a finger while the tape is secured to the other side. 5. Wound tapes should have gaps of 1/16 to 1/8 inch (2–3 mm) between them to allow for serous drainage. 6. Cross-stays of tape can be placed perpendicular over the tape ends to prevent them from peeling off. 7. Additional glue can be applied to the tape edges every 24 hours to reinforce adhesion.

Clinical studies of the use of staples to close traumatic lacerations have found various advantages of stapling over suturing: wound tensile strength is greater, there is less inflammation, time required for closure is shorter, and fewer instruments are needed.32 Most important, cosmetic outcome is not compromised.18 Staplers are lightweight, presterilized, and easy to use.

Wound Taping Skin Tapes. Skin tapes are useful for shallow, nongaping wounds and have several advantages over suturing, including reduced need for anesthesia, ease of application, decreased incidence of wound infection, and availability. Any strong tape can be used to improvise skin tape strips, but duct tape works especially well (Box 21-4). Puncturing holes in the tape before application helps prevent exudate from building up under the tape. Wipe the skin with a solvent such as acetone to remove oil and sweat. Then, apply benzoin to the skin before the tape to augment adhesion. Wound taping does not work well over joints or on hairy skin surfaces unless the hair is first removed.

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Box 21-5. Technique for Gluing Lacerations

Dental floss

1. Irrigate the wound with copious amounts of disinfected water. 2. Control any bleeding with direct pressure. Place a gauze pad moistened with oxymetazoline (Afrin) nasal spray into the wound to help control bleeding. 3. Once hemostasis is obtained, approximate the wound edges using fingers or forceps. 4. Paint the tissue glue over the apposed wound edges using a very light brushing motion of the applicator tip. Avoid excess pressure of the applicator on the tissue because this could separate the skin edges, forcing glue into the wound. Apply multiple thin layers (at least three), allowing the glue to dry between each application (about 2 minutes). 5. Glue can be removed from unwanted surfaces with acetone, or loosened from skin with petroleum jelly.

Tie floss around crossed hair twists

Figure 21-45. Scalp laceration closed using dental floss.

Hair-Tying a Scalp Laceration. If you are faced with a bleeding scalp laceration and the injured person has a healthy head of hair, you can tie the wound closed using the victim’s own hair and a piece of suture (0-silk works best), dental floss, sewing thread, or thin string. Take the material and lay it on top of and parallel to the wound. Twirl a few strands of hair on each side of the wound and then cross them over the wound in opposite directions so that the force pulls the wound edges together. Have an assistant tie the strands of hair together with the material while you hold the wound closed with the strands of hair. A square knot works best (Fig. 21-45). Repeat this technique as many times as necessary along the length of the wound to close the laceration.

Gluing The concept of gluing wounds is not new; the U.S. Army used a quick-sealing glue to treat battlefield wounds in Vietnam, and Histoacryl (N-butyl-2-cyanoacrylate) tissue adhesive has been used in Europe and Canada for sutureless skin closure for more than a decade.41 The U.S. Food and Drug Administration (FDA) has approved a topical skin adhesive to repair skin lacerations. Dermabond (2-octyl cyanoacrylate) is packaged in a small single-use applicator. Tissue glue is ideal for backcountry use because it precludes the need for topical anesthesia, is easy to use, reduces the risk of needle stick injury, and takes up much less room than a

conventional suture kit. When applied to the skin surface, tissue glue provides strong tissue support and peels off in 4 to 5 days without leaving evidence of its presence.31 It provides a faster and less painful method for closing lacerations than does suturing and has yielded similar cosmetic results in children with facial lacerations (Box 21-5).30 Tissue glue evokes a mild acute inflammatory reaction with no tissue necrosis.39 Dermabond has four times the three-dimensional breaking strength of Histoacryl and forms a more flexible bond, thus providing a stronger and longer bond than its European counterpart. Petroleum-based ointments and salves, including antibiotic ointments, should not be used on the wound after gluing because these substances can weaken the polymerized film and cause wound dehiscence. Tissue glue has also been used successfully to treat superficial painful fissures of the fingertips (“polar hands”), which commonly occur in cold climates and at high elevations.4


IMPROVISED BLISTER MANAGEMENT

To dress blisters without moleskin, molefoam, or other commercial blister dressing, you can improvise one with a piece of duct tape. Duct tape’s smooth outer surface provides protection from friction, while its adhesive side adheres strongly to skin. A sandwich bag can be used to improvise another type of blister dressing. It simulates the Blist-O-Ban, which was developed by SAM Medical Products as an innovative technique (BursaTek technology) to prevent blisters. The smooth, gliding surface of the bag helps to stop friction and reduce development of hot spots and blisters. Cut the corner of the sandwich bag and apply a lubricant between the two surfaces. Secure the piece of bag to the blister site with tape or glue (Fig. 21-46).


RING REMOVAL Rings should always be removed quickly after injury to fingers and trauma to the hands; progressive swelling may cause rings to act as tourniquets. If a ring cannot be removed with soap or lubricating jelly, the string wrap technique can be used. Pass a

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A

B

Figure 21-46. A–C, Blister dressing improvised with plastic sandwich bag.

C

20-inch (51 cm) length of fine string, dental floss, umbilical tape, or thick suture between the ring and the finger. Pull the string so that most of it is on the distal side of the digit. Then wrap it around the swollen finger from proximal to distal, beginning next to the ring and continuing past the proximal interphalangeal joint. Place successive loops of the wrap close enough together to prevent any swollen skin from bulging between the strands. Remove the ring by unwinding the proximal end of the string and forcing the ring over the distal string. If the string is not long enough, the technique may require repeated wraps (Fig. 21-47).


IMPROVISATIONAL TOOLKIT Some people, convinced they could whittle a Swan-Ganz catheter from a tree branch, enter the wilderness with nothing more than a Swiss Army knife. However, a little foresight and preparation make improvisation much easier. Efficiency trans-

lates into speedy preparation and assembly, which ultimately results in better care. The following section lists items that facilitate improvisation in the field.

Knife The knife can be a fairly simple model, but it should have an awl for drilling holes into skis, poles, sticks, and so on. The awl on a Swiss Army knife works quite well for this purpose. This allows one to create well-fitted components during improvisation (e.g., a drilled cross-bar attached to ski tips for an improvised rescue toboggan).

Tape Carry some form of strong, sticky, waterproof tape. This item cannot be improvised. Use either cloth adhesive tape (already in the medical kit) or duct tape. Duct tape is ideal for nearly all tasks, even being useful on skin when needed (e.g., to close wounds, treat blisters, or tape an ankle). Note, however, that some persons may be sensitive to the adhesive. Fiberglass

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Box 21-6. Uses of a Safety Pin Safety pins can be used: • To pin the anterior aspect of the tongue to the lower lip (use two pins) to establish an airway in an unconscious victim whose airway is obstructed (see Figure 21-1) • To replace the lost screw in a pair of eyeglasses to prevent the lens from falling out • To improve glasses: Draw two circles in a piece of duct tape where your eyes would fit. Use a pin to make holes in the circles, then tape this to your face. The pinholes will partially correct myopic vision and protect the eyes from ultraviolet radiation. Slits can also be used for improvised sunglasses. • To perform neurosensory skin testing • To puncture plastic bags for irrigation of wounds • To remove embedded foreign bodies from the skin • To drain an abscess or blister • To relieve a subungual hematoma • As a fishhook • As a finger splint (mallet finger) • As a sewing needle, using dental floss as thread • To hold gaping wounds together • To replace a broken clothing zipper • To hold gloves or mittens to a coat sleeve • To unclog jets in a camping stove • To pin triage notes to multiple victims • To remove a corneal foreign body (with ophthalmic anesthetic) • In a sling and swath for shoulder or arm injuries • To fix a ski binding • To extract the clot from a thrombosed hemorrhoid • To pin a strap or shirt tightly around the chest for rib fracture support • To remove ticks Figure 21-47. String technique for removing a ring from a swollen finger (see text).

strapping tape has greater tensile strength and is ideal for joining rigid components, such as taping two ice axes together. However, it is less sticky than duct tape and not as useful for patching torn items. Extra tape can be carried by wrapping lengths of it around pieces of gear.

Plastic Cable Ties Lightweight cable ties can be used to bind almost anything together (e.g., binding pack frames together for improvised litters or ski poles together for improvised carriers). They are also perfect for repairing many items in the backcountry.

Parachute Cord Parachute cord has hundreds of uses in the backcountry. It can be used for trucker’s hitch traction and for tying complex splints together. Parachute cord is light; carry a good supply.

Safety Pins See Box 21-6 for various uses for safety pins.

Wire Braided picture-hanging wire works well because it is supple and ties like line. Its strength makes it superior for repairing and

improvising components under an extreme load, such as fabricating improvised rescue sleds or repairing broken or detached ski bindings.

Bolts and Wing Nuts Bolts and wing nuts make the job of constructing an improvised rescue sled much easier (see Improvised Rescue Sled or Toboggan section). Bolts are useful only if holes can be created to put them through. Therefore, a knife with an awl is needed for drilling holes through skis, poles, or other improvised items.

Prefabricated Cross-Bar The prefabricated cross-bar can be used for double ski pole traction splint systems. A cross-bar is easily fabricated from a branch or short section of a ski pole, but carrying a prefabricated device, such as a 6-inch (15 cm) predrilled ski pole section, saves time (see Figure 21-24).

Ensolite (Closed-Cell Foam) Pads Since the introduction of Therm-a-Rest types of inflatable pads, closed-cell foam has become increasingly scarce; however, closed-cell foam (Ensolite) is still the ultimate padding for almost any improvised splint or rescue device. The uses for

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closed-cell foam are virtually unlimited. Even die-hard Therma-Rest fans should carry a small amount of closed-cell foam, which is lightweight and doubles as a comfortable seat cushion. Furthermore, unlike inflatable pads, Ensolite will not puncture and deflate. Therm-a-Rest pads also have their place, being useful for padding for long bone splints and immobilizers (e.g., an improvised universal knee immobilizer). An inflatable pad can also be used to cushion pelvic fractures. First, wrap the deflated pad around the pelvis. Then secure the pad with tape and inflate it, creating an improvised substitute for military antishock trousers (MAST device).

Fluorescent Surveyor’s Tape Surveyor’s tape can be used much like Hansel and Gretel’s breadcrumbs to help relocate a route into or out of a rescue scene. It is also ideal for marking shelters in deep snow and can serve as a wind sock during helicopter operations on improvised landing zones. Surveyor’s tape is not biodegradable, so it should always be removed from the site after the rescue is completed.

A

Space Blanket or Lightweight Tarp For improvising hasty shelters in times of emergency, some form of tarp is essential. In the snow, a slit trench shelter can be built in a matter of minutes using a tarp. Otherwise, the complex and time-consuming construction of improvised structures, such as snow caves, igloos, or tree branch shelters, might be necessary. Typically, little time or help is available for this task during emergencies. In addition, tarps are essential for “hypothermia wraps” when managing injured persons in cold or wet conditions. The only advantage of a space blanket over other tarps is its small size, which means there is a good chance it was packed for the trip.


IMPROVISED EYEGLASSES Exposure of unprotected eyes to ultraviolet radiation at high altitudes may produce photokeratitis (snow blindness). Symptoms are delayed, and the victim is often unaware that an eye injury is developing. When sunglasses are lost at 14,000 ft (4267 m) in the snow, photokeratitis can develop in 20 minutes. One can improvise sunglasses from duct tape, cardboard, or other light-impermeable material that can be cut. Cardboard “glasses” with narrow eye slits can be taped over the eyes for protection. Slits can also be cut into a piece of duct tape that has been folded over on itself with the sticky sides opposing. After a triangular wedge is removed for the nose, apply another piece of tape to secure the glasses to the head. If a sunglass lens is broken or lost, the above technique can be used over the existing frame (Fig. 21-48). Pinhole tape glasses can improve vision in a myopic person whose corrective lenses have been lost. With myopia, parallel light rays from distant objects focus in front of the retina. The pinhole directs entering light to the center of the cornea, where refraction (bending of the light) is unnecessary. Light remains in focus regardless of the refractive error of the eye (Fig. 21-49). Pinhole glasses decrease both illumination and field of vision, so puncture a piece of duct tape or cardboard repeatedly with a safety pin, needle, fork, or other sharp object until enough light can enter to focus on distant objects. Secure the device to the face (Fig. 21-50).

B Figure 21-48. Improvised lens for sunglasses (see text).


IMPROVISED TRANSPORT Carries Two-Hand Seat* Two carriers stand side by side. Each carrier grasps the other carrier’s wrists with opposite hands (e.g., right to left). The victim sits on the rescuers’ joined forearms. The carriers each maintain one free hand to place behind the back of the victim for support (support hands can be joined). This system places great stress on the carriers’ forearms and wrists.

Four-Hand Seat Two carriers stand side by side. Each carrier grasps his or her own right forearm with the left hand, palms facing down. Each *Both the two-hand seat and the four-hand seat are useful only for very short carries over gentle terrain.

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A

Figure 21-49. Pinhole in cardboard to improve vision in person with myopia.

B Figure 21-51. Ski pole seat.A, Ski poles are anchored by the packs.B, The victim is supported by the rescuers.

carrier then grasps the forearm of the other with his or her free hand to form a square “forearm” seat. With the forearm seat, the victim must support himself or herself with a hand around the rescuers’ backs.

Ski Pole or Ice Ax Carry Two carriers with backpacks stand side by side with four ski poles or joined ice ax shafts resting between them and the base of the pack straps (Fig. 21-51). The ski poles or ice ax shafts can be joined with cable ties, adhesive tape, duct tape, wire, or cord. Because the rescuers must walk side by side, this technique requires wide-open, gentle terrain. The victim sits on the padded poles or shaft with his or her arms over the carriers’ shoulders. Figure 21-50. Pinholes in duct tape to improve vision in person with myopia.

Split-Coil Seat (“Tragsitz”) The split-coil seat transport uses a coiled climbing rope to join the rescuer and victim together in a piggyback fashion (Fig. 21-52). The victim must be able to support himself or herself to avoid falling back, or must be tied in.

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A

Figure 21-52. Split-coil seat. A, Rope coil is split. B, Victim climbs through rope. C, Rescuer hoists the sitting victim.

B C

Two-Rescuer Split-Coil Seat The two-rescuer split-coil seat is essentially the same as the splitcoil Tragsitz transport, except that two rescuers split the coil over their shoulders. The victim sits on the low point of the rope between the rescuers (Fig. 21-53). Each rescuer maintains a free hand to help support the victim.

Backpack Carry A large backpack is modified by cutting leg holes at the base. The victim sits in it as would a child in a baby carrier. Some large internal frame packs incorporate a sleeping bag compartment in the lower portion of the pack that includes a compression panel. With this style of pack, the victim can sit on the suspended panel and place his or her legs through the unzipped lower section without damaging the pack, or the victim can simply sit on the internal sleeping bag compression panel without the need to cut holes.

Nylon Webbing Carry Nylon webbing can be used to attach the victim to the rescuer like a backpack (Fig. 21-54). At least 15 to 20 feet (4.6 to

6.1 m) of nylon webbing is needed to construct this transport. The center of the webbing is placed behind the victim and brought forward under the armpits. The webbing is then crossed and brought over the rescuer’s shoulders, then down around the victim’s thighs. The webbing is finally brought forward and tied around the rescuer’s waist. Additional padding is needed for this system, especially around the posterior thighs of the victim.

Three-Person Wheelbarrow Carry This system is extremely efficient and can be used for prolonged periods on relatively rough terrain. The victim places his or her arms over two rescuers’ shoulders (the rescuers stand side by side). The victim’s legs are then placed over a third rescuer’s shoulders. This system equalizes the weight of the victim very efficiently.

Litters (Nonrigid) Many nonrigid litter systems have been developed over the years. These systems are best suited for transporting non– critically injured victims over moderate terrain. They should

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Figure 21-53. Two-rescuer split-coil seat. Balance could be improved by using a longer coil to carry the victim lower.

never be used for trauma victims with potential spine injuries.

Figure 21-54. Webbing carry. Webbing crisscrosses in front of the victim’s chest before passing over the shoulders of the rescuer.

Blanket Litter A simple nonrigid litter can be fabricated from two rigid poles, branches, or skis and a large blanket or tarp. The blanket or tarp is wrapped around the skis or poles as many times as possible and the poles are carried. The blanket or tarp should not be simply draped over the poles. For easier carrying, the poles can be rigged to the base of backpacks. Large external frame packs work best, but internal frame packs can be rigged to do the job. Alternatively, a padded harness to support the litter can be made from a single piece of webbing, in a design similar to a nylon webbing carry.

Tree Pole Litter The tree pole litter is similar to the blanket litter described previously. In the tree pole litter, instead of a blanket or a tarp, the side poles are laced together with webbing or rope and then padded. Again, the poles may be fitted through pack frames to aid carrying. To give this litter more stability and to add tension to the lacing, the rescuer should fabricate a rectangle with rigid cross-bars at both ends before lacing.

Parka Litter Two or more parkas can be used to form a litter (Fig. 21-55). Skis or branches are slipped through the sleeves of heavy parkas, and the parkas are zipped shut with the sleeves inside. Ski edges should be taped first to prevent them from tearing through the parkas.

Internal Frame Pack Litter The internal frame pack litter is constructed from two to three full-size internal frame backpacks, which must have lateral compression straps (day packs are suboptimal). Slide poles or skis through the compression straps; the packs then act as a support surface for the victim.

Life Jacket Litter Life jackets can be placed over paddles or oars to create a makeshift nonrigid litter.

Rope Litter On mountaineering trips, the classic rope litter can be used, but this system offers little back support and should never be used for victims with suspected spine injuries. The rope is uncoiled and staked onto the ground with sixteen 180-degree bends (eight on each side of the rope center). The rope bends should approximate the size of the finished litter. The free rope ends are then used to clove hitch off each bend (leaving 2 inches [5 cm] of bend to the outside of each clove hitch). The leftover rope is threaded through the loops at the outside of each clove hitch. This gives the rescuers a continuous handhold and protects the bends from slipping through the clove hitches. The rope ends are then tied off (Fig. 21-56). The litter is padded with packs, Therm-a-Rest pads, or foam pads. This improvised

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Figure 21-55. Parka litter. On the right, the sleeves are zipped inside to reinforce the litter.

To build an improvised rescue sled or toboggan, the rescuer needs a pair of skis (preferably the victim’s) and two pairs of ski poles; three 2-foot-long (61-cm) sticks (or ski pole sections); 80 feet (24.4 m) of nylon cord; and extra lengths of rope for sled hauling. The skis are placed 2 feet (0.6 m) apart. The first stick is used as the front cross-bar and is lashed to the ski tips. Alternatively, holes can be drilled into the stick and ski tips with an awl, and bolts can be used to fasten them together. The middle stick is lashed to the bindings. One pair of ski poles is placed over the cross-bars (baskets over the ski tips) and lashed down. The second set of poles is lashed to the middle stick with baskets facing back toward the tails. A third rear stick is placed on the tails of the skis and lashed to the poles. The lashings are not wrapped around the skis; the cross-bar simply sits on the tails of the skis under the weight of the victim. Nylon cord is then woven back and forth across the horizontal ski poles. The hauling ropes are passed through the baskets on the front of the sled. The ropes are then brought around the middle cross-bar and back to the front cross-bar. This rigging system reverses the direction of pull on the front cross-bar, making it less likely to slip off the ski tips.38 Another sled design utilizes a predrilled snow shovel incorporated into the front of the sled. A rigid backpack frame can also be used to reinforce the sled. This requires drilling holes into the ski tips and carrying a predrilled shovel. This system holds the skis in a wedge position and may offer slightly greater durability.34 Figure 21-56. Rope litter (see text).

litter is somewhat ungainly and requires six or more rescuers for an evacuation of any distance. A rope litter can be tied to poles or skis to add lateral stability if needed.

Improvised Rescue Sled or Toboggan A sled or toboggan can be constructed from one or more pairs of skis and poles that are lashed, wired, or screwed together. Many designs are possible. Improvised rescue sleds may be clumsy and often bog down hopelessly in deep snow. Nonetheless, they can be useful for transporting a victim over short distances (to a more sheltered camp or to a more appropriate landing zone). They have sometimes been used for more extensive transports, but they do not perform as well as commercial rescue sleds.


A FINAL NOTE Under certain conditions, improvised systems are entirely suboptimal and may not meet standard-of-care criteria. It would, for example, be ill advised to fabricate a litter for transporting a victim with a suspected spine injury when professional rescue is only a few miles away. An improvised litter system might be entirely appropriate, however, if the injured person is 40 miles out and needs transport to a sheltered camp or potential helicopter landing zone. The context of the situation should be considered. At times, persons are obligated to do whatever they can, and a resourceful approach to problem solving combined with a little ingenuity could save a victim’s life.

The references for this chapter can be found on the accompanying DVD-ROM.

Chapter 22: Hunting and Other Weapons Injuries

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22

Edward J. Otten and David G. Mohler

Even as Nimrod the mighty hunter before the Lord. Genesis 10 : 9 Anthropologists have many theories concerning the origins and importance of hunting in the evolution of the human species. The physical attributes of bipedal locomotion, binocular vision, and an opposable thumb all make humans more efficient hunters. Whether these exist because humans have an innate compulsion to hunt or whether humans are hunters because of these traits is debatable. There is no debate, however, that human social evolution, language, the use of tools, and domestication of animals are directly related to more efficient hunting. In a survival situation, and in some ways with regard to evolution, hunter–gatherer animals have a distinct advantage over strictly vegetarian animals because of the relative food value of meat over plants. Hunters tend to be males. Approximately three fourths of all calories in modern hunter–gatherer groups are derived from plants, and this portion of the food is usually supplied by the women in the group. Even in Eskimo tribes where plants make up little of the diet, the women do most of the fishing while the men hunt. Hominids were at a disadvantage, even in groups, when hunting large animals or driving off other predators from their kills until they began using stones, long bones, and sticks to enhance their relatively weak teeth and claws. Implements for hunting and skinning animals were the earliest tools found by anthropologists. Human cultural evolution followed closely the technological changes in weapons, although sports, business, and war had replaced the need for hunting in most cultures even by the time Nimrod walked the earth. Bows and arrows, slings, spear throwers, nets, harpoons, traps, and firearms were designed to extend the reach and increase the lethality of the human hand. Unfortunately, humans discovered that they could kill each other with these weapons. Since the discovery of gunpowder, the development of weapons technology has surpassed all other forms of human endeavor, including medicine and transportation.6,7,15 Only a few cultures still depend on hunting as their primary food-gathering method. Examples are the Mbuti tribe of the Ituri Forest in Zaire, Andaman Islanders in the Bay of Bengal, and Eskimos. Many cultures, however, use hunting to supplement agriculture, plant gathering, or raising livestock. Most hunting in the United States is done for sport or pleasure, although in some areas of the country hunting and trapping are still the primary source of income for a few people.


HUNTING IN THE UNITED STATES

The total number of hunters and trappers is unknown. Some participate illegally and are not licensed. In 2003, throughout the United States, 14.7 million individuals purchased hunting licenses at a cost of $679.8 million. Although hunting seasons are regulated and relatively short, hunters spent 16 million visitor-days in the national forests. The North American Association of Hunter Safety Coordinators, a division of the New York State Office of Wildlife Management, reported 860 fatal hunting injuries in the United States during the 4-year period of 1983 to 1986, with a total of 6992 injuries from firearms.35a Interestingly, 34% of the total injuries and 89% of the handgun injuries were self-inflicted. Shotguns accounted for 106 of the fatalities and 906 of the total injuries, whereas rifles accounted for 79 fatalities and 465 injuries. The New York State Department of Environmental Conservation reported that the average number of hunting injuries decreased from an average of 137 per year in the decade of the 1960s to only 48 in 2001 and 37 in 2002.24a They credit the institution of hunter safety programs in 1960. In 2001 Colorado reported nine injuries and one death per 500,000 licensed hunters.12a Michigan reported 2 deaths per 2,665,952 hunters in 2003, making hunting one of the lowest injury and fatality rates of any recreational activity.47a The type of hunting also influences the rate of injury. Smith and colleagues reviewed 1345 hunting injuries in Pennsylvania from 1987 to 1999.38 They showed that turkey hunters had the highest rate of injury (7.5 per 100,000 hunters) and grouse hunters the lowest (1.9 per 100,000 hunters). This was attributed to turkey hunters not wearing hunter orange clothing. Deer hunters had the highest casefatality ratio at 10.3%, and pheasant hunters the lowest at 1.3%. This higher fatality rate was largely because most deer hunting injuries were due to wounds caused by rifle bullets. They also noted that younger hunters suffered the highest rate of injuries, and the largest percentage of incidents occurred on opening day. Hunting-related shootings represent a very small portion of the total number of accidental firearm deaths in the United States. Of 131 unintentional firearm deaths in California from 1977 to 1983, only eight were the result of hunting accidents.8,12,27,35,44,47 Hunting injury data may be inaccurate for a number of reasons. Many minor nonfatal injuries may go unreported, and

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most states do not differentiate accidental firearm hunting deaths from deaths that occur during any other activity. Also, automobile and all-terrain vehicle accidents that occur while hunting, or gunshot wounds inflicted while “cleaning a gun” at home, may be classified as hunting or nonhunting injuries.

Types of Injuries Encountered Most injuries to hunters are the same types of injury seen in backpackers, fishermen, and climbers. Frostbite, sprains, burns, and fractures occur with the same frequency in hunters as in others who visit wilderness areas. Prolonged extraction times may increase the risks of hypothermia, wound infection, dehydration, missed medications, and other time-dependent secondary complications. Injuries that are unique to hunters are those caused by their weapons. Most hunting is done with firearms. Shotguns and rifles are more commonly used, although handguns are increasing in popularity. Use of bows and crossbows in hunting is also rapidly increasing. Hunters using these weapons frequently are permitted an extended hunting season that does not overlap with periods for rifle and shotgun hunting. Hunters who use bows and crossbows pose far less danger to people in the hunting area at long range compared with rifles and shotguns. Bow hunting requires more skill, use of camouflage, and stealth because of the short effective ranges of arrows and bolts. These factors place bow hunters at greater risk for being mistaken for a game animal at long ranges, which is why rifle and shotgun seasons rarely run concurrently with bow-hunting activity. Other weapons are used for hunting but are less likely to be encountered. For example, spears, harpoons, and nets are used by some hunters in the Arctic, Australia, and Africa. Spear injuries from gas-powered spearguns or rubber-band powered Hawaiian slings have been associated with fatal injuries, especially when occurring in ocean or lake environments where secondary drowning or shark attack may be an additional hazard. Harpoon and fishing spearheads may separate from the shaft and, depending on the force used, may penetrate the skull or a body cavity. Slingshots are rubber-band–powered devices that use the energy in a stretched piece of rubber to hurl a projectile, often a small rock or ball bearing, at 200 to 300 feet (61 to 91 m) per second. Although this is considered a low-velocity and thus low-energy projectile, injuries to the head and face, especially the eyes, have been reported. Blowguns, while mainly used by aboriginal hunters, have become popular with some recreational hunters of birds and small game. The blowgun varies in length, and a variety of darts can be projected 20 to 50 feet (6 to 15 m) by the exhaled breath. The darts have low energy and do not penetrate very deeply. Modern blowguns rarely cause serious injury unless striking the eye or possibly a blood vessel. To effectively kill small game, the darts generally must carry an immobilizing or poisonous toxin. Darts used by some tribes contain toxins such as curare or batrachotoxin, which can be fatal to humans. Trap injuries may be included in the definition of hunting injuries. Most traps are designed to catch and hold small game. Injuries usually occur when a trapper triggers a spring-loaded trap prematurely. Crush injuries and puncture wounds to the hands are most common. Hikers occasionally tread on unmarked traps, and domestic animals such as dogs are accidentally caught in poachers’ traps. Another problem with traps occurs when an animal (wild or domestic) is caught in a trap and attacks the trapper while being released.

Figure 22-1. The wrong way to use a tree stand.This hunter is not wearing a safety harness, is drinking alcohol, and is pulling his firearm into the tree stand with the muzzle pointing upward.

Many knife lacerations occur when hunters clean game. Lack of familiarity with the process or techniques for field dressing and cleaning game is the likely cause. Failing to wear protective gloves; using the wrong type of knife; working with bloody, slippery material; and having cold hands all contribute to accidents.

Tree Stand Injuries A frequent preventable cause of serious injury and death among hunters is not associated with firearms at all. It is the tree stand injury. Tree stands are small platforms designed to hold hunters high above the ground so they can more easily spot and kill large game while remaining undetected. Whether homemade or of commercial design, the platforms generally are small, portable devices that the hunter attaches to the trunk of a tree near game trails or water holes. The stands may have attached ropes or ladders for access, or the hunter may free-climb the tree for placement of the stand or fasten small climbing steps on the tree (Figs. 22-1 and 22-2). Hunters may fall asleep on the platforms and fall off, or fall while climbing up or down trees. At least half of these injuries could be prevented if all

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Figure 22-2. A commercially produced tree stand can be used to climb the tree and obviates the need for a ladder or steps, which are the cause of many falls.

Figure 22-3. The correct way to bring a firearm or quiver into the tree stand, with the muzzle or arrowheads pointing down and the hunter wearing a safety harness at all times.

hunters wore tree stand safety harnesses (Fig. 22-3). Although most of the injuries are similar to those seen with any type of fall, occasionally a hunter drops a firearm, which discharges, or falls on an arrow or rifle, causing an additional weapons injury. Over 10 years, injuries of this type in Georgia accounted for 36% of reported hunting injuries and 20% of hunting fatalities.9 A study from the University of Rochester, New York, looked at tree-stand injuries from 1996 to 2001.34 The authors noted that 51 injuries occurred, all in men with a mean age of 42. Alcohol was present in 10% of patients and 2 of 3 deaths. Spinal fractures were the most common injury (51%), followed by extremity (41%), head (24%) and lung injuries (22%). Only two patients had been using a safety belt (4%). Sixteen spinal cord injuries were reported from 1987 to 1999 in Oklahoma; the mean height of fall was 16 feet, and 18% were related to alcohol ingestion.41 Ninety percent resulted in paraplegia/ paresis, and 12.5% were fatal.34,41,43

wooden arrows. A number of types of arrowhead are in use, such as field points and target points, but most injuries are due to specially designed hunting arrowheads called broadheads. These razor-sharp metal points come in a variety of sizes and shapes and are designed to kill game by lacerating tissue and blood vessels, causing bleeding and shock. Unlike hunting firearms projectiles, which are designed to kill quickly through massive tissue damage and rapid incapacitating hemorrhage, arrows usually kill more slowly with less tissue damage (Fig. 22-4).4,22,24 Arrows are propelled by a conventional bow, which may be straight, recurved, or compound, or by a crossbow. Crossbow projectiles may be called arrows or bolts and generally are shorter and heavier than arrows fired from a bow. The force used to propel the arrow is usually measured in draw weight, which is the number of foot-pounds necessary to draw a 28-inch (71.1 cm) arrow to its full length. The higher the pound draw, the more powerful the bow and the deeper the penetration the same type of arrow will have. Arrows have a much shorter range than bullets do, and arrows must be more accurately placed to kill the animal quickly; therefore, most shots are taken under 164 feet (50 m).

Arrow Injuries Modern arrows are usually made from aluminum, graphite, or fiberglass, although many beginners still use inexpensive

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS and colleagues estimated 21,840 injuries in 2000 from nonpowder firearms, with a 4% hospitalization rate.28 There were 39 resultant deaths between 1990 and 2000. Care must be taken not to trivialize these injuries, especially in the pediatric patient where softer, thinner bone may lead to deep penetration of even lightweight projectiles.

Figure 22-4. Types of arrows.Top, Aluminum shaft arrow with hunting broadhead.Middle (left to right), Four field points of various weights: two types of broadheads and small game blunt hunting head with spring claws to prevent arrow loss from burrowing into the ground. Bottom, Fiberglass shaft for interchangeable heads.

Because brush and tree branches can easily deflect an arrow, most shots are taken with a clear field of view. For these reasons, bow hunters rarely mistakenly shoot another hunter they presumed was a game animal. Most arrow injuries occur when hunters fire illegally at night in heavy brush and are not sure of their target. Another common injury occurs when a hunter runs after a wounded animal and falls on an arrow that was to be used for a second shot or falls out of a tree stand onto an arrow. A loaded crossbow is similar to a loaded gun. Hunters have been accidentally shot when dropping the weapon or snagging the trigger on a branch or fence. Hunting arrowheads are quite sharp; self-inflicted injuries may occur when a hunter is sharpening the blades of the broadhead or returning an arrow to the quiver.

Injuries from Firearms Nonpowder Firearms. Although the word firearms technically defines guns that fire projectiles by ignition and burning of a propellant, similar designs referred to as “nonpowder” firearms using springs, compressed air, or compressed gas cartridges are in widespread use among sportsmen and children, and will be considered as firearms in practical use. Whereas traditional firearms discharge a projectile by the contained expanding gases generated in the gun barrel by modern fast-burning powders or old-fashioned black powder, nonpowder firearms use a spring, compressed air, or a carbon dioxide cartridge to accelerate the projectile out the barrel. Although air guns are quite accurate at short distances and can develop muzzle velocities in excess of 1200 feet per second, the small lightweight projectiles cannot usually penetrate skin at distances greater than 328 feet (100 m). Nonpowder firearms are commonly used by children, who cannot legally obtain or use other types of firearms. Uninformed parents buy them as toys, erroneously believing them to be harmless by design. Without supervision and proper training in gun safety, severe injury and death can result. The wounds they cause can be lethal, especially from high-powered air rifles, which can send out pointed projectiles at sufficiently high velocities to penetrate the skull and body cavities. In a recent technical report, Laraque

Powder Firearms. In older style weapons (black powder weapons), gunpowder is loaded directly into the barrel. In modern weapons, gunpowder is contained in a cartridge. Black powder weapons use a centuries-old slow-burning propellant that is ignited with a spark from flint striking steel or a percussion cap. The firearms are usually single shot and are loaded from the muzzle by pouring a measured amount of black powder down the barrel, and then inserting the projectile and tamping it down onto the powder charge. When ignited, the propellant is converted to a gas that expands and pushes the projectile out of the barrel of the weapon. With modern design and manufacturing techniques, these weapons are sufficiently accurate to hunt large game, such as deer and elk. The injuries from black powder weapons are similar to those from modern weapons and are discussed later. The same precautions should be used when hunting with or shooting any type of firearm, whether the propellant is air or gunpowder.29,33,46 The term cartridge is used to refer to the intact, unfired assembly of projectile and propellant loaded into the gun for firing. Rifle and pistol cartridges consist of a metal case that contains the gunpowder propellant and into which the bullet is seated and held by compressing the case around the bullet base at the time of manufacture. The base of the case contains a small metal primer filled with a small amount of high explosive that serves to ignite the fast-burning propellant when it is struck by the firing pin of the gun. The primer is in the center of the base of the case (center-fire ammunition) in all cartridges except in small-caliber .22 cartridges, where it is incorporated into the entire circumference of the cartridge base rim (known as rimfire ammunition). Rifle and pistol cartridges generally contain a single bullet, although some may be loaded with very small shot to increase the probability of hitting small objects at short distances. Shotgun cartridges consist of a center-fire metal base combined with a paper or plastic shell in the form of a closedend tube. Within this tube is placed the propellant and then the projectile(s) along with associated plastic, cotton, or paper materials collectively referred to as wadding. Shotgun projectiles consist of shot ranging in size from 1 mm to 10 mm (Fig. 22-5) or a single solid projectile known as a slug. Shot pellets used to be made of lead. Because of high lead levels in ducks and geese who ingested spent shot while feeding, lead shot for bird hunting was banned in 1991. Approved shot may be made of steel, tin, or various mixtures of tin, bismuth, and up to 15% iron. Steel shot can be identified on radiographs because it retains a perfect round shape, whereas lead and tin shot deforms inside the barrel during firing, resulting in nonspherical shapes. Determining the shot type can help clinicians decide about the safety and utility of MRI scans in the setting of steel projectiles, or the risk of lead toxicity. The wadding is commonly a single plastic cup with a thickened expandable base designed to contain the shot and serve as a seal inside the barrel to contain the expanding gases behind the shot cup for maximal muzzle velocity. Slugs also have a type of wadding known as a sabot, which surrounds the slug inside the barrel of the shotgun. In all cases, the wadding is fired from

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Chapter 22: Hunting and Other Weapons Injuries

Lead shot sizes:

Pellet diameter (inches) (mm)

Figure 22-5. Standard shot size number and letter system (with corresponding metric measurements) of hunting shotgun shell projectiles. The smaller the shot size, the more pellets loaded in a single shotgun shell. Larger pellets are heavier, lose less velocity per unit of flight time, and penetrate more deeply than smaller pellets.(From Shotgunworld.com.Used with permission.)

12

.05 1.27

9

81/2

8

71/2

.080 2.30

.085 2.16

.090 2.29

.095 2.41

Buck shot sizes:

No. 4

No. 3

No. 2

Pellet diameter (inches) (mm)

.24 6.10

.25 6.35

.27 6.86

Steel shot sizes:

6

Pellet diameter (inches) (mm)

5

.11 .12 2.79 3.05

4

3

6

.110 2.79

No. 1

.30 7.62

2

.13 .14 .15 3.30 3.56 3.81

1

5

4

.120 3.05

.130 3.30

2

BB

.150 3.81

.180 4.57

No. 0

No. 00

No. 000

.32 8.13

.33 8.38

.36 9.14

Air Rifle

.16 .177 4.06 4.49

BB BBB

T

.18 .19 .20 4.57 4.83 5.08

F

.22 5.59

Note: the size of shot, whether lead or steel, is based on American Standard shot sizes. Thus, a steel No. 4 pellet and a lead No. 4 pellet are both .13 inches (3.3 mm) in diameter.

the gun and immediately peels away from the slug or shot. Wadding is commonly found inside close-range wound channels but generally is not involved in wounds at ranges more than 16 to 23 feet (5 to 7 m). Besides the wadding and projectile(s), hot gas and unburned powder also exit the muzzle. In cases of close-proximity wounds, usually under 31/2 feet (∼1 m), powder stippling may appear on clothing or skin. The presence of wadding in a wound or powder stippling may have important forensic applications and should always be noted. With contact wounds where the muzzle is pressed into the skin at the time of firing, the escaping hot gases may enter the wound channel and expand inside the victim, causing burning, organ damage, bursting of the skin, and a stellate laceration around the point of entrance. Figures 22-6 to 22-8 show examples of gunshot wounds. Hundreds of types of cartridges are available for firearms. They may be factory loaded or hand loaded, which adds the variables of propellant amount and type. Rifle and pistol cartridges are initially classified according to caliber, or diameter, of the bullet. For example, .22 caliber means the diameter of the bullet is 0.22 inch (5.6 mm); .45 caliber is 0.45 inch; and so forth. The caliber may be expressed in metric measurement; for

Figure 22-6. Gunshot wound to the face and mandible showing extensive bone and soft tissue injury. Patient was initially able to protect his airway, but later required endotracheal intubation because of edema and bleeding.

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Figure 22-7. Shotgun wound to the upper arm. Initially, the wound looked benign. Both entrance and exit can be seen.

Figure 22-9. Examples of hunting bullets. Left to right, .50 caliber black powder lead bullet, .22 caliber lead bullet, .22 caliber long rifle lead bullet, .44 magnum semijacketed hollowpoint bullet, .44 magnum shotshell, .223 caliber (5.56 mm) full metal jacket bullet, .22/250 caliber semijacketed soft point bullet,.30/30 caliber soft point flat nose bullet,.270 caliber pointed soft point bullet, and .30-06 caliber round nose soft point bullet.

Figure 22-8. Radiograph of the same shotgun wound to the upper arm as seen in Figure 22-7. Extensive bone and soft tissue injury, as well as vascular and nerve damage, can be seen.

example, a 9-mm bullet is 9 mm in diameter, which also happens to be 0.357 inch. However, bullet diameter alone is insufficient to name a cartridge, because bullet length can vary, as do cartridge length and width. The U.S. Army M-16 service rifle fires a .22 caliber bullet weighing 62 grains at 3100 feet (945 m) per second. The common .22 rimfire rifle used by generations of young shooters fires a .22-caliber bullet weighing 40 grains at 1100 feet (335.3 m) per second initial velocity. Obviously, the wounding potential of these two projectiles is vastly different. Nomenclature for a particular cartridge is made more specific by including a measurement of cartridge length, name of the inventor or inventing company, amount of powder in the case, length of the entire cartridge, or the year the cartridge was invented. For instance, the M-16 round is generally referred to as a 5.56 × 45 mm (metric), or a .223 cartridge (English system of measurement), with the third digit differentiating it from the common low power .22 rimfire cartridge. Other common hunting cartridge names illustrating these variations are .45/70 (70 grains of powder), .30-06 (adopted in 1906), and .35 Whelen (the man who developed the round).

Figure 22-10. Examples of shotgun rounds. Left to right, 12-gauge slug round, empty 12gauge plastic round, plastic 12-gauge wadding, and number six shotgun pellets.

The recent introduction of the term magnum refers more to the type and amount of powder than to the size of the bullet used. Magnum cartridges are designed to give hunters the ability to successfully hunt large game with pistols by improving terminal ballistic performance of the bullet. Figure 22-9 shows some examples of different bullets. Shotgun terminology is a little less complicated, based on the number of lead balls, the diameter of the barrel, and how many lead balls it takes to make a pound. For example, a 12-gauge shotgun has a barrel that is the same diameter as a lead ball that weighs 1/12 pound; a 20gauge, 1/20 pound. The higher the gauge number, the smaller the barrel and the smaller the projectile. The only exception is the .410 shotgun, which is caliber .410 or 0.410 inch in diameter. Figure 22-10 shows some examples of shotgun rounds and the shot and wadding within them.

Chapter 22: Hunting and Other Weapons Injuries

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TABLE 22-1. Comparison of Bullet Caliber,Weight,Velocity, and Muzzle Energy MUZZLE VELOCITY CALIBER .22 .223 .44 magnum .30/60

WEIGHT (GRAINS)

Feet/sec

M/sec

MUZZLE ENERGY (FOOT-POUNDS)

40 55 180 150

1080 3250 1600 2750

329 991 488 838

90 1280 1045 2500

The type and severity of wounds inflicted by a firearm depend on several factors. The most often quoted factor, but the least important, is the amount of energy the bullet (projectile) has when leaving the firearm. The kinetic energy formula, KE = 1 /2 MV2, can be applied to any moving object and can be used to calculate the muzzle energy for a particular type of firearm. Energy increases much more as a function of the velocity of the bullet than as a function of the mass. For this reason, most firearms are classified according to muzzle velocity. The higher the velocity of the bullet, the greater the energy and the greater the potential for injury. Firearms with muzzle velocities greater than 2500 feet (762 m) per second are considered high velocity, 1500 to 2500 feet (457–762 m) per second are medium velocity, and less than 1500 feet per second are low velocity (Table 22-1). Bullets cause damage to tissue by crushing. The energy of a bullet may be transmitted to the tissue in part or in total depending on the surface area the bullet presents to the tissue. Bullets that yaw, expand, or fragment present more surface area than do bullets that stay in one axis and maintain one shape. By international agreement codified in the articles of the Hague Convention IV of 1907, military bullets are not to be designed in a manner to produce “superfluous” wounding effects by features that would encourage the bullets to flatten or expand on impact with tissue. They are typically completely encased in a copper jacket to prevent deformation of the soft lead core. Such rounds generally pass through an individual, leaving a permanent wound tract similar in diameter to that of the bullet. The ammunition is designed to wound a soldier and put him out of combat, but not to kill him. In contrast, hunting ammunition is designed to expand on impact up to 2 or 3 times its diameter, resulting in a much larger wound channel, greater tissue damage and rapid incapacitation and death (Fig. 22-11). This feature of planned deformation also promotes retention of the bullet within the target and reduces the risk of injury to unseen individuals downrange from the game animal. In fact, many states require the use of expanding ammunition for hunting large game, and this may increase the wound severity of hunting injuries compared to military and criminal shootings. In addition to direct tissue destruction by the deforming bullet, fragmentation may occur when a bullet strikes bone and sends bone and bullet fragments in several directions. These secondary missiles cause injuries within the body similar to those from bullet fragments and may even exit the body to injure bystanders. A second injury mechanism of terminal ballistic bullet behavior is temporary cavitation, which occurs at all velocities to some degree but becomes a significant wounding mechanism factor only at high velocities. The temporary

Figure 22-11. The .30-caliber Nosler 180 g Accubond Polymer Tip bullet fired into calibrated 10% ordnance gelatin is typical of the .30 caliber hunting bullets used for .30-06,.308,.300 Win Mag, and other cartridges.This photo shows this bullet fired from a .308 rifle with an 18-inchlong barrel. Muzzle velocity was 2,499 feet (762 m) per second. Penetration depth exceeded 20 inches (51 cm).Temporary cavity maximum width was 4.7 inches (11.99 cm) at a depth between 2.8 inches (7.11 cm) and 8.7 inches (22.1 cm). Diameter of the recovered bullet at the front surface was 0.56 inches.Weight of the recovered bullet was 149.5 g; 17% of the bullet turned into fragments. Terminal performance of this type is suitable for all medium to heavy game encountered in the lower 48 U.S. states, including moose, elk, black bear, pigs, and deer. Tencent coin (dime) is shown for comparison. (Courtesy of Gary K. Roberts, DDS.)

cavity is created by radial dispersion of tissue by the bullet surface as a result of acceleration of tissue away from its path. A permanent cavity occurs when a bullet or fragment crushes tissue. In high-velocity bullet wounds, the temporary cavity may be many times larger than the permanent cavity. This wave is well tolerated by most elastic tissue, such as muscle, bowel, and lung; however, inelastic tissues, such as liver or brain, do not tolerate it and may be severely damaged by the temporary cavity.

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

Bullet motion in flight is described by rotation, yaw, and pitch. The rifle grooves cut into the inside of the barrel cause the bullet to spin around its long axis, just like a football thrown in a tight spiral. Yaw and pitch describe bullet motion left or right, or up and down relative to the long axis of the bullet. In wound ballistics, yaw is used to describe both axes of motion. A rifle bullet will usually yaw after striking any object outside the body such as a tree branch, belt, or clothing and when striking skin and other tissue within the body. Yaw can result in complete end-over-end rotation of the bullet within tissue, causing the bullet to increase the area that is crushed as the entire side profile of the bullet passes through the tissue. Bullets with round ends, for example the .45 automatic Colt pistol bullet or round musket balls, routinely do not yaw, and produce wound channels equal to their caliber or expanded caliber. Yaw causes maximum damage at 90 degrees of rotation, when the entire side profile of the bullet crushes tissue. This factor, combined with any bullet expansion, can cause the exiting bullet to produce a much larger wound than when it entered. In order to allow laboratory comparison of projectile designs and to study the effect of velocity and expansion, experimental wounding profiles have been described using ballistic gelatin, which accurately simulates human muscle tissue. These wounding profiles show the various aspects of potential ballistic injury including the cavitation, yaw, and fragmentation (Figs. 22-12 and 22-13).13 The total effect of high energy, fragmentation, expansion, yaw, and temporary cavity formation results in

tissue injury. Although the kinetic energy formula yields the total energy available to cause injury, the physical behavior of the projectile(s) and the transited tissues are the actual determinants of the complete injury pattern. The type of tissue struck is the most important factor. As can be seen from Table 22-1, the .22-caliber long rifle rimfire bullet has a low mass and velocity and thus a low muzzle energy, yet more fatalities have occurred from this round than from any other. It is very inexpensive, can be fired from a number of rifles and handguns, is commonly used to hunt game, and is not thought of as particularly dangerous by inexperienced hunters. For these reasons, more people are shot by this cartridge than any other single bullet type. The bullet is highly lethal when striking the brain, heart, or major blood vessel.1,2,16–20,32,42,45 Rubber or plastic bullets, while generally not used for hunting, may be encountered. These bullets travel at about 200 feet (61 m) per second and will not usually penetrate skin, although at short ranges (under 50 feet [15 m]) can cause fractures, eye trauma, and other blunt injuries.13 Other rare problems associated with firearms are explosions that occur within the firearm itself. These can cause burns or fragment types of injuries. When firearms are loaded with excessive amounts of powder or when the wrong powder is used in reloading bullets, the resultant detonation may cause the frame or cylinder of the firearm to explode. The burning powder or fragments of metal can cause injuries to the shooter. These injuries usually occur to the face and hands; penetrating eye injuries are also common. Obstruction of the barrel of the firearm by snow, mud, or other foreign material may cause a similar explosion.

Trap Injuries

Figure 22-12. Wound profile of a .223 rifle bullet in 10% ballistic gelatin showing the permanent and temporary cavities and the effect of tumbling and fragmentation.

Figure 22-13. The path of a test bullet through ballistic gelatin suggests the amount of tissue damage that a hunting bullet can do inside the human body, even if entrance and exit wounds are small.The data for this bullet are given with Figure 22-11.(Courtesy of Gary K.Roberts,DDS.)

Traps are designed either to kill animals or to capture them alive and uninjured. The latter type poses no risk to humans unless they should happen upon a trap and attempt to free the animal or otherwise approach the trap. The trapped animal often will bite or claw anyone within range. Leghold traps designed to kill or injure an animal may occasionally cause problems for unwary hikers or campers. These traps have a spring-loaded jaw that closes when triggered by something touching the trigger plate, usually involving only 1 to 2 pounds (1/2 to 1 kg) of pressure. Most injuries involve the foot, but any area of the body that can fit between the jaws potentially can be injured. The jaws can be released by compressing the spring controlling the jaws (Fig. 22-14). Very large traps used to trap poachers or to catch large animals, such as tigers or bears, cannot easily be released without help. These traps may also be attached to large weights, such as logs or concrete blocks, to prevent escape. Fortunately, most of these large traps are now collector’s items and not used in the field. Many injuries occur when the person setting the trap inadvertently causes the trap to spring before being set in the ground. This often causes hand and finger injuries, especially with amateur trappers unfamiliar with the type of trap (Fig. 22-15). Unconventional traps, such as snares, deadfalls, and pit traps, may rarely be encountered, but the mechanisms and types of injuries are quite variable. Trap guns are illegal in most areas of the world; injuries are similar to gunshot wounds.

Treatment of Hunting Injuries Treatment of hunting injuries involves standard principles and priorities of trauma care. Airway, breathing, circulation, bleed-

Chapter 22: Hunting and Other Weapons Injuries ing control, immobilization of the spine and fractured extremities, wound care, and stabilization of the victim for transport should be performed in an expedient manner. The victim should always be disarmed to prevent accidental injury to the rescuer or further injury to the victim. Removing the firearm or arrow from

545

the vicinity of patient care is usually sufficient, but ideally the firearm should be made safe by removal of the ammunition and opening of the firing chamber. Arrows should be placed in a quiver, or the points may be wrapped in cloth to prevent injury.

A

B

C

D

E Figure 22-14. A, A leghold trap set. B and C, A leghold trap sprung. D and E, To release a trap that has been sprung, stand on each end of the trap and compress the spring.

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

Figure 22-16. Arrow wound to the left side of the neck near the mandible. The shape of the wound resembles the blades of the broadhead as shown in Figure 22-4. Figure 22-15. Spring traps must be set carefully to avoid injury to the person setting the trap.

The management of common traumatic injuries and illnesses, such as hypothermia and mountain sickness, is no different except for one important point: always disarm the victim. A victim with a charged weapon and a head injury or change in mental status for any reason presents an immediate danger to a well-meaning rescuer. If the person attempting to offer aid to an injured hunter is not familiar with weapons, it is usually best to move the weapon several feet from the victim and point it in a direction where an accidental discharge will do the least harm.

Arrow Injuries Lacerations from razor-sharp hunting points are not unusual and can be treated like any similar laceration. The wound should be irrigated, any foreign material removed, and the laceration closed primarily. Victims pierced by an arrow should be stabilized, and the arrow should be left in place during transport, if possible. Attempts to remove the arrow by pulling it out or pushing it through the wound may cause significantly more injury and should be avoided. It is acceptable to cut off the shaft of the arrow and leave 3 or 4 inches (8 to 10 cm) protruding from the wound to make transport easier if this can be accomplished with a minimum of arrow movement. A large pair of paramedic-type shears can usually cut through an arrow shaft if it is stabilized during cutting. The portion of the arrow that remains in the wound should be fixed with gauze pads or cloth and tape. A similar approach should be used for spears and knives. The victim should be transferred as quickly as possible to an operating room, where the arrow can be removed under controlled conditions. Radiographs are helpful to identify associated anatomic structures before removal is attempted in the operating room (Fig. 22-16).

Gunshot Wounds Myths about Gunshot Wounds. Many myths associated with the management of gunshot wounds should be repudiated. Myth 1: The size or caliber of the bullet can be determined by the size of the wound. In truth, the skin is quite elastic and has high tensile strength. Although a knife or arrow can cut the skin, a blunt bullet must crush the tissue by stretching. This

stretching occurs until the bullet passes through and then retracts, causing the wound in the skin to be smaller than the caliber of the bullet. Myth 2: The size of the wound determines whether it is an exit or entrance wound. Actually, the bullet usually tumbles or yaws after striking the skin and soft tissue; if the bullet exits while still tumbling, the exit wound may be larger than the entrance. This commonly occurs when a missile strikes an arm or leg where the bullet is in mid-tumble at 90 degrees when exiting. Often the bullet fragments, and only a small portion of the bullet exits, making the exit wound much smaller than the entrance. In addition, pieces of bone or tooth may exit, causing an odd-size wound. Myth 3: The path of the bullet can be determined by connecting the entrance and exit wounds. This myth may lead to inappropriate intervention in gunshot wounds. A case example: A gunshot-wound victim had two wounds about 6 inches (15 cm) apart on his upper thigh, and they were initially thought to be an entrance and exit wound. The patient developed abdominal pain, and on chest x-ray it was noted that there were two bullets in the left chest. Subsequent surgical intervention revealed injury to the colon, spleen, bowel, stomach, diaphragm, lung, and subclavian vessels. So what appeared to be entrance and exit wounds were actually two gunshot wounds sustained while the patient was lying supine. The outcome of most gunshot and blast wounds depends primarily on the body part that has been injured, and secondarily on the environment in which the injury occurred and the quality and timeliness of medical intervention. While knowing the type of weapon and the physics of ballistics and blast can help predict the extent of physical damage, there is no substitute for attention to detail when examining the patient.

Emergency Department Care. Emergency department care of the gunshot wound includes securing the airway, placing two intravenous lines in unaffected extremities, performing cardiac monitoring, and providing oxygen therapy. The patient with a neck wound and expanding hematoma should be endotracheally intubated as soon as possible. If endotracheal intubation is not possible, a needle cricothyrotomy followed by a tube

Chapter 22: Hunting and Other Weapons Injuries cricothyrotomy should be performed. Relief of tension pneumothorax with a needle or tube thoracostomy or occlusion of a sucking chest wound should be done immediately. Any external bleeding should be controlled by direct pressure. In a wilderness situation, a tourniquet may be the best means of controlling significant bleeding in a manner that is less labor intensive. A radiograph should be obtained of the involved area, and where there is a presumed entrance wound without an exit wound, multiple x-ray studies may be needed to find the location of the bullet. On rare occasion, bullets have been observed to embolize from the chest area via the aorta to the lower extremity arteries or to the heart via the vena cava. A type and crossmatch and basic trauma laboratory tests should be performed. Tetanus toxoid and immunoglobulin should be administered as indicated by the victim’s history. Broad-spectrum antibiotics should be administered to cover the wide range of pathogens associated with gunshot wounds, especially with complex wounds to the abdomen and extremities. The bacteriology of gunshot and blast injury wounds is quite complex. There are a number of environmental pathogens, including soil and water bacteria, such as Clostridium, Aeromonas, Staphylococcus, Streptococcus, Bacteroides, and Bacillus. These bacteria and associated bacteria on the victim’s clothing and skin account for the majority of infections in soft tissue. Wounds penetrating the abdomen increase the presence of Pseudomonas, Proteus, E. coli, and other coliforms. Systemic antibiotics should be started as soon as possible and continued for at least 24 hours. Although there is no specific antibiotic that will cover all organisms, selection of antibiotic should be on the basis of probable type of infection. Cellulitis and necrotizing soft-tissue infections can be treated with ceftriaxone plus metronidazole plus gentamicin. Intra-abdominal infections can be treated with the same regimen or cefotetan, and ampicillin– sulbactam can be substituted for ceftriaxone, clindamycin for metronidazole, and ciprofloxacin for gentamicin. There is no substitute for drainage of abscesses and empyemas, excision of devitalized tissue, and removal of foreign debris. Topical antibiotics have not been shown to be useful. Surgical debridement and systemic antibiotics are the mainstay of prevention and treatment of wound infection. Victims in shock should be taken to the operating room immediately to control bleeding. If this is not possible, type Onegative or type-specific blood should be transfused. Autotransfusion, when available, can be an ideal way to replace lost blood in the victim in shock. Starch or other blood substitutes may raise the blood pressure temporarily, but large amounts of crystalloid fluids may cause increased bleeding. Hypotensive resuscitation, which allows the patient to remain relatively hypotensive as long as organ perfusion is adequate, may be the best intervention if an operating room is not readily available. A systolic blood pressure of 80 mmHg may not be “normal,” but it may be sufficient for a supine patient. Increasing the blood pressure to 110 mmHg may seem “normal,” but it may also cause rebleeding and irreversible shock. Military antishock trousers or pneumatic antishock garments have not been shown to be beneficial in the treatment of shock secondary to penetrating trauma.5a Emergency thoracotomy is indicated for victims who have lost vital signs shortly before reaching the emergency department or while in the emergency department. Injuries to the heart or great vessels can be occluded with Foley catheter balloons, pericardial tamponade can be relieved, and the aorta can be cross-clamped. Hypothermia is commonly

547

unrecognized in the trauma victim and may lead to coagulopathy, cardiac arrhythmias, or electrolyte disturbances. Rectal temperatures should be obtained and only warmed fluids and blood given to the victim.13 Wounds from high-velocity bullets are similar to other types of wounds, and standard rules of debridement should be followed. Wide debridement of normal-appearing tissue is unnecessary and should not be done. In general, victims of gunshot wounds should be evacuated quickly and stabilized if possible. Most victims (80%) of gunshot wounds to the chest who survive the first 30 minutes can be treated with a thoracostomy tube and observation.26a The amount of blood that is drained from the thoracostomy tube determines whether operative intervention is necessary. Draining > 1500 mL of blood immediately or > 200 mL/hour for over 4 hours is an indication for thoracotomy. Signs of pericardial tamponade are an indication for immediate pericardiocentesis and operative repair. All gunshot wounds to the abdomen should be explored in the operating room. These include all penetrating injuries below the nipples and above the symphysis pubis. Radiographs should be used to identify bullets, bullet fragments, and bony injuries. Extremity wounds can be treated conservatively unless signs of vascular injury are present. Signs of arterial injury include pulsatile bleeding, expanding hematoma, absent pulses, presence of a thrill or bruit, or an ischemic limb. Experience in combat has shown that vascular injuries do best when identified and treated immediately. However, life takes priority over limb, and a tourniquet may be needed to control vascular bleeding that may ultimately lead to loss of the limb. Obviously, major bony injuries and nerve injuries eventually need operative therapy, but immediate intervention is rarely necessary. Most important, the underlying injury cannot be determined by examination of the external wound. Vascular injuries may not be identified during the initial examination; therefore noninvasive, portable, Doppler ultrasound studies can be extremely valuable in the emergency department. Contrast angiography should be performed on any victim with a suspected vascular injury. The removal of the bullet or bullet fragment is not necessary unless the bullet is intravascular, intra-articular, or in contact with nervous tissue, such as the spinal cord or a peripheral nerve. Bullets found during exploratory laparotomy or wound debridement should be removed, but it is unnecessary to explore soft tissue, such as muscle or fat, solely to remove a bullet. Shotgun pellets that have minimal penetration can be removed from the skin with a forceps. Often plastic or cloth wadding is found in superficial shotgun wounds and should be removed. Shotgun blasts may produce large soft tissue defects that need extensive debridement and either skin grafting or surgical flap rotation to maximize coverage. Patients with powder burns should have as much of the powder residue removed as possible with a brush under local anesthesia. The powder will tattoo the skin if it is not removed, and the deep burns may need dermabrasion or surgical debridement (Fig. 22-17).17,32,45 Retained lead bullets and shotgun pellets for the most part are not hazardous; however, when they are within joint spaces or the gastrointestinal tract, significant amounts of lead can be absorbed and toxicity can occur.40

Prevention of Hunting Injuries Most state fish and wildlife agencies have recognized that hunters are at risk for injuries and have tried to develop pro-

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A

B Figure 22-17. A, Close-range 12-gauge shotgun wound to the right side of the upper chest. The large central wound was caused by the plastic wadding, and the pellets have struck at an angle toward the shoulder.The patient was turning to the right when shot.The external appearance of the wound indicates a massive injury to the chest.B, Chest radiograph of the patient in A. No pellets have penetrated the chest, and there was no pneumothorax, pulmonary contusion,or vascular injury.The injury was totally superficial,and the patient was admitted for observation and local wound care.

grams to minimize morbidity and mortality. National organizations such as the Boy Scouts of America and the National Rifle Association have been teaching firearm and hunting safety for decades. The Hunter Education Association and the North American Association of Hunter Safety Coordinators (NAAHSC) have attempted to identify high-risk groups and situations by collecting data on both fatal and nonfatal huntingrelated injuries. NAAHSC-approved Hunter Safety Programs are available in every state, and all states except Alaska, Massachusetts, and South Carolina require the course before issuing a license to hunt. These courses are roughly 12 hours long and cover hunter responsibility, firearms and ammunition, bow hunting, personal safety, game care, and wildlife identification. They stress respect for the wilderness and a rational approach to game management. All hunters, potential hunters, and

Figure 22-18. Hunter wearing bright orange clothing, which is essential to distinguish a human from the background and avoid an accidental shooting.Many accidental shootings have occurred when one hunter’s movement was mistaken by another hunter for the movement of an animal.

persons going into hunting areas should take one of these courses. Approximately 650,000 hunters complete a hunter safety course annually. Since the first course given in Kentucky in 1946, more than 18 million hunters have been certified. Most injuries could probably be prevented by following a few simple rules. Nonhunters should be aware of hunting seasons and designated hunting areas and wear international orange clothing while in hunting areas (Fig. 22-18). Hunters should always be sure of their target before shooting, use safety harnesses in tree stands, and use appropriate technique and tools for cleaning game. Tree stands should be well constructed. Hunters should never consume alcohol or mind-altering drugs that might interfere with their judgment. Eye protection in the form of safety glasses should be worn while hunting or target shooting to prevent injuries from ricocheting fragments and shotgun pellets. High-frequency hearing loss is common in hunters because of the loud report of the firearm. Although earplugs and headsets can protect the hunter, they are impractical for most hunting and are used mainly for target shooting. Some hunters use a single ear plug for the ear closest to the muzzle of the firearm. This protects the ear most likely to be injured but still allows the hunter to hear approaching game

Chapter 22: Hunting and Other Weapons Injuries

549

and other hunters. Bow hunters should always use wrist and finger protection to prevent injuries from the arrow fletching and the bowstring. All arrows should be carried in a quiver until ready for use. The broadhead arrow should always be pointed away from the hunter. These few steps would probably eliminate most hunting injuries.36,37


FISHING INJURIES Sport fishing is associated with a large number of relatively minor injuries compared with hunting. The usual problems associated with outdoor recreation are common among fishermen: sunburn, frostbite, hypothermia, near drowning, sprains, fractures, motion sickness, and heat illness. Lacerations are relatively more common because of the use of knives to cut bait and fishing lines and to clean fish. These lacerations are often contaminated with a variety of marine and freshwater pathogens that may increase the incidence of wound infection. Thorough debridement of the wound and copious irrigation with sterile saline solution are the best initial methods to prevent infection.

Fishhook Injuries Fishhooks are designed to penetrate the skin of fish easily and to hold fast while the fish is played and landed. To perform this dual role, they are extremely sharp at the tip, have a barb just proximal to the tip, and are curved so that the more force applied to the hook, the deeper it penetrates. Fishhooks may be single or in clusters of two, three, or four to increase the chance of catching the fish. Some state fishing laws limit the number of hooks allowed on a single line when fishing for certain game fish to make it more sporting. Unfortunately, the greater the number of hooks on a lure or line means an increased chance of catching a fisherman. The most common fishhook punctures occur when fish are removed from hooks. The combination of sharp hooks, slippery fish, and an inexperienced fisherman leads to puncture wounds or embedded fishhooks. Many fishermen use commercial fishhook removers or large Kelly forceps to remove hooks. Some fishing guides simply cut the hook with a side-cutting pliers; they believe the remaining segment of hook will eventually oxidize in the victim and disintegrate. Often, fishhooks are stepped on with a bare foot or fishermen catch themselves or another person on the backcast. Fishhooks can penetrate skin, muscle, and bone, and they may pierce the eye or the penis. Care must be taken in removing a fishhook so that further damage to underlying structures is avoided. The first step is to remove the portion of the hook that is embedded from any attached lines, fish, bait, or lure. This is best done with a sharp side-cutting pliers. A bolt cutter may be needed for large, hardened hooks. A number of techniques are used for removing embedded fishhooks, but all involve a certain amount of movement of the hook, which causes increased pain. A local anesthetic should be infiltrated around the puncture site to minimize pain and movement of the patient. The following method can be used if the hook is not deeply embedded (Fig. 22-19E). Pressure is applied along the curve of the hook while the hook is pulled away from the point. Because the barb is on the inside of the curve of the hook, this enlarges the entrance hole enough to allow the barb and point to pass through. Sometimes a string looped through the curve of the hook facilitates the process. If the hook is deeply

A

B

D

C

E

Figure 22-19. A to D, Removal of a fishhook that has deeply penetrated a fingertip. E,“Pressand-yank” method of fishhook removal.

embedded, pressure can be applied along the curve of the hook until the point and barb penetrate the skin at another place, and then the barb can be cut off and the remainder of the hook backed out (Fig. 22-19A–D). Fishhooks embedded in the eye should be left in place, the eye covered with a metal patch or cup, and the victim referred to an ophthalmologist for further care. Rarely, hooks become embedded in bone or cartilage; this victim must be taken to the operating room to have the hook removed via a surgical incision.

Fishing Spear Injuries Fishing spears, like fishhooks, are designed to penetrate and hold fish. They may be jabbed, thrown, or propelled by rubber straps or carbon dioxide cartridges. The more force used to propel the spear, the deeper the penetration into tissue. Although arrows are designed to cause bleeding and bullets to cause crushing, fishing spears are designed to hold the fish until it drowns or is otherwise dispatched. Spears may penetrate the human chest or abdominal cavity, skull, or any other anatomic area. Some bleeding may occur, especially if major blood vessels are struck. The victim should be removed from the water as soon as possible and immediate attention given to airway, breathing, and bleeding control. The spear should be stabilized in place, and the victim immediately transported to a medical facility. Penetrating neck and chest injuries may require endotracheal intubation and tube thoracostomy. If a spear is embedded in the victim’s cheek and interferes with the his or her airway, cutting the spear off with a bolt cutter and removing it through the mouth is permitted. Spears in all other locations should be left in place, although they may be cut off to facilitate transportation or improve the victim’s comfort (Fig. 22-20).


UNEXPLODED ORDNANCE There are many areas in the world where unexploded ordnance can be found. Types of ordnance may include aerial bombs, rockets, artillery and mortar shells, grenades, and mines. Any area of the planet where a war has been fought within the past century or so has potential for harboring these items. Crews excavating streets in urban areas of England, France, and Germany often uncover unexploded ordnance from World War

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

Main charge

Fire assembly adapter plug

Soft metal plate

Wire

Striker Retaining wall Detonator Detonator adapter plug

Delay-arming mechanism

A Figure 22-21. An example of an antipersonnel mine manufactured by the Soviet Union.

B Figure 22-20. A, Male patient with a multipronged fishing spear through the foot.He said he saw something move and he speared it. B, Same patient with the spear being cut off in the emergency department with a bolt cutter.The patient was taken to the operating room to have the remainder of the spear removed.

I or World War II. Many areas of the United States that have been used for bombing or artillery ranges are adjacent to wilderness regions and, although they are usually well marked as impact areas, still pose a risk for the unwary traveler. Many areas of the shallow ocean accessible to scuba divers have sunken munitions transports and warships that contain massive amounts of unexploded bombs, shells, and torpedoes. Another problem that has arisen is the use of mines and booby traps to protect marijuana and opium fields and illegal drug laboratories throughout the world. Currently, unexploded land mines represent a significant health problem in Southeast Asia, the Balkans, Central America,

Egypt, Iran, and Afghanistan. The International Red Cross estimates that someone is killed or injured by a land mine every 22 minutes. The average number of mines deployed per square mile in Bosnia is 152, in Iran 142, in Croatia 92, and in Egypt 59. There are a total of 23 million mines in Egypt alone.39 Land mines may be commercially manufactured or produced locally from available materials (Fig. 22-21). Commercial land mines currently produced in United States have a limited active life and self-destruct after their active life has expired. Unfortunately, this is not true of older types of mines or mines produced by other countries. Locally produced mines have no standard size, shape, or detonation pattern and may be very difficult to detect and defuse. These types of land mines are used extensively in El Salvador, Malaysia, and Guatemala. Land mines have two primary functions, the first of which is to cause casualties, the so-called antipersonnel mines. These may be blast or fragmentation type. The fragmentation type may be either directional or nondirectional (Fig. 22-22). Antipersonnel mines may cause lethal or nonlethal injuries in several persons. Wounded soldiers require more care than killed soldiers do, and the tactical effect may be the same. The second primary function is to destroy vehicles, such as tanks, so these mines are usually much larger. All mines have three basic components: (1) a triggering device, (2) a detonator, and (3) a main explosive charge. The triggering device differs depending on the type of mine. Blast mines usually involve a pressure-type trigger and occasionally are command detonated, especially for antitank purposes. Many antitank mines will not explode unless a pressure of 300 to 400 pounds (136 to 181 kg) is applied. The M14 blast antipersonnel mine needs only 20 to 30 pounds (9 to 14 kg) of pressure to trigger the detonation. Fragmentation mines are usually triggered by trip wires or similar “touch” devices. The M18A1 fragmentation mine, or “claymore” mine, is designed to be command detonated by an electronic trigger. Booby traps other than land mines may be mechanical, chemical, or explosive. During the Vietnam War, venomous snakes

Chapter 22: Hunting and Other Weapons Injuries

Figure 22-22. Above, A directional type mine used against unarmored vehicles or personnel. Below, An improvised mine, or booby trap, manufactured from a hand grenade and materials at hand.

were used, as well as the notorious sharpened bamboo spikes known as “punji” traps. The distribution of mines usually entails spreading them on the surface of the ground; by air along roads, railways, and defensive positions; or hiding them by burying or camouflage along trails or suspected routes of approach. Injuries from land mines depend on several factors: type of mine (blast vs. fragmentation), position on the ground, method of detonation, whether it explodes above the ground, position of the victim, environment, and type of soil. Four general patterns of injuries occur with land mines. Pattern A injuries occur with small blast mines, such as the U.S. M14 and the Chinese Type 72. These injuries usually involve only the leg below the knee. Complete or partial foot amputations are most common, and trunk or head injuries are rare. Pattern B injuries are caused by larger blast mines, such as the Russian PMN. These mines contain 4 to 6 times as much high explosive material, and the cone of explosion is much larger. The injuries seen with this type of land mine usually involve massive soft tissue injuries to both legs below and above the knee and commonly the pelvis, abdomen, and chest. Pattern C injuries are generally caused by Russian PFM-1, or “butterfly,” mines. These mines are usually distributed by air, and the wings are designed to help spread the mines. They are triggered by pressure applied to the wings; handling the mine commonly does this. Most of the injuries involve amputation of the hand at the wrist, but often the head, neck, and chest are injured also. Unfortunately, the loss of one or both eyes is not uncommon with this mine. Pattern D injuries are caused by fragmentation mines. These may be bounding mines, such as the U.S. M16 or the Russian OZM, or directional mines, such as the U.S. M18A1 or the Russian MON. They are

551

designed to spread metallic fragments over a wide area at the height of a person’s waist. The fragments lose their energy much faster than a bullet projectile but at close range can be devastating. The lethal range is usually 82 to 164 feet (25 to 50 m), with casualties occurring out to 656 feet (200 m). The injuries are quite similar to gunshot wounds and are often multiple. Large, unexploded artillery shells or bombs may cause a combination of blast and fragment injuries but on a larger scale, sometimes involving scores of victims. Many military and civilian casualties are caused by improvised explosive devices (IEDs), which may be conventional explosives; improvised from fertilizer, propane, or other unconventional explosives; artillery, mortar or other ordnance; or explosive charges removed from said ordinance. The IEDs are commonly used by terrorist groups, which may detonate the devices either by timing mechanisms or by command, sometimes in suicidal attacks. These devices are usually detonated in crowded areas or near important political or military targets to create the greatest impact. Examples are attacks on the Oklahoma City Federal Building, the Beirut Marine barracks, and multiple incidents in Iraq. The treatment of these injuries can be very complex and involve vascular, orthopedic, soft tissue, abdominal, and craniofacial procedures. The wounds are usually highly contaminated with soil, clothing, and fragments that may be driven deep into tissue proximal to the obvious injuries.48 In most of these injuries, massive debridement is necessary. Rarely, unexploded ordnance may be imbedded in soft tissues and body cavities and must be removed in the operating room, possibly endangering the lives of medical personnel. Most victims who survive never completely regain normal function, especially if the initial treatment was delayed or inadequate. Postsurgical infection of mine injuries is common and greatly increases morbidity and mortality. Initial treatment involves airway control, treating tension pneumothorax, and controlling hemorrhage. Tourniquets are often necessary to control the bleeding from amputated limbs. Splinting the injured extremity and covering the wound to prevent further contamination is necessary. Initial debridement must be done carefully; removal of fragments may cause bleeding to recur. Penetrating injuries of the pelvis and abdomen usually require laparotomy, and soft tissue injuries may require multiple reconstructive procedures. Broad-spectrum antibiotics and tetanus prophylaxis are appropriate in all cases, and fluid resuscitation is usually indicated with extremity injuries. Blast injuries without fragmentation may cause tympanic membrane rupture, blast lung resulting from alveolar rupture, and intestinal rupture, although the latter is more common with underwater mine explosions. The mechanism is production of an overpressure wave that travels through tissue of various densities and causes tear injuries at membrane interfaces. These injuries must be suspected in any victim involved in a blast, whether from a land mine or other explosive device. Scuba divers and swimmers who are involved in underwater explosions may have more serious injuries because of the increased speed of sound in a liquid medium. This can cause more severe tearing of membranes at the fluid–air interface and additional trauma secondary to a “water hammer” effect and spalling. The position of the victim and the number of shock waves caused by reflection of the blast wave off of walls and ground may increase the amount of damage. Victims in contact with solid objects, such as the hull of a ship or vehicle, may have increased injuries because of increased velocity of the blast wave through solids. Burns and translational injuries, whereby

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the victim is thrown by the blast and has injuries similar to a fall or motor vehicle crash, also occur. Generally speaking, the closer the victim is to the blast, the greater the injury. The tympanic membrane will rupture at overpressures of 5 psi. This causes acute hearing loss, pain, and tinnitus. Blast lung is caused by the overpressure wave passing through the chest wall and may involve one or both lungs. Chest pain, dyspnea, and hemoptysis may present immediately or be delayed up to 48 hours. Chest x-ray may show patchy or diffuse infiltrates, pneumothorax, subcutaneous air, and hemothorax. Implosion of air into the vascular system may cause air embolism and sudden death. Abdominal injuries in air blast are uncommon but in water blast may present as abdominal pain, nausea, vomiting, and tenesmus. Sigmoid and transverse colon

23

injuries are most often seen, followed by small bowel and solid organ (such as liver and spleen) injuries from the water hammer effect. Abdominal injuries may have a delayed (up to several days) presentation. The key to therapy is to be suspicious of occult injuries in any victim of a blast, whatever the cause. Most injuries will present within the first hour; however, because injuries may be delayed in presentation, observation and close follow-up are critical. Treatment is generally supportive for ear and lung injuries and operative for abdominal injuries.3,5,10,11,14,21,23,25,26,30,31

The references for this chapter can be found on the accompanying DVD-ROM.

Tactical Medicine and Combat Casualty Care Lawrence E. Heiskell, Bohdan T. Olesnicky, and Lynn E. Welling

Tactical medicine can be defined as both emergent and nonemergent care provided to victims of illness or injury related to law enforcement or military operations, often in a hostile environment.56 Tactical medicine in the early years was often referred to as tactical emergency medical support (TEMS). The emergency medical services (EMS) and prehospital community called it tactical EMS, and the U.S. military coined the phrase combat casualty care. Numerous law enforcement agencies now have tactical medical teams composed of on-call physicians and prehospital care providers. Because many law enforcement agencies and branches of the U.S. military have embraced this concept, it is now commonly known as tactical medicine. Prior to 2001, there was a perception of professional separation between doctors in traditional medical practice and the tactical medicine physicians involved in law enforcement. This was probably related to what might be seen as competing priorities for physicians when dealing with sick or injured patients who are suspects in a police investigation. No other subspecialty in emergency medicine has experienced the growth rate of tactical medicine. In the past 15 years, more than 170 publications addressing tactical medicine issues have been written. Tactical medicine educational programs have trained thousands of emergency medical technicians (EMTs), paramedics, and physicians, who have responded to the call to provide on-scene emergency medical care to members of the law enforcement community or active duty military.51 Tactical medicine is very similar for both military and civilian tactical providers. Techniques, strategies, protocols, and equipment are

all virtually identical, with few differences. The military tactical medical provider must deal with long deployment times, therefore incurring a significant preventative medicine requirement. Although routine medical care and performance enhancement (e.g., conditioning, nutrition, rest) are important for both civilian and military tactical teams, they take on a longer-term function for the military tactical medicine provider. A civilian tactical operation typically takes hours to days. (The Waco and Ruby Ridge incidents were exceptions, more in concert with a military length of engagement). A typical tactical military operation may take days to months, and other aspects—disease and nonbattle injury—become as important as the tactical medical care (Table 23-1). Tactical medicine has been a mainstay of military operations since the beginning of modern warfare. The hospital corpsman, or combat medic, was deployed on the front lines with the warriors to provide basic medical care. This care was provided under fire, sometimes in the harsh environments of the jungle, the desert, high mountains, and underwater. As the science of medicine improved, the need to move higher levels of care further toward the forward edge of the battle area was recognized. Shock trauma platoons, manned by emergency physicians and support staff, were sent to the front lines to provide advanced resuscitative support. These units could be fully operational and seeing patients in less than 30 minutes. Mobile surgical teams and forward resuscitative surgical teams developed the technology to put trauma surgical teams within minutes of the location of a combat casualty. These teams are fully mobile

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

the victim is thrown by the blast and has injuries similar to a fall or motor vehicle crash, also occur. Generally speaking, the closer the victim is to the blast, the greater the injury. The tympanic membrane will rupture at overpressures of 5 psi. This causes acute hearing loss, pain, and tinnitus. Blast lung is caused by the overpressure wave passing through the chest wall and may involve one or both lungs. Chest pain, dyspnea, and hemoptysis may present immediately or be delayed up to 48 hours. Chest x-ray may show patchy or diffuse infiltrates, pneumothorax, subcutaneous air, and hemothorax. Implosion of air into the vascular system may cause air embolism and sudden death. Abdominal injuries in air blast are uncommon but in water blast may present as abdominal pain, nausea, vomiting, and tenesmus. Sigmoid and transverse colon

23

injuries are most often seen, followed by small bowel and solid organ (such as liver and spleen) injuries from the water hammer effect. Abdominal injuries may have a delayed (up to several days) presentation. The key to therapy is to be suspicious of occult injuries in any victim of a blast, whatever the cause. Most injuries will present within the first hour; however, because injuries may be delayed in presentation, observation and close follow-up are critical. Treatment is generally supportive for ear and lung injuries and operative for abdominal injuries.3,5,10,11,14,21,23,25,26,30,31

The references for this chapter can be found on the accompanying DVD-ROM.

Tactical Medicine and Combat Casualty Care Lawrence E. Heiskell, Bohdan T. Olesnicky, and Lynn E. Welling

Tactical medicine can be defined as both emergent and nonemergent care provided to victims of illness or injury related to law enforcement or military operations, often in a hostile environment.56 Tactical medicine in the early years was often referred to as tactical emergency medical support (TEMS). The emergency medical services (EMS) and prehospital community called it tactical EMS, and the U.S. military coined the phrase combat casualty care. Numerous law enforcement agencies now have tactical medical teams composed of on-call physicians and prehospital care providers. Because many law enforcement agencies and branches of the U.S. military have embraced this concept, it is now commonly known as tactical medicine. Prior to 2001, there was a perception of professional separation between doctors in traditional medical practice and the tactical medicine physicians involved in law enforcement. This was probably related to what might be seen as competing priorities for physicians when dealing with sick or injured patients who are suspects in a police investigation. No other subspecialty in emergency medicine has experienced the growth rate of tactical medicine. In the past 15 years, more than 170 publications addressing tactical medicine issues have been written. Tactical medicine educational programs have trained thousands of emergency medical technicians (EMTs), paramedics, and physicians, who have responded to the call to provide on-scene emergency medical care to members of the law enforcement community or active duty military.51 Tactical medicine is very similar for both military and civilian tactical providers. Techniques, strategies, protocols, and equipment are

all virtually identical, with few differences. The military tactical medical provider must deal with long deployment times, therefore incurring a significant preventative medicine requirement. Although routine medical care and performance enhancement (e.g., conditioning, nutrition, rest) are important for both civilian and military tactical teams, they take on a longer-term function for the military tactical medicine provider. A civilian tactical operation typically takes hours to days. (The Waco and Ruby Ridge incidents were exceptions, more in concert with a military length of engagement). A typical tactical military operation may take days to months, and other aspects—disease and nonbattle injury—become as important as the tactical medical care (Table 23-1). Tactical medicine has been a mainstay of military operations since the beginning of modern warfare. The hospital corpsman, or combat medic, was deployed on the front lines with the warriors to provide basic medical care. This care was provided under fire, sometimes in the harsh environments of the jungle, the desert, high mountains, and underwater. As the science of medicine improved, the need to move higher levels of care further toward the forward edge of the battle area was recognized. Shock trauma platoons, manned by emergency physicians and support staff, were sent to the front lines to provide advanced resuscitative support. These units could be fully operational and seeing patients in less than 30 minutes. Mobile surgical teams and forward resuscitative surgical teams developed the technology to put trauma surgical teams within minutes of the location of a combat casualty. These teams are fully mobile

Chapter 23: Tactical Medicine and Combat Casualty Care

Figure 23-1. Forward resuscitative surgical team. (Courtesy Lynn Welling, MD.)

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Figure 23-2. Patient transport. (Courtesy Lynn Welling, MD.)

TABLE 23-1. Nonbattle Conditions Encountered by Tactical Medical Personnel (Spring 2003)* PRIMARY ICD-9 DISEASE CATEGORY Digestive Symptoms ill defined Mental disorders Musculoskeletal Genitourinary Nervous system sense organs Skin Supplemental Infectious and parasitic Circulatory Endocrine, nutritional Neoplasms Respiratory Pregnancy Congenital Total

n

% OF TOTAL

44 38 29 29 21 17 15 15 10 10 8 6 5 3 3 253

17.4 15.0 11.5 11.5 8.3 6.7 5.9 5.9 4.0 4.0 3.2 2.4 2.0 1.2 1.2 100.0

*Navy/Marines Operation Iraqi Freedom from 21 March to 15 May 2003. ICD, International Classification of Diseases.

Figure 23-3. A high-velocity gunshot wound. (Courtesy Lawrence E. Heiskell, MD.)

and are able to set up or dismantle in 30 minutes, utilize tent shelters or shelters of opportunity within which to perform operations, and provide life-saving damage control surgery to multiple patients under the extreme conditions of modern warfare (Fig. 23-1). Systems are designed so that staff can resuscitate, treat, and transport patients in extreme hot or cold temperatures, over rough terrain and hostile territory, while the patient is paralyzed and intubated, while wounds are still open, and while attempts are made to prevent the hypothermia, dehydration, and coagulopathy inherent in postsurgical patients (Fig. 23-2). Tactical medicine has advanced to anticipate and react to changes in combat strategy. In Operation Iraqi Freedom, the initial injury patterns were primarily high-velocity penetrating wounds—that is, mostly gunshot wounds (Fig. 23-3 and Table

23-2).30 As the war has progressed, the weapon of choice of the insurgents has become the improvised explosive device (IED) (Fig. 23-4).79 This weapon produces significantly more trauma, including shrapnel, blast, and thermal injuries. It has also required a change in protective body armor as the injury patterns have changed to include more devastating extremity and head-and-neck wounds than torso wounds (Fig. 23-5).29 The IED has also continued to cause problems with torso injuries, as the blast patterns cause shrapnel to angle up under traditional body armor and through arm openings. This has promoted development of armor that helps better protect these areas. The terrorist attacks of September 11, 2001, and events such as the 1999 Columbine High School shootings heightened our nation’s awareness of the real threats of terrorism and violence

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on U.S. soil and diminished some of the resistance to medical providers being actively and closely involved in law enforcement special operations.80 Today, hundreds of fire and EMS agencies provide tactical emergency medical support to federal, state, and local law enforcement special operations teams.

Law enforcement special operations, often referred to as SWAT (special weapons and tactics) teams, are intended to deal with a wide range of high-risk criminal problems and threats.69 These include, but are not limited to, hostage rescues, terrorist acts, barricaded suspects, violent and suicidal suspects, takeover bank robberies, high-risk warrant services, and active shooter situations.18,43,45 Patient advocacy, with priorities of ensuring the best possible quality of care and patient confidentiality, can be at cross purposes with a police officer trying to gather important facts in

TABLE 23-2. Battle Conditions Encountered by Tactical Medical Personnel (Spring 2003)* MECHANISM OF INJURY

n

% OF TOTAL

Gunshot wound Shrapnel/fragmentation RPG (handheld antitank grenadelauncher)/grenade Motor vehicle accident Fall Explosion Unknown/not recorded Landmine Blast Mechanical/machinery Other Multiple (NOS [not otherwise specified]) Blunt Debris Total

76 65 39

24.1 20.6 12.4

28 17 16 16 14 11 13 10 4

8.9 5.4 5.1 5.1 4.4 3.5 4.1 3.2 1.3

3 3 315

1.0 1.0 100.0

*Navy/Marines Operation Iraqi Freedom from 21 March to 15 May 2003; wounded in action.

Figure 23-4. An example of an improvised explosive device (IED):a hand grenade wired to the undercarriage of a vehicle. (Courtesy Lawrence E. Heiskell, MD.)

Figure 23-5. Anatomic location of injury (wounded in action [WIA] only). (Courtesy Naval Health Research Center.)

Chapter 23: Tactical Medicine and Combat Casualty Care an investigation to ensure public safety and justice. Tactical medicine must respect both patient rights and mission goals. SWAT teams are found in most midsize and larger law enforcement departments. In some areas, a number of small departments have banded together to form multi-jurisdictional or regional SWAT teams.16 Harsh environmental conditions, including what many regard as wilderness, will increasingly provide a backdrop for incidents requiring tactical efforts.


HISTORY OF COMBAT CASUALTY CARE

Much of the training and tactics of civilian SWAT teams are based on the experience of military special operations teams. Such military teams have their origins in the U.S. Office of Strategic Services and the British Special Air Service during World War II (WWII). Some of the earliest military special operations teams incorporated tactical medical components. German Fallschirmjäger (paratroopers) incorporated a wellorganized medical support team with physicians. Dr. Heinrich Neumann jumped with the unit during the invasion of the island of Crete in 1942.37 During the Normandy Invasion of June 6, 1944, at Pegasus Bridge on the Orne River, the British, led by Major R. J. Howard, landed with medical support accompanied by a physician, Captain J. Vaughan of the Royal Army Medical Corps.2 The U.S. Armed Forces during WWII also incorporated physicians in their assault on fortressed Europe. Dr. Robert Franco and Dr. Daniel B. McIlvoy both parachuted into Sicily with the 82nd Airborne Division in April 1943 and jumped into Normandy in June 1944.26 During the 1950s, the Army Special Forces (77th Special Forces Group) was formed. As U.S. special operations teams evolved, other specialized teams, such as DELTA, America’s elite counter-terrorist force, were formed.36 Each of these special operations units has a plan for tactical medical support. The growth of terrorism in the 1970s resulted in the formation of other special operations groups worldwide. The Germans established a special unit within their border police, later presented to the world as GSG9 (Grenzschutzgruppe-9).99 This unit emerged after the 1972 tragedy at the Olympic Village in Munich, Germany. The French formed the Groupe d’Intervention de la Gendarmerie Nationale in 1974, and many other countries have since developed similar units. Medical providers in the combat environment were traditionally taught to perform with the principles of ATLS (advanced trauma life support). Although this training was instrumental in decreasing the morbidity and mortality of trauma victims in the noncombat scenario, it fell short of providing appropriate care for the patient and the combatant team members on the field of battle. Numerous reviews of past and recent conflicts have noted the inadequacies of this approach to battlefield medical care.6,8,15,104 Ninety percent of battle deaths occur in the field, prior to any medical intervention. Bellamy did a landmark review of wounds and death in battle.7,73 In this study,7 he noted that 31% of battlefield deaths resulted from penetrating head injury, 25% from surgically uncorrectable torso trauma, 10% from potentially correctable torso trauma, 9% from exsanguinating extremity wounds, 7% from mutilating blast trauma, 5% from tension pneumothorax, 1% from airway obstruction, and 12% from various wounds (sepsis and shock off the battlefield) (Fig.

555

23-6A). Potentially preventable battlefield causes of deaths include bleeding to death from extremity wounds, tension pneumothorax, and airway obstruction.54 These statistics have proven true in today’s Global War on Terrorism conflicts and in most tactical medical scenarios. They gave rise to questions about the pure application of the basic advanced life support precepts of airway, breathing, and circulation (ABC) for battlefield and tactical situations. In 1993, led by the Naval Special Warfare Command, a multi-agency working group (Committee on Tactical Combat Casualty Care), including special operations physicians, medics, corpsmen, and operators, began a 2-year study of this issue. This led to the guidelines titled Tactical Combat Casualty Care in Special Operations.15 The committee meets regularly and reviews new equipment, practices, and current operations for lessons learned, and then revises the guidelines as appropriate. These guidelines, which evolved from the special operations community, are currently being evaluated and implemented in most combatant units of the U.S. military, and of many other countries.14 The need for civilian SWAT teams in the United States evolved from high-profile criminal acts that resulted in shocking losses of human life. The seminal incident involved a sniper at the University of Texas at Austin. On August 1, 1966, Charles Whitman shot and killed 15 people and wounded 31 others.70 In the midst of this tragedy, it became apparent that the law enforcement agencies called out were ill equipped to deal with the threat, hampered by inadequate weaponry and not trained to respond in a timely and optimal fashion. After this incident, many law enforcement agencies began developing specially trained and equipped tactical units to respond rapidly to such threats to public safety.31 The Los Angeles Police Department and the Los Angeles County Sheriff’s Department were among the first law enforcement agencies in the United States to organize and develop full-time tactical units specifically trained to handle high-risk incidents. Before 1989, there existed great diversity in the ways emergency medical care was provided during law enforcement tactical operations. Early on, most law enforcement agencies relied on regular civilian EMS providers staged at a safe location removed from the area of operation, or they simply called 911. Although this took advantage of an already established prehospital care system, care for injured officers was delayed.103 Other agencies trained full-time SWAT officers as EMTs or paramedics. This concept of getting medical care “close to the fight” was also realized in the Gulf War, and the military put this new concept in place during Operation Iraqi Freedom. Information obtained from interviews with military emergency physicians who served in Iraq has suggested success of the new model of battlefield care.101


PRINCIPLES OF TACTICAL

COMBAT CASUALTY CARE

Tactical combat casualty care (TCCC) varies from ATLS in several distinct ways, primarily because the victim and the medical provider are not in a safe environment. Additionally, medical care of the victim may not be the highest priority, and the team may be hours from higher levels of care and operating in the open under extreme environmental conditions.

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A

Figure 23-6. A, How people die in ground combat.B, Intubation.(A courtesy Col.Ron Bellamy; B courtesy Lawrence E. Heiskell, MD.)

B The premise of TCCC is to do the right things at the right times. Underlying this basic statement is the suggestion that good hospital-based medicine is often not good battlefield medicine,14 as logically follows from these three statements: 1. Good medicine can be bad tactics. 2. Bad tactics can get everyone killed. 3. Bad tactics can cause the mission to fail. The ultimate goals of TCCC are the following: 1. Treat the casualty. 2. Prevent additional casualties. 3. Complete the mission. TCCC is divided into three main stages of care14: care under fire, tactical field care, and combat casualty evacuation care. These are defined in the following paragraphs.

Care under Fire Sometimes care is rendered by the medic or corpsman at the scene of the injury while he is still under effective hostile fire.

The medical equipment available is limited to what the individual operator or the corpsman or medic can carry in the medical pack. The most effective medical care during this stage of TCCC is fire superiority—that is, winning the battle, or at least keeping enemy heads down and weapons ineffective. The medical provider (and the casualty if able) must work to suppress hostile fire and eliminate the threat as directed by the mission commander, and, if possible, to protect the injured fighter from further harm. For many reasons, this is undoubtedly the most difficult phase of TCCC. First, the traditional provider, trained to be a “medic first,” may find it hard to direct attention to the threat and not maneuver to respond to the casualty. Second, this phase usually occurs in the most exposed environment, where the provider cannot use his normal assessment tools. For example, during nighttime he cannot use a light, as it would draw more fire, and listening for lung sounds with a stethoscope in an explosionrocked firefight is useless. In earlier conflicts, it was noted that

Chapter 23: Tactical Medicine and Combat Casualty Care

Figure 23-7. CATS (Combat Application Tourniquet System) tourniquet. (Courtesy Lawrence E. Heiskell, MD.)

many medics and corpsmen who responded to casualties instead of suppressing fire were wounded or killed, and that a significant number of the victims that they were trying to rescue were already dead. The priorities for the provider during this phase of care, therefore, are as follows14: 1. Return fire as directed or required. 2. Try to keep yourself from getting shot. 3. Try to keep the casualty from sustaining additional wounds. 4. Stop any life-threatening external hemorrhage with a tourniquet. 5. Take the casualty with you when you leave. Airway and breathing problems are not addressed during this phase. The key action is to stop exsanguinating hemorrhage. A tourniquet is the primary means to stop the bleeding on an extremity (Figs. 23-7 through 23-10). The tourniquet can be applied and left in place by the injured operator or medic, who can then return fire in support of the team. If a tourniquet cannot be placed because of the location of the wound, then direct pressure and a hemostatic dressing are recommended as the appropriate actions. As soon as possible, the casualty is moved to a safer location, and the next phase of TCCC is instituted. This movement is performed with techniques dictated by the tactical situation. It can be done by, for example, vehicles, pack animals, buddy lifts, or dragging. Another departure from traditional ATLS teaching is that cervical spine protection is not routinely provided in this phase of care. Studies of penetrating neck injuries in Vietnam demonstrated that only 1.4% of patients with penetrating injuries would have benefited from cervical spine immobilization.4 Although not all combat-related injuries are penetrating, the complexities of moving a patient in an environment where the patient and provider are under fire often preclude even rudimentary cervical spine immobilization.

Figure 23-8. Mechanical advantage tourniquet. (Courtesy Lawrence E. Heiskell, MD.)

Figure 23-9. Chitosan hemostatic dressing. (Courtesy Lawrence E. Heiskell, MD.)

Tactical Field Care The tactical field care phase consists of care rendered once the medic or corpsman and the casualty are no longer under effective hostile fire. It also applies to situations in which an injury has occurred on a mission but there has been no hostile fire. Available medical equipment is still limited to that carried into the field by mission personnel. Time prior to evacuation to a medical treatment facility may vary considerably. In this phase, the medic has a short time to evaluate and treat the wounded. The medic assesses injuries, performs medical

Figure 23-10. Emergency bandage. (Courtesy Lawrence E. Heiskell, MD.)

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care as able (equipment still limited to what was carried onto the battlefield), and then informs the mission commander of the findings. The mission commander then determines what action will be taken (evacuation, abort, continue). This again may be a major departure from nontactical medical care, in that the medical provider is not the ultimate authority on patient disposition. The mission commander decides how much time is taken to care for the casualty in any phase of the operation, if and when MedEvac will occur, and what assets will be allocated from the primary mission toward care of the injured. During this phase, the provider must assume not only that hostile fire may occur at any time but also that any injured team member with altered mental status may become a threat. The provider must therefore disarm the team member, an action that most warriors resist. This is the first step in the tactical field care phase. The second step is to address airway compromise. Airway actions are usually rendered as follows: if the victim is unconscious without obstruction, utilize a nasopharyngeal airway (better tolerated and less likely to become dislodged with movement)1 and a rescue position if able. If airway obstruction is present and cannot be alleviated with these maneuvers, the next recommended treatment is to move directly to a surgical cricothyrotomy. Endotracheal intubation is not recommended at this level of care for several reasons: (1) It requires the medic to carry onto the battlefield, equipment that has no other purpose, (2) the medic must practice regularly to maintain his skills, (3) success rates under austere conditions are believed to be significantly less than those done in a controlled or semicontrolled setting, and (4) the laryngoscope light may compromise team safety on the field.84,96,97 Emergency cricothyrotomy is the best option in this phase of TCCC. Because of distorted anatomy, it is the best way to protect the airway of a patient with maxillofacial wounds. Blood and tissue in the airway preclude visualization of the cords and make endotracheal intubation difficult or impossible.14,92 The third step is to treat breathing difficulties. Any severe progressive respiratory distress is assumed to be due to a tension pneumothorax (the number-two cause of preventable battlefield deaths). One cannot wait for the classic signs (which are unreliable at best and most often impossible to ascertain on the battlefield) of diminished breath sounds, hyperresonance, and tracheal deviation to make this diagnosis.76 Therefore, faced with victims in increasing respiratory distress and with unilateral penetrating chest trauma, the medic will go directly to a needle thoracostomy. This is the definitive procedure in this phase. A chest tube is not usually needed, it is difficult to perform on the battlefield, and it would only further complicate patient care, transportation, and mission completion.14 The fourth step is to readdress bleeding. The medic rapidly locates uncontrolled hemorrhage and any wounds where a tourniquet has been placed. If possible, a hemostatic dressing is placed; the tourniquet may be discontinued if the wound and tactical scenario permit. Even if the bleeding appears controlled, further “rough” evacuation may necessitate keeping a tourniquet in place to prevent rebleeding. Each action that the medic takes is designed to save life with minimal further care by the medic. For example, a medic who is holding pressure on a bleeding wound cannot return fire, take care of other casualties, or perform other procedures on this patient. The patient is not optimally prepared for transportation, which may consist of being thrown over someone’s back and carried out. Thus, a

tourniquet that would be a last-ditch effort in a noncombat environment becomes the method of choice in the tactical combat situation. Each operator in the field carries, and knows how to use, at least one tourniquet that can be self-applied. This allows the operator to self-administer life-saving bleeding control and then continue with the fight until treatment by the medic is possible. The fifth step is for the medic to determine whether an intravenous (IV) line or a saline lock is beneficial. The advantages would be that the patient could receive fluid resuscitation and IV antibiotics. Disadvantages include a probable delay in transportation, the additional equipment required (and the bulky apparatus that could become dislodged or tangled during evacuation), and difficulty in placing a line under austere tactical conditions. If an IV is deemed necessary but cannot be expeditiously placed, the intraosseous route is utilized. Several devices can be used to achieve this, including large-bore hypodermic needles, traditional intraosseous needles, and devices such as the FAST-1 (fast access for shock and trauma) and BIG (boneinjection gun), which quickly and accurately place the needle in the sternum or in another appropriate location. The medic’s sixth step is to determine whether fluid resuscitation is required. In general, if the patient is not in shock (the best indicators of shock in the field are altered mental status in the absence of head injury, and weak or absent pulses), then no IV fluids are necessary. If the patient is conscious, oral rehydration is permissible and preferred in many tactical scenarios. If the patient is in shock, the medic can give Hextend67 as a 500mL bolus and reassess after 30 minutes. If the victim is still in shock, the Hextend is repeated once. Usually, no more than 1000 mL of Hextend is given, and further efforts at resuscitation are determined by the tactical scenario. If the patient has a traumatic brain injury and is unconscious and pulseless, fluid resuscitation is given to restore the pulse. This protocol maximizes survivability of the patient and limits the amount of equipment necessary to be carried onto the battlefield. After exsanguinating hemorrhage, airway compromise, and breathing difficulties have been addressed, the seventh step in the tactical field care medical plan is to inspect and dress known wounds. The medic locates and appropriately treats wounds already identified but not yet treated because of tactical considerations and then proceeds with a quick but thorough headto-toe assessment for additional wounds. This is analogous to the secondary survey of ATLS, with a couple of notable exceptions. First, the patient is not exposed. This is because the patient may have to be moved quickly if the tactical situation changes, and because the patient must be kept warm and protected from further injury for a much longer time than in an urban setting. The medic often does this examination by feel in order to avoid using white light, to keep the victim’s body armor as intact as possible, and to avoid cutting off protective clothing that may be required during evacuation. Step eight is to assess for pain control. Analgesia is administered in this phase of care with the following considerations. If the victim is able to fight, non-narcotic preparations are used. These do not affect mental status, allowing the victim to remain armed and responsive. If the victim is unable to fight, morphine and promethazine, IV or intramuscular (IM), are given as needed. Step nine: If not already done, fractures are splinted and neurovascular status is rechecked. Step ten, the early administration of antibiotics for open combat wounds, significantly reduces the rate of infection.12

Chapter 23: Tactical Medicine and Combat Casualty Care Again, oral medication is preferred if the patient is conscious, and gatifloxacin has been shown to be highly effective and with minimal risks. Gatifloxacin is a broad-spectrum fluoroquinolone that is active against gram-positive and gram-negative microbes, aerobes, anaerobes, and fresh and salt water pathogens, is a once-a-day drug, and has a long shelf life. If the victim is unable to take oral medication or has significant abdominal trauma, IV/IM antibiotics are utilized, with cefotetan being the current drug of choice. In many units, the operators are given a “wound pack,” consisting of an antiinflammatory, acetaminophen, and gatifloxacin, and instructed to take the entire pack as soon as possible after being wounded. Step 11 in the tactical care medical plan is to continue to communicate with the victim, giving encouragement, explaining the care given, and giving updates on the tactical scenario if appropriate. Traumatic cardiac arrest is treated on the battlefield just as it is in the civilian setting. If the victim is pulseless, apneic, and has no sign of life, resuscitation is not attempted. After these measures have been taken, or if medical evacuation is now available, the last phase of TCCC, combat casualty evacuation care, is entered.

Combat Casualty Evacuation Care This phase of care is rendered once the casualty (and usually the rest of the mission personnel) has been picked up by an aircraft, land vehicle, or boat. Additional medical personnel and equipment that have been prestaged in these assets should be available at this stage of casualty management. The management plan aligns closely with that of the tactical field care phase, with the addition of more equipment and perhaps higher levels of medical providers. This phase is also the phase most similar to ATLS, although it may occur in the back of a moving conveyance and is still somewhat limited by available equipment and the tactical scenario. The basic medical plan for combat casualty evacuation care is as follows: 1. Airway management: Same as for tactical field care, with the addition of laryngeal mask airway (LMA)/Combitube/endotracheal intubation for definitive airway management prior to cricothyrotomy if the operators are trained and the patient can be intubated (e.g., has no midface injuries). Spinal immobilization is still not deemed necessary for casualties with penetrating trauma for the reasons stated earlier. 2. Breathing: Same initial considerations as for tactical field care. A chest tube can be placed if needle thoracostomy has produced no improvement in breathing, or if long transport is anticipated. Most combat casualties do not require oxygen, but its administration may be of benefit in the following situations: low oxygen saturation by pulse oximetry, injuries associated with impaired oxygenation, unconscious patient, and traumatic brain injury (to maintain oxygen saturation >90%). Sucking chest wounds should be treated with petroleum gauze applied during expiration, covering it with tape or a field dressing, placing the victim in the sitting position, and monitoring for development of a tension pneumothorax. Asherman seals are also ideal for quickly securing chest tubes and for sucking chest wounds. 3. Bleeding: Same as for tactical field care. 4. IV: Same as for tactical field care. 5. Fluid resuscitation: Same as for tactical field care, with blood and/or lactated Ringer’s solution possibly available.

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6. Monitoring, wound care, re-inspection for additional wounds, analgesia, reassessment of fractures, antibiotics: All the same as for tactical field care. The following scenario exemplifies the concepts of TCCC and the various phases of care. Consider a Special Forces team on a night mission. They jump from an aircraft at night into hostile territory. They are then to travel by foot over 4 miles of rocky, mountainous terrain to secure the objective, and then move to the shoreline for a waterborne extraction. On the initial jump, one of the operators sustains an open femur fracture. The medic and the team leader must consider (at a minimum) the following issues: • How to treat the injured member with the equipment they carried in (keeping in mind that a potentially long evacuation wait time precipitates the need to minimize injury, control pain, prevent infection, avoid shock, defend selves, and maintain concealment) • How or whether to continue the mission

Option 1. MedEvac the injured member, breaking operational security and calling for helicopter extraction. Option 2. Commandeering a local vehicle and driving to a pickup site, taking the patient to the planned extraction site, and continuing with the mission. Option 3. Aborting the mission and leaving the injured member and possibly some of the team behind to provide security until they return with help. Thus, a single injury throws a lot of variables into the mission commander’s decision tree. Preplanning for medical situations is essential, and the medical member of the team is essential in the planning and execution of the mission. A main precept of TCCC is to move the medical care from being the sole responsibility of the combat medic, to involve each operator and each level of leadership. Each fighter carries a tourniquet that can be self-placed. Each fighter is trained in basic combat lifesaving skills so that the effects of wounds can be minimized (within defined limits) and fire can be returned until the medic can arrive and perform the appropriate advanced medical care. Each leader, from the squad level up, is trained to evaluate medical concerns as an integral part of the mission execution and is able to decide when to abort the mission, when to continue, and when to alter the plan, based on the mission objective and the issues that the injured team member or members bring to the fight.


PRINCIPLES OF TACTICAL MEDICINE

The tactical environment presents unique challenges to law enforcement officers, and the same is true for personnel providing EMS in that environment. Tactical medical care providers must have an understanding of and consideration for law enforcement tactics and mission-specific objectives when planning and providing medical support (Fig. 23-11).55 Traditional EMS doctrine maintains that rescuer and scene safety are first priorities, and that patient care is a secondary concern.78 The nature of tactical operations requires that law enforcement officers and tactical medical personnel operate in unsecured environments and situations with significant potential for violence and injury (Fig. 23-12).74 Tactical scenes are

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Figure 23-11. Tactical medics placing a suspect under arrest during a tactical operation. (Courtesy Lawrence E. Heiskell, MD.)

Figure 23-12. At the International School of Tactical Medicine,law enforcement tactical medics train for high-risk vehicle assaults. (Courtesy Lawrence E. Heiskell, MD.)

rarely safe from the civilian standpoint, but tactical medical personnel are trained to conduct concise and limited medical evaluations and interventions in potentially threatening areas.85 What sets tactical EMS apart from standard EMS is the ability to render immediate care in an environment that may not be completely secured from threats (Fig. 23-13). When a SWAT team relies on traditional EMS to provide medical care and an operator or civilian is acutely injured during the mission, the EMS unit must wait until either the victim is brought out to the safe (“cold”) zone (Fig. 23-14) or for the entire scene to be secured by law enforcement before moving to the patient. When a tactical medical unit is present, care can generally be rendered to the victim in a timely manner, and when the injuries involve acute airway issues or life-threatening hemorrhage, lives may be saved by faster access to care.

Figure 23-13. Advanced airway management in the tactical environment.(Courtesy Lawrence E. Heiskell, MD.)

Other differences between tactical EMS and conventional EMS include limitations in medical equipment at hand, performing in adverse or austere environments (e.g., while maintaining light or sound discipline), and performing patient assessment from remote locations.90 “Medicine across the barricade” involves remote evaluation and management of patients, such as when a hostage has become ill or injured and the provider attempts to assist the victim by using the eyes, ears, and hands of someone closer to the situation.35 The tactical medical provider must use skills not unlike those of an EMS dispatcher handling an emergency over the radio. In addition, standard EMS medical care performed in specific clinical scenarios may require a different approach when the same situation is encountered under tactical conditions.34 Tactical medicine can be provided by EMTs, paramedics, registered nurses, mid-level providers (physician assistants, nurse practitioners), or physicians who serve on police tactical teams.47 Mid-level providers and physicians traditionally have training in advanced surgical and medical procedures beyond what is normally allowed for traditional EMS personnel.22 The primary goal of tactical medicine is to assist a tactical team in accomplishing its mission. This is achieved through team health management—keeping the tactical team members healthy before, during, and after operations.21,62 A full tactical medicine program encompasses the provision of preventive and acute medical and dental care, and for some teams even canine support veterinary care.50 Ready access to such care has a positive effect on team morale. One of the most important roles of the provider is to create a formal medical threat assessment for each training and operational deployment. This includes consideration of issues such as environmental conditions (heat, cold, wind) (Fig. 23-15),41,42 fatigue (and the possible need for rotating operators), nutritional issues,23 plant and animal threats, and a plan for extrication and transport of patients.11 When operational, this medical plan should include any medical intelligence that can be gathered prior to or during the mission, including issues such as who is involved, ages of those involved, medical history and

Chapter 23: Tactical Medicine and Combat Casualty Care

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Figure 23-14. The zones-of-care concept of tactical emergency medical services. (Courtesy Bohdan T. Olesnicky, MD.)

Figure 23-15. Tactical operators overcome with heat exhaustion receive cooling measures from a tactical physician. (Courtesy Lawrence E. Heiskell, MD.)

background, preexisting medical conditions, geographic location, and even the weather.20 SWAT teams and their tactical medical teams are important community resources not only for their response to major emergencies (e.g., weapons of mass destruction) but also in planning for them. Tactical medical operators, in conjunction with local medical control, EMS, and public health officials, should take a leadership role to ensure that aggressive, proactive planning

for these future threats is completed before the resources are needed.17,105 Although no one doubts that some terrorists, outlaw states, and even organized criminals have the capability to produce or access chemical and biological agents, the question is whether they will use them.39 The use of explosive devices is on the rise worldwide. The potential for terrorist acts against the United States is immeasurable. As a result, domestic preparedness and proper training for blast injuries is essential.27,32,38,75,98 It is advantageous to have more than one provider as a part of a tactical team. In the event of a serious injury or when multiple casualties are involved (e.g., in a raid on a clandestine drug laboratory),48,61 one of the team’s responsibilities is to lessen the agency’s liability exposure with adequate written, photographic, diagrammatic, or video documentation.66 Another benefit of having multiple providers is the ability to send a provider to the hospital with an officer who becomes ill or injured during a mission. This provider can serve as a concerned advocate for the officer and as a go-between with hospital personnel, which provides significant reassurance to the entire tactical team.44,46,71

Team Health Management Tactical medical providers ensure that everyone on the team is healthy and optimally fit for duty.49 The team’s medical officer is responsible for the team’s physical fitness, diet, exercise, sleep, stress management, and preventive medicine. The tactical unit can be viewed as a group of elite operators who are “occupational athletes.” Strength training for many tactical operators consists of traditional bodybuilding exercises. However, this type of physical conditioning does not duplicate the actions needed to perform as a tactical operator. A SWAT team member never does a bench press on a tactical entry. Tactical operators, like professional

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athletes, need a broad-based program of training and physical conditioning tailored to the specific actions they will perform. The team’s medical officer should stress regular physical conditioning. A comprehensive plan of proper nutrition and exercise must be established and maintained. This should include a balance of aerobic and anaerobic exercises and stretching. Cardiovascular fitness workouts, such as running or swimming, are excellent for the tactical team. Full-body or resistance circuit weight training is excellent for strength training, but it must be a total body workout. Training some parts of the body but ignoring others can lead to costly injuries and a lower level of fitness than desirable.93 Flexibility training is one of the best ways to prevent injuries in the field. Unfortunately, it is frequently ignored. Regular stretching or yoga has been long recognized as beneficial in athletic physical conditioning. In this respect, the tactical unit is no different from any other group of athletes. When the physical conditioning program encompasses all these points, the team operates at its peak potential with fewer injuries. A sound diet should be stressed and maintained, but diet is often a controversial topic. In response to the obesity problem in the United States, the Food and Drug Administration (FDA) and many other researchers have looked at diets worldwide and their effects on the human body. Randomized clinical trials studying the risks and benefits of various individual diets are only recent works.10,28,83,102 The FDA studied the traditional food pyramid (based on four food groups and no longer considered a valid nutritional program72), and Mediterranean, high-carbohydrate, high-fat, high-protein, low-fat, lowcarbohydrate, Atkins, Zone, Weight Watchers, Ornish, and South Beach diets.25 They revised their food pyramid to a more balanced program designed for variations in age, sex, and level of physical activity, and containing five food groups: grains, vegetables, fruits, milk, and meat and beans. Fats, sugars, sodium, and total caloric intake are restricted. The FDA has an interactive website for the new food pyramid (www.foodpyramid.gov). Although our knowledge of diet and exercise is improved, data continue to be gathered, and the perfect dietary program for the tactical operator is not yet known. Nonetheless, fast foods and simple sugars should be deemphasized or eliminated from the tactical operator’s diet. The team medical officer essentially becomes the family physician for the tactical unit and should be prepared for this role. Regardless of the level of training, the team physician will be viewed as the medical advisor to the tactical unit. It is this relationship that fosters better team health overall, and better performance of the unit as a result. Preventive medicine should be stressed with regular physical examinations and treatment where appropriate. Smoking cessation, alcohol and drug counseling, and stress management are the responsibility of the team medical officer.

A

B Figure 23-16. A, Blackhawk Products Group Special Operations medical backpack. B, Ballistic vest,level IIIa,showing trauma plate worn for tactical operations.(Courtesy Lawrence E.Heiskell, MD.)

Tactical Medical Equipment In general, tactical EMS equipment comes from other areas of emergency medicine and law enforcement and is combined into field-expedient, multifunction toolkits. Looking at the gear as a whole, a modular approach may be most helpful (Fig. 23-16A). The gear differs depending on the roles of the providers and the tactical unit.33 Basic equipment for the operator includes essential items. Typically, an operator has a duty uniform consisting of a battle dress uniform or jumpsuit.95 The uniform may undergo appropriate modifications depending on weather con-

ditions. As with other areas of outdoor activity, it is wise to use a system of appropriate layers that can be easily adjusted to changing weather conditions. Waterproof and breathable outer layers may be a consideration, as are wicking underlayers. In addition to the standard duty uniform, a Nomex balaclava and gloves are worn to protect from exposure to pyrotechnic devices on many entries. Because this is an environment where gunfire may be encountered, ballistic protection is needed. For the tactical medical

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TABLE 23-3. U.S. Department of Justice Rating of Body Armor TEST VARIABLES

ARMOR TYPE I

TEST ROUND

TEST AMMUNITION

1

38 Special RN Lead 22 LRHV Lead 357 Magnum JSP 9 mm FMJ 357 Magnum JSP 9 mm FMJ 44 Magnum Lead SWC Gas Checked 9 mm FMJ 7.62 mm (308 Winchester) FMJ 30–06 AP *

2 II-A

1 2

II

1 2

III-A

1 2

III

—

IV

—

Special requirement

—

PERFORMANCE REQUIREMENTS REQUIRED FAIR HITS PER ARMOR PART AT 0° ANGLE OF INCIDENCE

NOMINAL BULLET MASS

MINIMUM REQUIRED BULLET VELOCITY

10.2 g 158 gr 2.6 g 40 gr 10.2 g 158 gr 8.0 g 124 gr 10.2 g 158 gr 8.0 g 124 gr 15.55 g 240 gr

259 m/sec (850 ft/sec) 320 m/sec (1050 ft/sec) 381 m/sec (1250 ft/sec) 332 m/sec (1090 ft/sec) 425 m/sec (1395 ft/sec) 358 m/sec (1175 ft/sec) 426 m/sec (1400 ft/sec)

8.0 g 124 gr 9.7 g 150 gr

426 m/sec (1400 ft/sec) 838 m/sec (2750 ft/sec)

4

10.8 g 166 gr *

868 m/sec (2850 ft/sec) *

1

4 4 4 4 4 4 4

6

*

MAXIMUM DEPTH OF DEFORMATION

REQUIRED FAIR HITS PER ARMOR PART AT 30° ANGLE OF INCIDENCE

44 mm (1.73 in) 44 mm (1.73 in) 44 mm (1.73 in) 44 mm (1.73 in) 44 mm (1.73 in) 44 mm (1.73 in) 44 mm (1.73 in)

2 2 2 2 2 2 2

44 mm (1.73 in) 44 mm (1.73 in)

2

44 mm (1.73 in) 44 mm (1.73 in)

0

0

*

*See section 2.2.7 of reference. g, grams; gr, grains. From U.S. Department of Justice National Institute of Justice: Ballistic Resistance of Police Body Armor. NIJ Standard 0101.03; 5.2.1, April 1987.

provider, levels I and IIa are not advised. Level II is the bare minimum if the body armor is concealed under a shirt or uniform, but levels IIIa to IV are better (Table 23-3, and see Figure 23-16B). These levels of protection have a good balance of bullet stopping power and ability to absorb blunt trauma. Many tactical operators combine body armor with ballistic plates made of metal or ceramic, which stop high-velocity rifle bullets. Body armor is chosen by the agency from a vast array of different types and styles produced by a host of manufacturers. Some tactical physicians also carry a Kevlar blanket or ballistic shield, which can be used to cover a patient in harm’s way or can be used as a mobile source of cover when providing care or extracting a downed victim. These blankets, although effective, are extremely heavy and bulky. The weight and bulk of all nonmedical tactical equipment hinders the ability to carry large amounts of additional material. The medic needs to decide how much can be carried and whether to wear a backpack or a load-bearing vest, or neither. In general, the tactical medical provider must be able to effectively carry equipment and operate in a tactical situation without hindering the rest of the team. Of the two general sets of medical equipment, one is carried for immediate care, typi-

cally worn in a small backpack or load-bearing vest, and the second is carried in a larger backpack or duffel bag in the support vehicle. The latter is used for more extensive treatment, multiple casualties, and prolonged transports.59

Communication Communication between team members and members outside the area of the operation is often essential. Radios with throat microphones and headsets are fairly standard on most tactical units. Radios tend to be on secure channels to ensure the security of a mission. Some communications may even be encrypted. Simple communication between members may involve standard or specialized sign language.

Entry and Breaching Tools Specialized entry tools are used to gain access to barricaded subjects or closed doors. Typical items, familiar to firefighters and EMS personnel, include pry bars, battering rams, sledge hammers, hooks on chains or rope, stop blocks, and halligan tools (Fig. 23-17). Ladders may be needed to gain access to an elevated or depressed point. In extreme cases, a variety of explo-

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Figure 23-17. Entry tools: two rakes, a halligan tool, a ram, and a sledge hammer are shown. (Courtesy Bohdan T. Olesnicky, MD.)

sive devices are available to trained explosive experts in the tactical unit to gain entry to an area.

Figure 23-18. At the International School of Tactical Medicine, law enforcement tactical medics train with the HK MP5 submachine gun. (Courtesy Lawrence E. Heiskell, MD.)

Weapons Systems Whether a team medic should be a sworn law enforcement officer or an armed civilian has been a subject of much debate. Regardless, a provider must be familiar with the unit’s weapons systems. For offensive or defensive purposes, weapons systems are constantly encountered in the tactical arena. A provider who is a sworn officer has a primary role as an operator on the unit and a secondary role as a medical provider.77,81 However, a provider who is first a medical officer would still have to protect himself in a hostile situation and therefore would be armed defensively. In another scenario, the provider may be unarmed but may have to take charge of an officer’s weapon in a medical or tactical situation. An armed officer who is disoriented may become a danger to the team, so the provider would need to take charge of all of the officer’s weapons and render them safe. In the worst case, the provider may have to defend a downed officer using the officer’s weapon. Weapons system familiarity is paramount for the tactical medicine provider. A provider should be familiar with every handgun, shotgun, rifle, submachine gun, assault rifle, and smoke or chemical agent gun used by the team. All tactical team members, whether providers or not, should be able to use any weapon a team member carries and render it safe.91 The provider should not be exempt from this requirement (Fig. 23-18). Different weapons systems use different ammunitions (see Chapter 22). Typically, there is a duty handgun, which shoots low-velocity handgun ammunition. This same ammunition may be used by a submachine gun, such as the Heckler and Koch (HK) MP5 UMP 40, or UMP 45. Calibers of the handgun and submachine gun should be matched to avoid the wrong caliber ammunition going into the wrong weapon, causing malfunction in a crisis situation. Assault rifles, such as the Colt AR 15 or Colt M16, shoot .223-caliber high-velocity cartridges. The provider may be exposed to shotgun ammunition, typically 00 buckshot. The team may have a sniper, who shoots with a .308 high-velocity

rifle that is bolt action for precision shots. The flight characteristics and ballistics of shotgun, rifle, and handgun ammunition vary depending on the weight, shape, and velocity of the ammunition. The provider should be familiar with the effects in order to treat field wounds appropriately. In addition to traditional ammunition, the provider may be faced with the use of distraction devices, chemical munitions, and less lethal munitions. Chemical munitions deliver a chemical agent to an intended target to disorient or incapacitate and facilitate capture or surrender without loss of life. Typical chemical agents used in tactical operations are tear gas or a derivative of pepper spray. Less lethal munitions are also fired to incapacitate and facilitate capture. Unfortunately, with this use of force, injury is common, so the provider should be familiar with the injuries and their treatments. These munitions are low-velocity projectiles of wood, hard rubber, foam rubber, plastic, or bean bags. They have enough force to cause pain and usually make an assailant stop aggressive action on contact. They usually cause minor blunt trauma, but they may achieve enough force and velocity to penetrate into body cavities, causing penetrating injures (Figs. 23-19 through 23-21). Explosive breaching techniques and distraction devices, such as “flash-bangs,” are often deployed during tactical operations. The small explosives used to gain entry into an area can create injuries that the medic must be prepared to recognize and to treat effectively.68 For example, the flash-bang is a device that is hand thrown into an area to deliberately disorient a suspect and divert attention toward the device and away from the entry team. These devices usually have a nonexploding canister and a small explosive charge. The device is activated and thrown much like a military hand grenade, but it causes a brilliant flash of light (6 to 8 million candlepower) and a thunderous noise (175 decibels). This is accomplished by venting explosive gases through multiple holes in the canister (Fig. 23-22). Medical problems caused by flash-bangs and explosive entries include the following:

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• Burns, both minor and major • Smoke causing bronchospasm • Vestibular dysfunction • Transient visual disorientation • Emotional upset and anxiety Of note, in general use, the flash-bang has not been reported to cause ear drum rupture. Explosive breaching is the role of the team’s explosives expert, with whom the medic should consult, as part of the medical threat assessment, about the types of explosives planned and the blast forces that may be encountered.

Vision Figure 23-19. A 37-mm less-lethal munitions launcher. (Courtesy Lawrence E. Heiskell, MD.)

Covert operations and low-light situations dictate the use of visual adjuncts. Binoculars, tactical mirrors, spotlights, periscopes, strobe lights, chemical lights, and headlamps are often deployed in a low-light tactical environment (Fig. 23-23). Proper training and discipline are required for use of these devices in the tactical environment, as they may give away one’s position and alert a hostile opponent to the team’s position. Similarly, electronic night vision equipment, which operates outside of the range of visible light, is also extensively used.


MEDICAL PERSONAL

PROTECTIVE EQUIPMENT

Universal precautions against infectious diseases must be deployed; tactical medicine is no different from any other venue in this respect. Medical personal protective equipment (PPE) includes masks, eye protection, gloves, and perhaps gowns. In remote locations, surgical treatment may be provided prior to transport to a tertiary care center. The basics for protection should be carried on the provider’s person in a readily accessible location. Some don surgical gloves underneath their shooting gloves prior to an operation so they will be ready if the need arises. Although not sterile, they provide protection from blood and body fluid–borne pathogens.

Personal Supply Module To reduce the amount of equipment carried by the medic and to help team members help themselves, each member of the tactical unit should carry a personal supply module (PSM), or “self-help kit,” with medical supplies. A team member can thus provide self-help or aid another member, and the medic may not have to be summoned until the scene is more secure. A typical PSM should be vacuum sealed and contain supplies for basic trauma care and for IV access (Table 23-4 and Fig. 23-24). Vacuum sealing these contents provides protection from the elements and makes them last longer. It also cuts down greatly on bulk, but it adds some weight.

Basic Medical Module

Figure 23-20. The stinger grenade has a small explosive charge that disperses many small rubber balls in a spherical blast pattern, causing compliance through pain. (Courtesy Lawrence E. Heiskell, MD.)

In addition to a PSM, a basic medical module (BMM) should be carried by team medics. Because every team member in a tactical unit should have at least basic EMT certification, a BMM could be used by any team member to provide initial care to a victim. The BMM should have basic splinting material and dressing material (Table 23-5). Basic airway tools, such as nasal airways and pocket mask, should be included. A bag-valve-mask or a more compact alternative is advisable in the tactical environment. A simple bagvalve-mask alternative device (BVMAD) can be constructed out

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Figure 23-21. Target areas for direct-fire or skipfire less-lethal projectiles. The orange areas are nontargets, the green areas are preferred targets, and the yellow areas should be targeted with caution only. (Courtesy Armor Holdings, Inc.)

Figure 23-23. A Surefire headlamp setup can use white light or LED light in low-light tactical situations. (Courtesy Lawrence E. Heiskell, MD.)

Figure 23-22. The Def Tec 25 flash-bang device. (Courtesy Lawrence E. Heiskell, MD.)

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Figure 23-24. Saline bullets remove the most common injury: foreign bodies in the eyes. (Courtesy Bohdan T. Olesnicky, MD.) Figure 23-25. The bag-valve-mask alternative device (BVMAD) as it is stored,with the mouthpiece (red arrow) over the exhaust port. (Courtesy Bohdan T. Olesnicky, MD.)

TABLE 23-4. Sample Contents of Personal Supply Module (PSM) Trauma dressing IV start kit Minor dressings Saline bullets

Medicines

Other wound items

Bandages such as the Israeli bandage can be easily self-administered by the victim on most extremity wounds. 100 mL IV fluid, an alcohol wipe, tourniquet, IV catheter (3), IV tubing, tape, flush and saline lock Adhesive bandages should be carried by all team members. Foreign bodies in the eyes are very common on entries, and a bottle of eye drops (saline bullets) may allow an operator to continue on a mission (see Figure 23-24). Pain: acetaminophen, ibuprofen, narcotic analgesics Antibiotics: ciprofloxacin, metronidazole, cephalexin Surgical staples or liquid tissue adhesive

TABLE 23-5. Sample Contents of Basic Medical Module (BMM) Splints Airway Litter Wound care Other

Two SAM splints Pocket mask, bag-valve-mask (BVM) or BVM alternative device, oral and nasal airways Fold-up stretcher Various trauma dressings Elastic (ACE) wraps and cravats

of respiratory supplies from a one-way valve, flexible tubing, and a mouthpiece (Fig. 23-25).5 This is the preferred ventilatory device in the tactical environment, as it allows a rescuer to provide ventilation without unnecessary bulk. Oxygen is rarely useful in the immediate tactical environment, so O2 cylinders are left in the support vehicle with a regular bag-valve-mask and retrieved when necessary. An automated external defibrillator (AED) should be carried in the support vehicle.3 A small collapsible litter for extrication of a downed person should be a part of every BMM.

Intermediate Medical Module An intermediate medical module (IMM) is intended to be used by paramedics and registered nurses. Unlike the BMM, it con-

TABLE 23-6. Sample Contents of Intermediate Medical Module (IMM) Airway Medications

Endotracheal tubes, laryngoscope, stylette, bougie, bag-valve-mask alternative device (BVMAD) IV setup and tubing, pain medication, rapid sequence intubation medications, antibiotics (see Figures 23-26 and 23-27)

tains equipment and supplies suitable for advanced life support (ALS). Under standing orders from a team physician, ALS providers may provide advanced cardiac life support to a victim. An IMM is much more extensive than a BMM. It contains medications, IV tubing, IV fluids, an endotracheal tube, a Combitube, a laryngoscope, a light wand, and, if protocol allows, a cricothyrotomy kit (Table 23-6 and Figs. 23-26 and 23-27). These facilitate placement of a definitive airway prior to transport, which, when used with a BVMAD, permits hands-free ventilation of a patient, allowing extrication by one or two team members. Proficiency with the airway toolkit is of high priority, as conditions in the tactical environment are difficult at best.

Advanced Medical Module The most complex module is the advanced medical module (AMM), intended for independent practitioners, such as nurse practitioners, physician assistants, and physicians. These practitioners can perform advanced surgical procedures and medical interventions that can make the difference between life and death on a long transport. Transport to definitive care should not be delayed unless medically necessary. However, if advanced care in the field is indicated, it can be provided by an independent practitioner with an AMM.

Major Trauma Module Lengthy surgical interventions in the field are not advised and have extremely poor prognoses. Although rapid transport to a trauma center should not be delayed, some surgical procedures may be of benefit when performed in the field: laceration repair to stop bleeding or facilitate evacuation, cricothyrotomy, and,

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Figure 23-28. A vacuum-sealed minor-surgery tray. Many procedures can be accomplished with a minimum of equipment. (Courtesy Bohdan T. Olesnicky, MD.)

TABLE 23-7. Sample Contents of Major Trauma Module (MTM) Figure 23-26. Vacuum-sealed intravenous start kit. (Courtesy Bohdan T. Olesnicky, MD.)

Israeli dressing Combine dressings Gauze pads Antibiotic packs Tourniquet

Figure 23-27. A well-stocked and functional intermediate medical module (IMM) airway kit, containing a laryngoscope, a bag-valve-mask alternative device (BVMAD), oral airways, a bougie, a stylette, endotracheal tubes, tape, and a surgical airway kit. (Courtesy Bohdan T. Olesnicky, MD.)

Wound closures Minor-surgery tray ACE wraps Splinting material IV fluids

Supplies

in critical situations, chest tube insertion. These types of procedures can usually be performed using only the essential equipment found in a vacuum-sealed minor-surgery tray (Fig. 23-28), which can be one component of the major trauma module (MTM) for advanced providers (Table 23-7). Many users include hemostatic dressings in trauma kits, but their use is not yet well studied.60,86 The efficacy versus the potential harm of hemostatic dressings is a subject of debate. Direct pressure with a sterile dressing is the initial approach to hemorrhage control. The traditional and time-tested approaches of pressure-point compression and tourniquets are useful adjuncts to any bleeding problem, so these materials should be included in the MTM. A set of combine dressings, gauze, petrolatum gauze, and Israeli dressings should also be carried.

Other

May be self-administered by the patient with one hand; combines an ACE wrap, combine dressing, and tourniquet in one device To control heavy bleeding or cover eviscerated bowel and open fractures Multiple uses Pre-prepared medication packs for major trauma, containing pain medication and antibiotics Several excellent devices are available for tactical use Sutures, staples, and wound adhesives For performing surgical procedures that cannot wait for extrication or transport Strains, sprains, and fractures are common SAM splint or a short sealed roll of fiberglass casting material. Bullet wounds frequently fracture long bones For infusion of medication and management of shock as needed. Also used for wound irrigation and eye irrigation. Several IV start kits should also be on hand Gloves, tape, trauma shears, tweezers, adhesive bandages, roll gauze, cravats, nasal airways, 60-mL syringes, headlamp Duct tape, biohazard bags, medical record sheets, and trauma tags for multiple casualties

Support Vehicle Module Additional supplies and equipment are kept in the support vehicle module (SVM). Consumable items should be kept in the SVM, so that other modules can be restocked from it (Table 23-8). The SVM contains equipment such as O2 cylinders, an AED, airway adjunct devices, fiberoptic scopes, nebulizers, surgical trays, chest tubes, cervical collars, backboards, peroxide, povidone-iodine, liter bags of crystalloid IV fluid, replacement filters for gas masks, and fiberglass splinting material.

Chapter 23: Tactical Medicine and Combat Casualty Care

TABLE 23-8. Sample Contents of Support Vehicle Module (SVM) Biohazard container Saline eye flush Elastic (ACE) wraps Splinting material

IV fluids

Ice packs

Wound dressings Advanced airway tools Spare uniforms

Oxygen cylinders Bag-valve-mask (BVM) Automated external defibrillator (AED)

Disposal container for used sharps and medical waste Foreign bodies in the eyes are common on entries Strains, sprains, and fractures are common Fairly bulky and difficult to carry in the medical pack. C-collars are frequently kept here and may be retrieved when needed For prolonged transport or massive hemorrhage, more IV fluid should be kept in the SVM and not carried on entries. Multiple IV start packs for use when necessary Ice packs are commonly used, as ice is not always available in the field. If the location has a freezer, bags should be kept to use existing ice Additional adhesive bandages, Israeli dressings, combine dressings, ABD pads, and burn dressings Difficult-airway tools may be needed in the cold zone prior to transport, to secure a definitive airway If decontamination is needed, the victim will need to be reclothed in a clean, dry uniform, particularly in cold or wet environments Best left in the support vehicle because of their weight Replaces the BVM alternative device when hooked up to oxygen in the cold zone The AED is proven to save lives but is too bulky to carry on entry

Field care is limited only by the equipment that can be transported and the training of the providers. Items carried by advanced providers include the following: • Central line • Tracheotomy set • Retrograde intubation set • Laryngeal mask airway • Chest tube set • Fiberoptic intubation set • Blood products or blood substitutes

CBRN Specialty Modules Depending on the role of the tactical unit, chemical, biologic, radiologic, or nuclear (CBRN) threats may be encountered. These incidents require tactical emergency medical care because they involve large crime scenes with casualties. Individuals trained in tactical emergency medicine are much more familiar with evidence collection and preservation, and they usually already have necessary security clearance to enter such an area. Until the scene is cleared, the tactical physician may be the only one who can provide medical care to victims inside. The chemical and biologic environments are specialized depending on the agent released. Various civilian and military protective gear and respirators or supplied air sources may need

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to be worn. Operating in CBRN protective gear requires extensive training in addition to regular tactical training. Antibiotic prophylaxis with ciprofloxacin, as well as agent detection equipment, may be carried by the medic in this case. Several biologic and chemical diagnostic kits and meters are available but costly. Radiologic incidents involve the dispersal of a radiologic agent with conventional explosives, the combination often referred to as a dirty bomb. Nuclear detonations refer to the splitting of a radioisotope and the resultant massive energy release from a nuclear bomb. Geiger counters are available for radiologic and nuclear situations. These situations require a great deal of additional training, but they are not beyond the realm of tactical emergency medicine. Hazardous material (hazmat) situations are frequently seen in civilian law enforcement raids on clandestine drug laboratories. Level A, B, or C protective suits with gas masks or supplied air may be required in these situations as well. Hazmat and CBRN situations are highly specialized in their nature and require extensive training, beyond the scope of this text.

Medical Threat Assessment Any mission planning must include a medical threat assessment (MTA). The SWAT commander uses information from many sources to create a tactical plan prior to execution of a mission, including the manpower available, building layouts, street layouts, support equipment needed, nature of the mission, available weaponry, and various sources of intelligence.65 An MTA is an important component of the intelligence the commander needs to properly execute the mission. It is the responsibility of the tactical medic to provide a concise and accurate medical briefing to the commander. MTA forms should be used on every mission to ensure systematic planning, as scenarios and problems may be unique. Only a systematic approach ensures complete assessment of the situation. The tactical medical team and its MTA are key factors in dealing with apocalyptic terrorist events, such as the Columbine school shootings and the school hostage crisis in Beslan, Russia.87 Other venues, such as protection details and the war on drugs, rely heavily on a team’s internal capacity for medical care, as evidenced by the U.S. Marshals Service Judicial Protection Training Program.88 A complete threat assessment should include these elements: 1. Location of the operation, with a brief description of the goals of the mission and the other teams involved, with their needs and resources (Table 23-9). 2. Locations of all surrounding hospitals and medical care facilities, such as designated burn and trauma centers, with phone numbers to facilitate communication. Local EMS numbers should be listed. 3. Helicopter flight plan. Before the mission, it should be ascertained that a helicopter is available and that there is an acceptable landing zone (LZ) for day or night conditions. This should include the exact global positioning system (GPS) coordinates of the LZ. Obstructions and debris should be cleared prior to the mission (Table 23-10 and Fig. 23-29). 4. Weather. Factors to be evaluated include temperature, rain, wind, humidity, wet-bulb temperature (TW), and windchill. Sunrise and sunset times should be recorded and logged. The TW is the lowest temperature to which air can be cooled by the evaporation of water into the air at a constant pressure, so it reflects the limit to which a person can shed heat

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

TABLE 23-9. Sample Form to Provide Operational Information Location Type of operation Other teams

Hostage # Tactical

Suspect # EMS/medics

Warrant # K9

TABLE 23-10. Sample Form for Helicopter Information Helicopter Landing zone (LZ)

Obstructions? LZ cleared prior to mission start? Address:

LZ coordinates Latitude Longitude

Figure 23-29. Air ambulance helicopter preparing for tactical casualty evacuation. (Courtesy Lawrence E. Heiskell, MD.)

through sweating in a hot environment. The TW is used to determine fluid requirements and the need for work–rest cycles. The weather-related components of the MTA are used to determine the appropriate uniform to wear and the shelter required to prevent overheating or hypothermia (Table 23-11). Water sources should be recorded prior to the mission as part of the MTA. 5. Plant and animal threats. Plant exposures, especially to poison ivy and poison oak, are common to snipers. Snakebites are common to team members working with police dogs. Anticipated animal threats should be recorded, along with telephone numbers for the police veterinarian, animal control, and poison control, including sources of antivenom (Table 23-12).

Forms and Documentation Medical records should be kept for the team and for anyone treated or evaluated as a TEMS patient. Records should be stored for a minimum of 10 years and have proved to be indispensable as defense documents in several antipolice liability lawsuits. Without a medical record, there is no proof that appropriate medical care was given.

Protection # Patrol

Open terrain search # Detective

Terrorist # FBI/other


THE TACTICAL MISSION Each mission has a number of phases55,94: 1. Warning order (issued when the tactical team is first requested, and establishes the situation and chain of command) 2. Gathering of intelligence a. Building intelligence (targets location and surrounding areas and includes avenues of approach, escape routes, and rally points, as well as natural and man-made obstacles, fields of fire, opportunities for cover and concealment) b. Suspect or hostage intelligence (as detailed as possible) c. Medical threat assessment (complete) 3. Operation order 4. Briefing phase a. Detailed planning b. Detailed briefing c. Equipment selection d. Move to staging 5. Execution phase a. Entry b. Secondary search c. Transfer to arrest team and investigation team d. End of mission 6. Debriefing phase a. All persons, weapons, equipment, injuries, shots fired, and ammunition must be accounted for. b. Any problems must be discussed. In general, a tactical mission follows this order, although it may differ somewhat between agencies and missions. Proper handling of each point is required in order for a mission to flow seamlessly. Without proper intelligence, a mission becomes hazardous.


RESERVE PROGRAMS The ways a tactical medical team is utilized by a law enforcement agency can differ widely, especially between the East Coast and the West Coast. For example, in the western United States, especially California, Arizona, Nevada, Washington, Utah, and Oregon, there are many reserve programs in the police and sheriff’s departments.63 In these programs, the tactical medical provider has additional, formal law enforcement training, such as found in the Peace Officer Standards of Training (POST) program in California. This program allows the provider to be a sworn peace officer, bringing about an enhanced comfort level for the department and potentially mitigating some issues of civil liability. On the East Coast, reserve opportunities are less common, and medical providers typically serve as auxiliary units borrowed from traditional fire and EMS agencies. The liability issues and expenses in this type of relationship are often resolved via a written “memorandum of understanding” between the participating agencies.82

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TABLE 23-11. Sample Form for Weather-Related Information Temp high Temp low Rain % Wind: MPH Humidity %

Wet-bulb temp H2O qt/hr Rest Min/Hr Cold casualties Heat casualties Uniform adjustments

90 2.0 40 Work cycles Yes/No Shelter: Y/N

Sunrise: AM Sunset: PM Night ops: Duration: Location:

TABLE 23-12. Animal and Plant Threats Animal Threats Yes/No Animals present? Yes/No Police dog? Yes/No # Types of animals Number: Do you anticipate wild animals? Poisonous snake exposure: Veterinarian address: Yes/No Animal Control: Poison Control: 973-470-2242 800-222-1222 Plant Threats Yes/No Exposure to poisonous plants likely? Yes Type No Tecnu or Ivy Block available? Yes No Uniform adjustments needed? Yes Recommendations: No

Yes/No

What type? Vet phone:

Selecting appropriate providers must be accomplished through interviews, psychological testing, background investigations, and physical fitness testing. The tactical team leaders should use a careful approach in the selection process for each candidate, just as they do for other members of the team.58


MILITARY COMBAT FIELD UNITS Field units vary significantly with the mission, service, and threat (Fig. 23-30). Most often, medical care is provided in the open, or in as secure a location as possible. It is done on the ground, on a table, in the back of a Humvee, or on an aircraft or a watercraft. Specific types of shelter and equipment are available, most often in the far-forward care under fire and the tactical field care phases, but generally the equipment is as noted earlier. When CBRN threats or high explosives are added to the scenario, the forward elements are the same, with the exception of the appropriately protective clothing. Once evacuation occurs, the injured team member is taken to a standard unit with the capability for decontamination and treatment, much as is done in the civilian setting. Most larger military transport planes have the capability to accept a critical care air transport team (CCATT), which has a physician trained in critical care (emergency medicine, anesthesiology, internal medicine), a critical care nurse, and a respiratory technician. Most larger Navy ships are equipped with fully functioning operating rooms and intensive care units, or they can expand to provide this service quickly. All the services have basic medical units, from the selfaid or buddy-aide, to an aid station (with a physician), to forward resuscitative systems (surgical and nonsurgical), to surgical companies, combat surgical hospitals, and their equiva-

Figure 23-30. Law enforcement tactical medical team during a training exercise. (Courtesy Lawrence E. Heiskell, MD.)

lents. All services also have teams that are available to move far forward to provide surgical capabilities quickly should the need arise. These units can operate on any semi-flat surface, do resuscitative surgery, and package the patient for expeditious transport for further care.13

Uniforms and Personal Protective Gear The standard military tactical operator carries between 40 and 60 pounds of equipment when heading into battle. For longer

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missions, gear is heavier. Clearly, the operator needs to be in excellent physical condition, and the mission commander must proactively manage nutrition, hydration, and exertion levels. From anecdotal reports, the military has seen a significant decrease in truncal injuries because body armor has improved. The medical personnel have noted that the insurgent combatants in Operation Iraqi Freedom have changed their IEDs to target the head, neck, and extremities more than the whole body. Continued development is underway to produce body armor that will protect against higher-energy weapons, protect extremities, and be lightweight and flexible enough to allow fieldwork. As protective clothing is not removed in the field, the medic must work under and around it. Vigilance is required to check all body areas for hidden wounds. This is clearly more difficult in the field, in the dark, with sound and light restrictions, and with clothing in place than when the patient is undressed on the trauma table. Because the medic carries all the usual combat equipment, medical equipment is additional. Stethoscopes are usually left behind, as the medic cannot use the earpieces under the helmet, the environment is not conducive to being able to hear anything, and the victim is usually wearing body armor. Advanced medical gear is usually found on the MedEvac vehicle, or further to the rear where it is safe enough to remove protective equipment and further evaluate and treat the patient.


EDUCATION AND

TRAINING PROGRAMS

Tremendous advancement in tactical medicine education over the last decade has resulted in numerous training programs, many providing formal continuing medical education (CME) credits. These courses focus on the core issues of tactical medicine. A unique aspect of tactical medicine is application of ALS in an austere environment. The traditional approach to providing EMS is often not feasible in a tactical situation.89 Cost-effective training is available and should be afforded to all involved medical personnel, including prehospital care providers and physicians, who should be trained to the highest level possible. Such training provides emergency medical personnel with an understanding of tactical procedures and an appreciation for why some routine prehospital care techniques may not be appropriate in the tactical environment.53,57 Tactical medicine training needs to be as realistic as possible with live teaching scenarios in full tactical gear. This allows the medical providers to more fully understand the unique aspects of law enforcement tactical operations and the roles and responsibilities of each team member, along with the integration and application of EMS. With an established body of knowledge and skills, graduates of such training programs are better prepared to effectively perform as safe tactical medical providers.64 The International School of Tactical Medicine, a law enforcement agency program, is based at the Palm Springs Police Department Training Center in Palm Springs, California. This school has conducted high-quality realistic tactical medical training courses since 1996 and offers a 2-week, 80-hour program. The training and educational courses are designed for the U.S. military and federal and local law enforcement agencies to enhance their provision of medical care in the tactical environment. The standard curriculum for each course can be seen in Tables 23-13 and 23-14. Both the basic and advanced

TABLE 23-13. Sample Curriculum for Basic Tactical Medicine (BTM) Training Day 1

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Introduction to Tactical Medicine Tactical Medical Equipment Tactical Equipment Team Concepts and Planning Slow and Deliberate Team Movement Introduction to Tactical Pistol Medical Aspects of Chemical Agents and Distraction Devices Forced Entry Techniques Dynamic Clearing Techniques Operational Casualty Care Wound Ballistics Hemostatic Techniques and Dressings Team Health Management Medical Aspects of Clandestine Drug Labs Tactical Medical Scenarios Introduction to MP5 Submachine Gun Special Operations Aeromedical Evacuation Medical Management of K-9 Emergencies Disguised Weapons and Street Survival Medical Threat Assessment Written Exam Safety Briefing Tactical Medical Scenarios

From International School of Tactical Medicine, copyright 1996–2005 (see www.tacticalmedicine.com).

courses offer category 1 CME credit through the American College of Emergency Physicians. The school is approved by the State of California Commission on Peace Officer Standards and Training (POST) (see www.tacticalmedicine.com). The Tactical EMS School of Columbia, Missouri, offers two TEMS educational programs. The Essentials of Tactical EMS is the basic entry-level course. The Tactical EMS Field Operations course is designed to augment the training offered in the essentials course and is scenario-based teaching with a focus on casualty care in the tactical environment (see www.tacticalspecialties.com). The Counter Narcotics Tactical Operations Medical Support program (CONTOMS) at the Casualty Care Research Center (CRC) is a multidisciplinary injury-control research and training facility in Bethesda, Maryland. It is based in the Department of Homeland Security, Federal Protective Service, Special Operations Division, forming the Protective Medicine Branch (see www.casualtycareresearchcenter.org).


THE FUTURE OF

TACTICAL MEDICINE

Tactical medicine will continue to grow as a medical discipline, and emergency medicine is the ideal specialty to lead its development. Since the fall of 2002, under leadership of the International Tactical EMS Association (ITEMS), a multidisciplinary group of subject matter experts has been working to achieve consensus on development of a standardized national curriculum for tactical medicine training.19 Emergency medicine residents and surgeons with no special interest in participating in tactical medicine should have an understanding of this discipline, as they may well have the opportunity to treat an injured

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TABLE 23-14. Sample Curriculum for Advanced Tactical Medicine (ATM) Training Day 1

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Pediatric Trauma Management Trauma Anesthesia Building Clearing Techniques Review Tactical Medical Scenarios Range Advanced Pistol–MP5 Advanced Airway Management Advanced Airway Management Skills Stations Environmental Injuries WMD Biological Weapons Part 1 WMD Biological Weapons Part 2 Medical Issues of Less-Lethal Weapons Low Light Tactics and Team Movement Tactical Medical Scenarios Pistol–MP5 Field Courses Explosive Entry Demonstrations Medical Management of Blast Injuries WMD Chemical Weapons WMD Nuclear and Radiation Injuries Written Exam Safety Briefing Tactical Medical Scenarios

From International School of Tactical Medicine, copyright 1996–2005 (see www.tacticalmedicine.com).

operator or victim of violence associated with a tactical law enforcement action.24,40 There is a need for research into the unique aspects of civilian tactical medicine, such as injury prevention during operations, methods of ensuring optimal mental and physical preparedness for tactical operators, and evaluation of various standard EMS therapies for their feasibility and efficacy in tactical scenarios.

Figure 23-31. Tactical medics provide medical support under any and all operative conditions. (Courtesy Lawrence E. Heiskell, MD.)

Tactical medicine is wilderness medicine taking place in both the urban environment and some of the most remote places on earth. In these times, when the threat of violence to civilians in our society is at its greatest, we rely on our law enforcement professionals and the military to do all they can to keep us safe and protected. It is the role of tactical medics, providing medical care under any and all operative conditions (Fig. 23-31), to give back to these professionals by ensuring that someone is there to care for them if they are injured in the course of doing their duty. The references for this chapter can be found on the accompanying DVD-ROM.

Wilderness Orthopaedics Julie A. Switzer, Thomas J. Ellis, and Marc F. Swiontkowski

Musculoskeletal and soft tissue injuries account for 70% to 80% of injuries that occur in a wilderness setting.4,10 Being able to identify and provide initial, acute treatment of the most common types of injury is particularly important. In the initial management of a musculoskeletal injury, the following must be considered: the etiology and time of the injury, the direction of the causative force in relation to the individual or limb, and the environment where the accident occurred. These factors may indicate the severity of the injury and help determine examina-

24

tion and treatment priorities that can affect outcome. Special considerations for injuries to the skeletal system that occur in the wilderness include the effect of weather (exposure to wind, cold, or heat), lack of usual devices for stabilization of bone or joint injuries, and increased time to initiation of a victim’s definitive care. Stabilization of a victim’s cardiovascular and pulmonary status is critical. Once this has been accomplished, examination of the musculoskeletal system should be undertaken in a sys-

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TABLE 23-14. Sample Curriculum for Advanced Tactical Medicine (ATM) Training Day 1

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Pediatric Trauma Management Trauma Anesthesia Building Clearing Techniques Review Tactical Medical Scenarios Range Advanced Pistol–MP5 Advanced Airway Management Advanced Airway Management Skills Stations Environmental Injuries WMD Biological Weapons Part 1 WMD Biological Weapons Part 2 Medical Issues of Less-Lethal Weapons Low Light Tactics and Team Movement Tactical Medical Scenarios Pistol–MP5 Field Courses Explosive Entry Demonstrations Medical Management of Blast Injuries WMD Chemical Weapons WMD Nuclear and Radiation Injuries Written Exam Safety Briefing Tactical Medical Scenarios

From International School of Tactical Medicine, copyright 1996–2005 (see www.tacticalmedicine.com).

operator or victim of violence associated with a tactical law enforcement action.24,40 There is a need for research into the unique aspects of civilian tactical medicine, such as injury prevention during operations, methods of ensuring optimal mental and physical preparedness for tactical operators, and evaluation of various standard EMS therapies for their feasibility and efficacy in tactical scenarios.

Figure 23-31. Tactical medics provide medical support under any and all operative conditions. (Courtesy Lawrence E. Heiskell, MD.)

Tactical medicine is wilderness medicine taking place in both the urban environment and some of the most remote places on earth. In these times, when the threat of violence to civilians in our society is at its greatest, we rely on our law enforcement professionals and the military to do all they can to keep us safe and protected. It is the role of tactical medics, providing medical care under any and all operative conditions (Fig. 23-31), to give back to these professionals by ensuring that someone is there to care for them if they are injured in the course of doing their duty. The references for this chapter can be found on the accompanying DVD-ROM.

Wilderness Orthopaedics Julie A. Switzer, Thomas J. Ellis, and Marc F. Swiontkowski

Musculoskeletal and soft tissue injuries account for 70% to 80% of injuries that occur in a wilderness setting.4,10 Being able to identify and provide initial, acute treatment of the most common types of injury is particularly important. In the initial management of a musculoskeletal injury, the following must be considered: the etiology and time of the injury, the direction of the causative force in relation to the individual or limb, and the environment where the accident occurred. These factors may indicate the severity of the injury and help determine examina-

24

tion and treatment priorities that can affect outcome. Special considerations for injuries to the skeletal system that occur in the wilderness include the effect of weather (exposure to wind, cold, or heat), lack of usual devices for stabilization of bone or joint injuries, and increased time to initiation of a victim’s definitive care. Stabilization of a victim’s cardiovascular and pulmonary status is critical. Once this has been accomplished, examination of the musculoskeletal system should be undertaken in a sys-

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PART FOUR: INJURIES AND MEDICAL INTERVENTIONS

tematic manner. Careful initial attention should be devoted to