Wilderness Medicine 4th edition (February 15, 2001) by Paul S. Auerbach (Editor) By Mosby
By OkDoKeY
Auerbach: Wilderness Medicine, 4th ed.,Copyright © 2001 Mosby, Inc. Frontmatter Title Page Copyright Page Contributors Foreword Preface Part 1 - Mountain Medicine Part 2 - Cold and Heat Part 3 - Fire, Burns, and Radiation Part 4 - Injuries and Medical Interventions Part 5 - Rescue and Survival Part 6 - Insects, Animals, and Zoonoses Part 7 - Plants Part 8 - Food and Water Part 9 - Marine Medicine Part 10 - Travel, Environmental Hazards, and Disasters Part 11 - Equipment and Special Knowledge Part 12 - Special Populations and Considerations Appendix: Drug Stability Information
Part 1 - Mountain Medicine 1 - High-Altitude Medicine 2 - Avalanches 3 - Lightning Injuries
Part 2 - Cold and Heat 4 - Thermoregulation 5 - Nonfreezing Cold Injuries 6 - Accidental Hypothermia 7 - Frostbite 8 - Immersion into Cold Water 9 - Polar Medicine 10 - Pathophysiology of Heat-Related Illnesses 11 - Clinical Management of Heat-Related Illnesses
Part 3 - Fire, Burns, and Radiation 12 - Wildland Fires: Dangers and Survival 13 - Emergency Care of the Burned Victim 14 - Exposure to Radiation from the Sun
Part 4 - Injuries and Medical Interventions 15 - Wilderness Injury Prevention 16 - Principles of Pain Management 17 - Emergency Airway Management 18 - Wilderness Trauma and Surgical Emergencies 19 - Wilderness Improvisation 20 - Hunting and Other Weapons Injuries 21 - Orthopedics 22 - The Eye in the Wilderness 23 - Dental and Facial Emergencies
Part 5 - Rescue and Survival
24 - Wilderness Emergency Medical Services and Response Systems
25 - Search and Rescue
26 - Litters and Carries
27 - Aeromedical Transport
28 - Wilderness Survival
29 - Jungle Travel and Survival
30 - White-Water Medicine and Rescue
31 - Cave Rescue
Part 6 - Insects, Animals, and Zoonoses 32 - Protection from Blood-Feeding Arthropods 33 - Tick-Borne Diseases 34 - Spider Bites 35 - Scorpion Envenomation 36 - North American Arthropod Envenomation and Parasitism 37 - Non-North American Arthropod Envenomation and Parasitism 38 - North American Venomous Reptile Bites 39 - Non-North American Venomous Reptile Bites 40 - Antivenins and Immunobiologicals: Immunotherapeutics of Envenomation 41 - Bites and Injuries Inflicted by Domestic Animals 42 - Bites and Injuries Inflicted by Wild Animals 43 - Bear Attacks 44 - Wilderness-Acquired Zoonoses 45 - Emergency Veterinary Medicine
Part 7 - Plants 46 - Seasonal Allergies 47 - Plant-Induced Dermatitis 48 - Toxic Plant Ingestions 49 - Mushroom Toxicity 50 - Ethnobotany: Plant-Derived Medical Therapy
Part 8 - Food and Water 51 - Field Water Disinfection 52 - Infectious Diarrhea from Wilderness and Foreign Travel 53 - Nutrition, Malnutrition, and Starvation 54 - Seafood Toxidromes 55 - Seafood Allergies
Part 9 - Marine Medicine 56 - Submersion Incidents 57 - Diving Medicine 58 - Emergency Oxygen Administration 59 - Principles of Hyperbaric Oxygen Therapy 60 - Injuries from Nonvenomous Aquatic Animals 61 - Envenomation by Aquatic Invertebrates 62 - Envenomation by Aquatic Vertebrates 63 - Aquatic Skin Disorders 64 - Survival at Sea
Part 10 - Travel, Environmental Hazards, and Disasters 65 - Travel Medicine 66 - Non-North American Travel and Exotic Diseases 67 - Natural Disaster Management 68 - Natural and Human-Made Hazards: Mitigation and Management Issues
Part 11 - Equipment and Special Knowledge 69 - Wilderness Preparation, Equipment, and Medical Supplies 70 - Selection and Use of Outdoor Clothing 71 - Backcountry Equipment for Health Care Professionals 72 - Ropes and Knot Tying 73 - Wilderness Navigation Techniques
Part 12 - Special Populations and Considerations 74 - Children in the Wilderness 75 - Women in the Wilderness 76 - Elders in the Wilderness 77 - Medical Liability and Wilderness Medicine 78 - Ethics of Wilderness Medicine 79 - The Changing Environment
Appendix: Drug Stability Information Acetaminophen (Elixir, Drops, Tablets) Acetaminophen with Codeine (Tablets, Elixir) Acetazolamide (Capsules, Tablets, Oral Solution, Injection) Acetic Acid Solution Albuterol (Tablets, Syrup, Inhaled Formulations) Aloe (Gel, Ointment, Laxatives) Aluminum Acetate (Otic and Topical Preparations) Antacids Aspirin (Tablets, Oral Solution, Suppositories) Atropine Injection Azithromycin (Tablets, Capsules, Suspension, Injection) Bacitracin (Topical, Injection) Bismuth Subsalicylate (Tablets, Suspension) Butorphanol Tartrate (Injection, Nasal Solution) Calcium Chloride Injection Cephalexin (Capsules, Tablets, Oral Suspension) Cetriazone Injection Charcoal, Activated Ciprofloxacin (Capsules, Tablets, Injection) Cyclopentolate Hydrochloride Ophthalmic Solution DEET-Containing (Diethyl Methylbenzamide) Insect Repellents Dermabond (2-Octyl Cyanoacrylate) Topical Skin Adhesive Dexamethasone Injection Dextroamphetamine (Tablets, Elixir, Capsules) Dextrose (Oral, Injection) Diazepam (Injection, Capsules, Tablets) Digoxin Injection Diltiazem (Capsules, Oral Solution, Injection) Diphenhydramine (Tablets, Elixir, Injection) Domeboro (Astringent and Otic Solutions) Dopamine Hydrochloride Injection Doxycycline (Capsules, Tablets, Syrup, Suspension, Injection) Epinephrine Injection (Salts, Solutions) Erythromycin (Tablets, Suspensions, Topical, Injection) Estazolam Tablets Fluocinolone Acetonide and Fluocinonide (Ointment, Shampoo) Furazolidone (Tablets, Liquid) Furosemide (Oral Formulation, Injection) Gamma Benzene Hexachloride (Lotion, Shampoo) Glucagon Injection Hydrocortisone (Tablets, Suspension, Topical Cream, Injection) Hydroxypropyl Methylcellulose Topical Ocular Solution Ibuprofen Tablets Intravenous Solutions (D5W, D5NS, etc.) Ketoconazole (Shampoo, Tablets) Lidocaine Injection Loperamide Hydrochloride Capsules Lorazepam (Tablets, Injection) Mannitol Injection Meperidine Hydrochloride (Injection, Oral Solutions) Midazolam (Injection, Oral Solution) Morphine Sulfate (Injection, Solution, Soluble Tablets) Nalbuphine Hydrochloride Injection Naloxone Hydrochloride Injection Neosporin Ointment Nifedipine (Capsules, Tablets, Injection) Nitroglycerin (Sublingual Tablets, Spray, Topical, Injection) Norfloxacin (Tablets, Ophthalmic Solution) Ofloxacin (Tablets, Otic Solution, Injection) Penicillin GK Injection Phenobarbital Injection Phenylephrine (Nasal/Ophthalmic Solutions, Injection) Phenytoin (Tablets, Injection) Polysporin Ointment Potassium Permanganate Astringent Solution
Povidone-Iodine Solution Prednisone (Tablets, Oral Solution, Suspension) Procaine Penicillin G Injection Prochlorperazine (Injection, Solution, Tablets, Capsules) Promethazine (Injection, Tablets, Solution, Suppositories) Pseudoephedrine, Pseudoephedrine/Triprolidine (Tablets, Capsules) Sodium Bicarbonate Injection Sodium Sulfacetamide (Ophthalmic Solution and Ointment) Temazepam Capsules Tetanus Toxoid Injection Tetracaine Hydrochloride Ophthalmic Solution and Topical Lidocaine/Epinephrine/Tetracaine (LET) Tetracycline (Tablets, Topical Solution, Injection) Tolnaftate Topical Antifungal Triazolam Tablets Trimethoprim/Sulfamethoxazole (Tablets, Suspensions, Injection) Zinc Salts ACKNOWLEDGMENTS SUGGESTED READINGS
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WILDERNESS MEDICINE
FOURTH EDITION PAUL S. AUERBACH MD, MS Clinical Professor of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California; Venture Partner, Delphi Ventures, Menlo Park, California
with 1248 illustrations Mosby A Harcourt Health Sciences Company St. Louis • London • Philadelphia • Sydney • Toronto
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Mosby A Harcourt Health Sciences Company Acquiring Editor: Judith Fletcher Senior Managing Editor: Kathy Falk Project Manager: Carol Sullivan Weis Senior Production Editor: Rick Dudley Designer: Mark A. Oberkrom Cover Photograph: Paul S. Auerbach FOURTH EDITION Copyright © 2001 by Mosby, Inc. Copyright © 2001 Chapter 29 by John Walden Copyright © 2001 Chapter 43 by Steven P. French Copyright © 2001 Chapter 64 by Michael E. Jacobs Previous editions copyrighted 1983, 1989, 1995 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission of the publisher. NOTICE Pharmacology is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. Permission to photocopy or reproduce solely for internal or personal use is permitted for libraries or other users registered with the Copyright Clearance Center, provided that the base fee of $4.00 per chapter plus $.10 per page is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA, 01923. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collected works, or for resale. Mosby, Inc. A Harcourt Health Sciences Company 11830 Westline Industrial Drive St. Louis, Missouri 63146 Printed in the United States of America International Standard Book Number ISBN 0-323-00950-6 01 02 03 04 05 TG/KPT 9 8 7 6 5 4 3 2 1
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Contributors
Javier A. Adachi MD Fellow, Department of Infectious Diseases, Center for Infectious Disease, The University of Texas-Houston Medical School and School of Public Health, Houston, Texas; Universidad Peruana Cayetano Heredia, Lima, Peru Michele Adler BPharm, Cert. Hoft. Hons. Post. Grad. Dip. Ed. Lecturer in Horticulture, Horticultural Consultant, University of Melbourne-Burnley College, Richmond, Victoria, Australia Robert C. Allen DO, FACEP Lt. Col. USAF, Group Surgeon, 720th Special Tactics Group, Air Force Special Operations Command, Hurlburt Field, Florida Christopher J. Andrews BE, MBBS, MEngSc, PhD, DipCSc, EDIC Clinical Associate Lecturer, University of Queensland, St. Lucia, Queensland, Australia; Registrar in Anaesthesia, The Mater Hospital, South Brisbane, Queensland, Australia Betsy R. Armstrong MA Chief Operating Officer, Women of the West Museum, Denver, Colorado Richard L. Armstrong Senior Research Scientist, Cooperative Institute for Research in Environmental Sciences, National Snow and Ice Data Center, University of Colorado, Boulder, Colorado E. Wayne Askew PhD Professor, Division of Foods and Nutrition, College of Health, University of Utah, Salt Lake City, Utah Dale Atkins BA Geography Avalanche Scientist and Forecaster, Colorado Avalanche Information Center, Boulder, Colorado Paul S. Auerbach MD, MS Clinical Professor of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California; Venture Partner, Delphi Ventures, Menlo Park, California Howard D. Backer MD, MPH Emergency Department, Kaiser Permanente Medical Center, Hayward, California; Currently, Medical Consultant and Epidemiologist, Immunization Branch, Division of Communicable Disease Control,
California Department of Health Services James P. Bagian BSME, MD Clinical Assistant Professor of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, Texas; Adjunct Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F. Edward Hebert School of Medicine, Bethesda, Maryland; Director, National Center for Patient Safety, Veterans Health Administration, Ann Arbor, Michigan; Colonel, U.S. Air Force Reserve 920th Rescue Group, Patrick Air Force Base, Florida H. Bernard Bechtel MD Staff, South Georgia Medical Center, Valdosta, Georgia Greta J. Binford PhD Research Associate, Department of Biochemistry and Center for Insect Sciences, University of Arizona, Tucson, Arizona
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Warren D. Bowman Jr. MD, FACP Clinical Associate Professor of Medicine Emeritus, University of Washington School of Medicine, Seattle, Washington; National Medical Director Emeritus, National Ski Patrol System, Denver, Colorado; Past President, Wilderness Medical Society, Colorado Springs, Colorado Leslie V. Boyer MD Assistant Professor, Department of Pediatrics, University of Arizona Health Sciences Center; Medical Director, Arizona Poison and Drug Information Center, Tucson, Arizona George Braitberg MBBS, FACEM Senior Fellow, Department of Medicine, Director of Emergency Medicine, Consultant Medical Toxicologist, University of Melbourne, Parkville, Victoria, Australia; Consultant Medical Toxicologist, National Poison Centre, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia Robert K. Bush MD Professor of Medicine, University of Wisconsin-Madison; Chief of Allergy, William S. Middleton VA Hospital, Madison, Wisconsin Sean P. Bush MD, FACEP Staff Emergency Physician and Venom Specialist, Associate Professor of Emergency Medicine, Loma Linda University Medical Center and School of Medicine, Loma Linda, California Frank K. Butler Jr. MD Director of Biomedical Research, U.S. Naval Special Warfare Command; Attending Ophthalmologist, Naval Hospital Pensacola, Pensacola, Florida Michael L. Callaham MD, FACEP Chief, Division of Emergency Medicine,
Professor of Emergency Medicine, University of California, San Francisco, San Francisco, California Steven C. Carleton MD, PhD Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine; Medical Director, University Air Care, University Hospital, Inc., Cincinnati, Ohio Betty Carlisle MD Emergency Physician, South Bend, Washington Richard F. Clark MD Associate Professor of Medicine, University of California, San Diego; Director, Division of Medical Toxicology, Department of Emergency Medicine, University of California, San Diego Medical Center, San Diego, California Loui H. Clem Littleton, Colorado David A. Connor MD Clinical Toxicologist, Department of Medical Toxicology, Good Samaritan Regional Medical Center, Phoenix, Arizona Donald C. Cooper BS, MS, MBA, NREMT-P Deputy Fire Chief, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio Mary Ann Cooper MD Associate Professor, Department of Emergency Medicine, University of Illinois at Chicago, Chicago, Illinois Larry I. Crawshaw PhD Professor, Department of Biology, Portland State University; Professor, Behavioral Neuroscience, Oregon Health Sciences University, Portland, Oregon Barbara D. Dahl MD Attending Physician, Kaiser Santa Clara Emergency Department, Stanford/Kaiser Emergency Medicine Residency Program, Santa Clara, California; Department of Emergency Medicine, St. Rose Hospital, Hayward, California
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Daniel F. Danzl MD Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky Richard C. Dart MD, PhD Associate Professor of Surgery, Medicine and Pharmacy, University of Colorado Health Sciences Center; Director, Rocky Mountain Poison and Drug Center, Denver Health Authority, Denver, Colorado
Kathleen Mary Davis BS Forestry, MS Forestry Chief, Natural Resources, Southern Arizona Office, National Park Service, Phoenix, Arizona Kevin Jon Davison ND, LAc Maui East-West Clinic, Ltd., Haiku, Maui, Hawaii Anne E. Dickison MD Clinical Associate Professor of Anesthesiology and Pediatrics, University of Florida College of Medicine; Faculty Pediatric Intensivist and Anesthesiologist, Shands Teaching Hospital at the University of Florida, Gainesville, Florida Mark Donnelly MD Resident, Department of Emergency Medicine, University of Rochester Medical Center, Rochester, New York Howard J. Donner MD Clinic Physician, Telluride Medical Center, Telluride, Colorado Herbert L. DuPont MD Chief, Internal Medicine Service, St. Luke's Episcopal Hospital; H. Irving Schweppe, Jr., M.D. Chair in Internal Medicine; Vice Chairman, Department of Internal Medicine, Baylor College of Medicine; Mary W. Kelsey Professor of Medical Sciences, The University of Texas Health Sciences Center at Houston, Houston, Texas Thomas J. Ellis MD Director of Orthopedic Trauma, Assistant Professor, Oregon Health Sciences University, Portland, Oregon John H. Epstein MD, MS Clinical Professor of Dermatology, Department of Dermatology, University of California, San Francisco, San Francisco, California William L. Epstein MD Professor of Dermatology, Emeritus, University of California, San Francisco, San Francisco, California Blair D. Erb MD Past President, Wilderness Medical Society, Colorado Springs, Colorado; The Study Center; Jackson-Madison County General Hospital, Jackson, Tennessee Timothy B. Erickson MD Director, Emergency Medicine Residency Program, Director, Division of Clinical Toxicology, Associate Professor, University of Illinois at Chicago, Chicago, Illinois Murray E. Fowler DVM Professor Emeritus, Zoological Medicine, University of California School of Veterinary Medicine, Davis, California Mark S. Fradin MD
Clinical Associate Professor, Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina Bryan L. Frank MD Senior Clinical Instructor, Medical Acupuncture for Physicians Program, Continuing Education Office, University of California, Los Angeles School of Medicine; President, American Academy of Medical Acupuncture, Los Angeles, California; President, Integrated Medicine Seminars, L.L.C., Richardson, Texas
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Luanne Freer MD Clinical Assistant Professor of Emergency Medicine, George Washington University, Washington, D.C.; Chief of Staff, Yellowstone Park Medical Services, Yellowstone National Park, Wyoming; Emergency Physician, Bozeman, Montana, Idaho Falls, Idaho Steven P. French MD Research Director, Yellowstone Grizzly Foundation, Jackson Hole, Wyoming; Member, Bear Specialists Group, World Conservation Union; ER Medical Director (Retired) Stephen L. Gaffin PhD Research Physiologist, Thermal and Mountain Medicine, U.S. Army Research Institute of Environmental Medicine, Natick, Massachussetts Douglas A. Gentile MD, MBA Attending Physician, University of Vermont College of Medicine, Burlington, Vermont Gordon G. Giesbrecht PhD Professor, Health, Leisure and Human Performance Research Institute; Associate Professor, Department of Anesthesia, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada Philip H. Goodman MD, MS, FACP Professor of Medicine, Chief, Division of General Internal Medicine and Health Care Research, University of Nevada School of Medicine, Reno, Nevada John Gookin Curriculum Manager, Senior Staff Instructor, The National Outdoor Leadership School (NOLS), Lander, Wyoming; Associate Faculty, University of Utah, Salt Lake City, Utah Kimberlie A. Graeme MD Clinical Assistant Professor, Section of Toxicology, Division of Emergency Medicine, Department of Surgery, University of Arizona College of Medicine, Tucson, Arizona; Fellowship Director, Department of Medical Toxicology,
Good Samaritan Regional Medical Center, Phoenix, Arizona; Attending Physician, Mayo Clinic Hospital, Scottsdale, Arizona Peter H. Hackett MD Affiliate Associate Professor, Department of Medicine, University of Washington School of Medicine, Seattle, Washington; Emergency Department, St. Mary's Medical Center, Grand Junction, Colorado Murray P. Hamlet DVM Chief, Research Programs and Operations Division, U.S. Army Research Institute of Environmental Medicine, Natick, Massachusetts Susan L. Hefle PhD Assistant Professor, Department of Food Science and Technology, University of Nebraska, Lincoln, Nebraska John P. Heggers PhD, FAAM, CWS (AAWM) Professor, Surgery (Plastic), ILT-UTMB Medical School, University of Texas Medical Branch; Director of Clinical Microbiology, Directory of Microbiology Research, Shriners Burns Institute, Galveston, Texas David Heimbach MD Professor of Surgery, University of Washington School of Medicine, Seattle, Washington Henry J. Herrmann DMD, FAGD Private Practice, Falls Church, Virginia Ronald L. Holle MS Meteorologist, Global Atmospherics, Inc., Tucson, Arizona
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Rivkah S. Horowitz MD, PhD Clinical Assistant Professor of Medicine, Brown University School of Medicine, Providence, Rhode Island; Attending Physician, Lawrence and Memorial Hospital, New London, Connecticut Frank R. Hubbell DO Clinical Instructor, University of New England College of Osteopathic Medicine, Biddeford, Maine Steve Hudson President, Pigeon Mountain Industries, Inc., LaFayette, Georgia Kenneth V. Iserson MD, MBA Professor of Surgery, University of Arizona College of Medicine; Director, Arizona Bioethics Program, University of Arizona, Tucson, Arizona Michael E. Jacobs MD Private Practice in Internal Medicine and Gastroenterology; United States Coast Guard Licensed Captain; Professional Sailor,
Martha's Vineyard, Massachussetts Elaine C. Jong MD Clinical Professor of Medicine, Director, Hall Health Primary Care Center/University of Washington Student Health Service, University of Washington School of Medicine, Seattle, Washington Lee A. Kaplan MD Associate Clinical Professor of Medicine/Dermatology, University of California, San Diego, San Diego, California; Private Practice in Dermatology, Dermatologist Medical Group, La Jolla, California James W. Kazura MD Professor, Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio Barbara C. Kennedy MD Assistant Professor, University of Vermont College of Medicine; Attending Physician, Fletcher Allen Health Care, Burlington, Vermont Sean Keogh MRCP, FRCSEd, FACEM, FFAEM Consultant, Emergency Medicine, Auckland Hospital, Auckland, New Zealand Kenneth W. Kizer MD, MPH Distinguished Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; President and Chief Executive Officer, The National Quality Forum, Washington, D.C. Judith R. Klein MD Resident, Emergency Medicine, Stanford University, Stanford, California Donald B. Kunkel MD (deceased) Associate in Pharmacology and Toxicology, Health Sciences Center, University of Arizona, Tucson, Arizona; Medical Director, Samaritan Regional Poison Center, Samaritan Regional Medical Center, Phoenix, Arizona Jason E. Lang MD Clinical Instructor, University of Vermont College of Medicine; Chief Resident in Pediatrics, Fletcher Allen Health Care; Burlington, Vermont Carolyn S. Langer MD, JD, MPH Instructor in Occupational Medicine, Lecturer in Occupational Health Law, Harvard School of Public Health, Boston, Massachusetts Patrick H. LaValla President, ERI International, Olympia, Washington
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Raúl E. López PhD Research Meteorologist (Retired), National Severe Storms Laboratory,
National Oceanic and Atmospheric Administration, Norman, Oklahoma Roberta A. Mann MD Medical Director, Torrance Memorial Burn Center and Wound Healing Center, Torrance Memorial Medical Center, Torrance, California Ariel D. Marks MD, MS, FACEP Staff Physician, Emergency Department, Sequoia Hospital, Redwood City, California Vicki Mazzorana MD, FACEP Clinical Assistant Professor of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California Robert L. McCauley MD Professor of Surgery and Pediatrics, University of Texas Medical Branch; Chief, Plastic and Reconstructive Surgery, Shriners Burns Institute, Galveston, Texas Jude T. McNally RPh, ABAT Managing Director, Arizona Poison and Drug Information Center, University of Arizona College of Pharmacy, Tucson, Arizona James Messenger Lieutenant, EMT-P, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio; Rescue Specialist, F.E.M.A. Ohio Task Force 1 (OH TF-1) Timothy P. Mier BA Lieutenant, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio Sherman A. Minton MD (deceased) Professor Emeritus, Microbiology & Immunology, Indiana University School of Medicine, Indianapolis, Indiana; Research Associate, Department of Herpetology, American Museum of Natural History, New York, New York James K. Mitchell PhD Professor of Geography, Rutgers University, Piscataway, New Jersey Daniel S. Moran PhD Visiting Lecturer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Head, Physiology Unit, Heller Institute of Medical Research, Chaim Sheba Medical Center, Tel Hashomer, Israel John A. Morris Jr. MD Professor of Surgery, Director, Division of Trauma, Vanderbilt University School of Medicine, Nashville, Tennessee Robert W. Mutch BA, MSF Fire Management Consultant, Fire Management Applications, Missoula, Montana
Andrew B. Newman MD, FCCP Clinical Associate Professor of Medicine, Stanford University School of Medicine, Stanford, California Eric K. Noji MD, MPH Chief, Epidemiology, Surveillance and Emergency Response Branch, Bioterrorism Preparedness and Response Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia Robert L. Norris Jr. MD Associate Professor of Surgery/Emergency Medicine, Stanford University School of Medicine; Chief, Division of Emergency Medicine, Stanford University Hospital, Stanford, California
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Edward J. Otten MD, FACMT Professor of Emergency Medicine and Pediatrics, Director, Division of Toxicology, University of Cincinnati, Cincinnati, Ohio Naresh J. Patel DO Fellow, Allergy/Immunology, Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin Claude A. Piantadosi MD Professor, Department of Medicine (Pulmonary), Duke University Medical Center, Durham, North Carolina Richard N. Rausch PhD Postdoctoral Fellow, Department of Biology, Portland State University, Portland, Oregon Sheila B. Reed MS Education Consultant, International Disaster Management, Middleton, Wisconsin Robert C. Roach PhD Research Associate Professor, New Mexico Highlands University, Las Vegas, New Mexico; Director, The Hypoxia Institute, Montezuma, New Mexico Martin C. Robson MD Professor of Surgery, Division of Plastic Surgery, Department of Surgery, University of South Florida, Tampa, Florida Sandra Schneider MD Professor and Chair, Department of Emergency Medicine, University of Rochester; Strong Memorial Hospital, Rochester, New York Bern Shen MD, MPhil Institute for Health Policy Studies, University of California, San Francisco, San Francisco, California David J. Smith Jr. MD Professor and Section Head, Department of Plastic Surgery, University of Michigan Medical Center,
Ann Arbor, Michigan Alan M. Steinman MD, MPH Fellow, American College of Preventive Medicine; Board of Directors, Marine Safety Foundation Robert C. Stoffel President, Emergency Response International, Inc., Cashmere, Washington Jeffrey R. Suchard MD Assistant Clinical Professor of Medicine, Division of Emergency Medicine, University of California, Irvine Medical Center, Orange, California Mark F. Swiontkowski MD Professor and Chairman, Department of Orthopaedics, University of Minnesota, Minneapolis, Minnesota Eric A. Toschlog MD Division of General Surgery, Department of Surgery, East Carolina University, The Brody School of Medicine, Greenville, North Carolina Kenneth F. Trofatter Jr. MD, PhD 3M Clinical Professor, Department of Obstetrics, Gynecology, and Women's Health, University of Minnesota Medical School, Minneapolis, Minnesota Karen B. Van Hoesen MD Assistant Clinical Professor, Department of Emergency Medicine; Director, Diving Medicine Center; Director, Hyperbaric Medicine Fellowship, University of California, San Diego, San Diego, California John Walden MD, DTM&H Professor and Associate Dean for Development and Outreach, Marshall University Joan C. Edwards School of Medicine, Huntington, West Virginia
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Kimberley P. Walker MA, NREMT-P, CHT Manager of Corporate Systems Education, Department of Information Technology, Duke University Medical Center; Trainer, Divers Alert Network, Durham, North Carolina Helen L. Wallace BS Research Associate, Department of Biology, Portland State University, Portland, Oregon Eric A. Weiss MD Assistant Professor of Emergency Medicine, Stanford University School of Medicine; Associate Director of Trauma, Stanford University Medical Center, Stanford, California Eric L. Weiss MD, DTM&H Assistant Professor, Emergency Medicine and Infectious Diseases, Director, Stanford Travel Medicine Service, Stanford University School of Medicine, Stanford, California; Chief Medical Officer,
Medicine Planet, Inc. Knox Williams MS Atmospheric Science Fort Collins, Colorado Sarah R. Williams MD Emergency Medicine Ultrasound Fellow, Chief Resident, Clinical Instructor of Surgery, Attending Physician, Division of Emergency Medicine, Stanford University Medical Center, Stanford, California; Attending Physician, Emergency Department, Kiaser Santa Clara Medical Center, Santa Clara, California Ian J. Woolley MBBS, FRACP Senior Lecturer, Department of Medicine, Senior Staff Specialist, Infectious Diseases Unit, Alfred Hospital, Monash University; Director, Infection Control Units, Senior Staff Specialist, Infectious Diseases, Peninsula Health, Melbourne, Victoria, Australia Steven C. Zell MD Professor of Medicine, Division of General Internal Medicine and Health Care Research, University of Nevada School of Medicine, Reno, Nevada
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Foreword
"Everything to hope, with but little to fear" Food was scarce and the hunter was determined to bring back meat for his hungry friends. Thousands of bison swarmed over the prairie, and it did not take him long to shoot a fat male. As he watched the animal die, blood pouring from its mouth, he failed to see the grizzly bear until it was 20 steps away. He had no time to reload his clumsy gun, but could only retreat. There was no good place to hide—no trees, no bushes, only the nearby river. As soon as he turned, the bear charged after him, roaring open-mouthed and covering the ground with frightening speed. Fortunately, the riverbank was low and the hunter plunged into the water and turned to face the bear, hoping it would not follow. The bear rushed to within 20 feet, sized up the situation, turned away and ran off as fast as it had charged. Meriwether Lewis had just escaped with his life. The Lewis and Clark Expedition had been 11 months on the trail and was more than a thousand miles from its base. There was no contact with the outside world and no possibility of help. Supplies of food had run low, and the group depended on their hunters for meat. The native population had not always been friendly. The explorers could not speak the local languages and relied on interpreters. Attacks by ferocious animals were a daily danger. On June 16, 1804, 2 days after the bear attack, a critical point was reached in their journey. The outcome would not depend on their hunting skills and luck but on their medical knowledge. The leaders described the situation later in their diaries: June 12, 1805: The interpreter's woman very sick. One man has a felon rising on his hand; the other, with the toothache, has taken a cold in the jaw, &c. (Clark) June 13, 1805: A fair morning. Some dew this morning. The Indian woman very sick. I gave her a dose of salts. We set out early. (Clark) June 14, 1805: A fine morning. The Indian woman complaining all night, and excessively bad this morning. Her case is somewhat dangerous. Two men with the toothache, two with tumors, and one with a tumor and light fever. (Clark) June 15, 1805: Our Indian woman sick and low spirited. I gave her the bark and applied it externally to her region, which revived her much. (Clark) June 16, 1805: Found the Indian woman extremely ill and much reduced by her indisposition. This gave me some concern, as well for the poor object herself—then with a young child in her arms—as from the consideration of her being our only dependence for a friendly negotiation with the Snake Indians, on whom we depend for horses to assist us in our portage from the Missouri to the Columbia River. (Lewis)
Sacagawea, a 17-year-old Shoshone Indian with a 6-month-old baby, was married to one of the interpreters, Toussaint Charbonneau. She had been critically ill for several days and was not responding to treatment. Meriwether Lewis, who was in modern terms the "trip doctor" and the leader, took over her care. He had studied medicinal botany and had sought advice from America's leading physician, Dr. Benjamin Rush, before taking command of the group, but he was not a physician. Nonetheless, his knowledge of medical problems in the wilderness was not much different from that of many doctors of the time. Few doctors had medical degrees, and many were only apprenticed to an older physician for a few years before practicing on their own. The decision not to have a physician on the trip was made with the agreement of President Thomas Jefferson, who was the moving force behind the expedition. Sacagawea was suffering from abdominal pain and vomiting. She was febrile and nearly unconscious. Clark had treated her empirically with bleeding, salts, and abdominal poultices. In taking control of the case, Lewis did everything that a modern doctor would do under the same circumstances. He took a history, examined the patient, came to a diagnosis, and prescribed such treatment as was available. He concluded that her problem was due to "an obstruction of the mensis in consequence of taking could"—a diagnosis strange to our thinking but one that suggests a careful and detailed history. At that time, men did not naturally discuss such intimate details of the lives of women. He prescribed poultices and doses of mineral waters and laudanum. Sacagawea improved greatly and was able to get up and take a walk. Within 2 days she was back to normal. Her recovery was vital for the expedition because she was the key to opening the route to the Pacific Ocean. She had been captured while a child, taken hundreds of miles to the East, and was now on the verge of returning to her own country. Without her ability to
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interpret the language of the Shoshones, the expedition might have failed. When they finally met the Shoshones, Sacagawea found that her brother, now grown to manhood, was the chief of the tribe. Further progress of the expedition was assured. Lewis had achieved his two aims: recovery of his patient and salvage of the expedition. For many years, President Jefferson had visions of opening a water route to the West Coast, wresting the lucrative fur trade from the British and French, and finding the mythical Northwest Passage. The Spanish and British had similar aspirations to send explorers to the West Coast. In 1793, Alexander Mackenzie crossed the spine of the Rocky Mountains farther north, through an area so inhospitable that it was useless for trade. In the same year, a French botanist, André Michaux, supported by the American Philosophical Society, tried to travel up the Missouri River but failed. Two obstacles prevented further American attempts from coming to fruition: Congress would not appropriate money, and France and Spain controlled the land west of the Mississippi River. Knowledge of the geography of the country was limited and naïve. No one—British, French, Canadian, Spanish, or American—understood the vastness and complexity of the land. They were all blind men feeling a continental elephant. The British and Spanish had superficially explored the West Coast as far as Alaska. In 1792, Captain Gray, an adventurous American sailor, had discovered and named the Columbia River, which obviously flowed from the distant peaks. Exploration was confined to the coast, and people could only guess at what lay beyond the mountains that divided the country. Since fur traders had long used the lower reaches of the Missouri River to bring their trophies to St. Louis and New Orleans, Jefferson thought, why not an expedition that would ascend the Missouri, make a short portage across the mountains, and continue down the Columbia to the coast? Until 1800, Spain controlled the territory west of the Mississippi through which an expedition would have to move. Rule of the land passed to France from 1800 to 1803, until Napoleon sold the territory to the United States in the Louisiana Purchase. Suddenly the United States had dominion over a vast expanse of land from the Missouri to the Pacific. In 1802, Jefferson secretly persuaded Congress to appropriate $2500 for an expedition "for the purpose of extending the external commerce of the U.S." The expedition was also called a "literary pursuit," slim camouflage for an act of commercial imperialism that amazingly achieved its objectives with almost no loss of life, and without starting a war with Britain, Spain, or the Indians. President Jefferson chose his private secretary, Captain Meriwether Lewis, to lead the expedition. Lewis was an experienced army officer with knowledge of wilderness travel and a proven record of leadership. In addition, he was a member of a distinguished Virginia family and a close friend of the President. Lewis, in turn, chose his former commanding officer, William Clark, to be his co-leader. Time proved them to be the perfect team, as leaders, scientists, observers, and diarists—and
occasionally as physicians. President Jefferson organized the preparations meticulously. Lewis was dispatched to Philadelphia by Jefferson to learn celestial navigation, botany, and zoology, and become proficient in the preservation of biologic specimens. He visited Benjamin Rush, the leading physician of his day and physician to President Jefferson, to find out what medications he should take and how to treat the diseases he might encounter. Rush prepared a list of 14 questions for Lewis to answer and gave him 10 pieces of advice on how to maintain his own health. The questions to be answered concerned the health, morals, and religious practices of the Indians. Rush wanted Lewis to inquire about the diseases of these people and how they were cured. When did their women start and stop menstruating? How long were their children suckled? What were their sexual mores and habits? Rush was particularly interested in knowing if any of the religious ceremonies of the Indians were similar to those of Judaism because there was a belief, in some circles, that the lost tribe of Israel had ended up in the American West. Rush advised rest after strenuous exercise, moderation in drink and food, and the liberal use of purges, to both prevent and cure ailments. He told them to wear flannel next to the skin, especially in cold and wet weather, and advised that the men wear shoes without heels, since they would be less fatiguing than shoes with higher heels. The advice about purging, bleeding, and sweating conformed with the current theories of medical practice. Rush outspokenly believed that blood, bowel contents, and sweat contained the causes of disease that could be removed. Based on advice from Rush, the medical dispensary of the expedition contained a liberal supply of Rush's Pills, a potent mixture of calomel and jalap, both laxatives strong enough to empty the bowels of the hardiest frontiersman. Numerous drugs, herbs, and instruments, including laudanum for pain, medications for eye problems, four penis syringes for treating venereal disease, and lancets for bleeding, were packaged in a specially constructed wooden chest. The total cost of the medical supplies was $96.69. The Corps of Discovery, as the expedition was called, spent the winter of 1803–1804 in Camp Dubois, north of St. Louis, on the east bank of the Mississippi River (the west bank was not yet in the United States) and opposite the mouth of the Missouri River, training and equipping for the long and uncertain journey.
XV
Captain Clark, 23 army privates, four sergeants, Drouillard (a French-Indian hunter), York (William Clark's slave), and Lewis' Newfoundland dog Seaman pushed out onto the Missouri River on May 14, 1804. Lewis joined the group a few days later. They sailed in a 55-foot keel boat and two smaller pirogues. They struggled upstream, poling, rowing, sailing, and hauling the boats by hand. The weather was hot, with frequent summer storms. Thick clouds of mosquitoes were a constant plague. The food was bad and often scarce. Although generous supplies of some foods had been taken, the prime source of meat was obtained by hunting. At first they were lucky. There were vast herds of buffalo, deer, and elk. Game could often be shot within a short distance of camp. Such profusion would not last long after the opening of the West. The men were young, strong, and chosen for their wilderness skills. There were hunters, boatmen, carpenters, interpreters, and French voyageurs, as healthy and adventurous a group of young men as could be found. However, despite their strength, diseases plagued them constantly: diarrhea, fevers, near starvation, skin infections and boils, cuts from knives, sunburn, snakebites, dislocated shoulders, and feet lacerated from cactus spines. Only luck saved them from being killed by grizzly bears. A sleeping sergeant was bitten on the hand by a wolf. Sacagawea had a difficult labor but gave birth 10 minutes after receiving a concoction of rattlesnake rattles. Diarrhea and intestinal infections came to be expected. The men took few sanitary precautions, although the army knew that troops that remained on the move and dug latrines far from camp remained healthier than did those that stayed in one camp for a long time. Perhaps their mobility saved them from some problems. During the two periods they stayed in camps, medical problems were more common than when they were on the move. On August 17, 1804, Sergeant Charles Floyd developed abdominal pain that progressed over the next 3 days. During that time, he continued to work on the boat, but the pain became worse, shock developed, and on August 20, he died. Before he died, he said to Captain Clark, "I am going to leave you. I want you to write me a letter." He died "with composure" and was buried with military honors on a bluff overlooking the river, where there is now a monument to his memory. He was the only fatality in the Corps and the first U.S. soldier to die west of the Mississippi. The diagnosis is uncertain, although his symptoms suggest a ruptured appendix. Lewis described the symptoms as "bilious cholic," but there was no record of an examination. We do not know if Floyd's abdomen was tense, distended, or painful. Neither Lewis nor Clark was a doctor, and although Lewis was knowledgeable about herbs and probably knew how to treat wounds and accidents, he was not trained to diagnose illnesses or to make a physical examination. If the diagnosis was, indeed, a ruptured appendix, Sergeant Floyd would not have survived, even had he been in Philadelphia under Benjamin Rush's care. The first winter was spent in a collection of huts surrounded by a wooden stockade, near a Mandan Indian village. The weather was bitterly cold, and the supply of food ran low. The Indians were friendly, but they too had very little food; some members of the expedition helped them by going out on hunting excursions. Although the temperature dropped to -38° F, none of the Corps members sustained damaging frostbite. A Mandan boy, stranded out overnight and left for dead, was brought in with frozen feet. After a few days, the boy's toes became gangrenous and Clark "sawed off his toes." The endurance of another Indian amazed the soldiers. Stranded overnight in freezing weather, with no food and only the clothes on his back, he had neither frostbite nor hypothermia. The Mandans slept with their feet towards the campfire, to prevent frostbite during the night, but could not stave off frostbite while hunting with only thin moccasins on their feet. Prairie plums, cherries, and gooseberries supplemented the protein diet and contained enough vitamin C to prevent scurvy. As winter gave way to spring, thousands of buffalo returned and meat became available. The strength and health of the men improved. When they were about to set out again on the river on April 7, 1805, Lewis was able to write to Jefferson, "I can foresee no material or probable obstruction to our progress, and entertain therefore the most sanguine hopes of complete success.... With such men I have everything to hope, and but little to fear." At the same time he wrote to his mother, "... not a whisper of discontent or murmur is to be heard among them, but all act in unison, and with the most perfect harmony." The Corps, which had experienced disciplinary problems, a desertion, and the need for floggings, was now a tough, unified group, confident in their officers and prepared to embark on an endeavor more difficult than they could ever imagine. The journey westward through the Bitterroot Mountains was a constant struggle. Food was scarce; sometimes there was none. After days of pushing their way through fallen timber, along barely discernible trails, they staggered, half starved, into the territory of the Nez Perce Indians. At first, the Nez Perce wanted to kill the strange intruders, but an old woman, who had been befriended by a white person while a prisoner in the East, persuaded them to spare their lives. The Indians became loyal friends, supplying and guiding the expedition. Like many others of his day, Jefferson thought the portage from the Missouri River to the Columbia River would be short; perhaps there would be a direct connection between the two rivers. The "connection" was,
XVI
in fact, 340 miles long, with 60 of them over "tremendious mountains" covered with snow. The journey down the Snake River and into the valley of the Columbia River was a relief, drifting downstream instead of hauling supplies on reluctant, stumbling horses, up mountains and through forests. Salmon became part of the diet and, in place of deer or elk, dogs became a common and, for many, a favorite food. On November 7, 1805, Clark saw the sea. "Ocian in view! O! the joy!," he wrote in his diary. The explorers searched a long time for a good campsite until choosing what became Fort Clatsop, their log cabin camp for the winter. Like Fort Mandan, it was built to keep out inquisitive Indians. Lewis had been ordered by Jefferson to take every precaution against fighting with the Indians and had been very successful in avoiding trouble. The Clatsop Indians were not aggressive and had already traded with western sailors; but in some ways, they were too friendly, bringing girls to the camp, a temptation the men could not resist. They paid for their indulgence with the acquisition of venereal disease, repeating their experiences of the previous winter at the Mandan village. The winter at Fort Clatsop was cold and wet. Between November 4 and March 25, only 12 days were free of rain and only six were sunny. The diet was often nothing but spoiled elk, alternated with pounded fish and a handful of roots. A whale washed up on the shore, and the blubber and oil provided a pleasant new taste. There was the usual toll of accidents. One man cut his leg badly with a knife. Another developed severe low back pain that crippled him for weeks until he was cured by a sweat bath, alternating heat with cold. In March 1806 the Corps of Discovery launched their canoes on the river and set their course for home. Their delight was great but their troubles were not over. Crossing the mountains at first proved to be impossible because of deep, lingering snows. The expedition had to wait for several weeks, bargaining and competing with the Nez Perce in athletic contests and horse races. The trinkets they had brought as trade goods had been used up. One service remained that could be traded for
food or horses—medical aid. Clark proved to be a popular doctor with the Indians. He treated their sore eyes, set their fractures, and tried to cure a chief who was paralyzed by treating him in a sweat bath. However, he did not always treat with grace, calling one patient "a sulky bitch." Lewis had twinges of conscience in allowing the Indians to think that Clark was a doctor but excused the mild deception as necessary to get the horses and food they needed to continue. After the expedition finally crossed the mountains and left the Nez Perce guides behind, they divided into two groups—one to explore the Yellowstone River, and the other, led by Lewis, to go north along the Marias River. All went well with Lewis and the three men with him until they met a party of Blackfoot Indians, the most warlike tribe in the area. After nervous greetings, the two groups spent the night around the same campfire. The next morning, the braves tried to steal a gun and horses. One of Lewis' men ran after the thief who had stolen his gun and stabbed him to death, and Lewis shot and killed the horse thief. It was the first time anyone in the Corps of Discovery had killed an Indian. Lewis and his men mounted their horses and made a dramatic escape, riding more than 100 miles in 24 hours before joining up with the rest of the expedition. A few weeks later, one of the hunters, Cruzatte, who had bad eyesight, and Lewis were hunting a wounded elk in thick willows and riverside brush. Cruzatte thought he saw an elk, shot, and hit the buckskin-clothed Lewis in the buttock. The treatment Lewis gave himself was as good as might be given today under similar circumstances. Drains were inserted into the entrance and exit wounds, which were dressed. The bullet was found in Lewis' clothing, so no attempt had to be made to find it in the wound, which was the standard treatment of the day. Fortunately, the wound did not become infected, and within a few weeks, before the end of the voyage, Lewis was completely healed. On September 23, 1806, the expedition reached St. Louis. They had been away for 2 years and 4 months and had journeyed more than 8000 miles. Lewis reported to the President: In obedience to your orders we have penitrated the Continent of North America to the Pacific Ocean, and sufficiently explored the interior of the country to affirm with confidence that we have discovered the most practicable rout which does exist across the continent by means of the navigable branches of the Missouri and Columbia Rivers. Looking back, one can only be amazed at the medical success of the expedition, which returned with the loss of only one man. Was it skill? Was it luck? Was the trip a tribute to the endurance and resistance of the human body to cold, heat, starvation, insects, injuries, and medications that could have done more harm than good? The bear that attacked Meriwether Lewis turned away at the end of a bluff charge. The wolf that bit the sleeping sergeant was not rabid. When rattlesnakes struck, no serious injuries resulted. The cuts by knives and wounds from prickly pears caused no major infections. No man became blind. No limbs were lost to frostbite. The lead ball shot into Lewis was recovered in his clothing, so there was no dirty surgery. Sacagawea recovered, perhaps because the water that Lewis gave her from a mineral spring restored her electrolyte losses. Pompey, Sacagawea's son, recovered from a life-threatening abscess in his neck without the benefit of antibiotics. When Lewis used his penknife to bleed a man, septicemia did not follow.
XVII
The medicine chest contained little of therapeutic value except opium and laudanum. Peruvian bark, related to quinine, could have been useful for malaria, but there is no evidence that malaria was a problem. The ferocious laxatives fortunately caused little but discomfort. Tartar emetic was not needed because no man ingested poison. The lancets for bleeding were, mercifully, used sparingly. Could a modern doctor have done better? Not much. Some illnesses might have been shortened, some pain relieved, but many more medications would have been dispensed, more lacerations sutured, and perhaps even snakebite antivenom administered. Sergeant Floyd might only have been saved by a heroic operation under imperfect circumstances. So, the expedition would still probably have returned with the loss of one man and the medical bill would have been much greater than 96 dollars and 69 cents. REFERENCES 1. Elliott Coues, editor: The history of the Lewis and Clark expedition, vols I–III, New York, 1893, Francis P Harper; unabridged reprint by Dover Publications, 1998. 2. Ambrose SE: Undaunted courage: Meriwether Lewis, Thomas Jefferson and the opening of the American West, New York, 1996, Simon and Schuster. 3. Dillon R: Meriwether Lewis, a biography, Santa Cruz, Calif, 1988, Western Tanager Press. Bruce C. Paton MD Emeritus Clinical Professor of Surgery, University of Colorado Health Sciences Center, Denver, Colorado
XVIII
XIX
Preface
This fourth edition of Wilderness Medicine is designed to be a great improvement over the previous edition. It is necessarily expanded in girth in order to accommodate additional topics of relevance to medical professionals called upon to rescue, diagnose, and treat victims in outdoor environments. The specialty of wilderness medicine continues to mature, as most of the active participants in its progress come to agree on the body of knowledge that must be mastered to promote its science and create effective practitioners. Outdoor pursuits comprise the fastest growing segment of recreational life in the United States, and perhaps the world. Men and women of all nationalities have become travelers and adventurers in unprecedented numbers, and the related encounters with risk and danger have kept pace. The widely publicized tragedies that afflict climbers on Mount Everest, victims of avalanches, and explorers in hazardous seas regularly heighten our awareness of the powerful natural forces that prevail despite our best intentions and preventive efforts. As we climb into rarified air, sled over thin ice, eschew safety ropes and helmets, and stretch the limits of our diving decompression algorithms, we will be reminded of our vulnerability and limitations on a planet that shows no mercy in its most terrifying moments. Therein lies the relevance, challenge, and opportunity for wilderness medicine. In seeking to understand the pathophysiology of high altitude, we witness the beauty of pristine rock faces and summits. While we learn to repel sharks, we marvel at the rainbow colors of the barrier reefs. In the quest for a cure for malaria, the tropical scientist gazes into the emerald canopy of the rainforest. As we battle forest fires and survive the lightning and fierce winds of a thunderstorm, our attention is drawn to a herd of bison stampeding across a grass prairie that stretches as far as the imagination. No medical specialty or healthcare-related avocation is more connected to this planet than is wilderness medicine. My colleagues and I, and everyone else involved in outdoor health and wilderness medicine, could not be more fortunate. Wilderness medicine is presented here by experts and devotees. For example, the integration of basic science and clinical art is blended brilliantly in the chapters on heat-related illness. In recognition of our aging population, a new chapter is devoted to elders. A significant upgrade to the content is embodied by the nonmedical topics, such as the information on navigation, clothing, backcountry equipment, and ropes and knot tying. Wilderness medicine practitioners have long recognized that essential survival skills may need to be deployed by healers when outfitters and guides cannot function at full capacity. The physician who can recite everything there is to know about exposure to the sun and treatment of dehydration must also be able to pitch in and gather water; knowing how to avoid a shark attack is just as important as knowing how to treat a shark attack victim. A new information age is upon us. The Internet allows us to link "many to many," and to collect information from disparate locations in a hugely expedited fashion. However, it isn't yet a perfect filter for the reliability of the content, and so there is still much to be said for sitting down with a good book. Wilderness Medicine is meant to be a reference, but also to be a stimulus for inquiry and adventure. The publisher and I have worked hard to keep it to a manageable size, and the addition of color images throughout the book and emphasis on practical matters make this the most complete and relevant edition to date. Wilderness Medicine has become a life's work, and will continue to grow. In addition, the Wilderness Medical Society; the journal Wilderness and Environmental Medicine (recently accepted into the Index Medicus); a plethora of continuing medical education programs in wilderness medicine, diving medicine, adventure and travel medicine, and outdoor health; Field Guide to Wilderness Medicine; the book for laypersons Medicine for the Outdoors; and all of the opportunities yet to come by virtue of television and the Internet have propelled this 20-year effort into an established medical discipline for as long as there will be wilderness. I am grateful for Kathy Falk and Rick Dudley, my editors for this fourth edition. The contributors, some of whom have been with this book since its inception and who continue to learn, teach, and enhance this field, share my enormous thanks and respect. With great pleasure, I can now observe the activities of my children, and the children of many of the contributors, as they continue to increase their appreciation for the wilderness and outdoor health. In the continuing endeavor of Wilderness Medicine, I am in many ways the luckiest editor on Earth. Paul S. Auerbach XX
1
Part 1 - Mountain Medicine
2
Chapter 1 - High-Altitude Medicine Peter H. Hackett Robert C. Roach
Millions of persons visit recreation areas above 2400 m (7874 feet) in the American West each year. Hundreds of thousands visit central and south Asia, Africa, and South America, many traveling to altitudes over 4000 m (13,124 feet).[234] Increasingly, physicians and other health care providers are confronted with questions of prevention and treatment of high-altitude medical problems ( Box 1-1 ), as well as the effects of altitude on preexisting medical conditions. Despite advances in high-altitude medicine, significant morbidity and mortality persist ( Table 1-1 ). Clearly, better education of the population at risk and those advising them is essential. 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. Much of the information presented in this chapter is drawn from major high-altitude physiology and medical studies of the last 40 years, with an emphasis on the last decade (see the recent reviews by Houston,[139] Nakashima,[246] Richalet,[272] and West[355] ).
DEFINITIONS High Altitude (1500 to 3500 m [4921 to 11,483 feet]) The onset of physiologic effects of diminished PIO2 includes decreased exercise performance and increased ventilation (lower arterial PCO2 ) ( Box 1-2 ). Minor impairment exists in arterial oxygen transport (SaO2 at least 90%), but high-altitude illness is common with rapid ascent above 2500 m (8202 feet) ( Table 1-2 ). Very High Altitude (3500 to 5500 m [11,483 to 18,045 feet]) Maximum arterial oxygen saturation falls below 90% as the arterial PO2 falls below 60 torr ( Table 1-3 ; Figure 1-1 ). Extreme hypoxemia may occur during exercise, sleep, and high-altitude illness. This is the most common range for severe altitude illness. Extreme Altitude (over 5500 m [18,045 feet]) Marked hypoxemia and hypocapnia manifest at extreme altitude. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no permanent human habitation is above 5500 m (18,045 feet). A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude illness.
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 (19,030 feet), barometric pressure is one half that at sea level, and on the summit of Mt. Everest (8848 m [29,029 feet]) the inspired pressure of oxygen is approximately 28% that at sea level (see Figure 1-1 and Table 1-2 ). The relationship of barometric pressure to altitude changes with the distance from the equator. Thus polar regions afford greater hypoxia at high altitude, as well as extreme cold. West[354] has calculated that the barometric pressure on the summit of Mt. Everest (27° N latitude) would be about 222 torr instead of 253 torr 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 low-pressure trough can reduce pressure 10 torr in one night on Mt. McKinley, making climbers awaken "physiologically higher" by 200 m (656 feet). The degree of hypoxia, then, is directly related to the barometric pressure and not solely to geographic altitude.[354] Temperature decreases with altitude (average of 6.5° C per 1000 m [3281 feet]), and the effects of cold and hypoxia are generally additive in provoking both cold injuries and altitude problems.[269] [351] Ultraviolet light penetration increases approximately 4% per 300-m (984-foot) 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. We have observed temperatures of 40° to 42° C in tents on both Mt. Everest and Mt. McKinley. Heat problems, primarily heat exhaustion, are often unrecognized in this usually cold environment. Physiologists have not yet examined the consequences of heat stress or rapid, extreme changes in environmental temperature combined with the hypoxia of high altitude. Above the snow line is the "high-altitude desert," where water can be obtained only by melting snow or ice. This factor, combined with increased water loss
3
STUDY GROUP Western State visitors
Mt. Everest trekkers
NUMBER AT RISK PER YEAR 30 million
6000
TABLE 1-1 -- Incidence of Altitude Illness in Various Groups SLEEPING MAXIMUM ALTITUDE AVERAGE RATE PERCENT * ALTITUDE (m) REACHED (m) OF ASCENT WITH AMS ~2000
3500
1–2
22
~=3000
27–42 5500
9
0.01
[134]
[68]
1–2 (fly in)
47
1.6
10–13 (walk in)
23
0.05
Not specified
Mt. McKinley climbers
18–20
~2500 3000–5200
PERCENT WITH HAPE REFERENCE AND/OR HACE
[106]
30–50
[243]
1200
3000–5300
6194
3–7
30
2–3
[111]
Mt. Rainier climbers
10,000
3000
4392
1–2
67
—
[188]
Mt. Rosa, Swiss Alps
†
2850
2850
1–2
7
—
[201]
4559
4559
2–3
27
5
[64] [201]
3000–5500
5500
1–2
†
2.3–15.5
[320] [321]
Indian soldiers
Unknown
AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema. *Days to sleeping altitude from low altitude. †Reliable estimate unavailable.
4
TABLE 1-2 -- Altitude Conversion, Barometric Pressure, Estimated Partial Pressure of Inspired Oxygen, and the Related Oxygen Concentration at Sea Level* m ft PB PIO2 FIO2 at SL Sea Level
759.6 149.1
0.209
1000
3281 678.7 132.2
0.185
1219
4000 661.8 128.7
0.180
1500
4921 640.8 124.3
0.174
1524
5000 639.0 123.9
0.174
1829
6000 616.7 119.2
0.167
2000
6562 604.5 116.7
0.164
2134
7000 595.1 114.7
0.161
2438
8000 574.1 110.3
0.155
2500
8202 569.9 109.4
0.154
2743
9000 553.7 106.0
0.149
3000
9843 536.9 102.5
0.144
3048 10000 533.8 101.9
0.143
3353 11000 514.5
97.9
0.137
3500 11483 505.4
95.9
0.135
3658 12000 495.8
93.9
0.132
3962 13000 477.6
90.1
0.126
4000 13123 475.4
89.7
0.126
4267 14000 460.0
86.4
0.121
4500 14764 446.9
83.7
0.117
4572 15000 442.9
82.9
0.116
4877 16000 426.3
79.4
0.111
5000 16404 419.7
78.0
0.109
5182 17000 410.2
76.0
0.107
5486 18000 394.6
72.8
0.102
5500 18045 393.9
72.6
0.102
5791 19000 379.5
69.6
0.098
6000 19685 369.4
67.5
0.095
6096 20000 364.9
66.5
0.093
6401 21000 350.7
63.6
0.089
6500 21325 346.2
62.6
0.088
6706 22000 337.0
60.7
0.085
7000 22966 324.2
58.0
0.081
7010 23000 323.8
57.9
0.081
7315 24000 310.9
55.2
0.077
7500 24606 303.4
53.7
0.075
7620 25000 298.6
52.6
0.074
7925 26000 286.6
50.1
0.070
8000 26247 283.7
49.5
0.069
8230 27000 275.0
47.7
0.067
8500 27887 265.1
45.6
0.064
8534 28000 263.8
45.4
0.064
8839 29000 253.0
43.1
0.060
8848 29029 252.7
43.1
0.060
9000 29528 247.5
42.0
0.059
9144 30000 242.6
40.9
0.057
9500 31168 230.9
38.5
0.054
10000 32808 215.2
35.2
0.049 2
*Barometric pressure is approximated by the equation PB = Exp(6.6328 - {0.1112 × altitude - [0.00149 × (altitude )]}), where altitude = terrestrial altitude in (meters/1000 or km). P IO2 is calculated as the P B - 47 (water vapor pressure at body temperature) × fraction of O2 in inspired air. The FIO2 at sea level related to the given altitude is calculated as PIO2 /(760 - 47). Similar calculations for F IO2 at different altitudes may be made by substituting ambient PB for 760 in the equation.
TABLE 1-3 -- Blood Gases and Altitude ALTITUDE POPULATION
METERS FEET
PB (torr)
PaO2 (torr)
SaO2 (%)
PaCO2 (torr)
Altitude residents*
1646
5400
630
73.0 (65.0–83.0)
95.1 (93.0–97.0)
35.6 (30.7–41.8)
Acute exposure†
2810
9200
543
60.0 (47.4–73.6)
91.0 (86.6–95.2)
33.9 (31.3–36.5)
3660
12020
489
47.6 (42.2–53.0)
84.5 (80.5–89.0)
29.5 (23.5–34.3)
4700
15440
429
44.6 (36.4–47.5)
78.0 (70.8–85.0)
27.1 (22.9–34.0)
5340
17500
401
43.1 (37.6–50.4)
76.2 (65.4–81.6)
25.7 (21.7–29.7)
6140
20140
356
35.0 (26.9–40.1)
65.6 (55.5–73.0)
22.0 (19.2–24.8)
6500‡
21325
346
41.1±3.3
75.2±6
20±2.8
7000‡
22966
324
8000‡
26247
284
36.6±2.2
67.8±5
12.5±1.1
8848‡
29029
253
30.3±2.1
58±4.5
11.2±1.7
8848§
29029
253
30.6±1.4
Chronic exposure
11.9±1.4
Data are mean values and (range) or ±SD, where available. All values are for subjects age 20 to 40 years who were acclimatizing well. *Data for altitude residents from Loeppky JA, Caprihan A, Luft UC: VA/Q inequality during clinical hypoxemia and its alterations. In Shiraki K, Yousef MK, editors: Man in stressful environments, Springfield, III, 1987, Charles C Thomas. †Data for acute exposure from McFarland RA, Dill DB: J Aviat Med 9:18, 1938. ‡Data for chronic exposure during Operation Everest II data are from Sutton JR et al: J Appl Physiol 64:1309, 1988. §The second data set for acclimatized subjects studied during acute exposure to the simulated summit of Everest is from Richalet JP et al: Operation Everest III (COMEX '97), Adv Exp Med Biol 474:297, 1999.
5
Figure 1-1 Increasing altitude results in decrease in inspired P O2 (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 (9840 feet). (Data from Morris A: Clinical pulmonary function tests: a
manual of uniform lab procedures, Intermountain Thoracic Society, 1984; and Sutton JR et al: J Appl Physiol 64:1309, 1988.)
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. POTENTIAL MEDICAL PROBLEMS OF 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 illness
Box 1-2. GLOSSARY OF PHYSIOLOGIC TERMS
PB
Barometric pressure (torr)
PO2
Partial pressure of oxygen
PIO2
Inspired PO2 [0.21 × PB - 47 torr (vapor pressure of H2 O at 37° C)]
PAO2
PO2 in alvedus
PaCO2
PCO2 in alveolus
PaO2
PO2 in arterial blood
PaCO2
PCO2 in arterial blood
SaO2 %
Arterial oxygen saturation % (HbO2 /total Hb × 100)
R
Respiratory quotient (CO2 produced/O2 consumed)
Alveolar gas equation: PaO2 = PIO2 - PaCO2 /R
ACCLIMATIZATION TO HIGH ALTITUDE Rapid exposure to the altitude at the summit of Mt. Everest causes loss of consciousness in a few minutes and death shortly thereafter. However, 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 improves their hypoxic tolerance. The severity 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 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. Successful initial acclimatization protects against altitude illness and improves sleep. Longer-term acclimatization (weeks) primarily improves aerobic exercise ability. These adjustments disappear at a similar rate on descent to low altitude. A few days at low altitude may be sufficient to render a person susceptible to altitude illness, especially high-altitude pulmonary edema (HAPE), on reascent. The improved ability to do physical work at high altitude, however, persists for weeks.[198] Persons who live at high altitude during growth and development appear to realize the maximum benefit of acclimatization changes; for example, their exercise performance matches that of persons at sea level.[237] No genetic adaptation to high altitude in humans has yet been confirmed, but recent reports of normal pulmonary artery pressures and normal birth weights in Tibetans suggest selection of genetic traits for life at high altitude.[100] [238] [372] Ventilation By reducing alveolar carbon dioxide, increased ventilation raises alveolar oxygen, improving oxygen delivery (see Figure 1-1 ). This response starts at an altitude as low as 1500 m (4921 feet) (PIO2 = 124 torr; 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 respiratory center in the medulla to increase ventilation. This carotid body function (hypoxic ventilatory response [HVR]) is genetically determined [352] 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 progesterone[182] and almitrine,[114] 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 illness[277] (see Acute Mountain Sickness and High-Altitude Pulmonary Edema). 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
6
altitude ( Figure 1-2 ). The plasma bicarbonate concentration continues to drop and ventilation continues to increase with each successive increase in altitude. This process is greatly facilitated by acetazolamide (see Acetazolamide Prophylaxis). A way to appreciate the importance of the ventilatory pump at increasing altitude is to plot values for alveolar oxygen and carbon dioxide on the Rahn-Otis diagram ( Figure 1-3 ). This approach clearly contrasts the effects of acute and chronic hypoxic exposure and can be used to assess the degree of ventilatory acclimatization.[265] As ventilation increases, the decrease in alveolar carbon dioxide allows an equivalent increase in alveolar oxygen. The level of ventilation (~PACO2 ) is therefore what determines alveolar oxygen for a given inspired oxygen tension, according to the alveolar gas equation: PAO2 = PIO2 - PACO2 /R. The paramount importance of hyperventilation is readily apparent from the following calculation: the alveolar PO2 on the summit of Mt. Everest (about 33 torr) would be reached at only 5000 m (16,404 feet) if alveolar PCO2 stayed at 40 torr, limiting an ascent without supplemental oxygen to near this altitude. Table 1-3 gives the measured arterial blood gases resulting from acclimatization to various altitudes.
Figure 1-2 Change in minute ventilation, (•VE ) end-tidal carbon dioxide (PACO2 ), and arterial oxygen saturation (SaO2 ) during 5 days' acclimatization to 4300 m (14,104 feet). (Modified from Huang SY et al: J Appl Physiol 56:602, 1984.)
Circulation The circulatory pump is the next step in the transfer of oxygen, moving oxygenated blood from the lungs to the tissues. Systemic Circulation.
Increased sympathetic activity on ascent causes an initial mild increase in blood pressure, moderate increase in heart rate and cardiac output, and increase in venous tone. Stroke volume is low because of decreased plasma volume, which drops as much as 12% over the first 24 hours[365] as a result of the bicarbonate diuresis, a fluid shift from the intravascular space, and suppression of aldosterone.[25] Resting heart rate returns to near sea level values with acclimatization, except at extremely high altitude. Maximum heart rate follows the decline in maximal oxygen uptake with increasing altitude. As the limits of hypoxic acclimatization are approached, maximum and resting heart rates converge. During Operation Everest II (OEII), cardiac function was appropriate for the level of work performed and cardiac output was not a limiting factor for performance.[268] [331] 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 pressures are low, and there has been no evidence of left ventricular dysfunction or abnormal filling pressures in humans at rest.[101] [158] On echocardiography, the left ventricle is smaller than normal because of decreased
Figure 1-3 Rahn-Otis diagram, with recent data from extreme high altitude. Note that after acclimatization, alveolar oxygen is higher because of lower alveolar carbon dioxide. Point A is average alveolar gases in unacclimatized subjects (1 hour's exposure) to 3800 m (12,464 feet). Point B is after acclimatization to 3800 m (12,464 feet). (Data from Malconian MK et al: Aviat Space Environ Med 64:37, 1993; Rahn H, Otis AB: Am J Physiol 157:445, 1949; and West JB et al: J Appl Physiol 55:688, 1983.)
7
stroke volume, whereas the right ventricle may become enlarged.[331] 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,[101] especially in persons with a previous history of HAPE. During OEII, Groves et al [101] demonstrated that even when associated with a mean pulmonary artery pressure of 60 torr, cardiac output remained appropriate and right atrial pressure did not rise above sea level values. This suggested that right ventricular function was intact in spite of extreme hypoxemia and 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. [101] [156] The explanation is likely vascular remodeling with medial hypertrophy. See Stenmark et al[328] for a recent review of molecular and cellular mechanisms of the pulmonary vascular response to hypoxia, including remodeling. 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 torr (altitude greater than 2800 m [9187 feet]). In a classic study, CBF increased 24% on abrupt ascent to 3810 m (12,501 feet) and then returned to normal over 3 to 5 days.[312] More recent studies have shown considerable individual variation,[30] [31] [166] but overall, cerebral oxygen delivery and global cerebral metabolism are well maintained with moderate hypoxia.[67] Blood Hematopoietic Responses to Altitude.
Ever since the observation in 1890 by Viault[345] 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 has no relationship to susceptibility to high-altitude illness on initial ascent. In response to hypoxemia, erythropoietin is secreted and stimulates bone marrow production of red blood cells.[309] 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 altitude[122] ( Figure 1-4 ). 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 (17,717 feet) with no decrement in maximum oxygen uptake and an increase in cerebral functioning.[299] 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 trade-off that might impair exercise performance. Longer-term acclimatization leads to an increase in plasma volume, as well as in red blood cell mass, thereby increasing total blood volume. Oxyhemoglobin Dissociation Curve.
The oxyhemoglobin dissociation curve plays a crucial role in oxygen transport. Because of the sigmoidal shape of the curve, SaO2 % is well maintained up to 3000 m (9843 feet) 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 ( Figure 1-5 ). In 1936, Keys et al[173] demonstrated an in vitro right shift in the position of the oxyhemoglobin dissociation curve at high altitude, a shift that favors the release of oxygen from the blood to the tissues. This change occurs because of the increase in 2,3-diphosphoglycerate
Figure 1-4 Hematocrit changes on ascent to altitude in men and in women with and without supplemental iron. (Modified from Hannon JP, Chinn KS, Shields JL: Fed Proc 28:1178, 1969.)
8
Figure 1-5 Oxyhemoglobin dissociation curve showing effect of 10-torr decrement in Pa O2 (shaded areas) on arterial oxygen saturation at A, sea level, and B, near 4400 m (14,432 feet). Note the much larger drop in Sa O2 at high altitude. (Modified from Severinghaus JW et al: Circ Res 19:274, 1966.)
(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 oxyhemoglobin dissociation curve. On the other hand, the marked alkalosis of extreme hyperventilation, as measured on the summit and simulated summit of Mt. Everest (P CO2 8 to 10 torr, pH greater than 7.5), shifts the oxyhemoglobin dissociation curve to the left, which facilitates oxyhemoglobin binding in the lung, raises SaO2 %, and is thought to be advantageous.[297] This concept is further supported by observing that when persons with a very left-shifted oxygen-hemoglobin curve, caused by an abnormal hemoglobin (Andrew-Minneapolis), were taken to moderate (3100 m [10,171 feet]) altitude, they had less tachycardia and dyspnea and remarkably had no decrease in exercise performance.[127] 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. Banchero[13] has shown that capillary density in dog skeletal muscle doubled in 3 weeks at a barometric pressure of 435 torr. A recent study in humans noted higher-than-normal muscle capillary density, although it was impossible to determine whether this was an adaptation to high altitude or to physical training.[253] Ou and Tenney[256] revealed a 40% increase in mitochondrial number but no change in mitochondrial size, whereas the study of Oelz et al[253] showed that high-altitude climbers had normal mitochondrial density. During OEII, a significant reduction in muscle size was noted, and although no de novo synthesis of capillaries or mitochondria occurred, capillary density and the ratio of mitochondrial volume to contractile protein fraction
increased, primarily as a result of the atrophy. [199] Nevertheless, this change decreased the diffusion distance for oxygen. Sleep At High Altitude Disturbed sleep is common at high altitude. Reite et al[270] studied six men during a 12-day stay at 4300 m (14,108 feet). All subjects complained of disturbed sleep. Compared with sea level control studies, stages 3 and 4 sleep were reduced, stage 1 time increased, and stage 2 did not change. More time was spent awake, with a significant increase in arousals and slightly less rapid eye movement (REM) time. The subjective complaints of poor sleep were out of proportion to the small reduction in total sleep time. Five of the six had periodic breathing. Interestingly, the arousals were not necessarily related to periodic breathing. One subject had periodic breathing for 90% of the night and no recorded arousals. With more extreme hypoxia, sleep time was dramatically shortened and arousals increased, without a change in ratio of sleep stages but with a reduction in REM sleep.[5] Presumably, the mechanism of the arousals is cerebral hypoxia. Periodic breathing appears to play only a minor role in altering sleep architecture at high altitude. [296] Periodic Breathing.
Periodic breathing is primarily a nocturnal phenomenon, characterized by hyperpnea followed by apnea ( Figure 1-6 ). Respiratory alkalosis during hyperpnea acts on the central respiratory center, causing apnea. During apnea, SaO2 % decreases, carbon dioxide level increases, and the carotid body is stimulated, causing a recurrent hyperpnea and apnea cycle. Persons with a high HVR have more periodic breathing, with mild oscillations in SaO2 %, [184] whereas persons with a low HVR have more regular breathing overall but may suffer periods of apnea with extreme hypoxemia distinct from periodic breathing.[114] As acclimatization progresses, periodic breathing lessens but does not disappear and SaO2 % increases (Figure 1-7 (Figure Not Available) ). [5] [333] Periodic breathing has not been implicated in the etiology of high-altitude illness, but a chaotic pattern without apparent periodicity was found in HAPE-susceptible subjects. [91] Eichenberger et al[81] have also reported greater periodic breathing in those with HAPE, secondary to lower SaO2 %. Acetazolamide, 125 mg at bedtime, diminishes periodic
9
Figure 1-6 Respiratory patterns and arterial oxygen saturation (SaO2 ) with placebo and acetazolamide in two sleep studies of a subject at 4200 m (13,776 feet). Note pattern of hyperpnea followed by apnea during placebo treatment, which is changed with acetazolamide. (Modified from Hackett PH et al: Am Rev Respir Dis 135:896, 1987.) Figure 1-7 (Figure Not Available) Sleep oxygenation improves with acclimatization to same altitude. Top line is maximum and bottom line is minimum Sa O2 in an acclimatized person. Shaded area is maximum and minimum SaO2 values for new arrival at 5360 m (17,581 feet). (Modified from Sutton JR et al: N Engl J Med 301:1329, 1979.)
breathing, improves oxygenation, and is a safe and superior agent to use as a sleeping aid (see Figure 1-6 and Figure 1-7 (Figure Not Available) ). If insomnia is due to causes other than periodic breathing, 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), can be used. However, these are potentially dangerous in ill persons at high altitude because of resulting respiratory depression, and they may decrease oxygenation even in persons who are acclimatizing
Figure 1-8 On ascent to altitude, ?VO2 max decreases and remains suppressed. In contrast, endurance time (minutes to exhaustion at 75% of altitude-specific ?V O2 max) increases with acclimatization. (Modified from Maher JT, Jones LG, Hartley LH: J Appl Physiol 37:895, 1974.)
well. Bradwell et al[44] 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. A new, nonbenzodiazapine hypnotic, zolpidem (Ambien, 10 mg) was recently shown to improve sleep at 4000 m (13,123 feet) without adversely affecting ventilation. [32] Exercise Maximal oxygen consumption drops dramatically on ascent to high altitude (see references [92] and [278] for recent reviews). Maximal oxygen uptake (?VO2 max) falls approximately 10% for each 1000 m (3281 feet) of altitude gained above 1500 m (4921 feet). Those with the highest sea level ?VO2 max values have the largest decrement in ?VO2 max at high altitude, but overall performance at high altitude is not consistently related to sea level ?VO2 max.[253] [273] [356] In fact, many of the world's elite mountaineers have quite average ?VO2 max values, in contrast to other endurance athletes.[253] Acclimatization at moderate altitudes enhances submaximal endurance time but not ?VO2 max ( Figure 1-8 ). [92] Preliminary recent work suggests that genetic factors may play a role in determining exercise performance in mountaineers at high altitude. Montgomery et al identified a polymorphism in the gene encoding angiotensin converting enzyme (ACE) that was strongly related to mountaineering performance in 25 British mountaineers.[233] The
10
mechanism by which an ACE gene polymorphism could enhance exercise performance at high altitude is unknown but provides interesting and important direction for further investigations. Oxygen transport during exercise at high altitude becomes increasingly dependent on the ventilatory pump. The marked rise in ventilation produces a sensation of breathlessness, even at low work levels. The following quotation is from a high-altitude mountaineer: After every few steps, we huddle over our ice axes, mouths agape, struggling for sufficient breath to keep our muscles going. I have the feeling I am about to burst apart. As we get higher, it becomes necessary to lie down to recover our breath.[222] 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).[268] Although related to decreased oxygen transport, the exact limiting factors to exercise at high altitude remain elusive. Wagner[350] has proposed that the pressure gradient for diffusion of oxygen from capillaries to the working muscle cells may be inadequate. Another concept is that increased cerebral hypoxia from exercise-induced desaturation is the limiting factor.[57] Mountaineers, for example, become lightheaded and their vision dims when they move too quickly at extreme altitude ( Figure 1-9 ). [353] Training at High Altitude.
Optimal training for increased performance at high altitude depends on the altitude of residence and the athletic event. For aerobic activities (events lasting more than 3 or 4 minutes) at altitudes above 2000 m (6562 feet), acclimatization for 10 to 20 days is necessary to maximize performance.[202] For events occurring above 4000 m (13,123 feet), acclimatization at an intermediate altitude is recommended. Highly anaerobic events at intermediate altitudes require only arrival at the time of the event,
although mountain sickness may become a problem. The benefits of training at high altitude for subsequent performance at or near sea level depend on choosing the training altitude that maximizes the benefits and minimizes the "detraining" inevitable when maximal oxygen uptake is limited (altitude greater than 1500 to 2000 m [4921 to 6562 feet]). Hence, data from training above 2400 m (7874 feet) have shown no increase in subsequent sea level performance. Balke, Nagle, and Daniels[12] returned subjects to sea level after 10 days' training at 2000 m (6562 feet) and demonstrated an increase in aerobic power, plasma volume, and hemoglobin concentration, with faster running times. More recent work suggests training benefits from intermittent altitude exposure[192] and from training at low altitude while sleeping at high altitude.[11] [194] [329] Coaches
Figure 1-9 Calculated changes in the P O2 of alveolar gas and arterial and mixed venous blood as oxygen uptake is increased for a climber on the summit of Mt. Everest. Unconsciousness develops at a mixed venous PO2 of 15 torr. DMO2 , Muscle O 2 diffusing capacity. (Modified from West JB: Respir Physiol 52:265, 1983.)
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.[10] [40] [71] The benefit appears to be due to enhanced erythropoietin production and increased red cell mass, which requires adequate iron stores, and thus usually iron supplementation.[204] [285] [330]
HIGH-ALTITUDE SYNDROMES High-altitude syndromes are illnesses attributed directly to hypobaric hypoxia. Exact mechanisms, however, are unclear. For example, all persons at a given high altitude are hypoxic and those with AMS are barely more hypoxemic than those who are well.[99] [132] Also, there is a delay from the onset of hypoxia to the onset of high-altitude illness. These two facts have led to the conclusion that hypoxia induces time-dependent processes that are responsible for AMS, in contrast to the syndrome of acute hypoxia. Considerable overlap exists among the high-altitude syndromes, and terminology and classification of high-altitude illness remain somewhat confusing. 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
11
of Bert.[37] 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. We find it useful to separate the syndrome into neurologic and pulmonary components. For the neurologic syndromes, the spectrum progresses from 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 and oxygen. Longer-term problems of altitude exposure include high-altitude deterioration and chronic mountain sickness. Neurologic Syndromes The numerous neurologic syndromes at high altitude reflect the nervous system's sensitivity to hypoxia. The spectrum of clinical effects ranges from subtle cognitive changes to death from gross cerebral edema. Acute hypoxia is also included here because it is essentially a neurologic insult. We consider AMS and HACE as manifestations of a common underlying pathophysiology of vasogenic edema, but we give special consideration to high-altitude headache, which might have a number of mechanisms. Acute hypoxia and cognitive dysfunction are related to neurotransmitter dysfunction, whereas the focal neurologic syndromes, such as transient ischemic attack (TIA) and stroke, are related to secondary ischemia. Acute 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, 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 torr. [36] 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 sus- pecting that perhaps I had already lost use of my movements. Towards 7,500 m, the numbness one experiences is extraordi- nary. The body and the mind weakens little by little, gradu- ally, 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 per- sonal impression, this vertigo appears at the last moment; it immediately precedes annihilation—sudden, unexpected, ir- resistible. 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 nee- dle 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.[37] The ascent to over 8000 m (26,247 feet) took 3 hours, and the descent less than 1 hour. When the balloon landed, Tissandier's two companions were dead. The prodigious work that Paul Bert conducted in an altitude chamber during the 1870s showed that lack of oxygen, rather than an effect of isolated hypobaria, explained the symptoms experienced during rapid ascent to extreme altitude: There exists a parallelism to the smallest details between two animals, one of which is subjected in normal air to a pro- gressive 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. [37] 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 oxy- genation of central and peripheral nervous organs.... The symptoms... disappear very quickly when the balloon de- scends from the higher altitudes, very quickly also ... the normal proportion of oxygen reappears in the blood. There is an unfailing connection here.[37] Bert was also able to prevent and immediately resolve symptoms by breathing oxygen. Acute hypoxia can be quickly reversed by immediate administration of oxygen; rapid pressurization or descent; or correction of an underlying cause, such as relief of apnea, removal of a carbon monoxide source, repair of an oxygen delivery system, or cessation of overexertion. Hyperventilation increases time of useful consciousness. High-Altitude Headache Headache is generally the first unpleasant symptom consequent to altitude exposure and is sometimes the only symptom.[134] 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. [281] One could 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. Whether an
12
Figure 1-10 (Figure Not Available) Proposed pathophysiology of high-altitude headache. CNS, Central nervous system; eNOS, endogenous nitric oxide synthase; NO, nitric oxide. (Modified from Sanchez del Rio M, Moskowitz MA: High altitude headache, Adv Exp Med Biol 474:145, 1999.)
isolated headache is any different from the headache of moderate to severe AMS is unsettled until we have a better understanding of the pathophysiology. Because moderate to severe AMS is associated with vasogenic edema, and because headache by itself might not be, we choose to consider high-altitude headache as a separate category, pending further investigation. 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; headache scores have been well validated.[164] In general, the literature suggests that HAH can be prevented by the use of nonsteroidal antiinflammatory drugs,[46] [50] 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.[46] [49] [51] A serotonin agonist (sumatriptan, a 5-HT1 receptor agonist) was reported to be effective for HAH prevention and/or treatment in some studies[48] [343] but not in others.[27] Interestingly, oxygen is often immediately effective for HAH in subjects with and without AMS, indicating a rapidly reversible mechanism of the headache.[22] [108] The response to many different agents might reflect multiple components of the pathophysiology or merely the nonspecific nature of analgesics in some studies. As Sanchez del Rio and Moskowitz[298] 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. They recently provided a useful multifactorial concept of the pathogenesis of HAH, based on current understanding of headaches in general. [298] 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 likely altered at high altitude (Figure 1-10 (Figure Not Available) ). [298] If AMS and especially HACE ensue, altered intracranial dynamics may also play a role, via compression or distension of pain-sensitive structures. Acute Mountain Sickness Although the syndrome of AMS has been recognized for centuries, modern rapid transport and the 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), length of altitude exposure, level of exertion,[283] and inherent physiologic susceptibility. For example, AMS is more common on Mt. Rainier because of the rapid ascent, whereas HAPE is uncommon because of the short stay (less than 36 hours). Age has a small influence on incidence,[106] with the elderly somewhat less vulnerable.[282] Women apparently have the same[280] or a slightly greater incidence of AMS[106] [134] but may be less susceptible to pulmonary edema.[64] [323] It is useful clinically to classify AMS as mild or moderate to severe on the basis of symptoms ( Table 1-4 ). Importantly, AMS can herald the beginning of life-threatening cerebral edema. Diagnosis.
The diagnosis of AMS is based on setting, symptoms, physical findings, and exclusion of other illnesses. The setting is generally rapid ascent of unacclimatized *References [ 27]
[ 46] [ 48] [ 49] [ 50] [ 108] [ 267] [ 343]
.
13
TABLE 1-4 -- Classification of Acute Mountain Sickness CLINICAL CLASSIFICATION
Symptoms
HAH
MILD AMS
MODERATE TO SEVERE AMS
HACE
Headache only
Headache + 1 more symptom (nausea/vomiting, fatigue/lassitude, dizziness or difficulty sleeping)
Headache + 1 or more symptoms ±Headache (nausea/vomiting, fatigue/lassitude, dizziness or difficulty sleeping) Worsening of symptoms seen in moderate to severe AMS
All symptoms of mild severity
Symptoms of moderate to severe intensity
LL-AMS score*
1–3, headache only
2–4
5–15
Physical signs
None
None
None
Ataxia, altered mental status
Findings
None
None
Antidiuresis, slight increase in temperature, slight desaturation, widened A-a gradient, elevated ICP, white matter edema (CT, MRI)
HAPE common: +chest x-ray, rales, dyspnea at rest; elevated ICP; white matter edema (CT, MRI)
Same as HAH, plus early vasogenic edema
Vasogenic edema
Advanced vasogenic cerebral edema
Pathophysiology Cerebral vasodilation, activation of trigeminovascular system†
*The self-report Lake Louise AMS score. †See Figure 1-10 (Figure Not Available) and a recent review (reference
[ 298]
).
persons to 2500 m (8202 feet) or higher from altitudes below 1500 m (4921 feet). For partially acclimatized persons, abrupt ascent to a higher altitude, overexertion, use of respiratory depressants, and perhaps onset of infectious illness[243] are common contributing factors. The cardinal symptom of early AMS is headache, followed in incidence by fatigue, dizziness, and anorexia.[106] [134] [321] The headache is usually throbbing, bitemporal or occipital, typically worse during the night and on awakening, and made worse by Valsalva's maneuver or stooping over. 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, 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 or the group's basic needs. Any symptom suggestive of AMS should be considered caused by altitude unless proven otherwise. 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.[209] However, any pulmonary symptom mandates careful examination for pulmonary edema. Specific physical findings are lacking in mild AMS. Early authors described tachycardia, but Singh et al[321] 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. Rales localized to one area of the chest are common (5% to 20% incidence)[201] and probably represent pulmonary vascular congestion. A slight increased body temperature with AMS was recently reported.[200] Funduscopic examination reveals venous tortuosity and dilation; retinal hemorrhages may or may not be present and are not diagnostic; they are more common in AMS than non-AMS subjects at 4243 m (13,921 feet).[105] Absence of the normal altitude diuresis, evidenced by lack of increased urine output and retention of
14
fluid, is an early finding in AMS although not always present.[25] [110] [284] [321] [335] 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 is the single most useful sign for recognizing the progression from AMS to HACE; all persons proceeding to high altitudes should be aware of this fact. Differential Diagnosis.
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 (see Alcohol and Altitude). 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 differentiate the two. AMS is not improved by fluid administration alone; body hydration does not influence susceptibility to AMS (contrary to conventional wisdom).[7] 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. 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.[342] 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. Persistent unconsciousness in the setting of carbon monoxide exposure at high altitude can be due to either severe carbon monoxide poisoning or high-altitude cerebral edema. The management is nearly the same and includes coma care, oxygen, descent, and evacuation to a hospital. Pathophysiology.
Although the basic cause of AMS is hypobaric hypoxia, the syndrome is different from acute hypoxia. Because of a lag time in onset of symptoms after ascent and lack of immediate reversal of all symptoms with oxygen, AMS is thought to be secondary to the body's responses to modest hypoxia. In addition, even though an altitude of 2500 to 2700 m (8202 to 8859 feet) presents only a minor decrement in arterial oxygen transport (SaO2 is still above 90%), AMS is common and certain 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 that relate to pathophysiology include relative hypoventilation,[212] [236] impaired gas exchange (interstitial edema),[99] [188] fluid retention and redistribution,[25] [284] [335] and increased sympathetic activity.[19] [23] In mild to moderate AMS, limited data suggest that intracranial pressure (ICP) is not elevated.[125] [366] In contrast, increased ICP and cerebral edema are documented in moderate to severe AMS, reflecting the continuum from AMS to HACE.[140] [180] [213] [321] [361]
Relative hypoventilation may be due primarily to a decreased drive to breathe (low HVR) or may be secondary to ventilatory depression associated with AMS.[236] [277] Persons with quite low HVR are more likely to suffer AMS than are those with a high ventilatory drive.[131] [212] [236] For persons with intermediate HVR values (most people), ventilatory drive probably has no predictive value.[225] [277] The protective role of a high HVR 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,[321] increased alveolar-arterial oxygen difference,[99] [132] decreased transthoracic impedance,[163] and a high incidence of rales.[201] 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. The fact that exercise can contribute to interstitial edema at altitude was recently confirmed.[6] 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 A-a oxygen gradient observed in AMS[132] speaks against the increased lung water of AMS being related to HAPE, but the issue deserves further study. 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.[128] [335] Persons with AMS had elevated plasma or urine AVP levels in some studies,[23] [321]
15
but cause and effect could not be established. Other studies showed no AVP elevation. [25] The usual decrease in aldosterone on ascent to altitude does not occur in persons with AMS, and this may contribute to the antidiuresis. [25] 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.[19] Atrial natriuretic peptide (ANP) is elevated in AMS. Although this is most likely compensatory, elevated plasma ANP levels may contribute to vasodilation and increased microvascular permeability. [19] [359] 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. [335] Increased sympathetic nervous system activity is also consistent with the greater rise in norepinephrine noted in subjects with AMS.[23] See Krasney[177] 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.[99] [321] Persons with moderate to severe AMS or HACE display white matter edema on brain imaging and elevated ICP.* Possible mechanisms include cytotoxic edema with a shift of fluid into the cells, or vasogenic (interstitial) edema from increased permeability of the blood-brain barrier (BBB), or both. The classic view that hypoxia causes failure of the adenosine triphosphate (ATP)-dependent sodium pump and subsequent intracellular edema[137] is untenable, given the newer understanding of brain energetics; ATP levels are maintained even in severe hypoxemia.[315] The evidence now favors vasogenic brain edema as the cause of AMS/HACE. Hackett et al[118] point out that reversible white matter edema, with sparing of the gray matter, is characteristic of vasogenic edema (see Figure 1-13 ). The fact that dexamethasone is so effective for AMS also suggests vasogenic edema because this is the only steroid-responsive brain edema. In addition, a model of AMS in conscious sheep exposed to 10% oxygen for several days supports the vasogenic brain-swelling hypothesis. Krasney et al[179] have shown that cerebral capillary pressure rises, which causes filtration of fluid across the BBB and an increase in wet-to-dry cerebral tissue ratio. The pathophysiology may be similar to hypertensive encephalopathy, in which loss of vascular autoregulation results in increased pressures transmitted to the capillaries with resultant white matter edema.[189] [190] Because prolonged cerebral vasodilation by itself, however, is not sufficient to induce vasogenic edema, Hackett[104] and Krasney [178] 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, endothelium-derived products, such as nitric oxide, and direct neural and humoral factors known to affect the BBB. For a complete discussion of the mechanisms of BBB permeability and their possible role in altitude illness, see the recent reviews by Drewes,[77] Hackett,[104] Hossman,[135] and Schilling[304] ( Figure 1-11 ). The question of whether mild AMS, especially headache alone, is due to vasogenic cerebral edema is not yet answered (see High-Altitude Headache). Recent magnetic resonance imaging (MRI) studies demonstrated brain swelling in all subjects ascending rapidly to moderate altitude, regardless of the presence of AMS. [162] [244] The change in brain volume was greater than that expected from increased cerebral blood volume alone (resulting from 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 et al[174] 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. Although 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? Correlations of AMS with HVR, ventilation, fluid status, lung function, and physical fitness have been weak at best. Ross[294] hypothesized in 1985 that the apparent random nature of susceptibility might be explained by random anatomic differences. Specifically, he suggested that persons with smaller intracranial and intraspinal cerebrospinal fluid (CSF) capacity would be disposed to develop AMS because they would not tolerate brain *References [ 118]
[ 140] [ 180] [ 194] [ 213] [ 321]
.
16
Figure 1-11 Proposed pathophysiology of acute mountain sickness. BBB, Blood-brain barrier; CBF, cerebral blood flow; CBV, cerebral blood volume; HVR, hypoxic ventilatory response; iNOS, inducible nitric oxide synthase; Pcap, capillary pressure; VEGF, vascular endothelial growth factor.
swelling as well as those with more "room" in the craniospinal axis. The displacement of CSF through the foramen magnum into the spinal canal is the first compensatory response to increased brain volume, followed by increased CSF absorption and decreased CSF formation. Studies have shown that the increase in ICP for a given increase in brain volume is directly related to the "tightness" of the brain in the cranium (the brain volume:intracranial volume ratio) and to the volume of the spinal canal. [313] Thus the greater the initial CSF volume, the more accommodation that can take place in response to brain edema. Increases in volume are "buffered" by CSF dynamics. In light of our present understanding of increased brain volume on ascent to altitude, his hypothesis is very attractive. Preliminary data that showed a relationship of preascent ventricular size or brain volume:cranial vault ratios and susceptibility to AMS support this hypothesis, and the idea deserves further study.[104] [373] 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. Singh et al[321] followed the illness in soldiers airlifted to altitudes of 3300 to 5500 m (10,827 to 18,045 feet). Incapacitating illness lasted 2 to 5 days, but 40% still had symptoms after 1 week and 13% after 1 month. Nine soldiers failed to acclimatize in 6 months and were considered unfit for duty at high altitude.[321] 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.[367] 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 3000 m (9840 feet) was 15 hours, with a range of 6 to 94 hours.[68] Most individuals treat or tolerate their symptoms as the illness resolves over 1 to 3 days while
17
acclimatization improves, but some persons with AMS seek medical treatment or are forced to descend if symptoms persist. A small percentage of those with AMS (8% at 4243 m [13,921 feet]) [106] go on to develop cerebral edema, especially if ascent is continued in spite of illness. Treatment.
The proper management of AMS is based on early diagnosis and acknowledgment that initial clinical presentation does not predict eventual severity ( Box 1-3 ). Therefore 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 changes (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 (125 to 250 mg twice a day orally) speeds acclimatization and thus terminates the illness if given early.[99] Symptomatic therapy includes analgesics such as aspirin (650 mg), acetaminophen (650 to 1000 mg), ibuprofen [46] or other nonsteroidal antiinflammatory drugs, or codeine (30 mg) for headache. Prochlorperazine (Compazine, 5 to 10 mg intramuscularly) can be given by an appropriate route for nausea and vomiting and has the advantage of augmenting the HVR.[255] Promethazine (Phenergan, 50 mg by suppository or ingestion) is also useful. Persons with AMS should avoid alcohol and other respiratory depressants because of the danger of exaggerated hypoxemia during sleep. 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 (1640 to 3281 feet) is usually sufficient. Exertion should be minimized. Oxygen, if available, is particularly effective (and supply is conserved) if given in low flow (0.5 to 1 L/min by mask or cannula) during the night. Hyperbaric chambers, which simulate descent, have been used to treat AMS and aid acclimatization. They are effective and require no supplemental oxygen. Lightweight (less than 7 kg) fabric pressure bags inflated by manual air pumps are now being used on mountaineering expeditions and in mountain clinics ( Figure 1-12 ). An inflation of 2 psi is roughly equivalent to a drop in altitude of 1600 m (5250 feet); the exact equivalent depends on initial altitude.[168] [279] A few hours of pressurization result in symptomatic improvement and can be an effective temporizing measure while awaiting descent or the benefit of medical therapy.[168] [242] [258] [286] [338] Long-term (12 hours or more) use of these portable devices would be necessary to resolve AMS completely.
Box 1-3. FIELD TREATMENT OF HIGH-ALTITUDE ILLNESS
HIGH-ALTITUDE HEADACHE AND MILD ACUTE MOUNTAIN SICKNESS Stop ascent, rest, 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 Nifedipine, 10 mg po q4h by titration to response, or 10 mg po once, followed by 30 mg extended release q12 to 24h Hyperbaric therapy or Immediate descent
PERIODIC BREATHING Acetazolamide, 62.5 to 125 mg at bedtime as needed
Figure 1-12 The HELP System (Live High, Boulder, Colo.) uses breathing bladder technology to minimize the pumping necessary to circulate air in the hyperbaric compartment.
18
The use of diuretics has a sound basis because of fluid retention associated with AMS. Acetazolamide is of unquestionable prophylactic value and is now commonly and successfully used to treat AMS as well. Acetazolamide may be helpful in part because of its diuretic action; its multiple modes of action are discussed later. Singh et al[321] successfully used furosemide (80 mg twice a day for 2 days) to treat 446 soldiers with all degrees of AMS; it has not since been studied for treatment. Furosemide induced a brisk diuresis, relieved pulmonary congestion, and improved headache and other neurologic symptoms. Spironolactone, hydrochlorothiazide, and other diuretics have not yet been evaluated for treatment. The steroid betamethasone was initially reported by Singh et al [321] to improve symptoms of soldiers with severe AMS. Since then, dexamethasone was found to be very effective for treatment of all degrees of AMS. Dexamethasone is effective for treatment of moderate to severe AMS. [86] [116] [171] Hackett et al[116] used 4 mg orally or intramuscularly every 6 hours, and Ferrazinni et al[86] 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.[289] Dexamethasone should be started in conjunction with descent or hyperbaric treatment,[171] if possible, and continued until the victim is down to low altitude. Although the mechanism of action of dexamethasone is not clear, it probably acts by improving brain capillary integrity and diminishing vasogenic edema.[65] Dexamethasone seems not to improve acclimatization because symptoms recur when the drug is withdrawn. Therefore an argument could be made for using dexamethasone to relieve symptoms and acetazolamide to speed acclimatization.[35] Prevention.
Graded ascent is the surest and safest method of prevention, although particularly susceptible individuals may still become ill. Current recommendations for persons without altitude experience are to avoid abrupt ascent to sleeping altitudes greater than 3000 m (9843 feet) and to spend 2 to 3 nights at 2500 to 3000 m (8202 to 9843 feet) before going higher, with an extra night for acclimatization every 600 to 900 m (1969 to 2953 feet) if continuing ascent. Abrupt increases of more than 600 m (1969 feet) in sleeping altitude should be avoided when over 2500 m (8202 feet). 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.[62]
[124] [337]
Exertion early in altitude exposure contributes to altitude illness,[283] whereas limited exercise seems to aid acclimatization.
ACETAZOLAMIDE PROPHYLAXIS.
Acetazolamide is the drug of choice for prophylaxis of AMS. A carbonic anhydrase (CA) inhibitor, acetazolamide slows the hydration of carbon dioxide:
The effects are protean, involving particularly the red blood cells, brain, lungs, and kidneys. By inhibiting renal carbonic anhydrase, acetazolamide reduces reabsorption of bicarbonate and sodium and thus causes a bicarbonate diuresis and metabolic acidosis starting within 1 hour after ingestion. This rapidly enhances ventilatory acclimatization. Perhaps most important, the drug maintains oxygenation during sleep and prevents periods of extreme hypoxemia (see Figure 1-6 ). [114] [332] [336] Because of acetazolamide's diuretic action, it counteracts the fluid retention of AMS. It also diminishes nocturnal antidiuretic hormone (ADH) secretion[56] and decreases CSF production and volume and possibly CSF pressure.[310] Which of these effects is most important in preventing AMS is unclear. Numerous studies taken together indicate that acetazolamide is approximately 75% effective in preventing AMS in persons rapidly transported to altitudes of 3000 to 4500 m (9843 to 14,764 feet).[84] Indications for acetazolamide prophylaxis include rapid ascent (1 day or less) to altitudes over 3000 m (9843 feet); a rapid gain in sleeping altitude, for example, moving camp from 4000 m (13,123 feet) to 5000 m (16,404 feet) in a day; and a past history of recurrent AMS or HAPE. Numerous dosage regimens have been effective.[74] [80] Smaller doses (125 to 250 mg twice a day) starting 24 hours before ascent work as well as higher doses started earlier.[223] A 500-mg sustained action capsule of Diamox taken every 24 hours is probably equally effective and results in fewer side effects because of lower peak serum levels.[363] Most authors recommend continuing for the first day or two at high altitude, and some suggest daily acetazolamide the entire time at high altitude.[43] This hardly seems necessary once acclimatization is established and the danger of AMS has passed. Spironolactone[165] [186] and other diuretics have shown equivocal results for AMS prevention. 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. A sulfa drug, acetazolamide carries the usual precautions about hypersensitivity, crystalluria, and bone marrow suppression.
19
DEXAMETHASONE.
Dexamethasone is also useful for prevention of AMS. The initial chamber study in 1984 was with sedentary subjects.[167] The drug reduced the incidence of AMS from 78% to 20%, comparable with previous studies with acetazolamide. Dexamethasone was not as effective in exercising subjects on Pike's Peak,[289] but subsequent work has shown effectiveness comparable with acetazolamide.[84] [195] [374] The combination of acetazolamide and dexamethasone proved superior to dexamethasone alone. [374] 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. High-Altitude Cerebral Edema HACE is characterized clinically by a progression to encephalopathy in the setting of AMS or HAPE. As discussed previously, AMS is essentially a neurologic disorder, probably related to brain swelling, and HACE appears to be the extreme form of AMS; the distinction between AMS and HACE is therefore inherently blurred. Clinical Presentation.
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 frequently, but not always, present. Hallucinations, cranial nerve palsy, hemiparesis, hemiplegia, seizures, and focal neurologic signs have also been reported.[120] [140] [321] 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. Cyanosis or a gray pallor is common. Arterial blood gas study or pulse oximetry reveals exaggerated hypoxemia. Clinical examination, chest radiography, and autopsy have often demonstrated pulmonary edema; indeed, isolated HACE without HAPE is uncommon.[103] [118] The following case report from Mt. McKinley illustrates a clinical course of HACE, in conjunction with HAPE: H.E. was a 26-year-old German lumberjack with extensive mountaineering experience. He ascended to 5200 m (17,061 feet) from 2000 m (6562 feet) in 4 days and attempted the summit (6194 m [20,323 feet]) on the fifth day. At 5800 m (19,030 feet) he turned back because of severe fatigue, headache, and malaise. He returned alone to 5200 m (17,061 feet), stumbling on the way because of loss of coordination. He had no appetite and crawled into his sleeping bag too weak, tired, and disoriented to undress. He recalled no pulmonary symptoms. In the morning H.E. was unarousable, slightly cyanotic, and noted to have Cheyne-Stokes respirations. After 10 minutes on high-flow oxygen H.E. began to regain consciousness, although he was completely
Figure 1-13 Magnetic resonance image of patient with high-altitude cerebral edema. Increased T2 signal in splenium of corpus callosum (arrow) indicates edema.
disoriented and unable to move. A rescue team lowered him down a steep slope, and on arrival at 4400 m (14,436 feet) 4 hours later he was conscious but still disoriented, able to move extremities but unable to stand. Respiratory rate was 60 breaths/min and heart rate was 112 beats/min. Papilledema and a few rales were present. SaO2 % was 54% on room air (normal is 85% to 90%). On a 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 H.E. was still ataxic but was able to stand, take fluids, and eat heartily. He was evacuated by air to Anchorage (sea level) at 12:00 PM. On admission to the hospital at 3:30 PM, roughly 36 hours after regaining consciousness, H.E. was somewhat confused and mildly ataxic. Arterial blood gas studies on room air showed a PO2 of 58 torr, pH of 7.5, and PCO2 of 27 torr. Bilateral pulmonary infiltrates were present on the chest radiograph. Magnetic resonance imaging of the brain revealed white matter edema, primarily of the corpus callosum ( Figure 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 as AMS (see Acute Mountain Sickness, Pathophysiology and Figure 1-11 ). The early brain swelling of AMS becomes much more severe. In cases similar to this, lumbar punctures have
20
revealed elevated CSF pressures, often more than 300 mm H2 O[140] [361] ; evidence of cerebral edema on CT scan and MRI[118] [176] ; and gross cerebral edema on necropsy.[72] [73] Small petechial hemorrhages were also consistently found on autopsy, and venous sinus thromboses were occasionally seen.[72] [73] Well-documented cases have often included pulmonary edema that was not clinically apparent.
Whereas the mild brain swelling of AMS and reversible HACE is most likely vasogenic, as the spectrum shifts to severe, end-stage HACE, gray matter (presumably cytotoxic) edema develops as well, culminating in death. As Klatzo[175] 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 ICP produces many of its effects by decreasing cerebral blood flow, and brain tissue becomes ischemic on this basis also.[219] Focal neurologic signs caused by brainstem distortion and by extraaxial compression, as in third and sixth cranial nerve palsies, may develop,[291] 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. Treatment.
Successful treatment of HACE 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 1-3 ). Oxygen can be titrated to maintain SaO2 at greater than 90% if oximetry is available. Comatose patients require additional airway management and bladder drainage. Attempting to decrease ICP by intubation and hyperventilation is a reasonable approach, although these patients are already alkalotic and overhyperventilation could result in cerebral ischemia. Loop diuretics, such as furosemide (40 to 80 mg) or bumetanide (1 to 2 mg), may reduce brain hydration, but an adequate intravascular volume to maintain perfusion pressure is critical. Hypertonic solutions of saline, mannitol, or oral glycerol have been suggested but rarely are used in the field. Controlled studies are lacking, but empirically the 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.[140] Sequelae lasting weeks are common[118] [140] ; longer-term follow-up has been limited. Prevention of HACE is the same as for AMS. Focal Neurologic Conditions without Cerebral Edema Various localizing neurologic signs, transient in nature and not necessarily occurring in the setting of AMS, suggest migraine, cerebrovascular spasm, TIA, local hypoxia without loss of perfusion (watershed effect), or focal edema. Cortical blindness is one such condition. Hackett et al[113] 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" have included transient hemiplegia or hemiparesis, transient global amnesia, unilateral paresthesia, aphasia, and scotomas.[41] [196] [274] [364] 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.[55] [138] [322] Factors contributing to stroke may include polycythemia, dehydration, and increased ICP if AMS is present; increased cerebrovenous pressure; cerebrovascular spasm; and perhaps coagulation abnormalities. Stroke may be confused with HACE. Neurologic symptoms, especially focal abnormalities without AMS or HAPE, suggest a cerebrovascular event and mandate careful evaluation. Clinical Presentation
E.H., a 42-year-old male climber on a Mt. Everest expedition, awoke at 8000 m (26,247 feet) with dense paralysis of the right arm and weakness of the right leg. On descent the paresis cleared, but at base camp (5000 m [16,404 feet]) severe vertigo developed, along with extreme ataxia and weakness. Neurologic consultation on return to the United States re- sulted in a diagnosis of multiple small cerebral infarcts, but none was visible on CT scan of the brain. The hematocrit value 3 weeks after descent from the mountain was 70%. Over the next 4 years, signs gradually improved, but mild ataxia, nystagmus, and dyslexia persist. The focal and persis- tent nature of the cerebral symptoms and signs, although multiple, indicates a cerebrovascular, rather than an ICP, cause. The hematocrit value on the mountain was greater than 70%, high enough for increased viscosity and microcir- culatory sludging to contribute to ischemia and infarction. 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 TIAs at high altitude should probably be started on aspirin therapy and proceed to a lower altitude. Oxygen may quickly abort cerebrovascular spasm and will improve watershed hypoxic events. When oxygen is not available, rebreathing
21
to raise alveolar PCO2 may be helpful by increasing cerebral blood flow. Cognitive Changes at High Altitude If cerebral oxygen consumption is constant, what causes the well-documented, albeit mild, cognitive changes at high altitude? The cognitive changes may be related to specific neurotransmitters that are affected by mild hypoxia. For example, tryptophan hydroxylase in the serotonin synthesis pathway has a high requirement for oxygen (Km = 37 torr).[61] [94] Tyrosine hydroxylase, in the dopamine pathway, is also oxygen-sensitive. Gibson [94] suggested that a decrease in acetylcholine activity during hypoxia might explain the lassitude. In a fascinating study, Banderet[14] showed that increased dietary tyrosine reduced mood changes and symptoms of environmental stress in subjects at simulated altitude. Further work with neurotransmitter agonists and antagonists will help shed light on their role in cognitive dysfunction at altitude and could lead to new pharmacologic approaches to improve neurologic function. High-Altitude Pulmonary Edema The most common cause of death related to high altitude, HAPE, is completely and easily reversed if recognized early and treated properly. Undoubtedly HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of "pneumonia" within days of arriving at high altitude. The death of Dr. Jacottet, "a robust, broad-shouldered young man," on Mt. Blanc in 1891 (he refused descent so that he could "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 suffoca- tive catarrh accompanied by acute edema of the lungs.... I have gone into the particulars of this sorrowful incident be- cause a case of inflammation of the lungs also occurred dur- ing our expedition, on the summit of Monte Rosa, from which, however, the sufferer fortunately recovered.[241] On an expedition to K2 (Karakorum Range, Pakistan) in 1902, Crowley [66] described a climber "suffering from edema of both lungs and his mind was gone." In the Andes, physicians were familiar with pulmonary edema peculiar to high altitude,[160] but it was not until Hultgren[147] and Houston[136] that the English-speaking world became aware of high-altitude pulmonary edema (see Rennie[271] for a recent review). Hultgren[157] then published hemodynamic measurements in persons with HAPE, demonstrating that it was a noncardiogenic type of edema. Since that time, many studies and reviews have been published,[16] [93] and HAPE is still the subject of intense investigation. The incidence of HAPE varies from less than 1 in 10,000 skiers in Colorado to 1 in 50 climbers on Mt. McKinley and was higher (15%) in some regiments in the Indian Army (see Table 1-1 ). Individual susceptibility, rate of ascent, altitude reached, degree of cold,[269] physical exertion, and use of sleeping medications are all factors implicated in its occurrence. Younger persons seem more susceptible.[324] Although HAPE occurs in both genders, it is perhaps less common in women.[64] [153] [323] 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 (10,007-foot) sleeping altitude the first night of his trip in the Sierra Nevada. He proceeded to 3700 m (12,140 feet) the next day, noticing more dyspnea on exertion when walking uphill, a longer time than usual to recover when he rested, and a dry cough. He complained of headache, shivering, dyspnea, and insomnia the second night. The third day the group descended to 3500 m (11,483 feet) and rested, primarily for D.L.'s benefit. That night D.L. was unable to eat, noted severe dyspnea, and suffered coughing spasms and headache. On the fourth morning, D.L. was too exhausted and weak to get out of his sleeping bag. His companions noted that he was breathless, cyanotic, and ataxic but had clear mental status. A few hours later he was transported by helicopter to a hospital at 1200 m (3937 feet). On admission he was cyanotic, oral temperature was 37.8° C (100° F), blood pressure 130/76 torr, 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 were reported as normal. Romberg's and finger-to-nose tests revealed 1+ ataxia. Arterial blood gas studies on room air revealed PO2 24 torr, PCO2 28 torr, and pH 7.45. The chest
radiograph showed extensive bilateral patchy infiltrates ( Figure 1-14, C ). 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 torr, PCO2 30 torr, 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 2500 m (4921 feet and 8202 feet). 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. HAPE usually occurs within the first 2 to 4 days of ascent to higher altitudes (above 2500 m [8202 feet]), most commonly on the second night.[103] The earliest indications of the illness are decreased exercise performance and increased recovery time from exercise. The victim usually notices fatigue, weakness, and dyspnea on exertion, especially when he or she is trying to walk
22
Figure 1-14 A, Typical radiograph of high-altitude pulmonary edema (HAPE) in 29-year-old female skier at 2450 m (8036 feet). B, Same patient 1 day after descent and oxygen administration, showing rapid clearing. C, Bilateral pulmonary infiltrates on radiograph of 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.
23
TABLE 1-5 -- Severity Classification of High-Altitude Pulmonary Edema SIGNS
GRADE
SYMPTOMS
CHEST FILM
1 Mild
Dyspnea on exertion, dry cough, fatigue while moving uphill
HR (rest) < 90–100; RR (rest) < 20; dusky nail beds; localized Minor exudate involving less than 25% of rales, if any one lung field
2 Moderate
Dyspnea, weakness, fatigue on level walking; raspy cough; headache; anorexia
HR 90–100; RR 16–30; cyanotic nail beds; rales present; ataxia may be present
Some infiltrate involving 50% of one lung or smaller area of both lungs
3 Severe
Dyspnea at rest, productive cough, orthopnea, extreme weakness
Bilateral rales; HR > 110; RR > 30; facial and nail bed cyanosis; ataxia; stupor; coma; blood-tinged sputum
Bilateral infiltrates > 50% of each lung
Modified from Hultgren HN: High altitude pulmonary edema. In Staub NC, editor: Lung water and solute exchange, New York, 1978, Marcel Dekker. HR, Heart rate; RR, respiratory rate. 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.[153] 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 to the victim the development of a serious condition. In contrast to the usual 1- to 2-day gradual onset, HAPE may strike abruptly, especially in a sedentary person who may not notice the early stages.[347] Orthopnea is uncommon (7%). Pink or blood-tinged, frothy sputum is a very late finding. Hemoptysis was present in 6% in one series.[159] Severe hypoxemia may produce cerebral edema with mental changes, ataxia, decreased level of consciousness, and coma. Hultgren[159] reported an incidence of HACE of 14% in those with HAPE at ski resorts. On admission to the hospital, the victim does not generally appear as ill as would be expected based on 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 ). [157] Rales may be unilateral or bilateral and usually originate from the right middle lobe. Concomitant respiratory infection is sometimes present. Pulmonary edema sometimes presents with predominantly neurologic manifestations and minimal pulmonary symptoms and findings. Cerebral edema, especially with coma, may obscure the diagnosis of HAPE.[107] Pulse oximetry or chest radiography confirms the diagnosis. The differential diagnosis includes pneumonia, pulmonary embolism or infarct, and sometimes asthma. Complications include infection, cerebral edema, pulmonary embolism or thrombosis, and such injuries as frostbite or trauma secondary to incapacitation.[16] [107] [154]
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 HAPE* RECOVERY* CONTROLS† SaO2 %
58.0
84.0
89.0
Mean pulmonary artery pressure (mm Hg)
63.0
18.0
21.3
Wedge pressure (mm Hg)
1.5
3.5
7.1
Cardiac index (L/m2 )
2.5
4.4
4.1
1210.0
169.0
169.0
Pulmonary vascular resistance (dyne/cm-5 ) Mean arterial blood pressure (mm Hg)
82.0
—
96.0
*HAPE and recovery values from Penaloza D, Sime F: Am J Cardiol 23:369, 1969. †Mean values from 31 normal subjects studied at 3700 m; from Hultgren HN, Grover RF: Annu Rev Med 19:119, 1968.
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 ).[155] [260] Echocardiography demonstrates high estimated pulmonary artery pressures, tricuspid regurgitation, normal left ventricular function, and variable right-sided heart findings of increased atrial and ventricular size.[117] [254] The electrocardiogram usually reveals sinus tachycardia. Changes consistent with acute pulmonary hypertension
24
have been described, such as right axis deviation, right bundle branch block, voltage for right ventricular hypertrophy, and P wave abnormalities.[16] [153] Atrial flutter has been reported, but ventricular arrhythmias have not.
Laboratory Studies.
Kobayashi et al[176] reported clinical laboratory values in 27 patients with HAPE. This report confirms typical 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 above 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 according to the authors may have indicated brain damage.[176] Arterial blood gas studies consistently reveal respiratory alkalosis and marked hypoxemia, more severe than expected for the patient's clinical condition. Respiratory or metabolic acidosis related to hypoxemia has not been reported. Therefore arterial blood gas studies are not essential if noninvasive pulse oximetry is available to measure arterial oxygenation. At 4200 m (13,780 feet) on Mt. McKinley, the mean value of arterial PO2 in HAPE was 28 ± 4 torr. Values as low as 24 torr in HAPE are not unusual. Arterial oxygen saturation values in our HAPE subjects ranged from 40% to 70%, with a mean of 56% ± 8%.[307] Arterial acid-base values may be misleading in patients taking acetazolamide because this drug produces significant metabolic acidosis. Radiologic Findings.
The radiologic findings in HAPE have been described in original reports.[157] [206] [348] [349] 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's lines. The pulmonary arteries increase in diameter.[348] Infiltrates are commonly described as fluffy and patchy with areas of aeration between infiltrates, 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 quite rare. The x-ray 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 the basis for a diagnosis of unilateral absent pulmonary artery syndrome.[109] The x-ray 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 one to several days. Infiltrates are likely to persist longer if the patient remains at high altitude, even if confined to bed and receiving oxygen therapy. Radiographs taken within 48 hours of return to low altitude may confirm a diagnosis of HAPE. Pathologic Findings.
More than 20 autopsy reports of persons who died of HAPE have been published.* Of those whose cranium was opened, more than half had cerebral edema. All lungs showed extensive and severe edema, with bloody, foamy fluid in the airways. Lung weights were two to four times normal. The left side of the heart was normal. The right atrium and main pulmonary artery were often distended. Proteinaceous exudate with hyaline membranes was characteristic. All lungs had areas of inflammation with neutrophil accumulation. The diagnosis of bronchopneumonia was common, although bacteria were not noted. Pulmonary veins, the left ventricle, and the left atrium were generally not dilated, in contrast to the right ventricle and atrium. Most reports mention capillary and arteriolar thrombi and alveolar fibrin deposits, as well as microvascular and gross pulmonary hemorrhage and infarcts. The autopsy findings thus suggest a protein-rich, permeability type of edema, with thrombi or emboli. Confirmation of HAPE as a permeability edema was obtained by analysis of alveolar lavage fluid by Schoene et al.[306] [307] 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.[307] 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 et al.[112] In addition, the lavage fluid contained vasoactive eicosanoids and complement proteins, indicative of endothelium-leukocyte interactions. Mechanisms of High-Altitude Pulmonary Edema.
The search continues for the mechanism triggering the pulmonary vascular leak. 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. One mechanism that is consistent with the facts is failure of capillaries secondary to overperfusion edema ( Figure 1-15 ). ROLE OF PULMONARY HYPERTENSION.
Excessive pulmonary artery pressure (PAP) is the sine qua non of *References [ 8]
[ 72] [ 247] [ 319] [ 321] [ 361]
.
25
Figure 1-15 Proposed pathophysiology of high-altitude pulmonary edema. HPV, Hypoxic pulmonary vasoconstriction; HVR, hypoxic ventilatory response; Pcap, capillary pressure; PHTN, pulmonary hypertension.
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, atelectasis, or some other cause, 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-perfusion matching at high altitude. The degree of HPVR varies widely among individuals (as well as among species). Presumably those with a greater HPVR have a greater percentage of muscularized arterioles, constrict more units (a greater amount) of the circulation, and have a more restricted vascular bed and a greater rise in PAP. Although other factors, such as the vigor of the ventilatory response and subsequent arterial PO2 , may help determine the ultimate degree of pulmonary hypertension, HPVR appears to be the dominant factor. Because all persons with HAPE have excessive pulmonary hypertension, but not all those with excessive pulmonary hypertension have HAPE, it appears that pulmonary hypertension is a necessary factor but in itself is not the cause of HAPE. OVERPERFUSION.
Hultgren[148] suggested that in those who develop HAPE, the hypoxic pulmonary vasoconstriction is uneven and the microcirculation in an unconstricted (relatively dilated) area is subjected to high pressure and flow, leading to 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.[148] Uneven perfusion is suggested clinically by the typical patchy x-ray appearance and is supported by lung scans during acute hypoxia that show uneven perfusion in persons susceptible to HAPE.[346] Persons born without a right pulmonary artery are highly susceptible to HAPE (see Figure 1-14, D ), [109] supporting the concept of overperfusion of a restricted vascular bed as a cause of edema, because the entire cardiac output flows into one lung. Staub,[326] in an accompanying editorial, supported the concept of overperfusion edema
26
but pointed out that hydrostatic edema generally produces a low-protein transudate. 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). PERMEABILITY FACTORS.
Endothelial damage from shear forces,[287] as well as stress failure of the capillary membrane,[357] [358] has therefore been invoked to explain the high-protein permeability
leak from overperfusion. A recent preliminary study has found activity of adhesion molecules on ascent to high altitude,[82] which indicates interaction of leukocytes and endothelium. The lavage fluid findings of inflammatory mediators also point to the possible endothelial involvement, as do a number of animal studies that failed to produce permeability edema with overperfusion alone but succeeded when the pulmonary vascular bed was embolized with microspheres. [98] The overperfusion hypothesis is consistent with recent clinical trials of vasodilators intended for prevention and treatment of HAPE. Presumably, when pulmonary vasoconstriction is relieved, flow becomes more homogeneous, and because overall PAP is reduced, microvascular pressure also drops. The rapid reversibility of the illness is also consistent with this mechanism. Other factors contributing to increased hydrostatic pressure, such as exercise or a high salt load with subsequent hypervolemia, could also play a role in HAPE. The effective use of diuretics and vasodilators also supports a rationale for reducing hydrostatic pressure. A recent study found that an intravenous a-adrenergic blocker, phentolamine, was effective in reducing PAP in HAPE, [117] which raises the possibility that pulmonary venous constriction, which is sympathetically mediated, could be a factor. Any degree of venous constriction could significantly contribute to increased microvascular pressure. Experiments that convincingly demonstrate the validity of the preceding hypotheses are obviously difficult to perform in humans and await a successful animal model of HAPE. For now, the exact site and mechanism of the leak in HAPE remain enigmatic. CONTROL OF VENTILATION.
As in AMS, control of ventilation may play a role in the pathophysiology of HAPE. Victims have been shown to have a lower HVR than persons who acclimatized well,[115] [211] 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.[103] [115] 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 CNS suppression. Such persons, when given oxygen, show a "paradoxical" increase in ventilation.[115] HAPE Susceptibility.
Persons susceptible to HAPE (HAPE-s) show an abnormal rise of PAP and pulmonary vascular resistance during a hypoxic challenge at rest[169] [370] and during exercise, and even during exercise in normoxia.[83] [169] The response of PAP in HAPE-s may be related to greater alveolar hypoxemia secondary to lower HVR.[115] [133] [214] Recent work established a direct link in HAPE-s between the rise in PAP and greater sympathetic activation (as measured by microneurographic recordings in the peroneal nerve during hypoxia).[78] The authors concluded that sympathetic overactivation might contribute to HAPE. Also, smaller and less distensible lungs have been noted in HAPE-s.[83] [133] [327] Another characteristic of HAPE-s is reduced nitric oxide synthesis during hypoxia, suggesting impaired endothelial function.[302] Additional preliminary studies suggest that HAPE-s subjects are characterized by impairment of respiratory transepithelial sodium and water transport, which in mice is related to a genetic defect in the amiloride-sensitive sodium channel (aEnaC).[300] [303] Further 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.[121] The HLA-DR6 and HLA-DQ4 antigens were associated with HAPE, and HLA-DR6 with pulmonary hypertension. These preliminary findings suggest that an immunogenetic susceptibility may underlie the development of HAPE, at least in some cases. In summary, overactivation of the sympathetic nervous system in response to hypoxia, a low HVR, small lungs, and impaired pulmonary nitric oxide synthesis apparently combine to render a person susceptible to HAPE. The role of genetically determined impairment of respiratory epithelial sodium and water transport and the link between components of the major histocompatibility complex and HAPE provide exciting avenues for further investigation into the pathophysiology of HAPE. TREATMENT.
Early recognition is the key to successful outcome, as with other high-altitude illnesses (see Box 1-3 ). The therapy for HAPE depends on the severity of the illness and on the environment. In the wilderness,
27
where oxygen and medical expertise may not be available, persons with HAPE should be evacuated to a lower altitude as soon as possible. However, because of augmented pulmonary hypertension and greater hypoxemia with exercise, exertion must be minimized. If the disorder is diagnosed early, recovery is rapid with a descent of only 500 to 1000 m (1640 to 3281 feet) and the victim may be able to reascend slowly 2 or 3 days later. In high-altitude locations with oxygen supplies, bed rest with supplemental oxygen may suffice,[208] but severe HAPE may require high-flow oxygen (4 to 6 L/min or more) for more than 24 hours. Hyperbaric therapy is equivalent to low-flow oxygen and can help conserve oxygen supplies.[279] Oxygen immediately increases arterial oxygenation and reduces PAP, 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. Because cold stress elevates PAP, the victim should be kept warm.[54] 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.[187] [305] 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.[38] 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 delayed. Singh et al[321] 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) has proved effective in reducing pulmonary vascular resistance and PAP,[24] as have hydralazine and phentolamine.[117] [254] The vasodilators can cause hypotension, but they avoid the danger of CNS depression from morphine and possible hypovolemia from diuretics. Nifedipine does not quickly improve oxygenation, however, and clinical improvement is much better with oxygen and descent than with any of these drugs. Nifedipine and perhaps other vasodilators appear to be useful adjunctive therapy but are no substitute for definitive treatment (see Box 1-3 ). 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%), and 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.[376] 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 (9023 feet), might require further investigation, such as echocardiography, to rule out an intracardiac shunt. In children, undiagnosed congenital heart disease is worth considering ( Figure 1-16 ). 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 torr or an 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 or nifedipine for future ascents. An episode of HAPE is not a contraindication to subsequent high-altitude exposure, but education to ensure proper preventive measures and recognition of early symptoms is critical.
Figure 1-16 Chest x-ray of severe HAPE in a 4-year-old girl with a small previously undiagnosed patent ductus arteriosus that predisposed her to HAPE.
28
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. The role of exertion in HAPE may be overemphasized. Reports from North America have included hikers, climbers, and skiers, all of whom were exercising vigorously. Menon et al[221] clearly showed that sedentary men taken abruptly to high altitude were just as likely to become victims of HAPE. Nonetheless, because PAP rises with increasing level of exercise, prudence dictates no overexertion for the first day or two at altitude. Considerable clinical experience (but no data) suggests that acetazolamide prevents HAPE in persons with a history of recurrent episodes. Nifedipine (20 mg slow release every 8 hours) prevented HAPE in subjects with a history of repeated episodes.[24] 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. Reentry Pulmonary Edema In some persons who have lived for years at high altitude, HAPE develops on reascent from a trip to low altitude.[79] Authors have suggested that the incidence of HAPE on reascent may be higher than that during initial ascent by flatlanders,[19] [150] but data on true incidence are difficult to obtain. Children and adolescents are more susceptible than adults.[79] Hultgren[149] found a prevalence of HAPE in Peruvian natives of 6.4 per 100 exposures in the 1-to-20 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,[308] but reports are conspicuously absent from Nepal and Tibet, perhaps because such rapid return back to high altitude is not readily available.[368] Severinghaus[311] has postulated that increased muscularization of pulmonary arterioles that develops with chronic high-altitude exposure generates an inordinately high PAP on reascent, causing the edema.
OTHER MEDICAL CONCERNS AT HIGH ALTITUDE High-Altitude Deterioration The world's highest human habitation is at approximately 5500 m (18,045 feet), and above this deterioration outstrips the ability to acclimatize. [172] The deterioration is more rapid the higher one goes above the maximum point of acclimatization. Above 8000 m (26,247 feet), deterioration is so rapid that, without supplemental oxygen, death can occur in a matter of days. Life-preserving tasks, such as melting snow for water, may become too difficult, and death may result from dehydration, starvation, hypothermia, and especially neurologic and psychiatric dysfunction.[295] 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. Pugh[262] 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 AMREE still lost an average of 6 kg.[42] 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).[141] [292] At 4300 m (14,108 feet), weight loss was attenuated by adjusting caloric intake to match caloric expenditure.[52] Thus significant weight loss with prolonged exposure to high altitude may be overcome with adequate caloric intake, but decreased appetite is a problem.[170] [341] At very high altitudes, an increase in caloric intake may not be sufficient to completely counteract the severe anorexia and weight loss. At extreme altitude, Ryn[295] reported an incidence of acute organic brain syndrome in 35% of climbers going above 7000 m (22,966 feet), in association with high-altitude deterioration. This syndrome, which includes impaired judgment or frank psychosis, 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.[250] 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.[360] High-altitude residence does not clearly affect eventual stature, but growth and development are slowed.[69] [235] In the developing world, confounding factors such as nutrition and socioeconomic status make these issues difficult to assess.[145] 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. Lowland children traveling to high altitude are just as likely to suffer AMS as are adults. No data indicate that children are more susceptible to altitude illness, although diagnosis can be more difficult in preverbal children. [371] Despite this somewhat reassuring fact, very conservative recommendations are made regarding taking children to high altitude; it should be made clear that these opinions are not based on the science.[28] [261] Durmowicz et al[79] showed that children with respiratory infections were more susceptible to HAPE.
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Children can be given acetazolamide or dexamethasone as necessary for AMS/HACE. The dosage of acetazolamide for prevention or treatment of AMS in children is 5 mg/kg/day in divided doses. High-Altitude Syncope Syncope within the first 24 hours of arrival appears to be common at moderate altitude[248] but is rarely 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.[89] An unstable state of cerebral autoregulation may also play a role.[375] 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 might be contributing factors. Altitude syncope has no direct relationship to high-altitude illness. 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? A recent epidemiologic study indicated that 64% of tourists ingested alcohol during the first few days at 2800 m (9187 feet).[134] The effect of alcohol on altitude tolerance and acclimatization might therefore be of considerable relevance. Roeggla et al[290] determined blood gases 1 hour after ingestion of 50 g of alcohol (equivalent to 1 liter of beer), at 171 m (561 feet) and again after 4 hours at 3000 m (9843 feet). A placebo-controlled, double-blind paired design was used. For the 10 subjects, alcohol had no effect on ventilation at the low altitude, but at 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). [290] Whether this degree of ventilatory depression would contribute to AMS, and whether repeated doses would have greater effect, was not tested. Nonetheless, the authors argue that alcohol might impede ventilatory acclimatization and should be used with caution at high altitude. Conventional wisdom proffers an additive effect of altitude and alcohol on brain function. McFarland,[216] 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 ft." 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 ft."[216] His original observations were made on two subjects in the Andes in 1936. He found that blood alcohol levels rose more rapidly and reached higher values at altitude but noted no interactive effect of alcohol and altitudes of 3810 and 5335 m (12,501 and 17,504 feet).[217] Most subsequent studies refuted the increased blood alcohol concentration data except at the highest altitudes, over 5450 m (17,881 feet). Higgins et al,[129] [130] in a series of chamber studies, found blood alcohol levels were similar at 392 m (1286 feet) and 3660 m (12,008 feet), and they noted no synergistic effects of alcohol and altitude. Lategola et al[191] found that blood alcohol uptake curves were the same at sea level and 3660 m (12,008 feet), 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 (12,501-foot) altitude, with blood alcohol level of 88 mg%.[59] Performance was not affected by hypoxia, only by alcohol, and older subjects were more affected. When more demanding tasks were tested, Collins[58] found that a blood alcohol level of 91 mg% affected performance, as did an altitude of 3660 m (12,008 feet) during night sessions when the subjects were sleep deprived, but there was no significant altitude/alcohol interaction. In the one study in which Collins et al[60] were able to discern some altitude effect, there was a simple additive interaction of altitude (hypoxic gas breathing) and alcohol. He concluded that performance decrements resulting from alcohol may be increased by altitudes of 3660 m (12,008 feet) if subjects are negatively affected by that altitude without alcohol. All of these aviation-oriented studies used acute hypoxia equivalent to no more than 3500 m (11,483 feet). Perhaps the highest altitude (without supplemental oxygen) at which alcohol was studied was 4350 m (14,272 feet), on the summit of Mt. Evans in Colorado. Freedman et al[88] found that alcohol affected auditory evoked potentials the same as in Denver; that is, no influence of altitude was detectable. In summary, the possibility of interactions between alcohol and altitude deserves study. The limited data on blood gases at altitude after alcohol ingestion support the popular notion that alcohol could slow ventilatory acclimatization. Considerable data, however, refute the belief that at least up to 3660 m (12,008 feet), 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 Autopsy findings of widespread thrombi in the brain and lungs have led to investigations of the clotting mechanism at high altitude. Changes in platelets and coagulation have been observed in rabbits, mice, rats, calves, and humans on ascent to high altitude.[126] A report from OEII found no changes in concentration or inhibition of coagulation factors; significant altitude illness did not develop in OEII subjects. A remarkable case illustrating coagulation abnormalities at high altitude
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was reported by O'Brodovich et al.[252] In one of the women in this chamber study, disseminated intravascular coagulation developed within 1 ½ hours of exposure to
hypobaric hypoxia (PB = 410 torr, about 4600 m [15,092 feet]). The platelet count had decreased by 93,000/mm3 , and the activated partial thromboplastin time (aPTT) had shortened by 10 seconds. When symptoms of AMS developed, the study was discontinued. The exact mechanism is unknown. The woman and other subjects showed a shortening of the aPTT, perhaps secondary to the increase in procoagulant VII:C. Singh et al[318] reported that patients with HAPE had increased fibrinogen levels and prolonged clot lysis times, attributed to a breakdown of fibrinolysis. These authors also reported thrombotic, occlusive hypertensive pulmonary vascular disease in soldiers who had recently arrived at high altitude.[317] These findings, plus autopsy data, prompted Dickinson et al[72] to conclude that "hypercoagulability of the blood and sequestration of platelets in the pulmonary vascular bed provoke pulmonary thrombosis, and may contribute to the pathogenesis of HAPE." A series of experiments by Bärtsch et al[17] [18] [20] [21] however, carefully examined this issue in well subjects and in those with AMS and HAPE. They concluded that HAPE is not preceded by a prothrombotic state and that only in "advanced HAPE" is there fibrin generation, which abates rapidly with oxygen treatment. They considered the coagulation and platelet activation as an epiphenomenon rather than as an inciting pathophysiologic factor. Fibrin formation would, however, contribute to worsening of edema because of vascular obstruction, increased vascular permeability, and derangement of surfactant function.[26] Thrombotic and embolic events in mountaineers may be explained on the basis of dehydration, polycythemia, cold, constrictive clothing, and venous stasis from prolonged periods of weather-imposed inactivity. A role for hypoxia-induced abnormal clotting in the pathogenesis of these events, especially stroke, is not established. Peripheral Edema Edema of the face, hands, and ankles at high altitude is common, especially in females. Incidence of edema in at least one area of the body in trekkers at 4200 m (13,780 feet) was 18% overall, 28% in females, 14% in males, 7% in asymptomatic trekkers, and 27% in those with AMS.[105] 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 may also be merely due to exercise.[224] Immunosuppression Mountaineers have observed that infections are common at high altitude, slow to resolve, and often resistant to antibiotics.[243] On AMREE 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."[299] A suppurative hand wound and septic olecranon bursitis did not respond to antibiotics but did respond to descent to 4300 m (14,108 feet) from the 5300-m (17,389-foot) base camp. Nine of 21 persons had significant infections not related to the respiratory tract. Most high-altitude expeditions report similar problems. Data from OEII indicated that healthy individuals are more susceptible to infections at high altitude because of impaired T lymphocyte function; this is consistent with previous Russian studies in humans and animals.[220] 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 ß-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 in which 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 [18,045 feet]).[209] All 21 members of AMREE suffered these problems.[299] 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 (21,325 feet). Only four had sore throat. Obviously, factors other than hypoxia are involved. In the field, these problems usually appear without fever or chills, myalgias, lymphadenopathy, exudate, or other signs of infection. Whether these are infections is debatable. 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
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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; two climbers on AMREE had such fractures. 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. A recent study of high-altitude bronchitis on Aconcagua revealed that bronchitis developed in 13 of 19 climbers above 4300 m (14,108 feet).[264] Mean sputum production was 6 teaspoons per day. All reported that onset was after a period of excessive hyperventilation associated with strenuous activity. Although an infectious etiology is possible, experimental evidence suggests that respiratory heat loss results in purulent sputum and sufficient airway irritation to cause persistent cough.[215] This is supported by the beneficial effect of steam inhalation and lack of response to antibiotics. Many climbers find that a silk balaclava or similar material that is porous enough for breathing but that traps some moisture and heat effectively prevents or ameliorates the problem. Chronic Mountain Polycythemia In 1928, Carlos Monge[231] described a syndrome in Andean high-altitude natives that was characterized by headaches, insomnia, lethargy, plethoric appearance, and polycythemia greater than expected for the altitude. Known variously as Monge's disease, chronic mountain polycythemia, or chronic mountain sickness, the condition has now been recognized in all high-altitude areas of the world.[183] [229] [259] 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).[369] The incidence in Leadville, Colorado, is also high in men over 40 and distinctly low in women.[181] The increased hematopoiesis is apparently related to greater hypoxic stress, which may be due to a number of causes, such as lung disease, sleep apnea syndromes, and idiopathic hypoventilation. A diagnosis of "pure" chronic mountain polycythemia excludes lung disease and is characterized by relative alveolar hypoventilation and respiratory insensitivity to hypoxia.[229] Some studies suggest that even for the degree of hypoxemia, the red blood cell mass is excessive, implying excessive amounts or overactivity of erythropoietin.[362] Increasing age is also an important factor.[230] Regardless of the exact mechanism, therapy is routinely successful. Descent to a lower altitude is the definitive treatment. Supplemental oxygen during sleep is valuable. Phlebotomy is a common practice, provides subjective improvement (without significant objective changes), and is generally recommended when hematocrit is greater than 60% or hemoglobin level is greater than 20 g/dl blood.[362] The respiratory stimulants medroxyprogesterone acetate (20 to 60 mg/day) and acetazolamide (250 mg twice a day) have also been shown to reduce the hematocrit value by improving oxygenation.[182] The response to respiratory stimulants emphasizes the contribution of hypoventilation to chronic mountain polycythemia. High-Altitude Flatus Expulsion High-altitude flatus expulsion (HAFE) is the unwelcome spontaneous passage of colonic gas at altitudes above 3000 m (9843 feet).[9A] The mechanism has been postulated to relate to the expansion of intraluminal bowel gas at the decreased atmospheric pressure of altitude. Affected individuals may benefit from the oral administration of digestive enzymes or simethicone and a preferential carbohydrate diet. High-Altitude Retinopathy and Ultraviolet Keratitis See Chapter 22 . Fingernail Changes
A white transverse band visible across the fingernail plates may correspond to duration of altitude-related hypoxia. This has been observed (Figure 1-17 (Figure Not Available) ) in a 34-year-old climber who spent approximately 6 weeks at or above 5500 m (18,045 feet) climbing on Mt. Everest.[161] It Figure 1-17 (Figure Not Available) This photograph was taken 3 months after return to low altitude. A white transverse band grew out from the nail beds and was due to exposure to extremely high altitude. (From Hutchison SJ, Amin S: N Engl J Med 336:229, 1997.)
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was hypothesized that the white band may have been an effect of hypoxia and catabolic stress.
COMMON MEDICAL CONDITIONS AND HIGH ALTITUDE Persons with certain preexisting illnesses might be at risk for adverse effects upon ascent to high altitude, either because of exacerbation of their illnesses or because these illnesses might affect acclimatization and susceptibility to altitude illness. Certain populations also require special consideration, such as the pregnant and the elderly. 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 recent review by Hackett[102] for a more complete discussion. Conditions that can be aggravated by high-altitude exposure are listed in Box 1-4 . Respiratory Diseases Chronic Lung Disease.
Although oxygen saturation remains above 90% in a normally acclimatizing, healthy, awake person until at an altitude over 3000 m (9843 feet) (see Figure 1-1 ), persons with hypoxemic lung disease reach this threshold at a lower altitude that depends on the baseline blood oxygen values. As a result, these persons might have altitude-related problems at lower altitudes than would healthy individuals. In terms of their lung disease, improved airflow will result from decreased air density at high altitude, but hypoxemia, pulmonary hypertension, disordered control of ventilation, and sleep-disordered breathing could all become worse. Unfortunately, few data are available to guide the clinician advising such a person undertaking a trip to altitude. Hypoxic gas breathing at sea level can predict oxygenation at high altitude, but this does not always correlate with symptoms and is not convenient. Sea level PO2 values of 68 and 72 torr successfully classified more than 90% of the subjects with a PaO2 greater than 55 torr at simulated altitudes of 1525 m (5004 feet) and 2440 m (8006 feet), respectively.[95] [96] Such predictions have been further refined with the addition of spirometry.[76] A PaO2 of 55 torr 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 study to date, Graham and Houston[97] found that eight subjects with chronic obstructive pulmonary disease (COPD) tolerated 1920-m (6300-foot) altitude quite well. Persons with cor pulmonale or angina were excluded. The subjects had only minor symptoms on ascent, despite the fact that mean PaO2 declined from 66 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. The authors concluded that travel to this moderate altitude is safe for such patients. They speculated that these persons might have been partially acclimatized because of their hypoxic lung disease and were therefore less likely to develop AMS. Unfortunately, no further investigations with sicker patients or at higher altitudes have yet been reported.
Box 1-4. 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 Obesity Diabetes After coronary artery bypass grafting (without angina) Mild chronic obstructive pulmonary disease (COPD) Asthma Low-risk pregnancy Controlled hypertension Controlled seizure disorder Psychiatric disorders Neoplastic diseases Inflammatory conditions
CAUTION Moderate COPD Compensated congestive heart failure (CHF) Sleep apnea syndromes Troublesome arrhythmias Stable angina/coronary artery disease High-risk pregnancy Sickle cell trait Cerebrovascular diseases Any cause for restricted pulmonary circulation Seizure disorder (not on medication) Radial keratotomy
Seizure disorder (not on medication) Radial keratotomy
CONTRAINDICATED Sickle cell anemia (with history of crises) Severe COPD Pulmonary hypertension Uncompensated CHF
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.[33] To adjust oxygen therapy at altitude for persons already on supplemental oxygen, FiO2 is increased by the ratio of higher to lower barometric pressure (see Table 1-2 ). Oxygen also improved hemodynamics (lowered blood pressure) and decreased pulsus
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paradoxus and pulse pressure in COPD patients at a simulated altitude of 2438 m (7999 feet).[34] 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 persons with COPD developing altitude illness are absent from the literature. On the other hand, the issue has not been specifically addressed. Any degree of pulmonary hypertension might be expected to increase the likelihood of HAPE, and although this has been clearly demonstrated in other conditions (see High-Altitude Pulmonary Edema), 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,[325] and hypoxic testing has also tried to predict the need for supplemental oxygen upon ascent in this condition. [251] As with COPD, such tests are not particularly useful and tend to underestimate the oxygen requirements because they are done only during rest and while awake. Supplemental oxygen should be available for these children, and oxygen saturation monitoring might be desirable in certain circumstances. The physician should be liberal with the use of antibiotics and adjunctive therapy for exacerbations at high altitude, given the likely danger of greater hypoxemia and greater difficulty treating infections at high altitude. Asthma.
The available literature suggests that asthmatics do well at high altitude, both residents and sojourners, primarily because of decreased allergens and pollution.[39] [316] [344] Indeed, high altitude as a treatment for asthma has been popular in Europe for many decades. However, because altitude exposure often includes exercise (and cold), asthmatics with exercise-induced bronchospasm rather than allergic asthma might have problems at altitude. Matsuda et al[210] investigated the effect of altitude on 20 asthmatic children with exercise-induced bronchospasm in a hypobaric chamber simulating 1500 m (4921 feet) 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 sea level. The authors concluded that the modest altitude of 1500 m (4921 feet) does not exacerbate exercise-induced asthma. Future work will hopefully evaluate asthmatics at higher altitudes and in the field, where humidity and temperature are lower. 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[227] investigated the effect of acetazolamide in 16 asthmatic patients taken to 3200 m (10,499 feet). Acetazolamide showed the same benefits as in nonasthmatics, with higher oxygen saturation and fewer AMS symptoms compared with the placebo control group. Seven of the eight asthmatics in the control group developed symptoms of AMS, a rather high incidence, but without a nonasthmatic control group for comparison, whether this incidence was abnormal is unknown. Persons with asthma ascending to high altitude should be advised to be at maximum function before ascent; to continue on their usual medications, including steroids; and to have steroids 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 is unproven.[293] In summary, the available data, although limited, suggest that high altitude does not exacerbate asthma, and it actually improves allergic asthma. Further work needs to determine if asthma might have any influence on susceptibility to AMS and HAPE; anecdotally, this does not seem to be the case. Although it seems likely that a severe asthma attack at high altitude would be more dangerous than at low altitude, no data are available to answer this question. Although caution and adequate preparation are necessary, asthma is not a contraindication to high-altitude travel. Sleep Apnea and Sleep-Disordered Breathing Persons with snoring, sleep apnea syndrome, and sleep-disordered 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. Fujimoto et al[91] suggested that SDB at high altitude was related to altitude illnesses, including HAPE, but whether the SDB was present before altitude exposure was not determined. The chaotic breathing pattern during sleep that these investigators found in HAPE-s subjects was clearly different from the usual periodic breathing of high altitude. In fact, periodic breathing (Cheyne-Stokes) is considered benign, has not been related to AMS or HAPE, and is associated with a brisk HVR, which is generally considered beneficial at altitude.[114] 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
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pressure-compensating features. Therefore they might need to adjust their machines. The error is greater the higher the altitude and the higher the initial pressure setting.[90] For those not being treated with CPAP 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 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.[266] One well-controlled study showed an increase in blood pressure at 3500 m (11,483 feet) from a mean of 105/66 mm Hg at sea level to 119/77 mm Hg at 3 days, 111/75 mm Hg at 3 weeks, and back to 102/65 mm Hg on return to sea level.[207] Pugh[263] reported transient increases in blood pressure in athletes at the 1968 Olympics in Mexico City. Certain individuals, however, appear to have a pathologic response upon induction to high altitude. For example, arterial hypertension develops in 10% of lowland Chinese who move to Tibet.[314] 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 months, however, down-regulation of adrenergic receptors results in attenuation of the initial blood pressure response. This mechanism is thought to be the reason that long-term residents of high altitude have lower blood pressure than their sea level counterparts.[151] [288] Apparently for the same reason, chronic altitude exposure has also been shown to inhibit progression of hypertension.[228] As for the effect of short-term altitude exposure on preexisting hypertension, studies have generated mixed results. In general, the response in hypertensives is similar to those without hypertension, 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 the change in blood pressure. Altitudes less than 3000 m (9843 feet) seem to result in little if any change.[282] Palatini et al[257] studied 12
normotensives and 12 untreated mild hypertensives with 24-hour ambulatory blood pressure monitoring at sea level, after 12 hours at 1210 m (3970 feet), and after 1 ½ to 3 hours at 3000 m (9843 feet). The authors concluded that the increase of blood pressure in both normotensives and hypertensives was not important at 1210 m (3970 feet) but could become so at 3000 m (9843 feet). However, individual variability was great; the maximum change was 17.4 mm Hg for systolic and 16.3 for diastolic blood pressures. Two other studies were able to demonstrate a slightly greater blood pressure response in hypertensives compared with normotensives upon ascent to 2572 m (8439 feet) and 3460 m (11,352 feet).[69A] [301] Again, these authors also noted important individual variation, with some subjects increasing their systolic blood pressure by as much as 25 mm Hg at rest and 40 mm Hg during exercise, compared with sea level measurements. The important question of whether the blood pressure would continue to increase over the first 2 weeks at high altitude, as it does in normotensives, has not yet been addressed. At a more modest altitude, Halhuber[119] claimed a significant reduction in the blood pressure of 593 persons with hypertension after 14 days at 1700 to 2000 m (5578 to 6562 feet) in the Alps. A similar study of hypertensives at higher altitude will hopefully be accomplished. Patients receiving antihypertensive treatment should continue their medications while at high altitude. Because some persons may unpredictably become markedly hypertensive acutely,[152] blood pressure monitoring should be considered, especially in those with labile hypertension or those who become symptomatic at altitude. Hypertension in short-term high-altitude sojourners for the most part should be considered transient and should not be treated because it rarely reaches dangerously high levels and will resolve on descent. Given the large number of hypertensive patients visiting ski resorts and trekking at high altitude, however, the occasional person with an exaggerated response will require treatment.[152] Because the mechanism appears to be increased a-adrenergic activity, an a-blocker might be the best choice of therapy for these individuals. A preliminary report also suggested that nifedipine might useful and superior to atenolol.[70] There is no evidence to date to suggest that hypertensive patients are more likely to develop high-altitude illnesses. Although requiring some caution, hypertension does not seem to be a contraindication to high-altitude exposure. Arteriosclerotic Heart Disease.
Lifelong residence at high altitude appears to offer some protection from coronary artery disease (CAD) and the attendant acute coronary artery events, [226] perhaps in part resulting from increased myocardial vascularity.[53] Other factors that might explain this finding, such as genetics, fitness, and diet, have not been adequately evaluated. The effect of acute, transient exposure to high altitude on the healthy heart also appears to be benign. Various avenues of research have indicated that the healthy heart tolerates even extreme hypoxia quite well, all the way to the summit of Mt. Everest (PaO2 less than 30 torr). 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 be due to the marked reduction in maximal exercise with increasing altitude,
35
which reduces maximal heart rate and myocardial oxygen demand, and also due to the increased coronary blood flow. A person with CAD, however, may not have the same adaptive capacities. For example, diseased coronary arteries might have limited ability to vasodilate and might actually constrict because of unopposed sympathetic activation.[193] What, then, are the risks, and what to advise 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[119] reported an incidence of only 0.2% for myocardial infarction in 434 patients with CAD taken to altitudes between 1700 and 3200 m (5578 and 10,499 feet) for 4 weeks in the Alps. He also reported a very low incidence of sudden death in 151,000 vacationers in the Alps, 69,000 of whom 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.[47] However, the altitudes were rather low (1000 to 2100 m [3281 to 6890 feet]), and no increased risk was evident in men who participated regularly in sports. The authors suggested that abrupt onset of exercise in sedentary men combined with altitude stress might induce cardiac sudden death, but whether altitude contributed at all is unclear. In summary, limited data suggest no increased risk for sudden cardiac death or myocardial infarction at altitudes up to 2500 m (8202 feet). Another important question is whether altitude will exacerbate stable ischemia. The slight increase in heart rate and blood pressure on initial ascent to altitude might exacerbate angina in those with coronary artery disease, as described by Hultgren.[152] One study evaluated nine men with stable exercise-induced angina by exercise treadmill test at 1600 m (5250 feet; Denver), and within the first hour of arrival at 3100 m (10,171 feet). [239] Cardiac work was slightly higher for a given workload at high altitude compared with low altitude, and as a result, the onset of angina was at a slightly lower workload. They found that a heart rate of 70% to 85% of the rate that produced ischemia at low altitude was associated with angina-free exercise at 3100 m (10,171 feet), and they suggested that angina patients at altitude adjust their activity level based on heart rate, at least on the day of arrival. [239] Brammel et al[45] reported similar results and also suggested that those with angina need to reduce their activity at high altitude to avoid angina episodes. In a more recent study, Levine et al[193] investigated 20 men who were much older than those in the previous investigations (mean age 68 ± 3 years) and performed symptom-limited exercise tests. With acute exposure to 2500 m (8202 feet), the double product (heart rate times systolic blood pressure) required to induce 1 mm ST depression was decreased about 5%, but after 5 days of acclimatization at 2500 m (8202 feet), this value was unchanged from sea level. The degree of ischemia (maximal ST segment depression) was the same at sea level, with acute altitude exposure, and after 5 days at 2500 m (8202 feet). Also, no new wall motion abnormalities on echocardiography were seen at high altitude. Only one subject exhibited increased angina at altitude, and one person with severe CAD developed a myocardial infarction after maximal exercise at 2500 m (8202 feet). The authors concluded that CAD patients who are well compensated at sea level do well at a moderate altitude after a few days of acclimatization, but that acutely angina threshold may be lower and activity should be reduced.[193] Finally, a study of 97 elderly persons visiting 2500 m (8202 feet), 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.[282] Taken altogether, these various investigations indicate that those with CAD, including the elderly, generally do well at the modest altitude of 2500 m (8202 feet), but that reducing their activities the first few days at altitude is wise. To address the question of whether altitude might provoke cardiac arrhythmia, Levine et al,[193] in their study mentioned above, found that premature ventricular contractions (PVCs) increased 63% on acute ascent but returned to baseline after 5 days of acclimatization. A simultaneous rise in urine norepinephrine in these subjects indicated that sympathetic activation was the cause of the increased ectopy. They observed no increase in higher-grade ectopy, however, and no changes in signal-averaged ECG suggestive of a change in fibrillation threshold; in other words, the PVCs appeared benign. Halhuber[119] also found increased ectopy in his subjects and also no serious adverse events. In addition, Alexander[2] described asymptomatic PVCs and ventricular bigeminy in himself while trekking to 5900 m (19,358 feet). Subsequent evaluation found no evidence of heart disease, and the event prompted him to thoroughly review the subject of altitude, age, and arrhythmia. Although no dangerous arrhythmias have ever been reported in high-altitude studies, persons with troublesome or high-grade arrhythmia have not been evaluated upon ascent to high altitude. The available evidence would suggest that patients whose arrhythmias are well controlled on medication should continue the medication at altitude, whereas those with poorly controlled arrhythmias might do better to avoid visiting high altitude. In terms of advising persons with CAD or high likelihood of CAD about altitude exposure, the stress of
36
high altitude on the coronary circulation appears to be minimal at rest but significant in conjunction with exercise. Ideally, no one with known CAD or even risk factors for CAD should undertake unaccustomed exercise at any altitude and especially at high altitude. Therefore advising an exercise program at sea level before exercising at altitude is prudent. The same technique of risk stratification that is commonly used at sea level can be applied for providing advice for high altitude.[146] 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 before exercising at high altitude and then further evaluation as indicated. Patients with previous myocardial ischemia, bypass surgery, or angioplasty are considered high risk only if they have a strongly positive exercise treadmill test. Patients with multiple-vessel bypass grafts who were asymptomatic and with normal exercise tests at sea level have successfully visited altitudes over 5000 m (16,404 feet). High-risk patients may require coronary angiography to establish appropriate management. Alexander[1] 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. For these persons, he recommends ascent to no more than 2500 m (8202 feet) and proximity to medical care. Both sets of recommendations, although reasonable, need to be validated with outcome studies. HEART FAILURE.
Although information on the effect of high altitude on heart failure is scant, physicians in resort areas have noted a tendency toward acute decompensation in those with a history of heart failure within 24 hours of arrival. Those with CAD and low ejection fractions (less than 45%), but without active heart failure, actually did quite well, as gauged by exercise tests during acute exposure to 2500 m (8202 feet).[85] Compared with 23 control subjects, the decrement in exercise performance was similar, and no complications or signs of ischemia developed. Although these results are encouraging for such patients, they made no observations past the first few hours at altitude. One concern is that 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 et al[3] found that ejection fraction declined at altitude during an exercise study in patients with angina, with an increase in end-diastolic and systolic volume as measured by two-dimensional echo. 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, and they need to continue their regular medications and be prepared to increase their diuretic should symptoms of failure exacerbate. Acetazolamide prophylaxis may be useful to consider in terms of speeding acclimatization, inducing a diuresis, and preventing AMS, but its efficacy in these patients remains untested. PULMONARY VASCULAR DISORDERS.
Because of the danger of HAPE, pulmonary hypertension (of any etiology) is at least a relative contraindication to high-altitude exposure. In addition, hypoxic pulmonary vasoconstriction will most likely exaggerate preexisting pulmonary hypertension and could lead to greater symptomatology 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.[109] [275] [340] As Hultgren [152] 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. A recent report 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.[245] The first episode was at 2300 m (7546 feet) and the second one at only 1850 m (6070 feet), with skiing up to 2350 m (7710 feet). Other conditions warranting caution include bronchopulmonary dysplasia, recurrent pulmonary emboli, mitral stenosis, and kyphoscoliosis. 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. Sickle Cell Disease Sickle cell crisis is a well-recognized complication of high-altitude exposure.[87] Even the modest altitude of a pressurized aircraft (1500 to 2000 m [4921 to 6562 feet]) causes 20% of persons with hemoglobin SC and sickle-thalassemia genetic configuration to have a vasoocclusive crisis.[203] High-altitude exposure may precipitate the first vasoocclusive crisis in persons previously unaware of their condition. Persons with sickle cell anemia and a history of vasoocclusive crises are advised to avoid altitudes over 1800 m (5906 feet) unless they are taking supplemental oxygen. Persons with sickle cell disease who live at high altitude in Saudi Arabia have twice the incidence of crises, hospitalizations, and complications
37
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 (5921 feet).[185] [203] 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.[185] Treatment of splenic syndrome consists of intravenous hydration, oxygen, and removal to a lower altitude.[339] 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. [75] Pregnancy In high-altitude natives, pregnancy-induced hypertension is four times more common than in low-altitude pregnancies, preeclampsia is more common, and full-term infants are small for gestational age.[234] [235] These problems raise the issue of whether short-term altitude exposure may also pose a risk. So far, there is no evidence that these problems, or others such as spontaneous abortion, abruptio placentae, or placenta previa, can result from a sojourn to high altitude.[249] Unfortunately, however, few data exist on the influence of a high-altitude visit during pregnancy on the mother and the fetus. For moderate altitude, the research to date has been reassuring.[143] [144] Artal et al[9] studied seven sedentary women at 34 weeks gestation. Maximal and submaximal exercise tests were completed at sea level and 6000 feet (1829 m) after 2 to 4 days of acclimatization. They reported the expected decrease in maximal aerobic work but found no difference from sea level in fetal heart rate responses, or in maternal lactate, epinephrine, and norepinephrine levels. In a small number of subjects, the authors considered it safe for women in their third trimester of pregnancy to engage in brief bouts of exercise at moderate altitude. A similar conclusion was reached in a study of 12 pregnant subjects who exercised after ascent to 2225 m (7300 feet). The authors found no abnormal fetal heart rate responses and considered the exercise at altitude benign for both mother and fetus.[29] Huch[143] also concluded that short-term exposure, with exercise, was safe during pregnancy. In summary, the available data, though limited, indicate that short-term exposure to altitudes up to 2500 m (8202 feet), with exercise, is safe for a lowland woman with a normal pregnancy. Another avenue of research has been alteration of blood gases during pregnancy. Human and animal studies with acute hypoxic challenge, as well as oxygen-breathing studies, have drawn two conclusions: (1) that a compromised placental-fetal circulation could be unmasked at high altitude, and (2) that a fetus with a normal placental-fetal circulation seems to tolerate a level of acute hypoxia far exceeding a moderate altitude exposure.[15] [63] [276] Based on the available research, it seems prudent to recommend that only women with normal, low-risk pregnancy undertake a sojourn to altitude. For these women, exposure to an altitude at which SaO2 will remain above 85% most of the time (up to 3000 m [9843 feet] 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 before 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 HAPE at 2500 m (8202 feet), for example, is much more hypoxemic than a healthy woman at 5000 m (16,404 feet). Therefore a strategy for preventing altitude illness, especially pulmonary edema, must be explained and implemented. Similarly, carboxyhemoglobin from smoking, lung disease, and other problems of oxygen transport will render the pregnant patient at altitude more hypoxemic and physiologically at a higher altitude. Consideration of a high-altitude sojourn in the developing world, or in a wilderness setting, raises other issues that may be more important than the modest hypoxia. These include remoteness from medical care should a problem arise, the quality of available medical care, the use of medications for such important things as malaria and traveler's diarrhea (many of which are contraindicated in pregnancy), and the risks of trauma.
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Chapter 2 - Avalanches Knox Williams Betsy R. Armstrong Richard L. Armstrong Dale Atkins
An avalanche is a mass of snow that slides down a mountainside. In the United States, approximately 100,000 avalanches occur annually, of which about 100 cause injury, death, or destruction of property. Based on reported incidents in the 1990s, about 200 people a year are caught in avalanches (that is, they are bodily involved in the moving snow or its effects). Of these, 75 are partly or wholly buried, 18 sustain injury, and 24 are killed. Average annual property damage is approximately $520,000. 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 of time. 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 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 feather-shaped 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 ( Figure 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 airspace within an ice skeleton of snow crystals. In a typical layer of new snow, 85% to 95% of the volume is empty airspace. 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 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 rounded and suitable for closer packing. Intricate crystals change because they possess a shape
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Figure 2-1 International classification of solid precipitation. (From the International Association of Scientific Hydrology.)
that is naturally unstable. New snow crystals have a large surface area/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, 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 ( Figure 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
Figure 2-2 Settlement. As the crystal shapes become more rounded, they can pack more closely together and the layer settles or shrinks in thickness.
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.
or downward in the snow layer, called the temperature gradient. 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 ( Figure 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 does 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
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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 totally new crystals.
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 airspace diminishes. Some vapor changes to ice and is deposited on the surrounding ice grains. We witness a similar process when warm, moist air in a heated room comes in contact with a cold windowpane. The invisible water vapor is cooled to its 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 totally 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 temperature-gradient 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
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. (A and B, Polarized-light photos by Doug Driskell.)
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 10° 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 than about 10° C per meter, there is still a vapor pressure difference and upward movement of vapor through the snow layers, but 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
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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.
Figure 2-7 Equitemperature grain growth. In the presence of weak temperature gradients, bonds grow at the grain contacts.
grain contacts (concavities), as well as over the remaining surface of the grain (convexity) ( Figure 2-6 ). Connecting bonds formed at the grain contacts give the snow layer strength over time ( Figure 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. Rounded 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 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
Figure 2-8 Bonded or sintered grains resulting from equitemperature metamorphism. Grain size: 0.5 to 1 mm. (Polarized-light photo by Doug Driskell.)
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 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 point-release, or loose snow, avalanche ( Figure 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 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 near-surface 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 ( Figure 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
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Figure 2-9 Loose snow or point-release avalanche. (USDA Forest Service photo.)
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
Figure 2-10 Slab avalanche. (From USDA Forest Service: The snowy torrents. Photo by Alexis Kelner.)
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
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to slab formation. One scenario involves thick layers of weak snow, which result from 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 mountains, 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 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 densities 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 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. Downslope movement within the snow cover occurs at all times, even on gentle slopes. The speed of movement is slow, generally on the order of a few millimeters per day 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
Figure 2-11 Snow layer combinations that often contribute to avalanche formation.
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
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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.
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. The slab avalanche provides the best example of elastic deformation in snow cover. Although the deformation cannot actually be seen, evidence of the resultant brittle failure is clearly present in the form of the sharp, linear fracture line and crown face of the slab release ( Figure 2-13 ). 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 downslope, but throughout most of the winter the strength
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.)
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 ( Figure 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 tug-of-war team were to let go of the rope. If the remainder of the team were 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 propagate, allowing entire basins, many acres in area, to be set in motion within a few seconds.
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Figure 2-14 Slab avalanche released by a skier. (Photo by R. Ludwig.)
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Figure 2-15 The three parts of an avalanche path: starting zone, track, and runout zone. (Photo by B. Armstrong.)
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 obvious that opportunities for making measurements inside a moving avalanche are extremely limited. Although avalanche paths exist in a variety of sizes and shapes, they all have three distinct parts with respect to dynamics ( Figure 2-15 ). 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 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
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of a gorge or ravine. As a general rule, the slope angle of starting zones is 30 to 45 degrees, of the track is 20 to 30 degrees, and of the runout zone 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, with rare examples in the range of 150 to 200 mph. 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. During spring conditions when the snow contains large amounts of liquid water, speeds may reach only about 25 mph ( Figure 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 ( Figure 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 medium-sized 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 only comprise a few inches of settled snow yet contributes significantly to the total impact force. The presence of snow crystals can increase the air density by a factor of three or more. A powder cloud traveling at a moderate dry avalanche speed of 60 mph could have the impact force of a 180-mph wind, well beyond the destructive capacity of a hurricane.
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.
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
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Figure 2-17 The large powder cloud associated with a fast-moving dry-snow avalanche. (Photo by R. Armstrong.)
be a consistent producer of avalanches, a mountain and its weather must work in harmony. Elevation Mountains must be at high enough latitudes or high enough in elevation to build and sustain a winter snow cover 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 treeline. 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 causes, such as a streambed or rockslide area, or from human-made causes, 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 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. Dry-snow 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 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 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 do north slopes, which frequently leads to radically different snow covers. North slopes have deeper and colder snow covers, often with a substantial layer of depth hoar near the ground. South slopes usually carry a shallower and warmer snow cover, 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 longer-lasting snow cover. At high latitudes, such as in Alaska,
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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 factor. 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, 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, will not usually produce avalanches early in the winter, since it takes considerable snowfall to cover the ground anchors. Once most of the rocks are covered, avalanches will 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, since 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 state of the weather and snowpack changes 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 seldom produce avalanches. Snows of 6 to 12 inches usually produce a few small slides, and some of these harm skiers who release them. Snows of 1 to 2 feet 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 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 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. Snowfall Intensity The rate at which snowfall accumulates is almost as important as the amount of snow. A snowfall of 3 feet in one 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
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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 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. A layer of heavier-than-normal 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 is sufficient to pick up freshly fallen snow. Higher speeds are required to dislodge older snow. Speeds of 20 to 50 mph 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 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 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 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 downslope. The new snow layer settles, becomes more dense, 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
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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, this 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 of snow covers the ground at the University of Colorado's snow study site. At Alta, Utah, once 52 inches of snowpack have 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 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, 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, since 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 the snow surface is hoar frost, or surface hoar. This is the solid equivalent of dew. 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 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.
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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, being able to recognize and avoid avalanche terrain is sufficient education. 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. The ability to travel 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 of pitch, judging angle is a prime skill in recognizing potential avalanche areas. An inclinometer is an instrument 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 identifies avalanche slopes: the presence of fracture lines and the rubble of avalanche snow on the slope or at the bottom. Other clues are swaths of missing trees or trees that are bent downhill or damaged, especially with the uphill branches removed. Above treeline, steep bowls and gullies are almost always capable of producing avalanches. Route Finding Good route-finding techniques are necessary for safe travel in avalanche terrain ( Figure 2-18 ). 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 when choosing 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 deep and 3 feet wide should be dug. With the shovel, the uphill wall is shaved until it is smooth and vertical. Now the layers of snow can be observed and felt. The tester can see where the new snow touches the layer beneath, poke the pit wall with a finger to test hardness, and brush the pit wall with a 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 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
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Figure 2-18 Four ski-touring areas showing the safer routes (dashed lines) and the more hazardous routes (dotted lines). Arrows indicate areas of wind loading. (From USDA Forest Service: Avalanche handbook, Agricultural Handbook 489, USDA. Photo by Alexis Kelner.)
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
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shortcoming is that it is not a true test of stability, since 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 wide. By cutting into the pit wall, the skier isolates a block of snow that is about 7 feet wide (a ski length) and goes back 4 feet (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 by jumping harder until the block eventually shears loose or crumbles apart. The interpretation of the results is: "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, since 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 lengths as part of their rescue caches. The recreationist can buy probe poles of tubular steel that come in 2-foot sections that fit together to make a full-length 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 Cord.
An avalanche cord is orange or red rope, approximately 50 feet long, that can be coiled and attached to a belt. When traveling in avalanche terrain, a skier or climber strings the cord out behind. The idea is that if an avalanche releases and the victim is buried, the cord will float and some portion of it will come to rest on the surface. Rescuers follow the cord, or probe in the immediate area, to locate the victim. Avalanche cords have saved many lives in the past, but now they are obsolete and have virtually disappeared from use. They have been replaced as personal rescue devices by avalanche beacons, which are far more reliable. Avalanche cords always had severe limitations: tests done in the early 1970s by the International Vanni Eigenmann Foundation of Milan, Italy, showed that avalanche cords were only marginally effective. In tests performed by attaching an avalanche cord to a sandbag dummy tossed onto an avalanche path, a portion of the avalanche cord was visible on the surface only 40% of the time. Avalanche Rescue Beacon.
Avalanche rescue beacons, or transceivers, have become the most-used personal rescue devices 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 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 30 lives. Beacons save at least two or three lives per winter. Transceivers act as transmitters that emit a signal on a frequency of 457 kHz. (This is now the world-standard frequency. The old frequency of 2.275 kHz is no longer used, and all beacons using this frequency have been—or should be—retired.) A buried victim's unit emits this signal, while 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 improving the beacons on the market. 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 to display a digital read-out of the range to the buried unit. Both types operate on the same frequency and therefore are compatible with one another. However, different search techniques may be necessary to use each type most efficiently. Therefore special training and
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practice are required before the user attains proficiency. The main brands available in the United States are Ortovox, Pieps, Tracker, and SOS. Merely possessing a beacon does not ensure its lifesaving capability. Frequent practice is required to master a beacon-guided search, which may not be straightforward. Skilled practitioners can find a buried unit in less than 5 minutes once they pick up the signal. Since speed is of the essence in avalanche rescue, beacons are obvious lifesavers. The best proven rescue equipment is a beacon for a quick find and a shovel for a quick recovery ( Box 2-1 ).
Box 2-1. AVALANCHE TRANSCEIVER SEARCH
INITIAL SEARCH 1. 2. 3. 4. 5. 6.
Have everyone switch their transceivers to "receive" and turn the volume on "high." If enough people are available, post a lookout to warn others of further slides. Should a second slide occur, have rescuers immediately switch their transceivers to "transmit." Have rescuers space themselves no more than 30 m (100 feet) apart and walk along the slope parallel to one another. For a single rescuer searching within a wide path, zigzag across the rescue zone. Limit the distance between crossings to 30 m. For multiple victims, when a signal is picked up, have one or two rescuers continue to locate the victim while the remainder of the group carries out the search for additional victims. 7. For a single victim, when a signal is picked up, have one or two rescuers continue to locate the victim while the remainder of the group prepares shovels, probes, and medical supplies for the rescue.
LOCATING THE VICTIM With practice, the induction line search is more efficient than the conventional grid search. An induction line search requires a 457 kHz transceiver.
Induction line search (preferred method) When an induction line search is used, the rescuer may initially follow a line that leads away from victim ( Figure 2-19 ). 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 2-19, A ). 2. Holding the transceiver in this position, turn until the signal is maximal (maximum volume), then walk five steps (about 5 m [16 feet]), stop, and turn again to locate the maximum signal (see Figure 2-19, B ). 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 described above, and then stop and orient the transceiver toward the maximum signal. Reduce the volume. 4. Continue repeating the above steps. You should be walking in a curved path along the "induction line" toward the victim (see Figure 2-19, C ). 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 below).
Grid search 1. When a signal is picked up, stand and rotate the transceiver, which is held horizontally (parallel with the ground), to obtain the maximum signal (loudest volume). Maintain the transceiver in this orientation during the remainder of the search. 2. Turn the volume control down until you can just hear the signal. Walk in a straight line, down the fall line from the victim's last-seen location, until the signal fades. 3. When the signal starts to fade, turn 180 degrees and walk back toward the starting position. The signal will increase in volume and then fade again. Walk back to the point of loudest volume/maximum signal, which should be in the middle of two fade points. 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. This time, when you return to the middle of the fade points (maximum signal strength), 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. Maintain the transceiver in this orientation and sweep the transceiver from side to side and back and forth just above the surface of the snow. c. Find the signal position halfway between fade points (i.e., 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.
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Figure 2-19 Induction line search. (From Auerbach PS et al: Field guide to wilderness medicine, St Louis, 1999, Mosby.) Airbag.
In 1995 a new rescue device made in Germany was introduced in Europe. It was the ABS Avalanche Airbag System and was designed specifically for guides and ski patrollers. The user wears the airbag in a pack and deploys it by pulling a rip cord. This releases a cartridge of nitrogen gas that escapes at high velocity and draws in outside air through jets; it is capable of inflating two 75-L airbags in 2 seconds. This gives the avalanche victim buoyancy and cushioning against impact with trees or rocks. To operate the device, the user must be able to grab and pull the rip cord. By 1999, there had been 18 documented avalanche incidents in the Alps that involved 31 people equipped with airbags. In one case the airbag failed to work, and three other people failed to pull the rip cord, but all four survived anyway. There were 27 people with inflated airbags, and of these, 14 were not buried, 9 were partially buried, and 4 were bodily buried but a portion of the airbag remained on the surface, allowing for a quick recovery. All 27 survived. Airbags will be available in the United States by 2000. They are an additional rescue device available to the backcountry adventurer and someday may become
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a viable alternative to beacons, although they should never replace good judgment. 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. Called the AvaLung, it is worn as a vest by the user. If buried, the victim can breathe through a mouthpiece and flex-tube connected to the vest. The victim can inhale oxygenated air coming from the surrounding snow, which passes through a membrane in the vest. The exhaled air, rich in carbon dioxide, passes through a one-way valve and into
another area of the snow surrounding the victim to slow the effects of carbon dioxide narcosis caused by contaminating the air space. The AvaLung will be marketed by Black Diamond Equipment, Ltd., in 2000. It has worked well in simulated burials, allowing the victim to breathe for 1 hour in tightly packed snow. It has yet to be proven in an actual avalanche burial. In time, the AvaLung may prove to be a lifesaver among avalanche professionals, but only as an instrument of last resort. 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. A person should be padded and insulated if trapped. 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 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 a 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 far to the 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 out to the side or grabbing a tree, should be kept in mind. Survival of Victims Escaping to the Side.
The moment the snow begins to move around the person, he or she has a split second to make a decision or make a move. 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, since the avalanche invariably overtakes its victims. The person should shout and then close the mouth. Shouting alerts companions to what is happening. Clamping the mouth shut and breathing through the nose prevents inhalation of a mouthful of snow. Swimming.
A person knocked off his or her feet should attempt to swim with the avalanche. Cumbersome or heavy gear should be discarded. Ski poles should be tossed away; with luck, the avalanche will strip away the skis. The victim should get away from the snow machine. Swimming motions with the arms and legs increase the freedom to maneuver the body. The purpose is to maintain a position near the surface. Any swimming motions will do, but if the person has been thrown forward and is being carried head first downhill, the breast stroke with the arms (similar to body surfing) should be used; if being carried down feet first, the person
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should try to roll onto his or her back and attempt to "tread water" with the arms and legs. Reaching the Surface.
Avalanches come to a stop when they flow out onto more gentle terrain. A victim may have a second or two when he or she feels the sensation of slowing down. This is a crucial point in the ordeal, the best chance to reach the surface. The person should thrust upward with swimming motions and try to burst through to the surface. Unless very deeply buried at this time, the person will probably know which way is up. All possible strength should be exerted to get the head, an arm, or even a hand above the surface. Even if the person cannot get his or her head out, being near the surface greatly improves the odds for survival. If any clue is on the surface, it gives the rescuers something to see. A hand should be used to clear a breathing space over the mouth. Rescue by Survivors Marking the Last-Seen Point.
A survivor or eyewitness to an accident needs to act quickly and positively. The rescuer's actions over the next several minutes may mean the difference between life and death for the victim. First, the victim's last-seen point should be fixed and marked with a piece of equipment, clothing, a tree branch, or anything that can be seen from a distance downslope. It is most often safe to move out onto the bed surface of the avalanche that has recently run. It is dangerous when the fracture line has broken at mid-slope, leaving a large mass of snow still hanging above the fracture. Searching for Clues.
The fall line should be searched below the last-seen point 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 give the victim's trajectory and 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 is concentrated. 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 survivors must immediately switch their units to receive mode. While making the fast scuff-search for visual clues, survivors should at the same time search the debris, listening for the beeping sound coming from the buried beacon. When they pick up the signal, they will be able to narrow the search area quickly. If skilled in this kind of search, they will pinpoint the burial site in a few minutes. Probing.
Probing avalanche debris is a simple but slow method for searching for buried victims. A probe line is composed of up to a dozen rescuers with avalanche probes, or sounding rods, who stand elbow to elbow on the avalanche debris. Ideally, probes should be 3 to 4 m (10 to 13 feet) long. Once the whole area is probed without a find, the proper decision is to do it again. In rescues with enough manpower, shovelers stand nearby to check out any possible strike. The line does not stop in such an event but continues to march forward with its methodical "down, up, step" cadence.
Coarse probing is 4 to 5 times faster than the more thorough technique called fine probing. For a coarse probe, probers straddle a distance of 50 cm and are spaced 75 cm apart ( Figure 2-20 ). This leaves 25 cm between the toes of adjacent probers. Probes are pushed into the center of the straddled span. Upon command from the leader, the line advances one step, about 70 cm. (Where terrain is steep or probers are few, an alternative is to stand "fingertip-to-fingertip." Probers probe first on one side of their body, then on the other.) This method gives about a 70% chance of finding the victim. After several passes of coarse probing with no results, a fine probe is done, usually when the objective is body recovery. For this method the line is arranged as for coarse probing. Each searcher probes in front of the left foot, in the center of the straddled position, and in front of the right foot. On signal the line advances 30 cm and repeats the three probes. This method gives a 100% probability of finding a victim. The probe holes are spaced 25 by 30 cm, or 13 probes per square meter. On average, 20 searchers can fine probe an area 100 × 100 m (328 × 328 feet) in 16 to 20 hours. 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 in dangerous conditions, and self-preservation should be a major consideration. 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 rescuers, one person can be sent to notify the ski patrol immediately. If only one rescuer is present, the correct choice becomes harder. The best advice is to search the surface hastily but thoroughly for clues before leaving to notify the patrol. If a patrol phone is close, the rescuer should notify the patrol and then return immediately to resume the search. If the avalanche occurs in the backcountry far from any organized body of rescuers, all party members should remain at the site. The guiding principle in backcountry rescues is that survivors search until they
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Figure 2-20 A, Coarse, and B, fine avalanche probing.
cannot or should not continue. When deciding when to stop searching, the safety of the search party must be weighed against the decreasing survival chances of the buried victim. One exception exists to the rule of all party members staying to search. When there are a large number of survivors, two people can go out to secure help and the search party will still have a sizable rescue force on hand. Three-Stage Rescue.
A full-scale operation is divided into three stages. The first stage is the hasty search column. This group, composed of as many people as are on hand, heads swiftly to the site carrying probes, shovels, and first-aid equipment. They scuff the avalanche for clues and probe likely areas in hopes of making a quick find. The person reporting the avalanche often accompanies this column back to the site. The second stage brings the main body of rescuers to the site. They carry bulkier equipment needed for search, resuscitation, and evacuation: more probes and shovels, toboggans, sleeping bags, resuscitation equipment, medical supplies, and a trained avalanche dog and handler, if available. Ideally, stage two should begin 10 to 15 minutes after stage one. The third stage brings in support for stages one and two, in the case of a prolonged rescue. Included are fresh rescuers to take over for cold and tired searchers, hot food and drink, tents, warm clothing, and lights.
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Avalanche dogs and handlers can provide additional search power.
THE MODERN AVALANCHE VICTIM Avalanche deaths have increased in the United States each decade since 1950. Figure 2-21 shows annual deaths; Figure 2-22 shows these numbers averaged over 5-year periods. From 1950 to 1999, 571 people have died in avalanches. Of these, 471 (82%) were men and 54 (10%) were women. (Interestingly, not all accident reports list the gender of the victim.) The average age of all victims is 28 years. The youngest was 6; the oldest, 66. Figure 2-23 shows the activity groups for the victims. Most victims (83%) were pursuing some form of recreation at the time of their accident, with climbers, ski tourers, snowmobilers, and lift skiers heading the list. The distinction between ski tourers and lift skiers is that lift skiers pursue their sport in and around developed ski areas and rely on lifts to get them up the hill. This category includes skiers who leave the area boundary or ski into "closed" areas within the ski area boundary. The ski tourers category includes ski mountaineers, backcountry skiers, helicopter skiers, and snowcat skiers. Miscellaneous recreation includes hikers, snowshoers, and persons playing in the snow. Among nonrecreation groups, avalanches strike houses (residents), highways (motorists and plow drivers), and the workplace (ski patrollers and others whose job puts
Figure 2-21 Avalanche fatalities in the United States from the winters of 1950–1951 to 1998–1999.
them at risk). Since 1950, 15 states have registered avalanche fatalities ( Figure 2-24 ). Statistics of Avalanche Burials Numerous factors affect a buried victim's chances for survival: time buried, depth buried, clues on the surface, safety equipment, injury, ability to swim with the avalanche, body position, snow density, presence of airspace, and size of airspace. A victim who is uninjured and able to fight and swim on the downhill ride usually has a better chance of ending up only partly buried, or if completely buried, a better chance of creating an airspace for breathing. A victim who is severely injured or knocked unconscious is like a ragdoll 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 third of all avalanche deaths are caused by trauma, especially to the head and neck. Second, snow burial causes suffocation in two thirds of avalanche deaths. The problem of breathing in an avalanche does not start with being buried. A victim being carried down in the churning maelstrom of snow has an extraordinarily hard time breathing. Inhaled snow clogs the mouth and nose; suffocation occurs quickly if the victim is buried with the airway already blocked. Snow
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Figure 2-22 Avalanche fatalities in the United States averaged by five-winter periods, 1950–1951 to 1998–1999.
Figure 2-23 Avalanche fatalities in the United States from 1950–1951 to 1998–1999 by activity categories.
Figure 2-24 Avalanche fatalities in the United States from 1950–1951 to 1998–1999 by state.
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Figure 2-25 Length of time buried for U.S. avalanche fatalities and survivors in direct contact with the snow (not in a structure or vehicle) from 1950–1951 through 1998–1999.
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. The snow is much less permeable to airflow, making it harder for the victim to breathe. Snow sets up hard and solid after an avalanche. It is almost impossible for victims to dig themselves out, even if 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 sometimes is so great that the victim is unable to expand his or her 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. It takes longer than snow-clogged airways, but the result is still death by suffocation. Another factor that affects survival is the position of the victim's head; that is, whether they were buried face up or face down. The most favorable position is face up. Data from a limited number of burials show the victim is twice as likely to survive if buried face up rather than face down. If buried face up, an airspace forms around the face as the back of the head melts into the snow; if buried face down, an airspace cannot form as the face melts into the snow. The statistics on survival are derived from a large number of avalanche burials. In compiling these figures, we have included only persons who were totally buried in
direct contact with the snow. We have not included victims buried in the wreckage of buildings or vehicles, since such victims can be shielded from the snow to allow sizable airspaces. Under favorable circumstances such as this, 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. Figure 2-25 shows decreasing survival with increasing burial time. In the first 15 minutes, more persons are found alive (87%) than dead. Between 16 to 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. The important point is that speed is essential in the search. In favorable circumstances, buried victims can live for several hours beneath the snow; therefore rescuers should never abandon a search prematurely. A miner in Colorado who was buried by an avalanche near a mine portal was able to dig himself out after being buried for approximately 22 hours and nearly 1.8 m (6 feet) deep. However, after several hours the diminishing probability of finding a live victim should be weighed against the safety of the search party. Survival is interrelated with both time and depth of burial, as shown in Figure 2-26 . Survival probabilities diminish with increasing burial depth. To date, no one in the United States who has been buried deeper than 2.1 m (7 feet) has been recovered alive. Statistics of Rescue A buried victim's chance of survival directly relates not only to depth and length of time of burial but also to
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Figure 2-26 Depth of burial for U.S. avalanche fatalities and survivors and percentage survival for victims in direct contact with the snow (not in a structure or vehicle) from 1950–1951 through 1998–1999.
TABLE 2-1 -- Type of Rescue for Buried Avalanche Victims in Direct Contact with Snow, Based on a Sample of 682 Burials in the United States from 1950–1951 to 1998–1999 SELF-RESCUE RESCUE BY PARTY MEMBERS RESCUE BY ORGANIZED TEAM TOTAL Found alive
49 (16%)
186 (64%)
57 (20%)
292
Found dead
—
84 (22%)
306 (78%)
390
type of rescue. Table 2-1 compiles the statistics on survival as a function of type of rescue. Buried victims rescued by party members or groups at the accident site have a much better chance of survival than those rescued by organized rescue groups, time being the major influencing factor. Of those found alive, 64% were rescued by party members and 20% by an organized rescue party. Table 2-2 describes methods of rescue for buried avalanche victims. Seventy-three percent of victims (108 of 147) who were 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 some cases this was simply good luck, but in many cases it was the result of actively fighting or swimming with the avalanche or of thrusting a hand upward when the avalanche began to slow down. 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 alone, with no one to spot the hand or ski tip and provide rescue.
TABLE 2-2 -- Method of Locating (First Contact) Buried Avalanche Victims, Based on a Sample of 748 Avalanche Burials in the United States from 1950–1951 to 1998–1999 METHOD FOUND ALIVE FOUND DEAD TOTAL Attached object or body part
108
39
147
Hasty search or spot probe
26
38
64
Coarse or fine probe
22
139
161
Rescue transceiver
36
58
94
Avalanche cord
1
0
1
Acoustic contact
26
1
27
6
34
40
17
14
31
0
41
41
Inside vehicle
30
10
40
Inside structure
22
28
50
Method not known
19
33
52
313
435
748
Avalanche dog Other (digging, bulldozer) Found after long time span
TOTAL
Organized probe lines have found more victims than any other method, but because of the time required, most victims (86%) are recovered dead. Only 22 people were found alive by this method, with 139 recovered dead. Rescue transceivers are an efficient method to locate victims, but two problems have limited the number of survivors who were wearing beacons. First, few who wear beacons are well practiced in the art of using them instantly and efficiently to save a life; and second, even with a quick pinpointing of the burial location, extricating
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the victim from deeper burials may take too long to save a life. Therefore, since the first transceiver rescue in 1974, only 38% (36 of 94) of buried victims found with transceivers have been recovered alive. The more practice and experience with transceivers on the part of the rescuers, the faster the find and recovery. Despite the sound-insulating properties of snow, 26 victims who were shallowly buried were able to yell and be heard by rescuers (acoustic 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 effected five additional live recoveries. A trained avalanche dog can search more effectively than can 30 searchers. Search dogs move rapidly over avalanche debris, using their sensitive noses to scan for human scent diffusing up through the snowpack. Dogs have found bodies buried 10 m (33 feet) deep but have also passed over some buried only 2 m (6 ½ feet) deep. They are not 100% effective. Search and rescue teams and law enforcement agencies work closely with search dog handlers, and trained avalanche dogs are
becoming common fixtures at several ski areas in the western United States. These statistics point out the extreme importance of rescue skills. Organized rescue teams, such as ski patrollers, must be highly practiced. They must have adequate training, manpower, and equipment to perform a hasty search and probe of likely burial spots within a minimum time span. For backcountry rescues the message is clear that a buried victim's best hope for survival is to be found by his or her companions. The need to seek outside rescue units practically ensures a body recovery mission.
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Suggested Readings
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Armstrong BR, Williams K: The avalanche book, Golden, Colo, 1992, Fulcrum, Inc. The Avalanche Review, P.O. Box 1032, Bozeman, MT 59771-1032 (official publication of the American Association of Avalanche Professionals). Daffern T: Avalanche safety for skiers and climbers, ed 2, Seattle, Wash, 1992, Cloudcap. Fraser C: Avalanches and snow safety, New York, 1978, Charles Scribner. Fredston J, Fesler D: Snow sense: a guide to evaluating avalanche hazard, ed 4, Anchorage, 1994, Alaska Mountain Safety Center. LaChapelle E: The ABC's of avalanche safety, ed 2, Seattle, Wash, 1985, The Mountaineers Books. Logan N, Atkins D: The snowy torrents: avalanche accidents in the United States 1980–86, Denver, Colo, 1996, Colorado Geological Survey Spec Pub 39. McClung D, Schaerer P: The avalanche handbook, Seattle, Wash, 1993, The Mountaineers Books.
APPENDIX: Public Information Twenty-four-hour regional avalanche information is available, generally from November through April, by calling the following Internet web sites or recorded telephone messages. California Internet: www.r5.fs.fed.us/tahoe/avalanche/ Truckee 530-587-2158 Mammoth Lakes 760-924-5500
Colorado Internet: www.caic.state.co.us Denver/Boulder 303-275-5360 Fort Collins 970-482-0457 Colorado Springs 719-520-0020 Summit County 970-668-0600 Vail 970-479-4652 Aspen 970-920-1664 Durango 970-247-8187
Idaho Internet: www.avalanche.org/~ciac/bulletin.txt Sun Valley 208-788-1200 x8027
Montana Internet: www.gomontana.com/avalanche Bozeman 406-587-6981 Cooke City 406-838-2341
New Hampshire Internet: www.mountwashington.org/avalanche Utah Internet: www.avalanche.org/~uafc/ Salt Lake City 801-364-1581 Provo 801-378-4333 Ogden 801-626-8600 Park City 435-658-5512 Logan 801-797-4146 Alta 801-742-0830 Moab 801-259-7669
Washington and Oregon Internet: www.nwac.noaa.gov Seattle 206-526-6677 Portland 503-808-2400
Wyoming Internet: www.untracked.com/forecast Jackson 307-733-2664
Canada Internet: www.avalanche.ca
APPENDIX: Avalanche Education Several organizations teach basic and advanced avalanche awareness and training courses. Beyond those listed here, many local colleges and universities, ski patrols, and recreation departments offer courses. Adventures to the Edge Box 91 Crested Butte, CO 81224 970-349-5219 Alaska Avalanche School Alaska Mountain Safety Center 9140 Brewsters Drive Anchorage, AK 99516 907-345-3566 American Avalanche Institute Box 308 Wilson, WY 83014 307-733-3315 Canadian Avalanche Association Training Schools Box 2759 Revelstoke, BC, Canada V0E 2S0 250-837-2435 Canadian Ski Patrol System 8 Vartown Place NW Calgary, AB, Canada T3A 0B5 403-938-2101 Federation of Mountain Clubs of British Columbia 336-1367 West Broadway Vancouver, B.C., Canada V6H 4A9 604-739-7175 National Avalanche School National Avalanche Foundation 133 South Van Gordon St., Suite 100 Lakewood, CO 80228 303-988-1111 National Outdoor Leadership School Box 345 Victor, ID 83455 208-354-8443 National Ski Patrol 133 South Van Gordon St., Suite 100 Lakewood, CO 80228 303-988-1111 Northwest Avalanche Institute 39238 258th Ave., SE Enumclaw, WA 98022 360-825-9261 Sierra Ski Touring Box 176 Gardnerville, NV 89410 702-782-3047 Silverton Avalanche School Box 178 Silverton, CO 81433 Summit County Rescue Group Box 1794 Breckenridge, CO 80424 Telluride Avalanche School Box 261 Telluride, CO 81435 970-728-3829 Colleges and universities that offer avalanche and snow related courses (mostly graduate level) and the E-mail contact: University of Arizona Department of Hydrology and Water Resources Dr. Roger Bales:
[email protected] Arizona State University Department of Geography Dr. Andrew Ellis:
[email protected] University of California, Santa Barbara Donald Bren School of Environmental Science and Management Dr. Jeff Dozier:
[email protected] University of British Columbia (Vancouver) Department of Geography & Civil Engineering
Dr. Dave McClung:
[email protected] University of Calgary (Calgary) Department of Geology and Geophysics Department of Civil Engineering Dr. Bruce Jamieson:
[email protected] University of Colorado (Boulder) Department of Geography Institute of Arctic and Alpine Research (INSTAAR) Dr. Mark W. Williams:
[email protected] Colorado State University (Fort Collins) Department of Earth Resources Dr. Kelly Elder:
[email protected] Montana State University (Bozeman) Department of Civil Engineering Dr. Ed Adams:
[email protected] Department of Earth Sciences Dr. Katherine Hansen:
[email protected] Northern Arizona University (Flagstaff) Department of Geography Dr. Lee Dexter:
[email protected] University of Oregon (Eugene) Department of Geography Dr. Cary Mock:
[email protected] Rutgers University (Piscataway, NJ) Department of Geography Dr. David A. Robinson:
[email protected] Sierra College Tahoe-Truckee Extension Center Box 2467 Truckee, CA 96161 530-587-3849 University of Utah (Salt Lake City) Department of Civil Engineering Dr. Rand Decker:
[email protected] Utah State University (Logan) Department of Forest Resources Dr. Michael J. Jenkins:
[email protected] University of Washington (Seattle) Geophysics Program Dr. Howard Conway:
[email protected] APPENDIX: Avalanche Safety Equipment Manufacturers and Suppliers Backcountry Access, Inc. 2820 Wilderness Place, Unit H Boulder, CO 80301 303-417-1345 Backcountry ski equipment, Tracker rescue beacons Black Diamond Equipment, Ltd. 2084 East 3900 South Salt Lake City, UT 84124 801-278-5552 Backcountry ski equipment, clothing, survival gear, rescue beacons, AvaLung Cascade Toboggan 25802 West Valley Highway Kent, WA 98032 206-852-0182 Shovels, probes, rescue beacons, other rescue equipment Climb High 1861 Shelburne Road Shelburne, VT 05482 802-985-5055 Backcountry ski and expedition equipment, rescue beacons, shovels, probes, and clothing Eastern Mountain Sports 1 Vose Farm Road Peterborough, NH 03458 603-924-9571 (or local retail store) Backcountry ski equipment, clothing, survival gear, rescue beacons Life Link International P.O. Box 2913 Jackson Hole, WY 83001 307-733-2266 Snowpit instruments, shovels, probes, rescue beacons, other rescue equipment Mountain Safety Research 4225 2nd Avenue South Seattle, WA 98134 206-624-857 Survival gear, probes, other rescue equipment Mt. Tam Sports Box 111 Kentfield, CA 94914 415-461-8111 Snowpit instruments, rescue equipment, first aid equipment Ortovox USA, Inc. 455 Irish Hill Road Hopkinton, NH 03229 603-746-3176 Ortovox rescue beacons, shovels, rescue equipment Recreational Equipment, Inc. P.O. Box 88125 Seattle, WA 98138-2125 206-323-8333 (or local retail store) Backcountry ski equipment, clothing, survival gear, rescue beacons Survival on Snow, Inc. Box 1, Site 218 RR2 St. Albert, AB, Canada T8N 1M9 403-973-5412 SOS rescue beacons, rescue equipment Wasatch Touring 702 East 100 South Salt Lake City, UT 84102 801-359-9361 Snowpit instruments, probes, shovels, rescue beacons
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Chapter 3 - Lightning Injuries Mary Ann Cooper Christopher J. Andrews Ronald L Holle Raúl E López
HISTORICAL OVERVIEW Humans have always viewed lightning with awe and trepidation. Priests, the earliest astronomers and meteorologists, became proficient at weather prediction, interpreting changes in weather as omens of good or bad fortune, sometimes to the advantage of their political mentors. As a spectacular celestial event, lightning was often depicted in ancient cultures and religions.[52] A roll seal from Akkadian times (2200 BC) portrays a goddess holding sheaves of lightning bolts in each hand.[52] Next to her, a weather god drives a chariot and creates lightning bolts by flicking a whip at his horses, while priests offer libations. A relief found on a castle gate in northern Syria (900 BC) depicts the weather god Teshub holding a three-pronged thunderbolt. Beginning around 700 BC, Greek artists began to incorporate lightning symbols representing Zeus's tool of warning or favor. Aristotle noted that lightning resulted from the ignition of telluric fumes that made up storm clouds. Roman mythology saw lightning as more ominous than did the Greeks, with Jupiter using thunderbolts as tools of vengeance and condemnation so that Romans who were struck were denied burial rituals. Several Roman emperors wore laurel wreaths or sealskin to ward off lightning strikes. Important matters of state were often decided on observations of lightning and other natural phenomena. Both Seneca and Titus Lucretius discussed lightning in their treatises on natural events, and Plutarch noted that sleeping persons, having no spirit of life, were immune to lightning strikes.[52] The Norsemen named their thunder god Thor. Thursday is named for him. In Chinese mythology the goddess of lightning, Tien Mu, used mirrors to direct bolts of lightning. She was one of the deities of the "Ministry of Thunderstorms" of ancient Chinese religion. Lightning also played a role in Buddhist symbolism. Although lightning is most frequently rendered as fire, it has also been represented as stone axes hurled from the heavens. French peasants carry a pierre do tonnerre, or lightning stone, to ward off lightning strikes. The Yakuts of eastern Asia regard rounded stones found in fields hit by lightning as thunder axes and often use the powdered stones in medicines and potions. In Africa the Basuto tribe views lightning as the great thunderbird Umpundulo, flashing its wings in the clouds as it descends to Earth. Some Native American cultures had the Thunderbird in their religions. The Navajo have a story about the hero Twins who used "the lightning that strikes straight" and "the lightning that strikes crooked" to kill several mythical beasts that were plaguing the People (Navajo) and in the process created the Grand Canyon. [13] The art of the native Australians incorporates lightning symbols as well.
MYTHS, SUPERSTITIONS, AND MISCONCEPTIONS [33] The Roman Pliny noted that a man who heard thunder was safe from the lightning stroke. In general this is true because the light and strike precede the noise, depending on the distance from the lightning strike. However, some victims of direct hits report a sledge-hammer-like effect of the force while seeing a bright light and occasionally hearing a loud noise. Others who receive side flashes or ground current report both seeing the flash and hearing the stroke, indicating that the main stroke was some distance away. Many myths about lightning still persist today, including the notion that lightning strikes are invariably fatal. According to an American study of cases reported in the lightning literature since 1900, lightning strike carries a mortality of 30% and morbidity of 70%.[29] A slightly different statistical interpretation of the same data yielded a mortality figure of 20%.[2] [8] Because literature reports are usually biased toward the severe or interesting cases, a review of cases will tend to overestimate the mortality rate. In reality, mortality may be as low as 5% to 10%.[25] Most people suspect that the major cause of death would be from burns. However, the only cause of immediate death is from cardiac arrest.[29] Persons who are stunned or lose consciousness without cardiopulmonary arrest are highly unlikely to die, although they may still have serious sequelae.[31] Unfortunately, delayed causes of death include suicide induced by the life changes from disabilities wrought by lightning. Most people know to seek shelter when storm clouds roll overhead. Few realize that one of the most dangerous times for a fatal strike is before the storm.[35] Lightning may travel nearly horizontally as far as 10 miles or more in front of the thunderstorm and seem to occur "out of a clear blue sky," or at least when the day is still sunny. The faster the storm is traveling and
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the more violent it is, the more likely that a fatal strike will occur. Another time underestimated for the potential danger of lightning is the end of a thunderstorm, which has been shown to be as dangerous as the start of the storm. The "30–30 rule" is now recommended for lightning safety. [37] If you see lightning and can count to 30 seconds before you hear the thunder, you are already in danger and should be seeking shelter. Activities should not be resumed for at least 30 minutes after the last lightning is seen and the last thunder heard.[37] [117] To calculate your distance from lightning, take the number of seconds between the "flash" and the "bang" (flash-to-bang method) and divide by 5 to find the number of miles.[116] The problem with the flash-to-bang method is that it is sometimes difficult to match the correct thunder to the correct lightning flash in an active storm. In addition, many people forget to divide by 5 and so overestimate the miles (and their safety factor) by a factor of five. The distance between successive lightning flashes may be as little as a few yards or as much as 5 miles plus or minus another 5 miles (a count of 50 seconds) depending on the terrain and other local geographic factors.[86] One way to teach children lightning safety is to use the following phrase: "If you see it, flee it; if you hear it, clear it." Winter lightning (thunderblizzard), although rare, is usually more dangerous because it tends to be much more powerful than summer lightning. Most people believe that they are immune from lightning strikes when inside a building. Unfortunately, a significant proportion of injuries occurs to persons who are in their homes or places of employment.[1A] [6] [43] [105] [110] Side flashes strike people through plumbing fixtures, telephones, and other appliances attached to the outside of the house by metal conductors.[1A] Portable cellular phones offer protection from the electrical effects, although victims may suffer acoustic damage from the static in the earpiece similar to having a firecracker go off next to their ear.[6] With a hard-wired phone, they may suffer neurocognitive deficits,[32] [36] [103] death, or a myriad of other lightning-related problems because the phone system in most houses is not grounded to the house's electrical system and acts as a conduit for lightning either to come into the home or to exit from it. Telephone companies include warnings in their directories against using telephones during thunderstorms. Taking shelter in small sheds, such as hikers' leantos or those on golf courses, especially above tree level on a mountain, can be especially dangerous when lightning splashes onto the inhabitants. Unfortunately, the most recently published NFPA Journal (National Fire Protection Association) discusses protection that may be effective for the shelter but may actually increase the lightning risk to any inhabitants who seek shelter in them. The "crispy critter" myth is the belief that the victim struck by lightning bursts into flames or is reduced to a pile of ashes.[35] In reality, lightning often flashes over the outside of a victim, sometimes blowing off the clothes but leaving few external signs of injury and few if any burns. Two other myths held by the public and many physicians are: "If you're not killed by lightning, you'll be OK," and, "If there are no outward signs of lightning injury, the damage can't be serious."[35] Medical literature, because of lack of follow-up case reports, also implies that there are few permanent sequelae of lightning injury. However, in the last few years it has become apparent that several permanent sequelae may occur.* In addition, many lightning victims with significant sequelae had no evidence acutely of burns. Peripheral neuropathy, chronic pain syndromes, and neuropsychologic symptoms, including severe short-term memory difficulty, difficulty processing new information, depression, and posttraumatic stress disorder, may be debilitating.[36] [102] [103] Further study is needed to elucidate how malingerers may be distinguished from real victims of lightning injury.[60] [61] Occasionally, lighting victims show pathognomonic skin changes that are not true burns but have a fernlike pattern. At one time, these patterns were thought to be imprints of the surrounding vegetation transferred onto the victim's skin by the lightning. Actually these fernlike patterns resemble fractals or the kind of pattern that can be obtained from placing a photographic plate in a strong electromagnetic field, which is what lightning produces for a short time around the victim.[62] [121] They do not follow the distribution of nerves or blood vessels. Although they have been photographed and well described in the literature, no histologic study has been reported to explain the structure of the marking. It has been postulated that the pattern is caused by the forceful extravasation of red blood cells from the capillaries as they contract, similar to a bruise, which would also explain the evanescent nature of the markings. A myth still prevalent is that the lightning victim retains the charge and is dangerous to touch, since he or she is still "electrified." This myth has led to unnecessary deaths by delaying resuscitation efforts.[35] Medical literature and practice are plagued by myths that grew out of misread, misquoted, or misinterpreted data and continue to be propagated without further investigation. Not the least of these is the tenet that lightning victims who have resuscitation for several hours may still successfully recover. This belief seems to be grounded in the old idea of suspended *References [ 1]
[ 5] [ 28] [ 30] [ 33] [ 36] [ 47] [ 98] [ 102] [ 103] [ 110] [ 115] [ 122] [ 123]
.
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animation—the concept that lightning is capable of shutting off systemic and cerebral metabolism, allowing rescuers a longer period in which to resuscitate the patient. This concept, credited to Taussig,[113] actually appeared some time before her article. In addition, the case recounted by Taussig that is the basis for this myth, when searched to its source, was a case report by Morikawa and Steichen.[94] The case does show a somewhat longer resuscitation period than usual, but not as miraculous as reported in Taussig's paper or as propagated in subsequent references to her paper. In a study of lightning survivors, Andrews, Colquhoun, and Darveniza [4] have shown increasing prolongation of the QT interval, bringing up the theoretic possibility of torsades as a mechanism for the suspended animation reports. There is new evidence from animal experiments to support the teaching that respiratory arrest may persist longer than cardiac arrest.[2] [38] [39] One study, in which Australian sheep were hit with simulated lightning strokes, showed histologic evidence of greater damage to the respiratory centers than to the cardiac center in the fourth ventricle.[2] Prolonged assisted ventilation may in some cases be successful after cardiac activity has returned.
Another series of animal experiments by Cooper and Kotsos[38] [39] with hairless rats has shown that it is possible to obtain the skin changes (keraunographic markings), primary and secondary arrest with prolonged respiratory arrest, and temporary lower extremity paralysis with simulated lightning strike. Several booklets listing precautions for personal lightning protection appeared in the late 1700s and early 1800s. One of the superstitions listed was that humans, by their presence, could attract lightning to a nearby object. A book of the times, Catechism of Thunderstorms, illustrated other myths. Lightning was said to follow the draft of warm air behind a horse-drawn cart, so that coachmen were cautioned to walk their horses slowly through a storm. Other precautions listed included seeking shelter away from tall trees and sheaves of corn if caught in the open and installing lightning rods for the protection of buildings and ships. Historically, many remedies for resuscitation of lightning victims have been offered. On July 15, 1889, Alfred West testified in a New York court that he was revived by "drawing out the electricity" when his feet were placed in warm water while his rescuer pulled on Mr. West's toes with one hand and milked a cow with the other.[10] Other early attempts at resuscitation included friction to the bare skin, dousing the victim with a bucket of cold water, and chest compression. An early attempt at cardiopulmonary resuscitation was given in 1807 when mouth-to-mouth ventilation was used for lightning victims and it was proposed that gentle electric shocks from galvanic batteries passed through the chest might be successful in resuscitating a victim of lightning.[16] Before that, Benjamin Franklin had purposely electrocuted a chicken during a lightning experiment and reported successful resuscitation with mouth-to-beak ventilation.[50] A myth in current treatment is that lightning injuries should be treated like other high-voltage electric injuries. Although lightning as an electric phenomenon follows the same laws of physics, the injuries seen with lightning are very different from high-voltage injuries and should be treated differently if iatrogenic morbidity and mortality are to be avoided.[9] [34] "Lightning never strikes the same place twice." In reality, the Empire State Building and the Sears Tower are hit dozens of times a year, as are mountaintops and radio-television antennas. If the circumstances facilitating the original lightning strike are still in effect in an area, the laws of nature will encourage further lightning strikes. Other myths[35] : 1. Victims may have "internal burns": There may be cellular damage and certainly nervous system damage but rarely, if ever, internal burns such as those suffered with high-voltage electrical injuries. However, some physicians use this euphemism with patients to explain their pain and neurologic injuries. 2. Wearing rubber-soled shoes, raincoats, etc., will protect a person: If lightning has burned its way a mile or more through the air, which is a superb insulator, it is foolish to believe that a fraction of an inch of rubber or composite material will serve as an adequate insulator. 3. The rubber tires on an auto are what protects a person from lightning injury: See entry 2 above. Electrical energy goes along the outside of a metal conductor (the car body) and dissipates through the rainwater to the ground or off the axles or bumper of the car. 4. Wearing metal around the head or as cleats on shoes will increase the risk or "attract lightning": There is no evidence to support this. Secondary burns on the soles of the feet where metal cleats or grommets heat up have been reported, but there is no evidence that a person increases his or her risk by wearing these. 5. Carrying an umbrella increases the risk: This is true if a person's height becomes greater by holding an umbrella. 6. Lightning always hits the highest object: False. Lightning only "sees" objects about 30 to 50 meters from its tip. In addition, several pictures exist of lightning hitting halfway down a flagpole or at the bottom of the space shuttle gantry. 7. There is no danger of lightning injury unless it is raining: False. Although lightning only occurs as 76
a result of thunderstorms, it can travel 10 or more miles in front of the thundercloud and seem to "come out of the blue" to strike a person or object long before the rain comes down in their area. Nearly 10% of lightning occurs when there is no rain falling in the area of the strike. It has also been known to reach over a mountain ridge and "hit out of the blue" from the thunderstorm that was on the other side of the peak and was neither visible nor audible to the victim. 8. Lightning may occur without thunder: Whenever there is lightning, there is thunder, and vice versa. Sometimes it will appear that there is lightning without thunder because thunder is seldom heard more than 10 miles from the lightning stroke or may be blocked by buildings or mountains.
INCIDENCE OF INJURY Spatial Distribution of Lightning in the United States The distribution of cloud-to-ground lightning across the United States is known because of deployment and operation for the last decade of automatic real-time lightning detection networks. On the average, over 20 million cloud-to-ground flashes are detected each year in the United States.[69] On a shorter time scale, more than 50,000 flashes per hour are sometimes detected during summer afternoons over the United States.[40] A multiyear climatology of lightning from detection network data shows that central Florida always has the greatest number of flashes per area in a given year ( Figure 3-1, A ). Flash density decreases to the north and west from there. Flash densities over Missouri, Iowa, and Illinois during the 1993 Mississippi River flood rivaled Florida. [93] In addition to the general features in Figure 3-1 , important local variations occur along the coast of the Gulf of Mexico, where sea breezes enhance lightning frequency.[81] [119] Additional important maxima and minima are found in and around the regions in the western United States with mountains and large slopes in terrain. [81] [89] Temporal Distribution of Lightning in the United States Lightning is most common in summer months ( Figure 3-2, A ). About two thirds of the flashes occur in June, July, and August. In the southeastern states, lightning occurs quite often during all months of the year. A primary ingredient for lightning formation is a significant amount of moisture in the lower and middle levels of the atmosphere; this fuel for thunderstorms is consistently found in humid subtropical and tropical regions. Mechanisms to lift the moisture into thunderstorms are necessary. Especially along coastlines and mountain slopes, updrafts are produced almost daily that provide favored locations for thunderstorms. Lightning is most common in the afternoon ( Figure 3-2, B ). Nearly half of all lightning occurs from 1500 through 1800 local standard time (LST). Figure 3-2, B , combines regional results during the summer for Arizona,[120] northeast Colorado and central Florida,[81] and central Georgia.[80] There is no publication to date showing diurnal variation of lightning over the entire United States with detection network data. Lightning is at a maximum in the afternoon because the updrafts necessary for thunderstorm formation are strongest during the hours of the day when surface temperatures are highest, which results in the greatest vertical instability. Lightning Around the World Lightning detection systems similar to the U.S. network have been installed over part or all of about two dozen countries on every continent except Antarctica. Some have been in operation for up to a decade. At this time, there is no compilation of cloud-to-ground lightning flashes from such networks covering more than one country. Instead, Figure 3-1, B , shows the worldwide map of total lightning developed from the satellite-borne Optical Transient Detector (OTD), which measures both cloud-to-ground and cloud flashes.[26] Flash densities have been calculated statistically using OTD data to estimate that there are over 1.2 billion lightning flashes of all types around the world every year. Most lightning is over tropical and subtropical continents, and there is far more lightning over land than the oceans. Some of the highest frequencies are much greater than found in the United States over Florida and other Gulf Coast locations. Lightning is an afternoon phenomenon nearly everywhere, as was shown for the United States. At higher latitudes, most lightning occurs during the summer months. In Southeast Asia and surrounding regions toward the equator, maximum lightning activity during the year is influenced primarily by the monsoon and coincides generally with the months of heaviest rainfall. U.S. Lightning Casualties in Storm Data Every month, each National Weather Service (NWS) office in the United States compiles a list of damaging or notable weather phenomena occurring within the office's area of responsibility. This list is sent to National Oceanic and Atmospheric Administration (NOAA) headquarters, then to NOAA's National Climatic Data Center (NCDC) in Asheville, NC. These lists are combined at NCDC and Storm Data is published. From 1959 to 1994, Storm Data had 3239 deaths, 9818 injuries, and 19,814 property-damage reports caused by
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Figure 3-1 A, Cloud-to-ground flashes per square kilometer per year in the United States from a network of lightning detection antennas from 1989–1996. B, Total flashes per square kilometer per year for the world from May 1995 to April 1999 from the Optical Transient Detector. (A from Huffines GR, Orville RE: J Appl Meteor 38:1013, 1999; B courtesy Hugh Christian, NASA/Marshall Space Flight Center.)
lightning. Each report has some or all of the following: year, month, day, time, state and county, as well as number, gender, and location of fatalities and injuries, and amount and type of damage. Lightning-related casualties and damages are often less spectacular and more dispersed in time and space than other weather phenomena. Therefore lightning deaths, injuries, and damages have been found to be underreported.[66] [88] [92] [111] Factors contributing to the underreporting include the fact that most casualty events involve only one person or object, the fact that Storm Data relies on newspaper clipping services for lightning events, internal inconsistency within Storm Data in tabulation of individual occurrences into summary tables, lack of an accepted definition of lightning vs. "lightning-related" deaths, and inconsistency in the listing of medical diagnoses.[84] [92] [111] Regardless, Storm Data is the only consistent national data source for several decades. Table 3-1 shows that lightning is second only to flash floods and floods in weather-related deaths during the 30-year record. Spatial Distributions of Lightning Casualties The lightning casualty distribution (deaths and injuries combined) is shown from 1959 to 1994 in Figure 3-3, A . The general pattern has similarities to the distribution of lightning in Figure 3-1 , but Florida has twice as many casualties as any other state. Many of the other high numbers of casualties are from populous eastern states. It is preferable to use casualties for these results because the number of deaths is not very large and there is no obvious reason to expect differences in the geographic distribution of deaths vs. injuries. The lightning hazard is shown better when population is taken into account ( Figure 3-3, B ). The maximum rate of lightning casualties shifts from populous eastern
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Figure 3-2 A, Monthly distribution of U.S. cloud-to-ground lightning from 1992 to 1995 from a lightning detection network. B, Hourly distribution of cloud-to-ground lightning from networks in four U.S. locations. C and D, Monthly and hourly distributions of lightning casualties from 1959 to 1994 in the United States. (A from Orville RE, Silver AC: Mon Wea Rev 125:631, 1997; B from López RE, Holle RL: Mon Wea Rev 114:1288, 1986; C and D from Curran EB, Holle RL, López RE: Lightning fatalities, injuries, and damage reports in the United States from 1959–1994, NOAA Tech Memo NWS SW-193, 1997.)
TABLE 3-1 -- Weather-Related 30-Year Average Deaths (1965–1994), and 1994 Weather Casualties; Order is by 30-Year Average Deaths, Then 1994 Deaths WEATHER TYPE DEATHS PER YEAR 1994 DEATHS 1994 INJURIES Flash flood
139
River flood
59
33
32
14
Lightning
87
69
484
Tornado
82
69
1067
Hurricane
27
9
45
Extreme temperatures
81
298
Winter weather
31
2690
Thunderstorm wind
17
315
Other high wind
12
61
Fog
3
99
Other
6
99
TOTALS
388
5165
states to Rocky Mountain and plains states. The top two rates are from Wyoming and New Mexico; these states were 35th and 21st in number of casualties. Wyoming had most of its casualties in the 1960s and 1970s, and almost none since then. Southeastern states often have high rankings in both casualties and casualty rates ( Figure 3-4, A and B ). The only states in the top 10 of both casualties and casualty rate are Florida, Colorado, and North Carolina. Detailed listings of deaths and injuries by state, as well as death and injury rates per state, are in Curran et al.[41] This reference also contains information on the distribution of lightning damage reports, which has a high concentration over the plains states. Two lightning fatality studies for the United States had substantially similar results to Figure 3-3 . Duclos and Sanderson[44] used data from the National Center for Health Statistics, and Mogil et al[92] used Storm Data. Single-state maps by county were compiled for Florida,[44] North Carolina,[75] Michigan,[48] and Colorado.[82] [87] In other countries, fatalities divided by political boundaries were
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Figure 3-3 Rank of each state in lightning casualties (deaths and injuries combined) from 1959 to 1994. A, Casualties per state. B, Casualties weighted by state population. (From Curran EB, Holle RL, López RE: Lightning fatalities, injuries, and damage reports in the United States from 1959–1994, NOAA Tech Memo NWS SW-193, 1997.)
Figure 3-4 A, Number of casualties, deaths, and injuries. B, Ratio of injuries to deaths from 1959 to 1994 in the United States. (From Curran EB, Holle RL, López RE: Lightning fatalities, injuries, and damage reports in the United States from 1959–1994, NOAA Tech Memo NWS SW-193, 1997.)
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developed for Canada by Hornstein,[68] for Singapore by Pakiam et al,[101] for Australia by Coates et al,[27] and for France by Gourbière et al. [55] Monthly Variations of U.S. Casualties By month, lightning casualties peak during July ( Figure 3-2, C ). The percentages increase gradually before July, then decline more quickly after the maximum. Cloud-to-ground flashes show similar features ( Figure 3-2,A ). Seasonal maps of lightning casualty rates in Curran et al[41] show the summer patterns to be similar to annual maps. During other seasons, lightning casualty rates are higher in southern states. Casualty rates in the northeast are low except during the summer, whereas they are highest on the West Coast during autumn and winter. A July maximum was also found in prior Storm Data studies, as well as a slower increase before and a faster decrease after July.[44] [48] [82] [87] [92] August maxima were found in Florida by Duclos et al[44] and Holle et al.[64] January has the largest number of Australian fatalities, resulting from the reversal of seasons from the United States.[27] The Singapore fatality maxima in November and April are similar to the annual cycle of local thunderstorms.[101] Time of Day Variations of U.S. Casualties By time of day, most lightning casualties occur in the afternoon ( Figure 3-2, D ); two thirds occur between 1200 and 1800 LST. They show a steady increase toward a maximum at 1600 LST, followed by a slower decrease after the maximum. Lightning flashes in Figure 3-2, B , showed a faster increase to the afternoon maximum than shown here for casualties. Lightning occurs most often in the afternoon because the ground is heated most strongly by the sun during that time period. As a result, vertical cumulus clouds form and produce lightning when they are tall enough to have tops colder than freezing temperatures. Narrower distributions of casualties centered in the afternoon are apparent in the Rockies, Southeast, and Northeast compared with the broader time series in the plains and Midwest.[41] In the evening and at night (1800 to 0559 LST), casualties are most frequent in the plains, upper midwest, and some populous eastern states.[41] Of the 29 deaths from 0000 to 0559 LST, 59% occurred when people were in a house set on fire by lightning, and 21% occurred when people were camping in tents. Casualties in the morning are spread widely across the country. Casualties during the afternoon resemble Figure 3-2, D , since these are the most frequent hours for deaths (67%) and
injuries (63%). In winter, casualties are spread erratically through the day. [41] Spring casualties occur during nearly the same afternoon hours as for the year, but there is a secondary peak before noon. Summer casualties follow the annual cycle. Autumn casualties have a broad afternoon peak and a secondary morning peak. The casualties are spread more widely through the day outside of the summer months. This spread can be attributed to two factors. First, lightning is less concentrated during the afternoon because the ground is not heated as much as in summer. As a result, more thunderstorms are formed by large-scale traveling disturbances. Second, the number of casualties, especially in winter, is much smaller, so that distributions are affected more by a small number of cases. Maximum lightning impacts from 1400 to 1600 LST were documented by Duclos and Sanderson,[44] Ferrett and Ojala, [48] and López and Holle.[87] Duclos and Sanderson[44] found an 1800 LST peak in North Carolina deaths. Additional Storm Data Information Table 3-2 shows that males were much more frequent lightning casualties than were females. Similar ratios were found in the United States,[44] [45] [64] [75] Singapore,[101] and England and Wales.[46] The most common situation was for only one victim to be involved in a lightning incident. This is an important contributor to the underreporting of lightning casualties. For incidents involving deaths only, 91% had just one fatality; the largest single case resulted from the 1963 crash of an airliner in Maryland that killed 81 people. The largest number of injuries at one event was 90 at a Michigan campground.[48] The same tendency for single victims was noted in the United States,[87] Singapore,[101] and Australia.[27] According to Storm Data, nearly half of all lightning damages are between $5000 and $50,000.[41] However, these amounts are much larger than insured losses paid for claims by homeowners and small businesses.[66] [73] Storm Data Trends in Lightning Casualties From 1959 to 1994, Storm Data shows a slow decrease in lightning deaths, while injuries increase ( Figure 3-4 ). As a result, the ratio of injuries to deaths steadily increases. The typical ratio of injuries to deaths had been between 2:1 and 4:1. However, an uncertainty exists, since more injuries are missed than are deaths.[66] [88] [92] Cherington et al[25] found that a ratio of 10 injuries to one death applied in a thorough search of Colorado hospital and emergency room visits. There are additional injuries TABLE 3-2 -- Casualty Information in Storm Data from 1959 to 1994 TOPIC
DEATHS INJURIES CASUALTIES
Males
84%
82%
83%
One victim per event
91%
68%
68%
81
to persons whose visits are not documented by a medical clinic or if they are not treated. As a result, it is likely that a 10:1 ratio of injuries to deaths is the better estimate. After population growth was taken into account (normalization), several major trends were identified.[83] [84] A 30% decrease in the number of deaths per million persons was attributed to improved forecasts and warnings, better awareness of the lightning threat, more substantial buildings available for safe refuge, and/or other socioeconomic changes. An additional 40% reduction in normalized deaths may be due to improved medical care and emergency communications. The injury rate decreased only 8%; this lowered rate may be due to transfer of some potential deaths into injuries as a result of better emergency communications, medical attention, and other factors. Notable decreases in deaths were documented with long-term data sets in England and Wales,[46] England and Wales compared with Australia,[53] and Singapore.[101] Australian deaths increased during the years 1825 to 1918, then decreased through 1991.[27] Twentieth-Century Trends in Lightning Deaths Another difficulty in determining the number of casualties and deaths is changes in reporting systems since the turn of the last century. Beginning in 1900, the Bureau of the Census established a national registration of vital statistics for deaths that included states, Washington, D.C., and large cities; annual death statistics, including lightning as a cause of death, have been compiled and published by the U.S. government. Although only 10 states and several cities reported to the Bureau of the Census in 1900, the number of states increased gradually until all states and Washington, D.C., were covered by 1935. Mortality Statistics was published before
Figure 3-5 A, Annual lightning deaths reported by Bureau of the Census and Public Health Service from 1900 to 1991 (red). Solid blue line is population of reporting states and District of Columbia; dashed is total population of contiguous United States and District of Columbia. B, Time series of lightning deaths normalized by population of reporting states (red) and exponential function (blue) fitted to data. (From López RE, Holle RL: J Climate 11:2070, 1998.)
1937 and the series Vital Statistics of the United States was published after that. Starting with the 1945 records published in 1947, data collection was changed from the Bureau of the Census to the Public Health Service. Since then, data have come from the National Center for Health Statistics, Centers for Disease Control and Prevention, Public Health Service, of the Department of Health and Human Services.[85] [104] The number of lightning deaths reported since 1900 is shown in Figure 3-5, A . During the first 20 years, annual deaths increased from less than 100 to about 450 because of an increase in reporting states. In comparing the increase in deaths with the increased reporting population, the fatality increase appears exceptionally large. During the 1920s and 1930s there were about 400 lightning deaths per year, whereas recently it has been less than 100 per year. There has been a persistent drop in deaths since 1944. The same dramatic decline since 1940 was noted by others. [12] [44] [92] The effect of changes in population can be taken into account by dividing by the population. Figure 3-5, B , shows the number of lightning deaths per million people per year. In the earlier part of the series, year-to-year fluctuations are relatively large, probably because of random inclusion of reporting states with different demographic and climatic conditions. However, since 1925, the fluctuations are consistently smaller and more regular, and they decrease as the death rate decreases. The normalized time series and an exponential curve fitted to the data indicate a decrease during the twentieth century from more than 6 to a low of 0.4 deaths per million people. Effect of Rural-to-Urban Migration Before the turn of the last century, lightning deaths appeared to occur often in rural settings.[63] Since then, the
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percentage of the U.S. population in rural areas (but not the actual population) has dramatically decreased. Figure 3-6, A , shows that the percentage of the population living in rural areas since 1890 decreased from 60% in 1900 to 25% in 1990. The only significant departures from the exponential decrease were a slowing in the 1930s and early 1940s during the Great Depression, and an acceleration of the trend in the 1950s and 1960s with increased urbanization after World War II and the Korean War. The rural population curve is superimposed on the adjusted normalized lightning-death plot in Figure 3-6,B . The remarkable agreement leads to a conclusion that the
secular exponential decrease in population-adjusted deaths is closely related to the relative reduction in rural population. This long-term decrease has been noted by several authors, and a decrease in rural population has been hypothesized as a factor, together
Figure 3-6 A, Percent of contiguous U.S. population living in rural areas since 1890 (solid line), and an exponential function fitted to data (dashed line). B, Adjusted yearly lightning deaths normalized by population, as in A. Dashed line, Percent of population in rural areas. (From López RE, Holle RL: J Climate 11:2070, 1998.)
Figure 3-7 Time series of yearly lightning deaths normalized by population for United States and Canada (A) and Spain (B).
with improved home electrical systems, which include substantial grounding, as well as medical treatment, education, and meteorologic warnings.[12] [44] [83] [87] [92] These factors are also linked to the decrease in rural population resulting from emigration to cities or enhanced urbanization of rural areas. Similar decreases in lightning death rates have been found in two other countries. Figure 3-7,A , shows the decrease for the last century in Canada compared with the United States. The Canadian death rate is probably less because of the lower flash rate for this higher-latitude country. Both the United States and Canada had a proportional shift of people from rural to urban regions. In contrast, the shift to urban population for Spain was delayed by several decades ( Figure 3-7, B ) because of a national policy of maintaining rural populations. However, when industrialization began, the lightning death rate plunged.
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Types of Lightning Casualty Incidents The preceding analyses suggest a link between the shift from rural to urban settings and the number of lightning casualties. Storm Data has the location of lightning victims since 1959, but the categories are not especially helpful because 40% of its locations are unknown. It is necessary to go beyond location to discover a person's activity to better identify the type of incident. A key to understanding the influence of the urban migration can be found in analysis of Kretzer (1895), who documented 1043 lightning deaths and injuries from 1891 to 1894. An overall impression was developed for each entry as to whether the situation was rural or urban.[63] It was not possible to make this determination in roughly one third of the cases. The verbal narratives in Storm Data from 1991 to 1994 were used in a similar analysis. Events were subdivided by type of incident based on both activity and location.[63] In the 1890s, rural deaths were much more frequent than urban ( Figure 3-8, A ). Indoor fatalities were the most frequent; 23% of all deaths were inside houses. The next largest types were outdoors and agricultural incidents, whereas recreation and sports incidents were virtually nonexistent. In the 1990s, rural settings account for a much smaller proportion of casualties ( Figure 3-8, B ), and agricultural incidents are much less frequent than 100 years ago. Only 2% of modern deaths were to people inside houses, one tenth of the percentage a century earlier. Outdoors has become the largest type of incident, with the most frequent incidents occurring under or near trees (15% of all deaths) and in the yard or garden of a house. A high percentage of incidents occurs during recreation; these cases are dominated by beach, water, and camping situations. Sports incidents involve participating in and observing sporting events; many involved golf.[63]
Figure 3-8 Types of U.S. lightning casualty incidents (%) from 1891 to 1894 compared with 1991–1994. (From Holle RL, López RE, Navarro BC: U.S. lightning deaths, injuries, and damages in the 1890s compared to the 1990s, National Oceanic and Atmospheric Administration Tech Memo, ERL pending, 2000.)
These comparisons agree with the influence of the rural-to-urban migration on lightning casualties in the United States. Rural casualties are now half as frequent as urban cases. The inside of a house is no longer as dangerous as it was. This trend is most likely a result of grounding by modern wiring and plumbing. Recreation and sports have become relatively greater contributors to the population at risk from lightning.[27] [82] [87] Worldwide Lightning Fatalities Cautious extrapolation of U.S. results to the world can be considered. There were over 400 lightning deaths a year early in the twentieth century in the United States, at a rate exceeding 6 deaths per million people (see Fig. 3-5 and Fig. 3-7 ). These often occurred in agricultural incidents in rural settings or inside buildings before widespread installation of wiring and plumbing. Since the rates and trends are similar in Canada and Spain, they can be considered typical of much of Europe and other industrialized, urbanized countries. However, many people around the world rely on labor-intensive agriculture and live in dwellings with minimal grounding. The earlier rates from the United States could be appropriate for populous tropical and subtropical areas of Africa, South America, and Southeast Asia, where there is frequent lightning. About 100 lightning deaths per year currently occur in the United States. This number would be approximately 1000 if the U.S. population was still rural, practiced labor-intensive agriculture, and lived in dwellings with minimal lightning protection. So it might be reasonable to expect that the worldwide lightning death rate is at least 10,000 per year, since a large number of people live in such situations. A ratio of 5 to 10 injuries per death gives a worldwide total of 50,000 to 100,000 injuries a year from lightning.
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EARLY SCIENTIFIC STUDIES AND INVENTION OF THE LIGHTNING ROD [49]
[ 50]
The study of electric phenomena is often traced to the publication of Gilbert's De Magnete in London in 1600. Experiments in France and Germany and by members of the Royal Society of London led to the invention of the Leyden jar in 1745. Benjamin Franklin is generally regarded as the father of electric science and during his lifetime was known as the American Newton. The reason he was accepted into the French and English courts around the time of the American Revolution was not because he was an ambassador from America but because he was considered to be one of the foremost scientists of his time. Franklin was elected to every major scientific society at the time and received medals of honor from France and England for his scientific contributions. Before his work, it was thought that two distinct types of electric phenomena existed. Franklin's work unified these two forces, and he is responsible for renaming them as positive and negative charges.[50] He also proved with numerous experiments that lightning was an electric phenomenon and that thunderclouds are electrically charged, as demonstrated by the famous kite and key experiment.[49] He invented the lightning rod and announced its use in 1753 in Poor Richard's Almanack: It has pleased God in his Goodness to Mankind, at length to discover to them the Means of securing their Habitation and other Buildings from Mischief by Thunder and Light- ning. The Method is this: Provide a small Iron Rod (It may be made of the Rod-iron used by the Nailers) but of such a Length, that one End being three or four Feet in the moist Ground, the other may be six or eight Feet above the highest Part of the Building. To the upper End of the Rod fasten a Foot of brass Wire the Size of a common Knitting-needle, sharpened to a fine Point; the Rod may be secured to the House by a few small Staples. If the House or Barn be long, there may be a Rod and Point at each End, and a middling Wire along the Ridge from one to the other. A House thus furnished will not be damaged by Lightning, it being attracted to the Points, and passing thro the Metal into the Ground with- out hurting any Thing. Vessels also, having a sharp pointed rod fix'd on the Tops of their Masts, with a Wire from the Foot of the Rod reaching down, round one of the Shrouds, to the Water, will not be hurt by Lightning. In the 1750s and 1760s, the use of lightning rods became prevalent in the United States for protection of buildings and ships. Some scientists in Europe urged the installation of lightning rods on government buildings, churches, and other high buildings. However, religious advocates maintained that it would be blasphemy to install such devices on church steeples, since the churches received divine protection. Because of this divine protection, some towns chose to store munitions in their churches, leading on more than one occasion to significant destruction and loss of life when the churches were hit by lightning. Part of the delay in installing lightning rods in England may have been due to British distrust of the scientific theories of the upstart, newly independent United States. Years and numerous unsuccessful trials with English designs were required before the Franklin rod became accepted on Her Majesty's ships and buildings.[16] At one time, lightning rods were theorized to be diffusers of electric charges that could neutralize a storm cloud passing overhead, thus averting a lightning stroke. This theory was in part an outgrowth of the observation of St. Elmo's fire, an aura appearing around the tip of lightning rods and ships' masts during a thunderstorm. This phenomenon is caused by an electron discharge that results from the strong electromagnetic field induced around the glowing object. Properly installed lightning rods and lightning protection systems do not "attract" lightning, but protect a building by allowing the current from a lightning strike that would have occurred, regardless of the protection system, to flow harmlessly through the system to the ground instead of into or through the building, which often causes more extensive damage.[51] It has not been uncommon for charlatans to take advantage of the fear of lightning and the danger of lightning-caused fires. In the past, they drove from farm to farm offering to "discharge" the lightning rods on the barns and homes for a fee. Lightning protection still remains an area of great controversy, with few of the lightning codes verified by true research. Some of the recent codes (written by the lightning protection industry) now do more to protect buildings and shelters but unfortunately may actually increase the risk for those seeking "shelter" in bus, pool, rain, or golf types of structures, not only by increasing the sheltering person's effective height but also by increasing the chances of side-flash from the lightning protection wiring. Systems that claim to "predict" lightning rather than detect it have yet to prove the scientific validity of their technology by achieving patents. The public is recommended to follow the caveat emptor principle whether it applies to protection of shelters or detection/prediction of lightning by "warning" systems. The first Lightning Rod Conference was held in London in 1882. Recommendations from this conference were published that year and again in 1905. Further progress in the study of the properties of lightning came with the technical development of Sir Charles Vernon Boy's rotating camera and Dufour's high-speed cathode ray oscillograph, which helped delineate physical properties of lightning, including the direction and speed of the strokes. Certain countries developed codes of practice for lightning protection (Germany 1924, United States
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1929, Britain 1943, British colonies 1965). A variety of materials, including copper, aluminum, and iron, are recommended by these codes, which also specify the measurements and construction of the protective system, depending on the height, location, and construction of the structure to be protected. The most recent U.S. code revision was the National Fire Protection Act of 1993, written by lightning protection practitioners. Lightning strokes vary in power and frequency, depending on the terrain and geographic location.[90] Complicated formulas have been devised to take into account the relative frequency of strikes in an area; the height, construction, and design of the building; and the degree of protection desired, depending on whether it is a storage shed, house, school, hospital, or munitions factory.[73] A lightning protection system should be designed to take into account these factors plus the economic considerations of construction. Including a system in the initial design and construction is always easier and less expensive than modifying a completed building. In addition, except where prohibited by code, the owner may decide that a lightning protection system is not worth the expense, for example, for a mountain retreat that is seldom visited.[73] [90] An excellent noncommercial source for discussion of these risks is www.lightningsafety.com.
PHYSICS OF LIGHTNING STROKE Lightning Discharge[51] [52] [53] [90] [114] [118] The study of lightning discharge and formation is extremely complex and involves an entire branch of physics and meteorology. We therefore illustrate here the simplified and most common mechanism of thundercloud formation and lightning strike. Thunderstorms can be created by a number of factors that produce vertical updrafts. These ingredients are usually caused by cold fronts, large-scale upward motions, sea and lake breezes, lifting by mountains, and afternoon heating of warm, moist air ( Figure 3-9, B ). [52] [114] As warm air rises, turbulence and induced friction cause complex redistribution of charges within the cloud ( Figure 3-9, C ). Water droplets and ice crystals within the cloud acquire and increase their individual charges. A complex layering of charges, with large potential differences between the layers, results from the interaction between charged particles and internal and external electrical fields within the cloud. Generally lower layers of the thundercloud become negatively charged relative to the earth, particularly when the storm occurs over a flat surface. The earth, which normally is negatively charged relative to the atmosphere, has a strong positive charge induced as the negatively charged thunderstorm passes overhead. The induced positive charge tends to flow as an upward current into trees, tall buildings, or people in the area of the thunderstorm cloud and may actually course upward as "upward streamers." Normally, discharge of the potential difference is discouraged by the strong insulatory nature of air. However, when the potential difference between charges within the clouds or between the thundercloud and ground becomes sufficient, the charge may be dissipated as lightning. A lightning stroke begins as a relatively weak and slow downward leader from the cloud ( Figure 3-9,D ). Although the tip of the leader may be luminous, the stepped leader itself is barely discernible with the unassisted eye. The leader travels at about one-third the speed of light (1 × 108 m/sec), and the potential difference between the tip and the earth ranges from 10 to 200 million volts. The leader ionizes a pathway that contains superheated ions, both positive and negative, thus forming a plasma column of very low resistance. It travels with relatively short branched steps, going down about 50 m (164 feet) and then retreating upwards. The next time it goes down, it fills the original ionized path but branches at the end to go down another 50 m and then retreat again. This up-and-down, poly-branching process continues until the leader comes to within 30 to 50 m (98 to 164 feet) of the ground. Since lightning follows this ionized path, its tip "sees" only objects within about a 30- to 50-m radius, meaning that the hill or tower 200 feet (61 m) away from a person will not be "seen" by the lightning as a potential target. As the tip of the lightning gets closer to the earth with the large potential at its tip, more concentrated areas of induced charge accumulate up on earth, particularly at the peaks of tall, relatively sharp objects. Several upward streamers ( Figure 3-9, E ) may rise vertically from these objects toward the downward leader head. Ultimately one, or a small number, of the upward streamers will contact the downward leader, thus completing a lightning channel of low resistance between cloud and ground. The process of the downward leader joining with the upward streamer(s) is called attachment. There is often more than one point of attachment to the ground.[107] As the low-resistance channel is formed by attachment, the potential difference between cloud and ground effectively disappears and the energy available is dissipated in an avalanche of charge between cloud and ground. This avalanche is referred to as the return stroke ( Figure 3-9, F ) and is highly luminous. Subsequent to the discharge through the return stroke, the channel remains attached for a small amount of time, and with quick redistribution of charge from other regions of the cloud to the top of the channel (via J- and K-intracloud streamers), further return strokes may occur. Thus a lightning flash may be made up of multiple
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Figure 3-9 A, Warm, low-pressure air rises and condenses into a cumulonimbus cloud. B, Typical anvil-shaped thundercloud. C, Water droplets within the cloud accumulate and layer changes. D, Relatively weak and slow-stepped downward leader initiates the lightning strike. E, Positive upward streamer rises from the ground to meet the stepped leader. F, Return stroke rushes from the ground to the cloud.
strokes (1 to 30, mean 4 to 5) and is perceived by the eye as flickering of the main channel. When a very tall building is involved, or when high mountains rise into the clouds, the leader stroke may initiate from the building or mountain rather than from the cloud. In such cases, a joining stroke is rarely seen initiating from the cloud. The channel of ions formed by the leader stroke is maintained as a continuous stroke as the return stroke (misnamed in this instance) travels in the same direction from the ground or object to the cloud, dissipating the charge difference. The tip of the downward leader is the most luminous of the sequence of strokes in each lightning discharge, since a huge amount of energy must be expended to overcome air resistance and ionize a channel. Because of the relative slowness and brilliance of the leader, lightning is perceived as traveling from the cloud to the earth, although the vast majority of energy is actually dissipated in the opposite direction with the return strokes. The direction of the return stroke is not visually perceived because of its tremendous speed and is recognized merely as an instantaneous brightening
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or flickering of the ionized pathway. Lightning may vary in color, either from the excitation of nitrogen atoms in the atmosphere (radiant light energy released as a bluish or reddish afterglow), or because the particles of dust through which the lightning passes are high in ion or mineral content. Diameter and Temperature of Lightning[52] [114] Many techniques could be used to measure the diameter or temperature of the lightning stroke. Unfortunately, all measurement techniques have artifact problems. Visual measurement of the stroke using standard photography usually shows the diameter of the main body of the stroke to be about 2 to 3 cm. The diameter of the arc channel is sometimes measured indirectly, using measurements of holes and strips of damage that lightning produces when it hits aluminum airplane wings, buildings, or trees. Measurements vary from 0.003 to 8 cm, depending on the material destroyed, with hard metallic structures sustaining smaller punctures than do relatively softer objects, such as trees. The ionized sheath around the tip of the bright leader stroke has never been measured but is estimated to be 3 to 20 m (10 to 66 feet) in diameter. The temperature of the lightning stroke varies with the diameter of the stroke and has been calculated to be about 8000° C (14,432° F). Others estimate the temperature to be as high as 50,000° C (90,032° F). In a few milliseconds the temperature falls to 2000° to 3000° C (3632° to 5432° F), that of a normal high-voltage electric arc. Forms of Lightning
Lightning occurs in many forms. As described previously, the most common is streak lightning ( Figure 3-10 ). Sheet lightning is a shapeless flash of light that represents lightning discharges within and between clouds. Sheet lightning may also be seen when lightning occurs over the horizon. Ribbon lightning is streak lightning driven by winds of the thunderstorm; the ionized air channel moves so rapidly across the earth that the successive secondary or return strokes seem to parallel one another. Bead lightning occurs when different areas of ionization and charge persist, lending a beadlike appearance to the afterstrokes. Another possible explanation of bead lightning may be perception of the bright end-on appearance of portions of a very jagged stroke. The most unusual, least understood, and least predictable type of lightning is ball lightning. Ball lightning is usually described as a softball-sized orange to white globe. It may enter a plane, ship, or house, travel down the hallway, injure some people and objects and not others that it encounters, and exit out another door, chimney, or window, explode with a loud bang, or exhibit other bizarre behavior. [9] [16]
Figure 3-10 Example of classic streak lightning.
Lightning may be either positive or negative in charge. Negative lightning is the more common. Positive lightning tends to occur during the winter, at the beginning of very violent thunderstorms, and with tornadoes, and may have a very different injury profile from negative lightning. Positive lightning may be more likely to occur when there is particulate matter in the air. Thunder Thunder is formed when shock waves result from the almost explosive expansion of air heated and ionized by the lightning stroke.[52] [114] The following are accepted statements: 1. 2. 3. 4. 5. 6.
Cloud-to-ground lightning flashes produce the loudest thunder. Thunder is seldom heard over distances greater than 10 miles (16 km). The time interval between the perception of lightning and the first sound of thunder can be used to estimate distance from the lightning stroke. Atmospheric turbulence reduces audibility of the thunder. The intensity of a pattern of thunder in one geographic location appears different from the pattern in another location. The pitch of thunder deepens as the rumble persists.
The thunder clap from a lightning flash that is close by is heard as a sharp crack. Distant thunder rumbles as the sound waves are refracted and modified by the thunderstorm's turbulence.[114] Using the difference in speeds between light and sound gives an estimate of the distance to the lightning stroke. To obtain the approximate distance to the flash in miles, a person can take the difference in seconds between the perception 88
of the flash and the rumble and divide by five (flash-to-bang method).[65] [116]
MECHANISMS OF INJURY BY LIGHTNING[8]
[ 9] [ 17] [ 34]
Lightning is directly dangerous for three reasons: electrical effects, heat production, and concussive force. In addition, lightning may injure indirectly via forest fires, house fires, and explosions or by felling objects such as trees onto occupied homes and automobiles. Only injuries directly caused by lightning are discussed here: direct hit, splash, contact, step voltage, blunt trauma,[34] and the newly described upward streamer.[1] A direct strike is most likely to hit a person in the open who has been unable to find a safe location. A more frequent cause of injury is a splash. Splash injuries occur when lightning that has hit a tree or building splashes onto a victim who may have found shelter nearby.[53] The current, seeking the path of least resistance, may jump to a person whose body has less resistance than the tree or object that the lightning had initially contacted. There are multiple reports of side flashes indoors from metal objects, including plumbing and telephones. [1A] [105] [110] Splashes may also occur from person to person when several people are standing close together. On occasion, splashes occur from a fence or other long conductive object that was hit by lightning some distance away. Groups of animals have been killed as they stood near a fence or sought shelter under trees.[53] Contact injury occurs when the person is holding onto an object that is either directly hit or splashed by lightning. Step voltage, also called stride voltage or ground current, is produced when lightning hits the ground or an object nearby.[10] The current spreads like a wave in a pond, diminishing as the radius from the strike increases. Contrary to the public's belief that the Earth's surface is a decent "ground" (a good absorber of electrical energy), in reality, it is an excellent resistor of electrical energy. As walking bags of saltwater, animals and humans often have less resistance than the ground. If a person has one foot closer to the strike and one foot further away, a large potential difference may exist between them. Often the current will pass up and through the lower resistance circuit made by the victim's legs and body rather than stay in the ground. Swimmers may also be affected by this mechanism as the current passes through them in the water. Four-legged animals with longer distances between their front and back legs are at even greater risk. Although ground current is less likely to produce fatalities than are direct hits or splashes, multiple victims and injuries are frequent. Large groups have been injured on baseball fields, at racetracks, while hiking, and during military maneuvers.[16] Persons may suffer blunt injury either by being close to the concussive force of the shock wave produced as lightning strikes nearby or if ground current or some other mechanism induces an opisthotonic contraction. Victims have been witnessed to have been thrown tens of yards by either mechanism. In addition, some have theorized that the person who is struck by lightning may suffer from explosive and implosive forces created by the thunderclap, with resulting contusions and pressure injuries, including tympanic membrane rupture. Injury caused by being the conduit for an upward leader, even though it may not contact a downward leader to complete a lightning pathway, has recently been described.[35A]
PATHOPHYSIOLOGY OF LIGHTNING INJURY * It is necessary to distinguish between lightning and generator-produced high-voltage electrical injuries, since there are significant differences between the mechanisms of injuries and their treatment. Although lightning is an electrical phenomenon and is governed by the laws of physics, it accounts for a unique spectrum of induced diseases that are best understood relative to specific physical properties of lightning. Kouwenhoven determined six factors that affect the type and severity of injury encountered with electrical accidents ( Box 3-1 ): frequency, duration of exposure, voltage, amperage, resistance of the tissues, and pathway of the current. The factor that seems most important in distinguishing lightning from high-voltage electric injuries is the duration of exposure to the current. Frequency Lightning is neither a direct nor an alternating current. At best, lightning is a unidirectional massive current impulse. The cloud-to-ground impulse results from breakdown of a large electric field between cloud and ground, measured in millions of volts. Once connection is made with the ground, the voltage difference between cloud and ground disappears and a large current flows impulsively in a very short time. The study of massive electrical discharges of such short duration, particularly their effects on the human body, is not well *References [ 7]
[ 9] [ 30] [ 31] [ 34] [ 70] [ 76] [ 77]
.
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advanced. Lightning is said to be a "current" phenomenon rather than a "voltage" phenomenon. Box 3-1. FACTORS AFFECTING SEVERITY OF ELECTRICAL BURNS Frequency Voltage Amperage Resistance Pathway Duration
Voltage, Amperage, and Resistance Lightning, being a current phenomenon, is not easily considered in terms of Ohm's law (V = I × R) and power calculation (P = V × I) terms. Because the voltage between cloud and ground disappears after lightning attachment, examining the particular voltage in these equations becomes difficult. Thus we must resort to alternative formulations of the equations. The energy dissipated in a given tissue is determined by the current flowing through the tissue and its resistance by: Energy (heat) = Current2 × Resistance × Time where a current flows through a resistance for time t. As resistance goes up, so does the heat generated by passage of the current. In humans when low energy levels are encountered, much of the electric energy may be dissipated by the skin, so that superficial burns are often not accompanied by internal injuries. Although lightning occasionally creates discrete entry and exit wounds, these are rare. Lightning more commonly causes only superficial streaking burns. The exception to this is when "hot lightning," or long continuous current (LCC), occurs. LCC is a prolonged stroke lasting up to 0.5 second that delivers a tremendous amount of energy, capable of exploding trees, setting fires, and acting like high-voltage electricity to produce injuries. Other factors not understood may contribute to the formation of deep burns, although deep burns similar to those of high-voltage electric injuries generally are quite rare with lightning. Pathway, Duration of Current, and Flashover Effect It takes a finite amount of time for the skin to break down when exposed to heat or energy. Generally, lightning is not around long enough to cause this skin breakdown. Probably a large portion travels along the outside of the skin as "flashover."[100] There is some experimental evidence that a portion of the current may enter the cranial orifices—eyes, ears, nose, and mouth.[2] [3] [7] This pathway would help explain the myriad eye and ear symptoms that have been reported with lightning injury. Andrews[2] further examined the functional consequences of lightning on cardiorespiratory function and concluded that entry of current into cranial orifices leads to passage of current directly to the brainstem. In a sheep study, he was able to demonstrate specific damage to neurons at the floor of the fourth ventricle in the location of the medullary cardiorespiratory control centers. It is postulated that current travels from there caudad via cerebrospinal fluid (CSF) and blood vessel pathways to impinge directly on the myocardium. Andrews [2] also showed histologic damage to the myocardium, consistent with a number of autopsy reports of inferior myocardial necrosis.[6] An alternative hypothesis can be tested with mathematical modeling. [2] [9] Certain assumptions are made in any model, usually based on principles accepted in the literature. [11] [76] Figure 3-11, A , shows a model for skin resistance, and its connection to the internal body milieu is shown in Figure 3-11, B . It will be noted that the internal body structures are regarded as purely resistive, whereas the skin contains significant elements of capacitance.[11] [76] The sequence of events during the strike started with the postulate that the stroke attached initially to the head of the victim. For a small fraction of time, current flowed internally as the skin capacitance elements became charged. At a voltage taken as 5 kV, the skin was assumed to break down. It is worth noting in the context of time scale that a lightning stroke is modeled as a current wave building to a maximum value in around 8 msec, although this may be "modulated lightning"—lightning that has passed through other structures, such as wiring. Others have measured the rise time of direct lightning as 1.2 to 1.5 msec. Once the internal current increased, the voltage across the body to earth built up, and external flashover across the body occurred when the field reached the breakdown strength of air. The results of mathematical modeling of these events are shown in Figure 3-12 , and the relative magnitudes of the various voltage components can be seen with their time scale. On this time scale the times to breakdown are short and most events occur early in the course of the stroke. In summary, in this model, lightning applies a current to the human body. This current initially is transmitted internally, following which skin breaks down. Ultimately, external flashover occurs. Andrews[2] draws support for this model from measurements made in the experimental application of lightning impulses to sheep. Further modeling of step voltage injury verified that for
the erect human, this mechanism is less dangerous than is a direct strike. Experimental evidence suggests that "a fast flashover appreciably diminishes the energy dissipation within the body and results in survival."[100] In addition, Ishikawa obtained experimental results with rabbits similar to the human data found by Cooper's study.[29] Cooper [38] [39] has carried her studies to animals in developing an animal model of lightning injury and has successfully shown primary cardiac arrhythmias, prolonged ventilatory arrest, secondary cardiac arrest, keraunographic skin changes, and temporary lower extremity paralysis. As current flashes over the outside of the body, it may vaporize moisture on the skin and blast apart
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Figure 3-11 A, Electrical model for human skin impedance. B, Model of human body for the purposes of examination of currents flowing during lightning strike.
clothes and shoes, leaving the victim nearly naked, as noted by Hegner[58] in 1917: The clothing may not be affected in any way. It may be stripped or burned in part or entirely shredded to ribbons. Either warp or woof may be destroyed leaving the outer gar- ments and the skin intact.... Metallic objects in or on the clothing are bent, broken, more or less fused or not affected. The shoes most constantly show the effects of the current. People are usually standing when struck, the current then en- ters or leaves the body through the feet. The shoes, especially when dry or only partially damp, interpose a substance of in- creased resistance. One or both shoes may be affected. They may be gently removed, or violently thrown many feet, be punctured or have a large hole torn in any part, shredded, split, reduced to lint or disappear entirely. The soles may disappear with or without the heels. Any of the foregoing may occur and the person not injured or only slightly shocked.
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Figure 3-12 Model of human body adapted for the circumstance of direct lightning strike. Responses of the body model are shown for cases of direct strike with and without subsequent flashover.
The amount of damage to clothing or to the surface of the body is not an index to the severity of injuries sustained within a human. Either may be disproportionately great or small. However, in unwitnessed situations, the first author (MAC) and others have found that forensic evidence of damage to shoes and clothing may be the most important and reliable indicator in determining if lightning caused a person's death.[72] Behavior of Current in Tissue High- or low-voltage electric current may be carried through tissue in a direct conduction fashion, obeying simple linear equations such as Ohm's law. The result is heating of tissues under Joule's law, with thermally induced cellular death and dysfunction. Simple passage of current may interfere with neural and muscular function.[76] Earlier in the previous century, electric injury was thought to occur not only because of thermal effects but
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also because of some mysterious cellular effects.[10] [70] Unfortunately, the technology was not available to investigate these effects and this idea was largely forgotten. In the last few years, the theory of electroporation has been proposed. Cell wall integrity, enzyme reactions, protein shape and structure, and cell membrane "gates" and pumps operate by changes on the order of microvolts. It is not beyond the realm of imagination that passage of an electric current too small to produce significant thermal damage still may cause irreversible changes in these functions, leading to cell death or dysfunction.[76] Induction of electric charges by external electromagnetic fields has been shown to force water molecules into cell walls, causing the occurrence of fatal "pores." Magnetic Field Effects Some persons contend that the injurious effects of lightning can in part be magnetically mediated.[24] The case cited in support of this contention was a golfer under a tree in company with three other persons. It was stated that death occurred without evidence of current entering or leaving the index case. On the other hand, one accompanying golfer showed evidence of current traversal but survived. It is stated that three methods of shock exist—direct strike, side flash, and ground potential—but no evidence of any was seen. It was apparently considered that contact potential was not relevant, and this may have been historically so. In this case, with persons under a tree, it would seem possible to explain deleterious effects without resort to a magnetic hypothesis, but nonetheless the hypothesis bears examination, since it is a recurrent question. In the case under consideration, the stroke was considered a line current 1 m distant from the victim, and calculation of peak fields and their effects were given. It is useful to consider the stroke as a single line current as referenced; however, we must also gain a feeling for how far from a victim such a stroke will act. If the stroke is close to a victim, then attachment to the victim will take place and electrical effects will apply. If further away, the magnetic field will be operative without attachment and magnetic effects need to be examined. Ground potential at this distance will also exist. To determine the magnitude of this effect, it is necessary to find the minimum distance away from a victim that a stroke reaches ground without attachment to the victim, to give the worst-case distance from (that closest to) a victim at which pure magnetic field acts. The standard striking distance formula gives such a distance. [42] The formula is: ds = 10I0.65 where ds (m) is the striking distance and I is the stroke current in kA. This represents the distance at the last turn of the downward stepped leader, such that if an object lies inside this distance, attachment of the leader to the object will take place. For illustrative purposes, let a stroke have a peak current of 20,000 A. This gives ds of 70.09 m (230 feet). Pure magnetic effects are applicable at this distance and beyond. Inside this distance, the victim will be subject to electrical current effects. By comparison, the ground potential between two points 1 m (3 feet) apart at 60 m
(197 feet) from a stroke of 20 kA is about 60 volts, assuming earth resistivity of 100 ohm-meters. In examining the magnetic fields involved at this distance, assume a 20 kA stroke at 70 m distance from an individual. The peak magnetic B field (the "magnetic induction," formally quantifying the force on a moving charge in its influence) is: B = µ0I/2pds = 57 × 10-6 w/m2 = 57 µT For comparison, the earth's magnetic field is about 1 µT, and the magnetic fields causing concern for power line fields are around the 1 to 100 µT range. The magnetic fields used in magnetic resonance imaging (MRI) scanning are around 2,000,000 to 5,000,000 times these levels. Thus, if concern is realistically held for power line fields in terms of field level, then the field of a lightning stroke must be regarded as dangerous. However, magnetic problems of the acute kind are not seen in this circumstance, and the major concern (if any exists) would only be in terms of chronic exposure. Similarly, if one is concerned about a lightning stroke magnetic field, he or she should be entirely concerned about MRI fields. Again, the concern is not seen in the same terms. Certainly, the time varying nature of any B field is important, both in terms of the rate of change of the field and of movement of a conductor within this field. If one assumes that the above B field is generated in about 2 µsec, then the time rate of change for the B field is about 30 T/sec. Suppose this is applied to an aorta of cross section 8 cm2 (8 × 10-4 m2 ). Then the magnitude of the induced electric field in this region is approximately 0.024 V/m. If the resistivity of blood is taken as 1 ohm-meter, then the current induced in the aorta has density of 0.024 A/m2 . The corresponding current is therefore approximately 20 µA in the cross section under consideration. It is stated elsewhere that the blood vessels represent the most likely conducting medium in the body, and the most likely danger of arrhythmia exists in the current-passing media around the heart, the ventricle being of the same order in dimension as the aorta. This current in the aorta broadly approximates that within the ventricle. This current is calculated under quite ideal circumstances, and if myocardial effects are to occur, then the current must penetrate into a tissue of considerably higher resistivity with good coupling. This is unlikely,
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and the current in itself is of arguable danger in any case. One therefore concludes that magnetic field danger in normal circumstances is slight. Certainly special circumstances might exist, such as the presence of a pacemaker or the presence of an arrhythmic pathway, but in normal terms, magnetic effects would not seem to be clinically significant during occurrences of lightning strike.
INJURIES FROM LIGHTNING Severity of Injury Some of the most common signs and symptoms are listed in Box 3-2 . Lightning is almost instantaneous in its action and seemingly unpredictable in its physical effects. Each case report of lightning injury has unique characteristics, and symptoms may vary from trivial to fatal. For prognostic purposes, victims generally can be placed in one of three groups. Minor Injury.
These victims are awake and may report dysesthesia in the affected extremity from a lightning splash or, in more serious strokes, a feeling of having been hit on the head or having been in an explosion. They may or may not have perceived lightning or thunder. They often suffer confusion, amnesia, temporary deafness or blindness, or temporary unconsciousness at the scene.[16] They seldom demonstrate cutaneous burns or paralysis but may complain of paresthesias, muscular pain, confusion, and amnesia lasting from hours to days. Victims may suffer tympanic membrane rupture from the explosive force of the lightning shock wave. Vital signs are usually stable, although occasional victims demonstrate transient mild hypertension. Recovery is usually gradual and may or may not be complete. Permanent neurocognitive damage may occur.
Box 3-2. LIGHTNING INJURIES
IMMEDIATE Ventricular asystole Neurologic signs Seizures Deafness Confusion, amnesia Blindness Contusion from shock wave Chest pain, muscle aches Tympanic membrane rupture
DELAYED Dysesthesias, peripheral neuropathy Neuropsychologic changes
Moderate Injury.
Moderately injured victims may be disoriented, combative, or comatose. They frequently exhibit motor paralysis, particularly of the lower extremities, with mottled skin and diminished or absent pulses. Nonpalpable peripheral pulses may indicate arterial spasm and sympathetic instability, which should be differentiated from hypotension. If true hypotension occurs and persists, the victim should be scrutinized for fractures and other signs of blunt injury. Spinal shock from cervical or other spinal fractures, although rare with lightning, also may account for hypotension. Occasionally, victims have suffered temporary cardiopulmonary standstill, although it is seldom documented. Spontaneous recovery of the pulse is attributed to the heart's inherent automaticity. However, respiratory arrest that often occurs with lightning injury may be prolonged and lead to secondary cardiac arrest from hypoxia or some other yet-to-be-elucidated cause. Seizures may also occur. First-and second-degree burns not prominent on admission may evolve over the first several hours. Rarely, third-degree burns may occur. Tympanic membrane rupture should be anticipated[44] and, along with hemotympanum, may indicate a basilar skull fracture. Whereas the clinical condition often improves within the first few hours, victims are prone to have permanent sequelae, such as sleep disorders, irritability, difficulty with fine psychomotor functions, paresthesias, generalized weakness, sympathetic nervous system dysfunction, and sometimes posttraumatic stress syndrome. A few cases of atrophic spinal paralysis have been reported. Severe Injury.
Victims with severe injury may be in cardiac arrest with either ventricular standstill or fibrillation when first examined. Cardiac resuscitation may not be successful if the victim has suffered a prolonged period of cardiac and central nervous system (CNS) ischemia. Direct brain damage may occur from the lightning strike or blast effect. Tympanic membrane rupture with hemotympanum and CSF otorrhea is common in this group. Victims with other signs of blunt trauma are likely to have endured direct hits, although sometimes no burns are noted. The prognosis is usually poor in the severely injured group because of direct lightning damage, often complicated by a delay in initiating cardiopulmonary resuscitation with resultant anoxic injury to the brain and other organ systems. Differences between Injuries from High-Voltage Electricity and Lightning[9] [34] There are marked differences in injuries caused by high-voltage electric accidents and lightning ( Table 3-3 ). Lightning contact with the body is almost instantaneous, often leading to flashover. Exposure to high-voltage
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TABLE 3-3 -- Lightning Injuries FACTOR
LIGHTNING
HIGH VOLTAGE
Energy level
30 million volts, 50,000 Å
Usually much lower
Time of exposure
Brief, instantaneous
Prolonged
Pathway
Flashover, orifice
Deep, internal
Burns
Superficial, minor
Deep, major injury
Cardiac
Primary and secondary arrest, asystole
Fibrillation
Renal
Rare myoglobinuria or hemoglobinuria
Myoglobinuric renal failure common
Fasciotomy
Rarely if ever necessary
Common, early, and extensive
Blunt injury
Explosive thunder effect
Falls, being thrown
generated electricity tends to be more prolonged because the victim often freezes to the circuit. With skin breakdown, electric energy surges through the tissues with little resistance to flow, causing massive internal thermal injury that sometimes necessitates major amputations. Myoglobin release may be pronounced, and renal failure may occur. In addition, compartment syndromes requiring fasciotomy may occur. This is not the case with lightning injuries, in which burns and deep injury are uncommon and fluid restriction and expectant care are usually the rule. Cardiopulmonary Arrest The most common cause of death in a lightning victim is cardiopulmonary arrest. In fact, a victim is highly unlikely (p Tamb ) maximizes heat loss from the skin[219] [420] by convection and radiation. Although heat is carried by convection and conduction from the body core to the skin, the main role of elevated BFsk in a warm environment is to deliver the heat necessary to vaporize sweat.[189] Evaporative Cooling.
Evaporative, "wet," or insensible heat exchange is usually a one-way heat flow from a body surface to the environment. The heat of vaporization (2.45 J/kg) is "absorbed" slowly with an undetectable change in temperature of the skin or blood. As water is converted from a liquid to a gaseous state in insensible heat exchange, the rate of evaporation of water from the skin, and hence the cooling effect, is proportional to the difference between vapor pressures of water in sweat on the skin surface and that of the surrounding air. A lowered NaCl concentration in sweat increases this difference, hence increasing the rate of evaporation. Since acclimatization leads to lower sweat NaCl concentrations, this increases the sweat evaporation rate. [231] If the body is unable to maintain thermal equilibrium by radiation, convection, and conduction and core temperature rises, sweating must occur to permit heat loss by vaporization of water.[189] Evaporative heat loss is accompanied by the loss of 580 kcal/L of water evaporated or heat loss of approximately 1 kcal/1.7 ml of sweat vaporized. Since rates of gastric emptying and delivery of water to the intestines can exceed 1 L/hr, a 1 L/hr sweat rate appears sustainable without significant dehydration if fluid is consumed. Higher sweat rates (e.g., 1500 ml/hr) could theoretically achieve greater rates of heat loss (1500 ml/1.7 ml/kcal = 882 kcal) but are almost never achieved because some of the sweat drips off the skin and thus has no cooling effect. Moreover, these high sweat rates are often at the expense of total body water, since gastric emptying does not keep pace. Knochel[288] has estimated that 650 kcal/hr is a more reasonable figure for an upper limit of heat dissipation. Certain parts of the body surface are more important than others in providing cooling through sweating. The scalp, face, and upper torso are most important. Only about 25% of total sweat is produced by the lower limbs.[512] Therefore, although wearing a shirt may be critical in the development of heat illness, wearing long or short pants is much less important. The wearing of protective headgear may be most important in the development of heat illness, as shown by a training exercise. In bareheaded persons, the exercise was merely grueling, but 33% of those wearing hats suffered heat illness casualties,[224] as cited in Porter.[397] The maximum rate of sweat vaporization depends on air dryness and movement. In a hot climate, the limit to heat dissipation is a function of sweat rate and the "atmospheric cooling power," or maximal evaporative cooling capacity of the environment.[190] [440] The environment's capacity to vaporize sweat varies primarily with humidity and also with wind velocity. As humidity approaches 100%, evaporative heat loss is minimized. The major effect of wind occurs in humid environments at a velocity between 0.5 and 5 m/sec.[141] Sweat that drips from the body provides no cooling, and sweat evaporated from clothing is considerably less efficient than sweat evaporated directly from
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skin.[141] Risk of hyperthermia increases with air temperature and humidity. As a result, military trainers and coaches tend to conduct early morning runs to avoid high Tamb and the increased incidence of heat illness in humid climates, despite the lower dry bulb temperatures (Tdb ). Sutton[482] pointed out that EHS is reported with increasing frequency during "fun runs" and marathons when the temperature is not particularly hot. This reinforces the simple definition that exertion-induced heatstroke occurs whenever the rate of heat production of an exercising individual exceeds the rate of heat loss, causing body temperature to rise to critical levels. Heat Stress Indexes.
The ability to work in a hot environment is inversely related to the prevailing heat stress level; the higher the heat stress level, the shorter the ability to carry out work and the greater the risk of heat illness. Safety in a hostile environment depends on following strict rules and limitations concerning exposure time and work intensity. The need for a quantitative index that combines environmental heat stress factors to provide a reliable and consistent correlation with the induced physiologic strain
was recognized 100 years ago.[203] In 1905, Haldane suggested the use of wet bulb temperature (Tw ) as an index of the severity of a warm environment in Cornish tin mines.[203] Tw is lower than Tdb because of the cooling effect of evaporation of water from the thermometer, which in turn, varies inversely with relative humidity (RH). However, the relationship between Tw and physiologic strain (rises in Tc , HR, respiratory rate, etc.) was not valid at high-humidity levels and in hot-dry climates.[33] In 1923, Houghten and Yaglou[238] developed the effective temperature (ET) index to define thermal comfort limits. This index was a combination of Tw , Tamb , and wind velocity (Va), and produced an equivalent thermal sensation. However, several deficiencies were recognized, including overestimation of the effects of Tamb at high temperatures and underestimation of Va in hot-wet climates. [33] In 1957, Yaglou and Minard[535] suggested the wet bulb globe temperature (WBGT) index, which consisted of combining Tamb , Tw , and black globe temperature (Tg ) according to unequal weights: For outdoor use: WBGT = 0.7Tw + 0.2Tg + 0.1Tamb For indoor use: WBGT = 0.7Tw + 0.3Tamb However, calculation of WBGT involves measuring Tg from a thermometer surrounded by a 6-inch blackened sphere, which is inconvenient and not practical under many circumstances. Nevertheless, the WBGT index is the most widely used index to describe environmental heat stress for outdoor and indoor use and is used for setting limits of U.S. military training exercises in hot weather.[69] [117] It is also used to set limits in industrial plants,[369] by sports associations as guidance to prevent heat injury,[33] [337] and by workers in different occupations as a safety index.[83] [164] [202] [463] However, WBGT is limited for two main reasons: (1) it cannot be applied to persons wearing different types of clothing (e.g., protective clothing), and (2) measuring Tg is inconvenient. Wearing protective clothing imposes a higher heat stress equivalent to adding 6° to 11° C (10.8° to 19.8° F) to the WBGT index.[392] As a result, for WBGT to accurately reflect environmental stress, corrections and adjustments must be made for the type of clothing worn and the metabolic rate.[228] [271] Thus attempts were made to develop alternatives to WBGT. In 1971, Botsford[53] suggested the wet globe thermometer (WGT), known also as the Botsball, which combined measuring Tamb , Tw , and radiation into a single reading. Unfortunately, the WGT index did not provide adequate precision values for hot climates, and its readings were significantly lower than the WBGT index.[335] In 1962, Sohar et al[470] suggested the discomfort index (DI), using a combination of Tamb and Tw , which has been used extensively in Israel. However, a recently modified DI (MDI) suggested altering constants to the parameters Tamb and Tw to achieve a better correlation with the WBGT index.[349] However, uncertainties in the radiation component in any heat stress index would limit its assessment (e.g., solar radiation measurement for the shade vs. open sky). The most widely used WBGT index is computed from three separate environmental measurements, and the equipment to measure this index is cumbersome and more suited to a fixed-site station than a mobile situation. Furthermore, measuring Tg by a black globe thermometer requires about 30 minutes for the instrument to reach equilibrium. Thus the need for a reliable portable field instrument for measurement of this heat stress index in a mobile situation (e.g., training in the field) is essential. In a Marine training base with 17,000 to 25,000 recruits per year, clinical studies from the 1950s reported a large number of heat casualties occurring upon strenuous physical exercise when the WBGT was higher than 26.7° C (80° F).[344] As a result, new regulations and guidelines were implemented for different heat categories, which reduced the numbers of casualties. However, Kark et al[266] reported 1425 cases of exertional heat illness during the period of 1982–1991 and showed that 25% of the cases occurred between 7:00 to 9:00 AM at WBGT level of 26.7° C. These cases occurred in spite of the preventive measures taken on Parris Island, South Carolina, which involved rescheduling of training and physical activity according to newly categorized WBGT values. In addition, further attention was given to clothing, equipment, workloads, and hydration. Exertional heat illnesses continue to be a common problem during training in a warm environment despite preventive
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measures taken.[266] The WBGT index provides for measurement of heat load, but its practical application in current army doctrine is limited. If the "weather station" was alongside the trainees at the training site and the environmental measurements were taken continuously and not every hour, this might help in preventing some of the heat casualties. Work and sports in a hot environment require a fairly accurate measurement of the stress index to prevent heat illnesses and to determine safety behavior patterns (e.g., water consumption rates and work/rest cycles). To implement the current guidelines and limitations for exercise in a hot climate, there is great need for development of an accurate, portable heat stress measurement device. We suggest that current technology, including very small electronic sensors to measure Tamb and RH, a miniature display, and a miniature programmable microprocessor for calculating and storing the MDI index, in a wristwatch format are already available to devise a new portable heat stress monitor. Such a tool could help in the decision-making process relating to permissible strain when working in a hostile environment, for use by medical monitors, leaders, or others directly exposed to heat stress. These measures would clearly help prevent heat illnesses and would decrease the dependency on weather station reports. Temperature Regulation (See Also Chapter 11 and Box 10-1 ) To prevent or appropriately manage heat illness, the clinician must understand thermal stress[161] and human thermoregulation. [189] [214] [480] Temperature regulation refers to both behavioral and autonomic thermoregulatory processes that modify the rates of heat production by shivering and variations in basal metabolism, and heat loss by sweating and peripheral vasomotor tone.[189] These processes act to maintain the temperature of the body within a restricted range with a variable internal or external heat load. The regulated temperature is generally considered that of the "body core," or Tc . Behavioral Thermoregulation.
Hyperthermia appears to represent a more serious problem than hypothermia, since humans have developed a greater capacity for heat elimination (vasodilation, sweating) than for heat conservation (vasoconstriction).[159] [214] To live, work, and reproduce successfully in arid or tropical climates, humans depend not only on physiologic mechanisms to acclimatize to heat but also on behavioral responses to assist temperature regulation. Thus humans possess two control systems (behavioral and physiologic) to regulate body temperature. Although behavioral responses augmenting shivering seem obvious in a cold environment (e.g., seeking shelter, wearing clothes, and building fires), behavioral factors for thermoregulation in the heat (resting in the heat of the day, seeking shade or water when thirsty) are also important. Behavioral responses are conscious actions, and therefore the subjective sensations of thermal discomfort inducing the behavior anticipate actual changes in Tc .[102]
Box 10-1. COMMONLY HELD FALLACIES REGARDING HEAT ILLNESS* 1. The sine qua non for diagnosis of heatstroke includes hot, dry skin; temperature greater than 42° C; and coma. 2. Unlimited access to fluids allows the exercising individual to maintain adequate hydration despite heat stress. 3. Development of salt depletion heat exhaustion requires 4 to 5 days of exposure to marked heat stress. 4. Consumption of commercially available electrolyte-containing beverages during exercise in the heat tends to return plasma potassium levels to resting values. 5. The primary underlying mechanisms for the development of heat cramps are hypokalemia and hypovolemia. 6. Consumption of excessive volumes of fluid to the point of development of nausea promotes the maximal clearance of free water by the kidneys. 7. When the patient is evaluated in the emergency department, a normal body temperature when combined with normal serum transaminases precludes the diagnosis of heatstroke. 8. The most physiologically appropriate method to achieve rapid reduction in body temperature from hyperthermia is the use of warm air spray. 9. The risk of dilutional hyponatremia should preclude consumption of fluids in the absence of thirst. 10. Endotoxemia is a rare complication of ultramarathon running in the heat. 11. Review of the medical literature reveals that an individual sustaining a single episode of heatstroke remains at increased risk for future heat injury. 12. A high degree of aerobic conditioning, when combined with an appropriate period of heat acclimation, prevents the development of heat illness. 13. Adherence to published guidelines using wet bulb globe temperature to modify physical activity in the heat prevents the development of heat illness. 14. Carpopedal spasm is a relatively rare complication of exercise-induced heat exhaustion. 15. Violent shivering is a common complication in response to whole body cooling of patients with heat exhaustion. *These fallacies are discussed in greater detail later in the chapter.
Heat Production.
The basal metabolic rate of the average (70 kg) man in a sitting position amounts to approximately 50 to 60 kcal/hr/m2 of body surface area or 100 kcal/hr.[292] With increased activity, metabolic heat production increases significantly (walking produces
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250 to 300 kcal/hr; walking rapidly with a load, up to 400 to 450 kcal/hr) and may reach 20 times baseline level with strenuous exertion. Depending on the exercise task, usually 70% to 85% of the metabolic rate is released as heat that must be dissipated to maintain thermal balance. If there were no means to dissipate heat, the addition of 70 kcal to a 70-kg person would theoretically be able to increase core temperature approximately 0.8° C (1.4° F), assuming the average specific heat of the human body is 0.8 (kcal/kg/° C). Cellular metabolism increases 13% for each 1° C (1.8° F) rise in temperature until the body approaches heatstroke temperature; at that point, cellular metabolism increases more rapidly. It is 50% above normal at 40.6° C (105.1° F).[71] Body Temperature Ranges.
Normal internal temperatures range from 36° to 38° C (96.8° to 100.4° F), whereas the limits of body temperature for efficient thermoregulation are 35° to 40° C (95° to 104° F).[479] However, during athletic events, Tc increases to 40° to 42° C (104° to 107.6° F).[120] [356] [532] One marathoner was able to maintain a Tc greater than 41.5° C (106.7° F) for at least 44 minutes during a race.[329] Survival limits of body temperatures are exceptions to these ranges. For example, one heatstroke victim survived a measured Tc of 46.5° C (115.7° F).[466] Sensing, Relaying, and Central Integration Functions.
Physiologic temperature regulation involves detecting changes in body temperature by sensory mechanisms and relaying thermal signals from central and peripheral locations to a central integrative area. This directs effector organs to increase or decrease heat storage appropriately[189] and is mediated by the autonomic nervous system. Sensitive nerve endings within the hypothalamus and near the skin surface of most of the body act as thermoreceptors [224] [361] to monitor Tc and Tsk . The primary means of regulating Tc are (1) vasomotor alterations in blood flow and its distribution, (2) shivering, and (3) sweating. The threshold temperatures for sweating, BFsk , and forearm venous volume depend on both Tc and Tsk . Heating the skin lowers these threshold temperatures.[94] [438] [517] At any given Tc heating the skin increases the effector response. Mathematical modeling suggests that Tc is nine times as important as Tsk in the reflex control of BFsk . [436] However, the importance of Tsk should not be minimized; whereas Tc varies over a narrow range of 7° C (12.6° F), the variation in Tsk is threefold to fourfold as great, enabling the system to accommodate to a wide range of environmental temperatures. During exercise, an increase in Tc elicits an effector response (sweating) with only a minimal change in Tsk . The rise in body temperature is proportional to the increased metabolic rate and does not depend on Tamb over a wide range.[368] However, as anyone who has experienced heat exhaustion knows, this relationship does not hold under extremely hot or humid conditions or conditions of maximum effort. This disparity between theory and common experience gave rise to the concept of "prescriptive zone," or a set of conditions in which the magnitude of the core temperature response for everyday work was independent of the environmental temperature.[314] The preoptic area of the anterior hypothalamus of the brain is generally believed to be the primary site for integration and generation of a "thermal command signal." This area contains many neurons that alter their firing rate in response to warming or cooling.[57] The brain is well perfused relative to its mass and responds rapidly to only a few tenths of 1° C (1.8° F) change in blood temperature.[40] [41] Sweating and skin vasodilation increased linearly above a "set point" temperature of approximately 37° C (98.6° F).[40] [41] Local heating accelerates sweating. Thus central and peripheral mechanisms cause sweating when skin temperature is elevated. Local heating may result in a greater release of neurotransmitter for a given sudomotor signal,[137] or heating increases the sensitivity of the gland to a given dose of neurotransmitter.[376] Conversely, lower skin temperatures may inhibit sweating during exercise.[40] Since sweating is not completely abolished by cervical cord transection, spinal centers for temperature regulation appear to contribute.[491] Set Point Hypothesis.
The concept that the central nervous system is a functional interface ("central integrative area") between the thermosensors and thermoregulatory effectors is not accepted by all physiologists.[461] However, it provides a rationale for envisioning a thermostat, or "set point," that shifts all effector thresholds in the same direction.[189] This concept of a central thermostat provides a conceptual framework that fits a variety of situations. The principal mechanisms involved in temperature regulation during exercise in the heat are venodilation, increased BFsk , and sweating. Dilation of superficial veins
increases the efficiency of heat flow from the core to skin and increases the time available for heat transfer between the blood and skin. The cutaneous vasculature is therefore an effector system in thermoregulation because BFsk controls the rate of heat transfer between the body core and surface.[189] [420] Unless the rate of heat storage exceeds the capacity of the thermoregulatory system (e.g., a breakdown of heat dissipation mechanisms), effector responses will increase until heat balance is restored. Vasomotor System.
The term vasomotor system refers only to the arterioles that control organ blood flow, vascular resistance, and arterial blood pressure.[420] Since arterioles
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and the heart together regulate blood pressure, a change in blood pressure is corrected by changes in vascular resistance or cardiac output (CO).[189] [215] [420] Vasomotor adjustments optimize and regulate the distribution of CO within and between different organ systems. Central thermal receptors alter vasomotor outflow to redirect blood flow to the skin. BFsk in humans exposed to cold can be reduced to 1 ml/100g skin/min and can increase during maximal heat stress to 150 ml/100g skin/min, greater in the extremities than in the trunk.[231] Blood flow to the skin is under dual vasomotor control. In the cold, adrenergic vasoconstrictor fibers reduce skin blood flow.[160] However, during heat exposure, blood flow increases to the hands, lips, nose, and ears as a result of vasodilation, largely because of the withdrawal of vasoconstrictor tone.[160] Active sympathetic vasodilation over most of the skin area[421] reduces vascular resistance below basal tone. There is a relationship between active sympathetic vasodilation and sweating, perhaps through the release of vasoactive intestinal polypeptide (VIP). [498] The simultaneous release of both transmitters (VIP and acetylcholine) could help explain the apparent relationship between eccrine sweat secretion and cutaneous vasodilation.[320] Venomotor System.
The venomotor system controls the veins; it should be noted, however, that there is a dual venous drainage of the limbs. The deep veins draining mainly from the muscles have relatively poor sympathetic innervation,[510] whereas the superficial veins draining the skin are richly innervated. Although venodilation and increased BFsk enhance heat transfer,[192] they increase the amount of blood pooled in compliant peripheral vessels. As a consequence, filling of these veins reduces central blood volume; at some point, the redistribution of blood could compromise venous return and cardiac filling.[420] [421] This system may be altered by fundamental changes in the smooth muscles of the various vessels. Heat increases the speed and extent of contraction of femoral arteries to K+ and catecholamines (i.e., increases vascular resistance) and may therefore inappropriately slow blood flow to and from the extremities.[382]
CLASSIC HEATSTROKE The pathologic features of heatstroke are similar irrespective of the cause of the heat illness and are manifested by swelling and degeneration of tissue and cell structures, and widespread microscopic to massive hemorrhages. [456] Most organs are congested, with increased masses and swollen cells. In the gastrointestinal tract, postmortem examination often shows massive ulcerations, hemorrhages, and engorged intestinal vessels.[456] A discussion of the gut is important in any discussion of heat illness for two reasons: (1) its function determines whether ingested fluid and solutes are delivered to the systemic circulation to correct losses and thereby attenuate hyperthermia, dehydration, and reductions in splanchnic blood flow and gut distress; and (2) heatstroke may result from or be exacerbated by gastrointestinal dysfunction, leading to "leakage" of gut-derived endotoxin into the circulation, endotoxemia, and circulatory collapse. There is an equivalence between the rehydration demand, the capacity of the stomach to deliver water (gastric emptying under optimal conditions can provide 1.8 L/hr) and the intestine to absorb (1.4 to 2.2 L/hr) ingested fluids. Classic heatstroke occurs when environmental heat stress is maximal. [134] [216] [476] Populations at risk include the elderly, the poor (who lack adequate air conditioning), those who suffer from malnutrition, and those who have chronic diseases or substance addiction.[216] In classic heatstroke, in contrast to EHS, physical effort is not a primary determinant of excessive heat storage and therefore the onset of classic heatstroke is slower. Predisposing factors commonly intervene over days rather than minutes or hours. As a result, there is often ample time for fluid and electrolyte imbalances to develop. Under some circumstances, passive hyperthermia can develop rapidly in extremely hot environments, such as when infants and small children are left in locked vehicles in the summer heat. This is also true for adults who are passengers in improperly ventilated or non-air-conditioned vehicles. Within minutes under desert conditions, cabins and cargo spaces of vehicles can reach 54° to 60° C (129.2° to 140° F), depending on environmental temperature (Tamb ) and solar radiation.[242] Similar high temperatures may occur in closed or confined spaces, such as enclosed attics, or in places where there is a high radiant load from machinery or power plants, such as boiler rooms.[292] Individuals who depend on others for fluid intake because of age (the very young or the elderly) or illness are at risk of involuntary dehydration. Infants are more heat labile because of their immature thermoregulatory systems.[442] (See later discussion of thermoregulation in children.) Epidemiology—Heat Waves When environmental heat stress is maximal, strenuous exercise is not necessary to produce heat illness.[134] [195] [216] [476] In Peking in 1743, a heat wave reportedly caused 11,000 deaths[456] ; 411 cases of severe heatstroke in Nanjing were reported.[326] During the July 1996 Atlanta Olympics there were 1059 heat casualties reported, of which 88.9% were spectators and volunteers.[520] In a separate heat wave,[150] 42 of 44 cases occurred within 8 consecutive days during which the maximum ambient temperature varied from 38.9° to 41.1° C (102° to 106° F). The patients' local environment temperatures were probably much higher, since air conditioning was not widely available at the time.
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Only 7 of 44 persons were less than 50 years of age, and the greatest frequency of age distribution was in the range of 60 to 70 years. In Boulder City, Nevada, July 8 to 18, 1936, Tamb reached higher than 38.3° C (100.9° F) daily. Forty-four heatstroke victims were admitted to the Boulder City Hospital with progressively increasing daily admission rates during that period.[119] The increasing number of admissions over time suggests that there is a progressive deterioration of the body with prolonged hot weather. This may be related to elevated cytokine levels. In a different heat wave near Dallas, Texas, lasting 26 days, the first case occurred on day 10 of the heat wave and the last case occurred 10 days after the end of the heat wave, with half the cases (14 of 28) occurring over a 3-day period on days 20 to 22. Age was a factor in both heat waves, with 8 of 72 victims above 80 years of age, and a mean age of 59 years in Boulder City and 70.5 years in Dallas. Alcoholism and degenerative diseases were contributing factors in both waves. The victims characteristically had a high rectal temperature (Tre ) and dry skin, and half of the Boulder City patients and 24 of 28 Dallas patients were comatose. Of the 44 Boulder City patients, 23 showed a fiery red skin rash over the body, particularly over the chest, abdomen, and back.[119] The most common presentation in Dallas patients was that of respiratory alkalosis, often accompanied by metabolic acidosis.[216] All Dallas patients with blood lactate greater than only 3.3 mMol/L (normal range 0.6 to 1.8 mMol/L) suffered a poor outcome, whereas those with initial lactate less than 3 mMol/L did well. That is, what in exercise studies would be only modest elevations in blood lactate become adverse prognostic indicators in classical heatstroke. Furthermore, 9 of 28 classic heatstroke patients arriving with normal serum potassium subsequently became hypokalemic, and all victims were hypokalemic at some point in their course.[216] A heat wave in Chicago in July 1995 resulted in more than 600 deaths, and more than 3300 emergency department visits and intensive care unit admissions for near-fatal heatstroke. In a group of 58 of these victims with classic heatstroke, 100% experienced multiorgan dysfunction with neurologic impairment, 52% showed moderate to severe renal insufficiency, 45% had disseminated intravascular coagulopathy, and 10% had acute respiratory distress syndrome. Fifty-seven percent of the victims had infections on admission. In-hospital mortality was 21%.[112] During a July 1988 heat wave in Nanjing, at least 4500 cases of heat illness cases were treated, with 411 of them classified severe.[538] (See Table 10-1 and Box 10-2 .) The mean age for males and females was 69.5 and 75.6 years, respectively, and persons over 60 years of age accounted for 77.4% of total deaths. Interestingly, some of these victims showed severe overhydration,
Tc ON ADMISSION (° C)
TABLE 10-1 -- Core Temperature of Heatstroke Victims in Nanjing, July 1988 DEATH RATE (%) NUMBER OF DEATHS*
42
83.3
36
Data from Zhi-cheng M, Yi-tang W: Chinese Med J 104:256, 1991. *Overall deaths = 124/411 (30.2%). Victims older than 60 years accounted for 77.4% of all deaths.
with electrolyte values falling to as low as Na+ 98, K+ 2.1, Ca2+ 1.52, and Cl- 97.4 mMol/L.
Box 10-2. COMPLICATIONS AND SYMPTOMS OF HEATSTROKE VICTIMS IN NANJING, JULY 1988
COMPLICATIONS (%) Various chronic diseases (24.5) Hypertension (24.3) Coronary artery disease (6.1) Diabetes mellitus (5.8) Obesity (5.3) Cardiac insufficiency (4.6) Cerebral vascular accidents (4.1) Chronic bronchitis (1.7) Neoplasm (1.7)
SYMPTOMS (RATE %) Headache (35.5) Dizziness (29.2) Weakness (29.2) Incontinence (19.2) Thirst (19) Numbness of extremities (14.4) Dysphagia and dysphonia (7.1) Kinetic imbalance (2.4) T >40° C (60.1) Delirium (14.8) Coma (45.3) Convulsions (31.6) Xerosis and hot skin (46.7) Moist skin (3.2)
Data from Zhi-cheng M, Yi-tang W: Chinese Med J 104:256, 1991.
During 5 heat wave years (1952–1955 and 1966) the average number of heatstroke or heat exhaustion deaths in the United States jumped from 179 to 820 deaths per year.[138] [139] In addition, the number of deaths classified as heat-precipitated was more than 8000 during heat wave years. There appears to be a reluctance to
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certify heatstroke or heat exhaustion as a cause of death, and epidemiologic estimates of the incidence are probably conservative.[456] As an example, heat-related death rates in the Chicago July 1995 heat wave were calculated by two methods: classification of heat-related deaths by the Cook County Medical Examiner's Office (CCMEO) and the excess mortality rates based on total mortality differentials during and before the heat wave. This analysis showed an underestimation of heat-related deaths in areas with high death rates. These results indicate that current practice does not adequately measure actual heat-related deaths. Nevertheless, those numbers may still be practical to use as an indicator to target specific communities for prevention and relief efforts.[455] Hyperthermia commonly occurs in the presence of numerous and varied host factors.[27] [242] These include many that affect thermoregulation through altering heat loss mechanisms (e.g., lack of acclimatization, fatigue, lack of sleep, dehydration, skin disorders), whereas others contribute to heat production (e.g., obesity, lack of physical fitness, dehydration, febrile illness, sustained exercise). Classic heatstroke tends to be a disease of the elderly, the alcoholic, and the infirm. EHS is different, typically affecting young, healthy, and even euhydrated men and women during exercise, and is a syndrome involving hyperventilation and respiratory alkalosis.[59]
EXERTIONAL HEATSTROKE Physical training increases heat tolerance, whereas a sedentary lifestyle decreases it. A sedentary lifestyle leads to a loss of muscle protein and strength and gain of fat. As a result, more energy is required to carry out any given physical task per gram of body mass, consequently increasing metabolic heat production. Physical training improves tolerance to heat mainly by improving efficiency of the cardiovascular system, increasing the rate of sweat production, and reducing the threshold Tc at which cooling mechanisms are activated. [16] Within certain body temperature limits, normal thermoregulatory mechanisms are capable of restoring Tc to 37° C (98.6° F) from either hyperthermia or hypothermia. However, if Tc rises to approximately 42° C (107.6° F), then metabolic pathways may be so altered that inappropriate physiologic responses occur. Vascular collapse, shock, and death can follow unless countermeasures such as cooling and volume therapy are initiated. It is not certain whether there is a single critical intracellular derangement occurring at 42° C that ultimately leads to the activation of many harmful metabolic pathways and heatstroke death, or if several harmful pathways become established independently at about the same time in response to the given Tc . EHS often affects fit and highly motivated individuals participating in sporting events or undergoing performance tests, such as those for military recruits and firefighter and police officer candidates. There will be increases in exertional heat illness because of the increased numbers of individuals participating in sports [216] [288] [289] and fitness activities, such as jogging,[212] fun-running, [246] [367] [408] [483] bicycling,[456] and long-distance sporting events.[215] [532] For example, an estimated 25 million Americans and 1 million Canadians participate in organized road races annually.[216] EHS has been reported during every season, even in winter. During a winter night a father totally covered his 9-month-old infant with a blanket and a thick quilt because its crying disturbed his sleep. In the morning the child was found dead with many petechial hemorrhages in the upper chest and thoracic viscera, the blood was concentrated (indicating dehydration), and the bedclothes were extremely wet with sweat. This was listed as an accidental death resulting from exertional self-overheating in bed.[539] Heat Storage Rate A temperature of 40.4° C (104.7° F) represents a threshold hyperthermia above which heatstroke mortalities occur in exercised, heat-stressed rats.[244] [245] The increase in an individual's heat storage, as shown by a rise in Tc , may be rapid (minutes to hours) and metabolic in origin because of overloaded heat loss mechanisms. For brief periods of intense effort, heat production may exceed 1000 kcal/hr.[390] An Olympic marathoner produced metabolic heat in excess of 1400 kcal/hr.[17] Under conditions that limit heat dissipation, such as high humidity or impermeable clothing, this rate of heat storage would cause body temperature to rise approximate 0.5° C/min (0.9° F/min) and produce heatstroke within 10 to 12 minutes. Even under a moderate workload (300 kcal/hr), a person who cannot sweat effectively and thereby dissipate heat can experience a rise in Tc of 5° C/hr (9° F/hr). [356] [390] Others at increased risk of exertional heat illness because of occupation include miners,[531] heavy industry workers, [123] [129] and individuals in the military.[70] [322] [323] [344] The yearly pilgrimage to Mecca has resulted in hundreds of fatalities from heat illness. [277] Wearing impermeable garments during physical activity leads to rapid loss of sweat, overload of heat loss mechanisms, and hyperthermia. These events may occur voluntarily (e.g., dieters, wrestlers) or by occupation (e.g., firefighters, hazardous waste handlers). Some cases of EHS have a genetic component. [381] Failed thermoregulation can have its origin in the dysfunction of either central (hypothalamic) control or peripheral responses of heat loss mechanisms (sweating and vasodilation). A variety of drugs and toxins can produce hyperthermia and are implicated in some cases of severe heat illness.[4] [5]
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Individuals at Higher Risk To preserve body temperature in its optimal range of 36.5° to 38.5° C (97.7° to 101.3° F), and to prevent an increase above 40.5° C (104.9° F), it is essential that the body delicately balance metabolic heat production, dry heat exchange, and evaporative heat dissipation. This requires highly developed and effective mechanisms of thermoregulation and temperature sensation. Heatstroke can be completely prevented by providing proper health education and following some simple regulations.[451] [452] Prompt recognition, attention, and treatment usually result in complete recovery from heatstroke. Preventive measures include acclimation to environmental conditions, adjusting physical efforts to match physical fitness, scheduling training to avoid the warmer hours of the day, establishing regulations to induce proper rehydration, and commanding adequate rest periods during activity. The medical team supervising the event should play a major role in preventing exertional heat illness during strenuous physical activity. It should also have the authority to cancel any strenuous activity whenever weather conditions are adverse. Before exercise, medical personnel must examine and evaluate each subject predisposed to heatstroke and, if necessary, exclude him or her from the activity. These measures were successfully implemented in the Israeli Defense Forces (IDF) and have been in practice there for many years. Recently these criteria also became an official position offered by the American College of Sports Medicine.[8] Heat-susceptible persons include those who are obese, unfit, dehydrated, unacclimated; (perhaps) those with a previous history of heatstroke; and those who suffer from acute febrile illness, diarrhea, or chronic disturbances of the sweating mechanism. These persons carry risk factors for heat illnesses and should be prevented from participating in strenuous exercise, particularly in hot environments.[142] Prescription drugs or drug abuse are among the acquired factors that underlie heat intolerance and may predispose individuals to excessive heat strain by altering thermoregulatory functions physiologically or behaviorally. Potentially harmful drugs include diuretics, anticholinergics, vasodilators, antihistamines, central nervous system inhibitors, muscle relaxants, tranquilizers and sedatives, ß-blockers, amphetamines, and tricyclic antidepressants.[380]
Box 10-3. EXERTIONAL HEATSTROKE IN THE FIELD The following historical narrative from the middle of the nineteenth century describes vividly the devastating impact of heat and dehydration on a military unit in Texas during the Indian Wars, excerpted from "A Cavalry Detachment Three and a Half days Without Water" by CPT J.H.T. King, Assistant Surgeon, U.S. Army Post Surgeon, Fort Concho, Texas: ... The next day found them still marching onwards, and the mid-day tropical heat causing great suffering. The desire for water now became uncontrollable. The most loathsome fluid would now have been accepted to moisten their swollen tongues and supply their inward craving. The salivary and mucous secretions had long been absent, their mouths and throats were so parched that they could not swallow the Government hard bread ... Vertigo and dimness of vision affected all; they had difficulty in speaking, voices weak and strange sounding, and they were troubled with deafness, appearing stupid to each other, questions having to be repeated several times before they could be under- stood; they were also very feeble and had a tottering gait. Many were delirious ... As the horses gave out they cut them open and drank their blood ... (which) was thick and coagulated instantly on exposure; nevertheless, at the time it appeared more delicious than anything they had ever tasted. This horse blood quickly developed into diarrhea, passing though the bowels almost as soon as taken; their own urine which was very scanty and deep colored, they drank thankfully, first sweetening it with sugar. The inclination to urinate was absent and micturition performed with difficulty. A few drank the horses' urine, although at times it was caught in cups and given to the animals themselves. They became oppressed with dyspnea and a feeling of suffocation as though the sides of the trachea were adhering ... prolonging the intervals between each inspira- tion as much as possible, ... their lips ... were ... covered with a whitish, dry froth and had a ghostly, pale, lifeless appearance as though they would never be opened again. Their fingers and the palm of their hands looked shriveled and pale; some who had re- moved their boots suffered from swollen feet and legs.
Most EHS victims are highly motivated, young, healthy individuals who exert themselves beyond their physiologic capacity ( Box 10-3 ). In a recent review of 82 cases of EHS in soldiers,[143] it was found that most cases occurred during basic training (57%) and an additional 21% occurred during screening tests for special forces—in which motivation is a key issue. Most of the EHS cases occurred in highly motivated but relatively unfit soldiers. Overmotivated soldiers misinformed the medical team regarding various issues that otherwise would have prevented their participation in the activity and therefore resulted in heatstroke.[451] Shapiro and Moran[451] concluded that in the young, active population, physiologic maladaptation is associated mainly with lack of acclimatization, dehydration, presence of infectious diseases or skin disorders, fatigue, and overweight. Although an internal "alarm system" should warn the human body to cease physical activity, during thermoregulatory maladaptation, it fails in the individual
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who is overmotivated and/or under peer pressure. The most common underlying factors for heat sensitivity that may lead to heatstroke are summarized in Box 10-4 . Mechanisms of temperature regulation have close functional relationships with other homeostatic mechanisms, that is, regulation of blood pressure, body fluid volumes, electrolytes, and acid-base balance.[451] When these are intact, the thermoregulatory system has the physiologic potential to cope appropriately with any strain resulting from exercise-induced metabolic heat production. This will protect the body from the hazards involved with excessive heat accumulation and elevated body temperature. The defense from the threatening combination of intense physical effort (high metabolic rate) and low environmental potential to evaporate sweat (high humidity) is expressed by several body alarms that ultimately should result with cessation of physical activity. The subjective "alarm" may be caused by the thermoregulatory system and expressed by elevated body temperature or by the cardiovascular system and manifested by elevated HR.[451] Heatstroke is a maladaptive state whereby the body temperature exceeds a temperature of 40.5° C (104.9° F) or greater, depending upon the severity of any recent exercise, as a result of the mismatch between heat production and heat dissipation.
Box 10-4. RISK FACTORS FOR EXERTIONAL HEAT ILLNESS
FUNCTIONAL-PHYSIOLOGIC Dehydration Poor physical fitness Lack of acclimatization Heat illnesses history (controversial) Obesity Age Fatigue Pregnancy
CONDITIONAL CIRCUMSTANCES Hot climate External load Inadequate rest periods Impermeable clothing Insulated materials Missed meals
CONCURRENT DISEASES AND CONGENITAL ABNORMALITIES CNS lesions Sweat gland dysfunction Infectious diseases Diabetes mellitus Skin disorders Diarrhea
DRUGS Drug abuse Medications Alcohol Caffeine
PSYCHOLOGIC STRESS Overmotivation Peer pressure
PSYCHOLOGIC STRESS Overmotivation Peer pressure
Imbalances in fluids and electrolytes are common during hot spells, especially when salt losses in sweat are compounded by loss of appetite. Fluid and electrolyte losses resulting from illness (diarrhea or vomiting) often contribute to heat illness. In some cases, dehydration is the primary cause of death.[456] Sleep deprivation has an insidious effect. Prolonged sleep deprivation is fatal in animals, leading to immunosuppression and a sepsis-like death. That is, sleep is essential for optimal immune function.[38] During hyperthermia, sleep deprivation increases the Tc threshold for the onset of sweating and, in women, reduces BFsk .[118] [303] During moderate-intensity exercise, this delayed sweating onset reduced BF sk in the heat, decreased total body sweat rate, reduced evaporative and dry heat loss, [435] and led to elevated Tc . On the other hand, hyperthermia may disrupt the sleep-state pattern, decreasing the duration of rapid eye movement (REM) episodes, thereby degrading the quality of sleep and imposing a psychologic stress.[175] Combinations of factors that create a threat may be subtle. The presence of air conditioning in the home, workplace, and transportation may decrease the risk for the development of classic heatstroke. However, by diminishing the state of heat acclimatization and respect for the environment, air conditioning may increase a person's risk for developing EHS. Intense and prolonged exposure during weekends and holidays accounts for many cases of sunburn and heat illness. Military Training From 1942 to 1944, there were at least 198 deaths from heat illness during military training in the United States.[440] Gardener et al[177] recently studied exertional heat illnesses in Marine recruits at Parris Island. During 12-week basic training of Marine recruits, the rate of exertional heat illness depended upon fitness. These rates correlated with body mass index (BMI) and time-to-complete a 1 ½-mile run during the first week of the training. Those recruits with a BMI greater than 22 kg × m-2 and a run-time greater than 12 minutes had eight times the risk for developing heat illness than those with lower values.[177] In this study of 217,000 Marine recruits (90% male, 80% age 18–20 years), there were 1454 cases of exertional heat illness, with 89%
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men and 11% women,[177] and with a peak rate of 2% of recruits in summer. The frequency of reported cases closely correlated with daily heat load (a combination of Tw , Tdb , and solar radiation) but did not correlate well with Tamb . Most cases occurred between 7:00 and 9:00 AM, during training that would have been restricted at elevated Tamb later in the day. During those hours, the rate of heat casualties increased substantially as WBGT increased, beginning at levels as low as 18.3° C (65° F). At WBGT of 23.9° to 26.7° C (75° to 80° F), heat illness rates increased 26-fold (over baseline rates at Tamb < 18.3° C [65° F]) and 39-fold for the day before exercise. Exposure to WBGT of greater than 80° F was infrequent (25%) among the early morning cases at the time of illness. However, a fascinating observation was made: on the day before illness, high Tamb was common (87%), suggesting a prolonged biochemical/physiologic effect of heat exposure.[266] Regardless of the current temperature, if the day before was cool, the frequency of heat cases was low; if it was hot, the frequency was high. Since the recruits were forced to drink large amounts of water, enough to keep them urinating during the night, elevated rate of heat casualties could not have been related to an accumulated dehydration from the day before. The presence of a high environmental temperature caused an unspecified physiologic predisposition to heatstroke lasting for at least a day. Thus even following widely published guidelines based on WBGT for physical activity does not preclude risks. Perhaps a better index should be developed. High rates of metabolic heat production (e.g., running) combined with conditions that limit evaporative heat loss (e.g., high relative humidity, impermeable garments) appear to present a significant risk regardless of Tdb . Furthermore, prevention is complicated by the observation that conditions on the prior day contribute to the current risk of heatstroke. Gender differences were found for the incidence of heat illnesses. Female rates were higher during the early hot season (May) and male rates were higher than those for females in the late hot season (September). Although May was cooler than September, there was a higher overall rate in May, probably reflecting less acclimatization in the spring. Comparing the days of the week, only 1.1% of casualties occurred on Sundays, reflecting decreased physical activity. In another study, obesity increased the risk of heat disorders in soldiers training in a hot and humid environment (Singapore).[89] In the IDF, 82 cases (of 150 suspected) were positively diagnosed as EHS from 1988 to 1996.[143] More than 50% of these cases occurred during the first 6 months in service, mainly in summer (June–September), but 30% of the cases occurred during the spring, and some cases occurred during the winter season. EHS was not related to time of the day. Many cases occurred during the night or early morning, even under mild heat load. Interestingly, evaluated by the heat load index,[470] 40% of the cases occurred during very short activities, whereas 60% occurred within the first 2 hours of exercise. The temperature regulation mechanism is efficient and the potential core-to-periphery conductance and sweating rate in the 82 heatstroke victims were higher than needed. Therefore EHS is more likely to occur when there is a severe thermal imbalance as a consequence of disturbance in the homeostatic mechanism aggravated by one or more predisposing factors[451] (see Box 10-4 ). Although heatstroke may be due to accident, lack of knowledge, poor judgment, or neglect, it is a preventable illness. Therefore cases of fatal heatstroke should be investigated for criminal intent. For instance, in the IDF, almost all cases of EHS occurred when regulations were not strictly followed.[143] In a most unusual incident, an herbalist was convicted of manslaughter in Australia [338] because he "treated" a young boy by immersing him for 40 minutes in a heap of fermenting horse manure, and the boy died of heatstroke. Educational efforts by both the media and the health care community aimed at parents of small children during heat waves should be made with the same enthusiasm as public service announcements of windchill factors during subzero temperatures. If participants develop heat injuries during sporting events that occur in hot weather outside the heat stress guidelines, coaches and organizers of the event should be held legally responsible. The military has long recognized the preventable nature of heat injuries that result from the intense physical activity in hot weather; a passage in the June 10, 1865 Lancet reads: "Commanding Officers of volunteers are very apt to err in this particular; and the spirit of their men is such that they shrink from complaint and persevere in efforts which may easily, under a burning sun, become dangerous to life." Sports EHS is a true sports emergency. There are several reports each year of heat illnesses with some fatal results, especially in competitive games. Incidence and mortality statistics for athletes are difficult to ascertain, but some have been reported. Undoubtedly, the incidences of unreported nonfatal heatstrokes are higher. From 1990 to 1995, there were 84 reported deaths resulting from heatstroke in athletes participating in American football.[399] In 1995, five American high school football players were reported to have died of heatstroke. [432] Interior linemen are at higher risk because of the their large muscle bulk. The uniform worn by football players covers almost the entire body and adds to heat load. In a 10-year study, 10% of 136 American high school and college athlete deaths were caused by EHS.[500] In the Falmouth, Massachusetts, road race, there are between 10 and 15 heatstroke victims every year.[432] Cyclists
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and tennis players, in particular, tend to have great problems with dehydration, the cyclists because their sweat evaporates rapidly as they ride causing them to underestimate their fluid loss.[222] In tennis, the duration of the game varies considerably and drinking is permitted only during changeover. The players' sweating rates can reach 2 L/hr, which presents a practical challenge for adequate fluid volume replacement.[43] In soccer, 4.5% of injuries in 480 games were related to heat illnesses.[279] Marathon runners thermoregulate at elevated core temperature (~40° C [104° F]) during a run, and approximately 0.6% of the runners suffer from heat illnesses. [396] Training Injuries Although it is clear that the rate of heat illnesses is greater in summer than in winter, the development of musculoskeletal and other injuries is a less obvious consequence of seasonal variations in climate. During basic military training, the incidence of musculoskeletal injuries severe enough to cause a time loss is higher in summer than in fall.[286] That is, the injury rate increases with temperature and at Tamb = 33.3° C (92° F) is 2.6 times as high as that at T amb = 16.7° C (61° F) for men and 1.8 times as high for women. This effect is also seen in elite athletes [296] and in British professional rugby players, with summer seasons showing almost double the injury rate of winter (696.8/1000 hours and 363.6/1000 hours, respectively).[393] In various studies, women had 1.5 to 3 times the injury rate of men.[287] Risk factors for injury are poor physical fitness, cigarette smoking, physical inactivity, longer running distances, and use of old running shoes (those 6 months to 1 year old more
than doubled the injury rate).[176] Other risk factors for injury include older age, high-arched feet, and being "knock-kneed." [286] Heat Strain Indexes How can one best quantify the dyshomeostasis and body injury, or the inability to maintain Tc at the level prescribed by the thermoregulatory center,[203] resulting from exercise and heat? Heat strain is not simply a matter of Tc alone because heatstroke and other heat illnesses could may occur at Tc less than 41° C (105.8° F). During the last century, environmental parameters and physiologic variables were combined to develop a unified heat strain index. Although more than 20 heat strain indexes have been described, none are accepted as a universal physiologic strain index. The main reasons for their lack of generality are related to the number and complexity of the interactions among recognized determining factors and their limited validity. The existing indexes can be divided into two main categories: (1) "effective" temperature (ET) scales[238] based on meteorologic parameters only (e.g., ambient temperature, Tw , and Tg ) and in which the WBGT index is derived[535] ; and (2) "rational" heat scales that include a combination of environmental and physiologic parameters (e.g., radiative and convective heat transfer, evaporative capacity of the environment, and rate of metabolic heat production). ET indexes have been widely applied to both assess and predict heat strain but cannot accurately account for different levels of metabolic rate, and different types of clothing (e.g., encapsulating). [271] [392]
In 1937 the operative temperature index was developed,[527] which combined the rates of metabolic heat production (M), heat transfer between the body and the environment (Hr+c ) and the evaporative capacity of the environment to dissipate heat (Emax ).[34] Its best known modification is the Heat Strain Index (HSI), which relates total evaporation required (Ereq , the sum of M and Hr+c ) to Emax . HSI is widely accepted because it combines environmental variables and body activity. However, in certain situations, the heat strain was seriously in error and further modifications have not been fully satisfactory.[34] [228] HSIs based on physiologic parameters were also suggested but found unsatisfactory.[304] Collectively, although many HSIs were developed, some simple to apply, others highly complex, all were found to be valid only under certain specific conditions. Recently, Moran et al[350] introduced a new physiologic strain index (PSI) based upon adding equally-weighted the individual strains of Tre and heart rate (HR), which represent the combined strains of thermoregulatory and cardiovascular systems. Each strain system was scaled 0 to 5. Thus the PSI is scaled 0 to 10 and can be calculated continuously on-line or during data analysis. The PSI can be applied at any time whenever Tc and HR are measured, including during rest or recovery periods, unlike some of the other indexes.[350] In a recent series of studies, PSI successfully evaluated the strains generated by different clothing ensembles, climatic conditions, different levels of hydration, and exercise intensity for gender during heat stress, for different age groups during acclimatization, and during acute exercise heat stress.[348] [351] Furthermore, this index, when adjusted for animal values, successfully rated and correctly discriminated between trained and acclimated rats exposed to exercise heat stress.[352] PSI differs from previous indexes. It is easier to interpret and use than other indexes available and includes the ability to assess rest and recovery periods. PSI overcomes the shortcomings of previously described indexes and can be used over a wide range of conditions. Heat strain is well known to correlate with environmental heat load and metabolic heat production, resulting in higher values of Tre , HR, and Tsk , and a reduced ability to maintain exercise. Various types of clothing with different degrees of water permeation create microclimates differing from that of the environment
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and lead to higher strains. The combination of different climates, impermeable garments, and hydration levels during different exercise intensities is a challenge for assessment of the individual physiologic strain. However, in two recent studies when different HSIs were applied to quantify the heat strain, PSI was successful at all levels of heat exposure while the other indexes were limited in their abilities.[350] The applicability of PSI was further successfully shown for various sweat rates and relative exercise intensities in different climates and for exercise heat stress and gender at different combinations of exercise intensity and climate.[348] Gender In many experiments, women exposed to acute heat stress and exercise thermoregulated less effectively than did men, resulting in the general conclusion that women are less heat-tolerant than are men.[340] [453] [459] However, in most studies, women generally had lower cardiorespiratory fitness, higher percentage of body fat, lower body weight, lower body surface area, and higher surface area-to-mass ratio than men.[316] [387] [391] Those physiologic differences are probably not intrinsically gender-specific but result from inequalities in fitness and acclimatization attributable to differences in lifestyle.[372] When such variables were controlled, most of the physiologic differences were narrowed, although mean sweat rate (msw) still remained lower for women.[10] [186] [340] [533] Stephenson and Kolka[474] suggested that the apparent physiologic differences in msw were based on comparing unmatched genders, mainly aerobically fit men to relatively unfit women. They argued that most of the studies comparing responses of men and women were not controlled for menstrual cycle phase and thus were limited in their conclusions. Furthermore, Sawka et al[437] concluded that when men and women were matched for aerobic fitness, they then had similar heat tolerances and body temperature responses during exercise in the heat. For instance, acclimatized men and women have comparable responses to rest and exercise in a desert environment.[514] However, hormonal fluctuations of estrogen and progesterone concentrations associated with the menstrual cycle may alter women's performance and tolerance to exertional heat stress.[316] In a recent study, Moran et al[351] applied the PSI in three climates to evaluate the strain of men and women who were matched for maximal aerobic power (ApV?O2 max) and intensity for 60 minutes. All subjects underwent a matrix of nine experimental combinations of three different exercises.[23] [260] [437] The PSI confirmed previous studies that when men and women were matched for ApV?O2 max and selected physiologic parameters, there is no difference in strain between the two groups. For middle-aged women, the effects of hormone replacement therapies on the thermoregulatory system were studied.[65] [66] [186] [489] The luteal phase, with its increased progesterone-to-estrogen ratio, was associated with an elevated Tc , whereas elevated levels of unopposed estrogen were associated with a lower Tc at rest and during exercise heat stress.[489] In summary, although mean physiologic responses to exercise heat stress suggest poorer thermoregulation for women, this is not necessarily an intrinsic gender difference but reflects a combination of social factors serving to reduce fitness in women. Aging In general, middle-aged and older men and women are less tolerant to heat and exercise, suffering more physiologic strain than younger individuals. [237] [505] They developed higher HR, Tsk , and Tc and lower msw than younger men and women during exercise heat stress. However, it is uncertain whether this is related to age per se or to other factors, such as disease states, decreased physical activity, and lowered aerobic fitness.[386] A subgroup of middle-aged men who were "habitually active" displayed the same strains to acute exercise heat tolerance and acclimated to heat at about the same rate and degree as when they were younger.[414] Some studies on aging emphasize the importance of aerobic fitness and physical characteristics, such as body fat and body weight in maintaining work heat tolerance. In one study, old and young men and women were matched for ApV?O2 max, surface area, and surface area-to-mass ratio but differed in age by 35 years. [272] During 75 minutes of light exercise at 37° C (98.6° F) and 60% RH, all groups showed the same degree of physiologic strain. In 1988, Pandolf et al[388] compared responses to acute heat tolerance between young and middle-aged men who were matched for ApV?O2 max and morphologic factors. The middle-aged mens' tolerance times were actually half an hour longer than the younger mens' during the first day of acclimation (49° C [120.2° F], 20% RH) and they were also at a thermoregulatory advantage during the few days of heat acclimation, although both groups eventually acclimated to the same absolute degree. However, in these studies the middle-aged men were more chronically active than the younger men before heat acclimation. Under different environmental conditions, such as 30° C (86° F) with 80% RH and 40° C (104° F) with 20% RH, no differences were seen between the two groups.[467] In summary, when properly matched subjects are studied, heat stress of middle-aged men resulted in either the same or reduced physiologic strain as that of younger men.
CELLULAR HEATSTROKE Whatever physiologic derangements occur in the whole body as a result of overheating, some primary derangements must first occur in individual cells.
253
Subcellular Disruption Heating alters subcellular structures in many cell types, including detachment of cortical microfilaments from the plasma membrane,[99] [133] collapse of the cytoskeleton, swelling of the mitochondria and the endoplasmic reticulum,[50] and disaggregation of polyribosomes and nucleoli.[80] [339] Furthermore, heating increases membrane fluidity, grossly distorting the plasma membranes and forming bulges known as "blebs."[30] [113] [402] Blebs alter membrane function,[13] increasing membrane permeability[494] with solute leakage.[404] [424] Such changes are not necessarily lethal; up to a point, the bleb formation may be adaptive, increasing cell survival.[51] [261] Red blood cells undergo rearrangements in their cytoskeleton with heat, but rather than forming blebs, they form spheroids at elevated temperatures.[206] These enlarged spherically shaped cells are much less efficient at gas exchange than are normal red blood cells and probably contribute to reduced PO2 in the tissues at elevated temperatures. Spheroid formation has been found in athletes during long-distance running and may contribute to their physical collapse during exercise.[206] Apoptosis Cells are destroyed within the body by the processes of apoptosis and necrosis. In apoptosis, certain individual cells within the body are genetically programmed to die. In this process, cells are broken into small vesicles containing condensed chromatin surrounded by intact cell membranes and are phagocytosed by neighboring cells. During necrosis, a variety of factors, including inflammation, cause swelling, destruction of the plasma membrane, and spewing of cell contents into the environment. [332] Apoptosis may be induced by a variety of stressors, including hyperthermia, aging, and certain toxins (Pseudomonas endotoxin, diphtheria toxin, and ricin).[131] A few minutes' exposure to temperatures of 41.5° to 42° C (106.7° to 107.6° F) triggers apoptosis in both cultured mammalian cells and experimental animals by activating Jun N-terminal kinase (JNK).[101] [428] The organs producing the greatest number of apoptotic cells from whole body hyperthermia are the thymus, spleen, lymph nodes, and mucosa of the small intestine. The heat shock protein HSP-70 (see below) prevents this activation and contributes to acquired thermotolerance in mammalian cells.[166] Ionic Changes Ions do not readily cross lipid bilayers despite their large concentration gradients across plasma membranes. In general, they require specialized channels or carriers to do so. Membrane channels are proteins that contain hydrophilic "pores" penetrating the lipid bilayer, permitting the diffusion of specific ions down their electrochemical gradients to enter or leave cells.[528] Cotransporters are fundamentally different types of pathways that move ions across the cell membranes up their electrochemical gradients by coupling the translocation of at least two ions (e.g., K+ and Cl- ) using the energy stored in adenosine triphosphate (ATP)-dependent preformed chemical gradients, such as those of H+ or Na+ (rather than the concentration gradients of the transported ions).[528] Potassium ions enter cells by at least two pumping mechanisms, the membrane Na+ K+ ATPase pump and the "ouabain-resistant pump." [207] [537] K+ exits cells through several types of membrane channels, including voltage-gated, ATP-gated, arachidonic acid-gated, and "leak" channels.[281] [364] [473] Although the rate of K+ transport by each pathway varies with temperature, during heating, the overall resultant flux is a net loss of intracellular K+ and a primary rise in plasma K+ .[174] [168] [425] [475] Hyperthermia increases the rate of Na+ influx, leading to a net rise in intracellular sodium (Nai) that is prolonged and not rapidly reversed by cooling. At a sufficiently high temperature, the Na transport mechanisms become denatured and, because of the increased "leakiness" of the plasma membrane and the transmembrane Na concentration gradient, Nai progressively rises until death.[171] Acidifying cells leads to an explosive influx of Na+ upon heating. Hyperthermia leads to at least mild cytoplasmic acidification,[523] and therefore the combined stresses of heating and acidification lead to increased intracellular Na+ . Moderate heat activates a Ca2+ ATPase pump to temporarily lower intracellular calcium (Cai). However, severe heating causes a net rise in Ca2+ through the activation of at least two transport systems and therefore is expected to alter a number of metabolic pathways. [294] Depending on the temperature, Ca2+ enters the cell from the extracellular fluid by means of the "reversed mode" of the plasma membrane Ca2+ -ATPase pump and enters the cytoplasm from intracellular Ca2+ stores. Some ionic changes in mammalian cells induced by heating, for example, in Ca2+ and Na+ , are mediated by inhibition of the Na-H exchanger, activation of Na+ K+ ATPase, and changes of membrane conductance for ions.[465] See Gaffin [168] for a review of these mechanisms. Although heating acts directly on the rates of fundamental cell processes, heat also has indirect effects by causing the release of a variety of hormones. These hormones, singly or in combination, further alter the activities of virtually all the ionic pathways. For instance, catecholamines stimulate the muscle membrane Na+ K+ ATPase (by approximately 100% in rat soleus), increasing both the intracellular K+ concentration (Ki)[92] and membrane potential.[67] Epinephrine in the presence of insulin stimulates active Na+ /K+ transport and hyperpolarizes membrane potential in muscle.[156] This effect may be so powerful that, for a time, it "masks" the primary decrementing effect of the heat-induced hyperkalemia on performance.
254
In addition to the effect of heat on pathway activities, the rise in activity of the various ion pumps provides more metabolic heat, which, near the limit of sweat secretion, increases body temperature still more. Increased membrane permeability from hyperthermia leads to rises in circulating enzymes. Creatine kinase is the first enzyme detected at Tc as low as 39.5° C (103.1° F) in monkeys (S. Constable and S.L. Gaffin, unpublished observations), and 42.5° C (108.5° F) in rats, followed by lactate dehydrogenase. [324] Stress Pathways Early unicellular forms of life were preyed upon by their neighbors and, over geologic time, they developed an immune system for protection. This is a nonspecific immunity and is basic to all phyla today. The original mechanism destroyed the invader's cytoplasm by active oxygen species, including free radicals, produced by the host. In modern mammalian species, specialized inflammatory cells, such as macrophages and
Figure 10-1 Stress and the hypothalamic-pituitary-adrenal axis. Under basal conditions (1) the anterior pituitary secretes the immunostimulants prolactin, growth hormone, thyroid-stimulating hormone (TSH), and gonadotropin-releasing hormone, leading to the secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone. Severe stress (2) acts on the paraventricular nucleus in the hypothalamus, producing CRF (3), downregulating the secretion of the immunostimulants and gonadal hormones, and (4, 5) upregulating the secretion of the immunosuppressors ß-endorphin, a-melanocyte-stimulating hormone, and ACTH, the latter of which upregulates the secretion of the immunosuppressor cortisol. Stress also (6) activates the sympathetic nervous system, and catecholamines are secreted. These further downregulate the production of immunostimulants and (7) may reduce splanchnic blood flow sufficiently to cause ischemia of the intestinal vascular bed, local damage to the gut wall, and the leakage of lipopolysaccharide (LPS) into the circulation. LPS in turn (8) causes the production of the powerful immunosuppressors TNF and IL-1. TNF and IL-1 are also secreted within the hypothalamus in direct response to stress, leading to their participation (9) in a positive feedback loop, augmenting the secretion of CRF and resulting in even greater immunosuppression. NOTE: Moderate stress may have the opposite effect and increase the secretion of immunostimulants. (From Gaffin SL, Hubbar RW: Wilderness Environ Med 4:312, 1996.)
natural killer (NK) cells, are especially enriched in those enzymes and chemical pathways producing the toxic free radicals. They also contain additional pathways that allow these cells to recognize invaders and penetrate tight epithelia so that they may easily reach and destroy them. The immune cells are activated by means of circulating and locally produced cytokines, such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), as part of a stress reaction mediated by the hypothalamus. Thus there exists a common stress reaction in vertebrates that is activated by stresses other than infections, such as hyperthermia, and that activates pathways producing toxic species, which may now be inappropriate and toxic to the organism.[169] Severe hyperthermia in mammals leads to a common response pathway involving the secretion of corticotrophin releasing factor (CRF, also called corticotropin releasing hormone [CRH]) by parvicellular neurons of the paraventricular nucleus of the hypothalamus,[31] [497] activation of the sympathetic nervous
255
system, and secretion of cortisol and catecholamines ( Figure 10-1 ). CRF is directly transported via the hypothalamo-hypophyseal portal system to the anterior pituitary, where it has two important effects: (1) it downregulates eosinophilic cells that secrete the immunostimulants (growth hormone, prolactin, gonadotropin stimulating hormone, luteinizing hormone, and follicular stimulating hormone),[15] [127] and (2) it upregulates the pro-opiomelanocortin (POMC) gene in basophilic cells, leading to the secretion of immunosuppressors (ß-endorphin, a-melanocyte stimulating hormone, and adrenocorticotropic hormone [ACTH], in turn leading to the secretion of the immunosuppressor cortisol) (see Figure 10-1 ). A rise in IL-1 is part of a positive feedback loop, causing a further rise in CRF and ACTH.[249] [257] These are not just theoretic predictions based on animal studies. In human subjects, circulating levels of CRF, ACTH, cortisol, and arginine vasopressin (AVP) rose during graded work rates until exhaustion. It appears that high-intensity exercise favors AVP release, whereas prolonged duration favors CRF release.[250] Energy-Depletion Model During hyperthermia and continued heat stress, cellular Na+ K+ ATPase pumps operate at elevated rates, hydrolyzing ATP more rapidly and liberating waste heat into the body faster. If the body cannot dissipate this heat through radiation, conduction, convection, and sweat evaporation, then according to the laws of thermodynamics, Tc must rise further, leading to still greater rates of the Na+ K+ ATPase pumps-an ominous positive feedback loop. The amount of energy available to a cell is limited. Therefore, at a certain elevated temperature, ATP utilized by the activated Na+ K+ ATPase pump can no longer be resynthesized sufficiently rapidly to be available for normal cellular processes and the cell becomes "energy-depleted." Experimental support for this concept is the presence of swollen cells (implying a slowing of ion pumps, which affect water transport) and the rapid development of rigor mortis (caused by depletion of ATP) at the end stage of heatstroke pathophysiology. Persons exercising in the heat develop lethal heatstroke at lower Tc than do those at rest. This can be explained by the concept that exercise lowers ATP stores (i.e., creatine phosphate) and therefore less is available for other important cellular processes.[241]
CARDIOVASCULAR STRAIN AND EXERCISE Severe heat illness involves every system and affects the regulatory (cardiovascular), the integrative (neuroendocrine), and ultimately the basic cellular systems of the body. Probably no greater strain is put on the human body than heavy physical exertion in the heat. This impact of heat stress on the cardiovascular system represents the strain resulting from increased demand for cardiac output to transfer heat and water to the skin for evaporative cooling. Severe and prolonged exercise leads to changes in body compartments and the cardiovascular system, persisting for hours to days. For instance, a group of men carrying 20-kg backpacks during a 110-km march under warm conditions, eating and drinking ad lib, lost 3.4% of body weight and their plasma volume (PV) fell by 6.1%. However, the next day their PV dropped still further to -8.4%, even though they were not exercising. During the following day, PV rose to +3.7% above baseline and remained elevated 4 days after the march.[21] The hemodynamic displacement of blood to the periphery is aggravated by gravitational displacement of blood volume resulting from upright posture. In an upright human, about 70% of the blood volume is below heart level. Venous pooling of blood in the skin and in the great veins below the level of the heart leads to reduced venous return to the heart and consequent reduced cardiac filling.[421] If active skeletal muscle then vasodilates to supply the increased demands for blood flow in support of muscle metabolism, the competing demands for blood flow between vascular beds translate into a major regulatory problem.[420] The potential conductance of the vasculature (skin 8 L/min-1 , viscera 3 L/min-1 , and muscle 65 to 70 L/min-1 ) is enormous and far exceeds the pumping capacity of the normal human heart (about 22 L/min-1 ). [255] [422] Since the combined blood flow requirements of these vascular beds cannot be met, an inherent competition takes place between the mechanisms that maintain blood pressure and those that maintain blood flow to support metabolism and thermoregulation.[243] The existence of a variety of types of heat illnesses suggests: (1) the physiologic strain resulting in homeostatic failure produces heat illness; (2) a certain biologic variability is expressed in the response to heat and exercise; (3) hemodynamic stability often takes precedence over thermoregulation; (4) volitional behavior, expressed as exercise performance, is often maintained even as the risk of heat injury increases; and (5) the onset and increase in hyperthermia are not painful.[242] Not surprisingly, the physiologic threat to homeostasis is worsened when accompanied by fluid/electrolyte imbalance. [240] [383] Treatment is then directed at the major sources of homeostatic failure: cease the activity, lie down, cool down, and rehydrate. Sometimes the cause of collapse or the other symptoms involved (such as headache, nausea, vomiting, and vertigo) is obvious; sometimes, it is not readily appreciated. Sweating Although human eccrine sweat glands generally behave physiologically and pharmacologically as if under parasympathetic or cholinergic control, they also
256
respond to adrenergic stimulation.[434] There are 2 to 3 million sweat glands distributed with decreasing density in the skin of the palms and soles, head, trunk, and extremities, with an average density of about 100 to 200/cm2 . One g of sweat glands can secrete up to 250 g of sweat per day. Eccrine sweat is always hypotonic, contains variable concentrations of sodium, and is generally 99.5% water by weight.[141] That 0.5% of sweat solids is important, since 1 L of 0.5% sodium chloride contains 5 g of salt, a potential cause of serious salt depletion. The process of sweat secretion and sweat rate depend on activation of the sweat center in the hypothalamus, which discharges over the cholinergic fibers of the sympathetic nervous system. Rising blood temperatures increase both the number and the rate of sweat glands responding, until the body reaches a thermal equilibrium or the maximum sweat rate occurs.[189] Dehydration and hyperosmolality each leads to reduced sweat rates,[439] with hyperosmolality the more effective ( Figure 10-2 ). One of the highest sweat rates ever recorded in a human was in a world-class Olympic runner.[17] He produced
Figure 10-2 Effect of reduced plasma volume or increased osmolarity on sweat rates in six individuals. (Modified from Sawka MN et al: J Appl Physiol 59:1394, 1985.)
sweat at a rate of 3.71 L/hr after 19 days of heat acclimation training. Because the maximum rate of gastric emptying is much less than the maximum sweat rate (1.2 vs. 3.7 L/hr), rehydration cannot keep pace with sweat losses under those conditions [18] and an athlete faces significant risk of dehydration despite frequent drinking.[19] [20] [243] Since rates of gastric emptying can exceed 1 L/hr, as a rule of thumb, a 1 L/hr sweat rate appears sustainable without significant dehydration. Fluid and Electrolyte Imbalance Heatstroke Model.
Determining the time courses of changes in various physiologic and biochemical parameters caused by heatstroke is difficult or impossible in humans for ethical considerations. Use of rodents precludes the determining of many parameters simultaneously because of lack of blood volume. Miniswine have been used as models because of their considerable physiologic similarities to humans and their practical size. When anesthetized miniswine were passive heated to Tamb = 43° C (109.4° F), HR and mean arterial pressure (MAP) rose only slightly until Tc reached 42° C (107.6° F) ( Figure 10-3, A ). At this Tc , the HR rose to a
257
Figure 10-3 A, Effect of hyperthermia on mean arterial pressure (MAP) and heart rate (HR) in anesthetized miniswine. After 1-hour baseline, environmental temperature was raised to 42° to 43° C (107.6° to 109.4° F). * = P 40° C [104° F]) that it be included as 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.[290] Since 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 phenothiazine.[293] In summary, heatstroke in a summertime vacation area might be complicated by the use of therapeutic or recreational drugs. 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).[98] [306] [511] The anesthetic binds to
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RyR and activates the Ca++ 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.[98] Rhabdomyolysis, hyperkalemia, and myoglobinemia[443] are commonly associated with malignant hyperthermia, with plasma K+ rising as high as 10 mmol/L.[341] 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.[360] A 41-year-old man susceptible to malignant hyperthermia developed an infection and self-medicated 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.[268] Neuroleptic Seizure The treatment of psychiatric patients with neuroleptic drugs, as well as with antidepressants, antiemetics, and others,[130] may lead to the uncommon but often fatal neuroleptic malignant syndrome, characterized by hyperthermia as high as 42° C (107.6° F),[7] "lead pipe" (skeletal muscle) rigidity, dyspnea, coma, extrapyramidal syndrome, rhabdomyolysis, severe metabolic acidosis, leukocytosis, and elevated creatine phosphokinase.[221] [258] [488] A number of factors predispose to neuroleptic seizure, including dehydration, exhaustion, aggression, and restraints[254] ; high environmental temperature; high doses of neuroleptics; abrupt discontinuation of antiparkinsonism agents; and administration of lithium.[130] 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. [130] 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 cocaine[120] and amphetamine derivatives, such as 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") and 3,4-methylenedioxyethamhetamine (MDEA, "Eve").[490] Other components of this syndrome include hyperkalemia, rhabdomyolysis,[462] sympathetic hyperactivity, convulsions, rectorrhagia, psychosis, disseminated intravascular coagulation in the absence of positive blood cultures, and acute renal failure.[223] 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.[511] 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.[230] A ryanodine contracture test has been proposed as an in vitro diagnostic test to screen for surgical patients susceptible to malignant hyperthermia.[230] 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 the development of the physical symptoms associated with heat stress.[78] Typically, heat stress causes distortion of the sense of time,[35] [36] [104] memory impairment,[525] deterioration in attention, and decreased ability to calculate mathematical problems.[85] [199] [524] 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.[78] Vasovagal Syncope.
Syncope is the cause of about 3% of emergency department visits and 6% of hospital admissions.[183] Vasovagal syncope is responsible for 28% to 38% of syncope patients aged 35 to 39 years.[108] [263] [331] Benign presyncope or syncope may result from diminished venous return to the heart because of blood pooling in the peripheral circulation. Syncope encompasses psychologic disturbances activating an autonomic vasodilation response; reflex syncope caused by heavy coughing, micturition, and pressure on an irritable carotid sinus; or reduced vasomotor tone caused by hypotensive drugs or alcohol.[132] Interestingly, the frequency of vasovagal syncope is greater in the young than in the elderly, whereas orthostatic hypotension is more common in older persons.[317] Propranolol does not prevent the vasovagal reaction in response to head-up tilt.[317] 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%.[262] Hyperventilation Dizziness.
A slight but prolonged increase in respiratory rate or tidal volume may accompany an increase in anxiety.[132] 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 the
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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 the effective blood volume can temporarily compromise venous return, CO, and cerebral perfusion. Patients are usually erect at the outset and sometimes report prodromal symptoms of restlessness, nausea, sighing, yawning, and dysphoria.[280] 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 remedied. Fainting is usually brief and responds to horizontal positioning and improved venous return. The patient should be allowed to rest in cooler, shadier surroundings and 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
CASE NO.
TABLE 10-3 -- Clinical Data in 17 Patients with Heat Exhaustion AGE ACTIVITY SYNCOPE CRAMPS
Tre (° F)
RR Na+ pH PCO2
1
19
Marching
Yes
Abd
99.6 24 142 —
—
2
20
Running mile
Yes
Legs/abd
98.4 30 145 —
—
3
20
Rifle range
No
No
99.4 24 143 —
—
4
21
Marching/running Yes
Hands
100.4 22 162 7.47 34.0
5
21
Marching
No
Severe abd/legs
102.4 35 141 7.50 32.4
6
22
Marching
No
Legs
100.0 22 152 7.70 14.8
7
20
Rifle range
No
Mild
100.0 22 140 —
8
20
Marching
Yes
Abd/legs
100.8 30 145 7.52 28.8
9
20
Marching
No
Abd
101.4 24 —
10
18
Marching
Yes
Chest
100.8 18 140 7.56 29.4
11
19
Marching
Yes
Tetany
101.5 30 160 7.44 34.2
12
18
Marching
Yes
Severe
100.6 30 130 7.71 17.2
13
20
Marching
No
Mild
14
19
Marching
Yes
Abd/legs
100.7 30 145 7.76 16.3
15
23
Rifle range
Yes
Abd/legs
101.0 32 148 7.66 19.7
16
18
Marching
Yes
Chest/legs
101.2 28 148 7.78 14.7
17
17
Marching
Yes
Abd
101.6 22 146 7.53 28.4
—
7.69 19.8
98.6 26 141 7.77 15.2
Abd, Abdomen; RR, respiratory rate. pooling and the predisposition to syncope. Consistent with this, nonfainters have higher intramuscular pressure than fainters. The 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 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 10-6 ), suggesting the importance of salt and water retention in preventing this disorder.[242] Thus individuals medicated with diuretics would be at high risk. Furthermore, potassium depletion and hypokalemia may lower blood pressure and blunt cardiovascular responsiveness.[292] 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 and body temperature measured. 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 exhaustion[247] ( Table 10-3 ). In contrast to hypovolemic salt depletion, this heat exhaustion 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
278
those classically described as the venous pooling or postural hypotension variety. [32] [368] 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 a 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 10-3 . Almost all the casualties occurred in the afternoon during July 1971 at Fort Polk, Louisiana. All were diagnosed as 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. Serum electrolytes were in the normal range in the majority of the victims. However, hemoconcentration with elevated serum sodium level was observed in four patients. Only 1 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 (not shown). The mean arterial pH for this group of patients was 7.62 ± 0.03 (SEM), and 5 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. [60] 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 physiological ventilatory response to thermal extremes."[60] Hyperventilation with its resulting decrease in cerebral blood flow[275] [457] [509] 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 spasms but 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.[302] [308] 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 vs. 1.5 L/hr) than do nonacclimated persons but also have increased tolerance to exercise. If both groups voluntarily work at maximum sweat rates for any given task, those who are heat-acclimated could produce higher salt losses, despite their reduced sweat sodium concentrations. Under such a scenario, the acclimated individuals would be predicted to be the more prone to heat cramps.[11] However, Table 10-2 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.[484] Heat-Induced Tetany It has long been known that in excessively hot environments, men at rest hyperventilate.[203] Adolph and Fulton [2] 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 experiencing spontaneous
hyperventilation and attacks of tetany.[526] 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 onset of symptoms ranging from slight tingling of the feet and hands to more severe carpopedal spasms.[247] [248] 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 as depicted in Figure 10-10 . There was a direct relationship between the rate of change of the four parameters and the incidence of symptoms. 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 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.[136] Heat cramps are brief, intermittent, and often excruciating muscle contractions and are a frequent complication of heat exhaustion and occurred in about 60% of 969 cases of heat exhaustion.[95] [308] [479] 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
279
Figure 10-10 Comparison of absolute change and rate of change of PCO2 , CO2 , pH, and Tre with incidence of heat-induced tetany. Rate of change values were obtained by dividing the absolute change during exposure by the exposure time in minutes and multiplying by 60. (From lampietro PF: Fed Proc 22:884, 1963.)
at the time of heat exhaustion is obviously 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. During the 1930s, steel workers, coal miners, sugar cane cutters, and boiler operators were among the most common victims of classic heat cramps.[486] [487] Three factors common to most reports are that cramps are preceded by several hours of sustained effort, are accompanied with heavy sweating in hot surroundings, and are combined with the 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). [487] Diagnostic of heat cramps are hyponatremia and hypochloremia that might be due to salt deficit or some degree of water intoxication. [292] If overdrinking causes gastric distention, nausea[405] could trigger vasopressin release and contribute to renal water retention. In an industrial setting, heat cramps occur most commonly late in the day, and after physical activity has ceased; they sometimes occur while a person is showering and occasionally occur in the evening.[308] Classic heat cramps are distinguished from hyperventilation-induced tetany in that they are limited to contractions of those voluntary skeletal muscle subjected to prior exertion and usually affect only a few muscle bundles at a time. As one bundle relaxes, an adjacent bundle contracts for 1 to 3 minutes. The cramp thus appears to wander over the affected muscle, but the pain can be excruciating in severe cases. Three precipitating conditions (exhaustive work, hemodilution, and cooling the muscle) can each depolarize the muscle cell.[292] This could explain the association of cramps with showering in cool water, since cooling slows sodium transport and depolarizes the cell and may thus reach excitation threshold.[464] The low incidence of heat cramps within the Indian Armed Forces[323] and the fact that Shibolet observed no cases within IDF 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.[487] Heat cramps generally respond rapidly to salt solutions. Mild cases may be treated orally with 0.1% to 0.2% salt solutions (2 to 4 10-grain salt tablets [56 to 112 mEq] or ¼ to ½ teaspoon table salt dissolved in a quart of water). Cooling and flavoring enhance its palatability. Oral salt tablets are gastric irritants and are 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. The 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.[16] [19] [242] Clinical descriptions include tachycardia, hyperventilation, hypotension, and syncope. Although
280
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 tenuous [217] or even considered artificial.[456] 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 the occurrence of electrolyte and water imbalance. The hyponatremia and hypochloremia of patients with either heat cramps or salt depletion heat exhaustion often develop over 3 to 5 days[307] and usually in the unacclimatized individual who has not fully developed his or her salt-conserving mechanisms.[468] [469] In salt depletion heat exhaustion, muscle cramps, nausea, and vomiting may be intense, but victims do not feel very thirsty. [242] [383] The major route of fluid and electrolyte imbalance (salt depletion, water depletion, water intoxication) involved in a particular heat exhaustion case can be discovered from the events surrounding the collapse and a careful history.[71] [292] [308] [499] The alternate 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 vs. intense, short-term exertion), the intensity of the hyperthermia, and the absence or form of CNS disturbance. For example, Table 10-4 is a theoretic demonstration of the impact of body weight loss as either pure water or sweat of varying salt concentrations. If external cooling does not rapidly lower Tc to normal or, conversely, precipitates severe
SIGNS AND SYMPTOMS
TABLE 10-4 -- Signs and Symptoms of Salt and Water Depletion Heat Exhaustion SALT DEPLETION HEAT EXHAUSTION WATER DEPLETION HEAT EXHAUSTION
DILUTIONAL HYPONATREMIA*
Recent weight gain
No
No
Yes
Thirst
Not prominent
Yes
Sometimes
Muscle cramps
In most cases
No
Sometimes
Nausea
Yes
Yes
Usually
Vomiting
In most cases
No
Usually
Muscle fatigue or weakness
Yes
Yes
No
Loss of skin turgor
Yes
Yes
No
Mental dullness, apathy
Yes
Yes
Yes
Orthostatic rise in pulse rate
Yes
Yes
No
Tachycardia
Yes
Yes
No
Dry mucous membranes
Yes
Yes
No
Increased rectal temperature
Yes
In most cases
No
Urine Na+ /Cl-
Negligible
Normal
Low
Plasma Na+ /Cl-
Below average
Above average
Below average
*Data from Armstrong LE et al: Med Sci Sports Exerc 25:543, 1993; and 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.
shivering, intercurrent illness is suspected. Anecdotal experience that in the field suggests that approximately 20% of persons with suspected heat exhaustion have some form of viral or bacterial gastroenteritis. This is especially true if untreated (nonchlorinated) water or ice is available. At any given loss of body weight (see Table 10-4 ) the decrement in PV 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 rentention of salt the greater the increase in osmolality, plasma, sodium, and thirst. Table 10-4 attempts to compare and contrast the various 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 It has long been known that coexistent illness or infection predisposes an individual to heatstroke.[185] In one study of heat illnesses, 11.2% of patients[522] also had gastrointestinal (choleraic) illness.[522] The reverse is also true: heat waves produce excess deaths from all categories of disease. For example, in one heat wave week in New York in the late summer of 1948, deaths from diseases of the heart and arteries and from diabetes more than doubled (1364 vs. 585), and pneumonia deaths tripled.[139] Infection predisposes to heat illness and heat stress exacerbates infections, leading to greater morbidity and
281
mortality.[312] Relatively few studies have been reported on the susceptibility to infection during heat exposure, or the influence of infection on heat tolerance, and there is a need for further research into the effects of diseases on thermoregulation.[273]
ACKNOWLEDGMENT
This chapter is, in part, a revision of Gaffin SL, Hubbard RW, Squires DL: Heat-related illnesses. In Auerbach P, editor: Wilderness medicine, St Louis, 1995, Mosby, pp 167–212, and Dr. Hubbard's original contribution to this chapter is recognized. The opinions or assertions contained herein are the private views of the authors and should not be construed as official or reflecting the views of the United States Army or Department of Defense. Citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement or approval of the products or services of these organizations. Human subjects participated in these studies after giving their free and informed voluntary consent. Approved for public release; distribution is unlimited.
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Chapter 11 - Clinical Management of Heat-Related Illnesses Daniel S. Moran Stephen L. Gaffin
This chapter discusses clinical observations of heatstroke victims, management of heat-related illnesses, and consequences of different levels of hydration on heat illnesses. In heatstroke, the most severe heat illness, early clinical signs are nonspecific. A common picture of heatstroke is sudden collapse of an individual during physical activity carried out 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. The severity of heat illness depends on the degree of elevation in Tc and its duration. 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. Updated descriptions of issues related to dehydration, hypohydration, hyperhydration, and rehydration are also presented.
CLINICAL AND LABORATORY OBSERVATIONS IN HEATSTROKE The clinical manifestations of heatstroke vary, depending on whether the victim suffers from classic heatstroke or exertional heatstroke (EHS) ( Table 11-1 ). Some overlap in presentation may occur; treatment with a medication that places an elderly person at risk for classic heatstroke also places an exercising individual at risk for EHS. The clinical picture of heatstroke usually follows a distinct pattern of events in three phases.[76] Acute Phase The acute phase is characterized by central nervous system (CNS) disturbances. Since brain function is very sensitive to hyperthermia, this phase presents in all heatstroke patients. Signs of depression of the CNS often appear almost simultaneously in the form of irritability, aggressiveness, stupor, delirium, and coma.[3] [37] [214] Seizures occur in 60% to 70% of heatstroke cases. After a return to normothermia, the persistence of coma is a poor prognostic sign.[126] [214] Other symptoms include fecal incontinence, flaccidity, and hemiplegia. Cerebellar symptoms, including ataxia and dysarthria, are prominent and may persist.[153] [214] [242] In over 60% of heatstroke cases, pupils were constricted to pinpoint size.[126] [243] Papilledema was found to present in cases of cerebral edema. However, cerebrospinal fluid and pressure were usually within normal values.[3] [126] [214] Other common disturbances for the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dysfunction, including diarrhea and vomiting, often occurs. The latter, however, may reflect translocation of toxic gram-negative bacterial lipopolysaccharide (LPS) from the lumen of the intestines because of poor splanchnic perfusion, as well as from CNS impairment.[34] [94] [214] Hyperventilation and elevation of Tc primarily lead to respiratory alkalosis, which in EHS may be masked by metabolic acidosis as a result of increased glycolysis and the development of hyperlactemia.[39] [172] Hypoxemia may be present in cases of respiratory complications.[44] [172] [222] Hematologic and Enzymatic Phase In the hematologic and enzymatic phase of heatstroke, hematologic, enzymatic, and other blood parameters are altered. In humans and experimental animals, hyperthermia results in temporary leukocytosis[107] and changes in lymphocyte subpopulations—both in absolute numbers and in percentages. [1] Leukocytes may range from 20 to 30 × 103 /mm-3 and higher.[21] [110] In one study, all fatal cases of exertional heatstroke had disturbances in the blood coagulation system.[215] [216] Prothrombin time, partial thromboplastin time and the level of fibrin split products increased with a fall in thrombocytes.[76] Clotting dysfunction peaked 18 to 36 hours after the acute phase of heatstroke, and 2 to 3 days after heatstroke prothrombin levels fell to 17 to 45% of normal. Depending on the severity of heatstroke, thrombocyte values range between 110 × 103 /mm-3 and zero.[215] [216] These clotting disturbances resemble those of gram-negative bacterial sepsis, and it has been suggested that LPS participates in the pathophysiology of heatstroke.[101] Significant lay interest, scientific research, and commercial product development and marketing have focused on electrolyte abnormalities associated with physical exertion under various conditions. The marked variability in electrolyte content of sweat and intensity
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CLASSIC
TABLE 11-1 -- Comparison of Classic and Exertional Heatstroke EXERTIONAL
Age group
Elderly
Men (15–45 yr)
Health status
Chronically ill
Healthy
Concurrent activity
Sedentary
Strenuous exercise
Drug use
Diuretics, antidepressants, antihypertensives, anticholinergics, antipsychotics
Usually none
Sweating
May be absent
Usually present
Lactic acidosis
Usually absent; poor prognosis if present
Common
Hyperkalemia
Usually absent
Often present
Hypocalcemia
Uncommon
Frequent
Hypoglycemia
Uncommon
Common
Creatine phosphokinase/aldolase
Mildly elevated
Markedly elevated
Rhabdomyolysis
Unusual
Frequently severe
Hyperuricemia
Mild
Severe
Acute renal failure
41° C [105.8° F]), CNS disturbance, and cessation of sweating.[43] This symptom complex represents the extreme or full-blown heatstroke presentation and is now recognized to be too rigid and possibly delaying institution of critical interventional measures. We consider each of these criteria in turn. • The body temperatures reported in heatstroke victims in the field may be significantly higher (41.1° C [106.9° F] vs. 37.8° C [100° F]) than those documented in the hospital emergency department. [213] Failure to obtain or record on-site rectal temperatures may hinder prompt diagnosis; similarly, documentation of only mild elevation in body temperature should not preclude the diagnosis of heatstroke. • The victim's altered mental status may adversely affect the ability of emergency department personnel to obtain a detailed history regarding precipitating events. Lack of such information may also delay diagnosis. Emergency medical transport personnel should attempt to obtain this history before evacuating the victim and communicate the information to the appropriate medical staff. • Recent investigations have shown that cessation of sweating is a late phenomenon of heatstroke.[187] [216] At the time of collapse, most heatstroke victims continue to sweat profusely. Failure to consider the diagnosis of heatstroke in a diaphoretic patient could be fatal. • Unless an alternative cause is obvious, the previously healthy individual who collapses after physical exertion in hot weather should be considered to have EHS.[41] [214]
Diagnosis.
Shibolet[213] noted that a delay in measurement of Tc or inaccurate methodology in obtaining initial temperature values often led to inappropriately low initial temperature determinations when compared with actual Tc at the time of collapse. Loss of consciousness is an unvarying feature of heatstroke. With cessation of physical activity, the rate of metabolic heat production markedly decreases and Tc will fall if skin temperature (Tsk ) is greater than Tamb and sweating persists. Shapiro and Seidman[210] proposed that the diagnosis of heatstroke should be considered in any person who has lost consciousness during exertion and demonstrates clinical and laboratory signs of heatstroke, even if body temperature was not markedly elevated several hours after collapse. A history of prodromal symptoms as described for heat exhaustion should markedly increase the suspicion for heatstroke. CNS disturbances (coma, convulsions, confusion, or agitation) accompanying hyperthermia may also be due to CNS infections, sepsis, or other disease processes. Evaluation for these disorders should proceed only after the diagnosis of heatstroke is ruled out. Markedly elevated levels of AST, ALT, and LDH may help in differential diagnosis.[123] However, the clinician should bear in mind that elevation of these enzymes may not occur for 24 to 48 hours after heat injury.[214] Complications.
Observed complications of heatstroke reflect the results of both direct thermal injury and cardiovascular collapse. Autopsy of persons with EHS showed multiple hemorrhages, congestion, and cellular degeneration in most or all of the organs examined.[216] In EHS in particular, rhabdomyolysis is usually present.[137] A brief overview of the specific pathology found should provide a framework for discussion
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of the therapeutic and supportive management of heatstroke. CENTRAL NERVOUS SYSTEM.
The brain is particularly susceptible to thermal injury. CNS dysfunction is directly related to the duration of hyperthermia and to circulatory failure. The underlying pathology observed on autopsy is brain edema and congestion, with petechial hemorrhage and neuronal degeneration.[150] Cerebrospinal fluid pressure and hematologic features are normal.[214] In Shibolet's study,[213] all patients presented with confusion or agitation or both and 72% had convulsions, but all eventually became comatose. Agitation, delirium, and hallucinations reflect CNS hyperirritability. Pupillary constriction was present in 66% of cases.[127] Seizures occur in approximately 50% of cases.[127] Decerebrate rigidity, oculogyric crisis, and opisthotonos may develop; other findings may include loss of rectal sphincter tone, loss of skeletal muscle tone, and hemiplegia. [214] Cerebellar findings of dysarthria and ataxia are common.
Complete recovery occurs in most cases. However, chronic disability may develop in the form of mental deficiency, dysarthria, ataxia, aphasia, and hemiparesis. CARDIOVASCULAR SYSTEM.
Hypotension does not always occur in heatstroke but is usually present in fatal or severe cases.[216] This hypotension, which may persist even after large volumes of fluid therapy along with vasopressors, is an ominous late feature of heatstroke and may reflect failure of compensatory vasoconstriction of mesenteric blood vessels. As vital organs are hypoperfused, shock develops. Left ventricular subendocardial hemorrhage and focal necrosis of cardiac muscle fibers are commonly found on autopsy.[150] [214] The extreme stress placed on the cardiovascular system of victims with heatstroke results in a universal finding of sinus tachycardia, often with rates exceeding 140 beats/min.[216] Pulse pressure is elevated in the face of low cardiac output (CO) and low diastolic blood pressure. [214] Electrocardiographic findings include ST segment and T wave abnormalities and conduction disturbances.[56] In microswine and monkeys, during heating, HR rose to a plateau shortly after heating and commenced to rise still further at Tc of 41° C (105.8° F), peaking a few minutes before death. Blood pressure was stable or even rose until HR peaked at Tc of 41° C and then declined until death.[90] PULMONARY SYSTEM.
Hyperventilation is a common finding, particularly in EHI. Persistent hyperventilation may lead to respiratory alkalosis and tetany. Coma or seizures may predispose to pulmonary aspiration with consequent lung injury.[214] Pulmonary edema may become severe or fatal; DIC may lead to adult respiratory distress syndrome.[72] Pulmonary infarctions have been found on autopsy.[150] RENAL SYSTEM.
Acute renal failure develops in approximately 25% of heatstroke victims.[133] Hypotension and resultant decreased renal blood flow constitute the primary underlying etiology. As in the CNS, thermal injury may cause direct cellular damage.[202] DIC and myoglobinuria exacerbate the insult to renal tissue. Hematuria, pyuria, proteinuria, and hyaline and granular casts are seen on urinalysis. Eventually, oliguria and anuria may develop. HEPATIC SYSTEM.
Within 12 to 24 hours after heatstroke collapse, elevated AST, ALT, and serum bilirubin levels can be detected.[125] Levels of AST greater than 1000 U/ml are commonly seen in severe heatstroke.[233] Prothrombin level reaches its nadir 48 to 72 hours after heat injury.[201] Cholestasis and hepatocellular necrosis may develop. GASTROINTESTINAL SYSTEM.
Vomiting and diarrhea are common symptoms of heatstroke. Compensatory mesenteric vascular constriction may produce localized areas of gut ischemia and mucosal injury with consequent breakdown of its permeability barrier and translocation of LPS into the circulation.[93] Direct thermal damage to the gut wall may also contribute to gut wall pathophysiology. As previously discussed, the subsequent increase in serum LPS and its role as inducer of potentially damaging cytokines may play a critical part in both the morbidity and potential therapy of heatstroke. In the presence of DIC, hematemesis and melena may develop.[214] HEMATOLOGIC SYSTEM.
White blood cell counts may be elevated to as high as 20,000 to 30,000/ml. Platelet count is depressed, as are levels of clotting factors V and VIII. The commonly seen bleeding diathesis may be manifested as conjunctival hemorrhage, melena, purpura, or hematuria.[214] The primary causes of this coagulopathy are believed to be release of thromboplastic substances secondary to endothelial damage, and endotoxemia resulting in intravascular thrombosis and secondary fibrinolysis.[213] Other contributing factors include direct inactivation of clotting factors by thermal injury, decreased hepatic production of clotting factors, and decreased production of platelets secondary to thermal injury to marrow megakaryocytes. Low levels of fibrinogen and elevated levels of fibrin split products, in the presence of thrombocytopenia, herald the onset of DIC. Clotting abnormalities most often peak 18 to 36 hours after acute heat injury.[213] ACID-BASE AND ELECTROLYTE ABNORMALITIES.
Early in the course of heatstroke, respiratory alkalosis secondary to hyperventilation may be present. As anaerobic or even aerobic glycolysis increases, serum lactate levels rise, generating metabolic acidosis.
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Hypernatremia reflects associated dehydration common in heatstroke; however, Na+ levels may appear normal. In the face of dietary deficiency of Na+ or profuse sweat losses, initial normonatremia may develop into hyponatremia upon rehydration. Potassium levels may be low or elevated, with hyperkalemia associated with tissue damage and renal compromise. Hypocalcemia, hypomagnesemia, and hypophosphatemia may also occur. Although hypoglycemia may develop in cases of EHS, hyperglycemia secondary to elevated catecholamine release may also be seen.
ON-SITE EMERGENCY MEDICAL TREATMENT Heatstroke is a medical emergency. Rapid reduction of elevated body temperature is the keystone of management of heatstroke; duration of hyperthermia may be the primary determinant of outcome.[133] [216] Nevertheless, it is important to follow the ABCs of stabilization while cooling efforts are initiated. See Box 11-2 for basic first aid. Early diagnosis of heat exhaustion can be vital. Early warning signs include flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion.[71] Pitfalls in the diagnosis of heat illness include confusion, preventing self-diagnosis.[71] Mainstays of therapy include emergency on-site cooling, intravenous (IV) fluids, treating hypoglycemia as needed, IV diazepam for seizures or severe cramping or shivering, and hospitalization if response to therapy is slow or atypical.[71] [138] Cooling should be energetically initiated immediately upon collapse and minimally delayed only for vital resuscitation measures in order to prevent or minimize expected complications. In the field, the sick individual should be placed in the shade and any restrictive clothing removed. The victim's skin should be kept wet by applying large quantities of tap water or water from any source and his or her body constantly fanned. However, it is of utmost importance that these measures do not 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 hypoxia commonly associated with aspiration, pulmonary hemorrhage, pulmonary infarction, pneumonitis, or pulmonary edema.[72] [150] Positive-pressure ventilation is indicated if hypoxia persists despite supplemental oxygen administration (Figure 11-1 (Figure Not Available) ). As discussed previously, resuscitative measures may rapidly lower body temperature. Monitoring and recording rectal temperature 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 evaluation before fluid infusion.
Box 11-2. BASIC FIRST AID FOR HEAT ILLNESSES 1. 2. 3. 4. 5. 6.
Place the victim in the shade. Remove restrictive clothing. Apply large amount of water on the victim and keep his or her skin wet. Improvise a fan and cool the victim. Measure rectal temperature to confirm diagnosis. Evacuate to the nearest medical facility.
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 begun. Recommendations regarding the rate of administration of fluids vary. Some authors advise a rate of 1200 ml over 4 hours,[180] but we consider this to be too conservative. Others encourage a 2-L bolus over the first hour and an additional liter of fluid per hour for the next 3 hours.[210] However, vigorous fluid resuscitation may precipitate the development of pulmonary edema, so careful monitoring is indicated. Ideally, 1 to 2 L of fluid should be administered during the first hour after collapse and additional fluids administered according to the level of hydration.[76] 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, skin temperature may decrease enough to cause shivering. IV administration of chlorpromazine (50 mg)[124] or diazepam are effective to suppress shivering and prevent an additional rise in body temperature from metabolic heat production. Cooling Methods Much debate exists in the literature regarding the best approach to cooling heatstroke victims.[46] [55] [102] [219] [239] 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. Khogali and co-workers[239] developed a body cooling unit designed to maximize evaporative cooling by maintaining cutaneous vasodilation and minimizing
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Figure 11-1 (Figure Not Available) Flow chart for on-site emergency medical treatment of exertional heat illnesses. DD, Differential diagnosis. (Modified from Shapiro Y, Seidman DS: Med Sci Sports Exerc 22:6, 1990).
shivering. The patient is suspended on a net and sprayed from all sides with water at 15° C (59° F). Warm air (45° to 48° C [113° to 118.4° F]) 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 ice water 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, the increased thermal conductivity of water results in reduction of Tc to less than 39° C (102.2° F) in 10 to 40 minutes.[56] 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 a similar rate of cooling of 0.13° C/min.[180] Cold water immersion is less uncomfortable for the victim than immersion in ice water. In hundreds of EHS victims in a military population, there were no fatalities or permanent sequelae after treatment with ice water immersion.[55] [56] [179] Although other cooling methods reduce the rate of mortality, none has been as successful as ice water-soaked sheets or immersion. [89]
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In discussing an alternative cooling method, Khogali[128] [239] 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. • Access to the patient for monitoring of vital signs or administration of cardiopulmonary resuscitation is more difficult. • There is difficulty maintaining sanitary conditions should vomiting or diarrhea develop.
Although the first two criticisms may appear physiologically appropriate, review of the medical literature fails to provide documentation for a rise in body temperature following ice water immersion or shivering as a problem.[56] In fact, vascular resistance decreased during ice bath cooling and persisted until normothermia.[180] This is an expected observation. The hypothalamic set point for temperature regulation is not raised during heatstroke (unlike during febrile illness), and brain temperature accounts for approximately 90% of the thermoregulatory response, compared with the skin's 10%.[196] The shivering response should only occur if body temperature is allowed to fall below normal. When shivering occurred, chlorpromazine treatment (25 to 50 mg intravenously) was effective.[117] Heatstroke victims rarely require cardiopulmonary resuscitation, so this concern should not preclude the 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 core temperature 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.[89] The tub should be deep enough for submersion of the neck and torso.[188] Rapidly falling core temperature may not be accurately reflected by measured rectal temperature,[44] so with any cooling technique, active cooling should be discontinued when core body temperature falls to 39° C to prevent inducing hypothermia. 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, in treating elderly classic heatstroke patients, a case-by-case judgment call should be made deciding whether the risk of a theoretic, but never-shown, harmful stress by ice water treatment is worth 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 in 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, since absorption of alcohol may lead to poisoning and coma.
HOSPITAL EMERGENCY MEDICAL TREATMENT If airway control has not been previously established, a cuffed endotracheal tube should be inserted to protect against aspiration of oral secretions (Figure 11-2 (Figure Not Available) ). Supplemental oxygen and, when necessary, positive-pressure ventilation should be provided. Temperature should be continually monitored (at 5-minute intervals) by 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 room, IV fluid should be administered to EHS victims as a bolus of 1 L. Additional fluid should be based on the clinical situation after laboratory results are obtained 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).[180] Patients with a low cardiac index, low central venous pressure, hypotension, and low pulmonary capillary wedge pressure should receive fluid.
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Figure 11-2 (Figure Not Available) Flow chart for hospital medical treatment of exertional heat illnesses. (Modified from Shapiro Y, Seidman DS: Med Sci Sports Exerc 22:6, 1990.)
Cardiac monitoring should be maintained during at least the first 24 hours of hospitalization. Use of norepinephrine and other a-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 urinary 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).[210] Early dialysis should be considered 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 both hypoglycemia and hyperglycemia may occur after heatstroke.[205] Oral and gastric secretions are evacuated via nasogastric tube connected to continuous low suction. Although
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antacids and histamine H2 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.[214] 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, and/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. The peak levels are seen 36 to 72 hours after collapse. These high levels may last for several days.[76] [159] [216] Muscle damage is displayed primarily by marked elevation of serum CPK activity levels, which peak 24 to 48 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 interventions (e.g., liver transplant) are rarely necessary. Prognosis Rapid reduction of body temperature, control of seizures, proper rehydration, and prompt evacuation to an emergency medical facility currently result in a 90% survival rate in heatstroke victims, with morbidity directly related to duration of hyperthermia.[209] A poor prognosis is associated with Tc greater than 41° C (105.8° F), prolonged duration of hyperthermia, hyperkalemia, acute renal failure, and elevated serum levels of liver enzymes. Full recovery without evidence of neurologic impairment has been achieved even after coma of 24 hours' duration and subsequent seizures.[216] The persistence of coma after return to normothermia is a poor prognostic sign. [214] In a few victims, some neurologic deficits may persist, but usually for a limited period of 12 to 24 months, and only rarely for a longer period.[5] However, one recent study of classic heatstroke reported that 33% of patients left the hospital with some neurologic impairment.[63] Dantrolene Dantrolene has been used very successfully in the treatment of several hypercatabolic syndromes, such as malignant hyperthermia, neuroleptic malignant syndrome, and other conditions characterized by muscular rigidity or spasticity. [224] [236] Dantrolene stabilizes the Ca2+ release channel in muscle cells, reducing the amount of Ca2+ released from the cellular calcium stores. This lowers intracellular Ca2+ concentrations, muscle metabolic activity, and muscle tone, and thus heat production.[40] [175] In some studies, dantrolene was claimed effective in treating heatstroke, whereas in others it neither improved the rate of cooling nor improved survival.[38] [64] [148] [228] In six rhabdomyolysis patients, intramuscular Ca2+ concentrations were 11 times higher than in controls and dantrolene successfully lowered this elevated Ca2+ .[145] 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. [30] [112] [141] [184] Recently, Moran et al[164] 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. [245] Prevention Prevention of heat illness relies upon 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 are 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 psychologic 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 Risk Factors Any underlying condition that causes dehydration or increased heat production, or decreased dissipation of heat, interferes with normal thermoregulatory mechanisms and predisposes an individual to heat injury. Older individuals are less heat tolerant than are younger persons to EHI and 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 (BFsk ). 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 other
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fiber types.[115] In principle, since women have a thicker subcutaneous fat layer and a Tc 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.[183A] [223A] BMR-to-surface area ratios of children are higher than those of 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.[113] 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, cardiovascular disease, and lack of acclimation all limit the cardiovascular response to heat stress. Obesity places an individual at risk from reduced CO, increased energy cost of moving extra mass, increased thermal insulation, and altered distribution of heat-activated sweat glands.[161] The elderly 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, 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 major risk factors for heatstroke in the general population.[131] 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.[15] [36] [112] [230] 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 also use other pathogenic weight control measures, such as self-induced vomiting, laxatives and diuretics, and exposure to heat (saunas and hot tubs or "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.[60] Box 11-3 highlights some of the 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.[16] 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
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conditioning, acclimation to heat stress, and attention to hydration.
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
DRUGS THAT DECREASE SWEATING Antihistamines (diphenhydramine) Anticholinergics Phenothiazines Benztropine mesylate
Clothing.
Different regions of the body are not equivalent in their sweat production.[111] 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 maximum 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 will also permit more effective heat dissipation is indicated. 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. Modification of physical activity should not be based solely on any individual parameter of Tamb , wet bulb temperature or relative humidity (RH), or solar radiation, since all of these contribute to heat load. The wet bulb globe temperature (WBGT) is an index of heat stress that incorporates all three factors. This value may be calculated ( Table 11-2 ) or obtained directly from portable heat stress monitors that measure all three parameters simultaneously and compute the WBGT. Alternatively, the heat index may be obtained from national weather stations. Current recommendations for prevention of thermal injuries during distance running from the American College of Sports Medicine (ACSM) are based on WBGT.[10] 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."[10] 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 minimize heat illnesses, calculations indicate that CFT should not be undertaken when the end WBGT is expected to be greater than 25° C (77° F).[33] 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 early morning. Recently, Montain et al[157] updated the replacement guidelines for warm weather training ( Table 11-4 ). It is TABLE 11-2 -- Wet Bulb Globe Temperature (WBGT) Heat Index TEMPERATURE (° F)
EXAMPLE
Wet bulb × 0.7 =
78 × 0.7 = 54.6
Dry bulb × 0.1 =
80 × 0.1 = 8.0
Black globe × 0.2 =
100 × 0.2 = 20.0
HEAT INDEX
82.6
Wet bulb reflects humidity. Dry bulb reflects ambient air temperature. Black globe reflects radiant heat load. Alternative equation: WBGT = (.567) Dry bulb temperature + (393) Environmental water vapor pressure + 3.94.
TABLE 11-3 -- Modification of Sports Activity Using Wet Bulb Globe Temperature INDEX (° F)
LIMITATION
Emax , it is "uncompensable." At an uncompensable heat load, minor levels of hypohydration impair exercise tolerance, even at lower metabolic rates. The impairment becomes evident as the duration of the exercise increases at lower metabolic rates. Hypohydration decreases PV and increases plasma osmolality and inhibits peripheral blood flow and the sweating response, resulting in increased rate of rise in Tc . The effects of hypohydration on heat strain are well documented. The new physiologic strain index (PSI) showed high correlation between strain and losses of
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body mass through sweating[160] [161] [163] (see Chapter 10 ). However, the effects on skeletal muscle performance and metabolism are less well known.[154] [198] [199] [201] Some studies indicated that hypohydration reduces muscle endurance,[27] [77] [165] whereas others found no difference.[4] [79] [114] Recently, Montain et al[157] reported that moderate hypohydration (4% body mass) decreased skeletal muscle performance by 15%. This disagreement with previous studies was explained by inadequate control of prior exercise, heat exposure, and caloric intake in previous studies.[157] Physiologic Consequences of Hypohydration.
Hyperosmolality per se, even without a fall in blood volume, increases the threshold temperatures for onset of skin vasodilation and sweating during exercise in the heat.[57] These effects may be neurally mediated, since preoptic anterior hypothalamic neurons are osmosensitive.[218] Moreover, hypovolemia reduces the rate of sweating during exercise in the heat. [80] [201] Decreased PV as a result of lost water and salt, concomitant with increased distribution of blood volume to skin vascular beds, can reduce venous return, central venous pressure,
Figure 11-3 Decrements of cardiac performance with 3% and 5% body weight loss. (From Montain SJ et al: Int J Sports Med 19:87–91, 1998.)
cardiac filling pressure, stroke volume, and CO.[132] [173] This would be followed by compensatory increases in HR[158] ( Figure 11-3 ). In addition, increases in plasma hematocrit and viscosity further reduce cardiac filling pressure as a result of increased resistance. In one series of patients with EHS,[213] 35% were hypotensive with systolic blood pressure below 90 torr. Similar findings have been reported for classic heatstroke.[103] Sinus tachycardia in response to excessive circulatory requirements is consistently present in heatstroke victims.[210] CO and diastolic blood pressure are low, while pulse pressure is high.[214] Depending on the degree of hypoperfusion of vital organs, shock may ensue.[133] Hypohydration compromises thermoregulation,[214] with linear increases in Tc of about 0.15° C (0.27° F) for each 1% decrease in body mass during exercise in the heat.[201] Additionally, hypohydration negates most of the thermoregulatory advantages conferred by high aerobic fitness and heat acclimatization,[35] increasing the risk of heat illness.[214] Sawka et al[199] reported that exhaustion from heat strain occurred at higher Tre for euhydrated than for hypohydrated subjects during uncompensable exercise heat stress.
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Some athletes use diuretics to reduce body weight to compete in a lower weight category. Diuretics increase the rate of urine formation and generally result in loss of solute and volume.[238] Relatively less intracellular water (approximately 65% of total body fluid) is lost after using diuretics because there is no excess of extracellular solute to stimulate redistribution of body water. Unlike either exercise or heat-induced hypohydration, diuretic-induced hypohydration generally results in isoosmotic hypovolemia, since there is a greater ratio of plasma loss to body water loss.[116] Among the common diuretics in use are thiazide, furosemide, and carbonic anhydrase inhibitors. Hyperhydration It had been hypothesized that consuming excess water before activity would improve performance during heat stress by expanding blood volume and reducing blood osmolality, thereby reducing cardiovascular and thermal strain during exercise. [86] [197] Earlier studies[105] [149] [167] [176] suggested that hyperhydration lowered HR and Tc compared with euhydration. Hyperhydration is usually achieved by drinking water in excess but can also be achieved by ingesting glycerol, since glycerol reduces free water clearance through the kidneys, thereby increasing retention of fluid.[86] In one study, glycerol/water ingestion improved thermoregulation during exercise heat stress.[149] The rise in Tre was attenuated by 0.7° C (1.26° F) and the sweat rate was elevated by ~300 to 400 ml/hr above control levels. More recently, Latzka et al[142] [143] studied hyperhydration induced by drinking either water or a water/glycerol mixture during compensable and uncompensable exercise heat stress. Surprisingly, compared with euhydration, hyperhydration did not alter Tc , Tsk , whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or HR responses. Furthermore, there were no differences in physiologic variables between those achieving hyperhydration with water or by water/glycerol. These data demonstrate that hyperhydration provides no thermoregulatory or cardiovascular advantages over the maintenance of euhydration during compensable or uncompensable exercise heat stress. Exercise and heat stress each reduce renal blood flow and free water clearance. Therefore the effectiveness of glycerol relative to water as a hyperhydrating agent may be masked. Latzka et al[143] concluded that hyperhydration per se only provides an advantage (over euhydration) in delaying hypohydration during either compensable or uncompensable exercise heat stress. Furthermore, glycerol ingestion caused nausea and headaches on several occasions. The reasons for the conflicting results with previous studies are uncertain but may be due to differences in experimental design. For example, Latzka et al carefully controlled for the initial baseline hydration status for both treatments, whereas earlier studies did not address this important independent variable.
Hyponatremia.
Symptomatic hyponatremia is diagnosed when serum Na+ is less than 130 mEq/L and is generally caused by hypervolemia secondary to drinking large volumes of water or markedly hypoosmotic fluids. This illness has been reported in psychiatric patients and in cases of water overload. However, nonpsychiatric cases are usually associated with enforced water drinking to prevent EHI or with being "too conscientious" in drinking at water stations during a marathon run. There have been several cases of hyponatremia from excessive fluid intake during prolonged exertion in the heat, especially in events such as ultramarathons, triathlons, and recreational hiking, as well as in military training.[23] [68] [87] Hyponatremia subsequent to water overload is potentially a cause of fatal cerebral and pulmonary edema.[92] [178] During the development of hyponatremia, ingested water is absorbed from the gut lumen, diluted blood circulates to the brain, and water enters relatively hypertonic brain tissue by osmosis. Since the brain is enclosed by bone, it cannot swell and intracranial pressure increases. This essentially "squeezes" the cerebrovascular system, reducing intracranial blood flow and occasionally leading to ischemic damage and regulatory collapse. Immediate medical treatment is required. In the U.S. Army, 125 cases of documented hypoosmolality/hyponatremia were reported over a 7-year epidemiologic study.[67] Many of these cases were associated with excessive water intakes relative to sweat loss, with average serum Na+ of 121 mEq/L (116 to 133 mEq/L). Such low serum Na+ values imply that total body water increased by 3 to 5 L.[155] As a result of this report, Montain et al [155] recently revised the U.S. Army fluid replacement guidelines, emphasizing on one hand the need for sufficient fluid replacement during heat stress, while on the other, concern for the danger of overhydration and water intoxication. To achieve an accurate guideline for fluid replacement during heat stress, a two-phase study was carried out by Shapiro et al,[208] who developed a computer model to predict sweating loss (m?sw ) during different exercise intensities, followed by validation in a laboratory study. The fluid replacement guidelines presented in Table 11-4 were designed to be a simple and practical tool. These recommendations specify an upper limit for hourly and daily water intake, which safeguards against overdrinking and water intoxication. TREATMENT OF HYPONATREMIA.
It is critical to differentiate between water intoxication and heat exhaustion/heatstroke because the treatments are very different. In the field, discriminating between hyponatremia and
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certain heat illnesses may be difficult because of considerable overlap of symptoms. [92] A major difference between water intoxication and heat illnesses would probably be in Tc . In heat illnesses, Tc is generally greater than 39° C (102.2° F), whereas in hyponatremia, Tc is usually normal or close to normal.[23] [92] Heat illnesses are treated by cooling and sufficient rehydration, whereas hyponatremia is treated by restricting fluids and gradually correcting Na+ concentration by infusion of hypertonic NaCl solution. Too rapid a correction of hyponatremia can cause the demyelinating syndrome known as pontine myelinolysis. Rehydration Optimal performance is attainable only with sufficient drinking during exercise to minimize dehydration. It is beyond dispute that even low levels of dehydration (1% loss of body mass) impair cardiovascular and thermoregulatory responses and reduce capacity for exercise.[171] Fluid replacement reduces the risk of heat illness and improves exercise performance by preventing or reducing dehydration. Consuming fluids in amounts directly proportional to sweat loss maintains optimal physiologic functions and significantly improves exercise performance, even with exercise lasting 1 hour. However, it is recommended that ingested fluid be cooler than Tamb (15° to 25° C [59° to 72° F]) and flavored to enhance palatability and promote fluid replacement. [11] Once heat injury has progressed to the point of heatstroke, IV replacement of fluid losses is required. Normal saline solution is the initial IV fluid of choice, providing excellent expansion of intravascular volume without risking too rapid a correction of undiagnosed hyponatremia. The rate of fluid administration should reflect preexisting or coexisting medical conditions. An initial rate of 1200 ml over 4 hours has been proposed.[180] Supplemental potassium should be withheld until serum electrolyte levels are known. This is important because some commercial beverages previously ingested by the victim contain additional K+ . Future choice of fluids should reflect the individual's electrolyte status and cardiac and renal function. Recommendations for maintaining oral hydration (or, more accurately, minimizing dehydration) are presented in the Prevention section. The inability to rely on the thirst mechanism to prevent dehydration cannot be overemphasized. Simple provision of fluids at the sideline during athletic practices and competitions and military training scenarios is not sufficient. Scheduled breaks in activity (every 20 to 30 minutes depending on the degree of heat stress) for required consumption of fluids should become more commonplace. Rehydration with and without Acclimatization.
Sweating and normal thermoregulation have another impact on the predisposition to clinical states that is widely unappreciated by trainers, coaches, and team physicians. In unacclimatized individuals, sweat salt losses can theoretically produce solute deficits having a profound impact on thirst and therefore on potential rehydration rates. On average, 60% of body mass is water, so that a 70-kg adult contains 0.6 × 70 kg = 42 L of total body water (TBW). If he now loses 6% of body mass by hypothetically sweating pure water, then he has lost a volume of 0.06 × 70 kg = 4.2 L, or (4.2 L/42 L) = 10% of TBW. Thus TBW has been reduced by 4.2 L to 37.8 L. Since, in this example, all salts are retained within the body, plasma Na+ rises in proportion to the ratio of euhydrated volume to the new dehydrated volume, (42 L ÷ 37.8 L) × 140 mEq/L; Na+ has risen to 155 mEq/L, (assuming two osmotically active particles per NaCl molecule) and 310 mOsm/L. If, however, that same sweat volume contained NaCl at a concentration of half the normal euhydrated value (0.5 × 140 mEq/L = 70 mEq/L), then there was a sweat loss of 70 mEq/L × 4.2 L = 294 mEq Na+ , as well as the 4.2 L of water. Since the normal euhydrated plasma Na+ concentration is 140 mEq/L, crude calculations indicate that the total amount of Na+ present is 42 L × 140 mEq/L = 5880 mEq. To calculate the crude final Na+ concentration, the original total amount of Na+ must be reduced (5880 - 294 mEq = 5586 mEq) by the 294 mEq lost in sweat, and therefore the final Na+ concentration (5586 mEq ÷ 37.8 L) becomes 148 mEq/L and 296 mOsm/L. This is high enough to reach the thirst threshold (295 mOsm), so the person feels moderately thirsty and will "desire" to consume only 80 ml of water (vs. 1270 ml; see later discussion) before osmolality is reduced to the thirst threshold. This represents only 1.9% (80 ml/4200 ml × 100) deficit of the water. Consumption of a solute-rich meal or a fluid-replacement beverage about 2 hours before exercise potentially counteracts the salt loss in sweat of a nonacclimatized individual. This probably also explains, by and large, why water balance is often not fully restored until mealtime in sweating, nonacclimatized individuals. Another clinically and physiologically relevant aspect of this calculation should be emphasized. It is generally appreciated that fully acclimatized subjects, compared with nonacclimatized ones, sweat sooner (at lower Tc and Tsk ), with lower sweat salt concentration and in larger volume. That is, acclimated persons sweat more and require larger volumes of replacement fluids than do unacclimatized ones for the same activity. If this sweat were to contain a Na+ concentration as low as 0.17% NaCl, the solute loss would be reduced to 235 mOsm, compared with 588 mOsm (see earlier discussion). The dehydrated plasma osmolality would be 305 mOsm/kg, and the thirsty subject would have to consume 1270 ml (a sixteenfold increase) to lower the
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osmolality to the thirst threshold (30.2% of the water deficit vs. 1.9% above). Although this theoretically important aspect of acclimation on thirst and rehydration volumes has not been experimentally verified, it could significantly improve resistance to heat illness by maintaining more adequate body water stores. Fluid Replacement Beverages.
A more widely investigated and hotly debated topic is appropriate fluid replacement during physical activity in the heat. Confusion has arisen over a need for replacing electrolyte losses, as well as the advantages of carbohydrate supplementation. The benefits of fluid replacement with electrolyte-carbohydrate-containing beverages vs. water was studied in athletes with 1.9% and 3.5% electrolyte losses. [241] No significant difference was found in the maintenance of PV between trials with water and the experimental formulations. During intense exercise lasting longer than 1 hour, the ACSM guidelines for exercise and fluid replacement recommend that
carbohydrates be ingested at the rate of 30 to 60 g/hr to maintain oxidation of carbohydrates and delay fatigue.[11] Early investigators promoted consumption of Na+ -containing fluid to prevent development of hyponatremia during exercise. The rehydration effectiveness of three commercial sports drinks was compared during 4 hours of physical activity. [118] The beverages consisted of prepared solutions containing component individual minerals and glucose. All solutions proved equally effective in maintaining water and electrolyte balance during moderate physical performance. A benefit of ingesting commercial sports drinks appears to be enhanced palatability that increases voluntary fluid consumption, thereby reducing dehydration.[170] The rate of rehydrating various body compartments depends on the rates of gastric emptying of ingested fluid and the intestinal absorption of water. Gastric emptying is the slower rate-limiting step and depends principally on osmolality and caloric content of the fluid.[74] Which factor predominates depends on physical activity and the temperature and volume of the beverage. Earlier studies suggested that there was a delay in gastric emptying and increased rehydration time when the beverage contained more than 2.5% glucose, sucrose, or fructose. However, more recent studies have reported that there is in fact little or no difference in gastric emptying rates between water and carbohydrate solutions as high as 7%.[62] [203] Other investigators have confirmed that under exercise conditions, 5% glucose polymer solutions show a gastric emptying rate similar to water. A frequent argument for including Na+ in fluid replacement beverages is to enhance intestinal water absorption, since Na+ transport is the major determinant of water absorption in the proximal small bowel. Active coupled transport of Na+ and glucose creates an osmotic gradient that pulls water from the lumen into epithelial cells. However, the rate of intestinal absorption of carbohydrate-electrolyte solutions is equal to, but not faster than, absorption of water.[170] [240] Cold fluids increase the motility of smooth muscles in the gastric wall, thereby speeding gastric emptying more rapidly than do warm drinks. The commonly held belief that consumption of cold water results in stomach cramps has not been confirmed. Such a phenomenon, if it occurs, is more likely related to the volume of the beverage than to its temperature.[50] Gastric emptying is speeded by stretching the gastric wall. Therefore large volumes of liquid empty from the stomach more rapidly than do small quantities. Athletes, however, are uncomfortable exercising with a nearly full stomach. Indeed, although there may be a benefit to rapid oral rehydration, if the nausea threshold is reached, a secondary increase in ADH secretion may impair the kidneys' ability to excrete excess fluid volume and result in hyponatremia and water intoxication. [19] By drinking smaller volumes (150 to 250 ml) at 15- to 20-minute intervals, athletes can maintain adequate hydration while minimizing gastric distension. A sports drink should contain 5% to 10% carbohydrate in the form of glucose or sucrose to enhance endurance.[58] However, many athletes suffer cramps, nausea, and diarrhea after drinking a 10% glucose solution. An isocaloric glucose-polymer solution has only one fifth the osmotic pressure. Its lower osmolality allows an increase in the carbohydrate content of a sports drink without risking the gastrointestinal side effects of a high osmolar drink. Several commercial polymer solutions are available. Carbohydrate feeding during prolonged exercise enhances performance, whether assessed by time to exhaustion or by time to complete a predetermined exercise task.[45] [170] Glucose polymer solutions given before and during a soccer game sustained blood glucose concentration and improved performance, although no difference in perceived exertion was found.[212] However, dehydrated soldiers who ingested fluids during exercise in the heat reduced their strain and the intensity of perceived exertion.[169] Whether use of these beverages spares muscle glycogen is a matter of current debate. A potential problem in using carbohydrate-rich beverages is that they may attract bees and yellow jackets into the vicinity of the athletes, placing them at risk for sting-induced allergic or anaphylactic reactions. Under normal conditions, use of electrolyte-carbohydrate-containing beverages offers little advantage over water in maintaining PV or electrolyte concentration or in improving intestinal absorption. Consumption of an electrolyte-containing beverage may be indicated under conditions of caloric restriction, prolonged exercise, or repeated days of sustained sweat losses. Drinking carbohydrate solutions during prolonged exercise
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may enhance performance; athletes who might benefit are those involved in soccer, field hockey, rugby, and tennis. For these athletes, use of glucose polymer solutions may be considered. Under no circumstances should carbohydrate-containing beverages be placed into canteens, since microbial contamination would be unavoidable and subsequent sterilization required. For the vast majority of individuals, however, the primary advantage of using electrolyte- or carbohydrate-containing drinks appears to enhance voluntary consumption. This factor should not be considered insignificant if regulated intake is impossible.
ACKNOWLEDGMENTS
This chapter is in part a revision of Gaffin SL, Hubbard RW, Squires DL: Heat-related illnesses. In Auerbach P, editor: Wilderness medicine, St Louis, 1995, Mosby, pp 167–212. The original contribution by Drs. Hubbard and Squire to this chapter is recognized. We thank Dr. Ralph Francesconi for his helpful suggestions and comments. The opinions or assertions contained herein are the private views of the authors and should not be construed as official or reflecting the views of the U.S. Army or Department of Defense. Citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement or approval of the products or services of these organizations.
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Part 3 - Fire, Burns, and Radiation
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Chapter 12 - Wildland Fires: Dangers and Survival Kathleen Mary Davis Robert W. Mutch
It is hard to know what to do with all the detail that rises out of fire. It rises out of a fire as thick as smoke and threatens to blot out everything. Some of it is true but doesn't make any difference. Some of it is just plain wrong. And some doesn't even exist, except in your mind, as you slowly discover long afterwards. Some of it, though, is true—and makes all the difference. Norman Maclean, Young Men and Fire, 1992
Describing the 13 fatalities in the Mann Gulch fire near Helena, Montana, in 1949, Norman Maclean wrote, "They were still so young they hadn't learned to count the odds and to sense they might owe the universe a tragedy." The Mann Gulch fire has been called "the race that couldn't be won."[27] Although the crew increased their pace ahead of the fire, the fire accelerated faster than they did until fire and people converged at the end of a race the firefighters could not win. Miraculously, three persons survived the fire. The foreman ignited an escape fire into which he tried to move the crew; two of the smoke jumpers found a route to safety. Many improvements in a person's odds of surviving an encounter with a wildland fire have occurred since 1949. These advances include improved understanding of fire behavior, increased emphasis on fire safety and fire training, and development of personal protective equipment. However, as events such as the Colorado fires of 1994 showed, tragedies continue to occur. Whether the Mann Gulch fire, the 1871 Peshtigo fire in Wisconsin that killed 1150 people, the Great Idaho fire of 1910 that left 85 dead ( Figure 12-1 ), the 1947 Maine fires that produced 16 victims, or the 1991 Oakland fire that killed 25 people, wildland fires are as much a threat to human life, property, and natural resources on the North American continent as are hurricanes, tornadoes, floods, and earthquakes. This chapter describes the current look of this historical force and discusses new federal fire management policies, the nature and scope of wildland fire hazards, behavior of fires, typical injuries, summary of fatalities (1990–1998), and survival techniques.
WILDLAND FIRE MANAGEMENT AND TECHNOLOGY Programs for dealing with the overall spectrum of fire are collectively termed fire management.[1] They are based on the concept that fire and the complex interrelated factors that influence fire phenomena can and should be managed. The scientifically sound fire management programs that respond to the needs of people and natural environments must also maintain full respect for the power of fire.[1] Since the early 1900s, federal, state, and local fire protection agencies have routinely extinguished wildland fires to protect watershed, range, and timber values, as well as human lives and property. Fire detection, fire danger rating systems, and fire suppression methods have been developed by fire science laboratories and two equipment development centers maintained by the U.S. Department of Agriculture (USDA) Forest Service. Patrol planes, some with infrared heat scanners, and other aircraft can deliver firefighters, equipment, and fire-retarding chemicals to the most remote fire. These firefighting resources are organized under an Incident Command System that can easily manage simple to complex operational, logistical, planning, and fiscal functions associated with wildfire suppression actions.[3] Modern fire suppression technology, however, cannot indefinitely reduce the number of hectares burned, as demonstrated by several large fires in recent years: the Greater Yellowstone Area fires in 1988; Mack Lake fire in Michigan in 1980; Foothills fire near Boise, Idaho, in 1992; Silver Complex in Oregon in 1987; and Stanislaus Complex in California in 1989. The hard lesson learned from these fires and others is that wildfires are inevitable. Several factors have coincided to produce massive forest mortality, including drought, epidemic levels of insects and diseases,[21] and unnatural accumulations of fuels as a result of fire exclusion. Many agencies are now using prescribed fire more frequently, deliberately burning under predetermined conditions to reduce accumulations of fuels and to protect human life and property. Research has indicated that fires are not categorically bad. In fact, many plant communities in North America are highly flammable during certain periods in their life cycles. For example, annual grasses, ponderosa pine, and chaparral plant communities are flammable almost every dry season. Other communities, such as jack pine or lodgepole pine forests, although fire resistant during much of their life cycle, eventually become fire prone when killed by insects, diseases, and other natural causes. The spread of nonnative grasses, such as cheat-grass and red brome, in the arid West has increased the frequency of fires in desert shrublands. Wildland fires can benefit plant and animal communities. Evolutionary development produces plant species
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Figure 12-1 Burned ruins of the foundry in Wallace, Idaho, furnish mute testimony to the destructive force of the 1910 fires. The cottage on the terrace was the only one left standing in that part of town. (Courtesy the USDA Forest Service. Photo by R.H. McKay.)
well adapted to recurrent fires. Fire tends to recycle ecosystems and maintain diversity. [15] Thus there is growing consensus that fire should be returned to wildland ecosystems where appropriate to perpetuate desirable fire-adapted plant and animal communities and to reduce fuel accumulations. A landmark report in 1963 to the National Park Service by the Advisory Board on Wildlife Management[14] described how the western slope of the Sierra Nevada had been transformed by fire protection: When the forty-niners poured over the Sierra Nevada into California, those that kept diaries spoke almost to a man of the wide-spaced columns of mature trees that grew on the lower western slope in gigantic magnificence. Today much of the west slope is a dog-hair thicket of young pines, white fir, incense-cedar, and mature brush—a direct function of over- protection from natural ground fires. Not only is this accu- mulation of fuel dangerous to the giant sequoias and other mature trees, but the animal life is meager, wildflowers are sparse, and, to some at least, the vegetative tangle is depress- ing, not uplifting. The board recommended that the Park Service recognize in management programs the importance of the natural role of fire in shaping plant communities. Federal Wildland Fire Management Policy Recent tragedies in the West focused attention on the need to reduce hazardous fuel accumulations. The events of 1994 created a renewed awareness and concern among federal land management agencies about wildfire impacts, leading to a combined review of fire policies and programs. The result was the enactment of a new interagency federal wildland fire management policy, which provided a common approach to wildland fire among federal agencies and called for close cooperation with tribal, state, and other jurisdictions. [37] The principal points of the new federal wildland fire policies are as follows: 1. Firefighter and public safety remains the first priority in wildland fire management. Protection of natural and cultural resources and property is the second priority. 2. Wildland fire, as a critical natural process, must be reintroduced into the ecosystem, accomplished across agency boundaries, and based on the best available science. 3. Where wildland fire cannot be safely reintroduced because of hazardous fuel accumulations, pretreatment must be considered, particularly in the wildland-urban interface. 4. Wildland fire management decisions and resource management decisions are connected and based on approved plans. Agencies must be able to choose from the full spectrum of actions—from prompt suppression to allowing fire to have an ecologic function. 5. All aspects of wildland fire management will involve all partners and have compatible programs, activities, and processes. 6. The role of federal agencies in the wildland-urban interface includes firefighting, hazardous fuel reduction, cooperative prevention and education, and technical assistance. Ultimately, the primary responsibility rests at the state and local levels. 7. Structural fire protection in the wildland-urban interface is the responsibility of tribal, state, and local governments. 8. Federal agencies must better educate internal and external audiences about how and why we use and manage wildland fire. Prescribed Fire and Fire Use Prescribed fire, the intentional ignition of grass, shrub, or forest fuels for specific purposes according to predetermined conditions, is a recognized land management practice. The objectives of such burning vary: to reduce fire hazards after logging, expose mineral soil for seedbeds, regulate insects and diseases, perpetuate natural ecosystems, and improve range forage and wildlife habitat. In some areas managed by the National Park Service, USDA Forest Service, and Bureau of Land Management, naturally ignited fires may be allowed to burn according to approved prescriptions; fire management areas have been established in national parks and wildernesses from the Florida Everglades to the Sierra Nevada in California ( Figure 12-2 ). Visitors are increasingly aware that wildland fires can provide an important environment for the enjoyment of park and wilderness experiences.
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Figure 12-2 Some lightning fires in wildernesses and national parks are now allowed to burn under observation to perpetuate natural ecosystems. (Courtesy the USDA Forest Service.)
WILDLAND-URBAN INTERFACE: NEW LOOK OF A HISTORICAL PROBLEM Just as resource agencies are attempting to provide a more natural role for fire in wildland ecosystems, the general public is increasingly living and seeking recreation in many of these areas. However, past fire exclusion practices have allowed abnormal fuel accumulations, and this fact has combined with the sacrifice of relatively safe perimeter fire suppression strategies in favor of directly protecting people and their possessions.[42] Direct suppression actions within the fire's perimeter place firefighters at a greater disadvantage from a safety standpoint. The new interagency policy that emphasizes firefighter and public safety as the first priority will result in less effort to save structures in dangerous situations. What is known of fire behavior and fire survival principles must be readily available to emergency medical personnel, wildland dwellers, and recreationists. In fact, fire protection agencies have been making such information more available to the general public. Nature of the Problem Hot, dry, windy conditions annually produce high-intensity fires that threaten or burn homes where wildland and urban areas converge. Can the historical levels
Figure 12-3 These burned-over and wind-thrown trees resulted from the intense behavior of the 1910 forest fire near Falcon, Idaho. (Courtesy the USDA Forest Service. Photo by J.B. Halm.)
of destruction, injury, and fatality be repeated today in the face of modern fire suppression technology? The answer requires an analysis of the conditions that created high-intensity fire behavior in the forests of Idaho and Montana in 1910 ( Figure 12-3 ). The Peshtigo, Michigan, Hinckley, Yacoult, and Maine fires burned hundreds of thousands of hectares and killed more than 2000 people between 1871 and 1947. On October 8, 1871, the same day that fire wiped out the town of Peshtigo, Wisconsin, the great Chicago fire devastated urban Chicago. Comparative statistics for those two fires highlight the destructive potential of wildland fires. The Peshtigo fire covered 518,016 hectares (1,280,000 acres) and killed 1150 people, whereas 860 hectares (2124 acres) burned and 300 lives were lost as a result of the Chicago fire.[41] The 1910 wildland fires had several common elements: many uncontrolled fires burning at one time; prolonged drought, high temperatures, and moderate to strong winds; and mixed conifer and hardwood fuels with slash from logging and land clearing. These large fires occurred primarily in conifer forests north of the 42nd meridian, or roughly across the northern quarter of the contiguous United States.[2] One of these critical elements that is not as likely to occur today as formerly is the simultaneous presence of many uncontrolled fires. The effectiveness of modern fire suppression organizations reaches the most remote wildland
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locations. High-velocity winds and more than 1600 individual fires contributed to the spread of the 1910 fires; it is unlikely that a multifire situation of that magnitude would occur today. Prolonged drought, high winds, and flammable fuel types, however, remain significant to the behavior of high-intensity fires. Some of the fires most potentially damaging to human lives and property occur in areas rich in chaparral shrub fuel in California. Wilson[42] described the severe 1970 fire year in California, in which official estimates showed that 97% of 1260 fires occurring between September 15 and November 15 were held to less than 121 hectares (300 acres). The other 3% of the fires, fueled by a prolonged drought and fanned by strong Santa Ana winds, produced 14 deaths, destroyed 885 homes, and burned more than 242,820 hectares (600,000 acres). Ten years later the situation recurred over 28,330 hectares (70,000 acres) in southern California, resulting in the deaths of 5 persons and loss of more than 400 structures. More recently, on October 20, 1992, a devastating fire occurred in the hills above Oakland and Berkeley, California. Burning embers carried by high winds from the perimeter of a small fire resulted in a major wildland-urban interface conflagration that killed 25 people, including a police officer and a firefighter, injured 150 others, destroyed nearly 2449 single-family dwellings and 437 apartment and condominium units, burned over 648 hectares (1600 acres), and did an estimated $1.5 billion in damage.[23] The scenario for disaster included a 5-year drought that had dried out overgrown grass, shrubs, and trees, making them readily ignitable. Other factors included untreated wood shingles, unprotected wooden decks that projected out over steep terrain, low relative humidity, high temperatures, and strong winds that averaged 32 km per hour (20 mph) and gusted up to 56 to 80 km per hour (35 to 50 mph). These severe conditions produced a voracious fire that consumed 790 homes in the first hour. Winds lessened to 8 km per hour (5 mph) by the first evening, and firefighters had the situation under control by the fourth day, but not before they had an awful glimpse of what future fires will be. Wildland fires that threaten human lives and property are not exclusively located in southern California, since the exodus to wildland regions has become a national phenomenon. Fires burned more than 80,940 hectares (200,000 acres) in Maine in October 1947, killing 16 people; another 80,940 hectares (200,000 acres) burned in New Jersey in 1963. On July 16, 1977, the Pattee Canyon fire in Missoula, Montana, destroyed 6 homes and charred 486 hectares (1200 acres) of forests and grasslands in only a few hours.[7] Fires at the wildland-urban interface also have increased internationally. For example, the Ash Wednesday fire disaster in 1983 burned more than 340,000 hectares (840,000 acres) of urban, forested, and pastoral lands in Victoria and South Australia, killing 77 persons, injuring 3500 persons, and destroying 2528 homes.[36] A May 1987 wildfire in northern China added a new perspective regarding the devastating impact wildland fires may have on human lives, property, and natural resources. This fire reportedly burned over 404,700 hectares (1 million acres), killed almost 200 persons, seriously injured another 200, destroyed or damaged 12,000 houses, and forced nearly 60,000 people to evacuate their homes—clearly it was a disaster of major proportions. Protecting lives and property from wildfires at the wildland-urban interface presents one of the greatest challenges faced by wildfire protection agencies. Large forest fires around the world during the intense El Niño drought conditions of 1997–1998 focused public and media attention once again on the need to evaluate public policies and practices in the forestry and nonforestry sectors that directly or indirectly contribute to the impact of forest fires. The size and damage attributed to these fires was so immense that the Christian Science Monitor termed 1998 "the Year the Earth Caught Fire." At times that seemed to be literally true as smoke palls blanketed large regional areas, disrupting air and sea navigation and causing serious public health threats. Seventy people were killed in Mexico alone as a result of the fires, and ecosystems that generally are not subjected to fires, such as the Amazon rain forest and the cloud forest of Chiapas, Mexico, sustained considerable damage. A global fire conference sponsored by the Food and Agricultural Organization of the United Nations (October 1998) brought together specialists from 33 countries to review the serious nature of worldwide fires. Participants at the conference in Rome concluded that governments needed to enact more sustainable land use policies and practices to reduce the impacts of wildfires on people and natural resources. More recently, as of the end of September, 2000, nearly 7 million acres had been scorched by approximately 80,000 fires in the United States. It is becoming increasingly rare to have a wildland fire situation that does not involve people. However, people are not fully aware of the fire risks and hazards of living and traveling in or near wildlands. Risk, in the jargon of the wildland fire specialist, is the probability that a fire will occur. Hazard is the likelihood that a fire, once started, will cause unwanted results. Risk deals with causative agents; hazard deals with the fuel complex.[9] The results of two surveys indicated a general feeling of overconfidence by most residents toward the potential danger of forest fire. Eighty percent of Seeley Lake, Montana forest residents who were interviewed thought that the forest fire hazard was low to moderate in their area.[8] Seventy-five percent of Colorado residents interviewed thought that the forest fire hazard was low or moderate in mountain subdivisions of their state.[13] Forest fire hazards in these two areas were much
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higher than the public estimates. There is a growing need for the general public, emergency medical personnel, and fire suppression organizations to be well prepared to deal with wildland fire encounters ( Box 12-1 ).
Box 12-1. RECOMMENDATIONS TO REDUCE LOSS OF LIFE AND PROPERTY IN THE WILDLAND-URBAN INTERFACE
FIRE PROTECTION SERVICES Remember that firefighter and public safety is the first priority in every fire management activity. Ensure that all personnel receive regular cross-training in fighting wildfires and structural fires. In urban departments, in particular, recognize the need to extinguish fires in wildland fuels by using thorough mop-up procedures. Recognize the need for close coordination of response efforts among neighboring departments or agencies. Develop specific mutual aid plans for coordinating resources to attack fires in the wildland-urban interface. Schedule and conduct regular mutual aid training exercises. Regularly schedule and conduct fire prevention and fire preparedness education programs for the general public and homeowners. Conduct an assessment of fire risks and prepare a strategic plan to reduce these risks. Work effectively with lawmakers and other government officials to help prevent unsafe residential and business development.
LEGISLATORS Examine existing laws, regulations, and standards of other jurisdictions that are applicable for local use in mitigating hazards associated with wildland fires. Adopt National Fire Protection Association Standard 299 for the Protection of Life and Property from Wildfire. (The purpose of this standard is to provide criteria for fire agencies, land use planners, architects, developers, and local government for fire-safe development in areas that may be threatened by wildfire.) Provide strong building regulations that restrict untreated wood shingle roofs and other practices known to decrease the fire safety of a structure in the wildlands.
PLANNERS AND DEVELOPERS Create a map of potential problem areas based on fuel type and known fire behavior. Evaluate all existing or planned housing developments to determine relative wildland fire protection ratings and advise property owners of conditions and responsibilities. Ensure that all developments have more than one ingress-egress route. Offer options for fire-safe buildings. Provide appropriate fuel breaks or green belts in developments. Ensure that adequate water supplies exist in developments. Follow specifications in NFPA Standard 299 for the Protection of Life and Property from Wildfire.
PUBLIC AND HOMEOWNERS Determine the wildfire hazard potential of the immediate area before buying or moving into any home. Contact federal, state, and local fire services for educational programs and materials regarding fire protection. Provide a defensible space around structures to help protect them. Design and build nonflammable homes. Urge lawmakers to respond with legislative assistance to require appropriate fire safety measures for communities.
Wildland Lessons Recommendations to reduce the loss of life and property in the wildland-urban interface will be useless unless they are implemented at the grassroots level by all stakeholders. An excellent example of a community-based program is one implemented at Incline Village and Crystal Bay in the Lake Tahoe basin.[32] The objective of this program is to "reduce the potential for natural resource, property, and human life losses due to wildfire by empowering the communities' residents with the knowledge to address the hazard, providing the resources necessary to correct the problem, and encouraging the cooperative efforts of appropriate agencies." The three major components of this defensible-space program include neighborhood leader volunteers, a slash removal project, and agency coordination. The key to protecting life and property in the wildland-urban interface is property owners' realization that they have a serious problem and that their actions embody a significant part of the solution. In the Incline Village/Crystal Bay Plan, neighborhood leader volunteers are trained in defensible-space techniques and are expected to teach these techniques to their neighbors and to coordinate neighborhood efforts. Such concerted community action will greatly minimize the threats from Oakland-type "fires of the future." It is also wise to have sensible land development practices, since tragedies arise not only from ignorance of fuels and fire behavior but also from a greater concern
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for the esthetics of a homesite than for fire safety. Several aspects of development detract from fire safety in the wildland-urban interface.[6] [7] : 1. 2. 3. 4. 5. 6.
Lack of access to adequate water sources Firewood stacked next to houses Slash (i.e., branches, stumps, logs, and other vegetative residues) piled on homesites or along access roads Structures built on slopes with unenclosed stilt foundations Trees and shrubs growing next to structures, under eaves, and among stilt foundations Roads that are steep, narrow, winding, unmapped, unsigned, unnamed, and bordered by slash or dense vegetation that makes them impossible to drive on
during a fire 7. Subdivisions on sites without two or more access roads for simultaneous ingress and egress 8. Roads and bridges without the grade, design, and width to permit simultaneous evacuation by residents and access by firefighters, emergency medical personnel, and equipment 9. Excessive slopes, heavy fuels, structures built in box canyons, and other hazardous situations 10. Lack of fuel breaks around homesites and in subdivisions 11. Living fuels that have not been modified by thinning, landscaping, or other methods to reduce vegetation and litter that contribute to fire intensity 12. Homes constructed with flammable building materials (wooden shakes, shingles)
FIRE BEHAVIOR Urban and Wildland Fire Threats Safety precautions for wildland firefighting crews are continually upgraded as new knowledge is gained about fire behavior. Fire sites where people were injured or killed are visited afterward to assess fuel conditions, terrain features, probable wind movements at the time of the fire, and actions of firefighters ( Figure 12-4 ). This information, as well as data about hazards in the wildland-urban interface, is not included in training programs and safety briefings. In reviewing fire tragedies, a sobering observation is that crew members are almost always experienced and well-equipped firefighters, trained to anticipate "blowup" fire conditions. However, when visibility is lowered to 6 m (20 feet), noise levels preclude voice communication, eyes fill with tears, and wind blows debris in all directions, a person's judgment is badly impaired. Previous training can give way to panic, leading to decisions that result in serious injury or death. This scenario is most evident in urban fires; the pattern of hysteria affecting persons trapped in burning
Figure 12-4 In an attempt to avoid the intense heat of this brush fire in southwestern Colorado, four firefighters took refuge in the fireline, in the foreground at point A. Affected by intense convective and radiant heat and dense smoke, one individual ran into the fire and died at point B. Another individual ran approximately 1000 feet down the ridge, where his body was found at point C. The third fatality was a person who remained at point A; he died a short time after this position was overrun by fire. The only survivor also remained in a prone position at point A with his face pressed to the ground. At one point he reached back and threw dirt on his burning pants legs. The survivor sustained severe burns to the back of his legs, buttocks, and arms. The deaths of the other three individuals were attributed to asphyxiation. (Courtesy the USDA Forest Service.)
buildings is familiar to fire chiefs. The way fire kills in the urban setting can be compared with wildland fires, as shown here[24] : Heat rises rapidly to upper stories when a fire starts in the basement or on the ground floor. Toxic gases and smoke rise to the ceiling and work their way down to the victim—a vital lesson for families planning protective measures. Smoke poses the double problem of obscuring exit routes and con- tributing to pulmonary injury and oxygen deprivation. As the fire consumes oxygen, the ambient oxygen content drops, impairing neuromuscular activity. When the oxygen content drops below 16%, death by asphyxiation will ensue unless the victim is promptly evacuated. Asphyxiation, not fire itself, is the leading cause of fire deaths. Ambient temperatures may rise extremely rapidly from even small fires. Temperatures of 149° C (300° F) will cause rapid loss of consciousness and, along with toxic gases, will severely damage lung tissues. Warning devices may offer the only possibility for survival due to the rapid onset of debili- tating symptoms. Obvious similarities and differences are seen: 1. Smoke, heat, and gases are not as concentrated in wildland situations as in the confined quarters of urban fires. 2. Flames are not a leading killer in either the urban or wildland situation. 3. Although oxygen levels may be reduced near wildland fires, there is usually sufficient replenishment 324
of oxygen in the outdoor environment to minimize deprivation. Asphyxiation, however, can also be an important cause of death in wildland fires. 4. Inhalation of superheated gases poses as serious a threat to life in wildland fires as in urban fires. 5. Wildland smoke does not contain toxic compounds produced by combustion of plastics and other household materials, but it does impair visibility, contain carbon monoxide, and have suspended particulates that cause severe physical irritation of the lungs. 6. Automatic early-warning devices and sprinkler systems may protect people from serious injury or death in the urban environment, but in the wildland environment people must rely on their senses, knowledge, and skills to provide early warning of an impending threat to life. Fire Behavior Knowledge: A Wildland Early-Warning System The science of fire behavior describes and predicts the performance of wildland fires in terms of rates of spread, intensity levels, ignition probabilities, spotting, and crowning potentials. Spotting is a fire spread mechanism resulting from airborne firebrands or embers. Crowning is a fire spread mechanism that moves horizontally through the canopies of shrubs or trees. Knowledge of current and predicted weather information and fire danger ratings can be obtained from local wildland fire protection agencies. Experienced firefighters routinely assess the probable behavior of fires using current and expected weather conditions in relation to local fuel and topographic conditions. The emergency medical person, backcountry recreationist, and wildland homeowner must also understand basic fire behavior principles to provide for adequate personal safety. A cardinal rule is to base all actions on current and expected fire behavior. Attention to simple principles, indicators, and rules should enable wildland users to anticipate and avoid fire threats. Heat, oxygen, and fuel are required in proper combination before ignition and combustion will occur ( Figure 12-5 ).[1] If any one of the three is absent, or if the three elements are out of balance, there will be no fire. Fire control actions are directed at disrupting one or more elements of this basic fire triangle. Physical Principles of Heat Transfer.
Heat energy is transferred by conduction, convection, radiation, and spotting, but generally only the last three processes are significant in a wildland setting. Although conduction through solid objects is important in the burning of logs, this process does not transfer much heat outward from a flaming front. Convection, or the movement of hot masses of air, accounts for most of the heat transfer outward from the
Figure 12-5 Combustion is a process involving the combination of heat, oxygen, and fuel. An understanding of the variation of these three factors is fundamental to an understanding of fire behavior.
fire. Convective currents usually move vertically unless a wind or slope generates lateral movement. Convection preheats fuels upslope and in shrub and tree canopies, which contributes further to a fire's spread and the onset of crown fires. Via radiation, heat energy is emitted in direct lines of rays; about 25% of combustion energy is transmitted in this manner. The amount of radiant heat transferred decreases inversely with the square of the distance from a point source. More radiant heat is emitted from a line of fire than from a point source. Radiant heat travels in straight lines, does not penetrate solid objects, and is easily reflected. It accounts for most of the preheating of surface fuel ahead of the fire front and poses a direct threat to people who are too close to the fire ( Figure 12-6 ). Many organized fire crew members carry aluminized fire shelters in belt pouches so that they can deploy them quickly when escape is not possible ( Figure 12-7 ). These shelters are used as a last resort to protect from radiant heat.
Spotting is a mass transfer mechanism by which wind currents carry burning or glowing embers beyond the main fire to start new fires ( Figure 12-8 ). In this manner, fire spread may accelerate, unexpected fires occur, and fire intensity and indraft winds may increase. Factors in Wildland Fire Behavior.
A wildland fire behaves according to variations in fuel, weather, and topography. Early warning factors that signal the onset of hotter and faster burning conditions appear in Box 12-2 . When a person encounters a wildland fire, the first
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Figure 12-6 Fuels and people upslope or downwind from a fire receive more radiant heat than on the downslope or upwind side.
Figure 12-7 An aluminized fire shelter, carried in a waist pouch, is deployed by firefighters as a last resort to provide protection from radiant heat and superheated air. (Courtesy the USDA Forest Service.)
step should be to review the principles and indicators of fire behavior, sizing up the situation in terms of fuel, weather, topographic factors, and observed fire behavior. After the fire's probable direction and rate of spread are estimated, travel routes that avoid life hazards can be planned ( Figure 12-9 ). The direction of the main body of smoke is often a good indicator of the direction the fire will take. FUEL.
The more fuel that is burning, the hotter the fire will be. Certain types of fuel, such as chaparral, pine, and eucalyptus, burn more intensely because of their fine foliage that contains flammable oils. The size and
Figure 12-8 Fuels and people on the slope opposite a fire in a narrow canyon are subject to intense heat and spot fires from airborne embers.
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Figure 12-9 The parts of a fire are described in terms of its left flank, right flank, head, and rear. There may also be unburned islands within the fire and spot fires ahead of the fire. The safest travel routes generally involve lateral movement on contours away from the fire's flank or movement toward the rear of the fire. Moving in front of a headfire should be avoided. The burned area inside the fire's perimeter can offer a safe haven, if the flaming perimeter can be safely penetrated by an individual.
arrangement of fuel also influence fire behavior. Small, loosely compacted fuel beds, such as dead grass, long pine needles, and shrubs, burn more rapidly than does tightly compacted fuel. Large fuels burn best when they are arranged so that they are closely spaced, such as logs in a fireplace. Scattered logs with no small or intermediate fuel nearby seldom burn unless they are old and rotten.
Box 12-2. EARLY WARNING SIGNALS FOR HOTTER, FASTER BURNING CONDITIONS
FUEL More fuel; drier fuel; dead fuel; flashy fuel (dead grass, pine needles, and shrubs); aerial fuel (combustible material suspended in crowns of high shrubs and trees, such as branches, needles, lichens, and mosses).
WEATHER Faster winds; unstable atmosphere (indicators: gusty winds, dust devils, and good visibility); downdraft winds from dry thunderstorms and towering cumulus clouds (erratic and strong winds); higher temperatures, drought conditions, and lower humidities.
TOPOGRAPHY Steeper slopes; south- and southwest-facing slopes; gaps or saddles; chimneys and narrow canyons ( Figure 12-11 ).
FIRE BEHAVIOR Rolling and burning pine cones, agaves, logs, hot rocks, and other debris igniting fuel downslope; spot fires that occur ahead of the main fire; individual trees that torch out, or areas of shrubs and trees that burn in a continuous crown fire; fires that smolder over a large area; many fires that start simultaneously; fire whirls that cause spot fires and erratic burning; intense burning with flame lengths greater than 1.2 m (4 feet); dark, massive smoke columns with rolling, boiling vertical development; lateral movement of fire near the base of a steep slope.
WEATHER.
The greater the wind, the more rapid the spread of fire. Drier air and higher temperatures cause fuel to dry out more quickly; fire burns more intensely because drying creates more fuel. Prolonged drought makes more fuel available. Fires tend to burn more vigorously when atmospheric conditions are unstable. The North American continent has been classified into 15 fire climate regions based on geographic and climatic factors ( Figure 12-10 ).[29] Major fire seasons, or periods of peak fire activity, can be used to warn emergency medical personnel and wildland users of the most probable times for life-threatening situations. Although the fire season for the southern Pacific coast is shown as June through September, critical fire weather can occur year round in the most southerly portion. Fire seasons are most active during spring and fall in the Great Plains, Great Lakes, and North Atlantic regions. TOPOGRAPHY.
The steeper the slope, the more rapid the spread of fire. Fire usually burns uphill, especially in daytime. Changes in topography cause changes in fire behavior ( Figure 12-11 ). On steep terrain, rolling firebrands may cause a fire to spread downhill. Extreme Fire Behavior.
Several years of drought combined with a national forest health issue that has produced many dead and dying forests has set the stage for extreme fire behavior conditions that threaten people, property, and natural and cultural resources. Protection from these conditions requires an understanding of the crown fire process. As the name implies, a crown fire is carried through the crowns, or foliage, of a forest or shrubland. Rothermel[26] described the conditions that produce a crown fire: 1. 2. 3. 4. 5. 6. 7. 8.
Dry fuels Low humidity and high temperatures Heavy accumulations of dead and downed fuels Small trees in the understory, or "ladder fuels" Steep slope Strong winds Unstable atmosphere Continuous crown layer
The two most prominent behavior patterns of crown fires are wind-driven fires and plume-dominated fires. Each type of crown fire poses a distinct set of threats to people. Fires are seldom uniform and well behaved, so these descriptions of wind-driven and plume-dominated fire behavior may not be readily apparent. The behavior of these types of fires can be expected to
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Figure 12-10 Fire climate regions of North America, based on geographic and climatic factors, are as follows: (1) interior Alaska and the Yukon, (2) north Pacific Coast, (3) south Pacific Coast, (4) Great Basin, (5) northern Rocky Mountains, (6) southern Rocky Mountains, (7) Southwest (including adjacent Mexico), (8) Great Plains, (9) central and northwest Canada, (10) sub-Arctic and tundra, (11) Great Lakes, (12) Central States, (13) North Atlantic, (14) Southern States, and (15) Mexican central plateau. The bar graphs show the monthly and annual precipitation for a representative station in each of the fire climate regions. Months on the map indicate fire seasons. (From Schroeder MJ, Buck CC: Fire weather, Agricultural Handbook 360, 1970, USDA Forest Service.)
change rapidly as environmental, fuel, and topographic conditions change.[26]
WIND-DRIVEN FIRE.
A running crown fire can develop when winds increase with increasing elevation above the ground, driving flames from crown to crown ( Figure 12-12 ). Steep slopes can produce the same effect. Spread rates can vary from 1.6 to 11 km per hour (1 to 7 mph) and possibly faster in mountainous terrain. [26] A running crown fire is accompanied by showers of firebrands downwind, fire whirls, smoke, and the rapid development of a titled convection column. As long as
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Figure 12-11 Chutes, chimneys, and box canyons created by sharp ridges provide avenues for intense updrafts (like a fire in a stove) and rapid rates of spread. People should avoid being caught above a fire under these topographic conditions.
Figure 12-12 Cross-sectional view of a wind-driven crown fire. People are most at risk on the downwind side of a wind-driven fire. This type of fire is caused by winds that increase in velocity with increasing elevation above the ground.
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the wind remains fairly constant from one direction, the flanks of the fire can remain relatively safe. The greatest threat is to people who are at the head, or downwind, side of the fire, although long-distance spot fires that ignite from flying embers as far as 1.6 km (1 mile) ahead of the main fire front also pose a risk. PLUME-DOMINATED FIRE.
An alternative form of crown fire develops with relatively low windspeeds or when windspeed decreases with elevation above the ground. This type of crown fire is called a plume-dominated fire because it is characterized by a towering convection column that stands vertically over the fire ( Figure 12-13 ). This type of fire poses a unique threat to people because it can produce spot fires in any direction around its perimeter. It can also spread rapidly as the combustion rate accelerates.
Figure 12-13 Cross-sectional view of a plume-dominated crown fire. People are at risk around the complete perimeter of this type of fire because the fire can spread intensely or spot in any direction. This form of crown fire develops when wind velocities are relatively low or when velocities decrease with elevation above the ground. The convection plume above this type of fire may rise to 7600 to 9100 m (25,000 to 30,000 feet) above the ground.
One form of a plume-dominated fire can be especially dangerous when a downburst of wind blows outward near the ground from the bottom of a convection cell. These winds can be extremely strong[12] and can greatly accelerate a fire. This type of wind occurred during the Dude fire north of Phoenix, Arizona, on June 26, 1990, when six firefighters were killed. Some indicators help signal the onset of a downburst from a plume-dominated fire. The surest indicator is the occurrence of precipitation of any amount, even a light sprinkle, or the appearance of virga (evaporating rain) below a convective cell.[26] Another indicator is the rapid development of a strong convection column above the fire, or nearby thunder cells. A third and very short warning is the calm that develops when the indraft winds stop before the turnabout and outflow of wind from the cell. This brief period of calm may be accompanied by a humming sound just before the reversing wind flow arrives. If any of these indicators is present, the area should quickly be evacuated. The downburst may also break or uproot trees, creating an additional hazard for people.
FIRE-RELATED INJURIES AND FATALITIES Most fatalities in wildland fires occur on days of extreme fire danger when people are exposed to abnormally high heat stress caused by weather or proximity to fires. Loss of life is dramatically highlighted under extreme burning conditions; however, many more people are injured than are killed by fires. One of the worst fire disasters in Australia occurred on February 7, 1967, when 62 persons died in Tasmania.[17] Analysis of location and age of 53 individuals at the time of death is instructive ( Table 12-1 and Table 12-2 ). Most people whose bodies were found within or near houses were old, infirm, or physically disabled. More than half of the houses vacated by the 11 people who traveled some distance before being killed were not burned. Most of these victims would probably have TABLE 12-1 -- Location of Bodies of 53 Persons Who Died in Tasmanian Fires, February 7, 1967 LOCATION
NUMBER OF DEATHS
Mustering stock
2
Firefighting
11
Traveling in a vehicle
2
Escaping from and found at some distance from houses
11
Within a few meters of houses
10
In houses
17
From McArthur AG, Cheney NP: Report on southern Tasmania bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer.
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AGE GROUP
TABLE 12-2 -- Age Distribution of 53 Persons Who Died in Tasmanian Fires, February 7, 1967 NUMBER IN GROUP
AVERAGE AGE
1–25
1
23
26–50
13
38
51–75
26
64
76–88
13
82
From McArthur AG, Cheney NP: Report on southern Tasmania bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer. survived if they had remained in their homes. Most of the 11 firefighters who died were inexperienced. Many might have survived if they had observed fire behavior and safety rules. A review of USDA Forest Service records between 1926 and 1976 shows that 145 men died in 41 fires from fire-induced injuries.[42] Large losses occurred in the Blackwater fire in Wyoming in 1937 (15 deaths), in the Rattlesnake fire in California in 1953 (15 deaths), and in the 1933 Griffth Park fire in southern California (25 fatalities and 128 injuries). Wilson's analysis of people lost to fires in areas protected by other federal, state, county, and private agencies indicated 77 fire-induced fatalities in 26 fires. Wilson[42] identified some common features connecting these fatal fires: 1. 2. 3. 4. 5.
Relatively small fires or isolated sectors within larger fires seemed associated with most fatal incidents. Flare-ups of presumed controlled fires were particularly hazardous. Fatalities occurred in the mop-up stage. Unexpected shifts in wind direction or speed occasionally caused flare-ups in deceptively light fuels. Gullies, chimneys, and steep slopes directed fires to run uphill. The violent wind vortices left by helicopters and air tankers may have caused flare-ups in previously controlled areas.
Wilson concluded that the hairline difference between fatal fires and near-fatal fires was determined by the individual's reaction to a suddenly critical situation. Escapes were due to luck, circumstances, advance planning, a person's ability to avoid panic, or a combination of these factors. Frequently, poor visibility and absence of concise fire information threatened survival opportunities by creating confusion and panic. Nature of Injuries and Fatalies Fire-related injuries and fatalities are a direct consequence of heat, flames, smoke, critical gas levels, or indirect injuries ( Figure 12-14 ). Injuries and fatalities associated
Figure 12-14 The annual death toll for persons who died from all causes while involved in fighting wildland fires from 1990 to 1998 (133 total deaths).
with wildland fires fall into categories of heat (direct thermal injury, inhalation, and heat stress disorders), flames (direct thermal injury and inhalation), smoke (inhalation and mucous membrane irritation), critical gas levels (oxygen, carbon monoxide, and carbon dioxide), and indirect effects (acute and chronic medical disability and trauma). Intense fires that produce very high temperatures generally last for only a short time. The duration of intense heat increases with fuel load, being greater in a forest fire where heavy fuels are burning than in a grass or shrub fire. Temperatures near the ground are lower because radiant heat is offset somewhat by inflow of fresh air and the fact that gases of combustion rise and are carried away by convection.[4] Close to the ground, within a few meters of flames reaching up to 11 m (36 feet), air temperatures may be less than 15° C (59° F) above ambient temperature. The breathing of heated air can be tolerated for 30 minutes at 93° C (199° F) and for 3 minutes at 250° C (482° F).[16] Death or severe pulmonary injury occurs when these limits are exceeded. Thermal injuries of the respiratory tract frequently contribute to the clinical picture of smoke inhalation. Persons trapped in a fire may have no choice but to breathe flame or very hot gases. This usually injures the tissues of the upper airway and respiratory tract, most commonly the nose, nasopharynx, mouth, oropharynx, hypopharynx, larynx, and upper trachea. These injuries may result in edema that obstructs the airway and produces asphyxia or that causes tracheitis and mediastinitis. Signs of thermal injury to the airway include thermal injuries to the head, face, and neck; singed facial hair; burns of the nasal, oral, or pharyngeal mucosa; and stridor or dysphonia.[19] [33] [45] Associated with a history of exposure to flame and hot gases in a closed space, these clinical findings strongly suggest the presence of a thermal injury to the airway. With the potential for acute airway obstruction, there is obvious urgency in establishing this diagnosis. Most experts who treat thermal injuries of the tracheobronchial tree advocate early visualization of the vocal cords by laryngoscopy and bronchoscopy.[20] Bronchoscopy is a useful
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predictor of the clinical course and urgency of intensive care unit intervention. In addition, one report shows a significantly greater incidence of pneumonia and late mortality in persons with facial burns than in those without them.[43] Burns of the lower trachea are rarely reported. In fact, injuries to and beyond the carina are difficult to produce when the trachea is cannulated and hot gases are delivered in the anesthetized dog.[18] [44] Air has a very low specific heat and is therefore a poor conductor of thermal energy. In addition, the thermal exchange systems of the upper airway are quite efficient. The hot gas or flame is cooled sufficiently in the upper airway so that it does not burn the bronchi or more distal structures. However, although water or steam in the hot gas mixture is probably rare, it is a far more efficient conductor of heat and permits significant thermal injury to the lower trachea and bronchi. A delayed onset (2 to 24 hours after smoke inhalation) of pulmonary edema and adult respiratory distress syndrome is widely reported and should be anticipated. Whether this results from direct injury to alveoli, prolonged hypotension, or cerebral hypoxia and cerebral edema is unclear. Heat stress[30] occurs when air temperature, humidity, radiant heat, and poor air movement combine with strenuous work and insulative clothing to raise body temperature beyond safe limits. Sweating cools the body as moisture evaporates. When water lost through sweating is not replaced, physiologic heat controls can deregulate and body temperature may rise, leading to heat exhaustion or heatstroke (see Chapter 10 ). Direct contact with flames causes thermal injury, and death is inevitable with exposure for long periods. Burns may be superficial, partial, or full thickness (see Chapter 13 ). Immediate death results from hypotension, hyperthermia, respiratory failure, and frank incineration. The common cause of asphyxia in wildland fire is smoke. Danger increases where smoke accumulates because of poor ventilation, as in caves, box canyons, narrow valleys, and gullies. Dense, acrid smoke is particularly irritating to the respiratory system and eyes. Excessive coughing induces pharyngitis and vomiting. Keratitis, conjunctivitis, and chemosis may make it impossible to keep the eyes open. There are concerns about the levels of oxygen, carbon monoxide, and carbon dioxide associated with fire. Critical levels readily occur in a closed space and near burning or smoldering heavy fuels, but the open space of a wildland fire usually contributes to continual mixing of air. Misconceptions about lack of oxygen or excessive carbon monoxide and carbon dioxide in a wildland fire abound in the lay literature. Flaming combustion can be maintained only at oxygen
Figure 12-15 Ranger Pulaski led 42 men and 2 horses to this mine tunnel near Placer Creek in northern Idaho to seek refuge from the 1910 fire. One man who failed to get into the tunnel was burned beyond recognition. All the men in the tunnel evidently were unconscious for a period of time. Five men died inside the tunnel, apparently from suffocation. The remainder of the crew was evacuated to the hospital in Wallace, where all recovered. (Courtesy the USDA Forest Service. Photo by J.B. Halm.)
levels that exceed 12%, a level at which life can also be supported.[4] [16] With continued indrafts of air that feed the flames, a fresh source of oxygen is usually present. Even mass fires, in which large tracts of land are burning, rarely reduce oxygen to hazardous levels. Low oxygen levels may occur, however, where there is little air movement, such as in caves ( Figure 12-15 ) or in burned-over land that continues to smoke from smoldering fuels. Concentrations of carbon monoxide exceeding 800 parts per million (ppm) can cause death within hours. Most fires produce small quantities, but atmospheric concentrations rarely reach lethal levels because of air movement. High concentrations appear to be associated with smoldering combustion of heavy fuels, such as fallen trees or slash piles, and carbon monoxide may also collect in low-lying areas or underground shelters.[5] Outdoors, the danger lies in continual exposure to low concentrations that can increase blood carboxyhemoglobin levels. Prolonged exposure affects the central nervous system, resulting in headache, impaired judgment, progressive lethargy, decreased vision, and other psychomotor deficits.[42] Carbon monoxide levels of 50 ppm were measured close to a prescribed burn in grass.[8] In another estimate, concentrations of 30 ppm were found roughly 61 m (200 feet) from the fire front. Studies on the 1974 Deadline
332
and Outlaw forest fires in Idaho showed that firefighters were exposed to levels above the standards proposed by the National Institute of Occupational Safety and Health (35 ppm over an 8-hour period).[34] Decreased ambient oxygen may contribute to hypoxia and the overall picture of smoke inhalation ( Table 12-3 ). This mechanism is at least variably operant. When standing gasoline was ignited in a closed bunker, the fire self-extinguished, while the ambient oxygen level remained at 14%, a survivable level.[18] Injecting burning gasoline or napalm into bunkers produced nearly complete and prolonged exhaustion of ambient oxygen. Conflicting data make it difficult to classify definitively situations in which decreased ambient oxygen and subsequent hypoxia of exposed individuals contribute to the clinical picture of smoke inhalation. Studies in which ambient oxygen was measured by scientists did not show significant depletion of the scene of the fire.[11] Few data are available on levels of carbon dioxide around wildland fires. Although it may be produced in large quantities, it apparently never reaches hazardous concentrations, even in severe fire situations.[4] [16] The quantity of burning fuel and the type of topography affect levels of oxygen and toxic gases. Danger is greater in forest fires where heavy fuels burn over long periods of time than in quick-moving grass and shrub fires. Topography has a major influence; caves, box canyons, narrow canyons, gulches, and other terrain features can trap toxic gases or hinder ventilation, thereby preventing an inflow of fresh air. Although most fatalities result from encounters with smoke, flames, and heat, critical gas levels can induce handicaps sufficient to render the victim more vulnerable to other hazards. Wildland Fires, Air Toxins, and Human Health In the United States about 80,000 firefighters are involved with suppression activities on 70,000 wildland
AMBIENT OXYGEN (%) 20.9
TABLE 12-3 -- Human Response to Decreased Ambient Oxygen at Sea Level HUMAN RESPONSE Normal function
16–18
Decreased stamina and capacity for work
12–15
Dyspnea with walking; impaired coordination; variable impaired judgment
10–12
Dyspnea at rest; consciousness preserved; impaired judgment, coordination, and concentration
6–8
Loss of consciousness; death without prompt reversal
2000
Blood loss (% blood volume)
Up to 15%
15%–30%
30%–40%
>40%
Pulse rate
100
>120
>140
Blood pressure
Normal
Normal
Decreased
Decreased
Pulse pressure (mm Hg)
Normal or increased
Decreased
Decreased
Decreased
Respiratory rate
14–20
20–30
30–40
>35
Urine output (ml/hr)
>30
20–30
5–15
Negligible
CNS/mental status
Slightly anxious
Mildly anxious
Anxious, confused
Confused, lethargic
Fluid replacement (3 : 1 rule)
Crystalloid
Crystalloid
Crystalloid and blood
Crystalloid and blood
Figure 18-1 Venous cutdown performed at the distal greater saphenous vein.
Figure 18-2 Intraosseous resuscitation performed by introducing needle through the periosteum of the tibia joint inferior to the tibial tuberosity.
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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 also called into question the efficacy of prehospital resuscitation.[71] Although further prospective trials are needed relative to fluid type and prehospital use, an impressive compilation of data has been amassed looking at resuscitative fluids in the trauma victim. Past studies have not only compared colloids with crystalloids[88] but have 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 in 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] [77] [86] However, they are expensive and not yet adequately studied in humans. Additional studies are needed concerning artificial blood products, since no benefit relative to crystalloid has yet been demonstrated in trauma victims. Their relatively experimental nature, cost, and lack of proven superiority over crystalloid preclude use in the wilderness setting at this time. Based on the current literature, it is clear that both colloids (including hetastarches and albumin) and crystalloids are efficient volume expanders. [79] Certainly, larger volumes of crystalloids than colloids are needed to achieve similar resuscitative endpoints, 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] [68] Additionally, no proven detriment, including increased extravascular lung water, impaired wound healing, or decreased tissue oxygen diffusion, has been proven 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] [56] Although these data are compelling, they have been accumulated in victims with penetrating injuries and short prehospital times, and the definition of prehospital resuscitation within these studies comprised widely varying volumes. Clearly, prehospital resuscitative protocols remain in evolution, and it is likely that current common practices will be altered in the future. However, application of these particular 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. 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. 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. Additionally, 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, since this 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
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condition warrants. Specific examinations will be 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 simultaneous with the primary survey. The degree of resuscitation depends on available resources, experience of the rescuer(s), and environmental conditions. Under optimal circumstances, resuscitation allows oxygenation, fluid administration, and cardiac and vital sign monitoring. As adjuncts to the secondary survey, it also includes placement of urinary and nasogastric (NG) catheters. 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. A nasogastric tube and indwelling urinary (Foley) catheter should be placed if available and appropriate. In a victim with depressed level of consciousness or nausea and vomiting, gastric decompression assists in protection against aspiration—which could prove catastrophic in a remote area. In addition, children can exhibit deterioration in hemodynamics secondary to massive gastric distention. Nasogastric 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. If there is suspicion of a facial fracture(s), an NG tube should not be placed through the nares. 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 trauma[42] [57] and retrospective data in blunt trauma[7] indicate an increase in mortality with its use. The PASG has theoretical benefits in the stabilization of hemodynamically unstable pelvic fractures, although no scientific evidence exists for this application.[71] Further prospective studies in blunt trauma are needed, and use of the PASG is not indicated in the wilderness setting for blunt trauma at this time. 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 oral, facial, and eye injuries is presented in Chapter 22 and Chapter 23 . Elements of the GCS are repeated. The wilderness eye is discussed in detail in Chapter 22 , but general examination principles are as follows. Significant periorbital edema may preclude examination of the globe, and assessment should be carried out rapidly. 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.[75] Recent studies of ocular injuries in trauma victims have emphasized underappreciation of ocular and periocular signs indicative of significant underlying injury by many disciplines involved in the victim's care.[70] Head Injuries Background.
Approximately 500,000 to 2 million cases of head injury occur in the United States yearly.[34] Of these, approximately 10% die before reaching a hospital.[5] Long-term disability and sequelae associated with head injury are 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. No standardized management guidelines for head injuries in a wilderness setting have been developed, and a wide range of clinical approaches are used in hospital settings.[34] However, available literature suggests that morbidity and mortality can be reduced by means of a protocol that includes early airway control with optimization of ventilation,[38] prompt cardiopulmonary resuscitation, and rapid evacuation to a trauma care facility. In the wilderness setting, triage, resuscitation, and initial management of the head-injured victim must focus
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on maintenance of ATLS protocol, attempts to prevent secondary brain injury, and expeditious evacuation to a neurosurgical center. First and foremost, secure the airway. 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 compromise exists. Because of the high incidence of concomitant cervical spine injuries in this patient population, optimal immobilization is paramount in prevention of further devastating neurologic injury. The focus must then be 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. Anatomy.
The scalp is comprised of 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 of importance 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 base. The calvaria is composed of frontal, ethmoid, sphenoid, parietal, and occipital bones. The calvaria is especially thin in the temporal region, whereas the skull base is irregular with outcroppings, such as the anterior temporal fossa. The covering of the brain within the skull is composed of three membranous layers: a thick and fibrous dura, a thinner arachnoid layer, and the innermost pia. In the wilderness environment, the layers have little clinical relevance, and their distinction—with the exception of defining a closed vs. open injury—bears little significance. Pathophysiology of Traumatic Brain Injury.
TBI can be divided into primary and secondary injury. Primary injury is comprised of the physical or mechanical insult at the moment of impact, and the immediate and permanent damage to brain tissue and cranium. Little can be done in the wilderness setting relative to primary brain injury. Secondary injury is the biochemical and cellular response to initial mechanical trauma and includes physiologic derangements that may exacerbate primary injury. Such physiologic alterations include hypoxia, hypotension, ischemia, and hypothermia. Elevated intracranial pressure (ICP) may cause and exacerbate secondary brain injury. Many forms of head injury cause elevated ICP, the duration of which is significantly correlated with poor outcome. Thus elevated ICP is not only is indicative of significant underlying pathology but also contributes negatively to the outcome. The Monro-Kellie doctrine states that the volume of intracranial contents must remain constant. If the normal compensatory response to increased volume, which consists of decreasing venous blood and cerebrospinal fluid (CSF) volume, is overcome, then small increases in volume cause exponential increases in ICP. The volume-pressure curve in Figure 18-3 relates the small but critical time period between decompensation and brainstem herniation. With ICP elevation directly correlating with secondary brain injury, it is evident that the field provider must attempt to keep the head-injured victim in the flat portion of the curve, minimizing ICP. The most important priority in minimizing secondary brain injury in the field is optimizing cerebral perfusion pressure (CPP). CPP is relates 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] [37] Cerebral blood flow (CBF) should be maintained at approximately 50 ml/100 g brain tissue/minute.[54] At 5 ml/100 g/min, irreversible damage and potential cell death occur.[5] Study data have shown a correlation between low CBF and poor outcome.[54] At a MAP between 50 mm Hg and 160 mm Hg, cerebral autoregulation maintains
Figure 18-3 Critical time period between decomposition and brainstem herniation after traumatic brain injury.
437
CBF at relatively constant levels. Not only is autoregulation known to be disturbed in injured regions of the brain but also a precipitous fall in MAP can additionally impair autoregulatory function, decreasing CBF and exacerbating ischemia-induced secondary injury. Intuitively, it can been seen that the field provider has a means to combat rises in ICP simply by optimizing the MAP through aggressive resuscitation. Diagnosis.
There are three useful descriptions of head injury that may be applied to field recognition. History.
The history, including the mechanism and timing, severity, and morphology of the injury, can assist in the decision-making process regarding resuscitation and evacuation.[5] The mechanism may be identified as blunt or penetrating. The anatomic demarcation between blunt and penetrating injury is traditionally defined by the dura mater. Blunt injuries in the wilderness setting most often result from falls. Falling objects and assaults comprise the remainder of the majority of blunt injuries. Penetrating injuries are most commonly gunshot or arrow wounds. Severity.
Severity of injury can be estimated by quantifying the GCS and the pupillary response. The generally accepted definition of coma is a GCS score of less than 8. With regard to the primary survey and the essential component of airway protection, it has been demonstrated that GCS score does not specifically correlate with need to intubate, and the airway may be acceptable below a score of 8. It is important to note the victim's best motor response, since it is most predictive of 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 suggests increased ICP, which demands attention to optimizing MAP and consequently CPP. Abnormal or asymmetric pupillary responses relative to size or responsiveness also suggest intracranial mass lesion and elevated ICP. Morphology.
Injury morphology may be difficult to assess in the wilderness setting and relies on level of suspicion and clinical signs and symptoms. Following attention to the primary survey, including airway and
PUPIL SIZE
TABLE 18-2 -- Interpretation of Pupillary Findings in Head-Injured Victims LIGHT RESPONSE INTERPRETATION
Unilaterally dilated
Sluggish or fixed
Third nerve compression secondary to tentorial herniation
Bilaterally dilated
Sluggish or fixed
Inadequate brain perfusion; bilateral third nerve palsy
Unilaterally dilated or equal
Cross-reactive (Marcus-Gunn)
Optic nerve injury
Bilaterally constricted
Difficult to determine; pontine lesion
Opiates
Bilaterally constricted
Preserved
Injured sympathetic pathway
immobilization, the physical examination of the secondary survey is imperative and can provide information as to the existence of TBI. Injury Classification.
Intracranial injuries range from concussion to massive subdural hematoma. Subdural hematomas are more common than are 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 improve 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. They may present loss of consciousness followed by a lucid interval before rapid deterioration, although this sequence is frequently not observed. Hemorrhagic contusion is also quite frequent, constituting 35% of traumatic injuries; this lesion has the propensity to result in significant increases in ICP. Diffuse axonal injury (DAI) is the term used to describe a prolonged posttraumatic coma not resulting from a mass lesion or ischemic insult. Similar to hemorrhagic contusion, DAI may result in elevated ICP. Physical Examination.
The physical examination should be done so that it does not delay evacuation. The GCS should be reassessed. The hallmark of TBI is altered level of consciousness. Physical signs that may denote underlying brain injury include significant scalp lacerations, contusions, scalp hematomas, facial trauma, and signs of skull fracture, including Battle's sign (see below) and periorbital ecchymosis (raccoon eyes). Hemotympanum and bleeding from the ears, or CSF rhinorrhea or otorrhea, also suggest skull fracture and underlying TBI. The pupillary examination may provide valuable data in the assessment of underlying TBI. Temporal herniation may be heralded by a mild dilation of the pupil and a sluggish response to light. Further dilation of the pupil followed by ptosis, or paresis of the medial rectus or other ocular muscle, may indicate third cranial nerve compression by a mass lesion. Table 18-2 relates pupillary examinations to possible underlying
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brain lesions. Most dilated pupils are on the ipsilateral side of the mass lesion. With direct globe injury, traumatic mydriasis may result. Additionally, 5% to 10% of the population has congenital anisocoria. Neither direct trauma nor congenital anisocoria should be assumed in a head-injured victim exhibiting mental status change in the wilderness. After quantification of GCS score, pupillary examination, and examination of the head and face for signs of external trauma, a concise neurologic examination should be performed. The goal of the field neurologic examination is to identify motor or sensory focal deficits suggestive of intracranial injury. Sensory
Figure 18-4 Dermatome pattern, the skin area stimulated by spinal cord elements. Sensory deficits following general dermatome patterns.
deficits follow general dermatome patterns shown in Figure 18-4 . 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. With the exception of the performance of gag and corneal reflex evaluations, the brainstem cannot be evaluated in the wilderness environment. The "doll's eyes maneuver" should never be performed without complete radiologic evaluation of the cervical spine. Ice 439
water irrigation of the tympanic membrane intended to evoke nystagmus adds nothing to an evacuation decision and should not be performed outdoors. Resuscitation.
Resources and circumstances permitting, resuscitation should be initiated as an adjunct to the primary survey. The primary focus for the head-injured victim, similar to any traumatized victim, is the airway. During the primary survey and performance of the ABCDE sequence, IV access should be established. If IV resuscitation is impossible, it is not advisable to administer fluids orally to the victim with head injury because of the likelihood of vomiting, airway compromise, and aspiration. Individuals sustaining head trauma have a high incidence of concomitant injuries. Up to 32% of persons with severe head injury will 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 be assumed to have a nonneurogenic etiology of shock. Resuscitation is critical in this setting for multiple reasons. First, management of a head injury should be secondary to other life-threatening injuries, which, if not addressed, may preclude survival. Second, as previously discussed, maintenance of MAP and thus CPP is critical in preventing secondary brain injury. The type of resuscitative fluid administered is controversial. Previously, recommendations existed warning of the dangers of overhydration in head injury, to the extent of implementing fluid restriction. Fluid restriction has not been shown to reduce ICP or edema formation in the laboratory, and hypotonic solutions do not decrease cortical water content.[87] The need for resuscitation and intravascular volume support is now well established. Possible resuscitative fluids now include primarily isotonic crystalloids, colloids, or hypertonic crystalloids. Hypotonic fluids are not appropriate in TBI because they can cause increased brain water and thus elevated ICP. Recent data from animal studies suggest that colloids offer no advantage over isotonic crystalloids, such as lactated Ringer's solution, in head injury in terms of augmenting CBF or preventing cerebral edema.[98] 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.[89] [94] However, an advantage has not been demonstrated in trauma victims overall, and expertise is necessary for their use. Thus the recommended resuscitative fluid for the head-injured victim in the wilderness setting is isotonic crystalloid. MAP should be optimized at 90 mm Hg based on cuff pressure or extrapolation from distal pulses. 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, thereby increasing CBF. However, if PaCO2 falls below 25 mm Hg, severe vasoconstriction ensues, effectively reducing CBF and promoting ischemia. Studies have demonstrated worse outcomes in victims with severe head injury who were hyperventilated.[64] Because of the inability to measure or titrate this variable in the wilderness, ventilation should be controlled to approximate 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. Although diuretics have been widely utilized 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 diagnose. 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 and 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 depress the neurologic examination.[4] Compared with minimizing ICP, they offer no proven benefit.[37] Approximately 15% of persons with severe head injury experience posttraumatic seizures. Phenytoin, if available, can be safely administered in the field, but
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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. Basilar skull fractures often manifest signs that aid in the diagnosis, including periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle's sign), CSF leaks, or eighth cranial nerve palsy. Skull 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 injuries are usually catastrophic. However, examples of survival exist in small caliber, low-velocity injuries and tangential wounds.[55] As with closed head injury, management priorities consist of maintenance of airway, prevention of secondary brain injury, and rapid evacuation. If the cranium has been violated, the victim should receive antibiotics and tetanus immunization in the same manner as for open skull fracture. Some authors recommend 7 days of anticonvulsant therapy.[55] 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 may be done easily and without displacement of the intracranial segment.
Evacuation.
Survival and outcome of head injury in the wilderness correlate directly with the 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 fractures is variable but significant throughout the literature. Recent data predict that 30% to 90% of persons with raccoon eyes or Battle's sign will have an abnormal computed axial tomography (CAT) scan. [11] [18] Similarly, any person who sustains a penetrating injury should be evacuated. The decision to evacuate victims who have sustained closed head injuries can be simplified by dividing the victims into three groups based on probability of injury. The high-risk group is composed of persons 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[11] [18] and may be closely observed. 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 computed tomography (CT) scans have demonstrated the significance of decreased GCS, 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 normalcy 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. [69] 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. Treatment is focused on establishing and maintaining
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an airway until evacuation can occur. Frequently, the airway will be in jeopardy, and because of the propensity for injuries of this type to result in significant and progressive edema, endotracheal or nasotracheal intubation is often necessitated. 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 cricothyroidotomy may be necessitated. A recent study of prehospital cricothyroidotomy demonstrated that success rates were high regardless of medical specialty as long as previous training had been instituted.[51] For further descriptions of airway management, refer to Chapter 17 . 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 will have a cervical spine injury. Additionally, 55% of spinal injuries occur in the cervical region.[55] In the wilderness setting, fractures or dislocations of the cervical spine are a result of falls from significant heights, or of high-velocity ski or vehicular injuries. Twenty-eight percent of persons with cervical spine fractures have fractures elsewhere in the spine.[10] ANATOMY.
The cervical spine consists of seven vertebrae. The anteriorly placed vertebral bodies form the weight-bearing structure of the column. The bodies are separated by intervertebral disks and held in place anteriorly and posteriorly by longitudinal ligaments. The paraspinal muscles, facet joints, and interspinous ligaments contribute as a whole to the stability of the spine. The cervical spine, based on its anatomy, is more susceptible to injury than are the thoracic and lumbar spine. The cervical canal is wide from the foramen magnum to C2, with only 33% of the canal comprised by the spinal cord itself. The clinically relevant tracts in the spinal cord include the corticospinal tract, the spinothalamic tract, and the posterior columns. CLASSIFICATION AND RECOGNITION.
Fractures of the cervical spine frequently result in neurologic deficit, with total loss of function below the level of injury.[50] 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. Generally, 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 at 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 below) is the most commonly seen serious neurologic picture. A careful neurologic examination in the field to grade motor strength and to 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 the 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 spine;[10] 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 (since 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 dermatomal and motor myotomal patterns is invaluable (see Figure 18-4 ). 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, and assessment should begin at C5. The examiner must 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.
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Motor function should be assessed by the myotomal distribution listed in Box 18-2 . 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.
Central cord syndrome is characterized by a disproportionate loss of motor power between the upper and lower extremities, with greater strength retained in the lower extremities. Sensory loss is variable. The mechanism of injury usually involves a forward fall with facial impact and hyperextension of the spine. Anterior cord syndrome is characterized by paraplegia and loss of pain and temperature sensation. It is the most common presenting syndrome caused by cervical spine injury and carries a poor prognosis. Brown-Séquard's 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.
Box 18-2. 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
IMMOBILIZATION.
After identification of injury, the caregiver faces a critical decision with important ramifications—whether or not to immobilize.[31] 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.[40] [53] All criteria for the exclusion of immobilization must be satisfied. These include normal mental status without chemical influence; lack of distracting injury; normal neurologic examination; and a reliable neck examination without midline neck pain, deformity, or tenderness. Figure 18-5 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 precedent over ease of evacuation.[58] A difficult balance must be struck in the wilderness between the likelihood of true injury and the danger to the expedition members and rescuers that may ensue when the victim is immobilized. If a rigid litter is not available, the victim should be maintained on the flattest surface possible. A rigid cervical collar should be placed. All collars allow some degree of movement, particularly rotation. Soft collars offer the least immobilization.[30] The Philadelphia collar
Figure 18-5 Clinical assessment of cervical spine stability. Failure of any criterion suggests need for immobilization.
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has been shown to allow 44% of normal rotation and 66% of normal lateral bending. [55] To achieve 95% immobilization, a halo and vest are necessary. Any number of materials may be used to improvise an immobilizing device. Restriction of flexion, extension, and rotation must be achieved to the greatest degree possible. Optimal immobilization consists of a long spine board or litter, rigid collar, bolsters to the sides of the head, and tape or straps restricting movement ( Figure 18-6 ). 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 over the next 23 hours.[13] 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
Figure 18-6 Proper spine immobilization.
bony instability; however, stability should not be assumed. Neurologic deficits, if present, can progress with further movement of an unstable spine. Projectiles should not be removed if embedded in the neck. Penetrating injuries to the neck may not directly injure the spine, but neurologic sequelae may result from blast effect. The same immobilization criteria should be implemented as when dealing with blunt injuries. Penetrating injuries to the neck are classified according to anatomic zones of injury ( Figure 18-7 ). 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 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 vs. radiographic evaluation. In the wilderness setting, such considerations are not irrelevant. A penetrating injury violating the platysma muscle indicates the possibility of significant neurovascular, esophageal, and/or tracheal injuries, so the victim should be evacuated with close attention to the airway. If hemorrhage uncontrollable by direct pressure is present, careful insertion of a Foley catheter into the wound with balloon inflation may provide temporizing tamponade.[21] Injuries to the Thorax Background.
The mortality from thoracic trauma is approximately 10%. Approximately 25% of all trauma
Figure 18-7 Zones in penetrating neck trauma.
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deaths in the United States are attributable to chest injury.[5] However, only 15% of persons with major thoracic trauma require thoracotomy. Early intervention can play a critical role in survival, and many deaths are preventable. Prompt identification of life-threatening injuries in the immediate postinjury period may facilitate proper, lifesaving intervention. 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. The hallmark of significant thoracic injury is hypoxia, which may sometimes be remedied in the field. 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), and/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, or intercostal muscular retraction are abnormal and may give clues to the underlying injury. Chest wall movement during respiration should be symmetric. Paradoxical chest wall movement is associated with flail chest. The chest wall should be inspected for contusions and abrasions, which may herald underlying bony or visceral injury. Distention of the external veins in a person who has just suffered thoracic trauma and is hypotensive or tachycardic (heart rate greater than 130 beats per minute) suggests impairment of 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, vertebral ribs, have no attachment to the sternum. Point tenderness over a rib can be associated with contusion or fracture. Displaced fractures can be palpated; occasionally, bone grating can be palpated during respiration. Subcutaneous emphysema may extend up into the neck and down to the level of the inguinal ligaments. In the trauma situation, subcutaneous emphysema is invariably associated with pneumothorax. Vocal fremitus describes palpation of vibrations transmitted through the chest wall. During speech, the victim's vocal cords emit vibrations in the bronchial air column that are conducted to the chest wall. Diminished vocal fremitus is associated with pneumothorax or hemothorax. To test for vocal fremitus, the examiner applies the palmar arch of the examining hand against the person's anterior chest wall. The person is asked to repeat "one, two, three" using the same pitch and intensity of voice with each repetition. If the vibrations are not well perceived, the patient is asked to lower the pitch of the voice. The chest should be symmetric, left to right. Percussion is used to detect changes in the normal density of an organ. Percussion of the chest is performed by placing the examining fingertip on the chest wall and sequentially striking the fingertip with the tip of the finger of the other hand. In the trauma victim, dullness replacing resonance in the lower lung suggests hemothorax. Hyperresonance or tympany 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 within 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 variable heights. Compression of the chest wall by moving or falling debris may also contribute to intrathoracic
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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. Isolated rib fractures are managed with oral analgesics and rest. Thoracic taping and splinting are not necessary or helpful. Multiple rib fractures are significant because of the potential seriousness of associated injuries and increased pain. However, 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 lengths 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. 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(s), 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 the 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 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 vena 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 form 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
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open pneumothorax. Ideally, a 14-gauge catheter is inserted percutaneously over the second rib in the mid-clavicular or anterior axillary line ( Figure 18-8 ). 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
Figure 18-8 Needle decompression of tension pneumothorax. This procedure is performed only for tension pneumothorax in patients with hemodynamic instability.
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. Having entered the pleural space, a tube (36 F or greater in size) is inserted apically and posteriorly.
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The tube should then be secured with suture or tape and 10 to 20 cm H2 O suction or underwater seal applied. A tube open to the atmosphere can accomplish decompression. The end of the tube can be covered with a rubber glove, finger cot, or plastic bag; one-way flow evacuating the chest is the goal. It must be emphasized that this procedure is not without morbidity and should only be used 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 may be placed if proper equipment is available and evacuation may be delayed. Needle aspiration of a hemothorax is unnecessary in the immediate postinjury period and may precipitate a pneumothorax. As in the case of pneumothorax, treatment is strictly based on clinical deterioration. Isolated hemothorax from blunt trauma leading to shock is unusual and commonly associated with other massive injuries. 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 to progressively impair ventilation and oxygenation over the succeeding 48 hours. Victims will 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. 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) 16- to 18-gauge needle with an overlying catheter is introduced through the skin 1 to 2 cm 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, nebulous 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 and hemodynamic instability. Chest pain is invariably present, usually resulting from musculoskeletal contusion. Morbidity results from ensuing arrhythmias. The diagnosis, if hemodynamically significant, is difficult to distinguish from blunt trauma-induced tamponade. Diagnosis can only be definitively made at autopsy. Electrocardiographic abnormalities after injury have correlated with subsequent arrythmias.[52] 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,
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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,[67] and mortality in natural disasters is consequently high.[32] 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.[32] Crush injuries and rhabdomyolysis are discussed in the Extremity Injury section of this chapter. The pathophysiology of traumatic asphyxia involves two elements. The crush injury results in acute increases in intrathoracic pressure and thus inferior and superior vena caval pressures. Venous flow is reversed in the veins of the head, which contain no valves. Venous hypertension leads to capillary rupture and the characteristic facial edema and petechiae. Recognition of the physical findings is imperative in diagnosing the syndrome and identifying concomitant injuries ( Figure 18-9 ). Treatment consists of carefully extracting and, if necessary, immobilizing the victim. Rapid extrication is the single most important factor in improving survival. Establishment and 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.
Figure 18-9 Typical clinical facial appearance of traumatic asphyxia.
Mortality 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 intraabdominal 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 the loss of negative intrathoracic pressure affects the good lung. Consequently, it is important to rapidly reconstruct chest wall integrity. Initially, this is most easily done by placing a hand over the sucking chest wound. Field treatment includes placing a petrolatum gauze on top of the wound, covering it with a 4 × 4 gauze pad, and taping it on three sides ( Figure 18-10 ). The untaped fourth side serves as a relief mechanism to prevent tension pneumothorax. Persons with sucking chest wounds should be rapidly evacuated to sophisticated medical care. Injuries to the Abdomen Intraabdominal injuries in the wilderness setting are unique because they are often difficult to recognize. However, once recognized or suspected, all intraabdominal injuries require rapid resuscitation and immediate evacuation.
Figure 18-10 Treatment of a sucking chest wound. Sealing the wound with a gel defibrillator pad works best because this pad adheres to wet or dry skin. Petrolatum gauze or Saran Wrap also works well. Note that one side is not sealed to allow egress of air.
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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 intraabdominal injury is commonly associated with falls. Abdominal injuries are often associated with fractures or closed head injuries. Often the decision for evacuation is made on the basis of other injuries; however, the wilderness physician must be attuned to the potential for intraabdominal hemorrhage as an occult injury. ANATOMY.
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 intraabdominal pressure with subsequent rupture of the liver or diaphragm. The true abdomen contains the small bowel, large bowel, and bladder. Isolated bowel injuries are rare in the wilderness setting. Blunt bladder or rectal injury usually occurs in conjunction with severe pelvic fracture and carries high mortality. The retroperitoneal abdomen contains the kidneys, ureters, pancreas, and great vessels. It is notoriously difficult to evaluate by physical examination. Life-threatening hemorrhage can occur into the true abdomen or the retroperitoneal space. DIAGNOSIS.
Although much progress has been made in the last decade to evaluate for the presence of blunt intraabdominal injury, modalities such as CT, ultrasound, 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. 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 intraabdominal hemorrhage or, conversely, absent in victims when extraabdominal 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 intraabdominal 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-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 intraabdominal injury. These injuries mandate immediate surgical intervention. A victim of gunshot wounds to the head, neck, chest, abdomen, or groin should undergo immediate evacuation accompanied by the administration of a single-agent broad-spectrum antibiotic, such as an oral fluoroquinolone (e.g., ciprofloxacin, 750 mg po bid). Gunshot wounds (hunting injuries) are discussed in Chapter 20 .
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SHOTGUN INJURIES.
Shotgun injuries to the torso are managed in the same manner as gunshot wounds. Shotgun injuries have 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 above 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. Since 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 intraabdominal organ. Whereas the odds of an abdominal gunshot wound injuring a visceral organ exceed 95%, the odds of a stab wound injuring a visceral organ are between 50% and 60%. 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.[65] This approach uses local wound exploration, diagnostic peritoneal lavage, and frequent physical examination. Although no data exist addressing the management of stab wounds in the wilderness environment, the following approach is practical and reasonable. If the wound extends into the subcutaneous tissue, the evacuation decision depends on local wound exploration. This procedure is simple to perform, even in the wilderness environment. The skin and subcutaneous tissue are infiltrated with local anesthetic, and the laceration is extended several centimeters to clearly visualize the underlying anterior fascia. It is helpful to use lidocaine (Xylocaine) 1% with epinephrine to minimize slight but annoying bleeding that can impair visualization. The wound should never be probed with any instruments, particularly if overlying the ribs. Wound exploration is confined to the area from the costal margin to the inguinal ligament. Local wound exploration is contraindicated in wounds that extend above the costal margin, because it is possible for such exploration to communicate with a small pneumothorax, potentially exacerbating respiratory distress. If thorough exploration of the wound shows no evidence of anterior fascial penetration, and if the victim demonstrates no evidence of peritoneal irritation, the wound can be closed with tape (Steri-Strips) or adhesive bandages, dressed, and the evacuation process delayed. Physical examination should be performed every few hours for the next 24 hours. If no peritoneal signs develop and the victim feels constitutionally strong, a remote expedition may resume with caution and an eye to evacuation should the victim become ill. In the wilderness environment, it is prudent to have a low threshold for evacuation because of technical difficulties in performing wound exploration—such as insufficient light and inadequate instruments. Persons who have been impaled by long objects, such as tree limbs or ski poles, should have the object left in place, and carefully shortened, if possible, to facilitate transport. Pelvic Trauma In the wilderness setting, fractures of the pelvis are generally associated with falls from significant heights, high-velocity ski accidents, or vehicular trauma. Pelvic fractures can be lethal. With opening of the pelvic ring, there may be hemorrhage from the posterior pelvic venous complex and occasionally branches of the internal iliac artery. For hemodynamically unstable victims with severe pelvic fracture, resuscitative efforts should be instituted. Additionally, 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
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or hip location. For more information on pelvic fracture, see Chapter 21 . Extremity Trauma The majority of wilderness-related extremity injuries involve fractures and sprains, which are discussed in Chapter 21 . This section focuses on the general field management of significant extremity vascular injury, traumatic amputation, and recognition and treatment of rhabdomyolysis. 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 ( Box 18-3 and Box 18-4 ). All victims with hard signs should be evacuated emergently. Based on current data, an isolated soft sign may warrant observation alone, depending on the remoteness of the expedition and the risks of evacuation. The data for observation of soft signs has 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
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safely, the victim should be transported and observed in a medical facility. Box 18-3. VASCULAR "HARD SIGNS" Pulsatile bleeding Palpable thrill Audible bruit Expanding hematoma Six "P's" of regional ischemia Pain Pulselessness Pallor Paralysis Paresthesia Poikilothermia
Box 18-4. VASCULAR "SOFT SIGNS" Injury in proximity to major vessel Diminished but palpable pulses Isolated peripheral nerve deficit History of minimal hemorrhage
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 only be completed 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 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 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 asphyxia[32] 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.[32] The common cellular derangement is interference of the normal function of muscle cell membrane sodium-potassium adenosine triphosphatase (ATPase) with intracellular calcium influx and cell death.[74] 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 the 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 failure[66] 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 intravenously 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 have been shown to improve clearance of myoglobin but not to alter survival. Additionally, 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 18-5 ).
Box 18-5. 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
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Wound Morphology.
Major lacerations are often the most obvious sign of trauma; however, injuries to the integument are rarely life-threatening. 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 are 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 Chapter 41 Chapter 42 Chapter 43 Chapter 44 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 life-threatening injuries. The ATLS primary survey should be performed in the usual fashion. Control of Hemorrhage.
The vast majority of bleeding will be 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 transiently restore perfusion and to assess if they are still necessary. Clamping bleeding vessels is not advised, since 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 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 16 . 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 1:2000, and cocaine 11.8% in saline) has been used with success as a topical anesthetic. Complications have included seizure and death.[90] 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 anesthetic 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 300 to 400 mg subcutaneously. 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.[60] 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 the 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,[44] buffering the solution with sodium bicarbonate to a concentration of 1%, and administering anesthetic slowly in small doses all minimize pain.
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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 easier to administer and is preferred 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 twentyfold when proper technique is used. The type of irrigation fluid and the technique utilized will be 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.[31] Any concentration of sterile crystalloid solution can be used, although normal saline remains the most readily available, economical, and cost-effective irrigant. Recent data suggest that tap water may be as effective as normal saline.[62] The amount of irrigation necessary is difficult to quantify. Some authors use 60 ml of irrigant per centimeter wound length as a guide,[44] 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 irrigants, 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 tissues[14] 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 irrigant 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. 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. Additionally, 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, [90] 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. The extent of tissue removal should be based on the experience and training of the caregiver. Tetanus Prophylaxis.
The 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.[76] This fact accentuates the preventable nature of tetanus infections and the essential role of proper immunization. If available in the wilderness setting, tetanus prophylaxis should be administered as outlined in Table 18-3 . 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 the scalp and face; are less than 6 hours old; and have no anatomic contraindications.
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TABLE 18-3 -- Tetanus Prophylaxis CLEAN MINOR WOUNDS
MAJOR DIRTY WOUNDS
HISTORY OF IMMUNIZATION (DOSES)
TOXOID*
TIG†
TOXOID TIG
Unknown
Yes
No
Yes
Yes
None to one
Yes
No
Yes
Yes
Two
Yes
No
Yes
No (unless wound older than 24 hours)
Last booster within 5 years
No
No
No
No
Last booster within 10 years
No
No
Yes
Yes
Yes
No
Yes
Yes
Three or more
Last booster more than 10 years ago
*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 to 500 units IM in limb contralateral to toxoid.
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 suture, 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. Additionally, 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.[90] 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.[90] 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, use of octylcyanoacrylate and similar synthetic agents have been shown to be equal in strength and cosmesis compared with sutures at 1 year.[78] Advantages of adhesives include ease of application, safety, patient comfort, and low cost.[91] Similar to tape, immediate tensile strength is poor and dehiscence is more likely compared with sutures.[90] 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 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.[41] Hair surrounding the laceration is removed only if absolutely necessary to clean the wound using a safety razor. Hair removal should be limited to the immediate area of the laceration, since the surrounding hair can later be twisted into strands and used to approximate the wounds 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.
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Minor scalp lacerations can be effectively treated in the wilderness setting, after following the aforementioned infection-minimizing 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. 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, since surrounding tissue planes can be mobilized for closure. Adipose tissue should not be approximated with suture, 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 20 . 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 irrigated. Wet-to-dry dressings with
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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 Chapter 41 , Chapter 42 , Chapter 43 , Chapter 44 .
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,[49] and mushroom ingestion can cause severe gastroenteritis.[82] Pain, anorexia, nausea, vomiting, and fever are characteristic manifestations of an acute abdominal disorder. Tenderness and guarding are the hallmarks of peritoneal irritation and suggest that surgery is needed.
DISEASE
TABLE 18-4 -- Differential Diagnostic Features of Abdominal Pain LOCATION OF PAIN AND PRIOR MODE OF ONSET AND ASSOCIATED ATTACKS TYPE OF PAIN GASTRO-INTESTINAL SYMPTOMS
PHYSICAL EXAMINATION
Acute appendicitis Periumbilical or localized generally to right lower abdominal quadrant
Insidious to acute and persistent
Anorexia common; nausea and vomiting in some
Low-grade fever; epigastric tenderness initially; later, right lower quadrant
Intestinal obstruction
Diffuse
Sudden onset; crampy
Vomiting common
Abdominal distention; high-pitched rushes
Perforated duodenal ulcer
Epigastric; history of ulcer in many
Abrupt onset; steady
Anorexia; nausea and vomiting
Epigastric tenderness; involuntary guarding
Diverticulitis
Left lower quadrant; history of previous attacks
Gradual onset; steady or Diarrhea common crampy
Fever common; mass and tenderness in left lower quadrant
Acute cholecystitis
Epigastric or right upper quadrant; may be referred to right shoulder
Insidious to acute
Anorexia; nausea and vomiting
Right upper quadrant pain
Renal colic
Costovertebral or along course or ureter
Sudden; severe and sharp
Frequently nausea and vomiting
Flank tenderness
Acute pancreatitis Epigastric penetrating to back
Acute; persistent, dull, severe
Anorexia; nausea and vomiting common
Epigastric tenderness
Acute salpingitis
Bilateral adnexal; later, may be generalized
Gradually becomes worse
Nausea and vomiting may be present
Cervical motion elicits tenderness; mass if tuboovarian abscess is present
Ectopic pregnancy
Unilateral early; may have shoulder pain after rupture
Sudden or intermittently vague to sharp
Frequently none
Adnexal mass; tenderness
The approach to someone with abdominal pain begins with a detailed history that includes the person's age, gender, systemic symptoms, and past medical history. This information provides a framework for more detailed questioning about the character of the pain, its mode and time of onset, severity, and precipitating and palliating factors. In persons 15 to 40 years of age, females are more likely to have abdominal pain, but males have a higher incidence of surgical disease. Common genitourinary causes for abdominal pain in men include epididymitis, renal colic, urinary retention, and testicular torsion. Common causes in women include pelvic inflammatory disease (PID), urinary tract infection, dysmenorrhea, ruptured ovarian cyst, and ectopic pregnancy. Pain is the hallmark of a surgical abdomen ( Table 18-4 ). It can be characterized by mode and time of onset, severity, localization, 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
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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. 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 herniae. 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, if practical. 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. Initiation of crystalloid resuscitation in the field is intuitively beneficial for persons 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 eventual perioperative morbidity. Nasogastric tube decompression of the stomach can prove beneficial in alleviating emesis secondary to abdominal pain or obstruction. Large-bore 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 after 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 under the age of 30 years. Acute appendicitis is really more than one 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 so 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 not well 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.
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Acute appendicitis mandates evacuation because untreated perforation retains significant mortality. Broad-spectrum antibiotics (if IV capability, cefotetan [Cefotan] 2 g IV q12h, or as an alternate, piperacillin/taxobactam [Zosyn] 4.5 g IV q8h; 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. Intravenous 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, since 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 and/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.[63] 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 suspicious for cholecystitis, particularly when accompanied by fever, more significant nausea and vomiting, and right upper quadrant rebound tenderness. Recent studies have shown that fever may be an unreliable predictor of severity of infection.[36] 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 PO alternative ciprofloxacin [Cipro] 750 mg po bid) should be given, directed at common biliary organisms, including Escherichia coli, 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, nasogastric 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, it is less often a disease seen by surgeons. The exception is perforation of 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 suspicious for perforation of an ulcer. The physical examination greatly assists in the 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 mandates evacuation. Dehydration may be significant. IV resuscitation should be started and the victim placed on bowel rest. Antibiotics are not indicated. 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, ranging from mild, localized infection to intraabdominal catastrophe. It is more common in middle age; one third of the population over the age of 45 have diverticula, 20% of which will develop diverticulitis.[86] 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 oral antibiotics,[80] such as broad-spectrum fluoroquinolones, such as cefotetan 2 g IV q12h, or an alternative oral fluoroquinolone such as ciprofloxacin 750 mg po bid. Antibiotic therapy is directed primarily
460
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. [48] Because of unpredictability of response to antibiotic treatment, evacuation is indicated. Mechanical Small Bowel Obstruction.
Small bowel obstruction is a true emergency in the wilderness. When the obstruction is complete, expedient surgery is the only treatment. Small bowel obstruction in the United States is almost invariably the result of adhesions from previous laparotomy or incarceration of abdominal hernias, 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 a nasogastric 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.[59] Hernias can become incarcerated or strangulated, which constitutes a surgical emergency. Seventy-five percent of hernias occur in the groin[83] ; the majority of incarcerated hernias presenting in the wilderness setting will be 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 elicit concern. The pain of inguinal hernias is usually intermittent. A description of constant pain is suspicious 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 or previous incision site, or below the inguinal ring, indicates possible incarcerated umbilical, incisional, or femoral hernia, respectively. Bowel within an incarcerated hernia sac can become gangrenous in as little as 4 to 5 hours;[59] therefore it is important to attempt to identify time of incarceration. The decision to evacuate is determined by the presence of contraindications to manual reduction (see below), which are essentially physical signs that progression to strangulation may be occurring. Femoral hernias should not be reduced. The danger is en masse reduction of compromised or gangrenous bowel. Contraindications to reduction include associated signs of toxicity, such as fever, tachycardia, or evidence of bowel obstruction in association with a painful irreducible mass. If the hernia itself is exquisitely tender to palpation and the overlying skin is erythematous and warm, the hernia should not be reduced. Victims with incarcerated hernias with signs of systemic or local toxicity should be evacuated. Similarly, victims with irreducible hernias—which require emergent surgery—should be evacuated. A newly incarcerated hernia without contraindications to reduction may be reduced by personnel experienced in such techniques. Gentle pressure is exerted on the hernia mass toward the inguinal ring, optimally with the victim flat and hips elevated. Analgesia and sedation may aid in reduction. Gangrenous bowel can rarely be reduced by this method.[90] 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 percussion of the flank is present. Diagnosis in the wilderness is assisted by the presence of gross hematuria. Management is directed primarily at pain control. Although almost universally deployed, forced diuresis may reduce ureteral peristalsis. Thus forced oral fluids or aggressive IV hydration are of questionable benefit.[97] The majority of calculi pass spontaneously in 4 to
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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.[97] Narcotic analgesics are most effective given parenterally; however, agents such as meperidine, codeine, and hydromorphone (Dilaudid) may be given orally. For symptoms uncontrolled by antiinflammatory agents, narcotics may be added. Antiinflammatory agents and analgesics can be combined. An antiemetic may be added to relieve nausea. When administering pain medication in the field, particular attention should be given to airway maintenance and induced nausea and vomiting. Any person whose symptom complex cannot be controlled must be evacuated. Additional indications for evacuation include calculus anuria and evidence of obstruction-induced infection. Urinary Retention.
Urinary retention is an unpleasant and painful experience that requires immediate medical, and often surgical, intervention.[12] The etiology of urinary retention ranges from prostatism[46] in men to atonic bladder in women. In general, causes have been broadly divided into four groups: obstructive, neurologic, pharmacologic, and psychogenic.[96] Twenty-five percent of men reaching 80 years of age will experience acute retention, [12] which has been shown to increase prostate surgery perioperative mortality.[73] 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. 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 catheter coudé 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. 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.[81] Drainage of greater than 300 ml/hr can induce mucosal hemorrhage. In addition, 10% of victims develop post-obstructive diuresis that may lead to dehydration, in which case crystalloid repletion should be undertaken. Finally, it must be recognized that the situation has been temporized and that 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.[47] 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 a torsed testicular appendage or epididymitis. It has been stated that victims who can ambulate with minimal pain are less likely to have a torsed testicle. In addition, nausea and vomiting may
accompany torsion, whereas fever, dysuria, and frequency are associated with epididymitis. Physical examination reveals a firm-to-hard testis frequently associated with bluish discoloration at the superior pole (blue dot sign).[47] 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,[85] which is relief of pain accomplished by elevation of the testicle. Because torsion twists the spermatic cord and elevates the testicle, pain in 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 is helpful in conjunction with other findings.[85] Treatment consists of surgical detorsion, which should be accomplished within 12 hours of torsion.[47] 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.[39]
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If manual detorsion is necessitated, the victim should be placed supine. If the left testis is affected, the right hand of the examiner should grip the testis between thumb and forefinger to elevate the testis toward the inguinal ring. A counterclockwise (epididymis turning medially) rotation should be used. If successful, the testis will descend to its normal position and relief will be felt by all. The right testis is grasped with the left hand and rotated counterclockwise. 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 proper follow-up. Prostatitis.
Fifty percent of men will experience prostatic symptoms in their adult life.[74] A number of forms of prostatitis have been defined, including viral, bacterial (5%), nonbacterial (65%), and chronic forms, as well as prostatodynia.[76] The acute bacterial form may potentially lead to severe infection. Bacterial prostatitis is an infection of the prostate caused primarily by gram-negative bacteria, with 80% attributable to Escherichia 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 not uncommon, and cystitis frequently accompanies the infection. On rectal examination, the prostate gland is usually boggy, warm, and tender. 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. Ciprofloxacin (750 mg po bid), ampicillin (500 mg po qid), or trimethoprim (80 mg with sulfamethoxazole 400 mg po bid) is an effective regimen. 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 who have 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 age 20 to 40 report having had a UTI.[43] Conversely, men between the ages of 15 and 50 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 urinary tract infection; 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.[43] 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 Escherichia coli (70% to 95%); Staphylococcus species (5% to 20%); and, less frequently, Klebsiella, Proteus, and enterococci. Fortunately, oral antibiotics are highly effective. Although resistant Escherichia 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.[43] For pyelonephritis, similar antibiotics 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 75 . Skin and Soft Tissue Infections Poor hygiene, superficial skin wounds, blisters, dermatologically significant plants, and insect bites contribute to disruption of the skin barrier. Most often seen are superficial pyodermas that do not extend beyond the level of the skin. These include erysipelas, impetigo, folliculitis, furunculosis, and carbunculosis. The majority of superficial skin infections are self-limited. However, with less than optimal hygiene and limited resources, skin infections may progress to deep soft tissue infections. Cellulitis.
Cellulitis is acute infection of the skin involving subcutaneous tissue. The superficial form of cellulitis, erysipelas, is identified 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. Clostridia species and other pathogens are ubiquitous in the soil, and
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proper initial wound care may be suboptimal. Under such conditions, cellulitis can progress to abscess formation and tissue necrosis, leading to septicemia. Wounds that develop erythematous, warm, and boggy margins should be treated with antibiotics and closely observed. The margins of erythema should be marked to gauge progression. Treatment consists of proper wound hygiene and antibiotic therapy. Local wound measures include elevation, application of moist heat every 4 to 6 hours, and immobilization. Antibiotic therapy is directed at common causative pathogens. Group A streptococci and Staphylococcus aureus are most commonly implicated. If complications occur and the cellulitis appears to be progressing, a mixed infection is likely. Because Gram's stain and culture-directed therapy are not possible, the most broad-spectrum antibiotic available should be administered. Parenteral antibiotics are indicated for serious or mixed infections. Penicillin G (1 to 2 million units every 2 to 3 hours) is recommended, with first-generation cephalosporins as an alternative. Because oral antibiotics may be the only available therapy, they should be initiated early in the field. Suggested agents include erythromycin (for the penicillin-allergic victim); cephalexin; a macrolide, such as clarithromycin; or a fluoroquinolone, such as ciprofloxacin or levofloxacin.
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.[84] Abscess Formation.
When untreated, many superficial skin infections convert to abscesses. Development of a raised, fluctuant mass with overlying warmth and erythema should raise suspicion that surgical drainage is necessary. Frequently, the lesion will "point" when purulent fluid has amassed below the dermis and rupture is impending. Warm soaks and observation are recommended by some clinicians, particularly if the presence of drainable pus is uncertain. However, the definitive treatment is drainage. Antibiotics are recommended if significant associated cellulitis is present, but penetration may be poor. Local anesthesia should be administered before incision. The lesion should be incised in line with tissue planes over the point of maximum fluctuance. The value of cruciate incisions over linear incisions is debatable; the important feature is assurance of adequate drainage to prevent recurrence. If drainage is undertaken, the incision must be large enough to adequately drain the cavity. All purulent material should be evacuated and the cavity copiously irrigated with saline or water. Packing is unnecessary if adequate continued drainage is ensured. The wound should be covered with a sterile dressing, changed 2 to 3 times per day with concurrent irrigation, and closely observed for reaccumulation of purulence. Necrotizing Infections.
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.[35] The incidence of necrotizing soft tissue infections is unknown, and there is no age or gender predilection. They most commonly occur on the extremities, abdominal wall, and perineum, within 1 week of the inciting event. Common pathogens include streptococcal species, Staphylococcus, Vibrio species, Clostridia, 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, and/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 necessitated is often striking.
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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 only be halted by aggressive surgical intervention.
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Chapter 19 - Wilderness Improvisation Eric A. Weiss Howard J. Donner
At the heart of wilderness medicine is improvisation, a creative amalgam of formal medical science and commonsense 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 you work with an improvised system, you should test your 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
Figure 19-1 Safety pinning tongue to open airway. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
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 ( Figure 19-1 ). 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 (Cricothyroidotomy) Cricothyroidotomy—the 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. Cricothyroidotomy 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 cricothyroidotomy by cutting a hole in the thin cricothyroid membrane and then placing a hollow object into the trachea to allow for ventilation ( Box 19-1 ). 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"), whereas the second (below the thyroid cartilage) is the cricoid cartilage.
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Figure 19-2 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.
The small space between these two, noted by a small depression, is the cricothyroid membrane ( Figure 19-4 ). 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 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 ( Figure 19-5,A ). Stabilize the larynx between the fingers of one hand, and insert the improvised cricothyroidotomy tube through the membrane with your other hand ( Figure 19-5,B ). Secure the object in place with tape. Box 19-1. IMPROVISED CRICOTHYROIDOTOMY 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 ( Figure 19-2 ). 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 ( Figure 19-3 ). 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.
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Figure 19-3 Improvised cricothyroid airway device can be created by cutting barrel of syringe at 45-degree angle at its midway point. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
Figure 19-4 Cricothyroid membrane is found in the depression between the Adam's apple (thyroid cartilage) and the cricoid cartilage. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
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
Figure 19-5 Cricothyroidotomy. 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. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
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 ( Figure 19-6 ).
EAR, NOSE, AND THROAT EMERGENCIES Epistaxis is a common problem in travelers. The reduced humidity in airplanes, cold climates, and high-altitude environments can produce drying and erosion of the nasal mucosa. Other etiologic factors include facial
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Figure 19-6 Improvised cardiopulmonary resuscitation (CPR) barrier is created using a latex or nitrile glove. Make a slit in the middle finger of the glove.
trauma, infections, and inflammatory rhinitis. Although most cases of epistaxis are minor, some present life-threatening emergencies.[32] Anterior epistaxis from one side of the nasal cavity occurs in 90% of cases.[7] 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. Vaseline-impregnated gauze
Figure 19-7 Anterior epistaxis from one side of the nasal cavity can be treated using nasal packing soaked in a vasoconstrictor. Vaseline-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.
or strips of a nonadherent dressing can then be packed into the nose so that both ends of the gauze remain outside the nasal cavity ( Figure 19-7 ). This prevents the victim from inadvertently aspirating the nasal packing.[32] 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 or the Rhino Rocket, is available commercially. A tampon or balloon tip from a Foley catheter can also be used as improvised packing.[32] Anterior nasal packing blocks sinus drainage and predisposes to sinusitis. Prophylactic antibiotics are usually recommended until the pack is removed in 48 hours.[32] If the bleeding site is located posteriorly, use a 14- to 16-Fr Foley catheter with a 30-ml balloon to tamponade the site.[10] Prelubricate the catheter with either 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 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
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Figure 19-8 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.
from sharp objects or pressure necrosis caused by large objects.[20] The use of a Foley balloon-tipped catheter can be a safe method for removing blunt esophageal foreign bodies.[4] [5] [12] Success rates of 98% have been cited.[4] Associated complications include laryngospasm, epistaxis, pain, esophageal perforation, and tracheal aspiration of the dislodged foreign body.[20] Sharp, ragged foreign bodies or an uncooperative victim precludes use of this technique ( Figure 19-8 ).[28] 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 expelled by coughing. Take care to avoid lodging the foreign body in the nasopharynx. Any significant impedance to withdrawal should terminate the attempt.[28] Use of this technique is recommended only in extreme wilderness settings or when endoscopy is not available.
IMPROVISED PLEURAL DECOMPRESSION OF A TENSION PNEUMOTHORAX 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. 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 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 19-2 ). 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 1 ½ to 2 ½ inches thick, depending on the individual's muscularity and the amount of fat present. A gush of air signals that you have entered the pleural space; do not push the penetrating object further. Releasing the tension converts the tension pneumothorax into an open pneumothorax.
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Box 19-2. 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
Figure 19-9 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. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
Leave the needle or catheter in place and place the cut-out finger portion of a rubber glove with a tiny slit cut into the end over the external opening to create a unidirectional flutter valve that allows continuous egress of air from the pleural space ( Figure 19-9 ). 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 or catheter into the open end of the glove finger and through the tip as shown (see Figure 19-9, A ). 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 19-9, B and C ).
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.
IMPROVISED SPLINTING AND TRACTION * Cervical Spine Injuries 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 with use of 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 increase pain or focal neurologic deficit or (2) movement of the head and neck results in any noticeable mechanical resistance. [17] All cervical spine injuries (or suspected injuries) deserve 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 the small of the back also add to the victim's comfort during a long transport.[9] Cervical Collars.
Cervical collars are always adjuncts to full spinal immobilization and never 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 *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.
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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 the soft cervical collars often used by urban plaintiffs trying to impress a jury. An improvised cervical collar works effectively only if it has the following features: 1. 2. 3. 4.
It is rigid or semirigid. It fits properly (many improvised designs are too small). It does not choke the victim. It allows the victim's mouth to open if vomiting occurs.
The following are improvisational approaches to cervical collars. 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 by being 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. PADDED HIP BELT.
A padded hip belt or fanny pack removed from a large internal or external frame backpack can sometimes be modified to work perfectly. Wider is usually better. Take up excess circumference by overlapping the belt, and secure the excess material with duct tape ( Figure 19-10 ). CLOTHING.
Bulky clothing, such as a fiberpile or fleece jacket, can be rolled and then wrapped around the victim's neck to make a cervical collar. The extended sleeves can be used to secure the collar. Prewrapping a wide elasticized (Ace) wrap around the jacket compresses the material 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 ( Figure 19-11 ). 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
Figure 19-10 Inverted pack used as spine board. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
with a long board; and (2) long board immobilization, used for definitive immobilization during extensive transport. Use all 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 Ensolite. Alternatively, a -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 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 and allow 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 ( Figure 19-12 ); in this context the shovel blade serves as a head bed. This system incorporates
the remainder of the pack suspension as designed (that is, 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).
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Figure 19-11 Malleable 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 SAM splint. D, Frontal view. The end is angled inferiorly to provide an adequate chin-to-chest distance.
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Figure 19-12 Head immobilized on a padded shovel.
Figure 19-13 Short board using an inverted pack system. The backpack waistbelt can be seen encircling the head. 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 ( Figure 19-13 ). 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 you can eliminate excess circumference 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 ( Figure 19-14 ). Pad the snowshoe and rig it for attachment to the victim as shown.[19] IMPROVISED LONG BOARD IMMOBILIZATION
Continuous loop system.
For the continuous loop system (also known as the daisy chain, cocoon wrap, or mummy litter), the following items are needed: 1. 2. 3. 4.
A long climbing or rescue rope A large tarp Sleeping pads (Ensolite or Therm-a-Rest) Stiffeners (such as skis, poles, snowshoes, canoe paddles, or tree branches)
Lay the rope out with even -shaped loops as shown in Figure 19-15, A . 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 laid rope. 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 ( Figure 19-15, B ). Add multiple foam pads on top of the stiffeners followed optionally with a sleeping bag ( Figure 19-15, C ). Place the victim on the pads. To form the daisy chain, bring a single loop through the pretied 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) ( Figure 19-15, D ). 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 Figure 19-10 and Figure 19-13 ). Backpack frame litters.
Functional litters can be constructed from external frame backpacks. Traditionally two frames are used, but three or four frames (as illustrated in Figure 19-16 ) 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.
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Figure 19-14 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 long board systems, such as the continuous loop system.
Figure 19-15a Continuous loop, or "mummy," litter made with a climbing rope. A, Rope is laid out with even -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.
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Figure 19-15 D, Loop of rope is brought over each shoulder and tied off (see text).
Figure 19-16 Backpack frame litter.
Figure 19-17 Improvised head bed. Improvised head bed.
A malleable 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 ( Figure 19-17 ). Traction Why are improvised traction systems so crucial? Traction can be lifesaving in certain situations.[6] The importance of femoral traction in urban emergency medicine is generally accepted. 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 cylindric 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.
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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. 2. 3. 4.
Does the splint provide inline traction? Or does the splint incorrectly pull the victim's leg off to the side or needlessly plantar flex the ankle? Is the splint comfortable? Be sure to ask the victim. Does the splint compromise neurologic or vascular function? Constantly check distal neurovascular function. 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, technical 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. 2. 3. 4. 5. 6.
Ankle hitch Rigid support that is longer than the leg Traction mechanism Proximal anchor Method for securing the splint to the leg 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 the circulation. 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 ( Figure 19-18, A ). Pass the long loop sides through
the short loop on both sides ( Figure 19-18, B ) and adjust as needed ( Figure 19-18, C ). 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. -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 other similar material over the upper part of the ankle (lower calf) in an -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 ( Figure 19-19 ). 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 ( Figure 19-20 ). 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 ( Figure 19-21 ). 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 potential for neurovascular complications and dermal ischemia. In addition, improvised Buck's traction has been used to manage backcountry hip fractures. However, recent literature indicates 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 pounds or less). 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 ( Figures 19-22 ).
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Figure 19-18 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.
Figure 19-19 S-configuration hitch for traction splinting.
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Figure 19-20 Traction using cut boot and cravat.
Figure 19-21 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 19-22 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.
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Figure 19-23 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 19-24 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.
Figure 19-25 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 19-26 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. 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 ( Figure 19-23 ). 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 ( Figure 19-24 ) in the end of the pole to provide an anchor for the traction system. Alternately, use a Prusik knot ( Figure 19-25 ) to secure the system to the end of the tent pole ( Figure 19-26 ). Miscellaneous.
Any suitable object, such as a canoe or kayak paddle (see Figure 19-26 ), 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. TRACTION MECHANISM.
The first modern popularized improvised traction mechanism was the Boy Scout-style Spanish windlass. Although these systems work and look good in the movies, they can be awkward to apply
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Figure 19-27 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.
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 is primarily a function of comfort. A general rule is to use 10% of body weight or about 10 to 15 pounds for the average victim. After the traction is applied, always recheck distal neurovascular function (circulation, sensation, movement). Cam lock or Fastex-like slider.
This simple, effective system uses straps that have a Fastex-like slider. 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 19-22 ). Trucker's hitch.
A windlass can be easily fashioned using small-diameter line (parachute cord) and a standard trucker's hitch for additional mechanical advantage ( Figure 19-27 ). Prusik knot.
Almost any system can be rigged with a Prusik knot (see Figure 19-25 ). 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. 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 at the foot end of the litter. If this system is used, ensure that the victim is immobilized
Figure 19-28 Proximal anchor using cam lock belt. The belt is applied as shown. A ski pole is used laterally as the rigid support. Duct tape is useful for securing components. Padding is helpful but is not always necessary if the victim is wearing pants.
Figure 19-29 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.
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 ( Figure 19-28 ). A cloth cravat can be used in a pinch. On the river a life jacket can be used ( Figure 19-29 ). 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 ( Figure 19-30 ). This is preferred over a circumferential
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Figure 19-30 Folding Ensolite padding often provides better visualization of the extremity than does a circumferential wrap.
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 Ace bandage wrapped circumferentially provides a comfortable and secure union. Finally, strap or tie the ankles or feet together to give the system additional stability. Tying the ankles together also prevents the injured leg from excess external rotation and jarring during transport. 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 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 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 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
Figure 19-31 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.
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 ( Figure 19-31 , Figure 19-32 , Figure 19-33 , Figure 19-34 , Figure 19-35 , Figure 19-36 ). Functional Splints Although most splints are designed to completely immobilize an injured extremity, 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 quickly improvised 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 ( Figure 19-37 ).
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Figure 19-32 Humerus splint. Used in conjunction with a sling and swath, this splint adds extra support and protection for a fractured humerus.
Figure 19-33 Forearm splint. These splints are used for the 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.
Figure 19-34 Lower leg and/or ankle splint. A sugar-tong splint can be used to immobilize fractures of the tibia, fibula, or ankle.
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Figure 19-35 Posterior arm splint. This splint is cut from of a 5- to 9-gallon plastic fuel or water can (jerry can). When used with appropriate padding, this forms an excellent splint for injured or fractured elbows.
Figure 19-36 Webbing sling. An 8-foot length of 1-inch 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. Functional Shoulder Immobilizer (Shoulder Spica Wrap).
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 evacuation. A
Figure 19-37 Functional knee and lower leg immobilizer. Wrap a sleeping pad around the lower leg from the midthigh 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.
more functional system can be made using a 6-inch elastic wrap. This method allows the victim limited function (e.g., ski poling or kayak paddling) while still preventing complete abduction of the arm. 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 ( Figure 19-38, B ). 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 ( Figure 19-38, A ). 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.
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Figure 19-38 Techniques for pinning the arm to the shirt as an improvised sling. A, 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. B, With a long-sleeved shirt or jacket the sleeved arm is simply pinned to the chest portion of the garment.
IMPROVISED 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. Wound Irrigation The primary determinants of infection are bacterial counts and amount of devitalized tissue remaining in the wound.[15] Ridding a wound of bacteria and other particulate matter requires more than soaking and gentle washing with a disinfectant.[18] Irrigating the wound with a forceful stream is the most effective method of reducing bacterial counts and removing debris and contaminants.[21] [27] The cleansing capacity of the stream depends on the hydraulic pressure under which the fluid is delivered.[14] [26] 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 , respectively.[14] [23] [26] The solution is directed into the wound from a distance of 1 to 2 inches 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.[14] Remember, "The solution to pollution is dilution."
Box 19-3. 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 of salt (9 g) 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.
Which irrigation solution is best for open wounds? Those who subscribe to the dogma that nothing should enter a wound that could not be instilled safely into the eye believe that normal saline is the best solution.[8] [16] 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 F-68 (Shur-Clens).[11] Tap water was recently 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.[2] 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 19-3 ). Wound Closure Before a wound is closed, remove all foreign material and grossly devitalized tissue. You can accomplish debridement
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using scissors, a knife, or any other sharp object. Close wounds 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. Box 19-4. WOUND TAPING TECHNIQUE 1. Obtain hemostasis and dry the wound edges. 2. Apply benzoin or cyanoacrylate glue to the skin adjacent to the wound. Benzoin should be left to dry until it becomes tacky, but the tape should be applied to the glue while the glue is still wet. 3. Tape should be cut to ¼-inch or ½-inch widths, depending on the size of the laceration, and to a length that allows for 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 2 to 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, the time required for closure is shorter, and fewer instruments are needed.[24] Most important, the cosmetic outcome is not compromised.[13] Staplers are lightweight, presterilized, and easy to use. Wound Taping.
Skin tapes are useful for shallow, non-gaping 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 19-4 ). 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 first 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. 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
Figure 19-39 Scalp laceration closed using dental floss. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby.)
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 ( Figure 19-39 ). 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 (butyl-2-cyanoacrylate) tissue adhesive has been used in Europe and Canada for sutureless skin closure for more than a decade.[31] The U.S. Food and Drug Administration (FDA) has recently approved a topical skin adhesive to repair skin lacerations. Dermabond (2-octyl cyanoacrylate) is packaged in a small single-use applicator and costs about $30 per tube. Tissue glue is ideal for backcountry use because it precludes the need for topical anesthesia, is
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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.[23] 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 19-5 ).[22] Tissue glue evokes a mild acute inflammatory reaction with no tissue necrosis.[30] Box 19-5. TECHNIQUE FOR GLUING LACERATIONS 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 petrolatum jelly.
Dermabond has 4 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, since 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.[3]
RING REMOVAL Remove rings quickly from injured fingers and after any 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 20-inch length of fine string, dental floss, umbilical tape, or thick suture between the ring and the finger. Pull the string so that
Figure 19-40 String technique for removing a ring from a swollen finger.
most of it is on the distal side of the digit and then wrap it around the swollen finger from proximal to distal, beginning next to the ring and continuing past the proximal interphalangeal joint. Place successive loops of the wrap close enough together to prevent any swollen skin from bulging between the strands. Remove the ring by unwinding the proximal end of the string and forcing the ring over the distal string. If the string is not long enough, the technique may require repeated wraps ( Figure 19-40 ).
IMPROVISATIONAL TOOLKIT Some people, convinced they could whittle a SwanGanz 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 translates into speedy preparation and assembly, which ultimately results in better care. The following section lists items that facilitate improvisation in the field.
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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 you 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 almost all tasks, even being useful on skin when needed (e.g., to close wounds, treat blisters, or tape an ankle). Some persons may be sensitive to the adhesive. Fiberglass 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 (for example, 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 Safety pins have various uses ( Box 19-6 ). 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, and so on. 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 predrilled ski pole section, saves time (see Figure 19-22 ).
Box 19-6. USES OF A SAFETY PIN Using two safety pins to pin the anterior aspect of the tongue to the lower lip to establish an airway in an unconscious victim whose airway is obstructed Replacing the lost screw in a pair of eyeglasses to prevent the lens from falling out Improvising glasses: Draw two circles in a piece of duct tape where your eyes would fit. Use the 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. Neurosensory skin testing Puncturing plastic bags for irrigation of wounds Removing embedded foreign bodies from the skin Draining an abscess or blister Relieving a subungual hematoma As a fishhook As a finger splint (mallet finger) As a sewing needle, using dental floss as thread Holding gaping wounds together Replacing a broken clothing zipper Holding gloves or mittens to a coat sleeve Unclogging jets in a camping stove Pinning triage notes to multiple victims Removing 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 Tick removal
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 closed-cell foam are virtually unlimited. Even die-hard Therm-a-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.
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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 bread crumbs 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. 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 4267 m (14,000 feet) in the snow, photokeratitis can develop in 20 minutes. You 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. 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 ( Figure 19-41 ). 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.
Figure 19-41 Pinhole in cardboard to improve vision in person with myopia.
IMPROVISED TRANSPORT Carries Two-Hand Seat.*
Two carriers stand side by side. Each carrier grasps the other carrier's wrists with opposite hands (for example, 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 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. *Both the two-hand seat and the four-hand seat are useful only for very short carries over gentle terrain.
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Figure 19-42 Ski pole seat. A, Ski poles are anchored by the packs. B, The victim is supported by the rescuers. 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 ( Figure 19-42 ). 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. 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 ( Figure 19-43 ). The victim must be able to support himself or herself to avoid falling back, or must be tied in. Two-Rescuer Split-Coil Seat.
The two-rescuer split-coil seat is essentially the same as the split-coil 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 ( Figure 19-44 ). 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 like 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 ( Figure 19-45 ). At least 4.6 to 6.1 m (15 to 20 feet) 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 never be used for trauma victims with potential spine injuries. 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,
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Figure 19-43 Split-coil seat. A, Rope coil is split. B, Victim climbs through rope. C, Rescuer hoists the sitting victim.
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 ( Figure 19-46 ). 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 16 180-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 of bend to the outside of each clove hitch). The
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Figure 19-44 Two-rescuer split-coil seat. Balance could be improved by using a longer coil to carry the victim lower.
Figure 19-45 Webbing carry. Webbing crisscrosses in front of the victim's chest before passing over the shoulders of the rescuer.
Figure 19-46 Parka litter. On the right the sleeves are zipped inside to reinforce the litter.
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Figure 19-47 Rope litter.
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 ( Figure 19-47 ). The litter is padded with packs, Therm-a-Rest pads, or foam pads. This improvised 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. To build an improvised rescue sled/toboggan, the rescuer needs a pair of skis (preferably the victim's) and two pairs of ski poles; three 2-foot-long sticks (or ski pole sections); 24.4 m (80 feet) of nylon cord; and extra lengths of rope for sled hauling. The skis are placed 0.6 m (2 feet) apart. The first stick is used as the front cross-bar and is lashed to the ski tips. Alternately, 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.[29]
Another sled design incorporates 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.[25]
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.
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Anderson GH et al: Preoperative skin traction for fractures of the proximal femur, J Bone Joint Surg 75B:794, 1993.
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Angeras MH, Brandberg A: Comparison between sterile saline and tap water for the cleansing of acute traumatic soft tissue wounds, Eur J Surg 158:347, 1992.
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Ayton JM: Polar hands: spontaneous skin fissures closed with histoacryl blue tissue adhesive in Antarctica, Arctic Med Res 52:127, 1993.
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Bancewicz J: Oesophageal bolus extraction by balloon catheter, BMJ 1:1142, 1978.
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Bigler FC: The use of a Foley catheter for removal of blunt foreign objects from the esophagus, J Thorac Cardiovasc Surg 51:759, 1966.
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Borschneck AG: Why traction? J Emerg Med Serv 10:44, 1985.
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Bryant CA et al: Search for a non-toxic surgical scrub solution for periorbital lacerations, Ann Emerg Med 5:317, 1984.
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Chan D et al: The effect of spinal immobilization on healthy volunteers, Ann Emerg Med 23:48, 1994.
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Cook PR, Renner G, Williams F: A comparison of nasal balloons and posterior gauze packs for posterior epistaxis, Ear Nose Throat J 64:446, 1985.
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Dire D: A comparison of wound irrigation solutions used in the emergency department, Ann Emerg Med 19:704, 1990.
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Dunlap LB: Removal of an esophageal foreign body using a Foley catheter, Ann Emerg Med 10:101, 1981.
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Dunmire SM et al: Staples versus sutures for wounds closure in the pediatric population, Ann Emerg Med 18:448, 1989.
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Edlich RF: Current concepts of emergency wound management, Emerg Med Rep 5:22, 1984.
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Edlich RF et al: Principles of emergency wound management, Ann Emerg Med 17:1284, 1988.
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Edlich RF, Sinkinson CA: Current concepts of emergency wound management. Part II, Emerg Med Rep 5:173, 1984.
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Isaac J, Goth P: The Outward Bound wilderness first aid handbook, New York, 1991, Lyons & Burford.
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Lammers RL et al: Effect of povidone-iodine and saline soaking on bacterial counts in acute, traumatic, contaminated wounds, Ann Emerg Med 19:709, 1990.
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Lyons S, Wilderness Professional Training, Crested Butte, Colo, personal correspondence, 1994.
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Nandi P, Ong GB: Foreign body in the esophagus: review of 2394 cases, Br J Surg 65:5, 1978.
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Peterson L: Prophylaxis of wound infections, Arch Surg 50:177, 1945.
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Quinn JV et al: A randomized, controlled trial comparing a tissue adhesive with suturing in the repair of pediatric facial lacerations, Ann Emerg Med 22:1130, 1993.
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Rodeheaver GT et al: Wound cleansing by high pressure irrigation, Surg Gynecol Obstet 141:357, 1975.
24.
Roth JH, Windle BH: Staple versus suture closure of skin incisions in a pig model, Can J Surg 31:19, 1988.
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Schimelpfenig T, Lindsey L: NOLS wilderness first aid, Wyoming, 1991, NOLS Publications.
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Sinkinson CA: Maximizing a wound's potential for healing, Emerg Med Rep 10:11, 1989.
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Stevenson T et al: Cleansing the traumatic wound by high-pressure syringe irrigation, J Am Coll Emerg Phys 5:17, 1976.
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Taylor RB: Esophageal foreign bodies, Emerg Med Clin North Am 5:2, 1987.
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Tilton B: The basic essentials of rescue from the backcountry, Merrilville, Ind, 1990, ICS Books.
30.
Toriumi DM et al: Histotoxicity of histoacryl when used in a subcutaneous site, Laryngoscope, April 1991.
31.
Watson DP: Use of cyanoacrylate tissue adhesive for closing facial lacerations in children, Br Med J 299:1014, 1989.
32.
Yonkers AJ et al: Etiology and management of epistaxis, Ear Nose Throat J 60:453, 1981.
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Chapter 20 - Hunting and Other Weapons Injuries Edward J. Otten
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 technologic 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]
HUNTING IN THE UNITED STATES Only a few cultures still depend on hunting as their primary food-gathering method. Examples are the Mbuti tribe, Andaman Islanders, 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. The total number of hunters and trappers is unknown. Many participate illegally and are not licensed. Throughout the United States, 30 million hunting licenses were sold in 1988. 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 during the 4-year period 1983–1986, with a total of 6992 injuries from firearms. 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. Hunting injuries are only a small portion of the total number of unintentional firearm deaths in California from 1977 to 1983, only eight were the result of hunting accidents.* Hunting injury data may be inaccurate for a number of reasons. Many minor nonfatal injuries may go unreported, and 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, could be considered 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. A common type of injury in hunters that is not associated with weapons is the tree stand injury. Tree stands are platforms designed to hold hunters several feet off the ground so that they can more easily kill large game. Whether homemade or of commercial design, the platforms generally are small and attached to the trunks of trees, with some method, usually a ladder or steps, for *References [ 8]
[ 10] [ 22] [ 29] [ 36] [ 40]
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Figure 20-1 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.
climbing the tree ( Figure 20-1 and Figure 20-2 ). Hunters often fall asleep in the platforms and fall off, or fall while climbing up or down trees. At least half of these injuries could be prevented if all hunters wore tree stand safety harnesses. 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 ( Figure 20-3 ). Over 10 years, injuries of this type in Georgia accounted for 36% of reported hunting injuries and 20% of hunting fatalities.[35] [37] 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. Other types of weapon include the bow or crossbow and arrow. These are popular because an extended hunting season is allowed in several states if this type of "primitive" weapon is used. The rationale is that these weapons are less dangerous to innocent bystanders at long range compared with rifles and shotguns, and that more skill is needed to hunt with this type of weapon. Other weapons are used for hunting but are less likely to be encountered. For example, spears, harpoons,
Figure 20-2 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.
and nets are used by some hunters in the Arctic, Australia, and Africa. 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. 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. Arrow Injuries.
Modern arrows are usually made from aluminum, graphite, or fiberglass, although many beginners still use inexpensive wooden arrows. A number of types of arrowhead are in use,
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Figure 20-3 The correct way to bring a firearm into the tree stand, with the muzzle pointing down and the hunter wearing a safety harness at all times.
such as field points and target points, but most injuries are due to broadheads. These come in a variety of sizes and shapes and are designed to inflict injury by
lacerating tissue and blood vessels, thereby causing bleeding and shock. Unlike firearms, which are designed to kill quickly by tearing tissue and transferring large amounts of energy, arrows usually kill more slowly with less tissue damage ( Figure 20-4 ). [4] [19] Arrows are propelled by a conventional bow, which may be straight, recurved, or compound, or by a crossbow. 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 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 and must be more accurately placed to kill the animal quickly; therefore most shots are taken under 50 m (164 feet). Because brush and tree branches can easily deflect an arrow, most shots are taken with a clear field of view. For these reasons, target identification is usually not a problem and a bow hunter is less likely to shoot another hunter. Most arrow injuries occur when hunters fire illegally at night in heavy brush and are not
Figure 20-4 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.
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 cross-bow 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; injuries commonly occur when a hunter is sharpening the blade of the arrow or returning an arrow to the quiver. Injuries from Firearms.
Firearms discharge a projectile by using air, modern fast-burning powders, or old-fashioned black powder. Air guns use a spring or carbon dioxide cartridge to push the projectile from the barrel. Although air guns are quite accurate at short distances, the projectiles cannot usually penetrate skin from distances greater than 100 m (328 feet). Air guns are commonly used by children, who cannot legally obtain or use other types of firearms. Well-meaning parents buy them as toys, erroneously believing them to be safe. The wounds they cause can be lethal, especially from the spring-propelled guns, which can send out lead pellets at sufficiently high velocities to penetrate bone. Black powder weapons use a solid propellant that is ignited with a spark from flint striking steel or a percussion cap. When ignited, the propellant is rapidly converted to a gas that expands and pushes a lead ball out of the barrel of the weapon. These weapons are quite accurate and are used 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 below. The same precautions should be used when hunting with or shooting any type of firearm, whether the propellant is air or gunpowder.[24] [28] [39] The powder (propellant) in weapons that use modern gunpowder is encased in a brass or aluminum shell for rifles and handguns and in a plastic or paper shell for shotguns. Shells are open on one end for the actual projectiles to be inserted, and in the case of shotgun
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shells, plastic or cotton wadding is used to keep the projectiles from moving around inside the shells. The powder is detonated from the opposite end by an explosive primer that is in either the rim of the shell, as with the .22 caliber long rifle cartridge, or the middle of the shell, as with the 12-gauge shotgun shell or 30/30 rifle cartridge. Detonation occurs when the firing pin on the weapon strikes the primer, igniting the powder. Upon detonation the powder produces a rapidly expanding gas that pushes the projectile (and wadding) out of the barrel of the weapon. Not all of the powder is burned, so that in case of close-proximity wounds, powder stippling may appear on clothing or skin. With contact wounds the escaping gases may cause bursting of the skin and a stellate laceration near the point of entrance. The projectile may vary in size and shape from 1 mm in circumference and a few milligrams in weight to 2 cm in circumference and 100 g in weight. The projectiles are usually made of lead or steel and may be covered with a copper jacket. They are usually single when shot from a rifle or pistol and multiple when fired from a shotgun, although some hunters prefer large single (deer slug) rounds fired from shotguns. Hundreds of types of bullets or rounds are available for firearms. They may be factory loaded or hand loaded, which adds the variables of propellant amount and type. Small arms are classified according to caliber, which is expressed in fractions of an inch; for example, .22 caliber means the diameter of the bullet is 0.22 inch; .45 caliber is 0.45 inch; and so forth. The caliber may be expressed in metric measurement; for example, a 9 mm bullet is 9 mm in diameter, which also happens to be 0.357 inch. This system can be made more complicated when considering the amount of powder used, the year the bullet was adopted, or the name of the person who first introduced the round. Examples of these types are .45/70 (70 grains of powder), .30-06 (adopted in 1906), and .35 Whelen (the man who developed the round). 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 20-gauge, 1/20 pound. The higher the gauge, the smaller the barrel and the smaller the round. The only exception is the .410 shotgun, which is caliber .410 or 0.410 inch in diameter. The recent introduction of the term "magnum" refers more to the type and amount of powder than to the size of the bullet used ( Figure 20-5 and Figure 20-6 ). 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 = ½ MV2 , can be applied to any moving object or to calculate the
Figure 20-5 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 shot-shell, .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 20-6 Examples of shotgun rounds. Left to right, 12-gauge slug round, empty 12-gauge plastic round, plastic 12-gauge wadding, and number six shotgun pellets.
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/sec are considered high velocity, 1500 to 2500 feet/sec medium velocity, and less than 1500 feet/sec low velocity ( Table 20-1 ). 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 strike at an angle, yaw, mushroom, or fragment present more surface area than do bullets that stay in one axis and maintain one shape. Hunting bullets are designed to manipulate shape and composition to maximize surface area. By the Geneva Convention, military bullets must have a full metal jacket and be less than .50 caliber. This is designed 499
CALIBER
TABLE 20-1 -- Comparison of Bullet Caliber, Weight, Velocity, and Muzzle Energy MUZZLE VELOCITY (feet/sec) MUZZLE ENERGY (foot-pounds)
WEIGHT (g)
.22
40
1080
90
.223
55
3250
1280
.44 magnum
180
1600
1045
.30/60
150
2750
2500
to minimize surface area. However, most military rounds travel at such high velocities (greater than 2700 feet/sec) that fragmentation reliably occurs even with full metal jackets. Fragmentation may also occur when a bullet strikes bone and sends splinters in several directions. The bone fragments cause injuries within the body similar to those from bullet fragments and may even exit the body to injure bystanders. Another phenomenon is temporary cavitation, which occurs at all velocities to some degree but becomes a factor only at high velocities. A permanent cavity occurs when a bullet or fragment crushes tissue. The bullet also creates a radial dispersion wave as a result of acceleration of tissue away from its path, which creates a temporary 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. In high-velocity bullet wounds the temporary cavity may be several times larger than the permanent cavity. The total effect of high energy, fragmentation, mushrooming, yaw, and temporary cavity formation injures tissue. Although the kinetic energy formula cannot be denied, the other factors are probably more important to injury production. The type of tissue struck is the most important factor. As can be seen from Table 20-1 , the .22 caliber long rifle 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, most people are shot by this round. The bullet is highly lethal when striking the brain, the heart, or a major blood vessel.* 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 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.
Traps are designed to either 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 will often bite or claw anyone within range. Leg hold 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 touching a trigger plate usually only involving 1 to 2 pounds of pressure. Most injuries involve the foot, but any area of the body that can fit between the jaws can potentially be injured. The jaws can be released by compressing the spring controlling the jaws ( Figure 20-7 ). 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. Nonconventional 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. Unexploded Ordnance.
There are many areas in the world where unexploded ordnance can be found. This may include aerial bombs, rockets, artillery and mortar shells, grenades, and mines. Any area of the planet where a war has been fought in this century has potential for harboring these items. Crews excavating streets in urban areas of England, France, and Germany often uncover unexploded ordnance from World War 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 munition 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 *References [ 1]
[ 2] [ 12] [ 13] [ 14] [ 15] [ 16] [ 27] [ 34] [ 38]
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Figure 20-7 A, A leghold trap set. B and C, A leg hold trap sprung. D and E, How to release a trap that has been sprung by standing on each end of the trap and compressing the spring.
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. Land mines may be commercially manufactured or produced locally from available materials ( Figure 20-8 ). Commercial, currently produced United States land mines 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; these are so-called antipersonnel mines. These may be blast or fragmentation type; the fragmentation type may be either directional or nondirectional ( Figure 20-9 ). These 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 501
Figure 20-8 An example of an antipersonnel mine manufactured by the Soviet Union.
Figure 20-9 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.
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 pressure types of triggers and occasionally are command detonated, especially for antitank purposes. Many antitank mines will not explode unless a pressure of 300 to 400 pounds is applied. The M14 blast antipersonnel mine needs only 20 to 30 pounds 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 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 or 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 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 25 to 50 m (82 to 164 feet), with casualties occurring out to 200 m (656 feet). 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
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on a larger scale, sometimes involving scores of victims. 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, so 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 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 density 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 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/or 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 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.* Treatment of Hunting Injuries The treatment of hunting injuries involves standard principles and priorities of trauma care. Airway, breathing, circulation, bleeding 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 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. 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 *References [ 3]
[ 5] [ 9] [ 11] [ 17] [ 18] [ 20] [ 21] [ 23] [ 25] [ 26]
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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 protruding from the wound to make transport easier if this can be accomplished with a minimum of arrow movement. A large pair of paramedic types of 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 then 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 ( Figure 20-10 ). Gunshot Wounds.
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 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. 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
Figure 20-10 Arrow wound to the left side of the neck near the mandible. The shape of the wound resembles the blades of the broad-head as shown in Figure 20-4 .
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. Victims in shock should be taken to the operating room immediately. If this is not possible, type O-negative or type-specific blood should be transfused. Autotransfusion, when available, can be an ideal way to replace lost blood in the victim in shock. Military antishock trousers or pneumatic antishock garments have not been shown to be beneficial in the treatment of shock secondary to penetrating trauma. 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 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. Many myths associated with the management of gunshot wounds should be repudiated. The size or caliber of a bullet cannot easily be determined from the size of the wound; skin is quite elastic and stretches before being torn by a blunt bullet. The path of the bullet cannot be determined by connecting the entrance and exit wounds, since bullets may bounce and only a fragment may exit. The exit wound may be larger or smaller than the entrance wound, and the point of entrance or exit is not easily determined by looking at the wound. 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. All gunshot wounds to the abdomen should be explored in the operating room. 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. Experience in combat has shown that vascular injuries do best when identified and treated immediately. 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.
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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, intraarticular, 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 the 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,
Figure 20-11 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.
and the deep burns may need dermabrasion or surgical debridement ( Fig. 20-11 ).[12] [27] [38] 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.[33] Prevention of Hunting Injuries Most state fish and wildlife agencies have recognized that hunters are at risk for injuries and have tried to develop programs 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 hunting-related 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 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 articles while in hunting areas. 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 and other hunters. Bow hunters should always use wrist and finger protection to prevent injuries from the arrow
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fletching and the bowstring. All arrows should be carried in a quiver until ready for use. The arrow broadhead should always be pointed away from the hunter. These few steps would probably eliminate most hunting injuries.[30] [31]
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 (see Chapter 60 Chapter 61 Chapter 62 ). 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 increased number of hooks on a lure or line also increases the 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. 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
Figure 20-12 A to D, Removal of a fishhook that has penetrated a fingertip. E, "Press-and-yank" method of fishhook removal.
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 first method can be used if the hook is not deeply embedded. 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 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 ( Figure 20-12 ). 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 or thrown or propelled by rubber straps or carbon dioxide cartridges. The more force used to propel the spear, the deeper 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
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Figure 20-13 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.
intubation and tube thoracostomy. If a spear is embedded in the cheek and interfering with the victim's airway, cutting it 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 ( Figure 20-13 ).
References 1.
Adams DB: Wound ballistics: a review, Mil Med 147:831, 1982.
2.
Amato JJ et al: Bone as a secondary missile: an experimental study in the fragmentation of bone by high-velocity missiles, J Trauma 29:609, 1989.
3.
Argyros GJ: Management of primary blast injury, Toxicology 121:105, 1997.
4.
Bear F: Fred Bear's world of archery, Garden City, NY, 1979, Doubleday.
5.
Belvoir Research, Development, and Engineering Center: Mine/countermine guide for low intensity conflict environment in Central America, Fort Belvoir, Va, 1989, Countermine Systems Directorate.
6.
Blumenschine RJ, Cavallo JA: Scavening and human evolution, Sci Am 267:90, 1992.
7.
Campbell BG: Hunting and the evolution of society. In Humankind emerging, Boston, 1979, Little, Brown.
8.
Carter GL: Accidental firearm fatalities and injuries among recreational hunters, Ann Emerg Med 18:406, 1989.
9.
Cernak I et al: Recognizing, scoring and predicting blast injuries, World J Surg 23:44, 1999.
10.
Cole TB, Patetta MJ: Hunting firearm injuries, North Carolina, Am J Public Health 78:1585, 1988.
11.
Department of the Army: Field manuals FM 20–32 mine/countermine operations and FM 5–34 engineer field data, Washington DC, 1989, US Government Printing Office.
12.
Fackler ML: Wound ballistics: a review of common misconceptions, JAMA 259:2730, 1988.
13.
Fackler ML, Bellamy RF, Malinowski JA: Wounding mechanism of projectiles striking at more than 1.5 km/sec, J Trauma 26:250, 1986.
14.
Fackler ML, Ballamy RF, Malinowski JA: The wound profile: illustration of the missile-tissue interaction, J Trauma 28:S21, 1988.
15.
Fackler ML, Malinowski JA: The wound profile: a visual method for quantifying gunshot wound components, J Trauma 25:522, 1985.
16.
Fackler ML et al: Bullet fragmentation: a major cause of tissue disruption, J Trauma 24:35, 1984.
17.
Giannou C: Antipersonnel landmines: facts, fictions, and priorities, BMJ 315:1453, 1997.
18.
Guy RJ et al: Physiologic response to primary blast, J Trauma 45:983, 1998.
19.
Hain WH: Fatal arrow wounds, J Forensic Sci 34:691, 1988.
20.
Jeffrey SJ: Antipersonnel mines: who are the victims? J Accid Emerg Med 13:343, 1996.
21.
Krug EG et al: Preventing land mine related injury and disability: a public health perspective, JAMA 280:465, 1998.
22.
Lambrecht CB, Hargarten SW: Hunting-related injuries and deaths in Montana: the scope of the problem and a framework for prevention, J Wilderness Med 4:175, 1993.
23.
Landmine related injuries, 1993–1996, MMWR Morb Mortal Wkly Rep 46:724, 1997.
24.
Lawrence HS: Fatal nonpowder firearm wounds: case report and review of the literature, Pediatrics 85:177, 1990.
25.
Lein B et al: Removal of unexploded ordnance from patients: a 50 year military experience and current recommendations, Mil Med 164:163, 1999.
26.
Liebovivi D, Ofer NG, Shmuel CS: Eardrum perforation in explosion survivors: is it a marker for pulmonary blast injury? Ann Emerg Med 34:168, 1999.
27.
Lindsey D: The idolatry of velocity, or lies, damn lies and ballistics, J Trauma 20:1068, 1980.
28.
Lucas RM, Mitterer D: Pneumatic firearm injuries: trivial trauma or perilous pitfalls? J Emerg Med 8:433, 1990.
29.
National Safety Council: Accident facts 1987, Washington, DC, 1987, The Council.
30.
Ohio hunter safety education student handbook, Ohio Division of Wildlife, Seattle, 1981, Outdoor Empire.
31.
Pryce D: Safe hunting, New York, 1974, David McKay.
32.
Strada G: The horror of land mines, Sci Am p 40, May 1996.
33.
Stromberg BV: Symptomatic lead toxicity secondary to retained shotgun pellets, J Trauma 30:356, 1990.
34.
Sykes LN, Champion HR, Fouty WJ: Dum-dums, hollow-points, and devastators: techniques designed to increase wounding potential of bullets, J Trauma 28:618, 1988.
35.
Tree stand-related injuries among deer hunters—Georgia, 1979–89, MMWR Morb Mortal Wkly Rep 38:697, 1989.
36.
US Department of the Interior, Fish and Wildlife Service: 1985 national survey of fishing, hunting and wildlife associated recreation, Washington, DC, 1988, US Government Printing Office.
37.
Urquhart CK et al: Deer stands: a significant cause of injury and mortality, South Med J 84:686, 1991.
38.
Walker ML, Poindexter JM, Stovall I: Principles of management of shotgun wounds, Surg Gynecol Obstet 170:97, 1990.
39.
Walsh IR et al: Pediatric gunshot wounds—powder and non-powder weapons, Pediatr Emerg Care 4:279, 1988.
40.
Wintemute GJ et al: Unintentional firearm deaths in California, J Trauma 29:457, 1989.
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Chapter 21 - Orthopedics Thomas J. Ellis Marc F. Swiontkowski
SKELETAL SYSTEM INJURIES In the wilderness, initial management of a person with a musculoskeletal injury must consider the cause of the injury; the direction of force in relation to the individual or limb so the victim can be checked for injuries to adjacent bones and joints; the time of the injury, because the length of time to treatment may determine prognosis; and the environment where the accident has occurred, including cold, wind, or heat exposure, especially with open wounds that communicate with fractures. Once the victim's condition is stabilized, examine the skeletal system closely beginning with the spine, moving to the pelvis, and ending with the extremities.
SPINAL INJURIES Cervical Spine In the wilderness, cervical spine fractures or dislocations result from falls off significant heights or high-velocity ski or vehicular injuries. Because head and cervical spine injuries are highly associated, individuals with significant head injuries are considered to have a cervical spine injury, especially if unconscious. Ideally, a person with a suspected cervical spine injury is placed on a backboard, with neck immobilization, and evacuated. Neurologic deficit often results from cervical spine fracture. Fracture of the C1-2 complex results from axial loading (a C1 ring fracture—Jefferson's fracture) or an acute flexion injury (a C2 posterior element fracture—hangman's fracture). Complete neurologic injury at this level is fatal because of paralysis of the respiratory muscles, so surviving victims generally have partial deficits or are neurologically intact. Axial cervical spine fractures may result from flexion (most common), extension, rotational forces, or a combination of these, and most commonly occur at C5-6.[3] Fractures and dislocations may result in neurologic insult distal to the bony injury. Because flexion injuries are the most common cervical spine injuries, the neurologic deficit is generally an anterior cord syndrome. The victim suffers complete motor and sensory loss but retains proprioception. The field examination aims to grade motor strength, document sensory response to light touch and pinprick, and note the presence or absence of Babinski's reflex. When appropriate supplies are available, do a rectal examination. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicate spinal cord injury. When transporting an individual with a cervical spine fracture or dislocation, stabilize the neck to prevent further injury. Because 28% of persons with cervical spine fractures also have other spinal fractures, protect the entire spine.[3] A pure flexion event may dislocate one or both posterior facets, producing neck pain and limitation of motion. Because the interspinous ligament is ruptured, transport this victim with the neck rigidly immobilized to accommodate the posterior instability. Thoracolumbar Spine Thoracolumbar spine fractures occur most frequently at the thoracolumbar junction. Because the thoracic spine is well splinted by the thoracic cage, when an axial or flexion load is applied, the ribs diminish forces on the thoracic vertebral bodies and transmit the force to the upper lumbar levels. In the wilderness, falls from significant heights or high-velocity sporting vehicular trauma produce these fractures ( Figure 21-1 ). Thoracolumbar spine fracture is frequently associated with major hindfoot fractures (particularly of the calcaneus). With these mechanisms of injury and unilateral or bilateral calcaneus fracture, assume there is a spine fracture and transport the victim with spine precautions. Perform a careful neurologic examination as part of the secondary survey, paying close attention to the dermatomal response to light touch and pinprick, motor function, and the presence or absence of cord level reflexes. With significant head injury, assume a spinal injury is present. Logroll the victim, maintaining perfect spinal alignment, and carefully place him or her on a backboard, or use the scoop stretcher (see Chapter 26 ). Because significant fluctuations in sympathetic tone may occur, monitor blood pressure and body temperature, taking appropriate steps to cool or warm the victim.
PELVIC INJURIES Pelvic fractures generally occur in a fall from significant height, high-velocity ski accident, or vehicular trauma. The direction of force is directly related to the fracture and influences definitive management.[9] [11] Penna and Tile[5] [11] divide pelvic fractures into anteroposterior (AP) compression injuries, lateral compression (LC) injuries, and vertical shear (VS) injuries. In
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Figure 21-1 Wedge compression fracture from axial or flexion loading at the thoracolumbar junction.
addition, there are simple, nondisplaced inferior or superior ramus fractures and avulsion fractures. On clinical examination, these latter fractures are generally seen as an area of tenderness but no instability. The key factor in pelvic fracture is identification of posterior injury to the pelvic ring, which is associated with significant hemorrhage, neurologic injury, and mortality. Posterior ring fractures are revealed by instability of the pelvis associated with posterior pain, swelling, ecchymosis, and motion. Immediately evacuate this victim on a backboard, taking care to minimize leg and torso motion. Bleeding associated with a pelvic injury is from cancelleous bone at fracture sites, retroperitoneal lumbar venous plexus injury, or, rarely, pelvic arterial injuries. LC injuries are usually stable, with impaction of the posterior structures but seldom any complications. AP compression injuries demonstrate anterior instability, palpable ramus fractures, or public symphysis gapping. These fractures are often accompanied by bladder, prostatic, or urethral injury. Transport the victim on a backboard with the feet internally rotated to help reduce the anterior pelvic diastasis. With severe injury and hemodynamic instability, medical antishock trousers (MAST) provide stability and decrease intrapelvic blood loss. Keep them inflated until transfer to a definitive care center. If MAST are not available, tie a garment securely around the pelvis. Because vertical shear injuries are both rotationally and vertically unstable, definitive care is directed toward providing posterior stability, as it is for those few lateral compression injuries with unstable posterior fractures. In an AP injury, symphyseal widening exceeding 2.5 cm indicates injury to the anterior capsular structures of the sacroiliac joint, requiring stabilization with internal or external fixation.
EXTREMITY INJURIES Physical Examination Physical examination addresses circulatory, nerve, skeletal, and joint function. Circulatory Function.
Penetrating or blunt trauma can injure the major vessels supplying the limbs. Fractures can produce injury by direct laceration (rarely) or by stretching, which produces intimal flap tears that can occlude distal flow or lead to platelet aggregation and delayed occlusion. Thus circulatory function examination is done before and after the victim's arrival at the definitive care center. Assess the color and warmth of the skin or distal extremity; pallor and asymmetric regional hypothermia may indicate vascular injury. In the upper extremity, palpate the brachial, radial, and ulnar arteries, using hand-held, battery-powered sound Doppler units if available. If blood loss, hypothermia, or obesity makes these pulses difficult to assess, evaluate temperature and color. Any suspected major arterial injury mandates immediate evacuation after appropriate splinting. Nerve Function.
Nerve function may be impossible to assess in an unconscious or uncooperative person. If possible, establish nerve function to the distal extremity after the victim's condition is stabilized. Then compare these initial findings periodically with repeat examinations during transport, noting any deterioration. Carefully document the results of light touch and pinprick tests. For spinal and pelvic injuries, assess the dermatomal distribution of spinal nerves, and evaluate muscle function by observing active function and grading the strength of each group against resistance. Skeletal Function.
The long bones of the lower extremity serve as the major structural supports for locomotion, whereas those of the upper extremity stabilize the soft tissues, enabling positioning of the hand in space. A visible angular deformity reveals a fracture; palpable crepitus confirms the diagnosis. Perform appropriate splinting after aligning the limb with axial traction. Other than noting the degree and orientation of the limb's position when the victim is found, do not delay aligning and splinting fractures. Distinguishing joint injuries and intraarticular or very proximal or distal fractures must wait for the definitive care facility. Similarly, distinguishing wrist or ankle ligamentous injury from a fracture is not required for initial treatment.
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Joint Function.
Muscle forces act across joints to improve the position of the lower limbs for ambulation and the hand for handling objects. Each joint has a certain minimum function to allow for stability and a normal range of motion. Making the diagnosis of a joint injury in the field allows appropriate splinting and prevents further damage during transport. Begin palpation of long bones distally and proceed across all joints. Apply a splint if there is palpable crepitus, swelling, deformity, or a block to motion. If the victim can cooperate, take each joint through an active range of motion to quickly locate the injury. When this is not possible, evaluate passive motion of each joint after palpation for crepitus and swelling. Reduce any dislocations after completing the neurocirculatory examination. This generally relieves the victim's discomfort considerably. Next, evaluate stability by careful, controlled motion. Joints with associated fractures or interposed soft tissues are frequently unstable after reduction. Take great care in applying splints to prevent redislocation. Report details of the reduction maneuver, including orientation of the pull, amount of force involved, amount of sedation, and residual instability of the joint, to the definitive care physician. Splinting Techniques (see also Chapter 19 ) With suspected cervical or thoracolumbar spine trauma, transport the victim on a hard surface. Backboards or scoop stretchers (see Chapter 26 ) are most effective, but improvisation with any hard piece of wood, fiberglass, or straight tree limbs lashed together may be needed. If cervical spine injury is suspected, place a roll of clothes or a water bottle as high as the victim's mid face on either side of the head to prevent rotational movement. Apply tape from the supporting stretcher across the objects and the victim's forehead to add stability. Transport victims with a suspected major pelvic injury in similar fashion, stabilizing the lower extremities. For shoulder fractures or dislocations, use a commercially available sling or improvised triangular bandage to take the weight of the arm off the injured structures. Whenever possible, splint the upper extremity in the position of function. It may be difficult to place an injured elbow in 90 degrees of flexion and neutral pronation-supination. Securely fix the limb to the splint with tape or elastic bandages. Air splints, when inflated, can adequately splint the upper extremity in this position. These splints are lightweight and compact but should be used with caution under conditions such as heat and rapid increase in altitude in which they might expand and compress the limb. Splints may also be made from plaster or fiberglass, which can be applied over cotton softroll. Lightweight fiberglass splints, such as Orthoglass (Smith and Nephew), are easy to use and effective in
Figure 21-2 Improvisation of an ankle wrap to be used for traction.
the initial management of these injuries. These splints are prepadded and can be applied with either cold or warm water. The warmer the water, the faster the fiberglass sets and the greater the exothermic reaction. Avoid hot water because it may generate an excessively exothermic reaction and possibly burn the skin. Immerse the fiberglass in the water, gently squeeze out the excess, and apply the splint. An elasticized bandage helps hold the splint where desired until the fiberglass is hard. Wooden or metal splints, custom made or improvised, also work. Splints are used to immobilize the limb securely in functional position until definitive care is reached. Apply hand splints with the metacarpophalangeal (MCP) joints flexed 90 degrees and the interphalangeal (IP) joints extended. This position places the collateral ligaments at maximum length and prevents later joint contracture. Position the lower extremity for transport with the hip and knee extended and the ankle in neutral position. With hip or femur fractures or dislocations, apply traction whenever possible, improvising when necessary ( Figure 21-2 ). Usually, a Thomas splint with a Spanish windlass is available. The ring of the splint rests against the victim's ischium and pubis, and traction is applied through the windlass, stabilizing the
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joint or fracture fragments. The Kendrick traction device is lightweight and packaged for easy transportation. If commercial splints are unavailable, strap the injured leg to the noninjured leg, placing a tree limb or walking stick between them. If possible, transport the victim on a backboard. For the lower leg, air splints provide adequate immobilization of tibia-fibula fractures or ankle fractures and dislocations. Splints made from plaster or fiberglass may be applied over cotton padding with elasticized wraps. Custom-made or improvised metal splints can be stabilized with elastic bandages or tape. Hold the ankle in neutral and apply the splint firmly. Transport victims with unstable lower extremity fracture or dislocation in the recumbent position with the limb elevated. Open Fractures Recognizing an open fracture is imperative; without prompt surgical treatment, the incidence of osteomyelitis is high. In an open fracture, the fractured bone communicates with a break in the skin. Consider all lacerations near a fracture as open. With subcutaneous bones (tibia), open fractures are easily identified, but with other bones (humerus, femur, pelvis) that have more surrounding soft tissue, identification is more difficult because the fractured bone end usually retracts once it punctures the skin and is then covered by soft tissue. Most open fractures persistently ooze blood from the laceration, which may facilitate diagnosis. Fat globules may be extruding from the wound. General care of an open fracture outdoors depends on evacuation time. Open fractures require prompt operative irrigation, debridement, and stabilization. If evacuation can be completed within 8 hours, realign the fracture, give a broad-spectrum antibiotic, and splint the extremity. If the fractured ends of the bones are sticking out of the skin, try to realign the fracture and reduce the bone ends under the skin. If bone ends extrude through the skin, cover the exposed bone with a povidone-iodine solution-soaked gauze sponge, splint the extremity, and arrange for prompt evacuation. If evacuation time exceeds 8 hours, attempt irrigations, limited debridement, and stabilization with a splint in the field. Antibiotic options are listed in Box 21-1 . Amputation In the wilderness, the amputation victim requires immediate evacuation. Control hemorrhage using direct pressure; tourniquets are virtually never indicated. Without cooling, an amputated part remains viable for only 4 to 6 hours; with cooling, viability may be extended to 18 hours. Cleanse the amputated part with saline or water, wrap it in a moistened sterile gauze or towel, place it in a plastic bag, and transport it in an ice-water mixture. Do not use dry ice. Keep the amputated part with the victim throughout evacuation.
Box 21-1. ANTIBIOTIC OPTIONS
INTRAVENOUS Cefazolin (Ancef) 1 g q8h and gentamicin (5 mg/kg) q24h or ticarcillin (Timentin) 3.1 g q8h
INTRAMUSCULAR Ceftriaxone (Rocephin) 1 g q24h Oral ciprofloxacin 750 mg BID and cephalexin (Keflex) 500 mg QID
WATER EXPOSURE Ciprofloxacin 400 mg IV/750 mg po BID or sulfamethoxazole (Bactrim) DS 1 po BID and cefazolin (Ancef) 1 gm IV q8h/cephalexin (Keflex) 500 mg po q6h
DIRT OR BARNYARD Add penicillin 20 million units IV qd/500 mg po q6h
PENICILLIN ALLERGIC Use clindamycin 900 mg IV q8h or 450 mg po q6h in place of penicillins and cephalexin (Keflex)
ALTERNATIVES Erythromycin 500 mg q6h or amoxicillin 500 mg po q8h
Compartment Syndrome A compartment syndrome begins when locally increased tissue pressure reduces arterial blood flow to a muscle compartment. When local blood flow is unable to meet metabolic demands of the tissue, ischemia ensues. In the wilderness, compartment syndromes most frequently occur in association with fractures or severe contusions. This syndrome can occur when the victim has been lying for some time across a limb so that the body weight occludes the arterial supply. Elevated local tissue pressure (compartment pressure within 10–20 mm Hg of diastolic arterial blood pressure) can occur with acute hemorrhage or after revascularization of an ischemic extremity. Hypotension can lower the risk of a compartment syndrome. The lower leg and forearm are the most common sites for a compartment syndrome because of the tight fascia in these regions, but it also occurs in the thigh, hand, foot, and gluteal regions. The conscious victim complains of severe pain out of proportion to the injury. The muscle compartment feels extremely tight, and applied pressure increases the pain. There is deceased sensation to light touch and pinprick stimuli in the areas supplied by the nerves traversing the compartment. Stretching muscles within the compartment produces severe pain. The most reliable signs of a compartment syndrome are pain, tight compartments, hypesthesia, and pain on passive stretch. Pulselessness,
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pallor, and slow capillary refill may not be observed, even with a severe compartment syndrome. Emergency evacuation is required. The victim must be definitively treated in the first 6 to 8 hours after onset to optimize return of function to the involved limb. Emergency fasciotomy, the treatment of choice, relieves the pressure. Limited fasciotomies can be performed in the field by an experienced surgeon if evacuation will require more than 8 hours. RICE Principle The general principle in the acute management of all extremity injuries is rest, ice, compression, and elevation (RICE). For unstable fractures, immobilization is also indicated. Avoid heat for the first 72 hours after injury. Premade chemical cold packs work well, but cold packs made from ice or snow suffice. If ice is used, mix some water in a bag with the ice to more evenly distribute the cold. Wrap the cold pack to the injured area with an elasticized bandage. Place a thin piece of fabric between the cold pack and the victim's skin to prevent burning of the skin. Apply the ice to the elevated (above the level of the heart) extremity for 30 to 45 minutes every 2 hours, or, if cold packs are unavailable, immerse the extremity intermittently in a cold mountain stream. A compressive dressing also helps decrease swelling, but should not be used if compartment syndrome is possible. In this situation, keep the limb at the level of the heart and avoid compressive dressings.
UPPER EXTREMITY FRACTURES Clavicle Fracture of the clavicle usually occurs in the middle or lateral thirds of the bone and is associated with a direct blow or with a fall onto the lateral shoulder. Clavicle fractures are common with snow skiing. The victim complains of shoulder pain, which may be poorly localized. Arm or shoulder motion exacerbates the pain. To localize the problem, gently palpate the clavicle to identify the area of maximum tenderness. The presence of crepitus at the clavicle confirms the diagnosis. Although rare, a clavicle fracture can be associated with a pneumothorax because the cupula of the lung is punctured; therefore auscultate the chest for breath sounds. Shortness of breath and deep pain on inspiration increase suspicion for a pneumothorax. Clavicle fracture may also accompany injury to the brachial plexus and axillary artery or subclavian vessels. Perform a thorough neurocirculatory examination of the affected extremity and examine the skin carefully. Approximately 3% to 5% of clavicle fractures may be open because of the bone's subcutaneous location. Evacuate the victim if there is a significant open wound, suspected pneumothorax, or nerve or vascular injury. Field treatment
Figure 21-3 To control pain, a fractured humerus should be stabilized manually until a splint can be applied.
for a clavicle fracture consists of a figure-eight bandage or sling and judicious use of analgesics. Humerus Fracture of the humeral shaft may result from a direct blow or torsional force on the arm. This fracture frequently occurs with a fall, rope accident, or skiing accident. Fractures of the midshaft and junction of the middle and distal third of the humeral shaft violate the spiral groove path of the radial nerve. If there is arm pain with deformity and crepitus, stabilize the arm, and carefully check the sensory and motor function of the radial nerve as part of the overall neurocirculatory examination ( Figure 21-3 ). Evaluate radial nerve function by checking sensation in the dorsal thumb web space and MCP extension with the proximal and distal IP joints flexed. When fracture of the humeral shaft is suspected, firmly apply an appropriate coaptation splint made of plaster, fiberglass, or wood with an elastic bandage on the medial and lateral sides of the humerus. Use a sling for comfort. Acute reduction of the fracture is not routinely required. Fracture of the proximal humerus is often difficult to differentiate from shoulder dislocation in the acute phase. The mechanism is frequently a high-velocity fall onto an abducted, externally rotated arm, or a direct blow to the anterior shoulder. The victim complains of severe pain around the shoulder with palpation or any arm motion. Palpable crepitus confirms the diagnosis. This fracture does not routinely require acute reduction; application of an arm sling is appropriate field management. Fracture-dislocation of the proximal humerus can also occur, with most dislocations being anterior. Anterior or posterior fullness, with crepitus on the injured side compared with the uninjured side, suggests the diagnosis. This is a more severe injury, so perform a very careful neurocirculatory examination. Any significant nerve or vascular injury should prompt evacuation to a definitive care center. If the injury is identified and definitive care
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Figure 21-4 Nursemaid's elbow most commonly occurs when a longitudinal pull is applied to the upper extremity. Usually the forearm is pronated. There is a partial tear in the orbicular ligament, allowing it to subluxate into the radiocapitellar joint. (From Rockwood CA Jr, Willkins KE, King RE, editors: Fractures in children, ed 3, Philadelphia, 1991, JB Lippincott.)
is more than 1 to 2 hours away, attempt reduction. Using available sedation, stabilize the trunk while applying firm longitudinal traction in line with the arm. Have an assistant apply anterior pressure to the humeral head to ease it back into the glenoid joint space. Avoid any maneuver that compresses the brachial plexus (i.e., a foot in the axilla for countertraction). Fracture of the distal humerus is more frequently extraarticular in children and intraarticular in adults. Children generally sustain supracondylar fractures after falls from heights. Extension-type injuries are much more common than flexion-type, and they most commonly occur in children ages 4 to 8 years. Deformity, swelling, pain, and crepitus are present, and the diagnosis is fairly obvious. Perform a careful neurocirculatory examination, then focus the motor examination on flexion of the thumb and distal IP joint of the index finger, because injury to the anterior interosseus nerve is frequently associated. If the radial pulse is absent, try to flex or extend the elbow while palpating the radial pulse. If the pulse improves, splint the limb in that position for transport. If the pulse does not improve and definitive care is more than 1 hour away, perform a reduction. After available sedation is given, extend the supinated elbow with gentle longitudinal traction. Reduce the fracture by flexing the elbow while maintaining longitudinal traction, then splint the elbow in 90 degrees of flexion. Evacuation should be performed promptly. For the adult with pain, crepitus, deformity, and swelling after a fall, perform the neurocirculatory examination, then apply a splint with the elbow at 45 or 90 degrees of flexion, depending on the victim's comfort. Do not attempt reduction without radiographic confirmation because crepitus is more often associated with a fracture than with a dislocation. Evacuate the victim promptly if there is an open fracture or neurocirculatory deficit. Subluxation of the radial head in children (nursemaid's elbow) occurs when a longitudinal pull is applied to the upper extremity ( Figure 21-4 ). The orbicular ligament partially tears, allowing a portion of it to slip over the radial head. An audible snap may be heard at the time of the injury. The initial pain from the injury subsides rapidly, and the child does not seem distressed, but refuses to use the extremity. Any attempt to supinate the forearm brings about a cry of pain and distress. If a definitive care center is nearby, splint the injury and arrange for evacuation. Otherwise, if the history and examination are consistent with the diagnosis, attempt a reduction. First supinate the slightly flexed forearm; if this fails to produce the characteristic snapping sensation of reduction, maximally flex the elbow in supination until the snapping sensation occurs ( Figure 21-5 ). If the reduction is successful, the child is usually content and playing within 5 to 10 minutes, and no immobilization of the joint is indicated. If the reduction is unsuccessful, the child continues
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Figure 21-5 Reduction of nursemaid's elbow injury. Left, the forearm is supinated. Right, the elbow is then hyperflexed. The rescuer's thumb is placed laterally over the radial head to feel the characteristic snapping as the ligament is reduced. (From Rockwood CA Jr, Willkins KE, King RE, editors: Fractures in children, ed 3, Philadelphia, 1991, JB Lippincott.)
to avoid using the involved arm and should be evacuated for definitive care.
Radius Radial shaft fracture is commonly associated with a motor vehicle or industrial accident but may occur with a fall involving angular or axial loading of the forearm. A radial shaft fracture may be associated with dislocation of the distal radioulnar joint (Galeazzi's fracture), so examine the wrist for tenderness, swelling, and deformity. The victim generally complains of pain, and deformity and crepitus are noted over the radial shaft after a fall or direct blow, with any arm motion exacerbating the pain. When both the radius and ulna are fractured, forearm instability is marked. Always examine the joint above (elbow) and the joint below (wrist) for tenderness, crepitus, and deformity. Once a fracture of the radius or both bones of the forearm is identified, splint the wrist, forearm, and elbow in the position of function. Fractures of the radial head generally occur in young to middle-aged adults who fall onto outstretched hands. The victim complains of pain about the elbow, with loss of full extension, and pain at the radial head on the lateral side of the elbow with gentle pressure and rotation of the forearm. Fracture of the radial head frequently produces an elbow hemarthrosis, which is identifiable by fullness posterior to the radial head and anterior to the tip of the olecranon. A fluid wave can be ballotted. If equipment is available and you are confident of the diagnosis, aspirate the hemarthrosis and instill 5 ml of lidocaine. Gently move the elbow through a range of motion and then place it in a posterior splint in 90 degrees of flexion with the forearm supinated. On a prolonged expedition when definitive care cannot be reached, remove the splint after 5 days and have the victim perform intermittent range of motion exercises (both flexion/extension and pronation/supination), reapplying the splint for comfort. With more comminuted radial head fractures, attempts at motion produce pain and crepitus and motion remains restricted. These injuries require operative treatment. With nondisplaced or minimally displaced radial head fractures, early motion prevents permanent loss of motion, although most individuals lose some extension and pronation/supination. Splint the arm in supination to prevent contracture of the intraosseus ligament and loss of supination. Fracture of the distal metaphyseal radius is generally associated with a fall onto the outstretched hand of an older osteoporotic individual. In the wilderness, these fractures occur in younger adults with falls from significant heights onto outstretched hands. Intraarticular distal radius fracture often accompanies fracture of the ulnar styloid. Pain, deformity, and crepitus are obvious. Perform a distal neurocirculatory examination, focusing on the sensory function of the median nerve. When there is neurocirculatory compromise, and definitive care is more than 1 to 2 hours away, perform a gentle reduction. Place one hand on the forearm to provide countertraction and the other around the wrist of the involved extremity. Dorsiflex the wrist and apply longitudinal traction as the wrist is returned to a neutral position. Apply a splint that immobilizes the wrist and elbow. Distal radius and ulna fractures occur most commonly in girls ages 11 to 13 years and in boys ages 13 to 15. These fractures are not usually comminuted but can be difficult to reduce ( Figure 21-6 ). In cases involving an open fracture, significant distal neurologic deficit, or abnormal circulatory examination, splinting and evacuation should be prompt. Keep the limb elevated above the heart during transport. Ulna Ulna shaft fracture is most often associated with fracture of the radial shaft at the same level. When isolated, it usually occurs as a result of a direct blow, the so-called nightstick fracture. Fracture of the ulnar shaft can be associated with dislocation of the radial head (Monteggia's lesion), so assess elbow function carefully. In the wilderness, the most frequent mechanism of injury is bracing a fall or collision with the forearm. Pain, localized swelling, and crepitus are present. Apply a long-arm splint in the position of function. An open fracture is an indication for prompt evacuation. Fracture of the proximal ulna (olecranon) results from a fall onto the posterior elbow, or avulsion with
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Figure 21-6 Technique for reduction of a complete fracture of the forearm. A, Initial fracture position. B, Hyperextend fracture to 100 degrees to disengage the fracture ends. C, Push with the thumb on the distal fragment to achieve reduction. (B and C modified from Levinthal DH: Surg Gynecol Obstet 790, 1933. A to C from Green N, Swiontkowski MF: Skeletal trauma in children, vol 3, ed 2, Philadelphia, 1998, WB Saunders.)
violent asymmetric contraction of the triceps muscle. The victim may be unable to extend the elbow actively against gravity if the triceps is dissociated from the forearm with a complete olecranon fracture. On initial examination, the victim has pain, significant swelling, and a palpable gap in the olecranon. With severe trauma, olecranon fracture may be associated with an intraarticular fracture of the distal humerus, which can only be diagnosed radiographically. Do a complete distal neurocirculatory examination, examine the shoulder and wrist, then apply a splint in the position of function and comfort. An open fracture, absent pulse, severe swelling, or neurologic deficit should prompt immediate evacuation. Wrist Wrist fractures occur with significant rotational forces or high axial loading forces, as occur in falls onto the
Figure 21-7 The scaphoid (navicular) bone sits in the "anatomic snuffbox" of the radial aspect of the wrist
hand. The victim first complains of pain and later wrist swelling. Hand use or forearm rotation produces significant pain. Many carpal bone fractures are associated with wrist dislocation. Reduction of dislocations is described later. Carpal bone fractures cannot be diagnosed without radiographs. Scaphoid (navicular) fracture is the most common fracture and is suspected when the patient's area of maximum tenderness is in the "anatomic snuffbox" ( Figure 21-7 ). If appropriate splinting materials are available, apply a thumb spica splint, immobilizing both the radius and the entire thumb. With fracture of the hook of the hamate bone, the victim complains of pain at the base of the hypothenar eminence. This injury occurs when the hand is used to apply significant force to an object with a handle on it, such as an ax or hammer, and great resistance is met. A short-arm splint suffices for this injury, and for other suspected carpal injuries, until definitive treatment is obtained. With open fractures or those accompanied by median nerve dysfunction, promptly evacuate the victim. Metacarpals Fracture of the metacarpal base or shaft occurs with crush injuries or with axial loads when rocks or other immovable objects are struck. Fractures at the base of the digit metacarpals are suspected when tenderness, crepitus and, occasionally, deformity are present. Manage these with a short-arm splint. Fractures of the metacarpal necks also occur by the same mechanism and usually involve the fifth and fourth metacarpals. These fractures occur at the base of the knuckles and can be associated with significant flexion deformity. Up to 40 degrees of flexion in the
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fifth and fourth digits can be accepted without compromising hand function, so these fractures rarely require reduction. Rotational deformity of the metacarpal is poorly tolerated and should be anticipated with suspected metacarpal fractures. With the MCP and the IP joints flexed 90 degrees, the fingernails should be parallel to one another and perpendicular to the orientation of the palm. The terminal portions of the digit should point to the scaphoid tubercle.
When malalignment or significant shortening with a suspected shaft fracture is noted, reduce the fracture with longitudinal traction on the involved digit. Immobilize a fractured metacarpal shaft or neck by applying an aluminum splint (or stick) to the volar surface and taping the involved digit to the adjacent digit, with the MCP joint at 90 degrees. This is the point of maximum length of the collateral ligaments. Immobilizing the joint in this position prevents contractures that can lead to subsequent loss of motion. Fracture of the base of the thumb metacarpal often occurs with an axial force directed against a partially flexed thumb metacarpal. If the fracture extends into the joint, it often requires operative fixation. If this fracture is suspected, immobilize the thumb and wrist in a thumb spica splint. An open metacarpal fracture needs cleansing, debridement, and presumptive antibiotic therapy for 48 hours or until definitive care is obtained. Phalanges Fractures of the digital phalanges occur with crush injuries or when the digits are caught in ropes or within equipment being used to haul objects. Angular or rotational deformity and crepitus make these fractures obvious. Without radiographs, an intraarticular fracture with subluxation or dislocation is difficult to differentiate from an IP joint dislocation. Angular deformities in these fractures can be reduced using a pencil or thin stick placed in the web space as a fulcrum to assist in reduction. Reduce a fracture of the shaft of a phalanx by applying traction and correcting the deformity. Immobilize the fractures by taping the injured digit to the neighboring uninjured digit or to a volar splint. Cleanse nail-bed fractures or crushes with soap, apply a sterile dressing, and apply a protective volar splint to prevent further injury.
UPPER EXTREMITY DISLOCATIONS AND SPRAINS Sternoclavicular Joint Traumatic dislocation of the sternoclavicular joint generally requires tremendous force, either direct or indirect, applied to the shoulder, and consequently it is rare. Anterior dislocation is most common, with the medial head of the clavicle going anterior to the manubrium of the sternum. The victim complains of pain around the sternum and frequently has difficulty taking a deep breath. When the dislocation is posterior, significant pressure may be placed on the esophagus and superior vena cava. The victim may complain of difficulty swallowing and have engorgement of the veins of the face and upper extremities, representing superior vena cava obstruction syndrome. A step-off between the sternum and the medial head of the clavicle (compared with the uninjured side) confirms this diagnosis. Unreduced anterior dislocation does not produce neurocirculatory compromise and is treated with a sling. It is usually unstable after reduction. Attempt reduction of a posterior dislocation as soon as possible if any neurocirculatory compromise is present. Place the victim supine with a large roll of clothing or other firm object between the scapulae. Apply traction to the arm against countertraction in an abducted and slightly extended position. You may need to manually manipulate the medial end of the clavicle to dislodge the clavicle from behind the manubrium ( Figure 21-8 ). If this fails, apply sharp, firm pressure posteriorly to both shoulders. Repeat this maneuver several times, placing a larger object between the scapulae if reduction attempts are initially unsuccessful. Alternatively, seat the victim and place your knee between the shoulders, then pull back on both shoulders. If the victim remains in extremis, grasp the midshaft clavicle with a towel clip or pliers and forcefully pull it out of the thoracic cavity. Once reduced, the injury is usually stable. This type of dislocation requires evacuation. Acromioclavicular Joint The acromioclavicular joint is injured by a blow on top of the shoulder ( Figure 21-9 ). Because using the hand increases pain, place the arm on the affected side in a sling. As long as the individual can tolerate the discomfort associated with such an injury, evacuation is not necessary. Glenohumeral Joint The head of the humerus at the shoulder joint is generally dislocated anteriorly and inferiorly. The usual mechanism of injury is a blow to the arm in the abducted and externally rotated position. This frequently occurs in skiing as the individual crosses his or her ski tips or goes forward on a mogul and lands face first with the arms in this position. Recurrent dislocations and dislocations in younger patients may be easier to reduce than first-time dislocations in older patients. Do a thorough motor, sensory, and circulatory examination of the involved extremity. Carefully assess axillary and musculocutaneous nerves because they are the nerves most commonly injured with an anterior dislocation. Do serial examinations of distal pulses, capillary refill, and forearm compartments. The preferred method of reduction is linear traction along the axial line of the extremity while stabilizing
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Figure 21-8 Technique for closed reduction of the sternoclavicular joint. A, The patient is positioned supine with a sandbag placed between the two shoulders. Traction is then applied to the arm against countertraction in an abducted and slightly extended position. In anterior dislocation, direct pressure over the medial end of the clavicle may reduce the joint. B, In posterior dislocation, in addition to the traction it may be necessary to manipulate the medial end of the clavicle with the fingers to dislodge the clavicle from behind the manubrium. C, In a stubborn posterior dislocation, it may be necessary to sterilely prepare the medial end of the clavicle and use a towel clip to grasp around the medial clavicle to lift it back into position. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
the torso with a blanket or rope ( Figure 21-10 ). Narcotic or benzodiazepine premedication can be extremely helpful, but avoid this in a multiply-injured victim if you are concerned about altering mentation or adversely affecting blood pressure. You may tie a sheet, belt, webbed strapping, or avalanche cord around your waist and the victim's bent forearm, so that you (standing or kneeling) can lean back to apply traction, keeping your hands free to guide the head of the humerus back into position ( Figure 21-11 ). Place padding in the armpit and bend of the elbow to prevent pressure injury to sensitive nerves beneath the skin. In the Milch technique, place the patient prone or sitting upright. Place your right hand in the axilla for a dislocated right shoulder and hold the victim's hand with your left. Gently abduct the victim's arm and apply pressure to 517
Figure 21-9 Acromioclavicular joint surgery. A, Normal anatomy. B, Second-degree injury. C, Third-degree injury.
Figure 21-10 Traction and countertraction for dislocated shoulder reduction.
Figure 21-11 Pulling on the hanging arm to relocate a dislocated humerus. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.)
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Figure 21-12 Milch technique of closed reduction of anterior glenohumeral dislocation with the patient prone. The arm can be manipulated in the same manner with the patient supine. (Redrawn from Lacey T II, Crawford HB: J Bone Joint Surg 34A:108, 1952. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, WB Saunders, 1998.)
the humeral head. When the arm is fully abducted, rotate it externally and apply gentle traction to reduce the humeral head. This slow process can be highly successful in the acute setting because it usually does not require analgesics or muscle relaxants ( Figure 21-12 ).[6] The success of this maneuver decreases as the time after dislocation increases. Scapular manipulation is also minimally traumatic and highly successful. [2] Place the victim prone and apply 5 to 15 pounds of traction on the arm. Once relaxation is obtained, raise the inferior angle of the scapula and rotate it toward the spine; rotate the superior aspect away from the spine (Figure 21-13 (Figure Not Available) ). This can also be done with the victim in the standing position ( Figure 21-14 ). If the victim is standing, it may help to pull the arm forward, as well as down. This technique generally requires excellent relaxation, but can be highly successful. An alternative method is to have the victim lie prone so that the injured arm dangles free. Place a thick pad under the injured shoulder. Attach a 10 to 20 lb (4.5 to 9 kg) weight to the wrist or forearm (do not have the victim attempt to hold the weight) and allow it to exert steady traction on the arm, using gravity to relocate the humeral head (Figure 21-15 (Figure Not Available) ). A standing victim can bend forward at the waist as you pull steadily downward on the arm to simulate the gravity effect. Use gentle side-to-side motion at the wrist to assist with the reduction ( Figure 21-16 ). Avoid the Hippocratic maneuver (Figure 21-17 (Figure Not Available) ) of placing a foot in the axilla of the injured limb to achieve countertraction because of increased pressure on the structures within the axillary sheath. Figure 21-13 (Figure Not Available) Scapular manipulation technique for closed reduction of anterior glenohumeral dislocation. (Redrawn from Anderson D, Zvirbulis R, Ciullo J: Clin Orthop 164:181, 1982. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1998, WB Saunders.)
Posterior dislocation of the glenohumeral joint makes up less than 5% of shoulder dislocations. It may occur with adduction and axial loading of the shoulder, a direct blow to the anterior aspect of the shoulder, or as a result of marked internal rotation accompanying a grand mal seizure. Frequently, the dislocation is associated with either a humeral head impaction injury or a glenoid fracture. The victim complains of significant pain and loss of shoulder motion. Generally, external rotation is completely lost. On palpation of the shoulder, you can usually detect posterior fullness not found on the uninjured side. This dislocation can be more difficult to reduce than an anterior dislocation, so excellent analgesia is generally required. Flex the arm forward, rotate it internally, and adduct it to disengage the head from the posterior glenoid rim. Occasionally, lateral traction on the humeral shaft is also required. With longitudinal traction and anterior pressure on the humeral head from behind, reduction is achieved. If the reduction maneuver is successful, place the arm in a sling until definitive care is reached. If possible, hold a posterior dislocation in neutral or slight external rotation. Because of the significant incidence of fractures with these injuries, radiologic examination is required to make the diagnosis, and evacuation is mandated.
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Figure 21-14 Repositioning a dislocated shoulder. Attached to the victim's forearm with a strap, rope, or sheet, the rescuer uses his body weight to apply traction, leaving his hands free to manipulate the victim's arm. A second rescuer applies countertraction, or the victim can be held motionless by fixing the chest sheet to a tree or ground stake. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.) Figure 21-15 (Figure Not Available) Stimson technique. (Redrawn from Rockwood CA, Green CP, editors: Fractures in adults, vol 1, Philadelphia, 1984, JB Lippincott. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1998, WB Saunders.)
Figure 21-16 A, Pushing the lower edge of the scapula toward the spine while an assistant pulls downward on the hanging arm to assist in the relocation of a dislocated humerus. B, The downward pull on the arm may be slightly forward to help put the humerus back in the shoulder socket. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.) Figure 21-17 (Figure Not Available) Hippocratic technique of closed reduction of anterior glenohumeral dislocation. The foot is placed against the proximal humerus, and longitudinal traction is applied to the upper extremity. (Redrawn from Rockwood CA, Green CP, editors: Fractures in adults, vol 1, Philadelphia, 1984, JB Lippincott. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1991, WB Saunders.)
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Elbow Dislocation of the elbow occurs with hyperextension or axial load from a fall onto the outstretched hand. It is generally posterior and lateral. The diagnosis is obvious, with posterior deformity at the elbow and foreshortening of the forearm. After carefully assessing distal sensory, motor, and circulatory status, perform reduction. With countertraction on the upper arm, apply linear traction with the elbow slightly flexed and the forearm in the original degree of pronation and supination. Downward pressure on the proximal forearm to disengage the coronoid from the olecranon fossa may be helpful. Avoid hyperextension. Adequate analgesia can be extremely helpful. An alternative method is to place the patient prone over a log or makeshift platform and apply gentle downward traction on the wrist for a few minutes. As the olecranon begins to slip distally, lift up gently on the arm. No assistant is needed, and if the maneuver is done gently, no anesthesia is required ( Figure 21-18 ). A modification of this maneuver is to hang only the forearm over the platform and apply gentle downward traction via the wrist. Guide the reduction
Figure 21-18 Parvin's method of closed reduction of an elbow dislocation. The patient lies prone on a stretcher, and the physician applies gentle downward traction on the wrist for a few minutes. As the olecranon begins to slip distally, the physician lifts up gently on the arm. No assistant is required, and if the maneuver is done gently, no anesthesia is required. (Redrawn from
Parvin RW: Closed reduction of common shoulder and elbow dislocations without anesthesia, Arch Surg 75:972, 1957. In Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
of the olecranon with the opposite hand (Figure 21-19 (Figure Not Available) ). Reduction provides nearly complete relief of pain and restoration of normal surface anatomy. Apply a posterior splint with the elbow in 90 degrees of flexion and the forearm in neutral position, using a sling for comfort. If reduction is not successful after three attempts or if a nerve injury is suspected, apply a splint to the arm as it lies and initiate evacuation. Wrist Wrist dislocations, which are frequently associated with carpal fractures, are generally produced by a fall onto the outstretched hand. A wrist dislocation may be difficult to differentiate clinically from a fracture of the distal radius. However, in either case, perform a reduction maneuver after careful assessment of distal neurocirculatory function, emphasizing median nerve function. The reduction maneuver is similar to that for a distal radius fracture. Use one hand to stabilize the forearm and the other to grasp the hand. First, dorsiflex the wrist if the dislocation is dorsal (most common) or volarflex it if the dislocation is volar, then apply longitudinal traction. In general, significant dorsiflexion is required to obtain reduction, and premedication can be Figure 21-19 (Figure Not Available) In Meyn and Quigley's method of reduction, only the forearm hangs from the side of the stretcher. As gentle downward traction is applied on the wrist, the physician guides reduction of the olecranon with the opposite hand. (Redrawn from Meyn MA, Quigley TB: Reduction of posterior dislocation of the elbow by traction on the dangling arm, Clin Orthop 103:106, 1974. In Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
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extremely helpful. If reduction is unsuccessful after three attempts or if there is median nerve dysfunction, initiate evacuation. Apply a short-arm splint if reduction is successful, and elevate the arm above the level of the heart until definitive care is procured. Consider pain and tenderness about the wrist with no significant deformity an intercarpal ligamentous disruption or a carpal fracture and apply a short arm splint. Metacarpophalangeal Joint MCP joint dislocation is rare, being produced by a crush injury or when the hand is caught in a rope. This dislocation may be dorsal or volar, with dorsal dislocation being most common. Clinically, the joint is hyperextended and the phalanx shortened. Most dorsal dislocations are easily reduced. First, hyperextend the proximal phalanx 90 degrees on the metacarpal, then push the base of the proximal phalanx into flexion, maintaining contact at all times with the metacarpal head to prevent entrapment of the volar plate in the joint ( Figure 21-20 ). Avoid straight longitudinal traction because it may turn a simple dislocation into a complex dislocation (see below). Flex the wrist and IP joints to relax the flexor tendons, and the joint usually reduces easily with a palpable and audible clunk. Apply a dorsal-volar splint, with the joint held at 90 degrees of flexion. Irreducible or complex dislocations also occur when the volar plate is interposed in the joint. Clinically, the joint is only slightly hyperextended and the volar skin is puckered over the joint. These dislocations are most common in the index, thumb, and little finger. A single attempt at reduction using the technique just described is indicated, but these dislocations usually require open
Figure 21-20 The single most important element preventing reduction in a complex MCP dislocation is interposition of the volar plate within the joint space, and it must be extricated surgically. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
reduction. If reduction of an MCP joint dislocation is unsuccessful, splint the joint in the position of comfort and obtain definitive treatment as soon as possible. The thumb MCP joint is most commonly injured. Dislocations are reduced as already described. Injury to the ulnar collateral ligament of this joint (skier's or gameskeeper's thumb) results from a valgus stress, as may occur when an individual falls holding an object in the first web space. The victim complains of tenderness over the ulnar aspect of the MCP joint. There may be instability to radial stress with the joint held in 30 degrees of flexion, an indication for surgical repair. In the field, apply a thumb spica splint and seek definitive care within 10 days. If splinting material is not available, tape the thumb until definitive care can be obtained ( Figure 21-21 ). Proximal Interphalangeal Joint Proximal interphalangeal (PIP) joint dislocations may be dorsal, volar, or rotatory, with dorsal dislocation by far the most common. Dorsal dislocation occurs with hyperextension, and the volar plate is always ruptured. It can be associated with fracture of the volar lip of the middle phalanx, creating instability after reduction. Perform reduction as described for dorsal MCP dislocation. Avoid straight longitudinal traction to prevent entrapment of the volar plate into the joint. After reduction, tape the finger to an adjacent finger to avoid hyperextension and allow early motion ( Figure 21-22 ). As with MCP dislocation, a complex dislocation can occur, but it is rare. This is difficult to reduce closed and often requires open reduction. Volar dislocations are rare. For this injury to occur, the central slip must be disrupted, and the potential for a boutonniere deformity is present. Reduce the digit by flexion of the PIP joint, pushing the base of the middle phalanx dorsally. Treat the PIP joint like a rupture of the central slip, with the PIP joint splinted in extension. Leave the distal interphalangeal (DIP) and MCP joints free to allow motion.
Figure 21-21 Taping the thumb for immobilization. A, The buddy-taping method. B, A thumb-lock; if possible, padding should be placed between the thumb and forefinger. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.)
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Figure 21-22 Buddy-taping method to immobilize a finger. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.)
Figure 21-23 Rotary subluxation of the PIP joint. The condyle of the head of the proximal phalanx is button-holed between the lateral band and central slip, both of which remain intact. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
Rotatory subluxation of the PIP joint is also rare ( Figure 21-23 ), occurring after a twisting injury. The condyle of the head of the proximal phalanx is buttonholed between the lateral band and the central slip, both of which remain intact. This injury can be difficult to reduce. With both the MCP and PIP joints flexed, apply gentle
traction to the finger. This relaxes the volarly displaced lateral band and allows the band to be disengaged and slip dorsally when a gentle rotary and traction force is applied. You can achieve further relaxation of the lateral band by dorsiflexion of the wrist. After reduction, buddy tape the finger and begin early motion. With any dislocation of the PIP joint, seek definitive care promptly to ensure adequate reduction of the injury. "Jammed" fingers may be just as debilitating and painful as dislocated digits. With these injuries, stress the involved joint both radially and ulnarly to ensure collateral ligament integrity. If the joint is stable, the finger can be buddy taped to an adjacent digit and immediate care is not indicated. If the finger is unstable, seek definitive care.
Figure 21-24 The three types of injury that cause a mallet finger of tendon origin. Top, The extensor tendon fibers over the distal joint are stretched without complete division of the tendon. Although there is some drop of the distal phalanx, the patient retains weak active extension. Center, The extensor tendon is ruptured from its insertion on the distal phalanx. There is usually a 40- to 45-degree flexion deformity, and the patient has loss of active extension at the distal joint. Bottom, A small fragment of the distal phalanx is avulsed with the extensor tendon. This injury has the same clinical findings as that shown in the center drawing. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
Distal Interphalangeal Joint The DIP joint is less frequently injured than the PIP joint. Pure dislocations are rare and are usually dorsal and associated with an open wound. The reduction maneuver is similar to that used for dorsal PIP joint dislocation, and the injury is stable after reduction. More commonly, a mallet-finger injury occurs when the extensor tendon is taut, as when striking an object with the finger extended. The basic injury is incompetence of the extensor tendon at its insertion into the distal phalanx. The three types of mallet injuries are shown in Figure 21-24 . Individuals with this injury lack full extension of the DIP joint when the MCP and PIP joints are kept in extension. Holding these joints in extension isolates the extensor tendon by neutralizing the intrinsic muscles. If an extension lag is noted, splint the joint in slight extension for 6 to 8 weeks, leaving the PIP and DIP joints free ( Figure 21-25 ). Obtain a radiograph within the first 10 days to ensure that the joint is reduced. Occasionally, the flexor digitorum profundus (FDP) tendon is avulsed from its insertion on the distal phalanx.
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Figure 21-25 Mallet finger can be treated by immobilizing the DIP joint with a dorsal padded aluminum splint (A), a volar unpadded aluminum splint (B), a Stack splint (C), a modified Stack splint (D), or an Abouna splint (E). Note that each of these splints uses a three-point fixation principle. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green's Fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
This occurs with forced hyperextension of the DIP joint while the FDP is maximally contracted. The ring finger is most commonly injured. The diagnosis is made by demonstrating inability to flex the DIP joint with the PIP joint held in extension. Pain and local tenderness are more common over the PIP joint, where the retracted end of the tendon usually lies. Splint the digit in flexion, and seek care within 7 days from a surgeon specializing in the upper extremities.
LOWER EXTREMITY INJURIES Femur and Patella In general, healthy, active individuals sustain fractures of the proximal femur only in falls from significant heights or from high-velocity injuries sustained during water or snow skiing. These fractures occur in the femoral neck or intertrochanteric region. When the head and spinal cord are uninjured, the victim complains of pain within the proximal thigh. In all but the thinnest individuals, there is little local reaction in terms of swelling or deformity around the hip region to aid in diagnosis. Any movement of the affected limb produces significant pain. In many cases, the affected limb is noticeably shortened and externally rotated. Following a careful sensory, motor, and circulatory examination, realign the limb and apply a Kendrick, Thomas, or REEL splint, if available. An improvised traction splint can be fabricated (see Chapter 19 ). If none is available, transport the victim on a backboard, with the limbs strapped together or tied to a board with a tree limb placed between them. Fracture of the femoral neck is associated with a significant risk of posttraumatic femoral head necrosis. Without a radiograph, this fracture is impossible to distinguish from an intertrochanteric hip fracture. Because there is evidence that emergency treatment of a fracture of the femoral neck decreases the risk of posttraumatic avascular necrosis,[10] arrange rapid evacuation of any victim in whom this injury is suspected. Fracture of the femoral shaft occurs by similar mechanisms. Crepitus and maximum deformity are noted in the midportion of the thigh. After neurocirculatory examination, place the limb in traction or protect it as noted previously. Correct any gross deformity of the shaft with gentle traction, and repeat the neurocirculatory examination. This fracture may be an open injury, so split the victim's pants to complete the examination. Discovery of an open wound should prompt rapid evacuation. Fracture of the distal end of the femur is frequently intraarticular and occurs with high-velocity loading when the knee is flexed. With axial loading on the femur, the patella becomes the driving wedge and the femoral condyles suffer direct impact, producing either a patella fracture or a fracture of the femoral condyles or distal metaphysis. With a patella fracture, the injury may be obvious on deep palpation. This is often an open injury because there is very little soft tissue overlying this sesamoid bone. Instability of the distal femur with crepitus indicates a supracondylar femur fracture, not a patella fracture. The definitive diagnosis is made radiographically. After initial neurocirculatory examination, realign the limb to avoid compression of the popliteal artery and vein. Apply a posterior splint to the realigned limb for transportation. As with all fractures, open wounds in the region of the fracture, or an
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abnormal nerve or vascular examination should prompt immediate evacuation. Tibia and Fibula The tibial plateau is the broad intraarticular surface of the upper tibia that articulates with the distal femur. This area can be fractured with a fall or leap from a height. Frequently, angulatory moments across the knee are associated. A valgus moment produces a fracture of the lateral tibial plateau, whereas a varus moment produces a medial plateau fracture. Pain, swelling, and deformity are obvious on initial examination. With a tibial plateau fracture, significant hemarthrosis develops quickly. Because of anatomic tethering of the popliteal artery by the fascia of the soleus complex, arterial injury may result from this fracture, especially when associated with a knee dislocation. Assess distal pulses and capillary refill at 1-hour intervals, keeping in mind the possibility of a compartment syndrome. After initial examination, carefully realign the limb and apply a posterior splint for transportation. Tibial shaft fractures are associated with fibular shaft fractures in 90% of cases. These fractures result from high-impact trauma. Before the development of higher, anatomically conforming ski boots, these fractures were the most common ski injuries. The injury was sustained when the body rotated around a fixed foot (occurring with a ski caught against a rock or tree stump), which produced a torsional, spiral fracture of the tibia and fibula. Tibial shaft fracture is the most common type of open fracture in the wilderness setting. When this injury is suspected, inspect the entire limb for distal sensory, motor, and circulatory function before realignment. Apply a posterior splint for transport. Take great care in serially examining the limb for the possibility of a compartment syndrome because this is the most common anatomic location for this problem. Ankle The intraarticular distal tibia, medial malleolus, and distal fibula, or any combination of these, may be involved in an ankle fracture, which is generally produced by large torsional moments about a fixed foot. With the distal tibia, axial loading from a fall or jump may also be involved. Note if there is significant pain and swelling as the shoe is removed. Palpation along the medial and lateral malleoli confirms the clinical suspicion. After the shoe is removed to inspect the skin for open wounds, perform a neurocirculatory examination. If there is a rotational deformity in the ankle, realign the ankle with gentle traction before applying a posterior splint with the ankle in neutral position. During transport, elevate the limb above the level of the heart. Tarsal Bones The calcaneus and talus are usually fractured during falls or jumps from significant heights when the victim lands on his or her feet. With a calcaneus fracture, significant heel pain, deformity, and crepitus are immediately evident after the boot is removed. A talus fracture may be impossible to differentiate from an ankle fracture on clinical grounds. An ankle fracture is tender at the malleolus level, whereas with a talar fracture, the tenderness is located distal to the malleoli. Talus fracture occurs when the foot is forced into maximum dorsiflexion. Knowing the point of the foot's impact with the ground is helpful in differentiating a talus fracture from an ankle fracture. Talus fracture may be associated with subtalar or ankle joint dislocation, but this deformity is more severe. Arrange for emergency evacuation because these injuries are very difficult to reduce closed, and pressure on the skin from the displaced talar body can produce significant skin slough. Fractures of the other tarsal bones are exceedingly rare but can be defined by localizing the tenderness to a specific site. Apply a short-leg splint with extra padding and elevate the limb during transportation. If a talus fracture is suspected, expedite evacuation because posttraumatic avascular necrosis of the talar body is a common complication. Metatarsal Bones Fractures at the base of the metatarsals often accompany midfoot dislocation (Lisfranc's dislocation). These injuries occur across the entire midfoot joint and are commonly associated with fractures at the bases of the second and fifth metatarsals. The mechanism usually occurs with axial loading of the foot in maximum plantar flexion as a result of vehicular trauma, most frequently snowmobiling. The victim complains of midfoot pain and swelling; on removing the shoe, crepitus and tenderness are noted at the base of the metatarsals (especially the first, second, and fifth metatarsals) and plantar ecchymosis may be present. Overall foot alignment is maintained, but stressing the midfoot by stabilizing the heel and placing force across the forefoot in the varus and valgus directions reveals instability. Place the foot in a well-padded posterior splint and elevate it whenever possible. Do not allow the victim to ambulate. Swelling associated with this injury can produce a compartment syndrome. Metatarsal shaft fracture occurs with a crush injury or a fall or jump from moderate height. Midshaft metatarsal fractures also occur as "fatigue," or so-called "march" fractures, which often occur with prolonged hiking or running with poor preconditioning. Pain and localized tenderness are the hallmarks of this diagnosis. The dull pain at the midshaft of a metatarsal (often the second or fifth) may be converted to more severe pain with associated crepitus by a jump from a log or a
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rock. You can temporarily manage these fractures with a stiff-soled boot or orthotic insert. If there is fracture instability or extreme pain, apply a short-leg splint and allow no further weight bearing.
Phalanx Toe phalanges are fractured by crush injuries and can be prevented by the use of steel-toed or hard-toed boots. A great-toe phalanx fracture can be a significant problem because force is placed on this digit during the toe-off phase of gait. Manage phalanx fractures by buddy taping the toe to an adjacent uninjured digit with cotton placed between the toes. Displaced intraarticular fracture of the proximal phalanx of the great toe may need operative fixation. Stiff-soled boots minimize discomfort during weight bearing.
LOWER EXTREMITY DISLOCATIONS AND SPRAINS Hip Posterior hip dislocation is produced by axial loading of the femur with the hip flexed and adducted.[7] It generally occurs in vehicular trauma but can follow a fall or sledding or skiing accident. With posterior dislocation, the victim complains of severe pain about the hip and the affected limb appears shortened, flexed, internally rotated, and adducted. Any hip motion increases the pain. It is not clinically possible to determine if there is an associated acetabular or femoral neck fracture. With the rare anterior dislocation, the limb is externally rotated and slightly flexed and abducted. This Figure 21-26 (Figure Not Available) The Allis technique for reduction of a hip dislocation. The surgeon's position must provide a mechanical advantage for the application of traction. A, Internal and external rotation is gently alternated, perhaps with lateral traction by an assistant on the proximal thigh. B, In-line traction with hip flexed. C, Adduction is often a helpful adjunct to in-line traction. (A to C, redrawn from DeLee JC. In Rockwood CA Jr, Green DP: Fractures, vol 2, ed 2, Philadelphia, 1985, JB Lippincott. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1998, WB Saunders.)
type of dislocation is generally produced by wide abduction of the hip caused by significant force. Place the victim in a supine position to do a complete survey of all organ systems. Carefully examine the distal limb for associated fractures, and perform a thorough sensory and motor examination. The peroneal division of the sciatic nerve is most susceptible to injury with a posterior dislocation. Hip dislocations are an orthopedic emergency because time to reduction is directly linked to the incidence of avascular necrosis of the femoral head. Immediate transfer to a definitive care center is desirable because hip radiographs may reveal an associated femoral neck fracture that could become displaced if closed reduction is attempted. However, if it will be more than 6 hours before the victim can be evacuated to a definitive care center, attempt closed reduction. With the Allis technique (Figure 21-26 (Figure Not Available) ), position the victim supine on the ground or a stretcher. Stand above the victim and pull in-line traction on the extremity while an assistant applies counter traction to the iliac wings. With anterior dislocation, apply traction with the leg slightly abducted and externally rotated and the hip gently extended. Reduce posterior dislocations by flexing the hip 60 to 90 degrees. Internal rotation and adduction of the hip will facilitate the reduction. Successful reduction is usually indicated by an audible "clunk" and restoration of limb alignment. As with any reduction maneuver, adequate analgesia and a slow, progressive increase in traction force are helpful. The Stimson gravity technique (Figure 21-27 (Figure Not Available) ) may not be as practical in the wilderness. Position the patient prone on a makeshift platform. With a posterior dislocation,
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Figure 21-27 (Figure Not Available) The Stimson gravity reduction technique. This method has limited application in patients with multiple injuries. (Redrawn from DeLee JC. In Rockwood CA Jr, Green DP: Fractures, vol 2, ed 2, Philadelphia, 1985, JB Lippincott, 1985. In Browner BD et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1991, WB Saunders.)
the hip and knee are flexed 90 degrees. Apply longitudinal traction in addition to adduction and internal rotation. The reduction maneuver is actually the same for both techniques, with one performed with the victim supine and the other with the victim prone. Knee Knee dislocation is obvious because of the amount of deformity. The tibia may be dislocated in five directions: anterior, posterior, lateral, medial, and rotatory. The most common directions are anterior and posterior. This represents a true emergency because 5% to 40% of knee dislocations have associated vascular injuries.[1] [3] [4] [8] [12] In a large series, Green and Allen[4] reported an above-knee amputation rate of 86% for vascular injuries associated with knee dislocations that were not repaired within 8 hours of injury. The vascular injury occurs because of tethering of the popliteal vessels along the posterior border of the tibia by the soleus fascia. A knee dislocation is a high-velocity injury usually produced by vehicular trauma or a fall. When this injury is suspected, do a careful screening neurocirculatory examination. Intact distal pulses do not definitively rule out an arterial injury. Intimal flap tears can produce delayed thromboses of the popliteal artery. In addition, injury to the peroneal nerve can occur. Many knee dislocations spontaneously reduce and may lead the examiner to underestimation of the seriousness of the injury. Instability in extension to either varus or valgus stress indicates disruption of at least one of the cruciate ligaments and should alert you to the potential for a knee dislocation. After initial examination, reduce the persistent dislocation. Anterior dislocation is reduced with traction on the leg and gentle elevation of the distal femur. Posterior dislocation is reduced with traction in extension and anterior elevation of the tibia. Posterolateral rotatory dislocation can be very difficult to reduce and usually requires open reduction. It occurs when the medial femoral condyle buttonholes through the medial capsule. A transverse furrow on the medial aspect of the knee is pathognomic for this injury. For transport, apply a posterior splint to the limb and move the victim on a backboard. Be vigilant to the possibility of an arterial lesion or emerging compartment syndrome. Emergency evacuation is advised because of the risk of amputation related to vascular injury. Isolated ligament or meniscal injuries can also occur. Anterior cruciate ligament (ACL) injury happens with a hyperextension or twisting injury to the knee, often associated with an audible "pop" and rapid onset of swelling and pain. On examination, the victim has both a pivot shift and increased laxity on a Lachman's test. Meniscal injuries also occur with a twisting mechanism. These injuries show a slower onset of swelling (24 to 48 hours), with pain to palpation over the joint line. The victims may complain of the knee catching, locking, or giving way, especially with twisting motions. Medial collateral ligament (MCL) injury occurs with a valgus stress to the knee. The victim complains of tenderness along the medial aspect of the proximal tibia and sometimes over the medial femoral condyle. Valgus stress with the knee in 30 degrees of flexion is painful. With a partial or complete tear, laxity will be
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present. It is difficult to determine if a concomitant meniscal injury is present acutely because both injuries can be painful over the joint line. Instability to valgus stress in full extension indicates injury to the MCL and at least one of the cruciate ligaments. Wrap the knee with an elasticized bandage to contain the swelling, and place in an immobilizer if instability is present. Transport the victim to a definitive care center. Frequently, the patellofemoral joint is dislocated. Because of the increased femorotibial angle in females, this injury is far more common in women. Generalized ligamentous laxity may predispose to this problem. Dislocation of the kneecap may result from a twisting injury or asymmetric quadriceps contraction during a fall. These mechanisms routinely occur with hiking, climbing, and skiing accidents. The patella winds up lateral to the articular surface of the distal femur. Although neurovascular injuries rarely occur in association with a dislocated patella, conduct a screening examination. The patella can often be reduced by simply straightening the knee. If this is not successful, apply gentle pressure to the patella to push it back up onto the distal femoral articular groove. Apply a knee splint with the joint in extension; weight bearing is allowed. Keep the knee in extension until definitive care can be obtained. A radiograph is ultimately required to rule out osteochondral fractures, which are frequently associated with this injury. Ankle Ankle dislocations are almost always accompanied by fractures of both malleoli. These dislocations generally occur with falls onto uneven surfaces or with twisting injuries of moderate velocity. Carefully examine the area about the ankle for open injuries and conduct a neurocirculatory examination to obtain a baseline status. Then align the ankle joint by grasping the posterior heel, applying traction with the knee bent (to relax the gastrocnemius-soleus complex), and bringing the foot into alignment with the distal tibia. After this maneuver, reexamine the foot, dress any wounds, and apply a posterior splint. During transport, elevate the limb above the level of the heart. The most common musculoskeletal injury occurring in the wilderness setting is an ankle sprain. Ligament sprain, or tearing of the fibers, is separated into three grades. Grade 1 injury is partial disruption of some of the ligament fibers, represented grossly by mild intersubstance hemorrhage. Grade 2 injury is complete disruption of a
portion of the ligament fibers. The main substance of the ligament remains intact, and the injury is characterized by moderate hemorrhage with grossly visible torn ligament fibers. Grade 3 injury is complete disruption of the ligament fibers, which can result in instability of the related joint. The medial ligament complex consists of the deltoid ligament, which runs from the medial malleolus to the talus ( Figure 21-28 ). The ligament complex on the lateral side is much more complex and consists of three separate ligaments named for their origins and insertions: the calcaneofibular ligament, the anterior talofibular ligament, and the posterior talofibular ligament (see Figure 21-28 ). The lateral ligament complex is the most frequent site of an inversion injury. When such an injury occurs, remove the shoe and sock and conduct a screening neurocirculatory examination. Palpate each ligament individually for tenderness, and then evaluate the ankle for instability with the anterior drawer test. This test is performed by stabilizing the tibia with one hand and grasping the posterior heel to pull the foot forward with the other hand. If the talus slides forward within the ankle mortis (using the uninjured side as a comparison), the injury represents a grade 3 injury. Place the foot and ankle into a posterior splint or air splint. If possible, keep the victim from bearing weight on the limb. If this examination does not reveal instability and is thus indicative of a grade 1 or 2 sprain, apply an elasticized bandage or ankle taping (see Chapter 19 ). All injuries should be acutely treated following the RICE principle. Commercially available stirrup air splints also aid in ambulatory management of these injuries. A more serious ankle sprain is the high ankle sprain, which affects the anterior inferior tibiofibular ligament (portion of the syndesmotic ligament) and occurs in up to 10% of ankle sprains. The victim complains of pain to palpation over the distal tibiofibular joint and also with dorsiflexion and external rotation of the foot relative to the tibia. Compression of the fibula and tibia in the proximal half of the calf produces pain over the syndesmosis. Unlike stable lateral ankle sprains, these injuries take 4 to 6 weeks to resolve. Treat initially with a short leg splint or walking boot. Failure to recognize this injury will produce prolonged disability. In the field, tape the ankle both to decrease pain and to limit swelling ( Figure 21-29 ; see also Chapter 19 ). During taping, keep the victim's ankle perpendicular to the tibial shaft. This makes walking easier, because the ankle is not plantar flexed, and it helps prevent development of an Achilles tendon contracture. If available, an Aircast ankle brace provides additional ankle support and can be used with a shoe or boot. A fracture of the lateral process of the talus may be confused with a lateral ankle sprain, so radiographs are generally needed to rule out this injury. Inversion injuries are also infrequently associated with fractures at the insertion of the peroneus brevis tendon. You can identify this injury by the point tenderness at the base of the fifth metatarsal, but a radiograph is required for definitive diagnosis. Early management is the same as for an ankle sprain.
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Figure 21-28 Ligament complexes of the ankle.
Figure 21-29 Taping a sprained ankle. A, Strips of adhesive tape are placed perpendicular to each other to (B) lock the ankle with a tight weave. C, The tape edges are covered to prevent peeling. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.)
Hindfoot The subtalar joint may infrequently be dislocated in a significant fall or jump when an individual lands off balance or on an uneven surface. The calcaneus may be dislocated medially or laterally relative to the talus, the latter being slightly more common. Assess the position of the heel relative to the ankle. With either dislocation, attempt a reduction if it will be more than 3 hours until the victim will reach a definitive care center. Medial dislocation is reduced more easily than is lateral dislocation, in which the posterior tibial tendon frequently becomes displaced onto the lateral neck of the talus, blocking the reduction. The maneuver is the same for both: grasp the heel with the knee flexed (relaxing the gastrocnemius-soleus complex), accentuate the deformity, apply linear traction, and bring the heel over to the ankle joint. This maneuver is generally successful for medial dislocation, but lateral dislocation, especially when associated with open wounds, often requires open treatment. After reduction is attempted, apply a posterior splint and elevate the limb above the heart. Even if the reduction is successful, do not allow the victim to bear weight until definitive care is obtained. Midfoot Midfoot fracture dislocation (Lisfranc's injury) is described in the metatarsal fracture section. Metatarsophalangeal and Interphalangeal Joints Metatarsophalangeal (MTP) joint dislocations of the toes are relatively uncommon but can occur when a moderate axial force is directed at the great toe. Crush
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injuries and rock-climbing accidents while the victim is wearing flexible-soled shoes can produce this injury; wearing boots with reinforced toe boxes of adequate depth generally prevents it. Injuries of this type at the great toe may be associated with fractures of the metatarsal or phalanx. The dislocation is generally dorsal. Because these may be open injuries, inspect the foot carefully. Reduce the joint in a manner similar to that used for dorsal PIP joint dislocation of the hand. MTP dislocation of the great toe can occasionally require open reduction if the head of the metatarsal buttonholes through the sesamoid-short flexor complex. The lesser MTP joints are generally dislocated laterally or medially. The most common mechanism for this injury is striking unshod toes on immovable objects. Relocate the toes by applying linear traction with the victim supine and using the weight of the foot as countertraction. Similar mechanisms produce dislocations of the IP joints, which are also reduced by applying linear traction with gentle manipulation. Once reduced, tape the injured toe to the adjacent toe for 1 to 3 weeks and have the victim wear a protective boot with a stiff sole and deep toe box.
OVERUSE SYNDROMES Plantar Fasciitis Plantar fasciitis is inflammation of the fascia (tough connective tissue) on the sole of the foot. An individual with plantar fasciitis complains of insidious onset of pain at the origin of the plantar fascia, which is located at the most anterior aspect of the heel pad. Any activities that stretch the plantar fascia elicit pain. The pain is worse when first getting up in the morning or after resting, and is accentuated when the ankle and great toe are dorsiflexed (i.e., during push-off). Conservative treatment consists of (1) heel cord stretching 20 minutes twice a day, (2) antiinflammatory medications, and (3) wearing an orthotic that cups the heel, has a soft spot under the tender area, and supports the arch. It may take several weeks for symptoms to improve, but conservative therapy is successful in 90% of cases. An ankle-foot splint worn at night may also help because it holds the foot in a neutral position, keeping the plantar fascia slightly stretched. The orthosis also provides significant pain relief if used while walking. In severe cases, taping the arch can provide pain relief ( Figure 21-30 ). A thin layer of benzoin or spray tape adhesive is applied to the bottom of the foot. Fix an anchor strip of ¾-inch adhesive tape in a shape around the heel from just under the malleoli (prominences of the ankles) up to just behind the level of the "knuckles" of the toes ( Figure 21-30, A ). Next, lay fairly tight cross-strips of ½-inch tape across the bottom of the foot, with their ends torn to lay on the anchor strip ( Figure 21-30,B ). This creates a "sling" of tape under
Figure 21-30 Taping for arch support. A, Fix an anchor strip under the heel. B, Attach strips across the bottom of the foot. C, Lock the crosspieces. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, The Lyons Press.)
the foot for the support. Finally, apply another U-shaped piece of tape around the heel that crosses under the center of the arch and locks down the crosspieces ( Figure 21-30, C ). Carpal Tunnel Syndrome Carpal tunnel syndrome (CTS) occurs when the median nerve is compressed within the carpal tunnel. The carpal tunnel is located on the palmar side of the wrist and is formed by the transverse carpal ligament volarly and the carpal bones dorsally. The FDP and superficialis tendons to the second through fifth digits, the long thumb flexor, and the median nerve pass through this canal. Individuals complain of pain and paresthesias along the palmar aspect of the radial digits. They also complain of frequently dropping objects. Symptoms are worse at night and aggravated with prolonged wrist extension or flexion. Phalen's sign, which is numbness and tingling in the median nerve distribution after sustained wrist flexion, is suggestive of CTS. Thenar muscle atrophy is only seen in severe cases. Consider other causes, such as more proximal sites of nerve compression (especially the cervical spine), dialysis, pregnancy, or acute and chronic trauma. Treatment consists of wrist splinting in slight extension (especially at night), activity modification, and antiinflammatory medications. Tibial Fatigue Fractures Tibial fatigue fractures can also occur in individuals who suddenly increase their activity. Victims complain of pain with weight bearing, swelling, tenderness to palpation, and increased warmth at the fracture site. The most common site in the tibia is the proximal two thirds of the tibial diaphysis. Fracture of the distal third of the fibula can also occur. Treatment consists of activity reduction, protective weight bearing, and avoiding activities that produce pain. Failure to decrease activity level completes fracture of the tibia. As the pain subsides, the activity level can be increased. Two to three months may be required for resolution of symptoms.
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EVACUATION DECISION The issues surrounding the decision to evacuate an orthopedically injured individual vary depending on the goals and support of the expedition. A group of 25 climbers in the Himalayas with physician support and a field hospital at base camp will have very different criteria for evacuating an injured person than will a family of four spending a week hiking in the Rockies. In all cases, party leaders should have a plan for contacting evacuation support teams if a serious injury occurs. Musculoskeletal injuries that warrant immediate evacuation to a definitive care center are listed in Box 21-2 . These include any suspected cervical, thoracic, or lumbar spine injuries. A victim who has a suspected pelvic injury with posterior instability, significant suspected blood loss, or injury to the sacral plexus should receive emergency evacuation on a backboard. Any open fracture requires definitive debridement and care within 8 hours to prevent development of deep infection and should prompt emergency evacuation. Victims with suspected compartment syndromes must be evacuated on an emergency basis. Joint dislocations involving the hip or knee warrant immediate evacuation because of the associated risk of vascular injury or posttraumatic avascular necrosis of the femoral head. Lacerations involving a tendon or nerve warrant urgent evacuation to a center where an upper-extremity surgeon is available. In all but the most serious wilderness expeditions, arrangements should be made to evacuate the victim when the treating individuals are not reasonably sure of the injury with which they are dealing or its appropriate management.
Box 21-2. INDICATIONS FOR EMERGENT EVACUATION Suspected spine injury Suspected pelvic injury Open fracture Suspected compartment syndrome Hip or knee dislocation Vascular compromise to an extremity Laceration with tendon or nerve injury Uncertainty of severity of injury
References 1.
Almekinders LC, Logan TC: Results following treatment of traumatic dislocations of the knee joint, Clin Orthop 284:203, 1992.
2.
Anderson D, Zvirbulis R, Ciullo J: Scapular manipulation for reduction of anterior shoulder dislocations, Clin Orthop 164:181, 1982.
3.
Bohlman HH, Ducker TB, Lucas JT: Spine and spinal cord injuries in the spine, Philadelphia, 1982, WB Saunders.
4.
Green NE, Allen BL: Vascular injuries associated with dislocation of the knee, J Bone Joint Surg 59A(2):236, 1977.
5.
Penna GF et al: Pelvic disruption: assessment and classification, Clin Orthop 157:12, 1980.
6.
Russell JA, Holmes EM, Keller DJ et al: Reduction of acute anterior shoulder dislocations using the Milch technique: a study of ski injuries, J Trauma 21:802, 1981.
7.
Schatzker J, Barrington TW: Fractures of the femoral neck associated with fractures of the same femoral shaft, Can J Surg 11:297, 1968.
8.
Shelbourne KD et al: Low-velocity knee dislocation, Orthop Rev 20(11):995, 1991.
9.
Slatis P, Huittinen VM: Double vertical fractures of the pelvis: a report on 163 patients, Acta Chir Scand 138:799, 1972.
10.
Swiontkowski MF, Winquist RA, Hansen ST: Fractures of the femoral neck in patients between ages twelve and forty-nine years, J Bone Joint Surg 66A:837, 1984.
11.
Tile M: Fractures of the pelvis and acetabulum, Baltimore, 1984, Williams & Wilkins.
12.
Varnell RM et al: Arterial injury complication knee disruption, Am Surg 5(12):699–704, 1989.
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Chapter 22 - The Eye in the Wilderness Frank K. Butler Jr.
In the practice of ophthalmology, where the diagnosis often rests primarily on what is seen with a slit lamp, any locale that does not afford ready access to this modality could be considered wilderness. Another aspect of wilderness medicine practice is unfavorable environmental conditions, such as extremes of temperature or exposure to hypoxic or hyperbaric stress. Remote locations often make determining the urgency with which a victim should be referred for specialty care one of the most challenging aspects of treating medical disorders in the wilderness. This chapter considers several commonly encountered types of eye disorders: periocular trauma; chemical injury to the eye; sudden vision loss in a white, quiet eye; acute orbital and periorbital inflammation; and the acute red eye. A diagnostic and therapeutic approach to these disorders suitable for the wilderness environment is presented. Finally, eye problems that are encountered in diving and altitude exposures are discussed.
PRELIMINARY PLANNING Pertinent ocular items in a preliminary medical survey include contact lens wear; previous episodes of nontraumatic iritis; previous episodes of herpetic keratitis; and a history of corneal transplantation, retinal detachment, radial keratotomy, or other ocular surgery. A positive response to these questions may alert the health care professional to specific ocular problems that may be encountered on the proposed trip. In addition, a basic wilderness eye kit (described below) should be assembled and taken on the trip.
THE WILDERNESS EYE KIT Box 22-1 contains the suggested items for a basic wilderness ocular emergency kit. A topical fluoroquinolone, such as ciprofloxacin or ofloxacin, is the antibiotic eye drop of choice. These medications are preferred for treatment of bacterial keratitis in a wilderness setting. Topical tetracaine and fluorescein strips are important for diagnosis. Topical prednisolone is an excellent ocular antiinflammatory medication. The choice of an oral antibiotic is based on the efficacy of the proposed antibiotic in treating preseptal cellulitis, orbital cellulitis, and penetrating trauma to the globe. The fluoroquinolone family of antibiotics offers several good choices for these indications. Trovafloxacin (500 mg tablets) is a systemic fluoroquinolone with excellent coverage against gram-positive, gram-negative, and anaerobic bacteria. [29] [80] It also offers the convenience of once-daily dosing, but currently there have been a number of unpublished reports of hepatotoxicity with trovafloxacin that may limit the usefulness of this medication.[57] Levofloxacin (500 mg tablets) is another systemic fluoroquinolone with very good activity against a wide variety of gram-positive and gram-negative organisms but less anaerobic coverage than trovafloxacin. [57] Ciprofloxacin has been shown to have excellent ocular penetration when given orally[40] but is less efficacious against gram-positive organisms than is levofloxacin. Weighing these factors, levofloxacin is my current recommendation for the preferred oral antibiotic. Bacitracin is an antibiotic ointment suitable for use in patching corneal abrasions. Ophthalmic ointments are best applied by using downward pressure on the lower lid to pull it away from the eye and then applying a 1-cm ribbon of ointment to the conjunctiva of the lower lid. When released, the lid returns to its normal position and normal blinking distributes the ointment over the corneal surface. Oral prednisone has three possible treatment uses in the wilderness—refractory iritis, giant cell arteritis, and orbital pseudotumor. Topical scopolamine (0.25%) is used to reduce ciliary muscle spasm, which causes much of the discomfort associated with iritis and corneal abrasion. Scopolamine, however, has the disadvantage of dilating the pupil (making the eye very sensitive to bright light) and preventing accommodation (making reading very difficult) for 5 to 7 days. Artificial tears are used to treat ocular surface drying and to flush conjunctival foreign bodies from the eye. Diclofenac 0.1% drops have been shown to decrease corneal sensitivity, especially when multiple drops are used.[68] [78] [79] They have been found helpful in reducing the discomfort associated with traumatic corneal abrasion[31] and excimer laser refractive surgery.[20] [81] [82] In the unlikely event of angle-closure glaucoma in a wilderness setting, 2% pilocarpine may be used. The medications in Box 22-1 are listed in my recommended priority order. In the spirit of making do in the wilderness, all of the disorders mentioned in this chapter can be managed with only the medications mentioned above, but alternative therapies are also discussed.
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Box 22-1. THE WILDERNESS EYE EMERGENCY KIT
MEDICATIONS Ciprofloxacin or ofloxacin 0.3% drops Tetracaine 0.5% drops Prednisolone 1% drops Levofloxacin 500 mg tabs Bacitracin ointment Prednisone 20 mg tabs Artificial tears Scopolamine 0.25% drops Diclofenac 0.1% drops Pilocarpine 2% drops
MISCELLANEOUS Penlight with blue filter Fluorescein strips Cotton-tipped applicators Metal eye shield Eye patches (gauze) Tape (1 inch, plastic or nylon) Near vision card Wound closure strips (¼ inch) Magnifying glass
VISUAL ACUITY MEASUREMENT IN THE WILDERNESS Evaluation of visual acuity is an essential element of the eye examination. Serial measurements of visual acuity are used to monitor an individual's progress while being treated for an eye disorder. Lack of an eye chart does not preclude the ability to obtain some quantitative measure of visual acuity. A near vision card can be used for this purpose. It should be held the prescribed distance—usually 14 inches—from the eye. If a near card is not available, the ability to read print in a book is a useful alternative measure. If glasses have been lost, use a piece of paper with a pinhole created by the tip of a pen or pencil to help compensate for the lost refractive correction. Remember that individuals 40 years of age and older may need a pinhole or reading correction to help them focus on a near target. Although a marked decrease in visual acuity can be an important warning of a significant ocular disorder, visual acuity cannot always be considered a reliable indicator of the severity of disease. A corneal abrasion victim may initially have worse visual acuity than a person with a retinal detachment or corneal ulcer, despite the fact that the latter two entities are much more serious disorders.
GENERAL THERAPEUTIC APPROACH The recommendations made in this chapter are not necessarily the preferred management of the disorders mentioned when one is not in the wilderness setting. Of special interest is the recommendation for a nonophthalmologist to use a topical steroid in the management of several of the disorders discussed. The use of topical ocular steroids is generally best undertaken by ophthalmologists for two reasons: first, steroids are usually indicated only for relatively serious ocular disorders, which should be followed by an ophthalmologist when possible. Second, topical steroid use may result in elevated intraocular pressure, cataracts, and exacerbation of certain eye infections. All of the disorders for which steroids are recommended below should be referred to an ophthalmologist for follow-up as soon as possible upon return from the wilderness. Caution should be exercised in prescribing a topical steroid for longer than 3 days. Although cataracts are typically associated with long-term steroid use, a significant rise in intraocular pressure may occur within just a few days after initiation of topical steroid therapy. [23] The requirement for expedited evacuation is one of the questions that must be answered when treating an eye disease in the wilderness. In the sections below, the need for evacuation may be considered nonurgent unless an emergent (as soon as possible) or expedited evacuation (as soon as is deemed reasonable given the resources required to accomplish the evacuation) is specified in the recommendations for treatment.
ACUTE PERIOCULAR INFLAMMATION Causes of acute periocular inflammation are listed in Box 22-2 . Preseptal cellulitis means that the infectious process is confined to the tissues anterior to the orbital septum. Preseptal cellulitis therefore presents as erythema and edema of the eyelids without restricted ocular motility, proptosis, pupillary change, or decrease in visual acuity. However, some of these findings may be difficult to appreciate in the presence of marked lid edema. Historical clues include antecedent periocular trauma or insect bite or sting. In the past, this disorder has been treated very aggressively because of the high incidence of Haemophilus influenzae infection, especially in pediatric patients, with subsequent septicemia and meningitis. The advent of H. influenzae type B vaccine has changed the microbiology of this disorder and may dictate changes in treatment strategies in the future.[15] Persons who present with this disorder may be treated with levofloxacin 500 mg once a day and should have an expedited evacuation. Alternative antibiotic choices include ciprofloxacin 750 mg twice a day, dicloxacillin 500 mg every 6 hours, or cephalexin 500 mg 4 times a day. Dacryocystitis (infection of the lacrimal sac) may mimic the findings of preseptal cellulitis, but erythema, edema, and tenderness are localized to the area inferior to the medial aspect of the eye, over the nasolacrimal sac and duct. The presence of this condition generally indicates obstruction in the opening between the lacrimal sac and the nasal cavity. Surgical intervention to restore the patency of this opening is usually undertaken after the acute infection is treated. The most common pathogens in acute dacryocystitis are Staphylococcus aureus, Streptococcus species, and (in children) H. influenzae.[52] Treatment should be initiated with
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levofloxacin 500 mg once a day and warm compresses. Alternative antibiotic choices include ciprofloxacin 750 mg twice a day or amoxicillin/clavulanate 875 mg/125 mg every 8 hours. Worsening of the condition after 24 to 48 hours should be managed with an expedited evacuation. Box 22-2. DIFFERENTIAL DIAGNOSIS OF ACUTE PERIOCULAR INFLAMMATION Preseptal cellulitis Orbital cellulitis Dacryocystitis Orbital pseudotumor Insect envenomation
Periocular insect envenomation is a preseptal cellulitis look-alike. Although secondary infection may follow envenomation, the envenomation itself may produce significant erythema and edema. Diagnostic clues include a history of insect bite or a periocular papular lesion at the site of the envenomation. Ice or cool compresses may be used to treat the envenomation, with levofloxacin 500 mg once a day, dicloxacillin 500 mg every 6 hours, or cephalexin 500 mg 4 times a day added if secondary infection is suspected. The term orbital cellulitis means that the infection has spread to or originated in the tissues posterior to the orbital septum. This may be manifest as diplopia or restriction in ocular motility as the extraocular muscles are affected, proptosis as edema in the orbit pushes the globe forward, decreased vision as the optic nerve is affected, or pupillary change if innervation of the pupil is affected. Fever is suggestive of orbital cellulitis in the differential diagnosis of periocular inflammation. This condition is more commonly associated with sinusitis than with periocular trauma as an antecedent disorder. [42] Most series report a 50% to 75% incidence of sinusitis or other upper respiratory infection in association with orbital cellulitis. [83] The bacteria that most commonly cause orbital cellulitis are Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus pneumoniae.[52] Anaerobes are frequently present in cases of chronic sinusitis and should be suspected in orbital cellulitis associated with long-standing sinus disease.[52] If not treated aggressively, orbital cellulitis may be associated with life-threatening infection of the central nervous system. Before antibiotics became available, approximately 19% of persons with orbital cellulitis died of intracranial complications and 20% of survivors became blind in the involved eye.[52] This disorder requires hospitalization and intravenous antibiotic therapy. Interim therapy should include levofloxacin 500 mg twice a day. Alternative antibiotic choices are ciprofloxacin 750 mg twice a day or amoxicillin/clavulanate 875 mg/125 mg every 8 hours. A decongestant should be added if sinusitis is present, and emergent evacuation should be undertaken. Orbital pseudotumor is an inflammatory disease of the orbit that may present very much like orbital cellulitis. The differentiation between these two entities may be difficult.[42] There would typically not be a history of preceding sinusitis. A reasonable approach in the wilderness is to begin therapy with levofloxacin 500 mg twice a day and arrange for emergent evacuation. Prednisone (80 mg a day) should be added if there is no response to antibiotic therapy, there is no fever or sign of central nervous system involvement, and evacuation has not been possible by 24 to 48 hours after presentation. If prednisone therapy is initiated, its efficacy should be evaluated after 48 hours. If there has been a decrease in pain, erythema, edema, or proptosis, therapy should be continued until evacuation is accomplished. If there has been no response after 48 hours, the prednisone may be discontinued without tapering.
PERIOCULAR TRAUMA Eyelid Laceration The most important aspect of managing an eyelid laceration is to carefully exclude the presence of penetrating injury to the globe. Clues to the presence of an open globe are noted in that section below. A lid laceration that is horizontally oriented on the eyelid, does not penetrate the full thickness of the lid, and does not involve the lid margin is relatively easily managed. In the absence of an ability to properly irrigate, disinfect, and suture the laceration, it should be managed by irrigation with the cleanest disinfected water available, application of topical antibiotic drops (ciprofloxacin, ofloxacin, or tobramycin) to the laceration, drying the surrounding skin surface, and then closing the laceration with tape strips. The wound may then be treated with antibiotic ointment (bacitracin or erythromycin) 4 times a day for 3 to 4 days. Alternatively, the laceration may be left open, treated with antibiotic ointment 4 times a day, and repaired 1 or 2 days later.[42] The laceration should be observed frequently while healing. If redness or discharge develops, the victim should be started on levofloxacin 500 mg once daily or dicloxacillin 500 mg every 6 hours, the wound closure tape should be removed from the laceration, and evacuation should be expedited, especially if the response to oral antibiotics is poor. Complicated lid lacerations, defined as stellate or complex, or involving the lid margin or the canthi (medial or lateral end of the palpebral fissure), are more difficult to manage. These lacerations may result in secondary functional difficulties if ocular lubrication or lacrimal drainage becomes impaired. In addition, cosmesis may be poor if a meticulous repair is not done. These
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wounds should be managed by irrigation with the cleanest disinfected water available, application of antibiotic ointment, and coverage with a sterile dressing. Evacuation for definitive repair should be expedited. Instillation of Adhesive Drops into the Eye Inadvertent instillation of a "superglue" (cyanoacrylate-type adhesive) compound into the eye may bind the lids tightly together. Overnight application of a pressure patch with eye pads presoaked with water has been reported to make manual separation of the lids possible and eliminate the need for general anesthetic and surgical separation of the lids.[58] Ophthalmic ointment inserted through any small opening in the adherent lids has also been reported to facilitate resolution.[48] Once the lids are separated, the eye should be checked for a corneal abrasion.[71]
CHEMICAL INJURY TO THE EYE The mainstay in the management of any chemical eye injury is immediate and copious irrigation of the ocular surface with water from whatever source is most readily available. In the wilderness, bottled water or intravenous solution is the best option. If neither of those is available, treated (filtered and disinfected) water from a drinking container is the next best option, with untreated water a last resort. Instillation of several drops of tetracaine will make the procedure much less uncomfortable for the victim. Irrigation should be continued for a minimum of 30 minutes.[42] The two most damaging chemicals are strong acids and alkalis.[42] Sulfuric acid from an exploding car battery is a typical acid, whereas cleaning products, such as drain cleaners, are typical alkalis. Caustic alkalis are more likely to damage the eye than acids because of their profound and rapid ocular penetration. Do not attempt to neutralize the corneal surface with acidic or alkaline solutions. Chemicals other than acids and alkalis may be uncomfortable when they are encountered but are less likely to produce significant long-term damage. After a minimum of 30 minutes of flushing has been completed, the eye should be examined for retained particles. These should be removed with a moistened cotton-tipped applicator.[42] Treatment for an acid- or alkali-induced injury includes ciprofloxacin or ofloxacin drops 4 times a day until fluorescein staining confirms that the corneal epithelial defect that typically accompanies these injuries has resolved. Topical prednisolone 1% should be added if there is significant inflammation. Prednisolone drops should be used every hour while awake for 3 days. Eye pain is managed with scopolamine drops 4 times a day for 3 days and oral pain medications.[69] Evacuation should be expedited if: (1) the cornea is found to be opaque, (2) a large epithelial defect is found on fluorescein staining, or (3) significant pain persists after 3 days. Another sign of serious injury is blanching of the conjunctiva in the limbal area.[42]
ACUTE LOSS OF VISION IN A WHITE, QUIET EYE Vision may be variably decreased with many of the disease entities that are noted later in the Acute Red Eye section. This section addresses sudden loss of vision that occurs in a white, quiet eye. A differential diagnosis is provided in Box 22-3 . Disorders that cause this symptom are often difficult to diagnose without ophthalmic instruments (none of which are included in the kit shown in Box 22-1 ). There are few treatments for most of these disorders likely to be effective in a wilderness setting. Although an afferent pupillary defect (Marcus Gunn pupil) may be present, this is a nonspecific finding that would be expected with most of the disorders in Box 22-3 , except for vitreous hemorrhage and high-altitude retinal hemorrhage. An important question that must be asked in the face of acute loss of vision in a white, quiet eye is "Does this person have giant cell arteritis?" Giant cell arteritis (GCA), also called temporal arteritis, can cause devastating anterior ischemic optic neuropathy, often first noted on waking and which usually becomes permanent.[24] Subsequent involvement of the second eye is common if GCA in the first-stricken eye is not promptly treated. [24] Although visual loss has been reported to occur in both eyes simultaneously, there is typically a delay of 1 to 14 days before the second eye is affected.[1] Loss of vision in the second eye can be prevented in most cases by the prompt initiation of high-dose corticosteroid therapy.[1] [24] [28] [55] Arteritic anterior ischemic optic neuropathy is typically a disease of older individuals, with one large study reporting a mean age of 70 years and the age of the youngest patient as 53 years.[1] Clues to diagnosis are temporal headache, jaw claudication, fever, weight loss, transient visual obscurations, and polymyalgia rheumatica (generalized myalgias).[55] The visual obscurations seen in GCA usually last 2 to 3 minutes.[55] If a person is felt to be
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suffering from GCA, he or she should be started on prednisone 80 mg qd and evacuation expedited. Box 22-3. DIFFERENTIAL DIAGNOSIS OF ACUTE LOSS OF VISION IN A WHITE, QUIET EYE Retinal detachment Central retinal artery occlusion Anterior ischemic optic neuropathy Optic neuritis Central retinal vein occlusion Arteritic anterior ischemic optic neuropathy Vitreous hemorrhage High-altitude retinal hemorrhage
If one suspects a retinal detachment based on a history of high myopia (extreme nearsightedness), floaters, or photopsias (flashing lights), expedited evacuation should be undertaken because of the need for surgical repair. Loss of central vision caused by a retinal detachment usually means that the macula is involved and that surgical repair is urgent rather than emergent. Ross and Kozy[65] found that a delay to surgery of up to 1 week in macula-off rhegmatogenous retinal detachments did not affect final visual acuity. Expedited evacuation to a facility that has retinal surgery capability will allow for more precise determination of the urgency for surgical repair. If the victim is at altitude (above approximately 3048 m [10,000 feet]), high-altitude retinal hemorrhage (discussed below) should be suspected and further ascent avoided.[10] Descent of at least 915 m (3000 feet) should be undertaken as soon as feasible.[10] Another potentially treatable cause of sudden loss of vision in a white, quiet eye is central retinal artery occlusion (CRAO). Previous conventional therapy for CRAO of ocular massage, pentoxifylline, and anterior chamber paracentesis has been reported to be unsuccessful in restoring vision in 40 of 41 patients with CRAO, even though 11 patients presented within 6 hours of visual loss and 17 presented within 12 hours.[66] Primate retinas can tolerate no more than 100 minutes of ischemia caused by a complete blockage of retinal blood flow.[27] However, fluorescein angiography has shown that in humans, CRAO is seldom complete, and that therapy begun up to 6 hours after visual loss may be successful in restoring vision.[66] Hyperbaric oxygen was reported successful in restoring vision on two separate occasions in one patient with recurrent branch retinal artery occlusions associated with Susac's syndrome.[41] Oxygen is supplied to the retina from both the retinal and choroidal circulations. Under normoxic conditions, approximately 60% of the retina's oxygen is supplied by the choroidal circulation. Under hyperoxic conditions, the choroid is capable of supplying 100% of the oxygen needed by the retina.[41] When retinal arterial flow is interrupted, the retinal tissue undergoes a period of ischemia. Blood flow may be spontaneously reestablished, as frequently happens with arterial obstruction, or ischemia may continue until cell death and necrosis occur.[45] The period of time during which the tissue is ischemic, yet capable of recovery, is called the ischemic penumbra.[45] Hyperbaric oxygen is not always required for a reversal of retinal ischemia. The author has treated a monocular patient who suffered a central retinal artery occlusion in his only seeing eye and presented to the emergency department within an hour of visual loss. The victim's vision improved from 20/400 to 20/25 within minutes on supplemental oxygen by mask. Unfortunately, however, his vision decreased rapidly to 20/400 whenever the supplemental oxygen was removed. The victim was heparinized and maintained on supplemental oxygen for approximately 10 hours, at which time the removal of oxygen no longer caused a decrease in vision. If oxygen is being carried for an extreme altitude summit attempt or for other purposes, a person with sudden painless loss of vision should be given a trial of oxygen administered in as high a concentration as possible to see if this therapy results in visual improvement. Care should be taken when monocular visual loss occurs. Although central vision may still be normal in the fellow eye, depth perception may be impaired and the victim may therefore be at increased risk of a fall during evacuation.
ACUTE RED EYE Box 22-4 provides a partial list of disorders that can result in an acute red eye. In the absence of a slit lamp, the diagnosis must rely on the basic techniques of history, penlight inspection, fluorescein staining, response to administration of topical anesthesia, and pupillary status. The discussion of the differential diagnosis of the acute red eye that follows uses these clinical findings to establish the diagnosis. A pictorial representation is shown in Figure 22-1 . The term fluorescein positive is used to denote an eye with a discrete area of staining noted with cobalt blue light after instillation of fluorescein dye. Some conditions, such as blepharitis, viral keratoconjunctivitis, and ultraviolet (UV) keratitis, may cause a pattern of punctate staining referred to as superficial punctate keratitis (SPK). Traumatic Ocular Disorders Obvious Open Globe.
If there is a history of trauma and penlight inspection of the eye reveals an obvious open
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Figure 22-1 Algorithm showing wilderness diagnostic procedure for the acute red eye.
globe (such as the eye in Figure 22-2 ), the examination should be discontinued and a protective shield placed over the eye. Do not apply a pressure patch or instill any topical medication. There are two primary concerns in the management of this condition. The first is to minimize manipulation or additional trauma to the eye that might raise intraocular pressure and result in expulsion of intraocular contents through the corneal or scleral defect. The second is to prevent development of posttraumatic endophthalmitis, an infection of the aqueous and vitreous humors of the eye. This typically has devastating visual results, with only 30% of victims in one study retaining visual acuity greater than or equal to 20/400.[38] Staphylococcus epidermidis is the most common pathogen implicated, but Bacillus cereus is a very aggressive pathogen often isolated in this condition. [38] After the shield is placed, the victim should be started on levofloxacin 500 mg twice a day. Trovafloxacin 200 mg once a day is a reasonable alternative choice for prophylaxis because of its very broad antibacterial spectrum[29] [80] and good ocular penetration.[50] Ciprofloxacin 750 mg twice a day is a third option. A person with an obvious open globe needs surgical repair as soon as possible and
Figure 22-2 Obvious open globe (corneoscleral laceration). (Courtesy Steve Chalfin, MD.)
should be evacuated emergently. Because there is a possibility that air may have been introduced into the eye, barometric pressure changes during evacuation should be minimized, if possible. However, this consideration is secondary to the need for expeditious transport to a facility where surgical repair can be performed. Box 22-4. DIFFERENTIAL DIAGNOSIS OF THE ACUTE RED EYE Obvious open globe Corneal abrasion Corneal ulcer Subconjunctival hemorrhage Traumatic iritis Hyphema Occult open globe Herpes simplex virus keratitis Corneal erosion Acute angle closure glaucoma Iritis Scleritis Conjunctivitis Blepharitis Ultraviolet keratitis Episcleritis Conjunctival foreign body Dry eye Contact lens overwear syndrome
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Figure 22-3 Occult open globe with uveal pigment at the limbus and a peaked pupil. (Courtesy Steve Chalfin, MD.)
Figure 22-4 Corneal abrasion. (Courtesy Steve Chalfin, MD.) Occult Ruptured Globe.
A penetrating injury to the eye or a ruptured globe may not always be obvious. Clues to occult rupture include large subconjunctival hemorrhage with chemosis, dark uveal tissue present at the limbus, distorted pupil ( Figure 22-3 ), fluorescein leak from a linear or punctate corneal epithelial defect, mechanism of injury (hammering metal on metal, impaling injury, etc.), or decrease in vision. If an occult globe rupture is suspected, the victim should be treated as described previously for an obvious open globe. The relatively less severe appearance of the injury does not eliminate the threat of endophthalmitis, so levofloxacin therapy should be initiated. Corneal Abrasion.
A corneal abrasion is disruption of the protective epithelial covering of the cornea ( Figure 22-4 ). This results in intense pain, tearing, light sensitivity (photophobia), and increased susceptibility to infection until the defect has healed (usually in 2 to 3 days). There is typically a history of antecedent trauma or contact lens wear. The sine qua non for this diagnosis is an epithelial defect on fluorescein staining. Standard treatment consists of bacitracin ointment followed by application of a pressure patch, although a recent study has shown that small (less than 10 mm2 ), noninfected, and non-contact lens-related abrasions healed significantly faster with less discomfort when they were not patched.[33] In a wilderness setting, the nonpatching option has the additional advantage of not rendering the victim completely monocular and adversely affecting visual field and depth perception. If the nonpatching option is chosen, the victim should be treated with topical fluoroquinolone drops or bacitracin ointment 4 times a day until the corneal epithelium is healed. Diclofenac drops 4 times a day should be helpful in reducing discomfort. Sunglasses help alleviate photophobia. Repeated use of a topical anesthetic for pain control is contraindicated. If the abrasion is contact lens-related, the eye should not be patched because of the increased risk of corneal ulcer present with a contact lens-related abrasion[60] ; contact lens-related corneal abrasions should be treated with topical fluoroquinolone drops every 2 hours while awake until the epithelial defect has resolved to ensure coverage against Pseudomonas. An abrasion associated with vegetable matter should also not be patched.[60] If the abrasion is large or the victim's discomfort severe, scopolamine drops once or twice a day may be added to the antibiotic. (Wait 5 minutes between each drop.) Much of the pain associated with corneal abrasion and ulcer is due to ciliary muscle spasm, which is relieved by scopolamine. The rationale for using scopolamine only with a very painful abrasion in the wilderness is that this medication will cause the pupil to dilate (and the eye to become very sensitive to light) and accommodation to relax (with a resultant decrease in near visual acuity) for approximately 5 to 7 days. An oral analgesic may be required for pain control. The victim should be monitored daily for development of a corneal ulcer (noted on penlight examination as a white or gray infiltrate on the cornea) and for progress in healing of the epithelium (as measured by resolution of fluorescein staining). Corneal Ulcer.
The term corneal ulcer, as used here, denotes acute bacterial, fungal, or protozoal infection of the cornea. Chronic corneal epithelial defects caused by a variety of autoimmune or inflammatory processes are also referred to as corneal ulcers at times, but these disorders are beyond the scope of this chapter. Although a corneal ulcer ( Figure 22-5 ) is an infectious process, it is often preceded by a traumatic corneal abrasion. The other predisposing condition for a corneal ulcer is contact lens wear, which results in microtrauma to the corneal epithelium and may allow bacteria or other microorganisms to infect the cornea. Corneal ulcers are typically significantly painful. A small white or gray infiltrate on the cornea can be appreciated by a careful penlight examination. If not treated aggressively, the small initial lesion may progress to the much larger infiltrate shown in Figure 22-5 with a correspondingly
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Figure 22-5 Corneal ulcer. (Courtesy Steve Chalfin, MD.)
more severe impact on visual acuity. Fluorescein staining reveals an epithelial defect overlying the infiltrate. The associated pain is usually significantly decreased by application of a topical anesthetic, but ciliary spasm may cause pain relief to be incomplete. An inadequately treated corneal ulcer may result in visual loss from dense corneal scarring or ocular perforation with subsequent endophthalmitis. Management of this disorder in the past included hospital admission for treatment with concentrated and frequently administered aminoglycoside and cephalosporin topical drops. Recently, outpatient therapy with fluoroquinolone eye drops has been shown to be comparable in efficacy with fortified antibiotic preparations.[30] [53] Treatment for corneal ulcer, then, should be with ciprofloxacin or ofloxacin, 1 drop every 5 minutes for 3 doses initially, then 1 drop every 15 minutes for 6 hours, then 1 drop every 30 minutes thereafter around the clock.[60] Scopolamine 1 drop 2 to 4 times a day may help relieve discomfort caused by ciliary spasm. Repeated use of topical anesthetics for pain control is contraindicated. Systemic analgesia may be required if pain is severe. Expedited evacuation is recommended. Traumatic Iritis.
Iritis refers to inflammation of the iris or, more accurately, the anterior uveal tract of the eye. It may also be called anterior uveitis or iridocyclitis. The sine qua non of this condition is inflammatory cells in the anterior chamber of the eye, which must be visualized with a slit lamp. In the wilderness, this diagnosis must be presumptive. Iritis may accompany a corneal abrasion or result from blunt trauma. The diagnosis rests primarily on the presence of significant posttraumatic pain without a corneal abrasion or ulcer noted on fluorescein staining, or on pain that persists after the abrasion is healed. Treatment is with prednisolone 1 drop 4 times a day for 3 days. Scopolamine 1 drop twice a day may be added if pain is severe enough to justify the blurred vision that scopolamine therapy will entail.
Figure 22-6 Subconjunctival hemorrhage. (Courtesy Steve Chalfin, MD.)
Figure 22-7 Hyphema. (Courtesy Steve Chalfin, MD.) Subconjunctival Hemorrhage.
Subconjunctival hemorrhage ( Figure 22-6 ) is a bright red area over the sclera of the eye that results from bleeding between the conjunctiva and the sclera. It is easily visible without the use of a slit lamp. This injury is innocuous and resolves over a period of several days to several weeks without treatment. In the presence of antecedent trauma, one should be alert for another, more serious injury. In particular, if hemorrhage results in massive swelling of the conjunctiva (chemosis), an occult globe rupture should be suspected. Hyphema.
The term hyphema is defined as blood in the anterior chamber. Although this is usually seen in the setting of acute trauma, it may also be caused by other conditions, such as iris neovascularization. The eye should be examined with the victim sitting upright. If enough blood is present, it collects at the bottom of the anterior chamber and is visible as a layered hyphema ( Figure 22-7 ). This may not be appreciated if the victim is examined while in a supine position or if the amount of blood is very small.
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Figure 22-8 Herpes simplex virus keratitis. (Courtesy Steve Chalfin, MD.)
Although most hyphemas resolve without sequelae, this disorder may be complicated by an acute rise in intraocular pressure or corneal blood staining. Treatment in the wilderness consists of activity restriction (walking only), prednisolone drops 4 times a day, avoidance of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), and use of an eye shield until the hyphema has resolved. Diamox 250 mg 4 times a day by mouth should be added if available to treat the potentially increased intraocular pressure. Retinal injury and/or an occult ruptured globe may accompany traumatic hyphema. A hyphema victim requires ophthalmologic evaluation, so expedited evacuation should be undertaken. Nontraumatic Fluorescein-Positive Acute Red Eye Herpes Simplex Virus Keratitis.
The essential element in this diagnosis is the characteristic dendritic epithelial pattern on fluorescein staining ( Figure 22-8 ). There will often be a history of previous episodes of herpes simplex virus (HSV) keratitis. Treatment is trifluorothymidine 1% drops 9 times a day.[60] Treatment is continued until the corneal staining has resolved, at which time the frequency of dosing is reduced to 4 times a day for 1 week. Trifluorothymidine was not included in the list of eye medications to be taken on the expedition because trifluorothymidine drops require refrigeration. If a significant delay is anticipated before evacuation, HSV keratitis may be treated by using tetracaine 3 to 5 drops given 1 minute apart to anesthetize the cornea and then performing a gentle Q-tip debridement of the epithelial lesion.[60] The resulting epithelial defect should then be treated as described in the Corneal Abrasion section. Corneal Erosion.
A corneal erosion is an epithelial defect caused by nontraumatic disruption of the corneal epithelium. The fluorescein staining pattern seen with corneal erosion may be identical to that seen with corneal abrasion; pain and photophobia are present with both disorders. The diagnosis is made when the apparent corneal abrasion has no history of trauma to explain its presence. There is often a history of previous similar episodes. The two primary causes for corneal erosion are corneal dystrophies and previous ocular trauma.[55] Recurrent corneal erosions are believed to be caused by a defect in healing between the hemidesmosomes of the corneal epithelium and the underlying basement membrane.[42] At night, the epithelium may become adherent to the closed eyelid during sleep. When the individual awakens and opens his or her eyes, the corneal epithelium is pulled away from the basement membrane by movement of the lid. This accounts for the typical history of acute onset of pain on awakening. Signs and symptoms include pain, tearing, and foreign body sensation.[42] Treatment of these lesions may be difficult. The cornea should be inspected for a loose sheet of epithelium that remains partially attached to the corneal surface. If this is present, try to debride it with a cotton-tipped applicator after topical anesthesia with tetracaine. The lesion is then managed initially in the same manner as a corneal abrasion. There is a high rate of recurrence if follow-up treatment with 5% sodium chloride ointment each evening or anterior stromal puncture is not undertaken. Corneal Abrasion and Corneal Ulcer.
Both lesions may occur as complications of contact lens wear. Management has been described above. Contact lens-related corneal abrasions have a relatively high incidence of progressing to corneal ulcers.[33] Therefore they should not be patched and should receive topical antibiotic therapy with ciprofloxacin or ofloxacin drops every 2 hours while awake until the epithelial defect has resolved. Contact lens wear in both eyes should be discontinued immediately. If an ulcer is related to contaminated lens solutions, infection in the first eye may be followed rapidly by a similar occurrence in the other eye. Nontraumatic Fluorescein-Negative Acute Red Eye (Pain Not Significantly Improved by Topical Anesthesia) Acute Angle-Closure Glaucoma.
This diagnosis is easily made when the intraocular pressure can be measured with a tonometer. Intraocular pressure is normally between 10 and 21 mm Hg. With acute angle-closure glaucoma, the pressure may increase to 50 or 60 mm Hg or higher. Although handheld tonometers are available, they will not often be present outside of hospitals or clinics. The most important clues to the diagnosis of angle-closure glaucoma in the wilderness setting are the characteristics of the pain and the status of the pupil. Angle-closure glaucoma victims do not have the mild burning or foreign body type of pain typically seen with conjunctivitis, blepharitis, or other external eye diseases. Angle-closure glaucoma produces a pain that is usually deep and severe. Although corneal abrasions
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and corneal ulcers may also be accompanied by severe pain, the pain in these two disorders is usually significantly relieved by topical anesthetics. This is not true of the pain seen with acute glaucoma, scleritis, or iritis. In these disorders, the pain is rarely if ever significantly relieved by topical anesthetics. In acute angle-closure glaucoma, the pupil is usually found to be mid-dilated (6 to 7 mm) and vision is usually decreased. This disorder generally affects persons over 50 years of age[42] and is more common in persons of Asiatic ethnic origins. There is often a history of previous transient episodes of eye pain. Nausea and vomiting may be present. An eye with acute angle-closure glaucoma is shown in Figure 22-9 . The usual treatment is topical antiocular hypertensive medications and laser iridotomy, which allows the aqueous humor to bypass the pupillary block. This relieves the angle closure with a resultant decrease in intraocular pressure. [42] In the wilderness setting, treatment should be with 2% pilocarpine one drop every 15 minutes for 4 doses,[55] then 4 times a day in both eyes, since there is a high rate of subsequent occurrence of angle-closure glaucoma in the fellow eye. Pilocarpine alone may be successful in relieving the angle closure and lowering the pressure, but this is not a reliably effective treatment because ischemia of the pupillary sphincter muscle may prevent pilocarpine from exerting its miotic effect. Diamox 250 mg 4 times a day by mouth should be added if available. Evacuation should be emergent if pain is not relieved, since even 1 day of very high intraocular pressure may result in permanent damage to the optic nerve and loss of vision. Nontraumatic Iritis.
Signs and symptoms of nontraumatic iritis that may be appreciated without a slit lamp include pain, redness, photophobia, limbal flush, and decreased vision.[55] There is often a history of previous episodes. An eye with nontraumatic iritis is shown in Figure 22-10 . (The pupil is iatrogenically dilated.) Iritis not associated with corneal trauma is typically more severe
Figure 22-9 Angle-closure glaucoma. (Courtesy Steve Chalfin, MD.)
than the traumatic variety but may range from mild to very severe and typically is not significantly relieved by topical anesthesia. Fluorescein staining is negative and the pupil is usually miotic, thus helping differentiate iritis from angle-closure glaucoma. Iritis is far more common than angle-closure glaucoma and may be associated with a number of systemic infectious and inflammatory diseases. In the wilderness setting, the emphasis should be on immediate treatment with prednisolone 1% 1 drop every hour while awake. Scopolamine 1 drop 1 to 4 times a day may be added for pain control and to prevent posterior synechiae (pupillary scarring) if inflammation is severe. If pain is not significantly decreased in 24 to 48 hours, oral prednisone 80 mg a day should be added to the treatment regimen and maintained until evacuation. Evacuation should be expedited, since posterior synechiae and elevated intraocular pressure may develop. Scleritis.
It may be difficult to differentiate between nontraumatic iritis and scleritis without a slit lamp, but scleritis is much less common than iritis. The characteristics of the pain are similar, with pain, photophobia, scleral injection, and tearing.[55] Scleritis is often associated with rheumatologic disease and may be either nodular or diffuse.[55] The diffuse form of scleritis is shown in Figure 22-11 . The initial treatment of scleritis in the wilderness setting is topical prednisolone drops 1 drop every hour while awake and an NSAID, if available. Prednisone 80 mg a day should be added if there is no improvement in 24 to 48 hours and maintained until an expedited evacuation. Nontraumatic Fluorescein-Negative Acute Red Eye (No Discomfort or Discomfort Improved by Topical Anesthesia) Conjunctivitis.
One of the most common disorders in this diagnostic category is conjunctivitis. Etiologic agents of infectious conjunctivitis include bacteria,
Figure 22-10 Nontraumatic iritis. (Courtesy Steve Chalfin, MD.)
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viruses, chlamydiae, fungi, and parasites.[42] Acute allergic conjunctivitis may also be encountered, especially in a wilderness setting. The keys to diagnosis are the presence of discharge or tearing, relatively mild burning or foreign-body type discomfort that is relieved by topical anesthesia, and a negative (or SPK) fluorescein staining pattern. The diagnosis of conjunctivitis should be questioned in the absence of discharge or tearing. The primary exception to this statement is allergic conjunctivitis, which may not generate a significant discharge. In this case, bilaterality, significant ocular itching, and a history of ocular or systemic allergies will help make the diagnosis. With infectious conjunctivitis, there are often signs or symptoms of an accompanying upper respiratory infection (URI) or a history of contact with other persons who have recently suffered from conjunctivitis. Treatment of conjunctivitis in the wilderness setting is with ciprofloxacin or ofloxacin drops (1 drop 4 times a day for 5 days) if there is a yellowish discharge. Tobramycin 0.3% drops or trimethoprim/polymixin B drops are acceptable alternatives.[42] This should be an adequate treatment time if conjunctivitis is bacterial. Symptoms that persist for more than 5 days suggest a viral etiology. These symptoms may take several weeks to clear, just as some viral URIs take several weeks to resolve. If there is only tearing or a watery discharge, suggesting a viral etiology, treatment with artificial tears and cool compresses may be substituted for antibiotic therapy. The victim should be instructed on infection precautions, since viral conjunctivitis can spread rapidly through a group. This is especially true if the discomfort caused by conjunctivitis is severe and accompanied by significant photophobia. These symptoms suggest epidemic keratoconjunctivitis (EKC), which, in addition to having a prolonged course, is very uncomfortable because of the corneal involvement. An eye with EKC is shown in Figure 22-12 . Sunglasses should be part of the treatment. Scopolamine 1 drop 2 to 4 times a day may be required to reduce discomfort.
Figure 22-11 Diffuse scleritis. (Courtesy Steve Chalfin, MD.)
As noted previously, if the predominant ocular symptom is itching, allergic conjunctivitis should be suspected. Allergic conjunctivitis may be treated with cool compresses and/or systemic antihistamines. Severe ocular itching may be treated with a 3-day course of prednisolone, 1 drop 4 times a day. Hyperacute conjunctivitis with marked lid edema, conjunctival hyperemia, chemosis, and copious purulent discharge should alert the care provider to the possibility of a gonococcal etiology.[42] Gonococcal conjunctivitis may progress to vision-threatening keratitis and should be treated aggressively with levofloxacin 500 mg once a day, ciprofloxacin or ofloxacin drops 4 times a day, and expedited evacuation. Bacterial and viral conjunctivitis are highly contagious. Individuals with infectious conjunctivitis should be informed of this fact and the importance of infection precautions emphasized. Blepharitis.
Blepharitis is probably the most common external eye disease seen in the general ophthalmologist's office.[16] It is often misdiagnosed as conjunctivitis. Differentiation may often be made by the history. Blepharitis tends to be a bilateral, chronic disease with recurrences and exacerbations. There is chronic flaking and irritation of the skin at the base of the eyelashes that may occasionally be complicated by bacterial superinfection. An eye with blepharitis is shown in Figure 22-13 . There may be an association with skin disorders, such as seborrheic dermatitis or acne rosacea.[16] The victim often has a history of chronic ocular itching and burning. Fluctuating vision may be present as well.[16] A history of excessive mucous discharge in the eyes on waking is often present. Treatment for blepharitis should focus on the lid margins. Bacitracin or erythromycin ophthalmic ointment should be applied thinly to the lid margins at bedtime for 4 weeks. Lid hygiene is directed at reducing the amount of debris on the lid margins and consists
Figure 22-12 Epidemic keratoconjunctivitis (EKC). (Courtesy Steve Chalfin, MD.)
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Figure 22-13 Blepharitis. (Courtesy Steve Chalfin, MD.)
of warm, moist compresses applied to the eyelids 1 to 4 times a day for 5 to 10 minutes, followed by gently wiping away the moistened lash debris. Artificial tears may relieve the sensation of "dry eye" that often accompanies blepharitis.[16] Ultraviolet Keratitis.
The diagnosis of ultraviolet keratitis is easy to make in the presence of a severely sunburned face and bilateral red, painful eyes. The discomfort typically does not start until 6 to 10 hours after UV exposure and may awaken the victim.[55] Symptoms range from mild irritation and foreign body sensation to severe pain, photophobia, and lid spasm.[55] Fluorescein staining usually reveals a punctate staining pattern. Treatment consists of bacitracin or erythromycin ophthalmic ointment applied to the eye 4 times a day (an acceptable alternative would be fluoroquinolone drops 4 times a day) and sunglasses. In a severe case, one or both eyes may be patched to aid in pain control, although it may be better to patch only the more severely affected eye so that the victim is not deprived of vision in both eyes.[10] Scopolamine (1 drop twice a day) may be added for pain control. Systemic analgesia may also be required. The victim should be reexamined every day until there is no longer an SPK pattern present on fluorescein staining, at which time antibiotic therapy may be discontinued. The duration of discomfort from UV keratitis is typically 24 to 48 hours.[55] Conjunctival Foreign Body.
The symptom of ocular foreign body sensation does not necessarily mean that a conjunctival or corneal foreign body is present. Although the presence of a conjunctival foreign body may be strongly suspected based on the abrupt onset of discomfort following a gust of wind or other mechanism for depositing foreign material in the eye, definitive diagnosis requires visualization of the offending material, which may sometimes be quite difficult. Figure 22-14 shows an eye with a conjunctival foreign body. The victim
Figure 22-14 Conjunctival foreign body. (Courtesy Steve Chalfin, MD.)
is often able to help with foreign body localization before the instillation of topical anesthetic drops. Treatment consists of a careful search for the foreign body using adequate lighting. Topical anesthesia makes the victim much more agreeable during the search and removal efforts. A handheld magnifying lens or pair of reading glasses will provide magnification to aid in the visualization of the foreign body. Eyelid eversion with a cotton-tipped applicator helps the examiner identify foreign bodies located on the upper tarsal plate. Once located, the foreign body should be removed with a cotton-tipped applicator after the eye has been anesthetized and the cotton-tipped applicator moistened with tetracaine. The eye is then stained with fluorescein to check for a corneal abrasion. If no foreign body is visualized but the index of suspicion is high, vigorous irrigation with artificial tears or sweeps of the conjunctival fornices with a moistened cotton-tipped applicator after topical anesthesia may be successful in removing the foreign body. Several types of foreign body merit special mention. If the foreign body identified is one that may have penetrated into the eye, such as a large thorn, the victim should be managed as described in the Obvious Open Globe section. Hot ashes or cinders from a campfire may strike the eye, resulting in both a foreign body and a thermal burn. Immediate instillation of topical anesthesia will provide temporary pain relief to facilitate foreign body removal and will also stop any ongoing thermal injury. After the foreign body has been removed, the corneal abrasion that typically results from a thermal injury to the cornea should be managed as outlined in that section. Dry Eye.
Symptomatic dry eye is commonly encountered in the wilderness, especially in mountainous areas where the air is very dry and significant wind is often present.[10] Dry eye is usually bilateral and may result in secondary tearing.[60] There may be a history of
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previous episodes of symptomatic dry eye. Individuals with chronic dry eyes are usually middle-aged or older and may have a history of autoimmune disorders. The discomfort is usually relieved by topical anesthesia. Treatment is with artificial tears used as often as needed to relieve symptoms. Dehydration may contribute to this condition, and adequate fluid intake should be maintained. The use of sunglasses may provide protection from the wind and be of significant benefit in managing this disorder. Contact Lens Overwear Syndrome.
The considerations here are much as described in the Dry Eye section, except that the symptoms are magnified by the presence of contact lenses. Contact lens rewetting drops and sunglasses are the first line of management. Should these measures be ineffective in relieving symptoms, the contact lenses should be removed. If significant SPK are present on fluorescein staining, ciprofloxacin or ofloxacin drops 4 times a day should be used until the SPK have resolved.[10] Contact lenses should not be replaced in the eye until the eye is symptom-free. An individual who wears contact lenses in the wilderness should always carry a pair of glasses that can be used if contact lens problems arise. Episcleritis.
Episcleritis is a benign, self-limited, inflammatory condition of the lining of the eye between the conjunctiva and the sclera.[42] There is usually sectorial redness without discharge ( Figure 22-15 ). There is often a history of previous episodes. Discomfort is typically mild or absent. The presence of severe pain, photophobia, or decrease in vision suggests another cause. Episcleritis is often misdiagnosed as conjunctivitis, but the lack of a discharge and the sectorial redness usually seen in episcleritis will help differentiate between the two disorders. Episcleritis is usually self-limited and resolves without treatment over 3 to 4 weeks.[42] If symptoms are troublesome, it may be treated with prednisolone drops 4 times a day for 3 to 5 days.
SOLAR RETINOPATHY The retina is protected from UV radiation damage because this high-energy radiation is absorbed by the cornea and the lens of the eye. However, visible and near-infrared light of sufficient intensity may reach the retina and cause photochemical damage.[42] In the wilderness setting, this would most likely occur as the result of staring at the sun or a solar eclipse. Shortly after such an exposure, the individual may experience blurred or distorted vision, a central scotoma, and/or a headache. Visual acuity is often reduced to the 20/40 to 20/70 range. There is no effective therapy for this injury, but visual acuity may return to normal over a period of several months in mild cases.
Figure 22-15 Episcleritis. (Courtesy Steve Chalfin, MD.)
LOCATING A DISPLACED CONTACT LENS Soft contact lens wearers may occasionally have one of their lenses become displaced, causing blurred vision and a foreign body sensation. Once the lens is displaced, it may be hard to locate. The conjunctival fornix of the lower lid is easily examined by distracting the lens from the globe with gentle downward finger pressure applied to the lower lid. If the contact lens has been displaced into the superior conjunctival fornix (usually the case), it may be more difficult to locate. If visual inspection with a penlight and a handheld magnifying lens is not successful in finding the lens, gentle digital massage over the closed upper lid directed towards the medial canthus often results in the contact lens emerging at that location. Several minutes of massage may be required. A few drops of artificial tears often facilitates the process. If this maneuver is unproductive, the eye may be anesthetized with a drop of tetracaine, the upper lid distracted from the globe with upward finger pressure, and the fornix swept with a moistened cotton-tipped applicator.
IMPROVISATION (see also Chapter 19 ) If you encounter a person with known or suspected globe rupture, it is of paramount importance to ensure that subsequent inadvertent trauma does not cause extrusion of ocular contents. If an eye shield is not available, one may be fashioned with duct or rigger's tape and any available rigid flat or concave object that can be placed over the eye. Examples include small cups or bowls to provide a good standoff distance between the eye and the improvised shield. Improvised wound closure strips can be made by tearing rigger's or duct tape into ¼-inch widths. Spectacles and sunglasses can be improvised by making a pinhole in a piece of paper or cardboard. (Make the pinholes before placing the paper or cardboard in front of the eyes!) Take note of the
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TABLE 22-1 -- Pressures and Equivalent Oxygen Fractions at Altitude FEET
METERS
Sea level Sea level
ATMOSPHERIC PRESSURE (mm Hg)
EQUIVALENT OXYGEN (%)
PARTIAL PRESSURE OF OXYGEN (mm Hg)
760
20.9
159
4,000
1,219
656
18.0
137
7,000
2,134
586
16.1
122
10,000
3,048
523
14.4
109
15,000
4,572
429
11.8
89
20,000
6,096
347
9.5
73
25,000
7,620
282
7.8
60
29,028
8,848
253
7.0
53
restriction in peripheral vision caused by using pinhole glasses. If the purpose is to improvise sunglasses rather than to achieve a refractive effect, the pinhole can be larger or fashioned into a horizontal slit to improve peripheral vision. Improvised magnifying glasses for examining the eye or other small areas may be made by simply using a pair of reading or hyperopic glasses. Another refractive improvisation technique involves a handheld magnifying lens. This convex lens with its plus refracting power can be used to provide a variety of hyperopic refractive corrections by moving the lens to various distances in front of the eye.
THE EYE AT ALTITUDE Ocular disorders associated with altitude exposures have been addressed in a recent review article.[10] The sections from that paper that address ocular disorders likely to be encountered in mountaineering are included below. Altitude Exposures and Ocular Physiology A number of significant effects on visual function resulting from the hypoxia of altitude were described by Wilmer and Berens[88] in their classic article. The decrease in ambient pressure at altitude causes a hypobaric hypoxia despite a constant oxygen fraction of 0.21 as noted in Table 22-1 . Retinal blood flow has been shown to increase by 128% after 4 days at 5300 m (17,384 feet).[22] This increase in blood flow results in clinically observable changes, such as increase in diameter and tortuosity of retinal vessels and optic disk hyperemia, which are seen in most unacclimatized persons at altitudes above 4573 m (15,000 feet).[22] [35] [46] [59] Because of its avascularity, the cornea receives most of its oxygen supply from the surrounding atmosphere,[74] so it may suffer hypoxic dysfunction even if the inspired gas mix is not hypoxic, as noted below in the Refractive Changes at Altitude after Refractive Surgery section. This is an important factor when considering topics such as the suitability of contact lenses and refractive surgical procedures for mountaineers and aviators.
Figure 22-16 High-altitude retinal hemorrhages. (Courtesy Dr. M. McFadden, UBC, Vancouver, BC, in association with Dr. C. Houston, Burlington, Vt.; Dr. G. Gray, DCIEM, Toronto, Ontario; and Drs. Sutton and P. Powells, McMaster University, Hamilton, Ontario.)
High-Altitude Retinal Hemorrhage There are many reports of retinal hemorrhages ( Figure 22-16 ) in mountain climbers.* These have been described as high-altitude retinal hemorrhages (HARH) or as part of the more inclusive term altitude retinopathy. [8] A classification for HARH has been developed by Weidman.[85] [86] Butler, Harris, and Reynolds[8] reported an incidence of HARH of 29% in climbers on a Mt. Everest expedition at altitudes ranging from 5300 to 8200 m (17,385 to 26,896 feet). McFadden et al[46] found that 56% of their subjects had HARH at an altitude of 5360 m (17,581 feet) and that one had a retinal nerve fiber layer infarct (cotton wool spot) ( Figure 22-17 ). They also reported that exercise at altitude was associated with both an increased incidence of HARH and fluorescein leakage from the retinal vessels. Hackett and Rennie[26] described HARH in 4% of 140 trekkers examined at 4243 m (13,917 feet) at Pheriche in the Himalayas. These authors also found a significant correlation of retinal hemorrhages with symptoms of acute mountain sickness (AMS). Kobrick and Appleton[35] found no retinal *References [ 8]
[ 21] [ 26] [ 37] [ 39] [ 46] [ 59] [ 61] [ 67] [ 70] [ 84]
.
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Figure 22-17 Cotton wool spots seen at 5400 m. This occurred in a climber after Valsalva maneuver and represents the most severe form of retinopathy. (Courtesy Dr. M. McFadden, UBC, Vancouver, BC, in association with Dr. C. Houston, Burlington, Vt.; Dr. G. Gray, DCIEM, Toronto, Ontario; and Drs. Sutton and P. Powells, McMaster University, Hamilton, Ontario.)
Figure 22-18 The normal fundus as sea level (left). The same fundus at 5400 m (right). Note the vascular engorgement and tortuousness at altitude. (Courtesy Dr. M. McFadden, UBC, Vancouver, BC, in association with Dr. C. Houston, Burlington, Vt.; Dr. G. Gray, DCIEM, Toronto, Ontario; and Drs. Sutton and P. Powells, McMaster University, Hamilton, Ontario.)
hemorrhages in eight subjects examined after 48 hours at 4573 m (15,000 feet) in a hypobaric chamber, although all subjects displayed the marked vascular engorgement and tortuosity typical of the eye at altitude ( Figure 22-18 ). Differences in the incidence of HARH for exposures at similar altitudes may be due to differences in time at altitude before examination, acclimatization schedule, exercise levels, examination techniques, and the presence of concurrent conditions that may predispose to HARH. HARH has been reported to be associated with both altitude headache and a history of vascular headache at sea level.[67] Rimsza et al[61] noted that HARH may occur at lower altitudes in individuals with chronic lung disorders that interfere with oxygenation. Their case report described a woman with cystic fibrosis who had climbed as high as 3049 m (10,000 feet) but was at 1677 m (5500 feet) when she noted a sudden decrease in vision associated with preretinal hemorrhage of the right eye. They also noted that the ocular findings of cystic fibrosis are similar to those seen with altitude retinopathy.[61] Although HARHs are often not associated with acute visual symptoms, [8] [59] [84] [91] they may result in a loss of visual acuity or paracentral scotomas.[21] [39] [70] [84] Lang and Kuba[39] reported a person who experienced decreased visual acuity and central scotoma from HARH resulting from a 7000-m (22,960-foot) altitude exposure. Permanent deficits in visual function are uncommon but have been reported.[70] [84] Shults and Swan[70] reported that four survivors of an ill-fated Aconcagua expedition in Argentina in 1973 were found to have severe HARH after an altitude exposure of 6860 m (22,500 feet). Two of the survivors suffered apparently permanent paracentral scotomas. No reports were found of a progressive decrease in visual acuity or progressive enlargement of paracentral scotomas as a result of remaining at altitude after the development of HARH.[10] Weidman[84] reported a case in which further ascent after the development of HARH resulted in additional lesions. HARH that results in decreased visual acuity should be a contraindication to further ascent.[10] Butler and Harris[8] recommended that evacuation of individuals with decreases in visual function resulting from HARH (in the absence of high-altitude cerebral edema [HACE] or high-altitude pulmonary edema [HAPE]) be considered nonemergent unless reexamination indicates a progressive deterioration of vision or increasingly severe retinopathy. HARH resolves over a period of 2 to 8 weeks after the altitude exposure is terminated.[84] Cortical Blindness at High Altitude Hackett[25] reported six cases of cortical blindness at high altitude. These victims were found to have intact pupillary reflexes. Descent, Gamow (hyperbaric) bag recompression, or supplemental oxygen breathing should be used in persons with neurologic dysfunction at altitude. Ocular Motility Kramar[37] reported that convergence insufficiency was found in women with altitude illness. Basnyat[2] noted that lateral gaze palsy and other focal neurologic deficits, often in the absence of other symptoms of AMS or HACE, are seen commonly by physicians in the Himalayan Rescue Association. Rennie and Morrissey[59] reported a person with nystagmus at altitude that was associated with ataxia and intention tremor. Ocular motility abnormalities should be managed in the same way as cortical
blindness at high altitude as described in the preceding paragraph. Contact Lenses in Mountaineering Contact lenses may be used successfully at high altitude.[11] [91] Clarke[11] noted that contact lenses were used successfully by five members of the British Everest Expedition in 1975 up to altitudes as high as 7317 m (24,000 feet). Use of contact lenses at altitude during trekking or mountaineering entails several considerations beyond those encountered in normal use. In general, overnight use of extended-wear contact lenses is
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not recommended because of the associated increased rate of microbial keratitis. Even soft contact lenses decrease the oxygen available to the cornea. Lid closure during sleep further accentuates corneal hypoxia. Removing contact lenses at night, however, presents logistical problems in the mountaineering setting. Practicing acceptable lens hygiene during an expedition is difficult. The mountaineer who leaves contact lenses in a case filled with liquid solution in the tent outside of his or her sleeping bag at night may awaken to find the solution and lenses frozen solid. Guidelines for military personnel using contact lenses in austere environments have been developed and apply to the expedition setting[10] : 1. Disposable extended-wear lenses may be left in the eye for up to 1 week. If the wearer is still in the field at the end of this period, the lenses should be removed and discarded. After an overnight period without lenses, new lenses may be inserted, with strict attention to contact lens hygiene. 2. Contact lens wearers should always have backup glasses available for use in the wilderness in case a lens is lost or becomes painful. 3. Individuals who wear contact lenses on expeditions should carry both fluoroquinolone eye drops and contact lens rewetting solution. Both types of drops may freeze if not protected from the cold. 4. Contact lens wearers often note that their eyes become dry. This discomfort may be alleviated with contact lens rewetting drops. 5. Contact lens wearers often note increased sensitivity to sunlight. Individuals who wear contact lenses in the field during daylight hours should carry sunglasses. Continuous wearing of disposable contact lenses for a week, followed by discarding of the lenses and insertion of fresh lenses after an overnight period without a lens, is a controversial approach to contact lens wear in an expedition setting. Whether or not the reduction in lens handling offsets the increased risk of microbial keratitis resulting from overnight wear is not known. The decision to wear contact lenses while mountaineering should be made carefully. Microbial keratitis (corneal ulcers) can pose a significant threat to vision under the best of circumstances. Should this disorder occur with a 7- to 10-day delay to definitive ophthalmologic care, the danger of permanent loss of vision is great. Any eye pain that occurs in contacts lens wearers in the wilderness should be managed as described previously in the Acute Red Eye section. Considering all the potential problems, a good pair of prescription glacier glasses or laser refractive surgery might be a more reasonable alternative than contact lenses as a long-term solution to the refractive needs of mountaineers. Refractive Changes at Altitude after Refractive Surgery An acute hyperopic shift in persons who have had radial keratotomy (RK) and then experience an altitude exposure was reported by Snyder in 1988[75] and White and Mader in 1993.[87] This effect has been observed at altitudes as low as 2744 m (9000 feet).[75] A dramatic example of this phenomenon was that experienced by Dr. Beck Weathers in the Everest tragedy of May 1996 in which eight climbers lost their lives. Dr. Weathers had undergone bilateral RK years before the expedition. He noted a decrease in vision, which started early during his ascent.[36] Author Jon Krakauer recalls that "... as he was ascending from Camp Three to Camp Four, Beck later confessed to me, 'my vision had gotten so bad that I couldn't see more than a few feet.'"[36] This decrease in vision forced Dr. Weathers to abandon his quest for the summit shortly after leaving Camp Four and nearly resulted in his death. Another report describes two expert climbers who experienced hyperopic shifts of three diopters or more during altitude exposures of 5000 m (16,400 feet) or higher on Mt. McKinley and Mt. Everest.[12] Mader and White[43] found that the magnitude of the hyperopic shift was 1.03 +/- 0.16 diopters after 24 hours at 3659 m (12,000 feet) and 1.94 +/- 0.26 diopters at 5183 m (17,000 feet). Ng[51] reported no refractive change after 6 hours in post-RK eyes at a simulated altitude of 3659 m, suggesting that the hyperopic shift requires more than 6 hours to develop. Further studies by Mader et al[44] at 4299 m (14,100 feet) on Pike's Peak revealed that: (1) subjects who had undergone RK demonstrated a progressive hyperopic shift associated with flattened keratometry findings during a 72-hour exposure; (2) control eyes and eyes that had undergone laser refractive surgery (photorefractive keratectomy [PRK]) experienced no change in their refractive state; (3) peripheral corneal thickening was seen on pachymetry in all three groups; and (4) refraction, keratometry, and pachymetry all returned to baseline after return to sea level. Winkle[89] demonstrated that exposing post-RK corneas to 100% nitrogen via goggles at one atmosphere for 2 hours caused a significant hyperopic shift of 1.24 diopters and corneal flattening of 1.19 diopters in post-RK eyes. Corneal thickness increased in both post-RK and control eyes but was not associated with a hyperopic shift in control eyes. This is strong evidence that the effect of altitude exposures on post-RK eyes is caused by hypoxia rather than by hypobarism and further illustrates that breathing a normoxic inspired gas mix will not protect against the development of hypoxic corneal changes. The effect of the post-RK hyperopic shift seen at altitude depends on the postoperative refractive state (undercorrected patients may actually have their vision improve) and the accommodative abilities of the individual.[43] The work of Mader and his colleagues has
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provided compelling evidence for myopic mountaineers that PRK instead of RK is their refractive surgical procedure of choice. Individuals who have undergone RK and plan to undertake an altitude exposure of 2744 m (9000 feet) or higher while mountaineering should bring multiple spectacles with increasing plus lens power.[43] To my knowledge, a post-RK hyperopic shift has not been reported in airline passengers or flight crew. This may be because the latent period required for this phenomenon to develop exceeds the duration of most commercial flights or because the approximate 8000-foot cabin pressure on most commercial flights does not produce sufficient corneal hypoxia for a hyperopic shift to occur. Ultraviolet Radiation Damage (see also Chapter 14 ) Ultraviolet radiation is divided into UV-A (320 to 400 nm), UV-B (290 to 320 nm), and UV-C (100 to 290 nm). Almost all UV-C radiation is absorbed by the earth's ozone layer.[54] [77] The cornea absorbs all radiation with wavelengths of less than approximately 300 nm, and the lens absorbs almost all of the remaining UV-B radiation that reaches it.[77] UV radiation is increased with high altitude, low latitude, and highly reflective environments.[54] Altitude exposures associated with mountaineering entail exposures to increases in the amount of both incident and reflected UV light. Acute exposure to high levels of UV radiation may result in UV photokeratitis,[14] [77] whereas chronic exposures may be associated with cortical lens opacities,[13] posterior subcapsular lens opacities,[4] pterygia, [3] and squamous cell carcinoma of the conjunctiva. [49] Diagnosis and management of UV keratitis are discussed previously in this chapter. The best strategy for dealing with UV radiation-induced disorders is prevention. Most experienced mountaineers and trekkers are well aware of the need for sunglasses with high rates of UV absorption. UV attenuation in sunglasses depends on the size, shape, and wearing position, as well as the absorption properties of the optical material used.[63] The use of a brimmed hat is another effective means of decreasing UV exposure to the eye.[54] [64] In conjunction with the use of topical sun-blocking agents, a hat may also help prevent a series of cutaneous neoplasms from being a lasting reminder of previous mountaineering expeditions. Sunglasses Selection in Mountaineering What type of sunglasses should be worn by individuals on mountaineering expeditions? Absorption of essentially all UV radiation is a key consideration, since radiation in this portion of the electromagnetic spectrum is not visible and serves only to produce adverse effects in the eye. Another critical consideration is the amount of visible light transmitted. Sunglasses that suffice for everyday use may not be adequate for use in the mountains, especially while on snow or glaciers. The comfort zone for luminance is approximately 350 to 2000 candelas/m2 . [77] An outdoor environment consisting of sunlit fields and foliage may have a luminance of 3000 to 7000 candelas/m2 ; a bright beach may have a luminance of 6000 to 15,000 candelas/m2 . Standard sunglasses that transmit 15% to 25% of visible light reduce the luminance in these situations to within the comfort range. In contrast, bright sun reflected off snow or clouds may result in luminances of 15,000 to 30,000 candelas/m2 . Sunglasses with visible light transmittance in the 5% to 10% range are needed to reduce luminance to a comfortable range in these circumstances. (The 1986 American National Standards Institute [ANSI] standards for nonprescription sunglasses recommend that tinted lenses with visible light transmittances of less than 8% not be used for driving.[77] ) Sideshields or deeply wrapped lens designs should be used.[77] Infrared absorption is important in certain industrial occupations, such as glass, iron, and steelworkers,[77] but is less important in protective eyewear to be used outdoors. Table 22-2 provides desirable characteristics in selecting sunglasses
for mountaineering or other environments with high levels of luminance and UV radiation.[10] Photochromic Lenses Photochromic lenses change transmittance or color when exposed to light or UV radiation.[77] They are designed to transmit a greater percentage of incident light TABLE 22-2 -- Sunglasses Selection Criteria for Mountaineering SUBJECT
CHARACTERISTICS
UV absorption
99% to 100%
Visible light transmittance
5% to 10%*
Lens material
Polycarbonate or CR-39†
Optical quality
Clear image without distortion‡
Frame design features
Large lenses; side shields or "wraparound" design; fit close to face; good stability on face during movement; lightweight; durable
Color
Gray§
*Glasses with less than 8% transmittance of visible light should not be worn while driving. Sunglasses or any tinted lenses with a visible light transmittance of less than 80% should not be worn while driving at night.[ 77] †Glass lenses typically have very good optical clarity and scratch resistance but are heavier and more expensive. ‡Hold the sunglasses at arm's length and move them back and forth. If the objects are distorted or move erratically, the optical quality is probably less than desirable. Also, compare the image quality between several different pairs of sunglasses to get a basis for comparison. §The use of colored lens tints can alter color perception and possibly compromise the visibility of traffic signals. Neutral gray absorbs light relatively constantly across the visible spectrum and avoids these problems.[ 77]
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when indoors or in conditions of reduced illumination and a reduced amount of light when exposed to higher levels of illumination. This is accomplished in one example of glass lenses by incorporating an inorganic silver halide into the lens. When the lens is exposed to sunlight, this compound decomposes into its component silver and halide ions and the lens turns dark gray.[77] When the lens is removed from sunlight, the process reverses. When selecting photochromic lenses, the adequacy of indoor light transmittance can be judged while trying them on. The outdoor transmittance should be approximately 5% to 10% as noted in Table 22-2 if the glasses are to be used for mountaineering. Most photochromic lenses have outdoor transmittances of approximately 20%, which should suffice for less highly reflective outdoor environments.[77] Several plastic photochromic lenses are now available. The darkening process in plastic lenses is accomplished by organic light-sensitive compounds that are suspended in a thin layer near the front of the lens. Plastic photochromic lenses generally do not darken well enough to be used as sunglasses in bright environments. In addition, unlike glass photochromic lenses, the photochromic reaction typically used in plastic lenses usually fades in 1 to 2 years.[77]
THE EYE AND DIVING The ocular aspects of scuba diving and other hyperbaric exposures were reviewed in a 1995 paper.[9] The sections from that paper that address the hyperbaric environment, ocular barotrauma, the ocular manifestations of decompression sickness and arterial gas embolism, ophthalmic considerations in fitness-to-dive evaluations, and the differential diagnosis of decreased vision after diving are included here. An expanded discussion of these items, as well as additional material on diving after eye surgery, the effect of common eye medications on fitness to dive, and the use of hyperbaric oxygen to treat ocular disorders, may be found in the review article. The Hyperbaric Environment (see also Chapter 59 ) At sea level, the body is exposed to one atmosphere (ATA) of pressure. This magnitude of pressure may also be expressed as 760 mm Hg, 33 feet of sea water (FSW), and 14.7 pounds per square inch (psi). The normal atmospheric pressure of 1 ATA is often used as a reference point from which other pressures are measured. When one states that the intraocular pressure (IOP) is 15 mm Hg, what is meant is that the IOP is 15 mm Hg more than the surrounding environment. In point of fact, the absolute pressure inside the eye at sea level is 775 (760 + 15) mm Hg. The IOP that is measured with a tonometer is therefore a "gauge" pressure, meaning that the pressure displayed is the actual pressure minus the atmospheric pressure. Ophthalmic Considerations in the Fitness-to-Dive Evaluation A diver should have adequate visual acuity to be able to read his or her gauges and function safely underwater. Possession of a driver's license is a convenient indication that a potential diver has sufficient visual acuity to meet this standard.[9] A person who has recently undergone ophthalmic surgery should refrain from diving until the recommended convalescent interval has passed.[9] Individuals who suffer from glaucoma may dive safely unless they have had glaucoma filtering surgery performed. [9] Systemic carbonic anhydrase inhibitors are best avoided in glaucoma patients who wish to dive because of possible confusion between medication-induced paresthesias and decompression sickness.[9] Any individual who is suffering from an acute ocular disorder that causes significant pain, decreased visual acuity, or other disabling symptoms should refrain from diving until these symptoms have resolved.[9] Underwater Refractive Correction If contact lenses are to be used for diving, soft contact lenses are preferred.[5] [17] [32] [47] Hard (polymethylmethacrylate) contact lenses have been associated with corneal edema during decompression and after dives.[72] [73] These changes are caused by formation of nitrogen bubbles in the precorneal tear film during decompression, which interferes with normal tear film physiology and results in epithelial edema. Bubble formation would be expected to be more common during dives with significant decompression stress. Although the increased gaseous diffusion properties of rigid gas-permeable contact lenses theoretically decrease the chance of bubble formation in the tear film, use of these lenses while diving has been demonstrated to cause bubble formation under the lens, leading to secondary corneal epithelial disruption.[76] The author has treated one diver with foreign body sensation and blurred visual acuity that occurred during ascent while wearing gas-permeable contact lenses. Symptoms resolved upon removal of the lens at the surface. Corneal edema was not observed in one series in which soft contact lenses were studied.[73] The most frequent complication of soft contact lens use in diving is loss of the lens.[32] [34] The risk of lens loss can be minimized by ensuring a good seal on the face mask and minimizing the amount of water that gets into the air space of the mask. Should the mask become displaced during the dive, narrowing of the palpebral fissures helps decrease the chance of the contact lens floating off the surface of the eye.[32] A prescription ground face mask is another refractive alternative, as is a face mask with a lens bonded onto the surface of the mask. Masks and lenses may be lost in high swells or rough surf, however, leaving a
549
diver without refractive correction. When contemplating the purchase of an expensive prescription face mask, one needs to be mindful of the corollary of Murphy's law that applies to diving: "Weight belts always fall on the face masks with prescription lenses." Ocular Barotrauma The eye is normally filled with noncompressible fluid and solid tissues and is therefore protected from barotrauma. However, once a mask is placed over the face, a different circumstance exists. The face mask is an air-filled space bounded on one side by the eyes and ocular adnexa. As a diver descends, if he or she does not expel gas through the nose into the airspace of the face mask, a relative negative pressure develops in this space. If this negative pressure becomes great enough, the eyes and ocular adnexa are drawn towards the space. Marked lid edema with ecchymosis and subconjunctival hemorrhage may develop as tissues and blood vessels are disrupted by this distention. These signs may be alarming to the diver but typically resolve without sequelae. In a more severe case, such as that which may occur when an unconscious diver sinks a significant distance in the water column, more serious injury, including hyphema, may occur.[19] A diver with face mask barotrauma is shown in Figure 22-19 . Barotrauma is also possible in persons with gas bubbles in the anterior chamber or vitreous cavity. Pressure-induced changes in the volume of this bubble may result in retinal, uveal, or vitreous hemorrhage, as well as partial collapse of the globe. Permanent loss of vision may ensue. One person who attempted to dive while an iatrogenic bubble was present in the vitreous cavity noted the immediate onset of very severe eye pain upon descent and quickly aborted his dive.[56] Persons with intraocular
Figure 22-19 Mask squeeze in a diver who descended to 45 FSW without exhaling into his mask. (Courtesy Kenneth W. Kizer, MD.)
gas should not be allowed to dive as long as the bubble remains in the eye. The necessity of adding extra gas to the face mask during descent makes it obvious that swim goggles, which cover only the eyes and not the nose, should never be used for diving. Decompression Sickness Ocular involvement in decompression sickness (DCS) was first reported by Sir Robert Boyle, who observed gas bubbles in the anterior chamber of the eye of a viper that had been experimentally exposed to increased pressure.[6] Ocular manifestations of DCS are infrequently reported in the ophthalmic literature, [9] but there are a number of reports of ocular involvement with DCS in the diving medical literature.[7] [9] [18] [62] Reported manifestations include nystagmus, diplopia, visual field defects, scotomas, homonymous hemianopias, orbicularis oculi pain, cortical blindness, convergence insufficiency, optic neuropathy, and central retinal artery occlusion.[9] The
incidence of visual symptoms in patients with DCS was found to be 7% in one large series.[62] Fluorescein angiography of divers has documented retinal pigment epithelial abnormalities indistinguishable from those seen in eyes with choroidal ischemia. These changes are attributed to decompression-induced intravascular gaseous microemboli. The incidence of these lesions was related to the duration of diving and a history of DCS. Although no diver was reported to have suffered a loss of visual acuity from these abnormalities, the long-term effects of this phenomenon remain to be studied.[9] DCS may also result when an individual without a hyperbaric exposure is suddenly exposed to a decrease in pressure. Altitude DCS presenting as optic neuropathy has been reported.[7] The risk of DCS may be increased if an altitude exposure is undertaken after diving without allowing a sufficient time interval for excess nitrogen taken up during the dive to leave the body.[9] DCS is treated with oxygen breathing and recompression on an emergent basis. Ophthalmologists seldom encounter this disease in an acute setting because most divers know to seek recompression therapy for signs or symptoms of DCS. Since treatment generally results in resolution of all symptoms, most persons with visual symptoms before treatment are asymptomatic after recompression treatment and are therefore not referred to ophthalmologists.[6] Should an ophthalmologist encounter a person with acute ocular disturbances consistent with DCS after a hyperbaric or hypobaric exposure, the victim should be referred emergently to the nearest available recompression chamber and diving medicine specialist, since DCS may worsen rapidly if not treated. Physicians unsure of the location of the nearest diving medicine specialist or recompression chamber can call the Divers Alert Network at Duke University (919-684-8111).
550
Incomplete response to treatment or recurrence of symptoms after treatment may bring a victim with ocular DCS to the ophthalmologist on a less emergent basis. The victim should be managed in conjunction with a diving medicine specialist. Recompression therapy and hyperbaric oxygen should be administered even when a significant delay has occurred between the onset of symptoms and initial evaluation of the victim, since treatment may be effective despite delays of up to several weeks.[7] [9] Arterial Gas Embolism Retrochiasmal defects, such as hemianopias or cortical blindness, are found with arterial gas embolism. Central retinal artery occlusion may result from gas emboli in the ophthalmic artery.[9] Management is similar to that for DCS, with emergent recompression and hyperbaric oxygen therapy indicated in all cases. Differential Diagnosis of Decreased Vision after Diving DCS and arterial gas embolism should be considered whenever vision is acutely decreased after diving because of the possible emergent need for recompression therapy, especially if any other manifestation of DCS or arterial gas embolism are present. Other disorders may also affect vision after a dive. Corneal edema resulting from the formation of gas bubbles under polymethylmethacrylate and rigid gas-permeable contact lenses may cause decreased vision. A soft contact lens wearer who complains of blurred vision after a dive may have a lost or displaced lens. Another possible cause of nondysbaric decreased vision after a dive is epithelial keratopathy induced by chemical agents used to reduce face mask fogging. The time-honored application of saliva or toothpaste to the interior surface of the mask reduces but does not eliminate fogging. This led to the development of commercial antifog agents designed to be applied to the inside surface of face masks. These agents may contain volatile compounds potentially toxic to the corneal epithelium, including glycols, alcohols, and phenol derivatives. Exposure to these compounds may result in blurred vision, photophobia, tearing, and blepharospasm that may not develop until several hours after the dive.[90] Slit lamp examination typically reveals diffuse superficial punctate keratopathy. Development of this syndrome commonly results from improper use of the antifog agent, such as overly generous application or failure to rinse the mask before use. The author has treated several persons with recurrent mild ocular irritation and blurring of vision after dives on which soft contact lenses were worn. The lenses were noted to be tightly adherent to the cornea, probably as a result of a decrease in water content in the lens after contact with hypertonic sea water. Symptoms were relieved with a few drops of isotonic artificial tears.
Box 22-5. DIFFERENTIAL DIAGNOSIS OF DECREASED VISION AFTER DIVING Decompression sickness Arterial gas embolism Bubbles under contact lenses Displaced contact lens Antifog agent keratopathy Contact lens adherence syndrome Transdermal scopolamine
A diver sometimes uses a transdermal scopolamine patch (placed behind the ear) to prevent motion sickness. This may result in mydriasis, decreased accommodation, and blurred vision in the ipsilateral eye. A differential diagnosis of decreased vision after diving is presented in Box 22-5 .
ACKNOWLEDGMENTS
I thank Drs. Steve Chalfin, Dave Harris, and Dave Perlman for their much-appreciated contributions to the preparation of this chapter.
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Chapter 23 - Dental and Facial Emergencies Henry J. Herrmann
Acute conditions involving the mouth and related structures can disrupt recreational activities in the outdoors. A simple toothache, although not life threatening, can cause disabling pain. At the other end of the spectrum, odontogenic infections or major facial trauma are associated with high morbidity and mortality. This chapter discusses toothaches, temporomandibular joint (TMJ) disorders, oral infections, maxillofacial trauma, local anesthesia for dental emergencies, the dental first aid kit, and prevention.
MAXILLOFACIAL PAIN The causes of maxillofacial pain are myriad, and the diagnosis of head and neck syndromes can be exceedingly difficult. Box 23-1 is a partial listing of pain-producing conditions. Fortunately, most of these syndromes are relatively rare. Only the most commonly encountered are covered in this chapter. Pulpitis The common toothache is caused by inflammation of the dental pulp. It may be difficult for the victim to identify the offending tooth because the pain often radiates to the eye or ear region, or is referred from one dental arch to the other. The painful tooth is rarely sensitive to percussion or palpation. An obvious cause, such as a large carious lesion, is sometimes found on examination of the mouth, but often all of the teeth appear intact. If the pulpitis is mild, the condition is characterized by pain that is only elicited by hot, cold, or sweets, and disappears within seconds when the stimulus is removed. Moderate pulpitis is characterized by greater discomfort and an increasing interval between removal of the stimulus and resolution of the pain. In its most severe form, pulpitis causes intense, continuous, and debilitating pain.[4] [17] Emergency treatment recommendations follow. Mild Pulpitis (Characterized by Transient Thermal Sensitivity).
Examine the mouth visually. Structures will likely appear within normal limits. However, if a defect in a tooth is found, it should be temporarily filled. Reassure the victim that although this condition is annoying, rapid progression is unlikely. Moderate Pulpitis (Longer Episodes of Pain).
Proceed as for mild pulpitis. Treat with a nonnarcotic analgesic (ibuprofen 600 mg PO q6h prn pain). Severe Pulpitis (Intense, Continuous Pain).
The preferred approach to severe pulpitis is pain relief using a local anesthetic, followed by evacuation of the victim. A nerve block with bupivacaine 2% with 1:200,000 epinephrine (Marcaine) can provide up to 8 hours of excellent pain relief without central nervous system (CNS) depression (see section on local anesthesia). Large doses of narcotics should not be used because they are likely to compromise the victim's ability to participate in evacuation. In an extraordinary circumstance, an experienced rescuer could locate the offending tooth, expose the pulp, remove the inflamed pulpal tissue with a barbed broach, and cover the opening with a temporary filling material. Extraction is also an option in a case of severe pulpitis, but is to be discouraged for a number of reasons (see section on exodontia). Periapical Osteitis Inflammation of the supporting structures at the root of a tooth is characterized by constant, often throbbing pain. Unlike pulpitis, the affected tooth is easily located. The victim can usually point to the exact source of the pain, or the examiner may gently tap individual teeth, observing for tenderness. The area over the apex of the tooth is usually tender to palpation, but there is no frank swelling. Although trauma to a tooth can result in periapical inflammation, the most common cause is egress of bacteria and breakdown products from the necrotic pulp. Minor swelling around the apex extrudes the tooth slightly, causing increased forces on the tooth during occlusion and thus intensifying the pain. Emergency treatment includes an analgesic (ibuprofen 600 mg PO q6h prn pain) and/or a local anesthetic and a soft diet. Ideally, the contacting areas of the opposing tooth are reduced to relieve occlusal forces. Because this is generally impractical in the field, the victim should be given a strip of leather or something similar to place between the teeth on the nonpainful side. This will keep the offending tooth out of occlusion and reduce the pain. Cracked Tooth Syndrome With cracked tooth syndrome (CTS), the victim complains of momentary, sharp pain when chewing certain foods. Often, the victim reports that the tooth feels "weak" or that "it only hurts when I bite on something hard just the right way." These symptoms occur when forces of the proper magnitude and direction open the incomplete fracture within the tooth. Significantly,
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there is no pain on chewing soft foods. This condition usually progresses slowly. The victim should be advised to avoid chewing on the affected side and to seek definitive dental treatment as soon as possible.
Box 23-1. SOME CONDITIONS THAT CAUSE FACIAL PAIN Pulpitis (acute, chronic, hyperplastic) Periapical osteitis (acute, chronic) Cracked tooth syndrome Periodontal infections Periodontal abscess Acute necrotizing ulcerative gingivitis Primary herpetic gingivostomatitis Pericoronitis Temporomandibular joint disorders Maxillary sinusitis Neurologic pain Trigeminal neuralgia Trigeminal neuritis Herpes zoster neuritis Postherpetic neuralgia Atypical facial pain Psychogenic facial pain Dental causalgia (atypical odontalgia) Vascular pain Migraine headache Temporal arteritis Cluster headache Referred pain Pulpitis Subacute thyroiditis Myocardial infarction or angina pectoris
Maxillary Sinusitis The pain of maxillary sinusitis is generally described as a relatively continuous, throbbing ache that is intensified by postural change. A typical statement is "My tooth really hurt when we were hiking down that hill. I could feel it pound with every step. When we got to camp, I lay down, but it got even worse." The pain may be unilateral or bilateral. It is usually located in the infraorbital region and is often referred to the cheek, frontal region, and the maxillary premolars and molars. A complaint of multiple toothaches in the maxilla, with little or no evidence of carious teeth, should immediately raise suspicion for maxillary sinusitis. In addition to pain, there is tenderness elicited by pressure infraorbitally or over the bony prominence above the first molar. The victim also generally has an elevated temperature and nasal or postnasal discharge. Treatment of maxillary sinusitis includes an analgesic (ibuprofen 600 mg PO q6h prn pain), inhalation of steam, oxymetazoline (Afrin) 0.05% in each nostril, 1 spray bid, to shrink the nasal membranes and improve sinus drainage, and an antibiotic. Appropriate choices include amoxicillin 875 mg with clavulanic acid 125 mg (Augmentin) PO bid for 10 days, or trimethoprim 160 mg with sulfamethoxazole 800 mg (Septra DS) PO bid for 10 days. Azithromycin (Zithromax), 500 mg PO the first day and 250 mg PO for four days, is a convenient alternative. Temporomandibular Disorders Considerable disagreement remains concerning the etiology, classification, and treatment of temporomandibular disorders (TMD). The subject is confusing because TMD is actually a cluster of unrelated conditions, multifactorial in origin and with overlapping symptoms, that often respond to a variety of therapies, including placebos. [6] Included under the classification of TMD are two groups of sufferers: those with masticatory muscle involvement (myofascial pain and dysfunction [MPD]) and those with TMJ problems. A brief summary follows. Myofascial Pain and Dysfunction.
Muscle hyperactivity is an important etiologic factor in MPD. In some persons this may result from parafunction (e.g., gum chewing, clenching or grinding the teeth). Occlusal interferences can also cause muscle hyperactivity. This occurs when a lower tooth contacts an upper tooth prematurely during mouth closure and a reflex causes jaw muscle contraction that shifts the mandible in such a way as to avoid the premature contact. Psychologic stress is also an important factor in causing excessive muscle tension. Participants in wilderness activities are exposed to many of the risk factors for MPD. The high physiologic and psychologic demands of many expeditions lead to considerable stress. Increased jaw function, such as that required to chew granola, jerky, and other dried foods common on wilderness expeditions, is another factor that may precipitate an acute episode of MPD. Symptoms of MPD include pain in the muscles of mastication, which is usually unilateral and increases with chewing, headache, earache, intermittent clicking of the TMJ, limitation of jaw movement, and a change in bite. The victim may have a history of acute onset, or a long saga of exacerbation, remission, and various treatments. The examiner may find objective signs, such as audible clicking of the TMJ, tenderness of the jaw muscles to palpation, tenderness of the TMJ to palpation, and abnormal jaw movements, such as inability to open the mouth widely, or deviation of the chin to one side on opening. Emergency treatment consists of resting the muscles (e.g., soft diet and control of tooth clenching and grinding habits) and the application of
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moist heat. Holding a soft material such as a folded gauze between the front teeth often gives immediate relief because it keeps the teeth from touching and allows the
muscles to relax. An analgesic (ibuprofen 600 mg PO q6h) should be given on a scheduled basis, rather than as needed, to break the cycle of muscle pain and spasm. A muscle relaxant, such as metaxalone (Skelaxin) 800 mg PO tid or cyclobenzaprine (Flexeril) 10 mg PO tid, or sedative, such as diazepam (Valium) 2 to 10 mg PO tid, may be helpful if primary treatment is ineffective. Muscle relaxants and sedatives, especially in higher doses, can cause significant CNS depression, so they should be used in the lowest effective dosage and only if more conservative therapy has failed. Mandibular Dislocation.
Dislocation of the mandible and inability to close the mouth can result from external trauma or sudden wide opening of the mouth, such
Figure 23-1 Open and closed lock vs. condylar fracture. A, The normal temporomandibular joint with cartilaginous disc, shown in blue. B, In a mandibular dislocation, the condylar head is anterior to the cartilaginous disc. No teeth are touching. C, In a condylar fracture, the joint is positioned normally, but the muscles of mastication have pulled the posterior portion of the mandible upwards, creating premature contact of the posterior teeth.
as occurs with yawning. The condition may be unilateral or bilateral. If there is a history of trauma, a condylar fracture should be suspected ( Figure 23-1 ). A dislocated mandible is reduced by placing the rescuer's thumbs on the victim's lower molars and moving the mandible down, then posteriorly, and then up. If muscle spasm is severe, sedation might be necessary.[6] After reduction of the mandible, the victim must avoid wide mouth opening. The victim should place one hand under the chin or position the chin against the chest when yawning. It is also helpful to place a bandage around the head and under the chin for several days to limit jaw movement. Anterior Disc Displacement.
Anterior displacement of the TMJ's cartilaginous disc with reduction to a normal position on mouth opening causes clicking in the joint. Generally, this is not associated with pain or severe dysfunction. However, if the disc is displaced and does not
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reduce on mouth opening, the victim may not only have pain, but also limited jaw movement (closed lock). Closed lock can occur suddenly while eating or talking, it may be present on awakening, or it can be associated with trauma. There is joint tenderness, and the chin deviates toward the affected side on attempted mouth opening. [6] Similar restriction of mandibular function may be caused by muscle spasm. However, with myospasm the affected muscles are firm and extremely tender, whereas in closed lock the muscles are usually normal. The victim can often reduce a closed lock. Have the victim close his or her mouth until the teeth almost touch, then move the mandible as far as possible to the affected side, and finally swing the mouth fully open. If these maneuvers fail after three attempts, consider manual reduction. The rescuer places his thumbs on the victim's lower molars, presses downward, pulls the mandible forward, then gradually moves the mandible up and back.[6] This may require sedation with oral diazepam (Valium) 2 to 10 mg.
MAXILLOFACIAL INFECTIONS Aphthous Ulcers The etiology of aphthous ulcers is unclear. One opinion is that they represent an autoimmune attack on the oral mucosa, followed by secondary infection. The lesions are round, superficial, and have a red halo. They occur on movable mucosa and can be quite painful. The victim usually gives a history of similar ulcerations. The lesions typically last 10 to 14 days. Many treatments have been proposed, but none have been found to be predictably effective. The best approach appears to be application of a topical steroid to reduce pain and hasten healing by 3 to 4 days. Mix fluocinonide 0.05% (Lidex) ointment with Orabase and place the mixture gently over each ulcer 6 to 8 times per day, especially after meals and before bedtime. Do not mix the medications until you are ready to apply them, and do not rub the mixture into the lesions. Other options include premixed preparations, such as Kenalog in Orabase, which can be applied to the ulcer 6 to 8 times per day; these preparations are more convenient but deliver only about 10% of the antiinflammatory effect. Dexamethasone (Decadron) elixir (0.5 mg/5 ml, rinse with 5 ml for 2 minutes and expectorate qid) or a systemic steroid (prednisone, 40 mg PO qd for 3 days, then taper) can be used for a very severe case.[20] If these preparations are not available, tincture of benzoin or a topical anesthetic (viscous lidocaine 2%) can be applied to the dried surface of the ulcer before meals and at bedtime to control the pain. Viral Infections Herpes labialis (cold sore, fever blister) is the most common oral viral infection. It is characterized by yellow, fluid-filled vesicles that rupture to leave ragged ulcers. Other locations for recurrent herpetic outbreaks include the palate, tongue, and buccal mucosa. The victim can be given acyclovir (Zovirax) 200 mg PO five times daily for 5 days. It is important to begin treatment as soon as the victim becomes aware of a prodromal "tingle" or paresthesia. Use of sun-blocking agents on the lips helps prevent herpes labialis (see Chapter 14 ). Primary herpetic gingivostomatitis is characterized by a thin zone of very red, painful gingiva just next to the teeth. Other areas of mucosa, such as the tongue, may also be involved, and close inspection may reveal tiny vesicles or ulcers. Sore throat, lymphadenopathy, and low-grade fever are also present. This and other viral infections of the oral cavity are self-limited. The victim should be reassured that the condition will resolve in about 10 days. Treatment involves the use of an analgesic (ibuprofen 600 mg PO q6h prn pain) and soothing mouth rinses such as warm saline or a mixture of equal amounts of diphenhydramine (Benadryl) elixir 12.5 mg/5ml with kaolin-pectin (Kaopectate) and viscous lidocaine 2% (rinse and expectorate 5 ml q2h). Yeast Infections Oral yeast infections occur most commonly in persons who are debilitated, immunocompromised, or taking an antibiotic. Classic oral candidiasis (thrush) is characterized by white patches on the mucosa that can be rubbed off, leaving a red and raw surface. Candidiasis can also present as an erythematous mucosa without any white patches, or as chronic angular cheilitis. Candidiasis is treated with an antimycotic mouth rinse (nystatin oral suspension 100,000 units/ml, rinse with 5 ml for 2 minutes and swallow qid for 10 days) or lozenges (clotrimazole [Mycelex] troche 1 qid, leave in mouth 5 minutes and expectorate remains). In the field, nystatin preparations meant for vaginal treatment can be used (Mycostatin vaginal suppository used as an oral lozenge tid for 10 days). Bacterial Infections A bacterial infection in the maxillofacial region can become a serious health threat. In a wilderness setting, it should be treated aggressively. The majority of odontogenic infections are caused by mixed populations of aerobic and anaerobic bacteria. These organisms are almost always present as normal oral flora, but because of a change in the relative numbers of various bacteria or because of a change in the oral environment, an infection can become aggressive. The behavior of an organism, such as the production of collagenase or hyaluronidase, determines the clinical presentation. Thus an infection may present as a diffuse cellulitis or localize as an abscess. Oral infections generally spread slowly, but rapid spread to a deep facial space can occur. Regional lymphadenopathy is common,
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whereas severe systemic symptoms are rare. Although bone is often involved, osteomyelitis is uncommon. Acute Apical Abscess/Cellulitis.
An acute apical infection begins with bacteria invading the dental pulp. The infection then spreads to surrounding bone through the apical foramen and then along the path of least resistance. Because the apices of most teeth are located closer to the facial aspect of the jaw, swelling is much more common in the facial soft tissues, as opposed to those on the lingual or palatal side. The victim presents with pain and swelling, often fluctuant and usually in the buccal vestibule. There is often a history of prior toothache, but at this stage tooth pain is often absent. The offending tooth can be localized by percussion, the site of the swelling, the condition of the teeth, and by using radiographs if available. The affected tooth does not respond at all to hot or cold. The victim may be dehydrated from decreased fluid intake. The primary treatment for an apical abscess ( Figure 23-2 ). is drainage.[5] [7] This can be accomplished with incision, extraction, or endodontic therapy. The treatment chosen depends on the equipment and personnel available, the advisability of retaining the offending tooth, and ultimately, on clinical judgment. An antibiotic is necessary only if complicating factors exist[5] [7] [17] ( Box 23-2 ). Penicillin (Pen VK 500 mg PO qid) is the most commonly used antibiotic in dental practice,[17] but a cephalosporin, such as cephalexin (Keflex) 500 mg PO qid, typically carried on wilderness expeditions, is acceptable. Combination antibiotic therapy is not indicated except for life-threatening sepsis or when organisms particularly sensitive to combination therapy have been identified. There is some evidence that hesitance to obtain drainage combined with over-reliance on chemotherapy can lead to serious exacerbation of dental infections. [7] Incision and Drainage.
Incision and drainage (I and D) is often the treatment of choice in an emergency situation. An I and D can be performed by someone other than a dentist using commonly available supplies. It is indicated for fluctuant swelling caused by an apical abscess, and it may also be effective for nonfluctuant swelling associated with infection. Infiltration of a local anesthetic helps to reduce the pain of incision. If a local anesthetic is unavailable, adequate anesthesia can often be obtained by applying cold to the area to be incised, using ice, snow, or frigid water. An incision is made down to bone in one swift motion and a knife blade or the beak of a hemostat is used to spread the incision. A -shaped drain may be improvised from a piece of latex glove (Figure 23-3 (Figure Not Available) ) and retained without sutures. Hydration, a soft diet, an analgesic (ibuprofen 600 mg PO q6h prn pain), and warm saline rinses are helpful postoperative measures.
Figure 23-2 The left side of the figure shows a periodontal abscess. A periapical abscess is depicted on the right.
Box 23-2. INDICATIONS FOR ANTIBIOTIC USE IN DENTAL EMERGENCIES Prophylaxis for persons at risk of bacterial endocarditis Prophylaxis for persons having prosthetic joint implants within the past 2 years Local infections If the victim is immunocompromised If drainage cannot be established If there will be a long delay to definitive care Disseminated infections Lymphadenopathy Fascial plane involvement Systemic symptoms (fever, chills, malaise) Compound maxillofacial fractures, including all fractures of tooth-supporting bone Exarticulation (avulsion) of teeth Soft tissue wounds open for 6 hours or more before closure Surgical procedures under nonsterile conditions
Deep Fascial Space Infections.
An acute apical infection occasionally spreads beyond the local region. The rescuer should be suspicious of any dental infection that causes swelling or tenderness in the floor of the mouth, swelling of the tongue, dysphagia, breathing difficulty, or trismus, or that fails to respond to appropriate therapy. The most commonly involved fascial spaces are the canine, buccal, masticator, and submandibular spaces.
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Figure 23-3 (Figure Not Available) Incision and drainage technique. A, Fluctuant abscess. B, Abscess incised with scalpel. Purulent drainage is removed by suction or caught in gauze sponges. C, Cross section showing incision carried to the bone. D, The incision is spread with a hemostat. E, A " " drain will often stay in place without sutures. F, Drain in place. (Redrawn from Ingle JI, Beveridge EE: Endodontics, ed 2, Philadelphia, 1976, Lea & Febiger.)
The canine space is located lateral to the nose. Infection originates in the maxillary canine tooth, and swelling causes the eye to close. The infection is drained through an intraoral approach over the root of the canine tooth. Buccal space infection is characterized by a rounded swelling of the cheek. The offending teeth are the maxillary and mandibular molars. Drainage is obtained extraorally through an incision below the lower border of the mandible that will hide the scar. The masticator space is divided into the masseteric, pterygoid, superficial temporal, and deep temporal spaces, all of which communicate. The hallmark of involvement is trismus. Swelling may be minimal because of the deep location of the abscess. The masseteric and pterygoid spaces are drained at the angle of the mandible, whereas the temporal space may be drained from an intraoral approach or through an incision just superior to the zygomatic arch. The mylohyoid muscle divides the floor of the mouth into the sublingual and submandibular spaces. These communicate posteriorly and with their counterparts across the midline. An infection originating in a mandibular tooth can involve these spaces. If only the sublingual space is infected, an intraoral approach is used for drainage, avoiding damage to Wharton's duct. If the submandibular space is involved, an extraoral approach is used. All incisions in the facial area are made parallel to the branches of the facial nerve.[8] [16] Fascial space infections are potentially life threatening. The likelihood of widespread sepsis increases, cavernous sinus venous thrombosis and mediastinitis are
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possible, and the airway may become compromised.[9] The most feared infection is Ludwig's angina, a bilateral submandibular space infection that elevates the tongue, obstructs breathing, and is associated with high mortality. A mild dental infection can progress to a life-threatening emergency in as little as 48 hours.[7] Treatment of fascial space infections includes airway management, proper hydration and electrolyte balance, aggressive I and D, intravenous antibiotics, and pain control.[7] [9] [19] Because these objectives are best met in a controlled environment, any person with a suspected fascial space infection should be evacuated immediately. Chronic Apical Abscess.
The hallmark of chronic apical infection is a draining fistula or "gum boil." Because the bacteria have a route to escape, they do not cause pressure or pain, although the tooth may be mildly sensitive when eating. Such an abscess is not truly an emergency, but if the victim is overly concerned that the condition may worsen before definitive care is provided, an antibiotic can be given. An infected deciduous tooth also usually presents with a fistula and a mild amount of swelling at most. Happily for the child, pain is rarely present. Emergency care involves an antibiotic, with the dosage adjusted for the child's weight; I and D is performed only if the abscess is not draining. Extract the tooth only if it is very loose and it will be weeks until comprehensive care is available. Periodontal Abscess.
A periodontal abscess is an accumulation of pus between the gingiva and the tooth (see Figure 23-2 ). Swelling is near the gingival margin rather than in the vestibule, as would be the case with a periapical abscess. The tooth is sensitive to percussion, but responds appropriately to hot and cold. There is always a potential communication between the abscess and the mouth. The passage can be found by probing the gingival margin with a small, blunt instrument, using a local anesthetic if available. Gentle probing will establish drainage; no incision is necessary. Hot saline rinses are prescribed, and a rapid recovery is almost invariable. Pericoronitis.
Pericoronitis is an infection of the gingival flap over a partially erupted tooth. The most common site is the mandibular third molar. Pericoronitis is usually caused by
streptococci and seldom produces purulence. The condition may mimic streptococcal pharyngitis or tonsillitis. The primary site of infection is always tender, and trismus is a common sign. Field treatment consists of saline irrigation of the space under the flap using a syringe. Place the victim on hot saline rinses every 2 hours and begin antibiotic therapy. Acute Necrotizing Ulcerative Gingivitis (ANUG).
ANUG, also known as trench mouth, is characterized by ulceration and blunting of the interdental papillae. The gingiva between the teeth appears punched out and is covered by a gray/white pseudomembrane, whereas the surrounding gingival tissue is very red. The victim's primary complaint is pain, but he or she may also report gingival bleeding, a metallic taste, and a foul odor. This infection is caused by fusiform bacteria and spirochetes. It usually occurs in young adults with poor oral hygiene, stress, and suboptimal nutrition (conditions that may be present during difficult wilderness expeditions). The most important treatment is gentle debridement of plaque, calculus, and food from around the teeth. Resolution may require several sessions of careful cleaning 1 to 2 days apart. Each session of debridement will result in some healing, which will allow more aggressive treatment the next time. The victim is also given an antibiotic (metronidazole [Flagyl] 500 mg PO qid) and analgesic (ibuprofen 600 mg PO q6h prn pain) and instructed to keep the area clean with good brushing, flossing, and rinsing (warm saline and/or diluted hydrogen peroxide, if available).[4]
EXODONTIA A dental extraction is considered definitive treatment and should be attempted in the field only under extraordinary circumstances ( Box 23-3 ). Extraction requires trained personnel, specialized instruments, and profound anesthesia, which may be difficult to obtain. Premedication with a sedative and/or narcotic may be necessary. Intra-operative and postoperative complications are common. Providers of emergency care should focus on treating
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pain and infection with local anesthetics, analgesics (ibuprofen 600 mg PO q6h prn pain or hydrocodone 7.5 mg and acetaminophen 750 mg [Vicodin ES] PO q4 to 6h prn pain), I and D, and/or antibiotics (see section on periapical abscess) as appropriate for each case. Extraction or other definitive care can then be rendered after evacuation, and the tooth can often be saved. Box 23-3. FACTORS TO CONSIDER BEFORE EXTRACTION OF TEETH Desires of the victim Victim's medical history Available alternative treatments Difficulty/desirability of evacuation Certainty of diagnosis (are you sure you have the correct tooth?) Possible complications if the tooth is not extracted Factors relating to the difficulty of the procedure Mobility or immobility of the tooth Position of the tooth Condition of tooth structure above the gingiva Patient's mouth-opening ability Available supplies and instruments Experience of rescuers Possible complications arising from the extraction Fractured root(s) Fractured alveolus Soft tissue injury Root tip lost in the sinus Prolonged bleeding Localized osteitis (dry socket)
Other factors to consider before exodontia are the degree of mouth opening possible, the relationship of the root to the maxillary sinus, the condition of the clinical crown, the alignment of the tooth in the dental arch, and a history of previous endodontic treatment (after root canal treatment, a tooth is usually very brittle).[14] If, after careful consideration of all factors, extraction is deemed the best course of treatment, proceed as follows. Review the victim's medical history. In a wilderness setting, it is unlikely you will be faced with a case complicated by medical conditions such as a blood dyscrasia, anticoagulant therapy, or severe cardiovascular disease, but you must be certain before the surgery begins. Persons with most types of heart murmurs or recent prosthetic implants should be premedicated with an antibiotic[10] ( Box 23-4 and Box 23-5 ). Consider the emotional state of the victim and decide if sedation is prudent.
Box 23-4. RECOMMENDATIONS FOR ANTIBIOTIC PROPHYLAXIS BEFORE INTRAORAL PROCEDURES LIKELY TO CAUSE SIGNIFICANT BLEEDING
CONDITIONS FOR WHICH PREMEDICATION IS RECOMMENDED Prosthetic joint replacement if within 2 years of placement, or if victim has insulin-dependent diabetes, previous prosthetic joint infection, or hemophilia Prosthetic heart valve replacement Previous endocarditis Complex cyanotic congenital heart disease Surgically constructed systemic pulmonary shunt or conduit Most congenital cardiac malformations other than those listed below Acquired valvular dysfunction (e.g., rheumatic heart disease) Hypertrophic cardiomyopathy Mitral valve prolapse with valvular regurgitation and/or thickened leaflets
CONDITIONS FOR WHICH PROPHYLAXIS IS NOT RECOMMENDED Isolated secundum atrial septal defect Surgical repair of atrial septal defect, ventricular septal defect, or patent ductus Previous coronary artery bypass graft surgery Mitral valve prolapse without valvular regurgitation Physiologic, functional, or innocent heart murmur Previous rheumatic fever without valvular dysfunction Cardiac pacemaker or implanted defibrillator Coronary artery stent
Box 23-5. REGIMENS FOR ANTIBIOTIC PROPHYLAXIS BEFORE INTRAORAL PROCEDURES LIKELY TO CAUSE SIGNIFICANT BLEEDING
STANDARD REGIMEN Amoxicillin 2 g PO 1 hour before procedure
CHILDREN Amoxicillin 50 mg/kg PO 1 hour before procedure, not to exceed adult dose
UNABLE TO TAKE ORAL MEDICATIONS Ampicillin 2 g IM/IV 30 minutes before procedure
PENICILLIN ALLERGY (CHOOSE ONE OF THE FOLLOWING) Clindamycin 600 mg PO 1 hour before procedure Clindamycin 600 mg IV 30 min before procedure Clindamycin 20 mg/kg PO 1 hour before procedure (for children) Clarithromycin 500 mg PO 1 hour before procedure Cephalexin 2 g PO 1 hour before procedure
From Dajani AS et al: JAMA 277:1794, 1997.
Plan the procedure and gather all necessary equipment. Secure a good light source and a means to keep the field dry—either suction or plenty of gauze. It is important to have the victim's head supported. Therefore it may be best to place the victim in a supine position with the head slightly elevated. Obtain good local anesthesia and test by touching the soft tissues with a sharp instrument. A 4 × 4-inch gauze curtain placed in the rear of the victim's mouth will prevent aspiration of teeth and debris. Teeth are inflexible and brittle. Heavy forces, especially if applied quickly (high acceleration), break teeth. Bone has more flexibility, the degree of which depends on the individual victim. Judiciously applied, moderate
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forces will slowly expand the bone. The exodontist must be attentive to feedback from the forceps because the bone and tooth will "tell you what they want to do." The tooth will eventually be delivered in the same direction as if it continued to erupt. However, do not attempt to "pull" the tooth in that direction initially. The direction of force needed to loosen a tooth depends on the anatomy of the root. A straight, conical root can be loosened by twisting forces. This technique often works well on the upper front teeth. Sometimes a tooth can be removed by alternating 30 seconds of steady pressure toward the cheek with 30 seconds steady pressure in the opposite direction until the root gradually loosens.[23] A variety of instruments can be used to apply force to the tooth. Elevators are firmly wedged between tooth and bone in the interproximal area. Avoid putting pressure on the adjacent tooth. Forceps should be applied as far apically as possible. Spend plenty of time working the forceps well under the gingiva. Lower molars are often removed with "cowhorn" forceps, which in addition to applying the usual forces, are designed to apply force to the tooth in a coronal direction simply by squeezing the handles. However, an experienced exodontist using careful technique and a single forceps (number 151 universal forceps) will have success extracting almost any nonimpacted tooth, whereas a reckless operator using dozens of specialized instruments will still have difficulty.[23] Despite the utmost care, a tooth may break during the extraction procedure. If this occurs, stop and take a minute to reevaluate the situation. The root canals will probably now be exposed. If you are treating a case of infection, perhaps drainage can be obtained through the root canal. If you are treating a case of severe pulpitis, perhaps the pulpal tissue can now be removed. Remember that you are rendering emergency care, and it may not be necessary to remove the remaining root at that time. Some teeth are impossible to remove without sectioning, or they can be removed in only one direction. Once the tooth has been removed, compress the expanded socket using the thumb and forefinger. If the gingiva is quite loose, placing a suture may help speed healing. Have the victim apply direct pressure to the wound by biting firmly on a gauze pack for 30 minutes while sitting in an upright position. Complete hemostasis may require several hours of steady pressure. Caution the victim to avoid rinsing, spitting, tooth brushing, and smoking for 24 hours. Application of cold and the use of an appropriate analgesic will reduce swelling and pain. Beginning the day after surgery, have the victim rinse with warm saline to cleanse the area. A common postoperative complication is persistent bleeding several hours after the extraction, accompanied by a poorly organized clot that looks like a piece of raw liver growing out of the socket. Remove the "liver clot" and have the victim apply firm, uninterrupted pressure to the socket by biting on a gauze pack for 20 minutes. If the victim cannot do this, the rescuer will have to apply manual pressure. If bleeding continues after 20 minutes, consider packing the socket (e.g., using Gelfoam, Surgicel, or sterile gauze) and/or suturing. Then resume direct pressure. A dry tea bag used as a compress may provide chemical hemostasis because of the tannic acid. Another postextraction complication is acute alveolar osteitis, or "dry socket." The victim reports moderate to severe pain, foul odor, and a bad taste, beginning about 3 days after a dental extraction. Examination reveals an empty socket and exposed bone caused by loss of the blood clot, but no suppuration. Treatment consists of gentle irrigation with warm saline followed by packing with a strip of gauze dipped in eugenol. Also administer an oral analgesic. Change the pack every 24 to 48 hours until the symptoms subside, which may take up to 10 days. The victim should avoid alcohol, smoking, and carbonated beverages during treatment.
TRAUMA TO THE FACE AND JAWS It is essential to quickly evaluate the general condition of an injured victim (see Chapter 18 ). [13] The primary survey identifies and corrects any inadequacy in respiration or circulation. The mouth and pharynx should be examined for foreign bodies, such as blood clots, tooth or bone fragments, or dentures. If the airway is still obstructed, it may be necessary to perform a chin lift or jaw thrust, or insert an oropharyngeal airway to hold the tongue forward (see Chapter 17 ). Care should be taken not to hyperextend the neck because of the possibility of a cervical spine fracture. If there is no indication of a neck fracture, sometimes merely placing a victim on his side rather than in a supine position facilitates respiratory exchange. If all of these measures fail, endotracheal intubation or performance of a cricothyroidotomy or, less commonly, a tracheotomy may be necessary. Once a victim's airway is secured and he is hemodynamically stable, perform a secondary survey. Injuries to the Teeth and Supporting Tissues Question the victim about the time and nature of the accident, symptoms, loss of consciousness, nausea, vomiting, visual disturbances, and headache. A baseline mental status examination and cranial nerve assessment may be warranted. Clean the face, mouth, head, and neck of blood and debris. This will unmask soft tissue injuries and facilitate diagnosis. Gently reflect the lips with teeth closed to examine soft tissues and occlusion. Carefully examine any lacerations to determine if they penetrate through the lip and/or contain foreign material. Examine all of the teeth for fractures.
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A blow to the chin or a whiplash injury may produce fractures of the posterior teeth as the mandible is forcibly closed. Examine fractured teeth carefully for pulp exposure. This will require drying the teeth with gauze. Tap each tooth with an instrument handle. Tenderness denotes injury to the periodontal ligament, whereas a high-pitched, metallic sound indicates ankylosis. Test each tooth for abnormal mobility. Electrical pulp vitality testing, dental radiographs, and soft tissue radiographs are obtained if available.[2] [11] [15] A classification of traumatic injuries to the teeth and supporting structures is given in Box 23-6 . Note that these injuries often occur in combination, with one tooth exhibiting two or more injuries, or several teeth exhibiting various sequelae of trauma. Each injury requires definitive treatment, but proper emergency care will improve the prognosis and make the victim more comfortable. Treatment of most injuries requires, or is at least facilitated by, infiltration of a local anesthetic.[2] Specific Dental Injuries CROWN INFRACTION.
Blows to the teeth sometimes produce small craze lines in the enamel. These superficial fractures look like tiny surface cracks on an old porcelain dish. Reassure the victim that minimal damage has occurred and treatment is not necessary.
Box 23-6. CLASSIFICATION OF DENTAL TRAUMA INJURIES TO THE HARD DENTAL TISSUES AND PULP Crown infraction Uncomplicated crown fracture Complicated crown fracture Uncomplicated crown-root fracture Complicated crown-root fracture Root fracture INJURIES TO THE PERIODONTAL TISSUES Concussion Subluxation Intrusive luxation Lateral luxation Extrusive luxation Exarticulation INJURIES TO THE SUPPORTING BONE Comminution of alveolar socket Fracture of alveolar socket wall Fracture of alveolar process Fracture of jaw INJURIES TO SOFT TISSUES
From Andreasen JO, Andreasen FM: Textbook and color atlas of traumatic injuries to the teeth, ed 3, St. Louis, 1994, Mosby.
UNCOMPLICATED CROWN FRACTURE.
In an uncomplicated crown fracture, the tooth has been fractured, but no pulp tissue is visible. The tooth may be sensitive to cold, but otherwise all tests are within
normal limits. No emergency treatment may be necessary. Irritating sharp edges can be smoothed with a fingernail file. If thermal sensitivity is moderate to severe, a soothing topical antiinflammatory dressing (e.g., Intermediate Restorative Material [IRM], L.D. Caulk Co., Milford, Delaware) can be held in place with aluminum foil or adhesive tape. UNCOMPLICATED CROWN-ROOT FRACTURE.
Diagnosis and treatment of an uncomplicated crown-root fracture is identical to the uncomplicated crown fracture, except that the fracture is nearly vertical, leaving a small, chisel-shaped fragment attached only by the palatal gingiva ( Figure 23-4 ). Removal of this mobile fragment will make the victim much more comfortable. COMPLICATED CROWN FRACTURE.
In a complicated crown fracture, the pulp has been exposed. A small exposure that has not been grossly contaminated is capped with calcium hydroxide (Dycal, L.D. Caulk Co., Milford, Delaware) or IRM. If the exposure is large, or if the pulp tissue has been exposed for more than 24 hours, amputate about 2 mm of tissue with a sharp, sterile instrument. If bleeding continues for more than a few minutes, use a cotton pellet soaked in local anesthetic solution, hydrogen peroxide, or Dycal to obtain hemostasis. Fill the top of the canal with Dycal or IRM and protect the tooth as for a crown fracture ( Figure 23-5 ). COMPLICATED CROWN-ROOT FRACTURE.
In a complicated fracture of the crown and root, the tooth has been fractured obliquely, resulting in a mobile fragment attached
Figure 23-4 Crown-root fracture. The mobile fragment (a) should be removed. The larger fragment (b) should be left in place.
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Figure 23-5 Complicated crown fracture. Treatment of a complicated crown fracture.
to the palatal gingiva and pulp exposure. First remove the mobile fragment as in a crown-root fracture. Then treat the pulp exposure as in a complicated crown fracture. [2]
ROOT FRACTURE.
A root fracture may be difficult to diagnose without radiographs. There will be slight to severe malposition of the crown, but this could be caused by luxation of the entire tooth or a root fracture with luxation of the coronal portion. Reposition the tooth as precisely as possible and splint rigidly (see section on splinting). Hard tissue union of the fragments usually occurs within 3 months. If the coronal portion of the tooth proves impossible to stabilize and definitive treatment is days away, remove the mobile fragment, but do not attempt to extract the apical fragment.[2] [15] CONCUSSION AND SUBLUXATION.
Concussion and subluxation injuries to the tooth's supporting structures (i.e., periodontal ligament, bone, and gingiva) cause sensitivity to percussion. The tooth remains in its proper position. However, in subluxation the tooth is abnormally mobile, whereas mobility is normal with concussion. Emergency treatment consists of shortening the opposing tooth so that the victim can occlude comfortably. INTRUSION.
A tooth that has been driven into the bone by a vertical force will demonstrate little mobility and a high-pitched, metallic tone on percussion. Emergency treatment is palliative only. Endodontic treatment (to prevent inflammatory root resorption) and orthodontic extrusion should begin within 2 weeks of injury. Intrusion is associated with a poor long-term prognosis.[2] EXTRUSION.
The extruded tooth is partially displaced from its socket and extremely mobile. Gentle, steady pressure is used to reposition the tooth, allowing time to displace the blood that has collected in the apical region of the socket. After reduction, the tooth is splinted for 2 to 3 weeks. The splint should allow physiologic movement of the injured tooth.
Figure 23-6 Technique used to reduce lateral luxation. LATERAL LUXATION.
In lateral luxation injuries, the tooth is often displaced by a horizontal blow, yet it is not mobile because the apex is locked into its new position in the alveolar bone. A high, metallic tone on percussion is another clue that this has occurred. This injury and its treatment are painful. Figure 23-6 shows how two fingers are used to reduce the tooth. One finger guides the apex down and back while the other repositions the crown.[2] This requires judicious, but sometimes quite firm application of force. The tooth may snap back into position and be quite stable. Splinting is necessary if mobility is present after reduction. EXARTICULATION.
When a tooth is totally avulsed from bone, the prognosis after replantation depends on the health of the periodontal ligament cells, some of which are still attached to the root surface and some
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of which line the socket wall.[3] To preserve the vitality of these cells, certain guidelines should be observed. Keep the time before replantation to a minimum. Immediate replacement is ideal. If the tooth must be stored, keep it moist. Less than 15 minutes in air is associated with a good prognosis; longer than 2 hours results in a poor prognosis.[3] [11] If possible, the tooth should be stored in a Save-A-Tooth container (Smart Practice, Phoenix), which uses a soft mesh to suspend the tooth in Hank's balanced salt solution. Alternative transport mediums are whole milk, saline, the victim's saliva, sports drinks, and water, in that order of preference. The concept is to preserve the health of the periodontal ligament cells in the most isotonic, pH balanced solution at hand. If no container is available, use a plastic bag, plastic wrap, or saturated cloth to keep the tooth from drying. Handle the tooth by the crown only. Never scrub, curette, or use a disinfectant on the root surface; gently rinse with saline to remove debris. When removing clotted blood from the socket, use gentle irrigation and suction, and avoid scraping the socket walls. Ease the tooth back into place with slow, steady pressure. After replantation, nonrigidly splint the tooth for 1 week. Administer an antibiotic for 5 days and give appropriate antitetanus prophylaxis. Endodontic therapy should be instituted within 2 weeks.[3] [11] [15] The preferred approach to tooth avulsion or severe luxation is immediate reduction in the field, followed by evacuation for definitive treatment. The next most desirable option is to store the tooth properly and transport victim and tooth for replantation within a few hours of injury. If field conditions prevent either course of action, a delayed replantation procedure is indicated. Store the tooth dry. Three weeks after the injury, the necrotic pulp tissue is removed and the tooth is disinfected, fluoridated, and surgically replanted. The aim of delayed replantation is to produce ankylosis between tooth and bone.[2] ALVEOLAR SEGMENT FRACTURE.
Alveolar segment fracture is characterized by displacement of two or more teeth as a unit. The teeth are not mobile with respect to one another. The apices may be locked into their abnormal position, as in lateral luxation. The segment is repositioned (this may be painful even with local anesthesia), and rigid splinting is placed for 4 to 6 weeks. Proper Reduction.
It is sometimes difficult to know when a displaced tooth has been returned to its proper position. Usually a tooth should be positioned similarly to its contralateral mate. Sometimes asking the victim can help; it may be that one tooth has always been longer than the others, or in a different position. However, occlusion is always the best guide to proper position. If the victim bites and contacts only the injured tooth, further positioning is necessary. In many cases, it is not possible to completely reposition the tooth because of swelling or organized clot formation. Therefore
Figure 23-7 Arch bar and wire splint,
Figure 23-8 Cross sectional view of an arch bar and wire splint. A, The widest part of the tooth. B, The position of the wire on the stable teeth. C, The position of the wire on the mobile tooth or teeth.
some adjustment of the opposing tooth (try using an emery board or file from your pocket knife) may be necessary to allow proper occlusion. If the injured tooth receives additional trauma each time the victim bites, it will be uncomfortable, and healing will not occur. Splinting.
When the goal of splinting is to establish a normal, fibrous union between the tooth and the bone, a short-term, nonrigid technique is used. When hard tissue union is desired (e.g., with root fracture or alveolar segment fracture), longer-term rigid splinting is used.[2] Ideally, a single avulsed or loosened tooth is usually bonded to the adjacent tooth or teeth with the acid etch and composite technique.[2] [15] For fractures of the jaws or alveolar segments, arch bars and wire splints are often used ( Figure 23-7 and Figure 23-8 ). The rescuer lacking adequate materials must use ingenuity and improvisation to splint teeth. During a very short evacuation, the victim could hold the tooth in approximate position
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Figure 23-9 Suture used to stabilize a loose or avulsed tooth. The suture also passes through the palatal tissue (hidden from view).
by closing on a gauze pad. Softened wax can be adapted to a loosened tooth and the teeth on either side to lend support. Figure 23-9 shows how a suture can be used to hold a tooth in place for a period of a few days. For a sturdier splint, a crude arch bar can be cut from a SAM splint or made from a paper clip and dead-soft wire obtained from copper wiring or twist ties. Note the proper positioning of the wire on the injured tooth and the anchor teeth (see Figure 23-8 ). Injuries to Primary Teeth.
Injuries to the deciduous teeth offer unique challenges, not the least of which is behavioral management of a young child. Splinting is very difficult because of the small amount of tooth structure available. In general, heroic efforts should not be made to save primary teeth.[2] Exarticulated deciduous teeth should not be replanted. Severely extruded teeth, infected teeth, or those intruded into the developing permanent tooth should be extracted. Because the permanent tooth follicle lies to the lingual side of the primary tooth root, the typical frontal impact displaces the crown toward the palate, but levers the root apex away from the permanent tooth ( Figure 23-10 ). Most minor subluxations and luxations require only symptomatic treatment. As long as the displaced tooth does not interfere with occlusion, reduction is contraindicated. Spontaneous repositioning often occurs over a period of weeks. Fragments of primary roots need not be extracted because normal resorption will still occur. Epistaxis Although most cases of nosebleed are trivial, some can become life threatening as a result of respiratory compromise secondary to aspiration of blood, or extensive blood loss resulting in hypotension. Therefore the condition should never be neglected. The nasal mucosa is laced with numerous superficial blood vessels that serve to warm and humidify inspired air. A particularly rich collection of vessels, and a common site of anterior nosebleed, comprise Kiesselbach's plexus on the nasal septum (Figure 23-11 (Figure Not Available) ). Spontaneous epistaxis is more
Figure 23-10 When a deciduous tooth is traumatized, the typical direction of force as the child falls forward is shown by arrow A, and the apex of the deciduous tooth is levered
away from the developing tooth bud, as shown by arrow B.
common in environments that are cold, dry, dusty, or smoke-filled. In evaluating a victim with epistaxis, first determine if the bleeding is unilateral or bilateral, and whether it is coming from an anterior or posterior site. A nosebleed usually occurs on one side of the nasal cavity. However, in a victim with profuse bleeding, the blood can pass behind the nasal septum and also appear on the unaffected side. Most victims bleed from an anterior site, which can be visualized on intranasal examination. Posterior epistaxis is usually caused by traumatic injury to the sphenopalatine artery (see Figure 23-11 (Figure Not Available) ). The bleeding point cannot be seen on intranasal examination. The first step in treating a person with a nosebleed is to have him sit upright with his head tipped slightly forward so that blood will drip passively out of the nose rather than flow posteriorly into the throat, causing choking and possible aspiration or vomiting of swallowed blood. Ask the victim to blow his or her nose to remove any clots. If suction and a nasal speculum are available, the nasal cavity can then be examined to determine the site of bleeding. When there is minor bleeding from the anterior aspect of the nose, the victim can be instructed to pinch the nostrils together for at least 10 minutes. Hold the soft tissues tightly against the septum. Pinching the bony bridge of the nose will not provide direct pressure on the bleeding vessels. If nose pinching does not stop the bleeding, apply a topical vasoconstrictor. Choices include cocaine 4%,
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Figure 23-11 (Figure Not Available) Nasal anatomy. Kiesselbach's plexus is the most common site of anterior epistaxis. The sphenopalatine artery is the most common site of posterior epistaxis. Insert tubes and instruments in the direction of the nasopharynx, not the cribriform plate. (From Fleisher GR, Ludwig S: Textbook of pediatric emergency medicine, Philadelphia, 1999, Lippincott Williams & Wilkins.)
ephedrine 5%, aqueous epinephrine 1:1000, phenylephrine 0.5% (Neo-Synephrine), or oxymetazoline 0.05% (Afrin). Vasoconstrictors can also be found in some local anesthetics, asthma medications, and southwestern desert plants of the genus Ephedra (e.g., Mormon Tea, joint-fir, canatilla, tepopote). Vasocontrictors can be applied by drip, spray, on a cotton pledget, or with a cotton-tipped applicator. Objects placed in the nose should have a string attached, or other method of easy removal, and should be aimed posteriorly. Avoid pushing material laterally into the turbinates or superiorly toward the cribriform plate (see Figure 23-11 (Figure Not Available) ). Leave the vasoconstrictor in place between 10 minutes and 24 hours. When there is more vigorous anterior nasal bleeding, nose pinching or the topical application of a vasoconstrictor may not be effective. In such an instance, the bleeding site can be injected with 0.5 to 1 ml of lidocaine containing 1:100,000 epinephrine, which will have a tamponading and a vasoconstricting effect. Alternatively, a small piece of oxidized regenerated cellulose (Oxycel or Surgicel), gelatin sponge (Gelfoam), or microfibrillar collagen (Avitene) can be placed directly over the bleeding site. Once the bleeding has stopped, the victim should be instructed not to blow the nose or probe the area for 48 hours. Increasing the humidity of inspired air may help prevent a recurrence of the bleeding. Placing the victim in a tent with several other persons, or with a pot of boiling water, and placing a handkerchief over the victim's nose while outside, will humidify and warm the air before it reaches the nasal mucosa. If the bleeding cannot be controlled by the previous methods, anterior nasal packing is required. This involves placement of ½-inch strip gauze impregnated with an antibiotic or petroleum jelly into the nasal cavity. The adult victim requires 3 to 4 feet of such gauze to adequately pack the nose and tamponade the bleeding. The gauze is layered in tiers starting on the nasal floor and proceeding to the roof of the nose. Both ends of the gauze are left outside the nose and taped to the face to prevent inadvertent aspiration. Expandable packing (Weimert Epistaxis Packing, Rhino Rocket), with an applicator device for rapid deployment, or a Foley catheter can also be used for anterior nasal tamponade. Because anterior nasal packing blocks sinus drainage and can predispose to sinusitis, the victim should be placed on prophylactic amoxicillin, 875 mg with clavulanic acid 125 mg (Augmentin) PO bid, until the packing is removed in 48 hours. Because it is not possible to visualize the site of posterior epistaxis, the victim requires a posterior nasal
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pack or placement of a Foley catheter or nasal balloon.[1] Placing the conventional posterior nasal pack involves first gently inserting a lubricated soft tube into each nostril until the ends can be visualized in the back of the throat, grasped with a hemostat, and brought out through the mouth. Use Foley catheters, nasogastric tubes, chest tubes, or improvised substitutes, such as one of the products used to hold sunglasses in place. A cylindrical pack of 4 × 4-inch gauze pads is prepared and held in shape by tying three silk sutures around it and leaving the ends long. The pack should be the same diameter as a circle made by the victim's thumb and forefinger (the "OK" sign). The two end sutures are attached to the oral ends of the catheters (Figure 23-12 (Figure Not Available) ). The nasal ends of the catheters are then pulled carefully back out of the nose until the pack is firmly positioned against the posterior aspect of the nasal cavity above the soft palate. The sutures are then detached from the catheters and tied over a bolster placed underneath the nose. The middle suture remains outside of the mouth and is secured externally to be used to remove the pack 48 hours later. A 14 to 16 French Foley catheter with a 30-ml balloon can also be used as a posterior pack. The lubricated catheter is inserted through the nose into the posterior pharynx, inflated 10 to 15 ml, and then gently pulled back into the nasopharynx and held in position by clamping the external end with a hemostat. Commercially available preshaped nasal balloons can also be used to treat posterior epistaxis.[1] Air is preferred over saline for inflating nasal balloons as a safety precaution in case of breakage. Nasal Fracture Because of the prominence of the nose, nasal fracture is the most common facial fracture. It is often accompanied by abrasions, lacerations, and epistaxis. Nasal bleeding should be managed first. Once this bleeding is controlled, any facial wound should be properly cleansed. Local anesthesia may be needed to accomplish removal of foreign material. Plain lidocaine or another local anesthetic without a vasoconstrictor is recommended when injecting the nose. Particulate matter is removed either by irrigation or scrubbing with a sterile brush. This is essential to avoid infection and prevent tattooing. Abrasions should be covered with an antiseptic or antibiotic ointment (e.g., mupirocin, bacitracin) and washed gently twice daily with a mild soap and warm water to prevent crusting. Small laceration edges can be reapproximated with tape closure. Deeper lacerations require interrupted sutures. Remove sutures in 3 to 5 days, at which time tape strips can be placed if additional stabilization of wound margins is necessary. Once soft tissue injuries have been managed, the nose should be assessed for possible fracture by observing it for symmetry from the front and from below. If swelling has already occurred, this may be difficult to determine. However, palpation of the bridge may reveal Figure 23-12 (Figure Not Available) Inserting a posterior nasal pack. (From Fleisher GR, Ludwig S: Textbook of pediatric emergency medicine, Philadelphia, 1999, Lippincott Williams & Wilkins.)
displacement that is not visible, and crepitus can sometimes be felt. Point tenderness may also be indicative of a fracture, but it can also be associated with soft tissue injury. After external examination of the nose, the interior of the nasal cavity should be examined for lacerations and septal hematoma. Remove blood clots with a swab or suction to improve visibility. Small lacerations may not require treatment, but large lacerations should either be closed with resorbable sutures or covered with Oxycel, Gelfoam, Surgicel, or Avitene to control bleeding. Any deviation, bulging, or widening of the nasal septum may be indicative of a hematoma. However, septal deviation may have been present before the injury. To determine if a hematoma is present, the area can be pressed with a cotton-tipped applicator. A hematoma will feel soft, and the area may be temporarily indented by the pressure. A septal hematoma needs to be drained to prevent pressure necrosis and loss of nasal support or the formation of a septal abscess, which can also produce destruction of the septum. The area is anesthetized by injection of a local anesthetic or the application of a topical anesthetic (benzocaine 20%), and a small incision is made in the most inferior aspect of the hematoma. The nasal passage should then be packed with ½-inch gauze impregnated with petroleum jelly or antiseptic to prevent recurrence of bleeding. Because most surgeons prefer to treat nasal fracture after the swelling has subsided (5 to 10 days after injury), such an injury does not require immediate treatment.[12] As long as there is no active bleeding, and any abrasions and lacerations have been treated, the victim has at least 3 to 5 days before definitive management is
indicated. If the nose appears straight as the swelling subsides, and the victim can breathe easily through
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both nostrils, there probably was no fracture, or a fracture exists with only minimal displacement and further treatment may not be necessary. In the interim, the nose can be protected from further injury by a splint made by cutting a triangular piece of a SAM splint large enough to fit the contour of the nose. Rest the splint on the adjacent part of the face without placing pressure on the nasal bridge. This shield is held in place by strips of adhesive tape. Nasal packing is not necessary unless it is used to control epistaxis or recurrent septal hematoma. Penicillin VK or amoxicillin 500 mg PO should be administered four times each day for 5 days. Jaw Fracture Any person who has suffered a head or facial injury should be examined for a jaw fracture.[13] First, evaluate occlusion by having the victim bite the teeth together. Any deviation of the bite or change in the level of the occlusal plane, especially in the mandible, should raise the suspicion of a fracture. Usually there will also be a tear in the gingival tissues and bleeding and ecchymosis at the site of the discontinuity. A sublingual hematoma is a common sign of a mandibular fracture. In edentulous areas, there will also be a discrepancy in the level of the bone, often accompanied by a disruption in the mucosa. If no obvious tooth or bone displacement is noted, bimanual examination of the body of the mandible should determine if any abnormal movement can be detected. It is particularly important to evaluate any area of contusion in the soft tissue. In addition to preternatural movement, a grating sound can occasionally be heard when a fracture is present. The mandibular condyles should be evaluated, especially if the chin has sustained a traumatic blow. A unilateral fracture is suspected when there is a shift of the midline of the mandible to the painful side on mouth opening. A bilateral fracture will often result in an anterior open bite (see Figure 23-1 ). Normally, the condyles can be palpated by placing a forefinger in front of the external auditory meatus. If the condyle cannot be palpated, or if it does not move significantly when the mouth is opened, a fracture may be present. [13] [21] The maxilla is examined for possible fracture by grasping the anterior segment between the thumb and forefinger and gently rocking the jaw anteroposteriorly and laterally. If a complete (Le Fort I) fracture is present, the entire maxilla will move ( Figure 23-13 ). With a unilateral fracture, only one half of the maxilla will move. If a complete maxillary fracture is detected, the presence of a pyramidal (Le Fort II) fracture extending to the nasal area needs to be considered. The maxilla should again be rocked gently while the bridge of the nose is grasped between the thumb and forefinger of the opposite hand. Any movement of the nasal complex is indicative of a pyramidal fracture. Because this fracture also extends through the infraorbital rim, this
Figure 23-13 Classification of midface fractures. (Redrawn from Oral and maxillofacial surgery services in the emergency department, Rosemont, IL, 1992, American Association of Oral and Maxillofacial Surgeons.)
area should be palpated for the presence of a step deformity. However, care must be taken not to confuse a fracture with the infraorbital foramen, which can also be felt in this region. If a fracture is present, the victim will feel numbness below the eye and in the upper lip and lateral aspect of the nose. This is caused by injury to the infraorbital nerve. The third type of midface fracture, the Le Fort III, involves detachment of the midface from the base of the skull. This is a complex injury often accompanied by intracranial trauma. There is generally subconjunctival hemorrhage and bilateral periorbital edema and ecchymosis. Usually the eyelids are swollen shut. Laceration of the meninges causes cerebrospinal fluid (CSF) to leak from the nose. To distinguish CSF from mucus, hold a clean, white handkerchief under the nose for a moment and then allow the material to dry. Mucus will stiffen the fabric, whereas CSF will dry as a double ring without stiffening the fabric. When CSF rhinorrhea is suspected, an antibiotic (penicillin VK 500 mg PO qid) should be administered, but the nose should not be packed. Fractures of the zygomaticomaxillary complex generally result from a blow to the cheek. The most common findings are subconjunctival hemorrhage and ecchymosis and swelling of the lids. There may be double vision caused by displacement of the globe and/or entrapment of extraocular muscles. As with a Le Fort II
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fracture, there is numbness in the distribution of the infraorbital nerve. Because of the depression of the cheekbone, the victim's face will have a flat appearance. Fracture of the zygomatic arch can occur as an isolated injury. Such a fracture results in a depression on the lateral aspect of the face. Because the coronoid process of the mandible is located beneath the zygomatic arch, this type of fracture can also result in inability to fully open the mouth.[13] The best treatment for a jaw fracture is immediate immobilization. Even if perfect alignment is not achieved, fixation will make the victim more comfortable, reduce bleeding, and avoid further displacement of the fragments. Fractures that pass through the tooth-supporting portion of the mandible may be quickly stabilized with a bridle wire, or more securely held with an arch bar (see Figure 23-7 ). Fractures in more posterior locations can be temporarily immobilized with a bandage ( Figure 23-14 ), which should pull the mandible in a superior direction. Do not pull the chin posteriorly, because this can displace the fracture and compromise the airway. More rigid fixation can be obtained with intermaxillary wiring, which involves placing arch bars on upper and lower arches, placing the teeth in proper occlusion, and then connecting the upper arch bar to the lower bar with elastics or thin wire. A posteriorly displaced Le Fort fracture should be disimpacted using forward traction. If the mandible is intact, the maxilla can be held in place by forcing mouth props (commercially available or improvised) between the upper and lower molars. Significant bleeding from the nasal cavities sometimes accompanies midface fractures. However, any tamponade of the nasal cavities will displace the mobile maxilla inferiorly unless it is first stabilized from below with mouth props. A victim with facial bone fractures should be evacuated to a hospital for definitive treatment. In the interim, an antibiotic (penicillin VK 500 mg PO qid) and pain medication should be given. However, strong narcotics should be avoided if there is an associated head injury to avoid respiratory depression in an already obtunded victim. Soft Tissue Injuries Wounds of the oral mucosa and face should be treated after repair of the dental injuries and jaw fractures. Lacerations are likely to be reopened if closed before intraoral manipulations. Soft tissue injuries should be thoroughly irrigated and cleansed of foreign debris to prevent infection and tattooing. Tissue debridement should be very conservative. The excellent blood supply to this region means that wounds can be closed with sutures or other wound closures with little fear of infection if treatment can be accomplished within 6 hours of the injury. Sutures should be removed in 3 to 5 days, after which tape strips can be placed for additional stabilization
Figure 23-14 A simple bandage can be used to temporarily stabilize a jaw fracture.
of the wound margins. Facial abrasions should be gently washed twice daily with mild soap and warm water and then covered with an antiseptic ointment to prevent crusting. Small lacerations of the oral mucosa need not be closed. Use direct pressure for hemostasis. Through and through lacerations, which are common in the lower lip, are first closed intraorally, after which the remainder of the wound is closed in layers from an extraoral approach. A laceration crossing the vermilion border of the lip requires careful alignment to avoid disfigurement. Deep lacerations of the soft palate will involve the muscles and must be closed in layers. Maintain traction on the tongue while lingual lacerations are sutured. Have an assistant or the victim grasp the tongue with gauze and hold it forward. After any intraoral repair, have the victim avoid rinsing for 24 hours and advise a liquid, nondairy diet. After this period, initiate rinsing four times a day with warm saline, chlorhexidine gluconate 0.12%, or diluted peroxide. A facial laceration may be complicated by damage to associated structures ( Figure 23-15 ). Injury to the lacrimal drainage system is present if a probe inserted into the punctum at the medial corner of the lid emerges into the laceration. Damage to the parotid duct should be suspected if there is leakage from the wound when Stensen's duct is irrigated with saline. Evidence of facial nerve damage is sought by observing the victim move the eyebrows, eyelids, and mouth. If facial nerve injury occurs behind a vertical line through the lateral canthus of the eye, evacuation for immediate repair is recommended.
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Figure 23-15 Structures that may be injured by facial lacerations. A, The lacrimal drainage system. B, The parotid duct. C, A line drawn through the lateral canthus of the eye. Facial nerve injuries posterior to this line should be repaired as soon as possible. 1–5, branches of cranial nerve VII. (Redrawn from Oral and maxillofacial surgery services in the emergency department, Rosemont, IL, 1992, American Association of Oral and Maxillofacial Surgeons.)
Orthodontic Emergencies Orthodontic appliances sometimes cause soft tissue irritation or ulceration. Cover the offending fixture with soft wax. Sometimes a protruding wire can be bent until the sharp portion faces away from the soft tissues. If a bracket or wire becomes excessively loose, it can usually be removed with judicious tinkering. If a wire needs to be cut and small wire cutters are unavailable, try repeatedly bending the appliance until the metal fatigues and breaks.
LOCAL ANESTHESIA Local anesthesia is a prerequisite to many emergency dental, oral, and maxillofacial procedures. Anesthesia of any upper tooth and the associated buccal soft tissues can be obtained by infiltration. Approximately 2 ml of a local anesthetic solution is placed as close to the apex of the tooth as possible, just above the periosteum. By holding the syringe parallel to the long axis of the tooth, the needle tip is guided in the proper direction ( Figure 23-16 ). Two percent lidocaine with 1:100,000 epinephrine is commonly used, although 2% bupivacaine with 1:200,000 epinephrine (Marcaine) is useful
Figure 23-16 Technique for infiltration of a local anesthetic.
Figure 23-17 Technique for blocking the inferior alveolar nerve near the mental foramen. The shaded teeth will be anesthetized.
for long-term pain relief. Other available local anesthetics can be substituted. The mental nerve block is a simple method for obtaining anesthesia of the teeth and buccal mucosa from the second premolar forward. Proceed as for the infiltration, except that the target area is the mental foramen, located between the apices of the lower first and second premolars ( Figure 23-17 ). After depositing the solution, gently massage the area for about 30 seconds.
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Figure 23-18 When administering the inferior alveolar block, the target area (A) lies on the medial surface of the mandibular ramus, halfway between the rescuer's thumb and forefinger. Keep the syringe parallel to the occlusal plane, as shown in B.
The inferior alveolar nerve block is more difficult to learn, but it produces anesthesia of all of the lower teeth up to the midline and the buccal soft tissues forward of the mental foramen. The lingual nerve is also blocked by this injection, producing numbness of the anterior two thirds of the tongue and lingual gingiva. Figure 23-18, A , shows how the deepest concavity on the anterior border of the mandibular ramus is palpated by the thumb while the deepest concavity on the posterior border is palpated by the index finger. The target area is then halfway between the rescuer's thumb and index finger.[22] In Figure 23-18, B , the syringe is kept parallel to the plane of the lower teeth, and the mucosa is punctured just medial to the rescuer's thumbnail. When bone is contacted in the target area, the anesthetic solution is deposited. Experienced dentists miss the target area, and thus fail to produce adequate anesthesia, in about 10% of injections.[22]
DENTAL FIRST-AID KIT Items necessary to manage dental emergencies can be added to a wilderness first-aid kit without a large sacrifice of space or weight. Cavit (Premier Co., Norristown, Pennsylvania) is temporary filling material that requires no mixing and is easy to use. Squeeze a small amount of the material from the tube and place it in the tooth. Wet a dental packing instrument (or cotton-tip applicator or toothpick) to prevent sticking and pack the Cavit well. Then remove any excess. Have the victim bite to displace material that would interfere with occlusion. The filling material will set in a few minutes after contact with saliva. Zinc oxide/eugenol cements (Intermediate Restorative Material [IRM], L.D. Caulk Co., Milford, Delaware) consist of a liquid and a powder. Start with two drops of the liquid and begin mixing in the powder. Keep adding powder to make a dough that is as dry as possible. Dip the instruments in some powder to keep the mixture from sticking. Insert and shape the filling material as explained previously. Zinc oxide/eugenol cements have several advantages compared to Cavit. They are significantly stronger and can be mixed to a doughy stage for filling or slightly thinner for use as a cement. Most important is the soothing effect of eugenol on teeth with pulpitis. However, the liquid often leaks from its container, lending a pervasive odor to the backpack and tent; wind tends to blow the powder away; and the material is difficult to mix and is a sticky mess to insert into the tooth. A more complete kit for extended expeditions should include a number 151 universal extraction forceps and a straight elevator for extracting teeth. A mouth mirror, orthodontic wax, dental floss, dental syringe, 30-gauge needles, and anesthetic cartridges complete the kit. These items fit in a small case and weigh about 14 ounces. A custom dental first aid kit is preferred over commercial dental "travel kits" that contain unnecessary items and lack essential ones. In an outdoor situation, techniques must often be adapted or improvised depending on the items available. For example, Figure 23-9 shows how a suture can be used to splint an avulsed or extruded tooth. A temporary filling can be fashioned from softened candle wax, an emery board can be used to smooth a sharp tooth, or a pocket knife can be used to perform a drainage procedure.
PREVENTION The vast majority of dental emergencies can be prevented, beginning with pretrip planning. Before any extended
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travel in a remote area, each person should have a thorough dental examination, radiographs, periodontal care, and treatment of potentially troublesome teeth. The Peace Corps requires certification that examination and treatment have been performed before assignment to developing countries. The National Science Foundation has similar requirements, and in addition requires impacted and unopposed third molars to be extracted before travel to Antarctica. Once in the wilderness, minimal precautions can have significant effects. Lip balm with sunscreen can inhibit herpes labialis outbreaks. Routine personal oral hygiene will prevent many odontogenic infections and painful inflammatory conditions. Ideal care should include twice daily tooth brushing and flossing. Toothpaste is not essential, because mechanical removal of plaque and stimulation of the gingiva are the most important aspects of oral care. The fuzzy end of a hickory twig can be used if a toothbrush is not available. In the wilderness, daily oral hygiene not only helps prevent dental emergencies, but it also contributes to an overall sense of well-being and helps buoy morale when, for example, an expedition is tent-bound by bad weather. Helmets are essential for preventing trauma in rock climbing, white-water kayaking, and mountain biking. It is estimated that custom-made mouth guards prevent over 200,000 injuries every year in interscholastic sports.[18] Their use in backcountry recreation, now almost nonexistent, would probably also be very beneficial in appropriate circumstances.
References 1.
Abelson TI: Epistaxis. In Paparella MM et al, editors: Otolaryngology, ed 3, Philadelphia, 1991, WB Saunders.
2.
Andreasen JO, Andreasen FM: Textbook and color atlas of traumatic injuries to the teeth, ed 3, St Louis, 1994, Mosby.
3.
Andreasen JO et al: Replantation of 400 avulsed permanent incisors: factors related to periodontal ligament healing, Endo Dent Traumatol 11:76, 1995.
4.
Antonelli JR: Acute dental pain. Part I. Diagnosis and emergency treatment, Compendium 11:492, 1990.
5.
Baker KA, Fotos PG: The management of odontogenic infections: a rationale for appropriate chemotherapy, Dent Clin North Am 38:689, 1994.
6.
Blank LW: Clinical guidelines for managing mandibular dysfunction, Gen Dent 46:592, 1998.
7.
Bridgeman A, Wisenfeld D, Newland S: Major maxillofacial infections: an evaluation of 107 cases, Aust Dent J 41:281, 1995.
8.
Bridgeman A, Wisenfeld D, Newland S: Anatomical considerations in the diagnosis and management of acute maxillofacial bacterial infections, Aust Dent J 41:238, 1996.
9.
Chow AW: Life-threatening infections of the head and neck, Clin Infect Dis 14:991, 1992.
10.
Dajani AS et al: Prevention of bacterial endocarditis: recommendations by the American Heart Association, JAMA 277:1794, 1997.
11.
Diangelis AJ, Bakland LK: Traumatic dental injuries: current treatment concepts, JADA 129:1401, 1998.
12.
Doerr TD et al: Nasal fractures. In Cummings CW et al, editors: Otolaryngology head and neck surgery, vol 2, St. Louis, 1998, Mosby.
13.
Haug RH, Likavec MJ: Evaluation of the craniomaxillofacial trauma patient. In Greenburg AM, editor: Craniomaxillofacial fractures, New York, 1993, Springer-Verlag.
14.
Hooley JR, Golden DP: Surgical extractions, Dent Clin North Am 38:217, 1994.
15.
Josell SD: Evaluation, diagnosis, and treatment of the traumatized patient, Dent Clin North Am 39:15, 1995.
16.
Laskin D: Anatomic considerations in diagnosis and treatment of odontogenic infections, JADA 69:308, 1964.
17.
Okeson JP, editor: Orofacial pain: guidelines for assessment, diagnosis, and management, Carol Stream, IL, 1996, Quintessense Publishing Co.
18.
Padilla R, Dorney B, Balidov S: Prevention of oral injuries, CDAJ 24:30, 1996.
19.
Sands T, Pynn BR, Katsikeris N: Odontogenic infections: microbiology, antibiotics, and management, Oral Health 85:11, 1995.
20.
Svirsky JA: Recurrent aphthous ulcerations, Va Dent J 69:8, 1992.
21.
Tiner BD: Facial fractures. In Montgomery MT, Redding SW, editors: Oralfacial emergencies, Portland, Ore, 1994, JBK Publishing.
22.
Trebus DL, Singh G, Meyer RD: Anatomical basis for inferior alveolar nerve block, Gen Dent 46:632, 1998.
23.
Zambito RF, Zambito ML: Exodonture: technique and art, NY State Dent J 58:33, 1992.
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Part 5 - Rescue and Survival
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Chapter 24 - Wilderness Emergency Medical Services and Response Systems Franklin R. Hubbell
When an accident or medical crisis occurs in the wilderness or backcountry away from access to immediate assistance, the chain of events set in motion will hopefully lead to a successful rescue. However, how it unfolds varies tremendously, depending on the part of the world in which the critical events occur. Currently, no national or international standard for wilderness emergency medical services (EMS) and response exists. Instead, the configurations of personnel and policies reflect local, national, and international influences. In the United States, wilderness EMS are the most diverse, since they are provided by a wide range of agencies and individuals with a wide variety of training and certification levels, ranging from first aid to paramedic. Canadian wilderness EMS are generally provided through the military, whereas in European wilderness situations, physicians have a prominent role. The American Alpine Club's Safety Committee gathers, reviews, and analyzes mountaineering accidents that have occurred throughout North America and publishes the annual report Accidents in North American Mountaineering. The data collected illustrate both the necessary diversity of wilderness and mountain rescues and current limitations ( Box 24-1 ). Several states have established (or are in the process of establishing) working protocols for providing care in the wilderness or "extended care" environment. With increased natural and human-made disasters, EMS systems worldwide have suddenly found themselves essentially operating in "wilderness" settings because of prolonged exposure to hostile environments, delayed evacuation and transport times, and lack of medical resources and direction. Prehospital personnel almost always provide care for much longer than the "golden hour" and have been hard pressed to utilize their street-oriented skills in these extended care situations. Internationally, the Union Internationale des Associations d'Alpinisme (or International Union of Alpine Associations [UIAA]) has established criteria and courses for postgraduate training for physicians in mountain medicine. This allows physicians in the European Union to become certified in wilderness medicine and to practice the relevant skills in an appropriate arena. The foundation has been set for national standards in providing emergency care and rescue by the adoption and implementation of the Incident Command System (ICS). This system has been used in coordinating forest firefighting tactics in the western United States. It has evolved into a template usable by any agency that may become involved with an emergency effort. The ICS was developed to coordinate the many departments and individuals responding to large-scale forest fires. Since these fires can involve hundreds of departments with thousands of individuals, a system is needed that establishes a hierarchy of command and a common language of leadership and communication. The assimilation of ICS into rescue and EMS offers a solution to the single biggest problem facing these services: how to coordinate and interface a variety of teams working on the same rescue effort. When each team follows its own set of operating procedures, standing orders, leadership protocols, terminology, and egos, it often makes it virtually impossible to effectively and safely coordinate a major rescue effort. The ICS works well, and organizations such as the National Fire Academy and various state EMS offices have tried to adopt and implement it at all levels of emergency response. The ICS is now increasingly the standard for responding to any emergency situation, ranging from a single department answering a call to a minor motor vehicle accident to a complex search and rescue effort involving many agencies and rescue teams. Chapter 25 discusses the basics involved in the ICS. As it becomes widely adopted and used, it will establish a national standard on which can be built national prehospital standards, including wilderness or "extended care" protocols. Wilderness emergency medicine is a combination of emergency medical training and outdoor wilderness skills. Blending these elements, although essential, is not necessarily natural or easy. The art and science of prehospital emergency medicine began over 30 years ago in the United States and has evolved into a highly regimented and well-defined subspecialty of emergency medicine. We now have first responders, emergency medical technicians (EMTs), and paramedics, and a well-organized EMS system exists nationwide. However, this last statement may be somewhat misleading because each state has an independent EMS system and regulations so that a truly national standard does not yet exist. The only national prehospital EMS standard that currently exists is via the National Registry of EMTs.
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This organization offers individual state EMS systems standardized written and practical examinations for first responders, EMT-basics, intermediates, and paramedics. This guarantees that, regardless of where someone was trained, he or she will be tested using the same standard. According to the Registry, there are approximately 110,000 EMT-basics, 11,000 EMT-intermediates, and 41,000 EMT-paramedics currently certified by their agency. However, since not all states recognize the National Registry certification or participate in this particular standardization, the actual numbers of certified emergency care providers are considerably higher.
Box 24-1. MOUNTAIN SEARCH AND RESCUE FACTORS IN THE UNITED STATES 1. Search and rescue is the responsibility of national parks, state parks, county sheriffs, or state conservation officers, depending upon the state or park. 2. The vast majority of backcountry and technical rescues are carried out by volunteer rescue groups. 3. Ninety percent of all rescues are carryouts on foot rather than airlifts by helicopter or fixed-wing aircraft. 4. At least 95% of rescues are performed without physicians present, instead using the skills of first responders, emergency medical technicians, and paramedics, who may or may not be trained in wilderness medicine and rescue techniques. 5. Only two of the major climbing areas, Yosemite and Grand Teton National Parks, use helicopters extensively. 6. Only Denali National Park uses fixed-wing aircraft extensively and helicopters occasionally. 7. Only three national parks have rangers who are trained specifically for technical rescue, advanced medical support, and helicopter operations: Yosemite, Grand Teton, and Mt. Rainier National Parks. 8. National and state parks are not mandated with a "duty to rescue." However, virtually all parks provide rescue service. Most parks have a budget for these activities. 9. Many roadside climbing areas and popular backcountry areas are not within the jurisdictions of parks. Technical and backcountry rescues carried out at these locations are often performed by local rescue squads, fire departments, and ambulance units, usually without the benefit of specialized training or technical backcountry skills.
Training programs that focus on rapid response, rapid intervention, and rapid transport to advanced care facilities exist nationwide. Prehospital personnel are prepared to work within the framework of the "golden hour," when time is precious and critical actions save lives. This is a nationally accepted urban standard to which all EMS personnel are currently trained. Although this standard is appropriate for evaluating and training urban EMS personnel and response systems, it is often not adequate for rural, wilderness, mountain, or "extended" EMS personnel and response systems. In these situations, patient care is measured in hours and days rather than minutes. Traditional EMS recognizes rapid notification (the 911 system), dispatch, response, assessment, thorough prehospital care, transport, evaluation, and critical care in a hospital emergency department. Rapidity is the most critical factor that distinguishes urban emergency medical care from wilderness emergency medical care. However, time is not the only difference. Wilderness emergency medicine is governed by a complex set of medical skills and protocols, equipment requirements, and other specialized skills, including different attitudes or psychologic requirements, each of which combine premeditated action with improvisation. A productive mental attitude comes largely from the individual's training, expertise, and experience in the outdoors. In mountain and wilderness outdoor activities, including mountain and wilderness rescue, haste truly makes waste, which may, in certain circumstances, cost lives. As a result, wilderness and mountain rescue teams must achieve a balance between the urgency of the situation and the necessity for adequate preparation. This is not an easy or natural blend of emotions and skills. On one hand, trained EMS professionals are always primed and ready to go, feel comfortable moving rapidly, act quickly, and think on their feet. On the other hand, skilled outdoorspeople are always eager and willing to travel into the backcountry but understand the necessity of thorough preparedness. This attitude ensures that not only is each team prepared but that each individual is prepared. The team must be organized from a leadership perspective and know where it is headed, what injuries to anticipate, and how weather will affect the rescue. The team counts on each individual member being physically and mentally prepared. This difficult task requires recognition of the differences between short-term and long-term care during a rescue so that a safe and successful extended care rescue can be achieved. Mountain rescue, wilderness rescue, rural rescue, white-water rescue, expedition medicine, disaster medicine, air-sea rescue, search and rescue, cave rescue, and avalanche rescue are all likely to be extended rescues. Once rescue personnel reach a victim, they will usually be with the person for hours, providing extended emergency care. The terms extended rescue and extended emergency care refer to rescue efforts that are outside that first golden hour, which has relevance mostly for acute and severe trauma situations. Many of the recommendations in Box 24-2 need further development and may be considered controversial.
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In particular, specialized wilderness medical training with standardized protocols has yet to be developed. Box 24-2. RESCUE PERSONNEL AND TRAINING IN THE UNITED STATES 1. Most technical rescue personnel in the United States are climbers or skiers who have added rescue techniques and medical training to their skills. 2. There are about 600,000 EMTs in the United States. 3. There are a growing number of wilderness EMTs trained in the skills of extended victim care in the backcountry environment. 4. Key skill elements of medical training for wilderness medical and rescue training include the following. a. Thorough victim assessment skills and monitoring b. Technical skills and the authority to perform the following: 1. Airway management, to include endotracheal intubation. 2. Shock management to include intravenous therapy 3. Use of the military antishock trousers (MAST) garment 4. Oxygen administration 5. Use of appropriate medications a. Epinephrine for anaphylactic reactions b. Antibiotics for compound fractures c. Acetazolamide, nifedipine, and furosemide for acute high-altitude problems d. Pain medications for musculoskeletal trauma 6. Field rewarming techniques 7. Field reduction of fracture-dislocations c. Victim packaging and transportation skills 5. Key skill elements of technical training for rescue personnel in the United States include the following: a. Appropriate climbing skills for terrain (rock, ice, snow, glacier) b. Radio communications skills and protocols c. Helicopter and fixed-wing protocols d. Training and expertise in using the Incident Command System in field protocols
SEQUENCE OF EVENTS IN BACKCOUNTRY RESCUE The principles and standards of a wilderness or mountain rescue (extended care rescue), including organization, specialized skills and knowledge, and essential components of the team, can best be illustrated by reviewing the sequence of events during a typical backcountry rescue in North America ( Box 24-3 ). Occurrence of the Critical Event The critical event occurs when an individual participating in an activity away from immediate help is suddenly stricken by injury or illness. The key factor is immobilization. The fact that the injured or ill person cannot self-evacuate or move to seek shelter or stay warm results in the need for a rescue. Once the victim or others in the party realize this, the need to seek help becomes obvious.
Box 24-3. SEQUENCE OF EVENTS IN BACKCOUNTRY RESCUE 1. The critical event occurs: an injury or illness that requires assistance and evacuation. 2. A decision is made to "get help" and someone goes for help. 3. The emergency medical system is notified of the emergency. 4. The emergency medical system is activated, or "dispatched." 5. Eventually, the "extended rescue team" is notified and mobilized. 6. The rescue team assembles and organizes, then leaves the trailhead (may be preceded by a "hasty team"). 7. The team locates the victim. 8. The team provides appropriate "extended emergency care." 9. The team organizes and evacuates the victim to the appropriate facility. 10. The team returns to base, is debriefed, and prepares for the next rescue.
Making the Decision to Get Help Before anyone leaves to seek assistance, the victim's companions should perform a physical examination, record vital signs, determine the level of consciousness, and provide appropriate emergency care, which may entail moving the victim into protective shelter. Victim information should be summarized in a note that accompanies the individual(s) going for help. A map depicting the victim's exact location and a list of the other party members, noting their level of preparedness to endure the environmental conditions, should be included. The individual(s) going for help should carry appropriate provisions. To prepare information adequately generally takes 30 minutes to 1 hour. However, thorough preparation rarely occurs. Often, someone suddenly yells, "I'll get help" and disappears, running down the trail with sparse vital knowledge. With the improvements and availability of communications technology, such as cellular phones and global positioning systems, backcountry adventurers may have more rapid access to the EMS system from the mountains. Whether this will increase the number of inappropriate callouts remains to be determined. Recent reports indicate that reliance on fallible technology may be responsible for outdoorspeople using poor
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judgment in terms of trip planning. Assuming that help is just a phone call away, hikers are taking more risks. Notifying the Emergency Medical System Eventually, the messenger notifies someone in authority that an emergency has occurred and help is needed. Usually, the request is made to a central 911 system. If no central service is available, a local dispatch agency is notified. The agency contacts the closest emergency medical service, which can be a rescue squad, ambulance corps, fire department, or first response team. Activating the Emergency Medical System.
Notification of an emergency usually occurs via pagers worn by individual members. An alert tone is followed by an oral message describing the emergency, its location, and type of response required. At this point, a wide variety of events can occur, involving agencies within and outside the EMS system. Even in areas of the United States with well-organized extended care rescue teams, the team may be notified last. Ideally, it should be notified immediately, but all too often this is not the case. Instead, local agency responders are notified and rush around trying to determine how quickly they can reach the victim. Notifying and Mobilizing the Extended Rescue Team.
The first step is to notify team members. In many parts of the United States, organized and coordinated extended rescue teams do not exist, so a "team" is created of relatively untrained volunteers willing to hike in and assist. The task of further organizing and coordinating the rescue effort generally falls on the shoulders of a local rescue squad, fire service, or police department, which may or may not be willing and prepared to manage and execute an extended or technical rescue. In the parts of the United States where backcountry use is common and backcountry accidents occur regularly, extended care rescue teams have generally evolved from local EMS squads with skilled outdoor enthusiasts. Some teams offering local search and rescue capabilities may be coordinated locally (such as the Appalachian Mountain Club, Stonehearth Open Learning Opportunies [SOLO], and Mountain Rescue Service in the White Mountains of New Hampshire); other teams may be part of a nationwide system responding to incidents throughout the country and be coordinated on a regional or national level (such as the National Cave Rescue Commission). Coordination of extended care rescue teams may also come under the jurisdiction of a law enforcement body, such as state conservation officers (e.g., New Hampshire Fish & Game), sheriff's department (e.g., the Los Angeles County Sheriff in California), or a statewide coordinating system (e.g., the Pennsylvania Search and Rescue Council). Organized teams can be quite sophisticated in their dispatching function so that all members can be notified simultaneously, or they may use a more "low-tech" telephone tree to call out members. Assembling and Organizing the Rescue Team Once members are notified, they assemble at a common location (rescue station) to organize the rescue effort. The first task is to define the type of rescue to establish equipment needs. Estimating the time it will take to effect the rescue and assessing the need for other agency involvement and assistance are also primary tasks. The questions to be answered and the variables to be considered may include the following: 1. Time of day: will this be a night rescue? 2. Weather: what are the current weather conditions at the rescue location and what is the forecast? 3. When did the accident occur?
4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
What are the supposed injuries? How many victims are there? How many people are in the party? How well prepared are they? Does anyone in the party have medical expertise? Do we know the exact location, or is this a search and rescue? Is a "hasty team" needed? Has it left for the scene yet? Is each of the team members prepared? Does each have personal equipment, a bivouac kit, head lamp, food, and water? Is each member trained and skilled in this particular type of rescue? Who is on the medical team? Who is on the evacuation team? Is the team equipment organized and divided up? How urgent is the situation? Is a helicopter required? Is one available? Are the weather conditions appropriate for an air rescue? Will multiple agencies be involved? If so, are radio frequencies coordinated?
Once the team is assembled and all pertinent issues have been addressed satisfactorily, the team is transported to the trailhead (launch point) to begin the search. Commonly, a hasty team starts out ahead of the main team. Once the hasty team has enough information to locate the victim, they travel as lightly as possible, with only enough gear to ensure their own safety and to equip them to manage the victim's primary injuries. The goal is to reach the victim as quickly as is reasonably possible and deliver primary care, then apprise the rest of the team of the victim's condition, equipment needs, and environmental concerns. Locating the Victim How long it takes to locate the victim varies tremendously, depending on distance, terrain, weather conditions, mode of transportation, and whether the victim's exact location is known. A general rule of thumb for a
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team responding on foot is that it will take 1 hour for each mile through the backcountry. If a search is involved, all bets are off. A search and rescue effort can involve many agencies, individuals, and days (see Chapter 25 ). Providing Appropriate "Extended Emergency Care" Once the victim is located, appropriate medical care can be provided. The rescue team should ensure its own safety; wet clothes should be replaced with warm, dry clothing, and members should check for emerging problems within their group. While the medical team cares for the victim, the evacuation team secures shelter, prepares warm drinks, establishes and maintains communications, and plans and organizes the evacuation. Companions with the victim may have been affected by the environment while waiting for the rescue team to arrive and require assistance. They may need to be assessed and treated for hypothermia, frostbite, heatstroke, heat exhaustion, and dehydration. Regardless of what transpired before the medical team arrived, a complete victim assessment is essential. Do not assume that all the injuries have been found or that all medical conditions have been managed properly ( Box 24-4 ).
Box 24-4. VICTIM ASSESSMENT
PRIMARY SURVEY: LOCATING AND TREATING LIFE-THREATENING PROBLEMS A—Airway Management Is the airway open? Is the airway going to stay open? B—Breathing Is air moving in and out? Is the airway quiet or silent? Is breathing effortless? Is the respiratory system intact? Is breathing adequate to support life? C—Circulation Is there a pulse? Is bleeding well controlled? Is capillary refill normal (less than 2 sec)? Is circulation adequate to support life? D—Disability Conscious vs. unconscious Level of consciousness—awake/verbal/painful/unconscious (AVPU) or Glasgow Coma Scale Cervical spine stabilization E—Environment Internal vs. external Is the victim warm and dry? Protected from the cold ground Protected from the elements
Is the victim warm and dry? Protected from the cold ground Protected from the elements
SECONDARY SURVEY: WHAT IS WRONG AND HOW SERIOUS IS IT? Vital signs: Indicate the condition of the victim RR—respiratory rate and effort PR—pulse rate and character BP—blood pressure (systolic/diastolic) LOC—level of consciousness (AVPU or Glasgow Coma Scale) TP—tissue perfusion: Skin color, temperature, and moisture Capillary refill (less than 2 sec) Victim examination: Head-to-toe examination to locate injuries AMPLE history: Allergies Medicines Past medical history Last food/drink Events leading up SOAP NOTE: To record and organize victim data Subjective: Age, gender, mechanism of injury, chief complaint Objective: Vital signs, victim examination, AMPLE history Assessment: Problem list Plan: Plan for each problem
In the extended care environment, the victim must be monitored for changing conditions that indicate an underlying problem. Awareness of environmental emergencies is particularly important, with constant care to prevent hypothermia, frostbite, heatstroke, heat exhaustion, and dehydration. To do this, it is necessary to monitor the victim and write a new SOAP note at least every 15 minutes: Subjective: Is the victim comfortable, too hot, too cold, hungry, thirsty, or in need of urination or defecation? Objective: Vital signs—are they stable? Record these. Victim examination—recheck all dressings, bandages, and splints; are they still controlling bleeding? Are they too tight or too loose? (Swelling limbs can cause bandages or splints to impede circulation, resulting in ischemic injuries or worsening frostbite or snakebite.)
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Assessment: Has the initial assessment changed? Plan: Is the rate of evacuation still the same?
Evacuating the Victim to the Appropriate Facility While providing emergency care, part of the team is designated as the evacuation team. This group has evaluated the various options for evacuation. To properly evaluate the situation, the first information they need is provided by the medical team leader, since they need to know the status of the victim to establish the pace. If the victim's condition is stable, time is less important; if the victim's condition is critical, time is critical. The evacuation team must explore different options. If speed is a consideration, weather conditions are reviewed and the availability of a helicopter-assisted rescue is determined. If a helicopter is not an option, the fastest route out is established. If time or speed is not critical, the safest means of evacuation that is easiest on the victim and rescuers is defined. A general rule for the duration of an evacuation is that it will take 1 to 2 hours for every mile to be covered, requiring six well-rested litter bearers for every mile. Thus a 4-mile carryout will require a 24-member litter team and can take 4 to 8 hours to complete. Eventually, the team reaches a trailhead and the victim is transferred to an ambulance for transport to a hospital emergency facility. Returning to Base The team returns to base to reorganize equipment in preparation for the next extended rescue, and to debrief. Because people are exhausted and hungry, the debriefing session is often canceled. However, establishing a mechanism to debrief the rescue effort is imperative so that they can learn from the shared experience, discuss victim care, and work through problems. Whenever several different emergency organizations with disparate rescue and emergency personnel combine to perform a complex rescue, there may be tension, bruised egos, and concerns about the medical care provided or evacuation plan used. These problems deserve to be discussed and managed in real time as expediently as possible so that teams will cooperate successfully in the future, improve their performance, and provide the best possible patient care on the next rescue. This process minimizes the burnout syndrome that can occur with volunteer teams.
TEAM ORGANIZATION AND FUNCTION The organization of an extended care rescue team is based on both training of individuals and type of rescue. The structures of teams can vary from loosely knit groups of friends with no leadership hierarchy to paramilitary organizations with rigid leadership roles. Team members require personal knowledge, experience, and expertise in the particular aspect of extended care and rescue in which they will participate, as well as knowledge and expertise in the principles of extended emergency care, extended rescue techniques, and technical rescue skills. Personal Knowledge, Experience, and Expertise Individuals who want to be part of an extended rescue team need to acquire outdoor skills before they become part of a rescue team. Every member must have extensive knowledge of likely environmental emergencies: hypothermia, frostbite, heat syndromes, snakebite, dehydration, lightning strike, and so forth. Each must understand general principles of weather behavior. Rescuers need to be comfortable with route finding, map and compass, personal preparedness, and bivouac and survival skills. The knowledge, skills, and equipment that a skilled outdoorsperson should possess are often referred to as "the ten essentials" (see Box 24-5 ). The
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same skills, knowledge, and equipment commonly used by the outdoor enthusiast are essential on a mountain rescue. Box 24-5. THE TEN ESSENTIALS 1. Attitude Positive belief that you can make things better Will to survive
2. Fuel to burn: food High-carbohydrate foods that require no preparation High-carbohydrate foods that can be made into a drink
3. Quench your thirst: water A minimum of 2 L/day if not active Up to 3 L/hr if active
Ability to make more pure disinfected water
4. Stay warm and dry: clothing Warm clothing that retains heat even if wet Waterproof raingear, top and bottom
5. Get dry: shelter Ability to improvise shelter or bivouac A bivouac ("bivy") kit (see Box 24-6 )
6. Get warm: fire Ability to warm water (stove, candle, fire) Ability to build a fire (waterproof matches and tinder) Ability to make kindling or tinder (folding knife)
7. Know where you are going: navigation Map and compass skills and route-finding skills Ability to move about at night (headlamp)
8. Know the environment: weather Basic understanding of weather patterns Knowledge of how to react to severe weather, lightning
9. Getting help: signaling Whistle, preferably plastic
9. Getting help: signaling Whistle, preferably plastic
10. Providing help: first aid kit Basic small personal trauma kit
Box 24-6. BIVOUAC KIT Two large garbage bags (emergency shelter or raingear) 10 × 10 foot sheet of plastic and 100 feet of parachute cord (shelter) Emergency space blanket (shelter, ground cloth) Stocking cap (warmth) Spare socks (warmth and can act as spare mittens) Metal cup (to warm liquids) Gelatin (to make a drink) Two plumber's candles (to warm water or start fire) Waterproof matches or lighter Knife Compass Whistle All of these items fit neatly into a small stuff sack that is 6 × 6 inches and weighs less than 1 pound when filled.
Extended Rescue Techniques and Skills Specific skills and techniques applicable to a particular situation include those of search and rescue, vertical and technical rock climbing, and white-water navigation. Snow or winter camping or avalanche rescue may be required, depending on the environment. Extended rescue teams should require their members to have, at a minimum, the working knowledge and equipment in Box 24-7 . Knowledge is acquired over time. Specific medical, rescue, and technical skills are obtained and retained through courses, continuous training, and refresher programs. Appendix A at the conclusion of this chapter provides a list of schools, institutes, and organizations that are involved in mountaineering research, standards development, and training programs. Wilderness and Mountain Rescue Team Organization Organization of wilderness and mountain rescue teams is where the greatest diversity exists, since no universal standard has been established. Teams vary from local mountain rescue teams with extreme skills and qualifications for providing mountain rescue care to informal collections of friends without leadership. Other, more "professional," teams are operated under the jurisdiction of law enforcement agencies with paramilitary hierarchy and leadership. This diversity is particularly noticeable in the United States because the vast majority of teams are composed of volunteers who are not reimbursed for their rescue efforts. In Europe, mountain rescue teams are professional and employ full-time personnel. They charge for rescue efforts, with the fees providing money for personnel, equipment, helicopters, technical gear, and ongoing training. As with any "profession," standards have evolved. As a result, there are more standards in Europe than in the United States. Still, there is variation from European country to country, especially in leadership and organization. In many parts of the world, especially remote and wild areas, organized and available rescue teams do not exist. If someone is in need of help, the expedition team necessarily becomes the rescue team.
TRAINING OF WILDERNESS EMERGENCY MEDICAL TECHNICIANS The best way to develop an appreciation for the vast difference between what is required of the traditional (urban) EMT and what is required of the extended care or wilderness emergency medical technician (WEMT) is to compare their respective course curriculums. The Department of Transportation (DOT) is responsible for developing and updating the EMT curriculum in the United States. This curriculum is considered the minimum national standard for EMT students to qualify for the National Registry or an individual state practical and written examination. Passage of such an examination enables a student to become certified as a National Registry or state EMT. A national standard for WEMT curricula does not yet exist. Despite the lack of a DOT-like standard, there are several similar curricula for wilderness emergency care at the EMT level. Based on the recommendations of the Wilderness Medical Society and other groups that address the issues of wilderness prehospital emergency medicine, these curricula adhere to the same principles of long-term patient care, which can be used for comparison with the standard DOT curriculum. A WEMT course typically contains all of the material in the DOT EMT course curriculum plus what is necessary to acquire the skills attendant to long-term wilderness emergency care. Typical EMT courses are approximately 100 hours with 10 additional hours of emergency department observation time. The WEMT module carries an additional 48 to 80 hours of training.
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Box 24-7. KNOWLEDGE, SKILLS, AND EQUIPMENT FOR EXTENDED RESCUE TEAMS
MOUNTAINEERING SKILLS Understanding fabrics and clothing systems and their seasonal variations (see Chapter 70 ) Fabrics and fibers Layering techniques Vapor barrier systems Waterproof fabrics, raingear systems Footgear Personal protection equipment Helmets Harnesses Gloves Goggles, sunglasses Hearing protection Backcountry equipment Internal or external frame packs and soft packs Shelter (natural and human-made) Specialty equipment: snow shoes, crampons, ice axes, stoves, skis Backcountry travel Route finding Map and compass: map reading, dead reckoning, types of maps, compass reading, bearings, magnetic vs. true bearing, triangulation, global positioning systems Survival skills: the ten essentials Shelter and warmth; emergency bivouac ("bivy") kits Food, water Understanding how backcountry travel and rescue vary with the seasons Understanding how backcountry travel and rescue vary with different environments Alpine Desert Forest Water (swamp, river, lake, ocean) Tropics High altitude Low-impact camping and rescue work Basics of weather and weather forecasting
High altitude Low-impact camping and rescue work Basics of weather and weather forecasting Principles of barometric pressure Clouds and their significance in weather forecasting Prevailing weather patterns in the rescue area Personal fitness Physical conditioning Nutrition and hydration requirements for different activities
MOUNTAIN AND EXTENDED EMERGENCY MEDICAL SKILLS Emergency medical training should be at a minimal level of first responder or higher (emergency medical technician, paramedic, registered nurse, nurse practitioner, physician's assistant, or physician). Regardless of the level, training must include specific information on wilderness and extended emergency care procedures. Topics of extended care training and principles should include the following: Patient assessment system Cardiopulmonary resuscitation Airway management, including endotracheal intubation and needle decompression for tension pneumothorax Shock and control of bleeding, including the use of intravenous (IV) therapy for fluid resuscitation Long-term wound care and prevention of infection Musculoskeletal injury management, including specific information on diagnosis and long-term management of the following: Sprains and strains Fractures, including how to reduce or realign angulated fractures Diagnosis and reduction of dislocations Management of compound fractures Management of chest injuries, including decompression of a tension pneumothorax with a needle thoracostomy Spinal cord injury diagnosis and management Head injury, including recognition and management of increasing intracranial pressure Management of environmental emergencies Hypothermia and frostbite, including the use of IV fluids Heatstroke and heat exhaustion, including the use of IV fluids Dehydration and nutrition, acute and during evacuation Lightning injuries Animal attacks, insect bites, and reptile and marine envenomations, including anaphylactic reactions and the use of epinephrine and antihistamines Contact dermatitis, such as poison ivy, oak, and sumac Sunburn and snowblindness High-altitude injuries, including acute mountain sickness, pulmonary edema, cerebral edema Near drowning Diagnosis and management of acute medical emergencies Chest pain (myocardial infarction, angina, costochondritis) Shortness of breath (asthma, anaphylaxis, pneumothorax) Seizures and cerebrovascular accidents Acute abdomen (peritonitis, constipation, diarrhea) Pyelonephritis and septic shock Victim lifting and handling techniques (body elevation and movement [BEAM], free of any movement [FOAM]) Improvising techniques: "emergency medicine barehanded" (see Chapter 19 ) Training in the use of the Incident Command System Bloodborne pathogens and infectious disease prevention
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Monitoring of bodily functions (hunger, thirst, and need to excrete) General understanding and appreciation for the difference between urban (short-term) and wilderness (long-term) emergency care
MOUNTAIN AND EXTENDED RESCUE SKILLS Understanding equipment used in wilderness search and rescue operations, including maintenance and care
MOUNTAIN AND EXTENDED RESCUE SKILLS Understanding equipment used in wilderness search and rescue operations, including maintenance and care Ropes, slings, carabiners, harnesses, helmets Litters, litter harnesses, haul systems Litter patient packaging equipment Basic radio communications Care and maintenance of communications equipment Procedures and protocols Basic helicopter operations and procedures Approach to a helicopter Safety considerations Landing zones Haul techniques Interagency relations Basic understanding of search procedures Basic understanding of rescue procedures Basic understanding of Incident Command System and its use in search and rescue management Basic rope handling and knot tying skills How to care for and handle ropes Rappeling, belaying, and braking techniques Knots Figure-8 Figure-8 follow through Figure-8 on a bight Double figure-8 Double fisherman's Prusik Tensionless hitch (round turn and two half hitches) Water Half hitch and full hitch Bowline Alpine butterfly Specific rescue training Water search White-water Avalanche Technical or vertical (rock) Cave
LEADERSHIP Leadership and followship training Ability to use the Incident Command System
A typical WEMT course outline appears in Box 24-8 . The topics in boldface are peculiar to a WEMT program, whereas the other topics are those required in a DOT EMT course. Hours per topic illustrate the time required for both EMT and WEMT training. This outline is arranged in the current DOT EMT recommended format, with the WEMT material added on a per topic basis; topics are not necessarily listed in the order that they would be taught for a particular course. An explanation follows of the extended emergency medical care material that WEMTs must learn. Introduction to Emergency Care "Wilderness vs. urban emergency care" is an introductory presentation to illustrate the differences between urban ("golden hour") emergency care and extended, or "wilderness," emergency care. For WEMTs, it will in certain instances be necessary to learn two different modalities of therapy, one for short-term (less than 1 hour) care and one for long-term or extended (several hours to days) care. "Backcountry rescue gear inspection" is a hands-on review of gear for the outdoor practice sessions and backcountry mock rescues. The course staff must inspect the participants' boots, clothing, raingear, and rescue equipment to determine their adequacy for the particular environment in which they will be deployed. Inspecting equipment not only ensures the safety of each individual in the course but also teaches a standard for preparedness, awareness, and attention to details that is critical
for wilderness travel and emergency care. "Medical legal issues" is usually offered early in a course so that the participants are aware of the legal concerns surrounding practicing medicine as EMTs and WEMTs. WEMTs need to be aware of protocols existing where they will become licensed. "The human animal—our natural physiologic limits" is an overview lecture of how humans fit into the natural environment and of their daily nutritional requirements and natural limitations. The WEMT must understand physiologic limits, such as those of endurance, temperature, and altitude, and the consequences when these limits are exceeded. Patient Assessment Systems "Patient assessment in the wilderness and practice" takes the newly learned skills of patient assessment and adapts them to the backcountry. The WEMT must be
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knowledgeable and skillful in wilderness patient assessment, a step-by-step approach to the first 5 minutes of scene safety and patient care. The WEMT will develop an awareness of potential life-threatening dangers in the environment, how to ensure personal safety and the safety of others, how to approach a victim safely, how to perform primary and secondary surveys to determine the extent and severity of injuries, and what impact the environment might have on the victim. Box 24-8. EMT AND WEMT COURSE CURRICULA AND HOURS PER TOPIC* 1. Introduction to emergency care Wilderness vs. urban emergency care (1 hour) Backcountry rescue gear inspection (1 hour) Medical legal issues (1 hour) Blood-borne pathogens Overview of human systems—anatomy and physiology (2 hours) The human animal—our natural physiologic limits (2 hours)
2. Patient assessment systems Primary survey—ABCs (1 hour) Secondary survey (1 hour) Patient assessment practice (2 hours) Patient assessment in the wilderness and practice (3 hours)
3. Cardiopulmonary resuscitation (8 hours) Mannequin practice and certification (8 hours) Cardiopulmonary resuscitation (CPR) teaching, practice, and testing to American Heart Association standards
4. Airways, oxygen, and mechanical aids to breathing (3 hours) Airways, oxygen, CPR, and mechanical aids to breathing in the wilderness environment—uses and limitations (6 hours) Airways: oropharyngeal, nasopharyngeal, esophageal obturator airway, endotracheal intubation Oxygen administration Suction techniques
5. Bleeding and shock (3 hours) Shock, intravenous (IV) fluids, and long-term patient care (4 hours) Practice starting IV infusions and fluid administration (4 hours) Use of pneumatic antishock garments (PASG) (3 hours) Use of PASG in the wilderness (1 hour)
6. Soft tissue injuries (3 hours) Long-term wound care (1 hour)
7. Principles of musculoskeletal care Fractures of the upper extremities (3 hours) Fractures of the pelvis, hip, and lower extremities (3 hours) Fracture laboratory—practice in assessment and management (3 hours) Musculoskeletal trauma management in the wilderness (3 hours)
Fractures of the pelvis, hip, and lower extremities (3 hours) Fracture laboratory—practice in assessment and management (3 hours) Musculoskeletal trauma management in the wilderness (3 hours)
8. Injuries of the head, face, eye, neck, and spine (3 hours) Practical laboratory: spinal cord injury management (SCIM) (3 hours) Head trauma, increasing intracranial pressure (1 hour) SCIM: Long-term care and improvising (1 hour)
9. Injuries to the chest, abdomen, and genitalia (3 hours) Chest trauma in the wilderness (3 hours)
10. Medical emergencies I (3 hours) Poisoning, bites and strings, heart attack, stroke, dyspnea Medical emergencies II (3 hours) Diabetes, acute abdomen, communicable disease, seizure, substance abuse, and pediatric emergencies Medical emergencies in the wilderness (3 hours)
11. Emergency childbirth (3 hours) 12. Burns and hazardous materials (3 hours) Long-term care of burns (1 hour)
13. Environmental emergencies (3 hours) Hypothermia, frostbite, immersion foot (4 hours) Heatstroke, heat exhaustion, dehydration (4 hours) Drowning (2 hours) High-altitude emergencies (2 hours) Barotrauma (2 hours) Animals that bite and sting (2 hours) Plants—contact dermatitis (2 hours) Marine animals that bite and sting (2 hours)
14. Psychologic aspects of emergency care (3 hours) 15. Lifting and moving patients (3 hours) Use of Stokes litters and improvising litters (3 hours)
16. Principles of vehicle extrication (4 hours) Practice laboratory (3–8 hours) Principles of backcountry evacuation (4 hours) Search and rescue organization and execution (4 hours) Wilderness mock rescue with or without overnight (8–12 hours)
17. Leadership and followship skills The Incident Command System
18. Ambulance operations I (3 hours) Ambulance operations II (3 hours) Helicopter-assisted rescues (3 hours)
19. Review (3–6 hours) Testing—written and practical examinations (16–20 hours)
20. Emergency department observation time (10 hours) *Topics in boldface are peculiar to WEMT programs, whereas the other topics are required topics covered in a DOT EMT course.
Airways, Oxygen, and Mechanical Aids to Breathing "Airways, oxygen, cardiopulmonary resuscitation, and mechanical aids to breathing in the wilderness environment—uses and limitations" addresses one of the most important lifesaving and life-maintaining skills in emergency medicine: the ability to establish and maintain a patent airway. Unfortunately, most EMTs are not provided with the training and tools they need to properly maintain an open airway in an unconscious victim. Failure to perform endotracheal intubation can be disastrous for such a victim. Endotracheal intubation is commonly used by EMT-intermediates and paramedics and other advanced life support (ALS) personnel in cardiac arrest settings and for unconscious, unresponsive victims. In the extended care environment, the use of intubation in a cardiac arrest situation is not nearly as common as it is for the normothermic, unconscious, and unresponsive person, who has probably suffered head trauma. In this situation, without intubation, the only way to maintain a patent airway while lifting, moving, and transporting a victim in a litter is to place the victim on his or her side. Gravity pulls the tongue forward and allows secretions to drain from the mouth. Oropharyngeal, nasopharyngeal, and esophageal obturator airways and tongue pin-pull techniques may temporarily keep the tongue from occluding the airway, but they are ineffective in preventing vomitus, blood, or saliva from entering the airway. Also, during evacuation in a Stokes litter, constant monitoring of a victim's airway is virtually impossible, which makes endotracheal intubation of paramount importance. The WEMT should know how to establish and maintain a patent airway, including the use of endotracheal intubation. "Oxygen administration" presents the use of supplemental oxygen, for which both EMTs and WEMTs follow the same general guidelines. Even though oxygen is important to prehospital care, its use has significant logistic limitations in the backcountry. The WEMT must realize that carrying large quantities of oxygen into the backcountry is impossible. Small D and E cylinders can be carried, but each provides high-flow oxygen for only 20 to 30 minutes. Oxygen is a compressed gas in a tank, so as it expands, it cools dramatically and may contribute to hypothermia. To prevent this, the gas should be preheated by wrapping the oxygen tubing around a chemical heat pack during administration. "Suction techniques" presents the use of suction devices to clear the airway, which is similar for EMTs and WEMTs. Hand-operated, as distinct from battery-operated, suction devices are usually used in extended care scenarios. Bleeding and Shock "Shock, intravenous (IV) fluids, and long-term patient care" and "Practice starting IV infusions and fluid administration" provide information about the care of victims in shock. In the urban management of shock, the essential component is recognition. Once shock is recognized, the victim can be rapidly transported to an emergency department or intercepted by paramedics for definitive care, namely fluid resuscitation. In the extended care environment, WEMTs must be able to manage the shock syndrome by providing appropriate definitive care. During extended evacuations, WEMTs should know how to administer IV fluids to stabilize hypovolemia. This includes starting a peripheral IV line, maintaining the catheter placement, using proper fluids, and prewarming the solutions before and during administration. "Use of pneumatic antishock garments (PASG) in the wilderness" discusses the use of these garments for victims in shock. The practice of treating shock using PASG has largely fallen out of favor. As long as an IV line can be established and maintained, fluid administration is the definitive method for managing shock. The WEMT must be aware that the PASG has other uses. In the extended care situation, use of the PASG may be invaluable in stabilizing a fractured pelvis to control internal blood loss and prevent shock. It may be useful in conjunction with a traction splint for a fractured femur. An added benefit is that the PASG may facilitate a comfortable and well-padded ride for the victim in a Stokes litter. However, WEMTs must recognize the limitations of a PASG. The primary drawback in the backcountry is the potential for cold injury. Once the apparatus is inflated, the decrease in peripheral circulation greatly increases the risk for cold injuries or frostbite to the lower extremities. This can be prevented by properly packing the feet with chemical heat packs and adequately insulating the lower extremities in the litter. Careful monitoring of the lower extremities every 15 minutes is essential. Soft Tissue Injuries "Long-term wound care" covers proper wound management once bleeding has been controlled, and further care if more than 12 hours will be required to bring the victim to definitive care. The principles of long-term wound care are to stabilize the wound and prevent and control infection.
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To prevent infection, the WEMT must know how to sterilize or disinfect fluid and how to properly debride and rinse out a contaminated wound. Once the wound is cleaned and debrided, the edges can be approximated but not tightly closed, since this may increase the risk of abscess formation and a life-threatening infection. Training in suturing techniques to close wounds is not currently recommended. Even the most fastidiously cleaned wound can still become infected, particularly in a remote setting, because of constant exposure to microbes. Recognition of wound infections and appropriate management are important. The WEMT must learn to use specific antibiotics in extended care settings of greater than 3 days and for prophylaxis with grossly contaminated wounds and compound fractures. Antibiotic therapy is not controversial, since various safe broad-spectrum antibiotics can cover most wound infections with minimal risk of a severe allergic reaction. In certain circumstances the benefits of antibiotic administration clearly outweigh the risks. Principles of Musculoskeletal Care "Musculoskeletal trauma management in the wilderness" presents the treatment of injuries. In an urban setting, the primary concern with fracture and dislocation care is that the injury site be splinted properly to prevent further injury. In the extended care environment, the primary concern is to maintain proper circulation distal to the site of the injury. This may require straightening an angulated fracture or reducing a dislocation. When an angulated fracture occurs, distal circulation can be impaired, putting the soft tissues at considerable risk for ischemic injury or frostbite. Under normal circumstances, it would take hours for moderate ischemia to cause irreparable soft tissue injury, but in the backcountry, prolonged time under hostile weather conditions frequently occurs, which decreases the amount of heat and oxygen being transferred to the extremity. Knowing how to properly straighten out an angulated fracture significantly decreases the risk of secondary ischemic injury and frostbite, controls bleeding at the fracture site, and diminishes pain. It is much easier to splint and stabilize a fracture in proper position if it is straight than if it is angulated. Approximately 3 additional hours of training are needed to teach a WEMT how to straighten an angulated fracture and reduce dislocations. Without an x-ray, it is impossible to see the exact positioning of bone fragments or disarticulated joints, making it difficult to know exactly how to manipulate the bone. The concern is that if a jagged bone end is moved improperly, secondary injury might occur: part of a neurovascular bundle might be severed, a fascial sheath surrounding a muscle might be cut, or the bone ends might erupt through the skin. Fortunately, all of these structures are richly endowed with pain receptors. If the sharp end of a bone fragment begins to impinge, it causes a dramatic increase in pain at the site. A commonly used technique is to straighten the angulated site slowly while maintaining constant gentle traction. With each 1 to 2 cm of movement, the victim is asked if the new position is better or worse (causes less or more pain). If the pain diminishes with movement, the reduction is proceeding properly; if pain increases, all movement is stopped and the extremity is returned to the previous position of improvement. While still under gentle traction, the extremity is repositioned and another attempt at reduction is made. As long as nothing is forced and movement is achieved slowly under gentle traction, angulated fractures can be easily realigned and dislocations reduced without the need for pain medication or any risk of further injury. Musculoskeletal injuries in the long-term care setting must be carefully monitored. It is essential to reinspect the injury site at reasonable intervals for circulation, sensation, and motion. Fracture sites swell; as a result, even the best splint can act as an inadvertent tourniquet. Immobilized extremities cool because of lack of activity and impaired circulation, also increasing the risk of ischemic injury or frostbite.
Injuries of the Head, Face, Eye, Neck, and Spine "Head trauma, increasing intracranial pressure" addresses one of the leading causes of death from backcountry accidents. Many who die of head trauma in the wilderness would have survived in an urban setting because of rapid access to definitive care. The WEMT must be able to recognize a potentially serious head injury long before the victim is at risk of brainstem herniation. In the extended care environment, there are few situations when the team should hurry. One such situation is the presence of significant head trauma, for which the only appropriate care may be rapid evacuation to a facility where the victim can be put into the hands of a neurosurgeon. It is important to establish and monitor the level of consciousness. The AVPU (awake, verbal, pain, unresponsive) scale is used. Within the primary survey, an initial evaluation of disability or neurologic status is made. After that, level of consciousness is reevaluated every 15 minutes to observe in particular for any evidence of increasing intracranial pressure. Injuries to the Chest, Abdomen, and Genitalia Chest trauma is significant for the WEMT because it can result in a pneumothorax that can evolve into a tension pneumothorax. WEMTs need to be taught how to inspect, palpate, percuss, and auscultate the chest for significant injuries to the respiratory system. It is not difficult to train an individual to detect breath sounds, determine the presence of a pneumothorax, and monitor a pneumothorax for its development into a tension
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pneumothorax. Unlike increasing intracranial pressure, for which there is little to do but evacuate the victim, a tension pneumothorax can be relieved, increasing the chance of survival. The easiest and most effective technique a WEMT may learn is needle thoracostomy in the fifth intercostal space in the midaxillary line. Medical Emergencies Diagnosing medical emergencies in the wilderness requires the WEMTs to be aware of essential signs and symptoms. Environmental Emergencies The typical EMT course includes 3 to 6 hours of training in management of environmental emergencies. A WEMT course will have a minimum of 22 hours of additional training in environmental emergencies. "Hypothermia, frostbite, and immersion foot" covers cold injuries, which are among the most common environmental injuries seen in the backcountry. The WEMT must understand principles of thermoregulation; heat production and heat loss; recognition of hypothermia, frostbite, and immersion foot; and appropriate care. "Heatstroke, heat exhaustion, and dehydration" provides necessary information about the balance of heat production and heat loss in a hot environment and the fluid requirements necessary to support physiologic cooling. WEMTs need to know how to recognize and provide long-term care for victims of heatstroke, heat exhaustion, and dehydration. Lifting and Moving Patients "Use of Stokes litters and improvising litters" discusses the primary device for evacuation from the backcountry. Even when a helicopter is used, the victim is usually "packaged" in a litter before being loaded. WEMTs must know the specific techniques for victim packaging in a litter to protect and support injuries. Use of the proper carrying techniques and methods of belaying a litter up or down a steep slope are critical to the safety of everyone involved. Ambulance Operations "Helicopter-assisted rescues" describes the use of helicopters in backcountry rescue efforts and evacuation. WEMT training should address the dangers, hazards, and limitations of helicopters.
Suggested Readings American Academy of Orthopedic Surgeons: Emergency care and transportation of the sick and injured, ed 7, Sudbury, Mass, 1999, Jones & Bartlett. Auerbach P: Medicine for the outdoors, New York, 1999, The Lyons Press. Bowman W: Outdoor emergency care, ed 3, Lakewood, Colo, 1998, National Ski Patrol System. Forgey W, editor: Wilderness Medical Society: practice guidelines for wilderness emergency care , Merrillville, Ind, 1995, ICS Books. Henry M, Stapleton E: EMT prehospital care, ed 2, Philadelphia, 1997, WB Saunders. Houston C: Going higher, ed 4, Seattle, 1998, The Mountaineers Books. Iverson KV, editor: Position statements of the Wilderness Medical Society, Point Reyes Station, Calif, 1989, Wilderness Medical Society. Lindsay L et al: Wilderness first responder, wilderness and environmental medicine, Lawrence, Kan, 1999, Alliance Communications Group McSwain N et al: The basic EMT: comprehensive prehospital care, ed 1, St Louis, 1997, Mosby. Mistovich J et al: Prehospital emergency care and crisis intervention, ed 6, Upper Saddle River, NJ, 2000, Brady. Schimelpfenig T, Lindsey L: NOLS wilderness first aid, Lander, Wyo, 1991, National Outdoor Leadership School. US Department of Transportation, National Highway Traffic Safety Administration: Emergency medical technician-basic: national standard curriculum, ed 4, Washington, DC, 1994, US Government Printing Office. Wilkerson J, editor: Medicine for mountaineering, ed 4, Seattle, 1993, The Mountaineers Books. Williamson J, editor: Accidents in North American mountaineering, Golden, Colo, American Alpine Club, published yearly.
APPENDIX: Research, Standards, and Program Resources The following is a list of organizations and committees dedicated to some aspect of extended medical, rescue, and technical training. Many are also active in mountain, wilderness, marine, or disaster rescue and management efforts. American Alpine Club 710 Tenth Street, Suite 100 Golden, CO 80401 303-384-0110 Resource: Publishes The American Alpine Journal and annual Accidents in North American Mountaineering. Has committees dedicated to establishing and promoting standards in safety and education in mountaineering. American Mountain Guides Association 710 Tenth Street, Suite 101 Golden, CO 80401 Resource: Dedicated to establishing and maintaining standards for mountaineering and professional mountain guides. Publishes quarterly Mountain Bulletin. Appalachian Mountain Club P.O. Box 298 Gorham, NH 03581 603-466-2727 Resource: Active mountain rescue team that offers a variety of workshops on outdoor skills, environmental issues, and wilderness medical and rescue skills. Publishes quarterly Appalachia. Appalachian Search and Rescue Conference P.O. Box 440, Newcomb Station Charlottesville, VA 22904 804-674-2400 (emergencies only) Resource: Wilderness EMS agency, search and rescue, course and materials development. Center for Emergency Medicine of Western Pennsylvania 230 McKee Place, Suite 500 Pittsburgh, PA 15213-4904 Resource: Offers various wilderness EMT and wilderness command physician training courses. International Society for Mountain Medicine Clinique Generale de Sion 1950 Sion, Switzerland Resource: An international organization dedicated to research and education in mountaineering. Publishes quarterly The Newsletter of the ISMM. Mountain Rescue Association 5301 D North 33rd Drive Phoenix, AZ 85017-2802 Resource: National wilderness rescue organization dedicated to the development of standards and certification of mountain rescue teams. Nantahala Outdoor Center US 19 West, Box 41 Bryson City, NC 28713 704-488-2175 Resource: Offers a variety of courses on white-water rescue and wilderness medical and rescue training.
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National Association for Search and Rescue 4500 Southgate Place Suite 100 Chantilly, VA 20151 703-222-6277 Resource: National information resource for search and rescue, as well as certifications in various search functions. Publishes quarterly journal Response. National Cave Rescue Commission c/o National Speleological Society Cave Avenue Huntsville, AL 35810 205-852-1300 EMERGENCY: National Rescue Coordination 1-800-851-3051 Resource: Active national cave rescue team. National Ski Patrol System, Inc. Ski Patrol Building, Suite 100 133 South Van Gordon Lakewood, CO 80228 303-988-1111 Resource: Active rescue teams and ski patrols. Offers an outdoor emergency care course, various ski patrol certifications, avalanche training, and introductory mountaineering training. Stonehearth Open Learning Opportunities (SOLO) and North American Rescue Institute (NARI) P.O. Box 3150 Conway, NH 03818 603-447-6711 Resource: An international organization dedicated to developing and offering a variety of courses and certifications in wilderness and marine medicine, rescue, leadership, and outdoor skills. An active mountain rescue team. Publishes bimonthly Wilderness Medicine Newsletter. Union Internationale des Associations d'Alpinisme (UIAA) (International Union of Alpine Associations) President of the UIAA Medical Commission Bruno Durrer, MD Dokterhuus 3822 Lauterbrunnen Switzerland Resource: An international organization dedicated to the promotion of standards, safety, awareness, and education in mountaineering worldwide. Produces multiple
publications on mountain safety and medicine. United States Coast Guard Headquarters 2100 Second Street, SW Washington, DC 20593-0001 202-267-1012 (Boating Operations) Resource: Active national marine rescue military organization. Source of information and various boating-related certifications. Wilderness Medical Associates RFD 2, Box 890 Bryant Pond, ME 04219 207-665-2701, 800-742-2931 Resource: Offers a variety of courses and certifications in wilderness medical and rescue courses. Wilderness Medical Society P.O. Box 2463 Indianapolis, IN 46206 317-631-1745 Resource: A physician-based national wilderness medical organization with various committees dedicated to education in wilderness emergency medicine. Particular attention to education for physicians. Publishes quarterly newsletter and Wilderness and Environmental Medicine (formerly Journal of Wilderness Medicine). Wilderness Medicine Institute of the National Outdoor Leadership School 300 Tenth Street P.O. Box 9 Pitkin, CO 81254 303-641-3572 Resource: Offers a variety of courses and certifications in wilderness medicine and rescue.
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Chapter 25 - Search and Rescue Donald C. Cooper Patrick H. LaValla Robert C. Stoffel
As ever-increasing numbers of outdoor users turn to the wilderness for recreation, the medical community and search and rescue (SAR) organizations will contend with a growing number of lost, sick, and injured persons. Wilderness search, rescue, and medical intervention are unique in several ways. All aspects of SAR are enormously time consuming. Simply raising the alarm for someone lost or injured in an isolated area may take hours, days, or even weeks. Organizing a response, including obtaining equipment and transportation for responders, requires a variable amount of time, depending on the level of preparedness of the response organization. Finding, gaining access to, stabilizing, and transporting a victim to definitive care can be a lengthy process. Because it takes many persons to perform a wilderness rescue (six or eight persons are required to carry a litter 1 mile), logistic considerations such as food, shelter, and transportation for responders quickly create their own problems. SAR personnel are subjected to the same risks and environmental stresses that compromise victims. To obviate further tragedy, they must have a heightened awareness of potential danger, adverse conditions, and personal limitations. In addition to basic and advanced life-support training, rescuers must have extensive wilderness experience that combines practicality with creativity and resourcefulness. SAR personnel must have training in survival, improvisation, communications, leadership, navigation (e.g., map, compass, and global positioning system [GPS]), first aid, and specific SAR techniques. Many interventions, such as cardiopulmonary resuscitation, defibrillation, tube thoracostomy, tracheal intubation, and intravenous therapy, are difficult—if not impossible—in the wilderness setting. Examinations may be hampered by the bulky clothing necessary to keep the victim warm and dry. Medications and equipment are subject to rough handling and extremes of temperature, which may render them ineffective, unsterile, or inoperative (see Appendix at end of this book). Finally, decision making that optimizes patient care while not unduly risking the well-being of SAR personnel requires experienced leadership grounded in both common sense and technical skill. Perhaps the demands of SAR were best summarized by the wise rescuer who said that climbers, divers, hikers, and other outdoor enthusiasts get to choose where they practice their skills, but SAR personnel have no such choice. The situation, usually urgent, dictates where and when rescuers practice their art. The same situation that already compromised at least one person's health or well-being subsequently endangers the SAR participants. This chapter introduces medical professionals to the unique search, rescue, and medical problems encountered in wilderness, remote (including urban disaster environments), and backcountry situations. The rudiments of SAR coordination, resources, and specialized problems will be discussed. This information will help medical personnel understand how the SAR community works and provide an educational foundation to help prevent situations requiring undue risk, or SAR personnel themselves from having to be rescued.
SEARCH AND RESCUE: AN OVERVIEW SAR systems provide the response for overdue, lost, injured, or stranded persons, usually in connection with outdoor activities and environments. In the context of SAR, "wilderness" can take on several meanings. For instance, most consider wilderness to be regions that are uninhabited and uncultivated. Personnel may be called out to search a natural area such as a large park or desert, but it is equally likely that a search will be urban, in an area devastated by a natural disaster such as an earthquake or hurricane. Because the majority of the population in the United States resides in urban areas, emergency responders and SAR personnel are far more likely to encounter urban wilderness than a natural one. However, this chapter focuses on the nonurban setting. Types of SAR emergencies vary nationally, as do the responders. Programs, equipment, and personnel differ geographically in accordance with local needs and available resources. SAR can probably be best defined as "finding and aiding people in distress—relieving pain and suffering."[15] SAR often involves a great many volunteers and entails a multitude of skills. For example, the eruption of Mt. St. Helens, one of the nation's most catastrophic disasters, resulted in the largest peacetime SAR operation in the history of the United States. SAR operations can benefit comprehensive emergency management, providing a training ground and experience builder for disaster response capability at the most elementary level. The management concepts used in SAR operations establish foundation principles for providing response capability to large-scale emergencies and disasters. Nearly every type of hazard mentioned in comprehensive emergency management plans (local and state disaster coordination plans developed
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in all states) requires search and rescue.[14] Management of these SAR operations can range from directing the actions of a few responders in a small community hit by a minor earthquake to managing an effort involving thousands of searchers in a large urban calamity. Often, large situations involve several political subdivisions and coordination of air and ground resources. Local governments and other agencies that participate in SAR response must coordinate diverse multiskilled responders. In addition, many agencies that collectively support multiorganizational SAR responses operate under their own specific statutory authority. SAR operations entail a motivating time factor that focuses on a successful conclusion: finding or rescuing a lost subject before he or she succumbs to the effects of the environment, injuries, or a specific hazard. To be effective, extremely diverse organizations must be drawn together in a life-threatening situation with a commonality of purpose; this is even more true during a community-wide disaster. Search and Rescue in the United States National Search and Rescue Plan.
SAR involves many agencies and volunteers, and the federal government assumes some responsibilities for overall coordination, especially of federal or military resources requested by local or state agencies. The U.S. National SAR Plan[20] (website: www.uscg.mil/hq/g-o/g-opr/icSAR/nsp.htm) was first published in 1956 and identifies federal responsibilities in search and rescue. It is also the basis for the National Search and Rescue Manual, which discusses SAR organization, resources, methods, and techniques. The National SAR Plan is implemented and maintained by the National SAR Committee (NSARC), formerly the Interagency Committee on Search and Rescue (ICSAR), which includes representatives from each of the six signatory federal agencies (Departments of Transportation, Defense, Commerce, and the Interior; the National Aeronautics and Space Administration [NASA], and the Federal Communications Commission [FCC]). NSARC reviews SAR matters affecting all agencies, including recommendations by participating agencies for plan revision or amendment, and makes appropriate recommendations. It encourages federal, state, local, and private agencies to develop equipment and procedures that will enhance the national SAR capability and promote coordinated development of all national SAR resources. There are three geographic regions of jurisdiction identified in the National SAR Plan: 1. Inland area: Continental United States, except inland Alaska and waters under jurisdiction of the United States. 2. Maritime area: U.S. waters, Hawaii, specific areas off the west coast of Canada (south of Alaska), the high seas, and those commonwealths, territories, and possessions of the United States lying within the "Maritime area," which has two parts: the Atlantic and the Pacific. 3. Overseas area: Overseas unified command areas, inland Alaska, areas not included in Inland or Maritime regions. A "SAR coordinator" or agency responsible for SAR in the specific region administers each of the areas. The United States Air Force (USAF) is the coordinator for the Inland area, the United States Coast Guard (USCG) is responsible for the Maritime area, and the appropriate overseas unified command (and the Alaskan Air Command) tracks its respective areas in the Overseas area. Each SAR coordinator establishes agreements with military, civilian, state, local, and private agencies to ensure the fullest practical cooperation and utilization in SAR missions. SAR coordinators maintain files of these agreements and lists of the agencies and the locations of their SAR facilities. Although the federal government provides guidance, national policy protects the desires of state and local agencies to direct and control their own SAR resources. Therefore each state and local government is encouraged to assume SAR responsibility within its geographic boundaries and capabilities. The federal role is to coordinate federal agencies in support of those at the local and state levels to create a cooperative national SAR network. The USCG and USAF both operate rescue coordination centers (RCCs) in the United States, but each service takes a slightly different approach. The Air Force RCC (AFRCC) coordinates inland SAR activities in the continental United States but does not directly conduct SAR operations. In most situations, the Civil Air Patrol (CAP), state police, or local rescue services carry out the actual SAR operations. In contrast, the USCG not only coordinates but also conducts maritime SAR missions. U.S. Air Force Rescue Coordination Center.
Established in 1947 to meet the growing demand for SAR and its legislated responsibility, the original three AFRCCs have evolved into a single RCC located at Langley Air Force Base in Hampton, Virginia, under the Air Combat Command (ACC). The peacetime mission of the AFRCC is to build a coordinated SAR network, ensuring timely, effective lifesaving operations whenever and wherever needed. As of August 1996, the AFRCC recorded the prosecution of over 58,000 SAR missions, resulting in over 12,800 lives saved.[21] The AFRCC functions around the clock and is staffed by people trained and experienced in the coordination of SAR operations. The center is equipped with extensive audio and digital communications equipment and maintains a comprehensive resource file listing federal, state, local, and volunteer organizations
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that conduct or assist SAR efforts in the United States, Canada, and Mexico. There are four types of authorized AFRCC missions: search, rescue, MEDIVAC, and mercy. SEARCH.
Once a distress situation is determined to exist but a location is unknown, federal SAR forces may be activated to search for, locate, and relieve the distress situation.
The object of these searches may take the form of overdue aircraft, emergency locator transmitters (ELTs), hunters, hikers, or children. RESCUE.
A rescue mission entails the use of federal SAR forces to recover persons in distress whose location in a remote area is known, but who need assistance. This may be in the form of transportation to safety or to an adequate medical facility. These requests are normally received by the AFRCC from park-service personnel or the local law-enforcement authority. MEDIVAC.
The transportation by federal assets of persons from one medical facility to another is defined as aeromedical evacuation, or MEDIVAC. Requests are normally received from a local hospital when no commercial transportation is available, the person's life is in jeopardy, and time is critical. Each request is evaluated, and the decision to use federal resources is weighted heavily by the attending physician's medical opinions. MERCY.
A mission to transport blood, organs, serum, medical equipment or personnel to relieve a specific time-critical, life-threatening situation is referred to as a mercy mission. Requests are normally referred from a local hospital authority or, in come cases, the American Red Cross when commercial transportation is not available. Although the AFRCC will accept and act on initial notification from any person or agency, it will attempt to determine the urgency and the facts pertaining to the situation before obliging itself. Several aspects of the situation are considered before a mission is opened, including the following: 1. 2. 3. 4. 5.
Medical evaluation and urgency State agreement requirements Posse Comitatus Act Conflict of interest with commercial resources Resource availability
The medical condition of the victim or victims is the most important aspect of mission consideration. The AFRCC will only consider a request valid when there is an immediate threat to life, limb, or sight. A mission will only be started to prevent death or the aggravation of a serious injury or illness. The observations and opinions of a physician at the incident site weigh heavily on the decision to open a mission, and a flight surgeon is on call at the AFRCC when a local physician is unavailable. Each state has an agreement on file in the AFRCC describing the responsible agency and coordinating requirements for the various types of SAR missions. Each request for federal assistance is evaluated to ensure the requirements stipulated in the relevant agreement are met. Title 18 USC 1385 (the Posse Comitatus Act) prohibits military participation in civil law-enforcement activities. Although there are some exceptions to the prohibition, as a general rule, Department of Defense (DOD) forces, including the CAP, will be restricted from participating in searches in which the person being sought is evading searchers, is a fugitive, or when foul play is considered. On MEDIVAC or mercy missions in which the patient is not eligible for DOD medical benefits, federal assets cannot be used when commercial resources are available. Even when a patient is unable to pay or is destitute, commercial resources will be checked for availability and provided the opportunity to accept the mission before allocating federal resources. Although any SAR-capable asset belonging to the federal government may be requested, each resource is evaluated for distance from the distress location, special equipment requirements, urgency of the situation, and which resource can best accomplish the mission. Military forces may be called on to assist in civilian SAR missions. However, their participation in these activities must not interfere with their primary military mission. Once the decision has been made to use federal resources, a mission number is assigned and SAR forces are selected based on the geographic location and mission requirements. The Air Force coordinator will then work closely with the responsible agency in an attempt to provide the resources best suited to accomplish the mission. The AFRCC can be contacted as follows: Mailing address: AFRCC, 205 Dodd Blvd., Suite 101C, Langley AFB, VA 23665-2789 For mission use and SAR requests only: (800) 851-3051 Administration (Monday-Friday during duty hours): (757) 764-8117 Website: www.acc.af.mil/afrcc email:
[email protected] U.S. Coast Guard Rescue Coordination Centers.
The USCG is designated as the federal SAR coordinator for the Maritime area, which is divided into two areas: Atlantic and Pacific. These areas are divided into several districts, which are further divided into groups (several per district) and stations. A 24-hour alert status is maintained year round at all levels, and Coast Guard resources can be underway or airborne within minutes of notification of a SAR mission. At its headquarters, each area and district maintains a fully staffed operations center responsible for coordinating operations
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within that area or district on a 24-hour basis. When coordinating SAR missions, these operations centers are called "rescue coordination centers" (RCCs). Although minor SAR incidents are often resolved at the station or group level, the district or area assumes the duties of the SAR mission coordinator (SMC) in more complex or large-scale missions. The USCG is arguably involved in more SAR missions than any other organization or agency on the face of the earth. It is also notable that the USCG is a separate federal agency under the Department of Transportation, not the Department of Defense as is the Air Force. An important global service of the USCG is the Automated Mutual-Assistance Vessel Rescue (AMVER) system. AMVER involves ships, regardless of flag, voluntarily providing information about their capabilities (i.e., medical personnel on board, rescue equipment) and regularly reporting their location to a global computer system that tracks their whereabouts. When a situation arises that requires SAR capabilities, a surface picture (SURPIC) is produced that graphically shows the location of all AMVER participants in the vicinity. The RCC can use this information to select the best one or several ships to respond to the emergency, allowing all others to continue their voyages. Today approximately 12,000 ships from over 140 countries participate in AMVER, representing approximately 40% of the world's merchant fleet. An average of 2700 ships are on the AMVER plot each day, with over 1 million voyages tracked annually. The AMVER system has saved over 1500 lives since 1990.[22] A "preventive SAR" service provided by the USCG as a direct result of the Titanic disaster is the International Ice Patrol, whose operations are funded by SOLAS (Safety of Life at Sea) Convention signatories. Since 1913, the Ice Patrol has amassed an enviable safety record, with not a single reported loss of life or property caused by collision with an iceberg outside the advertised limits of all known ice in the vicinity of the Grand Banks. However, the potential for a catastrophe still exists, and the Ice Patrol continues its mission using high-tech sensors and computer models. The USCG also performs or coordinates the medical evacuation of seriously ill or injured persons from vessels at sea if the patient's condition warrants it and USCG
assets are within range. For less serious situations, USCG flight surgeons will offer medical advice via radio. On rare occasion, the RCC may coordinate with a U.S. Navy (USN) ship to allow a USCG MEDIVAC helicopter to refuel to extend its range. Also on rare occasion, the RCC may coordinate with the USAF to dispatch pararescue personnel to parachute to the vessel and stabilize the patient. In either case, these actions are taken only in the most serious situations where one or more lives depend on such drastic actions. If a vessel is reported overdue or unreported (i.e., failed to check in when expected), USCG assets may or may not launch immediately, depending on whether the overdue craft is thought to be in immediate danger. Regardless, an extensive investigative effort will be initiated immediately. During this investigation, a preliminary communications check (PRECOM) and extended communications check (EXCOM) will likely take place. These actually include more than just contacting intended destinations. They also include interviewing persons who may be knowledgeable about the craft and dispatching USCG vehicles and/or small boats to physically check harbors, marinas, launching ramps, and the like. In addition, an urgent all-ships broadcast is initiated requesting information on any recent or future sightings that might be the missing vessel, and EXCOMs are repeated on a regular basis. If none of these communications and investigation efforts produce positive results (i.e., locating the vessel and/or indications that the persons on board are not in immediate danger), a search will be undertaken. Search planning is conducted by the RCC staff, but additional assets can be requested from other agencies (i.e., USAF and USN) and/or foreign governments in a position to assist. With the assistance of the USCG's Computer Assisted Search Planning (CASP) system, the RCC develops scenarios based on the available information. These scenarios are then weighted according to a subjective estimate of how likely each one is to represent the true situation. The further analysis of available information leads to the development of probability maps (using CASP), after which a search is planned and orders are issued to all participating units. The search continues until either the survivors are found and rescued, or it is deemed that further searching would be fruitless. [6] Because SAR regions are not construed as boundaries to effective SAR action, and much of the Inland area borders on the Maritime area, coordination between the AFRCC and the USCG RCC is a daily occurrence. Missions that traverse both areas will be coordinated through the AFRCC or the appropriate USCG RCC. It is not unusual for the USCG to call on the AFRCC for a particular resource needed to prosecute a mission in the Maritime area, or conversely, the AFRCC to utilize a USCG resource in the Inland area. The USCG RCC can be contacted as follows: Mailing address: USCG Headquarters, Commandant (G-OPR), 2100 Second Street SW, Room 3106, Washington, DC 20593-0001 Phone: (202) 267-1943 Fax: (202) 267-4418 Website (RCC location and contact information): www.uscg.mil/hq/g-o/g-opr/contacts.htm
U.S. Mission Control Center.
The U.S. Mission Control Center (USMCC), located in Suitland, Maryland, is the U.S. operational component of a multiagency, multinational
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program that uses satellites to detect and accurately position emergency beacon signals from aircraft, vessels, and people in distress. This program is called the SAR Satellite-Aided Tracking (SARSAT) program, and the USMCC is one of 23 interconnected MCCs around the world that handle data distribution for the system. The National Oceanic and Atmospheric Administration (NOAA) operates Earth-observing satellites that are used to carry, among other things, SARSAT instruments that can detect and relay emergency signals from beacons activated by people in distress. These SARSAT payloads are provided by Canada and France, but Russia operates very similar instruments, known as COSPAS, aboard satellites that are part of a navigation system. The USMCC is administered by the SARSAT Operations Division of NOAA, which also represents U.S. interests in international COSPAS-SARSAT meetings. The USMCC is staffed 24 hours a day, 365 days a year. However, the vast majority of alert data distribution is handled automatically. Together, the COSPAS-SARSAT system is being used in an international cooperative SAR effort in which the objective is to help save the lives of aviators, mariners, or anyone in distress who activates an emergency beacon. Aircraft carry ELT beacons that are normally triggered by the impact of a crash. Ships carry floating Emergency Position-Indicating Radio Beacons (EPIRBs) that are activated by immersion in water. Both devices can also be activated manually. These devices transmit on a radio frequency of 121.5 Megahertz (MHz) and/or 406.025 MHz. Using Doppler processing techniques, a beacon transmitting on the 121.5-MHz frequency can be located with an accuracy of about 10 to 25 km (5 to 12 miles) and may take as long as several hours to confirm. Alternatively, a beacon alerting on the 406 MHz frequency can be located within an accuracy of about 2 to 5 km (1 to 3 miles) and is usually confirmed in a matter of minutes. In addition, the 406-MHz devices have the capability of transmitting a unique identifier for which the MCCs maintain registration information about the owner of the device if the beacon was previously registered. In the near future, some 406-MHz devices will be coupled with electronic navigational receivers (such as GPS units) and will be able to provide both immediate alerting and accurate position information. The COSPAS-SARSAT system consists of a network of satellites, ground stations, MCCs, and RCCs. When an emergency beacon is activated, the signal is received by a satellite and relayed to the nearest available ground station. The ground station, called a Local User Terminal (LUT), processes the signal and calculates the position from which it originated. Once calculated, this position is transmitted to an MCC, where it is joined with identification data and other information on that beacon, if such information is available. The MCC then transmits an alert message to the appropriate RCC based on the geographic location of the beacon. If the location of the beacon is in another country's service area, the alert is transmitted to that country's MCC. Before the inception of COSPAS-SARSAT, monitoring of ELTs depended largely on airborne aircraft or aviation ground facilities. This method provided irregular coverage, particularly in remote regions. Rapid location by satellite significantly reduces SAR time, improves survival chances for accident victims, and reduces exposure of SAR teams to hazardous conditions often encountered during their missions. Federal Aviation Administration.
The Federal Aviation Administration (FAA), through its Air Route Traffic Control Centers (ARTCCs) and Flight Service Stations (FSSs), monitors and flight-follows aircraft filing flight plans in the inland area. In some cases, individual citizens contact an FAA facility when they have knowledge of a probable SAR situation involving aircraft. Therefore the FAA is usually the first agency to alert the AFRCC of a distressed or overdue aircraft. The AFRCC is tied directly into the FAA's computer network, and FAA facilities use this system to alert the AFRCC. Once the AFRCC is alerted, the FAA and AFRCC work together to determine the urgency of the situation and locate the aircraft. Initially, radio communications are reviewed to determine the last known location of the distressed aircraft. Concurrently, other FAA facilities begin a check of all possible airports where the aircraft might have landed. In the meantime, the AFRCC contacts relatives, friends, and business associates of the pilot or passengers aboard the missing aircraft, with the hope of establishing the whereabouts of the aircraft, or to gather information about the personnel aboard. Through these contacts, the AFRCC determines the pilot's intentions, flying capabilities, emergency equipment aboard, and other pertinent information that would assist if a search becomes necessary. Through experience, the FAA and AFRCC have learned that the majority of alerts for missing aircraft are due to the pilot failing to either close the flight plan or inform some person or agency of his or her intentions. For this reason, only a small percentage of alerts issued by the FAA result in an actual airborne search for a missing aircraft. All ARTCCs have the capability to recall recorded radar data. The National Track Analysis Program (NTAP) can identify and track targets that are at a sufficient altitude to be tracked by radar regardless of whether they are being controlled by the ARTCC. NTAPs requested by the AFRCC have been proven to be a key ingredient in aircraft searches, providing the route of flight and last radar position. With the congressional mandate requiring most aircraft to be equipped with an ELT, the FAA works very closely with the USMCC and the AFRCC to readily locate the source of ELT signals. All ELT signals reported to
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FAA facilities are immediately forwarded to the AFRCC and jointly investigated as probable distress signals. Civil Air Patrol.
In 1948 the CAP was permanently chartered by the U.S. Congress as the official auxiliary of the USAF. As such, this nonprofit organization of volunteers was charged with three primary missions: the development of aviation through aerospace education, a cadet youth program, and emergency services. Under their emergency services mission, the CAP provides SAR mission coordinators, search aircraft, ground teams, personnel on alert status, and an extensive communications network to emergency response efforts. Further, they provide services to national relief organizations during a disaster; the transportation of time-sensitive medical materials (e.g., blood and human tissue); and aerial reconnaissance, airborne communications support, and airlift of law-enforcement personnel in the national counter-drug effort. When CAP resources are engaged in a SAR mission, they are reimbursed by the USAF for communications expenses, fuel and oil, and a share of aircraft maintenance expenses. In addition, CAP members are covered by the Federal Worker's Compensation Act in the event of an injury while participating in a SAR mission. The CAP is the AFRCC's prime air resource for the inland area. The AFRCC maintains an alert roster provided by CAP wings in each of the 48 contiguous states and is the central point of contact for CAP participation in SAR missions. The AFRCC also works closely with CAP national headquarters and directly provides input for CAP training in emergency services. The CAP can be contacted as follows: National HQ Civil Air Patrol, 105 South Hansell Street, Bldg. 714, Maxwell AFB, AL 36112-6332 Unit Locator: (800)-FLY-2338 Membership Development: (334) 953-4260 Public Affairs: (334) 953-4287
U.S. Coast Guard Auxiliary.
The U.S. Coast Guard Auxiliary is to the USCG as the CAP is to the USAF. The auxiliary is made up of citizens who volunteer their time and boats or aircraft to enhance and maintain the safety of boaters. The passage of the Auxiliary and Reserve Act of 1941 designated that civilian volunteers of the USCG be referred to as auxiliary. When America entered World War II, some 50,000 auxiliary members joined the war effort. After the war, their attention returned to recreational boating safety duties in compliance with the auxiliary's four cornerstones: vessel examination, education, operations, and fellowship. Today, as in 1941, auxiliarists are civilian volunteers whose activities are directed by policies established by the commandant of the USCG. Although under the authority of the commandant, the auxiliary is internally autonomous, operating on four organizational levels (smallest to largest): flotilla, division, district regions, and national. When auxiliary resources are engaged under USCG "orders," they are reimbursed by the USCG for communications expenses, fuel and oil, and a share of vessel/aircraft maintenance expenses. In addition, auxiliary members are covered by the Federal Worker's Compensation Act in the event of an injury while participating in an authorized mission. Many members of the auxiliary spend their weekends providing free boating safety courses to the public and free courtesy safety inspections to boaters. However, members also respond to minor SAR incidents, and the local USCG station, group or district RCC coordinates their activities. Some auxiliarists have also become qualified to work in the RCCs or assist regular USCG facilities with regulating and patrolling regattas and other maritime events.[23] With its 33,000 members, the auxiliary saved nearly 500 lives in 1998 alone, in addition to assisting over 12,000 persons, performing over 139,000 courtesy marine exams, teaching over 6000 public and youth classes, and assisting the USCG in over 50,000 administrative and operational missions.[22] The USCG auxiliary website URL is: www.cgaux.org/cgauxweb/ Disaster Response in the United States.
The Robert T. Stafford Disaster Relief and Emergency Assistance Act (1988) provides the authority for the U.S. federal government to respond to disasters and emergencies to provide assistance to save lives and protect public health, safety, and property. The Federal Response Plan (FRP; available at www.fema.gov/r-n-r/frp/) was designed to address the consequences of any disaster or emergency situation in which there is a need for federal response assistance under authority of this legislation. The purpose of the FRP is to facilitate the delivery of all types of federal response assistance to states to help them deal with the consequences of significant disasters. The FRP outlines the planning assumptions, policies, concept of operations, organizational structures, and specific assignments of responsibility to the departments and agencies in providing federal response assistance to supplement the state and local efforts. It is applicable to natural disasters such as earthquakes, hurricanes, typhoons, tornadoes, and volcanic eruptions; technologic emergencies involving radiologic or hazardous material releases; and other incidents requiring federal assistance under the Stafford Act.[4] To facilitate federal assistance, the FRP breaks federal response into 12 functions called emergency support functions or ESFs. Each ESF is coordinated by a primary federal agency and assisted by multiple support agencies. FEMA serves as the lead agency for ESF-9 (Urban SAR, or US&R or USAR) and, as such, coordinates the
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National Urban SAR Response System. This system is a framework for structuring local emergency services personnel into integrated disaster-response task forces. These task forces, replete with the necessary tools and equipment and requisite skills and techniques, can be deployed by FEMA for the rescue of victims of disaster and structural collapse. Currently, there are 27 FEMA US&R task forces spread throughout the continental United States trained and equipped to handle structural collapse rescue. They encompass local emergency service personnel from 18 states and can be deployed by FEMA to a major area disaster. Two task forces have also responded to several international disasters under the auspices of the U.S. Agency for International Development, Office of Foreign Disaster Assistance. Each FEMA US&R task force contains 62 specialists, is designed to be self-sufficient for the first 72 hours of operation, and must be able to function for up to 10 days before being replaced. By design, there are two task-force members assigned to each position for the rotation and relief of personnel. This allows for round-the-clock task-force operations. In addition, all task-force members must be sufficiently cross-trained in their SAR skill areas to ensure depth of capability and integrated task-force operations. After a request for federal assistance from a governor is received and approved by the president, task forces may be activated or placed on alert when a major disaster threatens or strikes a community or region. There are three regions: East, West and Central. Upon activation, alerted task forces start locating personnel and organizing their mobilization. Each task force is tasked with having all its personnel and equipment at the embarkment point within 6 hours of activation (the mobilization window). Depending on the location of the disaster, a task force will respond to the scene either by ground, using its own trucks, or via a military or civilian aircraft. Generally, an operational task force can be heading to its destination in a matter of hours. When the task forces are not on a FEMA-requested response, they function as technical rescue teams in their own communities and, in many cases, provide a regional or state-wide urban SAR capability. A FEMA US&R task force includes four major functional elements: 1. 2. 3. 4.
Search: Canine, electronic, and physical capabilities to locate trapped victims. Rescue: Evaluate compromised areas, structural stabilization, breaching, site exploration, live-victim retrieval. Medical: Minimize health and safety risks, treat both task-force team members and trapped victims, provide critical incident stress debriefing. Technical: Provide hazardous materials specialists, structural engineers, heavy rigging, communications specialists, and logistics specialists.
Typically, FEMA US&R task forces conduct the following operations: • Perform physical SAR operations in damaged or collapsed structures • Provide emergency medical care to task-force personnel, entrapped victims, and search canines • Conduct reconnaissance to assess damage and needs and provide feedback to local, state, and federal officials • Assess and/or shut off utilities to damaged buildings • Conduct hazardous materials survey or evaluation • Conduct structural/hazard evaluations of buildings needed for immediate occupancy to support disaster-relief operations • Stabilize damaged structures, including shoring and cribbing operations A comprehensive equipment cache totaling 58,000 pounds supports each task force. The cache elements sent to the disaster scene include communications and locating equipment, rope, and materials for rigging, hauling, lifting, and pulling. In addition, devices to facilitate shoring, structural movement sensing, victim extrication, cutting, and drilling are included to address a wide variety of potential SAR challenges. The medical team includes four medical specialists and two physicians. Many of the medical specialists on US&R teams are both paramedics and firefighters and thus have experience in both rescue and prehospital medical care. Most of the physicians involved in US&R are emergency medicine specialists who have attended additional training in confined-space medicine, crush syndrome, hazardous materials, public health issues relevant to disaster management, and other issues important to the function of a US&R team. The medical team is designed to bring the emergency department to the field and carries all of the advanced life-support equipment available in any advanced life-support (ALS) ambulance. The State's Role: Coordination and Support.
All states have passed legislation that provides for direct support to local government entities during emergencies or life-threatening situations, and most states have a specific agency responsible for overall coordination and support for local SAR problems. This support can take many forms, but most often it is in the area of coordination and "one-stop shopping" for resources. Each state must establish an agency or central location that is familiar with all aspects of emergency management and the resources available to aid in life-threatening situations. Many of these resources belong to the state and can be used to aid local jurisdictions. A number of states, especially in the Northwest, have designated a state agency to be responsible for directing and coordinating air SAR activities. These state
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departments, or divisions of aeronautics, develop and maintain aviation SAR response programs with cooperation and support from local and federal agencies. Experience shows that this system usually works better than those in other areas of the country that rely on the federal government to initiate and carry out aircraft SAR activities. If a local emergency manager, sheriff, or fire chief requests outside assistance in the form of specialized teams, search dogs, air support, or enhanced communications, the state agency for civil defense, emergency services, or emergency management can in most cases locate the nearest resources available and coordinate the response. If any federal resources are needed, such as air support or military personnel, the state agency provides a direct link to that resource. For instance, the AFRCC at Langley Air Force Base in Virginia has working agreements with all states that are updated annually. Technically, the resources of local and state governments must have been exhausted or be unable to perform a task before federal support can be rendered. However, policy provides for immediate aid when time is critical and in life-or-death situations. Much discretion is given to military installation commanders regarding aid to civilian authorities as long as the primary (military) mission of the resource is not impaired. In fact, most commanders appreciate the opportunity to fly actual missions. Access to these resources must be gained through the state and the AFRCC. Every state's emergency management agency is responsible for providing support, guidance, training, and coordination to local political subdivisions within that state. As such, it produces a vital behind-the-scenes effort to help local jurisdictions prepare for emergencies, including SAR. The state also initiates the laws necessary to enhance effective actions for SAR response. Such legislation often indemnifies volunteer SAR teams, provides their medical coverage and insurance, and in some cases replaces personal property lost during SAR work. Although most volunteers work willingly until the job is done, this recognition and coverage by the state often provide additional incentives for volunteer participation. Local Response.
The official response to the call for a wilderness SAR situation is usually delegated to a political subdivision within the state. The legal responsibility for SAR is generally vested with the county sheriff or chief law-enforcement officer at the local level, but this varies by region and state. In some cases it is the responsibility of state police agencies, and in others it belongs to land management agencies. The SAR response for one jurisdiction may differ greatly from that of another. For instance, many national parks in some areas of the country handle all of their own SAR incidents. Others jointly manage the function, whereas some rely entirely on outside resources. National forest land is managed solely by forest-service personnel, but when it comes to SAR, the forest service usually only supports the functions of the local responders. In urban and suburban areas, police officers, firefighters, emergency medical technicians, and civil defense emergency organizations maintain some degree of disaster and emergency readiness through daily missions that involve SAR work. Fire departments have historically been responsible for rescue and response to emergencies within certain geographic or political areas, and volunteers augment many departments. Law-enforcement agencies also maintain full-time, efficient response systems designed for their particular SAR requirements. Ambulance and rescue vehicles operated by a variety of private enterprises and volunteer organizations augment existing local government services. Through local emergency response planning and coordination, these services respond to a spectrum of everyday emergencies, including fires, collapsed buildings, hazardous material spills, vehicle extrications, and home medical emergencies. County sheriffs, reserve law enforcement, volunteer fire departments, and a variety of volunteer and rescue units have been established to address local SAR problems. Delivery of SAR aid to rural and wilderness areas often presents many special logistic problems, which may be compounded by distance, terrain, and weather. The demand for wilderness SAR is often seasonal and unpredictable. Volunteer mountain rescue units, Explorer SAR groups, SAR dog teams, CAP squadrons, motorized units, and many types of volunteer composite teams (i.e., teams that have a variety of capabilities) are usually formed locally in response to the type and nature of recurring SAR problems. Regardless of who does it or what type of SAR emergencies occur, local resources and effort must be developed because they are closest to the problem. State and federal resources are subject to problems with time lag, distance, weather, logistics, and bureaucracy. The same storm or disaster that incapacitates a local area may also prohibit outside (and sometimes inside) emergency response and resupply. Although official agency responses differ greatly around the country, one major factor remains constant—the dedicated and unfailing willingness of volunteers to respond and work until the job is done. The volunteer effort in SAR nationwide is the backbone of aid to people in distress, as is stated in the rescue service motto: "These Things We Do That Others May Live." The volunteer response has proved crucial to wilderness-type situations. Volunteer organizations, communications, and special skills cannot be replaced by any "official agency" resources.
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ORGANIZATION OF A SEARCH AND RESCUE EVENT SAR requires people who take action and meet objectives to achieve a common goal, often with one or more lives in the balance. For any combination of actions to be effective in a particular situation, the enterprise must be systematically coordinated and organized. All participants must know their responsibilities, what is expected of them, who is in charge, and to whom they answer. If this knowledge is lacking, the effort can quickly become chaotic, ineffective, and, very probably, dangerous. Nowhere are these issues more important than in an emergency situation in which time is of the essence. Emergency response research is clear and specific. The four operational problems that continue to arise during emergency responses in the United States are ambiguity of authority, inability to communicate between agencies, poor use (or no use) of specialized resources, and unplanned negative interactions with the news media.[14] [15] Accordingly, the key elements for success in SAR operations continue to be good coordination of resources (the right people and equipment in the
Figure 25-1 Functional hierarchy of the Incident Command System commonly used in SAR in the United States. (From Cooper DC, LaValla PH, Stoffel RC: SAR fundamentals: basic skills and knowledge to perform search and rescue, ed 3 (rev), Cuyahoga Falls, Ohio, 1996, National Rescue Consultants.)
right place at the right time), effective communications, and good management practices with trained leaders.[14] Incident Command System The system designed to address the challenges of managing emergency incidents in the United States, including SAR, is called the Incident Command System (ICS). It has been in use in the United States for many years.[17] This function-based system was designed to be adaptable to various types and sizes of incidents in a proactive, rather than a reactive, manner. The system groups similar tasks into five functional areas: command, operations, planning, logistics, and finance/administration. Each of these functions is performed at every incident to one degree or another, and all can easily be expanded as the size and complexity of the situation dictate. This expansion, however, is based on the premise that the span of control (the ratio of the subordinates to each supervisor) should never exceed seven to one and should more commonly be five to one. When this is exceeded, another level is added to the hierarchy to maintain an acceptable span of control ( Figure 25-1 ). The command section is led by the incident commander and provides overall management of the organization.
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Within ICS, the command section is responsible for dealing with other agencies (liaison officer), the news media and other external influences (information officer), and for the overall safety of the operation and its participants (safety officer). If the incident is too small for these functions to be performed by separate individuals, the incident commander performs them. The operations section is led by the operations section chief, who is responsible for coordinating and performing all tactical operations. This role is commonly performed by the incident commander until the incident becomes large and complex enough that the function must be performed by another individual. When multiple casualties are involved in an incident, their triage, treatment, and transport fall under the purview of the operations section. In such an incident the operations section is divided into functional groups, often including at least triage, treatment, and transport groups. The person in charge of managing and coordinating the efforts of each group is called the group supervisor. If the operations section is better divided using geography, a division rather than a group is formed. For instance, injured persons at an auto accident might be found on two sides of a road. An east division and a west division might be established to deal with the geographic separation of the resources. In a small organization, the supervisor of each division would answer directly to the operations chief. To respond to specific challenges within an incident, a task force or strike team might be formed. A task force is any combination of single resources assembled for a particular tactical need, with common communications and a leader. For instance, FEMA combines search, rescue, and medical resources to form a US&R Task Force. A strike team, on the other hand, is a combination of a designated number of the same kind and type of resources with common communications and a leader. The number of resources used in the team will be based on what is needed to perform the function. For instance, four three-person hasty search teams may be combined to form a strike team. These two combinations of resources permit the necessary flexibility when allocating resources. The planning section is led by the planning section chief, who is responsible for collecting, evaluating, and distributing all incident information. As with the other sections, the incident commander performs this function unless the size and complexity of the incident dictate otherwise. In SAR the planning section is particularly important because it evaluates search evidence and determines, based on what has been learned, what future actions should be taken or how current actions should be modified. Because such interpretation and evaluation often require great technical knowledge, personnel such as hazardous materials specialists, physicians, structural engineers, and other technical specialists may be required to help the planning section develop and revise the incident action plan. The logistics section is led by the logistics section chief, who is responsible for providing personnel, equipment, and supplies for the entire incident. This awesome task involves ensuring that personnel are available, rested, and fed; that all equipment, including communications equipment, is available and operable; that vehicles are fueled and repaired; and that medical care is provided for all incident personnel. Basically, logistics is charged with seeing that the physical tools required to meet the overall objectives are available, operable, and maintained. If the size and complexity of the incident prevent the incident commander from monitoring finance and administrative issues, the finance/administration section is led by the finance/administration section chief. This section is responsible for tracking all financial data for the incident, such as personnel hours, resource costs, costs for damage survey, and injury claims and compensation. Because most agencies involved in SAR can handle financial issues on their own, and most incidents are small and of short duration, the incident commander usually performs the functions of this section. Only in the largest or most complex incidents is it necessary for the incident commander to assign an individual or staff to perform finance section duties.
FOUR PHASES OF A SEARCH AND RESCUE EVENT: THE INCIDENT CYCLE Every SAR event goes through four consecutive phases: locate, access, stabilize, and transport.[2] This sequence, however, could more accurately be described as a continuum that begins with planning or preplanning for the incident. Because planning for the next incident should be affected by what happened during the last, the incident cycle is actually continuous and only pauses between incidents. Once first notice of an incident has been received and the locate phase begins, the goal is to progress through the access, stabilize, and transport phases as quickly, safely, and efficiently as possible. Planning between incidents allows decisions to be made in a calm environment without the urgency that often accompanies a SAR operation. Such plans identify who will be in charge, the organization of the operation, specific procedures, viable alternatives, and other decisions that are best made before an incident occurs ( Figure 25-2 ). Locate Phase The first step in addressing any emergency situation is locating the subject or subjects in need of assistance. This may be as simple as asking for an address or as
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Figure 25-2 The time-specific components of a SAR event vary with the type of incident. Note that all components take place in both incidents but require different amounts of time. A, Typical rescue operation. B, Typical search operation.
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complex as conducting an extended search for a lost person or persons. If the subject is easily found, rescuers can quickly move into the access phase. However, if locating the subject is difficult, this phase may turn into the crux of the SAR problem. First Notice.
The first notice of an incident is often conveyed by relatives who report an injury or missing person, by a witness to an incident, by a government agency reporting distress signals (such as an ELT), by bystanders who perceive a problem, or by a 911 call. Once the initial notice is received, the individual taking the information must know what to do and whom to call next. Planning Data and Its Uses.
Information gathered at the onset of an incident begins an ongoing investigation. It is used to determine the appropriate response and to help predict how the subject or subjects might react to the situation. This information is called planning data and includes any information that might affect what should be done to resolve the situation. Examples of planning data include the name of the subject, the situation that caused the problem, the last known location of the subject, the subject's physical and mental condition, the subject's plans (where was he or she going?), what resources are available, weather information (present and predicted), geographic information, and the history of similar incidents in the area. The purpose of collecting all of this information is to help decide what to do next while predicting what the subject might do to help or hinder the situation. The investigation and gathering of information continue throughout the incident and are used to modify initial plans. As new information is acquired, an action plan is developed and revised until the end of the incident cycle, when planning for the next incident commences. Once information is gathered, the urgency of the situation is assessed. This assessment ultimately determines the speed, level, and nature of any response and may indicate whether a nonurgent or an emergency response is needed. The specific information used in urgency determination includes the age and condition of the subject, current and predicted weather, and relevant hazards. Figure 25-3 is an Urgency Determination Form, which can be used by SAR managers to determine how urgent their response should be.[15] Urgency also contributes to allowable risks and thus influences searcher safety—a primary consideration for search managers. Search Tactics.
During the initial "locate" phase of the incident, emphasis is on searching for the subject. Exactly how to accomplish this is a priority, especially if this part of the incident cycle is expected to be a problem. SAR managers first initiate techniques that increase the chances of locating the subject in the shortest time. These techniques are generally termed tactics and involve some action performed to find the subject. These actions can be passive (e.g., not requiring actual field searching) or active (requiring deployment of searchers in the field). Examples of passive tactics include confining the search area to limit movement of the subject and others into and out of the area, identifying and protecting the point last seen (PLS) or the last known position (LKP), and attracting the subject, if he or she is expected to be responsive. Generally, passive techniques are quicker and easier to apply, so they are started first. As the incident progresses, active tactics are initiated. In SAR management, efforts are almost universally made to apply quick response resources in areas likely to offer early success. The best resources are put in the most likely areas as early as possible. In addition, identifying and protecting the PLS or LKP are crucial passive techniques that can mean the difference between success and failure of the entire effort.[15] Active techniques include sending teams of searchers into an area to search for clues or the subject. They are categorized by level of thoroughness. For instance, a fast, relatively nonthorough search of high-probability areas is called a type I search ( Table 25-1 ). Type II techniques can be applied when relatively rapid searches of large areas are desired. Thoroughness may increase, but more important, efficiency improves because larger areas can be searched with the same or fewer resources. Thus success is achieved sooner. Type III techniques are applied only when the absolute highest level of thoroughness is required. Unfortunately, this is almost always at the expense of time and efficiency. Basically, the greater the thoroughness, the more resource-intensive and time consuming the technique. Clues and Their Value.
Clues are discovered during the investigative and tactical phases of a search. Their importance cannot be overemphasized. They may take the form of physical evidence such as a footprint or discarded item, an account by a witness, or information gleaned from the investigation. Clues serve as the rudder that steers the overall search operation. Relevant clues are the basis for all search strategy and can determine or modify all actions. Their powerful influence should be obvious; this is why searchers are taught to be "clue conscious" and to seek clues, not just subjects. There are many more clues than there are subjects. People generate clues. A person exudes scent, takes up space, and, when traveling, leaves evidence of passing. This evidence is often discoverable if the appropriate resource is applied in a coordinated, organized
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Figure 25-3 Urgency Determination Form.
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TYPE I
TABLE 25-1 -- Summary of Active Search Tactics TYPE II
TYPE III
Criterion
Speed
Efficiency
Thoroughness
Objective
Quickly search high-probability areas and gain information on search area
Rapid search of large areas
Search with absolute highest probability of detection
Definition
Fast initial response of well-trained, Relatively fast, systematic search of high-probability self-sufficient, and very mobile searchers, segments of the search area that produce high results who check areas most likely to produce clues per searcher hour of effort or the subject the soonest
Slow, highly systematic search using the most thorough techniques to provide the highest possible probability of detection
Considerations
Works best with responsive subject; offers immediate show of effort; helps define search area; clue consciousness is critical; planning is crucial for effective use; often determines where not to search
Often employed after hasty searches, especially if clues were found; best suited to responsive subjects; often effective at finding clues; between- searcher spacing depends on terrain and visibility
Marking search segment is very important; should be used only as a last resort; very destructive of clues; used when other methods of searching are unsuccessful
Techniques
Investigation (personal physical effort); check last known position for clues; follow known route; run trails and ridges; check area perimeter, confine area; check hazards and attractions
Open grid line search with wide between-searcher spacing; compass bearings or specific guides are often used to control search; often applied in a defined area to follow up a discovered clue; no overlap in area coverage; critical separation; sound sweeps
Closed grid or sweep search with small between-searcher spacing; searched areas often overlap adjacent teams for better coverage
Usual team makeup
Two or three very mobile, well-trained, self-sufficient searchers
May include three to seven skilled searchers, but usually just three
Four to seven searchers, including both trained and untrained personnel
Most effective resource
Investigators, trained hasty teams, human trackers, dogs, aircraft, any mobile trained resource
Clue-conscious search teams, human trackers and sign-cutters, dogs, aircraft, trained grid search teams
Trained grid search teams
search effort. Searchers must be sophisticated enough to discover this evidence and interpret its meaning before it is destroyed or decays. Because evidence important to a search effort is often easily destroyed once it is discovered, it is important to protect it from damage until it is completely analyzed. Search Resources.
Resources are defined as all personnel and equipment available, or potentially available, for assignment to incident tasks. Specific types of active tactics are categorized by the resource that performs them, such as dog teams, human trackers, ground search teams, and aircraft. Other common resources include management teams (e.g., overhead teams, public information officers), water-trained responders (e.g., river rescue, divers), cold weather responders (e.g., ice climbers, avalanche experts, ski patrollers), specialized vehicle responders (e.g., snowmobiles, four-wheel-drive trucks, all-terrain vehicles, mountain bikes, horses), and technical experts (e.g., communications experts, interviewers, chemists, rock climbers, physicians, cavers). In addition to these, other less common resources might also be available. These could include attraction devices (such as horns, flags, lights, sirens), mine detectors (military), noise-sensitive equipment (super microphones), infrared devices (forward-looking infrared [FLIR] on aircraft, night-vision equipment, thermal imagers), thermistors, and even witches, seers, prophets, and diviners. Just about any person or thing imaginable may be available for use in a SAR incident. Their use is limited only by the creativity of those in charge. Here we discuss a few of the most common. DOGS.
Dog teams are a common type of active search resource in the wilderness and are composed of a dog (occasionally more than one) and a human handler. The dog uses scent to search for and follow a subject while the handler interprets signals from the dog and searches visually for evidence. Three common categories are tracking, trailing, and air-scenting dogs.
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Tracking dogs follow scent on the ground from a person's footsteps and usually very closely follow the trail where a person traveled, regardless of the wind. Trailing dogs follow scent that has fallen onto the ground from the subject along the route of travel. Unlike the tracking dog, the trailing dog may follow the scent at some distance from the actual tracks of the subject, and may therefore be more affected by wind. Tracking and trailing dogs are most effective when used in areas that have not been contaminated by humans other than the subject. Also, weather and time tend to destroy scent available to these types of dogs, so the earlier they are used in a search, the better their chances of finding something. Air-scenting dogs work off-lead to follow a subject's scent to its source. Specifically bred and trained air-scenting dogs can even discriminate between individual humans. They may detect scent from articles of clothing and can often follow it to discover a person buried in rubble or snow or even submerged under water. Wind is very important to this type of dog, as are other environmental forces such as sun and rain. But as long as the source exists, an air-scenting dog can usually detect the scent carried in air currents and follow it to the source. HUMAN TRACKERS.
Human trackers use their visual senses to search for evidence left by a person's passing. Human trackers "cut" or look for "sign" or discoverable evidence by examining the area where the subject probably would have passed. This process of looking for the first piece of evidence from which to track is called "sign cutting." Following the subsequent chain or chronology of sign is called "tracking." [3] In SAR, most trackers use a stride-based approach called the step-by-step method. This simple, methodical approach emphasizes finding every piece of possible evidence left by a subject. However, its most important role is undoubtedly the ability to quickly determine the direction of travel of the subject and thus limit the search area. Ground Search Teams
Hasty teams.
A hasty team is an initial response team of well-trained, self-sufficient, highly mobile searchers whose primary responsibility is to check out the areas most likely to first produce the subject or clues (e.g., trails, roads, road heads, campsites, lakes, clearings, and so on). Their efficiency and usefulness are based on how quickly they can respond and the accuracy of initial information. Ideally, hasty teams should include two or three individuals who are knowledgeable about tracking. They should be clue oriented, familiar with the local terrain and dangers in the area, and completely self-sufficient. Also necessary are the ability to skillfully interview witnesses and to use navigational skills with pinpoint accuracy. Team members should be trained at least in advanced first aid. Hasty teams usually operate under standard operating procedures so they do not have to wait for specific instructions. They carry all of the equipment they might need to help themselves and the lost subject for at least 24 hours. Grid teams.
Grid searchers use a more systematic approach to searching. They usually examine a well-defined, usually small segment to discover evidence ( Figure 25-4 ). The classic approach to grid searching involves several individuals (almost always too many) standing in a line, shoulder to shoulder, walking through an area in search of either evidence or subjects. The distance between searchers can be varied to change thoroughness and efficiency (wide spacing is less thorough and more efficient). However, such resource-intensive approaches to searching are generally less preferred than those that use fewer personnel in a more efficient manner (such as tracking, dogs, or aircraft). In addition, close-spaced grid searching tends to damage evidence and is generally difficult to coordinate. Although grid searching may be an acceptable approach in certain limited circumstances, experience has shown that when the subject of a search is a person, searching in this thorough manner should be used only as a last resort. Experiments involving grid searching have suggested that it is better to place searchers farther apart. This is usually a more efficient use of resources. AIRCRAFT.
Aircraft serve the same purpose as grid searchers, only from a greater distance, at a greater speed, over a larger area, and usually with a lower level of thoroughness. Within a search effort, aircraft can serve both as a tactical tool to look for clues and as transportation for personnel and equipment. Both
Figure 25-4 Map used to brief ground team. (Photo courtesy Spectra Communications, Inc.)
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fixed- and rotor-wing aircraft have their place in SAR and, like other resources, have their advantages and limitations. Among the most obvious limitations are the expense and complex use requirements of aircraft. Aircraft not only require specialized personnel and cost a great deal to operate, they also have very strict weather and environmental restrictions. For instance, it would be difficult to search from an aircraft in a snowstorm, and terrain may prevent searching certain areas from the air. However, most of these difficulties can be adequately addressed and minimized in a well-developed preplan. Search Planning and Management Considerations.
State-of-the-art searching for lost persons has come a long way from the familiar lining up of volunteers shoulder to shoulder and walking in a straight line to search an area. Many new lifesaving concepts have been developed by the national SAR community. By borrowing from psychology, mathematics, and business and analyzing research on past incidents, search management has evolved into a sophisticated science. By studying human behavior, statistics, probabilities, leadership, and management, search managers have been able to improve search effectiveness and efficiency. [15] Search management is determined by two general considerations: where am I going to look for the lost person? (strategy) and how am I going to find the lost person? (tactics). To be effective, modern searchers follow several basic principles and techniques, including the following: 1. 2. 3. 4. 5. 6.
Respond urgently—a search is an emergency Confine the search area Search for clues Search at night Search with a plan in an organized manner Grid search (type III) as a last resort
Every day, firefighters, paramedics, police officers, and other emergency responders receive calls to perform their duties, and often they can only guess what they will find once they arrive. In response to this the concept of the "firehouse" response has evolved. This concept calls for emergency responders, much like emergency physicians, to assume the worst until proven otherwise. Thus they respond with "lights and siren" to most calls just in case the situation is serious. Furthermore, they often respond in this way even when the reporting party specifies that the situation is minor, claiming that a certain percentage of individuals reporting incidents are wrong in their assessment. Essentially, the situation is considered an emergency until proven otherwise. For years, searching has been considered less urgent than other emergencies. While emergency responders were running with lights and sirens to situations reported as "women not feeling well" or "dumpster on fire," reports of a lost child or an overdue hiker were relegated to the "let's wait and see" category. Through years of experience, search managers now know that a search is as much an emergency as any other call for help. Furthermore, if an urgent response is mustered, the situation can be resolved faster, more successfully, and usually with less effort. Thus a search should be considered an emergency that justifies an urgent response, a high priority, a thorough assessment, and immediate action. Search Theory.
The mathematical basis for searching and the study of search theory had its beginnings during World War II in the work of the U.S. Navy's Anti-Submarine Warfare Operations Research Group (ASWORG) and was originally based on searching for the wakes of warships as seen by aircraft flying over the ocean.[5] The results of this work were collected in a seminal report by B.O. Koopman in 1946, [12] but the report was not declassified and generally available until 1958.[1] In 1980 Koopman developed a somewhat expanded version of this work, which was published in his book Search and Screening: General Principles with Historical Applications.[13] Although Koopman's work is clearly aimed at naval interests, the general theory of search he established is applicable to virtually any type of search problem. Since this early work, search theory has undergone continuous research and development by agencies such as the USCG and USN in both the maritime and aeronautical environments, mining and oil businesses in the search for mineral and petroleum deposits, and even archeologists in the search for lost cities, such as Troy.[18] The fundamental usefulness of search theory lies in its ability to help determine where and how to search. It accomplishes this by (1) quantifying the likelihood of a lost subject being in a particular area, as well as the likelihood of searchers finding the subject; and (2) offering tools with which one can estimate the chances of success of a particular search. The application of search theory requires the appropriate use of probability theory, a branch of mathematics that is used for estimating the likelihood of uncertain events, in planning a search. The chances that the lost person or clue is in the search area is called probability of area (POA). The probability that a search resource will find the lost person or clue if it indeed is in the area being searched is called probability of detection (POD). The mathematical combination of these two important variables produces a product called probability of success (POS = POA × POD). The foremost objective, and major challenge, for search planners is to combine the appropriate search resources (sensors producing POD) with appropriate segments of the search area where the subject is likely to be (POA) to produce the most POS in the least amount of time. On the surface
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this seems to be a straightforward proposition. However, additional critically important factors, such as resource detection capability, environmental influences, search object characteristics, probability density, probability distribution, coverage and sweep width, conspire to make the most correct search action a complex, unintuitive series of difficult choices. Although software is available to assist in the mathematical decisions, less than optimum but historically acceptable results have been achieved when a search manager applies the principles of search management as an intuitive combination of hard science and sage experience. In the final analysis, search success is based on more than just science. At its finest, it involves the artistic application of science and a high degree of organizational and management skill sprinkled with intuition and punctuated with a bit of luck. Lost Subject Behavior.
Modern search management is also based on the use of what is called a complete "subject profile." Such a profile identifies as much as is known about the missing subject, including general state of health, past experiences, and state of mind, through the use of a form called the Lost Person Questionnaire. This information is collected and used by search managers to predict how an individual would react in various situations. Analysis of this information from past incidents and understanding how the involved individuals behaved in given circumstances have offered great insight for search managers. Although it is not difficult to appreciate the importance of predicting how a subject might react when lost, the scientific approach to the subject began with William G. Syrotuck's seminal paper in 1977, Analysis of Lost Person Behavior: An Aid to Search Planning.[19] This paper was based on the premise that individuals will have similar travel habits when compared with others in the same "category." The six categories Syrotuck described include small children (1 to 6 years), children (6 to 12 years), hunters, hikers, elderly (over 65 years), and "miscellaneous adults," such as nature photographers, fruit gatherers, bird watchers, and other outdoor enthusiasts. He also included two "special categories" (mentally retarded persons and despondents) for which he had very little data. In his study, Syrotuck described the behavioral characteristics of a representative member of each category and computed "probability zones" for each based on distances traveled. This distance was measured "as the crow flies," or as a straight-line distance, between the point where the subject was last seen and the location where the subject was eventually found. Realizing that there was likely a substantial difference between how far a lost subject actually traveled and the crow's flight distance, Syrotuck argued that, "it is more important to realize that a known percentage of all lost persons is found within a one- or two-mile radius than it is to know how they got there." Syrotuck studied 229 cases, most from wooded areas of Washington and New York states, and all involved subjects traveling on foot. [19] Beyond identifying categories, Syrotuck also documented and described six other factors that may affect the search plan. He suggested that search personnel in possession of the following information could more accurately predict the subject's location: 1. 2. 3. 4. 5. 6.
Circumstances under which the person became lost Terrain Personality Weather Physical condition at time of loss Medical problems
He went on to describe how one's general state of health, past experiences, and physical situation (e.g., hot, cold, altitude) contribute to predicting behavior patterns. How one reacts to being lost, he also suggested, can impact the type and quantity of clues (i.e., disrobing, discarding equipment), survivability (i.e., failure to build a fire), detectability (i.e., bright clothing, bad weather), and tendency to follow travel aids such as rivers, roads, and trails. In all, Syrotuck produced the first scientific description of how people might react to being lost, and how searchers could use this information to improve operations. Following the theme of lost-person behavior and using the crow's-flight distance, Koester and Stooksbury[9] performed a retrospective study of persons who suffered from dementia of Alzheimer's type (DAT) and who became the subjects of organized SAR efforts in Virginia. They studied 82 cases (initially) from the Virginia Department of Emergency Services' (DES) lost subject database and compared the DAT patient's behavior to that of elderly lost subjects that possessed normal cognitive abilities. Their findings were of great interest to search managers in that this was the first time research of this type had been conducted for the inland SAR community. Koester and Stooksbury also described a "subject profile summary" and suggested specific search techniques for lost DAT patients. Notable in their findings were the facts that none of the subjects in the cases they studied yelled for help, and they were usually found 0.5 miles (0.8 km) from the PLS. Since this initial research, Koester[10] [11] has continued to analyze the Virginia DES data ( Table 25-2 , Table 25-3 , Table 25-4 ). Also using the crow's flight distance, Hill[8] described distances traveled and probability zones for lost persons in Nova Scotia. However, Hill found it useful to modify and add to Syrotuck's categories of lost persons. For instance, Hill broke young people into four categories, children 1 to 3 years, children 4 to 6 years, children 7 to 12 years, and youths 13 to 15 years. He described characteristics for fishermen, skiers, and walkaways (i.e., people who walk away from a constant-care situation), and additional characteristics for those who are despondent.
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TABLE 25-2 -- Summary of findings from Koester, 1999 [10] and Koester, 2000[11] TYPE OF VICTIM STATISTIC
ALZHEIMER'S ELDERLY DESPONDENTS RETARDATION PSYCHOTIC
n
87
33
65
29
25
Age (S.D.)
76 (9.2)
70 (4.3)
37 (15.7)
30 (3.3)
43 (15.9)
Males
67%
67%
76%
60%
63%
Females
33%
33%
24%
40%
37%
Uninjured
51%
48%
34%
85%
72%
Injured
27%
15%
11%
11%
5%
Deceased
22%
37%
55%
4%
22%
Mean
1.0
2.9
2.2
1.4
2.2
S.D.
0.8
0.8
5.3
1.9
3.7
Median
0.8
0.8
0.3
0.8
0.8
Range
0–4.8
0–8.0
0–32.2
7.7
12.9
25%
0.3
0.2
0.2
0.2
0.2
50%
0.8
0.8
0.3
0.8
0.8
75%
1.1
4.0
2.6
1.6
2.0
Max zone
2.4 (94%)
7.7 (95%) 8.0 (96%)
4.0 (95%)
7.7 (92%)
Distance from PLS (km)
PLS, Point last seen. TABLE 25-3 -- Distance Traveled Data, from Koester, 1999[10] and Koester, 2000[11] TYPE OF SUBJECT
DISTANCE FROM THE PLS MILES (km) n
ALZHEIMER'S (ADRD)
DESPONDENTS
MENTAL RETARDATION
PSYCHOTICS
87
74
29
25
10%
0.1
0
0
0
20%
0.1
0.1
0.1
0.1
30%
0.25
0.1
0.2
0.25
40%
0.3
0.15
0.25
0.3
50%
0.5
0.2
0.5
0.4
60%
0.5
0.25
0.75
0.5
70%
0.7
0.75
1.0
1.0
80%
1.0
1.25
1.7
2.0
90%
1.25
4.0
3.0
4.8
100%
2.0
20
4.8
8.0
8%*
10%
11%
5%
Investigative finds PLS, Point last seen. *Investigative finds increase to 25% in urban areas.
TABLE 25-4 -- Subject Found Location Data, from Koester, 1999[10] and Koester, 2000[11] TYPE OF SUBJECT ALZHEIMER'S (ADRD)
DESPONDENTS
MENTAL RETARDATION
PSYCHOTICS
Structure
15%
8%
21%
23%
Yard (open field)
18%
4%
16%
—
Drainage
18%
8%
21%
7%
7%
33%
16%
30%
29%
—
11%
7%
Road
7%
—
11%
23%
Powerline/linear
—
13%
5%
—
Other
4%
8% (cliff bottom)
—
—
Woods Brush/briars
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Taking a slightly different approach, Heth and Cornell[7] published a study of 162 incidents of persons lost in wilderness areas in southwestern Alberta, Canada. They tabulated crow's-flight distance traveled and angular dispersion of travel (the angle from a line that connects the PLS with the intended destination) by different categories of wilderness users. They formed 10 categories of outdoor user ( Table 25-5 ) and included only subjects propelled by muscle (no machinery). Interestingly, Heth and Cornell found a behavioral distinction between "front country" users (i.e., front to parking lots, groomed trails, frequent signage, good and available maps attracted users with a large range of outdoor experience and skill) and "backcountry" users (i.e., remote areas, undeveloped, attracted prepared and experienced users). Not unlike Syrotuck and Hill, Heth and Cornell discovered that, with the exception of despondents, there is a similar distribution of distance traveled by persons lost outdoors. However, they went further and suggested that there might be a linear relationship between certain data sets. For instance, their analysis indicated that hikers travel about 2.3 times farther than campers, and cross-country skiers breaking trail travel about 5.4 times farther than cross-country skiers using groomed trails. The implication is that if archival data are possessed for one category in one region and are compared with categories of lost subjects similar to those described by Heth and Cornell, a scalar parameter could be applied to extrapolate crow's-flight distances for other subject categories. Such a possibility is exciting to search managers who only rarely have access to relevant and reliable archival data. Search managers have used these behavioral studies, and others, in a number of valuable ways. By direct analysis and limited extrapolation, search managers have been able to find answers to important planning questions that are helpful in determining where and TABLE 25-5 -- Formal Estimates of Crow's Flight Distance (in km) Between the PLS and the Point Found for (N) Persons Lost During Different Wilderness Activities PERCENTILE ACTIVITY GROUP
25
Campers (18)
.722 1.559
Cross-country skiers: break trail (5)
50
75
90
3.001
4.931
4.537 9.795 18.860 30.988
Cross-country skiers: groomed trail (18)
.842 1.819
3.501
5.753
Despondents (6)
.229
1.793
4.664
.656
Hikers (38)
1.691 3.650
7.028 11.548
Hunters (5)
1.222 2.638
5.079
Mountain bikers (18)
3.759 8.116 15.626 25.675
Scramblers (7)
1.165 2.515
Walkaways (14)
.701 2.007
5.486 14.274
1.765 3.812
7.339 12.058
Other (13)
4.843
8.345 7.958
From Heth DC, Cornell EH: J Environ Psych Dec 11, 1997. NOTE: Estimates for despondents and walkaways were based on a different Wakeby distribution than that used to estimate the percentiles of the other user categories. how to search. Such efforts have also taught search managers the importance of collecting behavioral data on lost persons, and the predictive value of such data. Access Phase After the subject is located, the search is over. Rescuers must now gain access to the subject to assess and treat injuries, evaluate the situation, and mitigate the problem. Accomplishing these objectives may be as simple as walking into a room with the subject or as complex as reaching an astronaut in space. Regardless, planning for this eventuality should be complete and ready to be carried out at the conclusion of the locate phase. Once rescuers reach a subject, the situation and scene must be assessed. In emergency services terminology, this is called the size-up. The size-up consists of identifying hazards to the subject and rescuers, then developing a strategy to deal with the problems. For instance, a subject might be trapped by a winter storm in a high alpine environment. Safety considerations for rescuers entering such a hostile and dangerous environment would certainly influence further actions and may well
take precedence over the entire rescue effort. Specialized skills may be required for rescuers to safely gain access to the scene. For instance, rescuers may need to rappel to a patient who has fallen onto a ledge in terrain such as the Grand Canyon. Or rescuers may need to climb sheer rock faces to reach an injured mountaineer on Half Dome in Yosemite National Park. These are examples of how complex the access phase of a rescue may be and point to the importance of thorough and proper planning. If the size-up indicates that the situation or environment is so hazardous that remaining on scene poses an immediate threat to the subject, accelerated rescue techniques may be required. Accelerated rescue techniques are immediate actions required to remove a subject
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from a dangerous environment without stabilization. They often entail deviations from local standard operating procedures and protocols. Examples of such situations include poisonous gas environments (e.g., in caves), fires, unstable terrain (such as avalanches and rock slides), adverse weather (hurricanes, thunderstorms, severe snowstorms), or any hostile environment that threatens the subject, rescuers, or both. Stabilize Phase The stabilize phase has three primary components: physical, medical, and emotional. Once rescuers have access to the subject, the scene must be quickly evaluated, or sized-up, for immediate physical hazards and threats from the environment or situation. Scene safety is an initial priority in the size-up, and risks to rescuers and the subject must be weighed against the benefits to be gained. An example of physical stabilization would include an occupied automobile teetering on the edge of a cliff. Before the occupant can be medically assessed, the situation (i.e., the automobile) must be stabilized to best protect the rescuers and the patient. Other examples of physical stabilization might include protecting the patient from further injury (e.g., removing them from the hazardous environment, applying a helmet) or removing the hazard (e.g., extinguishing the fire, securing the teetering auto). Once the physical environment is stabilized and free from immediate hazards, medical management and stabilization commence. This process usually follows accepted procedures, starting with primary and secondary physical examinations and basic and advanced life support. It should include full-body immobilization, usually in a litter; specific site immobilization of fractures and related injuries; treatment of shock and other hemodynamic compromise; and protection from the environment. The goal of medical stabilization is usually to prepare the subject for transportation to a definitive care facility. If medical care is not required, confirming this fact may be all that is required at this stage before moving into the transport phase. Emotional stabilization is necessary because an anxious victim is a hazard to rescuers and himself or herself. Again, the goal is to best protect both the rescuers and the victim. Simple, calm communication with the victim, slowly describing what happened and what rescuers are doing, is often enough to calm a nervous victim. Stabilization, like assessment, should continue throughout the transport phase. The overall objective is to prepare the victim for transport to definitive care while maintaining his or her comfort and safety. Transport Phase In the fourth phase of SAR, the subject is moved to definitive care. For this to occur, the stabilized subject must be "packaged" so that he or she can be moved safely and efficiently while stabilization and assessment continue. Transportation types range from foot travel, with the subject walking on his or her own, to evacuation by aircraft. The appropriate mode of transportation is determined by weather, type and severity of injuries, overall urgency, terrain, available resources, and other related factors. Rescue Equipment.
Today's rescues occur in many remote and unusual environments and often require extremely technical rescue equipment and skills. Responders trained in the appropriate techniques and technologies should be the only personnel to apply them. Much of the gear and many of the techniques have been derived from those first developed by mountaineers, climbers, cavers, and, more recently, white-water enthusiasts. Rescue equipment is generally broken down into three broad categories: personal gear, rescue software, and rescue hardware. Personal equipment includes such items as footwear, gloves, helmets, articles of clothing, eye protection, and other protective apparel. Software is equipment such as rope, webbing, slings, and harnesses that are made of soft, strong synthetic materials specifically designed and manufactured for rescue. Hardware is such equipment as carabiners, cams, friction devices, pulleys, and litters made of steel and alloys specifically designed and manufactured to endure the rigors of rescue. PERSONAL EQUIPMENT.
Rescuers must often wear special equipment to protect them from accidents and hazards. Head, eye, and hand protection is considered mandatory in virtually all rescue environments. Additional personal equipment requirements are dictated by the rescue environment and the specific needs of the situation ( Figure 25-5 ). Special gear.
In addition to the usual challenges of the rescue environment, certain hazards require specialized equipment. Examples of such equipment include fire-resistant clothing worn by structural and wildland firefighters, personal flotation devices (PFDs) used by rescuers in and around water ( Figure 25-6 ), netting used in outdoor settings when insects become a problem, bulletproof garments used by law-enforcement and military rescue personnel, and chemical protective suits worn when exposure to hazardous materials is possible. No clothing or protective gear meets all of the requirements for involvement in or around a rescue scene. Rescuers study situations so that they understand all hazards before anyone becomes involved. Their conclusions help them identify protective-equipment requirements. Gear that may be necessary for one environment can be dangerous in another. A firefighter's turnout gear may be required in a structure fire but can be deadly in a river rescue situation. Every
608
Figure 25-5 Even though the personal equipment necessary is dictated by both the rescue environment and the needs of the specific situation, it includes head, hand, foot, and eye protection as a minimum.
Figure 25-6 Rescuer wearing a personal flotation device (PFD) and helmet often used for rescue in and around moving water.
Figure 25-7 Example of ½-inch, nylon, static, kernmantle rope of the type commonly used in rescue. Rescue rope should be checked over its entire length for damage before use.
rescuer is responsible for understanding the rescue environment and how to best prepare for it. SOFTWARE
Rope.
Rope is by far the most versatile piece of rescue equipment and serves as the universal link in most rescue environments. The material from which the rope is made (such as nylon, polyester, or polyolefins) and the design (laid, kernmantle, flat) are important in the consideration of the use for which a rope is intended. In most rescue environments, nylon is preferred because of its overall strength, resistance to abrasion, and ability to stretch and absorb energy. Natural fiber ropes such as hemp are no longer considered for use in rescue—synthetic materials are far better. Although design and amount of materials used influence strength, new ½-inch diameter nylon rescue rope usually has a tensile strength in excess of 9000 pounds ( Figure 25-7 ). The most common design of rescue rope is kernmantle, a term derived from German, meaning "core in sheath." With this design, a core of material (often parallel fibers) is surrounded by a braided sheath. The sheath protects the inner core, which supplies much of the strength of the overall rope. Other designs such as laid (twisted) and braided are also used in rescue rope. Kernmantle rope is either "dynamic" or "static." Dynamic kernmantle stretches more than 4% of its length to
609
absorb the impact of a fall, and it is used primarily in lead climbing. Static kernmantle stretches less (no more than 4% of its length); it is used in rescues in which a great deal of stretch would be a nuisance or even dangerous. Because of the importance of rope in the rescue chain, frequent inspection, care, and maintenance are important. Rope used in rescue is kept clean, inspected often, and protected from sharp edges, high temperatures, sunlight, chemicals, and abrasion. In addition, a detailed history of rescue ropes is kept so that an educated decision can eventually be made regarding each rope's removal from rescue service (see Chapter 72 ). Webbing.
Flat rope or webbing is another common link in rescue systems. It comes in two common configurations: flat and tubular. Tubular webbing is manufactured as a tube in such a way as to seem flat when in use. In cross section, however, it is obviously tubular and a bit less stiff than true flat webbing. One-inch-diameter tubular webbing can be used in rescues to tie anchor slings and harnesses. It has a tensile strength of approximately 4000 pounds when new. Flat webbing is flat in cross section. Its strength is directly proportional to the amount of material used in its manufacture. Automobile seat belts are an example of the material used in rescue harnesses, anchor slings, and anywhere strong, flat software is beneficial ( Figure 25-8 ). Harnesses.
Harnesses come in many sizes and shapes; they are used to attach something (usually a rope) to a person's body. They may be "full-body," encompassing the thorax and the pelvis ( Figure 25-9 ); "seat," encompassing only the pelvis (see Figure 25-5 ); or "chest," encompassing only the thorax. Each type of harness has its use and associated advantages and disadvantages. Classically, the most common harness for climbing has been the seat harness. However, rescue practitioners have been trying to standardize the full-body harness for rescuer use, with the separate seat and chest harnesses having only limited special use by trained individuals. Webbing can be tied into a large loop (runner) and applied to a person in such a way as to serve as an improvised harness. Although this is not a preferred method of attachment to a rope, it can work if other harnesses are not available. HARDWARE
Carabiners.
Carabiners are large, safety pin-type mechanisms used to connect various elements of a rescue system, such as a rope and anchor. They are occasionally called "biners," "snap links," or "crabs," and consist of a spring-loaded gate that pivots open, a spine that supports most of the load and lies opposite the gate, a latch, and depending on the specific style, a locking mechanism. Steel and aluminum are the two materials from
Figure 25-8 Left, Tubular webbing with cross section visible. Right, Flat webbing used in anchor sling.
Figure 25-9 Full-body harness. Note that the harness encompasses both the pelvis and the thorax.
which carabiners are most commonly made. Size for size, steel is stronger and heavier, but aluminum is lighter and stronger pound for pound. In rescue, steel is almost always preferred unless weight is a factor, as in remote alpine situations. Common shapes of carabiners include oval, D, offset D, pear, and large offset D. The design best suited for any situation is dictated by the specific use. No matter what the shape, carabiners used in rescue usually have a mechanism for locking the gate closed so that opening it takes a special effort. This design feature not only
610
Figure 25-10 Various types of carabiners. Top to bottom: (1) RSI Big hook, steel, screw locking hinged gate; (2) alloy, offset D, screw locking hinged gate; (3) RSI Twist Link, steel, screw locking hinged gate; (4) SMC extra large, rescue, steel, screw locking hinged gate; (5) Tri-link, steel, triangular, screw lock; (6) Auto-lock, swivel-mount, steel, quarter twist locking hinged gate (NFPA 1983 certified). Note that locking carabiners should always be locked when in use.
Figure 25-11 Example of figure-8 plate descending device (with "ears") commonly used in rescue.
improves the strength of the device, but also reduces the chances that a carabiner will open accidentally at a bad time ( Figure 25-10 ). Descending/friction devices.
Many different descending devices exist today, but they all do primarily the same thing: apply friction to the rope to allow controlled lowering of a person or load. The most common descending devices in rescue are the figure-8 plate and the brake bar rack. The figure-8 plate gets the name from its general shape. It has two rings of different sizes. The larger ring produces friction on the rope, whereas the smaller ring is used primarily as an attachment for the load (e.g., the rescuer during rappel). Friction is produced by passing a bight of rope through the large ring and around the small ring, then attaching the small ring to either an anchor (for a lowering system) or a rescuer's harness (for a rappel or abseil) with a locking carabiner ( Figure 25-11 ). The brake bar rack, or simply "the rack," uses either steel or aluminum bars on a steel rack to produce friction on a rope. When the rope is threaded alternately around the bars and the load or rescuer is attached to the "eye" in the rack, friction is applied. The number of bars applied to the rope and the distance between them can be varied to change the friction. This variable friction allows versatility not available with the figure-8 plate; however, the rack takes a bit more training to use safely ( Figure 25-12 ).
Figure 25-12 RSI Super Rack brake bar rack in use.
611
Ascenders.
Ascenders are devices that grip or hold the rope. They have been adapted from climbing and caving equipment, with which they are used to ascend or climb a fixed rope. In rescue, they are used to climb fixed lines when necessary, but they can also be used in hauling systems to grip the rope. In this way, they hold fast when the rope is pulled in one direction and allow the rope to slide easily when it is pulled in the other direction ( Figure 25-13, A–D ). When ascenders are used to climb a rope, one is fixed to the rope and supports the load while the other is moved into position ahead. When this action is alternately repeated, a skilled climber can move up a rope with relative speed and ease. Selected rope hitches (e.g., a Prusik hitch) can be used in lieu of an ascender.
Figure 25-13 A, Gibbs ascender applied to rope. When the eye of the cam is pulled, the cam squeezes the rope and holds fast. When the cam is released, the device can be moved on the rope. B, Gibbs ascender dismantled with shell around rope. Note cam (upper left) and pin (bottom). C, Clog handled ascender. Although used where climbing a fixed rope is required, handled ascenders are rarely used in rescue. D, A 3-wrap Prusik hitch can often be used in lieu of a mechanical ascender. Pulleys.
Pulleys are simple machines that apply a turning wheel to reduce friction on a rope as it rounds a turn. In rescue, these metal devices serve primarily to change the direction of a rope, such as within a mechanical advantage system. The "sheave" is the wheel or pulley, and there may be more than one. The "side plate" or "cheek" is the side of the device that makes contact with the anchor at the "hook," which is usually the weakest part. The axle or "sheave pin" is what the wheel turns on; it is supported by the side plates. In rescue pulleys the side plates are movable so that the pulley can be attached to a rope anywhere along its length ( Figure 25-14 ). The larger the diameter of the pulley, the more efficient the device. That is, the bigger the pulley, the more
612
Figure 25-14 Two types of pulleys commonly used for rescue. Top, 2-inch double pulley. Bottom, 2-inch, "Prusik-minding." Note that rescue pulleys are applied to rope by removing the carabiner and swiveling the side plate to allow the introduction of the rope.
friction (theoretically) is reduced. A rule of thumb often used by rescuers is that a pulley with the largest diameter possible should be used, but never less than four times the diameter of the rope. Therefore, because ½-inch (11 mm) rope is commonly used in rescue, a pulley diameter of at least 2 inches should be used. A variation of the pulley is the edge roller. This device uses 4- to 6-inch open-face pulleys to both reduce the friction of a rope passing over an edge and reduce damage to the rope by protecting it from excess abrasion. Single units can protect the rope from 90-degree angles, and multiple units tied together can provide protection for complex projections. Litters.
Litters or stretchers are the conveyances in which victims are transported when they cannot travel under their own power. New high-technology materials and designs have greatly improved the choices available. In past years, rescuers were forced to settle for either wooden backboards, old military stretchers, the wire Navy Stokes basket, or the "scoop" stretcher. Today, strong, lightweight synthetic materials and inventive designs have improved the strength, weight, durability, and comfort of litters. The goals have not changed during the continuing evolution of the perfect wilderness transportation device. Rescuers still want a device that is comfortable for a person in pain, serves well as a platform for assessment and medical care during transport, allows for full-body immobilization while offering complete security, and protects its occupants from the rescue environment. See Chapter 27 for additional information regarding specific litters, packaging, handling, and evacuation techniques.
ANATOMY OF A SEARCH AND RESCUE INCIDENT To summarize how all of the previously discussed information fits together, it is convenient to dissect a SAR incident into its component parts and then analyze how all of the parts fit together ( Figure 25-15 ). From the SAR operative's perspective, an actual callout is merely an interruption of planning for an incident. That is, people involved in SAR are constantly in a state of readiness and prepared to respond. When a situation occurs, this planning stage is suddenly interrupted by the report of an incident or first notice. The individual taking the information is charged with conveying it to the appropriate authority. The authority determines the urgency, continues the investigation process, begins to develop an operational strategy, and generates an incident action plan. At the same time, those in charge begin to muster appropriate resources to carry out the action plan. In SAR, this is termed resource callout, or just callout. Once notified of an incident, individual resources are gathered at a collection point and signed in. The sign-in process enhances safety and allows tracking of resources, which helps those in charge determine the quantity and type of resources available. Once signed in, resources are allocated to assignments designed to meet the goals of the action plan within a reasonable time. This physical implementation of plans in the field is called tactics and is a direct outgrowth of the incident action plan. Allocation of resources in the field continues until there is reason to suspend a phase of the operation. If the subject is found, the search is suspended and the access phase can commence. Once rescuers have access to the subject, the focus turns to stabilization and transportation. If at any point the operation cannot be continued (e.g., the subject was never found, access cannot be gained, transportation is impossible), suspension and demobilization may occur without completion of the entire cycle. The decision to discontinue active search efforts is difficult and involves complex management issues, almost always of the no-win variety. When a situation is resolved, mission suspension and demobilization begin. In larger incidents this may involve structured deactivation of multiple resources, pulling teams out of the field, dismantling facilities, completing documentation, and returning resources to
613
Figure 25-15 Time progression or the "anatomy" of a search from a searcher's (operational) perspective. The process is actually a continuous cycle that pauses in the planning and preparation phase until an incident occurs.
service. Basically, everyone finishes what he or she was doing and gets ready to do it again. All of this takes planning and preparation and should be addressed in the overall preplan long before it is required. After every incident, participants realize that if they had it all to do again, they would do some things differently. If these thoughts and ideas are not documented, they can be lost, and future responses may be cursed to repeat past mistakes. This is one reason that every incident should contain some type of evaluation of the entire mission, known as the post-incident critique. The critique can be formal, involving every participant at a sit-down meeting, or informal, involving just a brief discussion of recent events. The critique documents lessons learned and provides a basis for revising the preplan. Thus the cycle continues, and lessons learned from one mission influence the next.
SEARCH AND RESCUE ENVIRONMENTS WITHIN THE WILDERNESS SETTING [4] SAR teams throughout the world are frequently called on to solve complex problems in a wide spectrum of environments. Even within the environments addressed in this text, widely diversified subenvironments exist that present unique sets of problems and hazards to SAR personnel. When confronted with the numerous and dangerous environmental conditions found in the wilderness setting, SAR personnel must be prepared to work where others have been unable to cope. A military motto becomes the SAR credo: "Adapt, improvise, overcome." Some of the specialized subenvironments and their associated conditions within which SAR team members may have to work are listed in Box 25-1 . It is beyond the scope of this text to discuss in detail how SAR personnel adapt to each of these environments, but it is important to note that adaptation and improvisation are required in nearly all wilderness situations. The particular improvisation depends on the situation, as well as the skill and experience of the individuals involved.
Box 25-1. SEARCH AND RESCUE CONDITIONS Mountainous terrain Vertical rock Vertical ice Flat ice and ice holes Snow fields and avalanches Crevasses Caves Mines Wells Booby-trapped stills and gardens Air shafts Fast water and white-water streams Coastal white-water surf Flash floods Slow-rising floods High winds and storms Seas and lakes Snow and blizzard conditions Hazardous material dump sites
Regardless of the type of rescue environment encountered by rescuers, the following general rules should be followed: 1. Use technical personnel for technical rescue. 2. If the subject is dead, evacuate only when there is no risk to team members, or at least when the hazard has been assessed and the risk justified. 3. Stabilize the subject before evacuating; continue stabilization during transport. 614
4. Find, plan, and use the easiest route for evacuation. 5. If a litter must be carried, appoint someone to serve as route finder, with a radio and markers, to report potential hazards and problems. 6. Litter teams of six to eight persons per team should be used, with three teams minimum. Normally, there should be no more than 20 minutes per shift. Additional personnel may also be required to carry equipment. 7. Use accepted procedures to care for and protect the victim. 8. A radio carrier brings up the rear. 9. If using a helicopter for evacuation, make sure: a. That the subject is briefed. b. That the subject is protected. c. That someone goes with the subject who knows what has been done medically. Special Environments in Search and Rescue Specialized SAR environments produce diverse problems and potential complications. Each environment presents its own obstacles to increase the complexity and difficulty of particular rescues. Technical Rock.
Mountaineering, rock climbing, and casual scrambling have created a need for specialized SAR expertise. Individuals and groups involved in rock rescue have refined and developed techniques for most situations. The hallmark of a technical rock rescuer is the ability to improvise and modify tools or techniques to meet any crisis. He or she must be comfortable using climbing gear and being exposed to heights. Once an individual is located in a rock environment and the situation is surveyed, it is necessary to gain access. Local groups familiar with particular well-known areas
will have already solved this problem. The solution will involve either climbing up or dropping down to the victim. Safety for all persons involved is paramount, because an accident during a rescue is almost always catastrophic. Climbing up to the victim requires knowledge of rock-climbing techniques, and proper equipment and familiarity with its use are critical. Local outing clubs or mountaineering stores can be contacted for more detailed assistance. Specialized technical rock rescue teams, such as those sanctioned by the Mountain Rescue Association, routinely practice climbing techniques and solving vertical rescue problems. Caves and Mines.
Standard obstacles in the environment include poor communications, extreme darkness, difficulty in lighting, small and wet spaces, and questionable atmosphere. The various environments included here are collectively termed confined spaces. The levels of moisture in a water, or "live," cave can vary over a considerable range. Some are merely muddy; others have flowing rivers. Caves in the western United States are generally drier than eastern caves; however, humidity, wetness, and cold temperatures create potential for hypothermia in both areas, a fact that is greatly underestimated. Flooding is often a great problem, and many cavers have died because of inattention to the weather on the outside. During heavy rains, the caves become natural drains for streams. Wind and temperature are other underestimated problems associated with cave and mine emergencies. It is not unusual for strong winds to develop along subterranean passages, which intensifies convective air chilling. Confined passages, low crawls, and squeezes pose unique problems for the rescue of injured cavers. The use of standard items such as litters, backboards, and splints may be impossible in such places. Confined passages with varying, often toxic, constituent gases can lead to difficulties for victims and rescuers alike. Occasionally, a self-contained breathing apparatus or surface-supplied air is required. The potential for toxic gases justifies extensive atmospheric monitoring while operating in the underground environment. An essential part of any cave or mine rescue operation is thorough orientation to the hazards associated with a particular underground area. This involves pinpointing the locations of pits, waterfalls, siphons, canyons, and other difficult formations that may pose problems in extrication, search, or safety. Many caves have been mapped by the National Speleological Society and the National Park Service. The real difficulties may begin only after a victim is located. The goal is to move the person rapidly, safely, and comfortably to the surface. Without practice underground, that task will be virtually impossible. Neoprene exposure bags similar to body bags have been used for this purpose and keep the individual dry and protected during what may be a very long and slow evacuation. Medical care procedures must be performed under dark, cold, and muddy conditions. Experienced cave rescuers agree that repackaging supplies and equipment for underground use is essential. Streamlining kits, packs, and containers is imperative for unobstructed passage through tight spaces in cold, damp conditions. Team members must carry a minimum of 24 hours of light in a helmet-mounted lamp; two additional sources of light, with spare bulbs and batteries; and waterproof matches and candles. Other equipment needed might include the following: 1. A high-quality helmet with chin strap and headlamp attachment 2. Sturdy, warm clothes and gloves for damp, dirty conditions for up to 24 hours; the material should be wool and the fit should allow good mobility 3. Lug-soled boots that are light and drain water 615
4. Nonstretch, specialized caving rope that is highly resistant to abrasion 5. Wrap-around-style litter (or even an old conveyor belt) that can aid in dragging an injured person through small passages: a common Stokes litter may not always work well 6. Wet suits for longer missions in extremely wet caves 7. Harnesses and slings resistant to chemicals and water 8. Plastic sheeting to divert water around a victim during evacuation 9. Small portable pumps, a siphon hose, and plastic to divert, dam, or pump water around areas during operations 10. Warm food and drink carried in thermally insulated containers Essential caving skills include all of the capabilities for rock climbing, including vertical rope technique, ascending, rappeling, belaying, and being comfortable working at the end of a rope. All of these skills must be practiced until they can be done in the cold and wet without the benefit of light. Team practices are conducted both on the surface and underground, with participants being forced to work in mud, suffocatingly tight squeezes, soaking waterfalls, and complete darkness. This may be a difficult evolution for even the most experienced rescuer to endure, but just another "hang in the hole" for a seasoned caver. White-Water River.
There are dozens of potentially dangerous problems in the river SAR (white-water) situation (see Chapter 30 ). Log and debris piles at various bends in the river can function as "strainers" for the recreational victim, but they may be death traps for the would-be rescuer. The banks of the stream may be deeply undercut, with treacherous overhanging debris and snags that can catch on clothing, equipment, and skin. Combined with muddy and rapidly rising water, these factors render river rescue difficult and unpredictable. In fast-moving water, the single greatest problem is that responders underestimate the power and threat of moving water. Foolhardy heroics and overenthusiasm frequently lead to further tragedy. Cold-water immersion, coupled with wind and cold temperatures, predisposes everyone to hypothermia. Wet clothing, darkness, and injury add to the insult. The noise of moving water may obviate clear communications, and poor contact between the victim and rescuers or among the rescuers leads to confusion and danger. All potential responders in this environment must know how to read the water for capsize points and other dangerous phenomena. The hydraulics of low-head dams, collapsed bridges, and other submerged structures can produce a drowning machine for unsuspecting individuals. Rescue team members must know how to protect themselves in fast-moving water at all times. Mandatory in this environment are good judgment, strong swimming ability, knowledge of all types of technical systems and equipment used in climbing, and a thorough understanding of river dynamics and hydraulic influences. WHITE-WATER AND RIVER RESCUE EQUIPMENT NEEDS.
In addition to standard rescue equipment, the following items should be considered when establishing rescue capability in the white-water and river environment: 1. Inflatable rafts or boats (Hard boats may not be as stable and are usually less preferred. Inflatables should be at least 14 to 16 feet long and 6 feet wide, with separate air chambers. The "spider boat," with two pontoons joined together in a catamaran-style craft, makes an excellent, stable rescue platform for moving water.) 2. A line gun or crossbow adaptation that will shoot a line at least 200 feet 3. Power winch or simple "come-along" that can be carried to remote sites 4. Lengthy (150 to 300 feet) durable floating ropes in rope bags 5. Floating throw-rope bags with approximately 60 feet of line 6. A lightweight litter with enough flotation to keep a packaged patient's head out of the water; standard rescue litters often have adaptations for this purpose 7. Fire-hose end caps with air-hose adapters, which allow the fire hose to be inflated with air and used in a shore-based rescue 8. PFDs for every rescuer who will be exposed to the water environment; wet suits and helmets for rescuers who will be directly involved in moving water 9. Dry extra clothing for victims and rescuers 10. Portable "loudhailer" or public address system 11. Portable lighting systems 12. Detailed maps, aerial photographs, or both, of the area, as well as information regarding river hazards during high, medium, and low water levels 13. Dry, buoyant storage bags for sensitive gear 14. Reliable, watertight communications capability for white-water noise and moisture conditions 15. Small surfboardlike Styrofoam boards ("boogie board") for swimming in moving water
White-Water Surf.
Like river white water, ocean surf can present some very different problems in rescue because there is no "average" beach. There are recurring rescue situations that pose unique problems in the white-water surf environment.
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Figure 25-16 Runout. A, This phenomenon begins with an offshore sandbar. As waves roll in, the water level builds up behind the bar until a section gives way. B, As the sandbar "dam" gives way, the water develops a very rapid current running seaward. The recommended action is to swim across the current until out of the pull.
Figure 25-17 Rip. A depression in the beach floor concentrates returning water into a strong current. To escape, a person should ride with the current or swim to the side and out of the pull.
Along with the potential for immersion hypothermia, lacerations and contusions can result from being dashed against barnacle-encrusted rocks in the wild and unpredictable ocean surf. Contact with venomous sea life is always a possibility. However, the greatest threat to ocean beach users is the action of the water itself and the possibility of drowning through inattention or unfamiliarity with ocean surf hazards in the form of runouts, undertows, and rips. RUNOUT.
A runout occurs when an offshore sandbar or ledge is built up over a long period. Millions of tons of water flow over the bar during daily tidal changes. Eventually the water may equal or exceed the level outside the bar. Any weak spot in the bar usually gives way, causing a funnel effect ( Figure 25-16 ). Water rushes toward the bar at a terrific rate, sweeping everything with it. This common phenomenon can be easily spotted from the beach. Usually 15 to 50 yards wide, it is characterized by choppy, jumbled-up, little waves. The water often has a dirty, foamy, or debris-laden surface moving seaward. If a bar is visible offshore, definite breaks can be seen where the water pours through. Surfers often seek runout currents for fast transportation out beyond shoreline waves. Swimmers caught in a runout have two options. They may swim parallel to the shoreline out of the strip of current, or if the bar is visible (usually characterized by breaking waves), they may relax and let the current complete its runout. About 25 yards beyond the bar the current dissipates. This is an offshore phenomenon—current force increases near the bar but is often negligible near shore. RIP.
A far worse problem close to the beach is a rip, which can knock children and even adults off their feet and carry them to deep water in seconds. Rips are caused by a slight depression on the beach where wave water rushes after breaking on shore. Water rushing to the depression soon becomes an irresistible seaward flow ( Figure 25-17 ). It may be as narrow as 15 yards at its source and usually does not travel as far as a runout. Rips generally dissipate a few yards beyond the breakers. A rip looks like a runout, with a streak of turbulent discolored water or a line of foam leading directly out from shore. A swimmer has the same options as in a runout, either to swim parallel to the beach or to relax and ride the current until it ebbs. A person who swims straight toward the beach will never make it. A beach with several rips moving up and down in unpredictable patterns is very dangerous. An unwary swimmer could panic and drown. UNDERTOW.
On narrow, steep beaches a type of current known as undertow can be found. It is caused by gravity acting on water thrown up on the beach by wave action. Water retreating back down the steep shore continues under oncoming waves ( Figure 25-18 ). Undertow is usually of very short duration and is ended by the next breaking wave. Wading near shore on a steep beach, an individual could be pulled under in this current and find himself or herself quickly in deep water. If the person resists the current, the next wave may break directly on the person's back. In some circumstances this could cause traumatic injury, especially to the neck
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Figure 25-18 Undertow. This hazard develops on a steep beach where the water returns rapidly seaward after being tossed up by the wave action. A person should never fight this action but should relax and rise on the next wave.
and back. A person caught in an undertow should let the current pull until it ceases, then swim to the surface and ride the next wave into shore. Cold, Snow, and Ice.
Perhaps no other type of SAR environment requires a more broadly based foundation of personal and team skills than winter snow and ice. These skills include downhill and cross-country skiing, snowshoeing, technical climbing, winter survival, and a good understanding of snow and ice physics. Unlike rock, snow and ice conditions change on a daily and even minute-to-minute basis. The effects of gravity, wind, temperature, slope, heat exchange, load factors, and avalanche (see Chapter 2 ) continually impose problems for missions under these conditions. Technical and nontechnical SAR problems in snow and ice environments take longer to address and are more taxing, technical, and complex. Combined with shorter days, extremes of weather, and the ever-present threat of hypothermia and localized cold injuries, technical missions of this type are unacceptable for all but the most experienced SAR personnel. Versatility and improvisation are essential components of the overall strategy that must be used in snow and ice. Transportation of the victim is often one of the most difficult problems, but it can usually be resolved through detailed preplanning. Innovations such as covering a litter with a canvas cover or improvising an attachment to cross-country skis are clever solutions to common winter problems. Commercial products such as the Hegg Sled and the Sked Litter (see Chapter 26 ) have streamlined the laborious task of transporting injured people through snow and ice.
MAGNITUDE AND CAUSES OF PROBLEMS IN WILDERNESS SEARCH AND RESCUE It is impossible to report the exact number of backcountry SAR missions that occur each year in the United States. Some estimates are in excess of 100,000. In the United States, no federal agency is charged with gathering these data. With rare exception, only in the last few years have some states and local jurisdictions begun to collect and analyze SAR mission numbers and related information. Through the efforts of organizations such as the National Association for Search and Rescue, this vital information is now being used as a database to predict victim behavior and to improve the efficiency of SAR management.
Box 25-2. FACTORS THAT CONTRIBUTE TO SURVIVAL SITUATIONS AND SEARCH AND RESCUE MISSIONS Improper clothing, foot gear, or both Lack of rest (fatigue) Lack of adequate water (dehydration) Hypothermia or hyperthermia Too ambitious an undertaking for skills or proficiency Poor physical condition, lack of motivation, or both Inadequate or improper food Little or no planning Inadequate party for the goal, and lack of leadership Itinerary confusing or not known to others Individuals could not recognize a physical, mental, or environmental threat No preparation for adverse weather Unfamiliarity with terrain and lack of map or compass "It can't happen to me" philosophy
Most wilderness accidents are the result of inexperience or lack of preparation, often aggravated by fatigue, lowered body temperature, and other medical management problems, rather than the direct result of natural phenomena such as avalanche or rock fall. In an effort to save lives through education, the Washington State Department of Emergency Management SAR Division has been recording statistics on SAR missions for over 20 years. The goal of this effort has been to find out what factors in each SAR mission may have caused a problem for the subject. Box 25-2 is an overview of that data, compiled in an attempt to create a preventive SAR subject profile. In addition to the factors listed in Box 25-2 , the data pointed out some extremely interesting characteristics. Using broad-based generalizations, the analysts were able to further describe a potential SAR victim. Although the data were gathered only from the state of Washington, they have application in nearly every state and have to some degree been substantiated by other statistics. The average SAR victim is a composite outdoorsman (e.g., hunter, fisherman, skier, hiker, climber, boater, photographer). Most do not do any of these activities well and are not members of organized groups that specialize in these pursuits. Most reside in densely populated areas and travel some distance for recreation
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and outdoor pursuits. They usually travel too fast and too far to acclimatize well to the terrain, altitude, and environmental conditions encountered. Interviews show that they also generally ignore signs of weather change, environmental hazards, body indicators, and written warnings concerning danger or safety. Most wilderness or backcountry emergencies are solved by either the victim or outside help within 72 hours. The decisions and actions taken by the victims during the first 6 hours of the situation (such as emergency shelter, improving clothing, firecraft, signaling) are the most critical and influence the outcome most heavily. Of all precipitating factors, weather contributes the most to misery, carelessness, and the ultimate SAR mission.
References 1.
Benkoski M, Monticino M, Weisinger J: A survey of the search theory literature, Naval Research Logistics 38:469, 1991.
2.
Cooper DC, LaValla PH, Stoffel RC: SAR fundamentals: basic skills and knowledge to perform search and rescue, ed 3 (rev), Cuyahoga Falls, Ohio, 1996, National Rescue Consultants.
3.
Cooper DC, Taylor A: Fundamentals of mantracking: the step-by-step method, ed 2, Cuyahoga Falls, Ohio, 1992, National Rescue Consultants.
4.
Federal Emergency Management Agency: The Federal Response Plan, PL 93-288, as amended, Washington, DC, 1991, Superintendent of Documents.
5.
Frost JR: Search theory enhancement study: prepared for interagency committee on SAR research and development working group, Fairfax, Va, 1998, Soza and Company, Ltd.
6.
Frost JR: Personal communication, March 3, 1999.
7.
Heth DC, Cornell EH: Characteristics of travel by persons lost in Albertan wilderness areas, J Environ Psych Dec 11, 1997.
8.
Hill KA: Distances traveled and probability zones for lost persons in Nova Scotia, 1996, unpublished data.
9.
Koester RJ, Stooksbury DE: Behavioral profile of possible Alzheimer's disease patients in Virginia SAR incidents, Wilderness and Environmental Medicine 6:34–43, 1995.
Koester RJ: (1999). Behavioral and statistical profile of lost mentally retarded and psychotic subjects in Virginia. Personal communication, July 7, 1999. Based on author's presentation with same title at RESPONSE '99, Annual Conference of the National Association for Search and Rescue, June 1999. 10.
11.
Koester RJ: Behavioral and statistical profiles of lost subjects in Virginia. Personal communication, June 6, 2000.
12.
Koopman BO: Search and screening (OEG Report No. 56, The Summary Reports Group of the Columbia University Division of War Research, 1946). Available from the Center for Naval Analyses.
13.
Koopman BO: Search and screening: general principles with historical applications, New York, 1980, Pergamon Press.
14.
LaValla PH, Stoffel RC: Blueprint for community emergency management: a text for managing emergency operations, Olympia, Wash, 1991, Emergency Response Institute.
15.
LaValla PH et al: Search is an emergency: a text for managing search operations, ed 4 (rev), Olympia, Wash, 1998, Emergency Response Institute.
16.
Miller AT Jr: Altitude. In Slonin NB, editor: Environmental physiology, St Louis, 1974, Mosby.
17.
National wildfire coordinating group: Incident command system, national training curriculum reference text, NWCG, October, 1994.
18.
Soza and Company, Ltd., United States Coast Guard: The theory of search: a simplified explanation, (rev), Fairfax, Vir, 1998, the authors.
19.
Syrotuck WG: Analysis of lost person behavior, Westmoreland, NY, 1977, Arner Publications.
US Coast Guard and The Joint Chiefs of Staff: National search and rescue manual, vol 1, National search and rescue system. Joint Pub 3–50, COMDTINST M16120.5A, Washington, DC, 1991, Superintendent of Documents. 20.
21.
United States Air Force: AFRCC history and mission, March, 1999, (www.acc.af.mil).
22.
United States Coast Guard: U.S. Coast Guard website: www.uscg.mil/hq/g-o/g-opr/, May, 1999.
23.
United States Coast Guard Auxiliary: U.S. coast guard auxiliary history and accomplishments, website: www.cgaux.org, May, 1999.
24.
Worsing RA Jr, editor: Basic rescue and emergency care, Park Ridge, Ill, 1990, American Academy of Orthopaedic Surgeons.
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Chapter 26 - Litters and Carries Donald C. Cooper James Messenger Timothy P. Mier
Every search and rescue event goes through a series of four consecutive phases. These phases are illustrated by the acronym LAST (locate, access, stabilize, and transport). This process ends with the movement of the patient (or patients) from the scene to either a medical facility or an area of comfort and safety (transport)[6] (see Chapter 25 ). In the United States the term stretcher suggests a flat, unsophisticated frame covered with canvas and used for carrying the sick, injured, and deceased short distances. The term litter can mean the same thing but usually suggests an apparatus specifically designed to immobilize and carry a patient longer distances. Over the years the subtle differences in the terms have been lost, and users have gravitated to one or the other. In the United States the term litter is used to describe all manner of rescue conveyance. In Great Britain, however, the preference is to use stretcher to describe the same devices. In this chapter the two terms are used interchangeably.
SIZE-UP To select the best method for getting a patient to definitive care, the rescuer must make a realistic assessment of several factors. Scene safety is the initial priority. The necessary evaluation, called the size-up ( Box 26-1 ), involves a (usually hasty) determination of whether the victim, rescuer, or both are immediately threatened by either the environment or the situation. Proper immobilization and patient packaging are always preferable, but sometimes the risk of aggravating existing injuries is outweighed by the immediate danger presented by the physical environment. In such a situation the rescuer has little choice but to immediately move the patient to a place of safety before definitive care is provided or packaging is completed. Evacuation options are limited by three rescuer-related variables: (1) the number of rescuers, (2) their level of fitness, and (3) their technical ability. Carrying a victim, even over level ground, is an arduous task. At an altitude where just walking requires great effort, carrying a victim may be impossible. The specific rescue situation or environment encountered also may present challenges beyond the capability of the available rescuers. Complex rescue scenarios requiring specially trained personnel and special equipment are called technical rescues and often involve dangerous environments, such as severe terrain, crevasses, avalanche chutes, caves, or swift water. To avoid becoming victims themselves, rescuers must be realistic when evaluating their ability to perform these types of rescues.
DRAGS AND CARRIES The most fundamental and expedient method of transporting an ill or injured person is by dragging or carrying them. Although these methods of transportation are far less than ideal and may not meet standard care criteria, the urgency of the situation may outweigh the risks involved. In addition, the process can be physically demanding, and rescuers can quickly become fatigued to the point of hazard. Therefore other options often should be considered before a victim is moved, especially a long distance. A drag or carry may be the best option when a person cannot move under his or her own power, injuries will not be aggravated by the transport, resources and time are limited, the need for immediate transport outweighs the desire to apply standard care criteria, the travel distance is short, or the terrain makes the use of multiple rescuers or bulky equipment impractical. A "blanket drag" ( Figure 26-1, A ) can be performed on relatively smooth terrain by one or more rescuers rolling the victim onto a blanket, a tarp, or even a large coat and pulling it along the ground. This simple technique is especially effective for rapidly moving a person with a spinal injury to safety because the victim is pulled along the long axis of the body. In extreme circumstances the "fireman's drag" ( Figure 26-1, B ) can be used. In this type of drag the rescuer places the bound wrists of the victim around his or her neck, shoulders, or both and crawls to safety. A carry should be considered only after it is confirmed that the victim cannot assist rescuers or travel on his or her own. Beyond simply lifting a person over one's shoulder in a "fireman's carry" ( Figure 26-2 ) or acting as a human crutch, a more efficient one-person carry can be accomplished by using equipment, such as webbing, backpacks, coils of rope, or commercial harnesses. Equipment-assisted carries are particularly effective when an injured climber or hiker must be evacuated across a short distance over rough terrain or when a person must be quickly removed from a hazardous environment. In the simplest equipment-assisted carry, 4.5 to 6 m (15 to 20 feet) of webbing is
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Figure 26-1 A, Blanket drag. B, Fireman's drag. Both techniques are intended to be used when expeditious transport over a short distance is required. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, Lyons Press.)
Figure 26-2 Classic fireman's carry: a single rescuer technique for short distance transport only. The rescuer must use his or her legs for lifting. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, Lyons Press.)
wrapped around the victim, who is "worn" like a backpack by the rescuer ( Figure 26-3 ). Similarly a backpack or split coil of climbing or rescue rope can be fashioned into a seat around the victim and hoisted by the rescuer. A rescuer can modify a large backpack by cutting holes in the bottom for the victim's legs, who then sits in it like a child would sit in an infant carrier ( Figure 26-4 and Figure 26-5 )
Box 26-1. EVACUATION SIZE-UP FACTORS What are the scope and the magnitude of the overall situation? Are there immediate life-threatening hazards? What is the location, and how many victims are there? What is the patient's condition? Is the subject able to assist rescuers?
a. b. c. d. e.
No injury (able to walk unassisted) Slight injury (able to walk unassisted) Slight injury (assistance required to walk) Major injury (requires considerable attention and assistance) Deceased
Is there a need for technical rescue? Is the scene readily accessible? What rescue resources (including rescuers and equipment) are available? How far must the patient (or patients) be transported? Are ground or air transport assets available?
A few commercial harnesses allow a lone rescuer and single patient to be raised or lowered together by a technical rescue system. A Tragsitz is one example ( Figure 26-6 ). For carrying infants and small children a papoosestyle sling works well and can easily be constructed by the rescuer tying a rectangular piece of material around his or her waist and neck to form a pouch. The infant or child is then placed inside the pouch, which can be worn on the front or back of the rescuer's body. If two rescuers are available, additional and often superior options for carrying a victim become possible. One option consists of two rescuers forming a seat by joining their hands or arms together. The victim sits on the "platform" and holds on to the rescuers for support. It is difficult to cover a long distance or rough terrain when using
this technique ( Figure 26-7 ). A coil of climbing or rescue rope can be used to form a "two-rescuer split coil seat," with each rescuer slipping a side of the rope coil around his or her outside shoulder ( Figure 26-8 ). The patient then sits on the "seat" formed by the rope. A similar approach involves using padded ski poles or stout limbs tied together and supported by backpacks worn by rescuers. The victim sits on the supported poles with his or her arms around the rescuers' shoulders. If the poles are properly padded and securely attached to sturdy rescuers, this technique can be quite comfortable for both rescuer and victim. This approach requires gentle terrain without narrow trails. Spine injuries generally prohibit the use of drags or carries because the victim cannot be properly immobilized,
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Figure 26-3 Web sling (tied into a loop) used to carry a victim. The rescuer must use his or her legs for lifting
Figure 26-4 Backpack carry.
Figure 26-5 Single-rescuer split coil carry. Note that the coil can be tied in front of the rescuer, and the wrists of the victim can be bound and wrapped around the rescuer's neck for more stability.
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Figure 26-6 Tragsitz harness in use.
Figure 26-7 A, Four-handed seat used to carry a person. In this technique the upper body is not supported. B, Alternative four-handed seat that helps support the victim's back. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, Lyons Press.)
Figure 26-8 Two-rescuer split coil seat.
but drags or carries may be acceptable when immediate danger outweighs the risk of aggravating existing injuries. Drags are particularly useful for victims who are unconscious or incapacitated and unable to assist their rescuer (or rescuers) but may be uncomfortable for conscious victims. When a drag is used, padding should be placed beneath the victim, especially when long distances are involved. The high fatigue rate of rescuers makes carries a less attractive option when long distances are involved.
LITTER IMPROVISATION The simplest improvised litter is made from a heavy plastic tarpaulin, tent material, or large polyethylene bag ( Figure 26-9 ). By wrapping the material around a rock, wadded sock, or glove and securing it with rope
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Figure 26-9 Improvised handled soft stretcher.
Figure 26-10 Tying an improvised rope (nonrigid) stretcher.
or twine, the rescuer can fashion handles in the corners and sides to facilitate carrying. The beauty of this device is its simplicity, but it can be fragile, so care must be taken not to exceed the capability of the materials used. As an additional precaution, all improvised litters
Figure 26-11 Improvising a stretcher from two rigid poles and a blanket or tarp.
should be tested with an uninjured person before being loaded with a victim. This type of nonrigid, "soft" litter can be dragged over snow, mud, or flat terrain but should be generously padded, with extra clothing or blankets placed beneath the victim. A coil of rope also can be fashioned into a litter, called a rope litter or clove hitch stretcher, but a 46- to 61-m (150- to 200- foot) climbing or rescue rope is required ( Figure 26-10 ). The rescuer constructs the litter by laying out 16 180-degree loops of rope (8 on each side of center) across an area the desired width of the finished litter. The running ends of the rope are used to tie a clove hitch around each of the loops, and then the unused portion of rope can be passed through the loops on the other side and tied off. The litter is then padded with clothing, sleeping pads, and similar material. Lateral stability can be added by tying skis or poles to the finished product. Because of its nonrigid construction, this litter offers little back support and is best suited for victims with injuries that do not require immobilization. A sturdy blanket or tarp can be used in combination with ski poles or stout tree branches. The blanket or tarp is stretched over the top of two poles, which are held about 1 m (3 feet) apart; tucked around the far pole; and folded back around the other pole. The remaining material lies over the first layer to complete the litter ( Figure 26-11 ). The weight of the victim holds the blanket in place. A similar device can be improvised by passing the poles through the sleeves of two heavy, zipped (closed) parkas.
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Figure 26-12 Packframe litter. Note that the sapling poles on the litter can be attached to the rescuer's pack frames to help support the victim's weight.
It may be necessary to transport victims with certain injuries (i.e., spine injuries; unstable pelvis, knee, or hip dislocations) on a more rigid litter. Ski poles, stout tree limbs, or pack frames can provide a rigid support framework for such a device. For example, three curved backpack frames can be lashed together to form a platform ( Figure 26-12 ). Ski poles or sturdy branches then can be fastened to the frames for use as carrying handles, and the platform can be padded with ground pads, sleeping bags, or a similar material. Combining a rope litter with a rigid litter can provide more strength and versatility. The rescuer fashions this type of litter by first building a platform of poles or limbs, using a blanket as in a rigid litter, and placing the victim in a sleeping bag on the platform. The patient and platform are wrapped and secured with a length of rope. Because a mummy sleeping bag is used to encapsulate the victim, this device is sometimes called a mummy litter. Although this type of litter offers improved support, strength, and thermal protection, careful thought must be given to the physical and psychological effects such a restrictive enclosure may have on the victim ( Figure 26-13 ). If long distances must be traveled or if pack animals are available, a litter may be constructed so that it can be dragged or slid along the ground like a sled. One such device is known as a sledge ( Figure 26-14 ). This litter is fashioned out of two forked tree limbs, with one side of each fork broken off. The limbs form a pair of sledlike runners that are lashed together with cross members to form a patient platform. The sledge offers a solid platform for victim support and stabilization. If sufficient
Figure 26-13 Mummy litter. (From Auerbach PS: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, Lyons Press.)
effort is put into fashioning a smooth, curved, leading edge to the runners, a sledge can be dragged easily over smooth ground, mud, ice, or snow. Ropes also can be attached to the front of the platform for hauling and to the rear for use as a brake when traveling downhill. A travois is a similar device that is less like a sled and more like a travel trailer (without wheels). A travois is a -shaped platform constructed out of sturdy limbs or poles that are lashed together with cross members or connected with rope or netting. The open end of the V is dragged along the ground, with the apex lashed to a pack animal or pulled by rescuers. Although the travois can be dragged over rough terrain, the less smooth the ground, the more padding and support necessary for comfort and stabilization. A long pole can be passed through the middle of the platform and used for lifting and stabilization by rescuers when rough terrain is encountered. When victims are transported in improvised litters, especially over rough terrain, they should be kept in a comfortable position, with injured limbs elevated to limit pressure and movement. To splint the chest wall and allow full expansion of the unaffected lung, victims
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Figure 26-14 A "sledge."
with chest injuries generally should be positioned so that they are lying on the injured side during transport. For a person with a head injury, the head should be elevated slightly, and for persons with dyspnea, pulmonary edema, or myocardial infarction, the upper body should be elevated. Conversely, when the victim is in shock the legs should be elevated and the knees slightly flexed. Whenever possible, unconscious patients with unprotected airways should be positioned so that they are lying on their side during transport to prevent aspiration.[1]
RESCUE LITTERS AND STRETCHERS The image most often associated with rescue immobilization and transportation devices in the United States is that of a traditional tubular steel and chicken wire-netted basket, which came to be known as the Stokes basket. Although this apparatus was and still is ubiquitous, many may recall the Thomas, Duff, Mariner, Brancard Piguillem, Perche Barnarde, Neil Robertson, MacInnes, and Bell stretchers for their evolutionary and robust designs. Today there are a variety of devices that meet the following two primary wilderness medical needs: 1. Immobilization and protection of a victim during transportation 2. Safe, comfortable, and stabilized transportation of a victim to definitive care
DESIRABLE CHARACTERISTICS OF A WILDERNESS STRETCHER Peter Bell,[2] rescue equipment historian and developer of Bell stretchers, has described several specific characteristics of a high-quality, useful rescue stretcher. Bell claims that "a good stretcher should": 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.
Be as strong and robust as possible, with materials compatible with the rescue environment Be as lightweight as possible Have smooth edges that will not snag Be devoid of small spaces that will trap or pinch fingers (rescuers' and patients') Be large enough to provide strength, security, and comfort for the largest of persons when the device is in any position (horizontal, vertical, on its side, upside down, etc.) Prevent worsening of injuries during use Provide security for the victim regardless of his or her condition (e.g., slippery, wet, muddy) Be comforting to the conscious victim Be easy to use in the dark and in temperature extremes (very hot or cold) Protect the victim from the environment (heat, cold, brush, rocks, etc.) Be reliable for many years after many uses in extreme conditions Be easy to carry and use when carrying a heavy, large person Be portable (can be carried in a car, boat, plane, helicopter, etc.) Be impossible to use improperly Be easy to clean and sterilize
STRETCHERS In the interest of brevity and with some technical latitude, this discussion describes stretchers in four categories: basket-style, flat, wrap-around, and mountain rescue. Basket-Style Stretchers The basket-style stretcher derives its name from its shape. The sides curve upward to protect the victim's sides and to prevent the victim from rolling out. Most basket-style stretchers combine a steel frame (solid, tubular, or both) with a shell of either steel wire netting ("chicken wire") or plastic. Many include wooden slats in the bottom to provide additional protection and support.
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Most likely, basket-style stretchers initially were adopted by wilderness rescue organizations because they met fundamental needs and were sufficiently robust to endure great abuse in severe terrain. The seminal basket-style stretcher, called the Stokes, first appeared in the late 1800s and likely got its name from the fact that it was designed to be used on naval and commercial ships to remove casualties from the "stokehold," a room in which the boilers were stoked ( Figure 26-15 ). However, at least one source makes an unsubstantiated claim that the device was invented in 1895 by Charles Stokes.[8] The significant influence of this device is reflected in the fact that the Stokes was the first commercially available basket-style stretcher in the United States. The original Stokes design included a leg divider meant to separate and support each leg individually. Many came to consider this configuration counterproductive when the use of long (16 × 72 inch) backboards and other spinal, full-body immobilization devices became widespread, especially for early treatment of trauma. Most current designs of the Stokes basket-style stretcher have eliminated the leg divider to allow full immobilization of a patient on a long backboard, which can be inserted into the basket. The Junkin Safety Appliance Company manufactures several Stokes basket-style stretchers, including models that break into two pieces and models with and without wooden slats or leg dividers, that meet the more robust military specifications (MIL-L-37957 and RR-L-1997) ( Figure 26-16 ). Although the traditional materials and design (i.e., tubular and flat, welded steel with a steel chicken wire covering) are still in use today, basket-style stretchers are more often constructed from tubular stainless steel or aluminum because of the added corrosion resistance, increased strength, and reduced weight. Manufacturers, such as Junkin and Ferno, offer basket-style devices in full-rectangular and tapered-rectangular shapes. Both are also available in break-apart versions for easy carrying. Narrower versions (usually 19 inches wide, instead of 24) are available for use in confined spaces or caves, although cave rescuers rarely prefer any type of chicken wire litter. Because of the importance of portability in wilderness areas, the break-apart capability is an adaptation to nearly all styles and types of litters. Junkin manufactures a version of the Stokes stretcher completely coated with a plastic material called Plastisol, which provides nonsparking, nonconductive, and antistatic properties. Junkin suggests that this coating allows improved purchase (handgrip) on the litter and offers insulation from the temperature of the metal. A collateral benefit of the coating is that it extends the life and integrity of the steel chicken wire netting. Taking advantage of substantial improvements in polymer research, some manufacturers began producing
Figure 26-15 Traditional tapered Stokes litter with leg divider. (Courtesy Junkin Safety Appliance, Inc.)
Figure 26-16 Break-apart Stokes litter with wooden slats. Many manufacturers also offer accessory straps or backpack devices that allow the rescuer to carry the litter halves on his or her back. (Courtesy Junkin Safety Appliance, Inc.)
Figure 26-17 Ferno model 71 stretcher. (Courtesy Ferno.)
a stretcher shell composed of rigid plastic instead of steel mesh. Ferno's model 71 stretcher has an orange plastic shell wrapped around an aluminum frame and secured with aluminum rivets. Brass grommets in the plastic serve as attachment points for a lifting harness ( Figure 26-17 ). At half the weight of a traditional steel Stokes, this device offers protection from snags and obstacle 627
penetration that cannot be provided by the wire netting of the Stokes. In addition, the plastic used is chemical resistant and the molded underside runners make it slide smoothly over flat ground, ice, and snow. Ferno offers a version with tow handles and a chain brake that is designed specifically for ski patrol applications so that a packaged victim can be "skied" down a slope or pulled along a snow-covered trail. The orange Ferno litter has a load limit of 270 kg (600 lb), but its usefulness in a vertical raise configuration depends on the integrity of the aluminum frame and the plastic shell; if one is compromised, both may fail. Because of this limitation and because of the lightweight materials used, bending or twisting the device should be avoided. International Stretcher Systems also builds a basketstyle stretcher with an aluminum frame but uses a different approach for combining the frame with the shell. Their plastic shell is similar to the shell in the Ferno model 71 (high-density polyethylene), but it is placed outside a full aluminum skeleton to facilitate sliding over the ground. Inside the stretcher, a spring-suspended victim "bed" that doubles as the victim retention system has been added to protect the victim from the internal frame members. This bed minimizes transport shock and features built-in shoulder straps, pelvic padding, a head and chin immobilizing harness, foot and ankle straps, and a large "double-security" Velcro body restraint flap that wraps around the victim. The stretcher is lightweight (weighing 10 kg, or 22 lb) and high strength (holding up to 1134 kg, or 2500 lb) ( Figure 26-18 ). The Junkin model SAF-200-B includes parallel stainless steel top rails. The top tube is larger to allow comfortable hand-gripping and to provide an attachment for lifting bridles, and the smaller solid steel lower rail allows attachment of patient retention straps. The twin rail configuration keeps patient straps and lifting systems from interfering with each other and helps protect the attached materials from abrasion during use. Unlike the International Stretcher Systems device, the stainless steel frame in the Junkin stretcher wraps around the exterior of the basket, which is lined with a smooth-surfaced, permanently padded plastic shell. This design offers comfort for the victim but makes it difficult to slide on the ground because of the external, exposed steel frame members. The unit is heavy (weighing 14.5 kg, or 32 lb) but breaks apart for packing and marries well with a litter wheel to allow easier handling. Bell Rescue Stretchers offers the Series 2 Ludlow stretcher, which is simply their strongest flat stretcher with deep basket sides added. This strong, stainless steel-framed design has fold-down sides, which simplify access with a backboard. The sides can be completely removed to revert the device back to a flat
Figure 26-18 International Stretcher Systems' "3-in-1" Basket Litter with flotation added. (Courtesy International Stretcher Systems.)
stretcher. Other available variations on this theme from Bell include versions with shorter sides (the Otterburn), an open foot end (the Newark), and a steel plate welded into the bottom of the stretcher to help protect the victim (the Manchester). The Manchester weighs nearly 22.5 kg (50 lb) by itself. The manufacturer claims that the Series 2 models can all accommodate a long spine board and have been "proof tested" to between 500 and 720 kg (1102 and 1587 lb). The "bed" of Bell's Series 2 stretchers is made of 14 polypropylene web straps that cross between the steel frame members. This webbing also passes through two movable stainless steel spinal supports (flat steel frame members that run the length of the caudal two thirds of the litter). Four patient retention straps attached to the outermost rails, a patient shoulder strap, and integral lifting rings are supplied with the device. A slightly smaller, lighter, and less robust version, called the Bell Emergency Stretcher (discussed in the next section), also is available. Flat Stretchers Flat stretchers are generally flat and have very short or no sides. Restraint straps or built-in tie downs serve as the physical means by which the victim is secured in the litter. Although the specific characteristics of these types of stretchers vary greatly (from extremely lightweight to high strength), generally they are used when specific benefit is derived from their low-profile shape. Although this style of stretcher has been modified to allow dragging or sliding (e.g., mountain rescue stretchers), the primary purpose of the flat design is to reduce weight and profile for carrying or for specific applications, such as loading into an aircraft. Although a simple, two-pole canvas litter is fine for use over short distances, uncomplicated terrain, or the battlefield (where haste is paramount), the lack of patient protection and immobilization capability limits it usefulness outside of the hospital or battlefield setting. A more modern version of this simple device is made of aluminum, folds for easy storage, and doubles as a long
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Figure 26-19 The Junkin Air Rescue Stretcher (SAF-350) was designed for use in Bell Jet Ranger helicopters. This lightweight, flat stretcher folds for easy storage but is not designed for long carries. (Courtesy Junkin Safety Appliance, Inc.)
backboard. Another version is hinged at one end so that it can be spread along its long axis and slid under a patient on the ground with little movement or rolling. This "scoop" stretcher was commonly used by emergency medical service providers but has been supplanted by the use of long backboards. In the final analysis, both the military and aluminum iterations of the flat stretcher are intended for carrying a person short distances in an environment with few terrain obstacles or where complete security and immobilization are not required. Several successful varieties of flat stretchers have evolved over the years, including the Brancard Piguillem, the Junkin Air Rescue Stretcher ( Figure 26-19 ), and a few of the Bell stretchers that are categorized as flat for the purposes of this discussion. The Brancard Piguillem (Brancard is French for "stretcher" and Peguillem is a proper name) is a flat, old-style stretcher consisting of a canvas patient bed lashed to a steel and aluminum frame (weighing 14 kg, or 30 lb), which folds in half for easy carrying by one person. The design, which has evolved over the years in the European and British mountain rescue communities, includes a patient bed with a permanently attached, integral casualty bag lashed to the frame to protect and secure the victim. Full-length runners raise the stretcher a few inches above obstacles and allow for easy bare-handed gripping. This folding, portable design with integral patient protection made the Brancard Piguillem popular with mountain rescuers and served as the impetus for the evolution of several of the current styles of mountain rescue stretchers. The Kendall Stretcher, from Bell Rescue Stretchers, has the same features as their Ludlow Stretcher without the basket sides (see the previous section). The Kendall has a stainless steel frame, integral lifting rings, a bed made of polypropylene web straps that cross between the frame members, color-coded patient retention (38-mm web) straps, and a detachable foot loop. The Kendall Stretcher can be used either side up; there is no top or bottom. A slightly less robust version of Bell's flat stretcher is their Basic Emergency Stretcher. This device is smaller and lighter (weighing 5.2 kg, or 11 lb, 8 oz) and works well in commercial and industrial settings where severe terrain is rarely encountered. Troll Safety and Rescue Equipment produces the Alpine Stretcher, a folding, one-piece, steel-frame
Figure 26-20 The steel-framed Troll Alpine Stretcher has an integral patient retention system and a polyolefin bed. (Courtesy Troll USA.)
stretcher that has a short spinal protection strip below a rigid polyolefin bed. It is strong and flat, making it suitable for wilderness and mountain rescues in which vertical evacuation is required. The integral, color-coded full-body harness and folding capability make it easy to transport into the wilderness and securely package a patient ( Figure 26-20 ). Mountain Rescue Stretchers Mountain rescue stretchers are essentially stronger, more robust flat litters with runners or skis attached to the bottom for easy movement over rugged terrain. Over the years, engineers and litter designers with mountaineering and rescue backgrounds have adapted rescue litter designs to meet specific practical needs of their environment. The result is the strongest and most robust platform available for patient treatment and transportation, but these benefits come at the cost of weight and size. The Thomas Stretcher is an early and beautifully simple example of the mountain rescue device. Invented in the U.K. in the 1930s by Eustace Thomas (no relation to Hugh Owen Thomas, who invented the Thomas "half-ring" splint), it consisted of wood (ash) runners, an aluminum frame, a canvas bed, and six or seven patient straps attached to the rails. It also had locking, tubular, retractable handles that stowed in the tubular rails.[5] The Thomas Stretcher is still manufactured, with some modifications, by Bell Rescue Stretchers in the U.K. In the late 1950s, Donald Duff, a pioneer of mountain rescue in Scotland, designed a stretcher with a steel
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tubular frame and no handles. Channeled steel runners extended along two thirds of the caudal end of the stretcher. It weighed about 13.5 kg (30 lb) and could be fitted with a wheel and undercarriage for easier movement over rocky terrain. Its profile was low and sleek, and the runners could be detached and the remainder folded in two for backpacking.[4] Although they have almost completely been replaced by more modern designs, two basket-style mountain rescue stretchers that evolved in Britain and Europe over the first half of this century deserve mention. The Perche Barnarde (Perche is French for "perch" or "pole" and Barnarde is a proper name) consists of a 2-m (7-foot)
square section of steel tube from which a canvas casualty bag is suspended. The tube breaks into three pieces for easy carrying. The bag is attached to the tube at each end. Where the patient's shoulders would fall, a spreader bar is placed to keep the bag open. From each end of the steel tube extend two removable, bicycle-type handlebars fitted with pads so that the handlebars can rest on rescuers' shoulders. Although this device has been used successfully in many difficult mountain evacuations over the years, its limitations regarding patient comfort, protection, and immobilization are obvious. The Mariner consists of a canvas bed attached to a steel sledlike frame. The bed functionally resembles a reclining chair in that the patient sits flexed at the hips and waist with the lower legs supported by a canvas platform. The frame is rounded from end to end and includes two steel runners to deflect obstacles. Two adjustable handles extend from each end of the frame for carrying. Today, the Mariner is used by several U.K. mountain rescue teams and contributed significantly to the evolution of the mountain rescue stretcher. The current British standard for mountain rescue stretchers includes two devices that are incredibly strong, durable, and unfortunately heavy. The Mark III Bell Rescue Stretcher (which weighs 24 kg, or 53 lb) and the model 6 MacInnes Rescue Stretcher (which weighs 22 kg, or 48 lb) ( Figure 26-21 ) are intended to survive years of use in extreme mountainous environments. Both have break-apart versions for easy packing into isolated areas, and both incorporate lifting rings, skids, and head guards. Flexible, Wrap-Around Stretchers A focus on improving stretchers for particular environments or situations has led to major developments in a number of litter design areas. It is difficult for a single device to excel in every situation because enhancing one capability or characteristic can be detrimental to another. For instance, it can be difficult to achieve a substantial increase in strength while decreasing overall weight. However, new innovative stretcher designs and materials allow structural flexibility to meet specific needs.
Figure 26-21 MacInnes MK 6 Mountain Rescue Stretcher. Note the extending handles, folding head guard, and optional twin (solid) tires. (Courtesy MacInnes Rescue Stretchers.)
Flexible, wrap-around stretchers can be folded, rolled, or otherwise compacted for storage and "wrap around" in that they contain the victim to provide protection, immobilization, and often sufficient support for vertical lifting. The Neil Robertson Stretcher was the impetus for this entire category of device. Adapted from a Japanese design and first produced between 1906 and 1912, this wooden and canvas stretcher was originally made of bamboo and sewn by hand. The "Neil Rob" supplanted the Mansfield military stretcher in the U.K. and was first given the name Hammock for Hoisting Wounded Men from Stokeholds and for Use in Ships whose Hoists are 2 feet, 6 inches in Diameter.[3] The Neil Rob consists of wooden slats covered with semirigid canvas that are sewn the length of the stretcher. These slats wrap around the patient in mummy fashion, with arms in or out, providing protection without bulk. Full-body immobilization, protection, and a small cross section combine to produce a device well suited for use in small spaces or for situations in which the victim must be moved through a small opening.[9] For situations requiring full-body protection for the victim without complex restraint systems, the Reeves Stretcher (model 321011) and Ferno Flexible Stretcher (model 131 and 137) almost totally encapsulate the patient ( Figure 26-22 ). Although not intended for vertical lifting, both include a durable, vinyl-coated fabric shell that wraps around the sides of the patient and integral wood or synthetic slats that provide longitudinal rigidity. When used in conjunction with a cervical collar and spinal immobilization, these devices provide environmental and mechanical protection while allowing the victim to be carried through narrow passages. The Reeves Sleeve (model 31220) is a compact immobilizing stretcher suitable for hand-carry situations or vertical environments. The device slides over a full backboard and depends on the backboard or short spinal immobilizer to provide rigidity ( Figure 26-23 ).
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Figure 26-22 Ferno Flexible Stretcher with storage case. (Courtesy Ferno.)
Figure 26-23 Reeves Sleeve in use. (Courtesy Reeves Manufacturing, Inc.)
Figure 26-24 SKED Stretcher in use. (Courtesy Skedco.)
Figure 26-25 Troll Evac II Body Splint and carrying bag. (Courtesy Troll USA.)
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Figure 26-26 The Smith Safety Products (SSP) HD Rescue Stretcher and carrying bag constitute the basic package. When the detachable plastic shell (shown) is added, it becomes the SSP USAR Stretcher. (Courtesy Smith Safety Products, Inc.)
Skedco's SKED stretcher provides wrap-around protection similar to the Neil Rob, but a combination of shape and material, rather than integral slats, provides longitudinal rigidity ( Figure 26-24 ). Light and compact when stored in its packable case, the flexible, low-density polyethylene plastic litter wraps around the victim to form a rigid sleeve that is superbly compact for maneuvering in tight quarters. A half-length version is available for moving persons from areas that are too confined for a full-length device when flexing the victim at the hips might facilitate extrication. The hard and smooth plastic material can be easily dragged over a variety of surfaces and offers substantial protection from penetrating obstacles. Though the SKED stretcher provides spinal protection, the manufacturer recommends using an Oregon Spine Splint (Skedco) or similar device when cervical spine immobilization is necessary. External lift slings are included with the SKED to allow vertical or horizontal lifting, and flotation is available for use in a marine environment. Troll Safety and Rescue Equipment produces the Evac II Body Splint, which is designed for use in confined spaces and for technical rope evacuations ( Figure 26-25 ). A flexible, heavy nylon moisture barrier gives moderate rigidity to the protective nylon covering with sewn-on web handles. The integral body harness eliminates the need for any additional casualty retaining straps, and the lightweight nature of the device allows superior portability in confined areas. However, the substantially tapered shape may make it difficult to package the victim with external splints. The device can be used horizontally, as a transportation device, or vertically, during technical evacuation. The Ferno Paraguard Rescue Stretcher (model 1411) is based on a narrow patient "bed," which gets its foundation from a stainless steel and aluminum frame. The bed includes color-coded straps and wraps for victim packaging. The stretcher folds in half when not in use. It may be used in vertical environments and includes removable "bicycle-type" handlebars and shoulder harness assist straps that allow two rescuers to carry the stretcher from each end. Smith Safety Products (SSP) manufactures a wraparound stretcher system that incorporates many of the features found individually in other products. The SSP HD Rescue Stretcher is based on a wrap-around shell made of multi-ply polyvinyl chloride (PVC) and closed-cell foam encased in a 1000-din Cordura nylon shell ( Figure 26-26 ). According to the manufacturer, this combination forms a comfortable, full-body splint that provides patient protection from temperature extremes. SSP's basic stretcher features built-in patient restraint straps (head, shoulder, and ankle) and a footrest. Their USAR Stretcher package offers, in addition to the basic
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Figure 26-27 The Medical Devices International Immobile-Vac Full Body Mattress is a full-body splint that can be carried or inserted into other litters. (Courtesy Medical Devices International.)
features, a detachable plastic shell that provides a smooth surface for dragging or sliding and protection from snags or penetration. The USAR Response Set adds a patient bag made of thermal fleece. Medical Devices International (MDI) makes the Immobile-Vac Full Body Mattress, which is a full-body vacuum splint on which the victim is carried ( Figure 26-27 ). The vinyl-coated, fabric patient bed contains loose polystyrene (Styrofoam) beads similar to those in a beanbag chair. Once the victim is positioned on the mattress, a small hand pump is used to expel air from within it. This process creates a rigid, full-body splint that conforms to the victim's shape. This "cocoon" immobilizes the spinal column and extremities while providing a comfortable platform. The mattress has integrated web carrying straps that can be used to carry the patient directly, or the mattress can be inserted into a basket-style stretcher for added versatility and strength. The use of a basket stretcher will be necessary for high-angle rescue because the MDI device is not designed for vertical rescue by itself.
TRANSPORTATION HARDWARE ACCESSORIES A number of wheeled devices can be attached to most basket-style stretchers. These devices take the carrying burden off rescuers in nontechnical evacuations and reduce the load on low-angle haul systems. One example is the Russ Anderson Litter Wheel, which incorporates a large, underinflated all-terrain vehicle tire into a lightweight aluminum frame that clamps to the underside of
Figure 26-28 The Stokes Chariot from Farrington Chariots. (Courtesy Farrington Chariots.)
the litter. This single wheel is positioned under the center of gravity, and the rescuers walk alongside the litter to steady and guide it, with the wheel carrying most of the load. When they encounter large obstructions, such as logs or trenches, rescuers simply lift the litter and continue rolling. One advantage of this device is that it reduces the number of rescuers required to move a litter safely over a long distance. When using this device, only two rescuers (one at each end) are required to tend the litter, but more may be used as necessary. To meet a similar need, the Stokes Chariot (Farrington Chariots) employs a collapsible stainless steel frame with two attached 16-inch (outer diameter) wheels. With no axle between the wheels, the tires can be set to the outside of the frame for greater side-to-side stability or to the inside and under the frame to negotiate narrow trails or doorways. The draw bar end of the "chariot" is set up to receive either the T bar handle, for towing by rescuers on foot, or a hitch adapter, for towing behind motorized vehicles ( Figure 26-28 ). International Stretcher Systems makes a similar device out of aluminum. It also can be folded for storage and employs wheels that can be repositioned on the frame. Junkin and CMC Rescue market two useful stretcher accessories. The CMC Rescue Stretcher Insert is based on Yosemite Search and Rescue's idea to replace the chicken wire in the Stokes litter with a nylon bed, because chicken wire requires padding to allow even minimal patient comfort. A nylon bed allows for an integrated patient restraint system (harnesses) and greatly improves patient comfort. Junkin's Comfo-Pad takes a slightly different approach to the same problem by supplying padding where it is needed in this type of uncomfortable stretcher. MacInnes and Bell integrate steel wire head protectors in their mountain rescue stretcher designs. This feature is important where falling rock is a hazard. CMC Rescue markets a similar aftermarket device
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Figure 26-29 The CMC Litter Shield protects the victim from falling debris while allowing access to the head and face.
made of clear polycarbonate under the trademark CMC Rescue Litter Shield ( Figure 26-29 ). It protects the victim's face from falling debris; allows for easy, rapid airway access; and can be moved out of the way because it hinges on the end of the litter. The shield stores compactly in the litter when not in use. Flotation systems are available for some litters. Ferno and Skedco each offer this option to make their devices safer and more versatile in swift or open water rescue situations. Most litter manufacturers offer specific devices or methods for carrying their devices into isolated areas. For instance, the SKED, Troll Evac II, and SSP HD Rescue Stretchers can be rolled up and carried in a special backpack by a single rescuer. Other manufacturers sell special backpacks or integral carrying harnesses for carrying half of their break-apart litters because of the greater weight. Carrying a Loaded Litter An evacuation is defined as high angle or vertical when the weight of the stretcher and tenders (stretcher attendants) is primarily supported by a rope and the angle of the rope is 60 degrees or greater.[7] This type of situation is often encountered when a rescue is performed on a cliff or overhang or over the side of a structure and usually requires only one or two tenders. In high-angle rescues, most often the stretcher is used in the horizontal position to allow only one tender and to keep the victim supine and comfortable. However, when the packaged victim and stretcher must be moved through a narrow passage or when falling rock is a danger, the stretcher may be positioned vertically. In a scree or low-angle evacuation, the slope is not as steep (less than 60 degrees), the tenders support more of the weight of the stretcher, and a rope system is still needed to help move the load. In this type of rescue, more tenders (usually four to six) are required and the rope is attached to the head of the stretcher. The head of the litter is kept uphill during a low-angle rescue. In a nontechnical evacuation, tenders completely support the weight of the stretcher during a carry out. Generally the terrain dictates the type of evacuation. If the stretcher can be carried without the support of a rope, it is a nontechnical evacuation. If rope is needed to support the load or to move the stretcher, it is either a low- or high-angle evacuation, depending on the angle of the slope. Carrying a litter in the wilderness is difficult and requires many resources. It takes at least six rescuers to carry a person in a litter a short distance (0.4 km, or ¼ mile, or less) over relatively flat terrain. With six rescuers, four can carry the litter while the other two clear the area in the direction of travel and assist in any difficult spots. However, depending on the terrain and the weight of the victim, all six rescuers may be needed to safely carry the litter any distance. If the travel distance is longer, many more rescuers are required ( Figure 26-30 ).
PATIENT PACKAGING Patients (victims) on stretchers must be secured, or "packaged," before transport. Packaging consists of stabilization, immobilization, and preparation of a victim for transport. Physically strapping a person into a litter is relatively easy, but making it comfortable and effective in terms of splinting can be a challenge. The needs of a person secured and transported in a litter are great and should not be overlooked or underestimated. The rescuer's goals are as follows: 1. 2. 3. 4. 5.
Package the person to avoid causing additional injury. Ensure the victim's comfort and warmth. Immobilize the victim's entire body in such a way as to allow continued assessment during transport. Package the victim neatly so that the litter can be moved easily and safely. Ensure that the victim is safe during transport by securing him or her within the litter and belaying the litter as necessary.
Generally, proper patient packaging must provide for physical protection and psychological comfort. Once packaged in a carrying device, a person feels virtually helpless, so transport preparation must focus on alleviating anxiety and providing rock-solid security. With this in mind, rescuers must provide for the victim's ongoing safety, protection, comfort, medical stabilization, and psychologic support.[6] Splinting and spinal immobilization are usually achieved by using a full or short backboard. The victim
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Figure 26-30 Litter-carrying sequence. A, Six rescuers are usually required to carry a litter, but rescuers may need relief over long distances (greater than 0.4 km, or ¼ mile). B, Relief rescuers can rotate into position while the litter is in motion by approaching from the rear. C, As relief rescuers move forward, others progressively move forward. D, Eventually the rescuers who are furthest forward can release the litter (peel out) and move to the rear. Rescuers in the rear can rotate sides so that they alternate carrying arms. Carrying straps (webbing) also can be used to distribute the load over the rescuers' shoulders. In most cases the litter is carried feet first, with a medical attendant at the head monitoring airway, breathing, level of consciousness, and so on.
is secured to the board, and then the victim (on the board) is placed into the litter. When the immobilized patient is finally placed into the litter, adequate padding (e.g., blankets, towels, bulky clothing, sleeping bags) placed under and around him or her contributes to comfort and stability. During transport, victims like to have something in their hands to grasp, to have pressure applied to the bottom of their feet by a footplate or webbing, and to be able to see what is happening around them. [6] Because persons are so vulnerable to falling debris when packaged in a litter, especially in a horizontal high-angle configuration, a cover of some type should always be used to protect the victim ( Figure 26-31 ). A blanket or tarpaulin works well as a cover to protect most of the body, but a helmet and face shield (or goggles) are also recommended to protect the head and face from projectiles. Alternatively a commercially available litter shield can be used and allows easy access to the airway, head, and neck ( Figure 26-29 ). Because the head and neck usually require immobilization, the technique and equipment used to protect them should allow this. Remember also that the conscious victim desires an unobstructed view of his or her surroundings. Carrying a person in the wilderness often requires that the litter be tilted, angled, placed on end, or even
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Figure 26-31 Smith Safety Products (SSP) Thermal Fleece Patient Bag (model 323) was designed to provide thermal protection for the SSP HD Rescue Stretcher but also offers limited protection from falling debris. (Courtesy Smith Safety Products, Inc.)
Figure 26-32 One 10-m (30-foot) web or rope can be used to secure a person into a litter.
inverted. In all of these situations the victim must remain effectively immobilized and securely attached to the litter, the immobilizing device within the litter, and any supporting rope. Poor attachment can cause patient shifting, exacerbation of injuries, or even complete failure of the rescue system. Manufacturers have taken several approaches to securing a person within the litter. Most integrate a retention or harness system directly into the litter. However, a few require external straps to secure the victim to the device. Many users suggest that an independent harness be attached directly to the victim to provide a secondary attachment point in case any link in the attachment chain fails. When a harness is not available, tubular webbing, strips of sturdy material, or even rope can be used to secure the victim. One approach uses tubular webbing slings in a figure eight at the pelvis and shoulders to prevent the victim from sliding lengthwise in the litter. A 10-m (30-foot) piece of 5-cm (2-inch) webbing or rescue rope can be used to achieve the same goal ( Figure 26-32 ). The rope or web is laced back and forth between the rails of the litter in a diamond pattern until the victim is entirely covered and secure. Such a technique also easily incorporates a protective cover and support of the victim's feet. Regardless of the techniques and equipment used, frequently checking vital signs (i.e., distal pulse and capillary refill) during transport can help ensure that any strapping does not obstruct circulation.
References 1.
Auerbach P: Medicine for the outdoors: the essential guide to emergency medical procedures and first aid, ed 3, New York, 1999, Lyons Press.
2.
Bell P: So, what makes a good stretcher? Bell Rescue Stretchers website, www.rescuestretchers.co.uk/study.html, April, 1999.
3.
Bell P: The Neil Robertson stretcher. Bell Rescue Stretchers website, www.rescuestretchers.co.uk/nrob.html, May, 1999.
4.
Bell P: Rescue stretchers in the U.K. Bell Rescue Stretchers website, www.rescuestretchers.co.uk/hist.html, May, 1999.
5.
Bell P: The Thomas stretcher. Bell Rescue Stretchers website, www.rescuestretchers.co.uk/thomas.html, May, 1999.
Cooper DC, LaValla PH, Stoffel RC: Search and rescue fundamentals: basic skills and knowledge to perform search and rescue , ed 3 (revised), Cuyahoga Falls, Ohio, 1996, National Rescue Consultants. 6.
7.
Frank JA, Smith JB: CMC rope rescue manual, ed 2, Santa Barbara, Calif, 1992, CMC Rescue.
8.
Hudson S, editor: Manual of U.S. cave rescue techniques, ed 2, Huntsville, Ala, 1988, National Speleological Society.
9.
U.S. Navy: Rescue and transportation. In Virtual naval hospital: standard first aid, www.vhn.org/StandardFirstAid/chapter11.html, May 1999.
APPENDIX: Comparison of Contemporary Available Stretchers and Litters
636
637
YES OR NO APPROX. DIMENSIONS WEIGHT FRAME SHELL RETAIL L×W×H lbs (kg) MATERIALS MATERIALS COST (US $)
RATED RUNNERS FOLDS, FLOTATION DESIGNED CAN STRENGTH OR ROLLS OR AVAILABLE FOR WHEEL(S) (R) OR SKIDS? BREAKS AS HORIZ. OR ATTACH? PROOF APART FOR OPTION? VERT. LOAD (P) CARRYING? LIFTING?
BASKET STRETCHERS Bell Series 2—Ludlow
2280
2080 × 585 mm
Poly web bed
500 kg (P)
N
N
Y
Y
Y
High-density polyethylene
600 lbs (R)
Y
Y
Y
Y
Y
Recyclable polyethylene shell; vinyl-coated nylon bed insert
2500 lbs (P)
Y
N
Y
Y
Y
1000 80.5 × 22.5 × 34 (15.4) Welded steel Steel 8 inches tube hexagonal mesh netting
1200 lbs (R)
N
Y
Y
Y
Y
Ferno Basket Model 71-S
655 85.25 × 24 × 8 inches
International Stretcher Systems "3-in-1" Basket Litter1
900
Junkin Basket, break-apart Model SAF-300-B Junkin Plastic Stretcher, break-apart Model SAF-200B
560
Junkin Confined Space Stokes Model SAF-300CS
81 × 25 × 8 inches
84.5 × 24 × 7.5 inches
38.5 (17.5)
Stainless steel
26 (11.8) Tubular aluminum
22 (10) Aluminum schedule 80 pipe, butt welded
32 (14.5) Steel tube
High-density polyethylene
1200 lbs (R)
Y
Y
Y
Y
Y
240 81.5 × 18.5 × 7.75 inches
23 Welded (10.45) stainless steel tube
Steel hexagonal mesh netting
1500 lbs (R)
Y
N
Y
Y
Y
Junkin Air Rescue SAF-350
300
73 × 16 × 7 inches
14 (6.3) Aluminum tube
Vinyl-covered nylon
400 lbs (R)
N
Y
N
N
Y
Medical Corp Stretcher ex: Junkin SAF-501-NA, Ferno 108
150
87 × 4.5 inches
14 (6.36) Anodized aluminum side poles with 4 hardwood handles
Vinyl-coated nylon
500 lbs (R)
Y
Y
N
N
N
"Scoop" stretcher ex: Junkin SAF-400, Ferno 65
515 79 × 16.75 × 3 inches
Aluminum
350 lbs (R)
N
Y
N
N
N
Troll Alpine Stretcher
975
6000 lbs (R)2
Y
Y
N
Y
Y
FLAT STRETCHERS
MOUNTAIN RESCUE STRETCHERS
78 × 23 × 3.25 inches
20 (9)
Aluminum tube
25 (11.3) Square Polyolefin bed tubular steel (16 g)
MacInnes Mountain Rescue Stretcher Mark 6
MacInnes Superlight Stretcher
Bell Mountain Rescue Stretcher Mark 3
1324 218 × 47 × 26 cm
44 (20) Stainless steel tube and rod
896 189 × 53 × 31 26.4 (12) Stainless cm steel and aluminum tube
3192
2000 × 578 mm
48.4 (22) Stainless steel, aluminum, titanium
Aluminum
1000+ kg (P)
Y
Y
N
Y
Y
Aluminum alloy
NP
Y
Y
N
Y
Y
Stainless steel wire mesh
1000 kg (P)
Y
Y
Y
Y
Y
350 lbs (R)
N
Y
N
N
Y
NA
400 lbs (R)
N
Y
N
Y
N
WRAP-AROUND STRETCHERS Ferno Flexible Stretcher Model 137
Ferno Paraguard Model 1411
350 76.5 × 27.25 × 1 inches
1828
72 × 11 × 4 inches
19 (8.6) Oak wooden Vinyl-coated slats nylon
36.5 (16.6)
Stainless steel and aluminum alloy slats
Reeves Flexible Stretcher Model 101
215
78 × 28 inches
14 (6.3) Wooden slats
Vinyl-coated nylon
300 lbs (R)
N
Y
N
N
N
Reeves Sleeve Model 122
400
73 × 24 inches
14 (6.3) NA
Vinyl-laminated Vertical: nylon 5000 lbs (P)
N
N
N
Y
N
NA
N
Y
N
N
N
Horiz.: 10000 lbs (R)3
N
Y
Y
Y
N
6000 lbs (P)3
N
Y
Y
Y
N
6000 lbs (R)6
N
Y
N
Y
N
Horiz.: 1250 lbs (P) MDI Immobile-Vac Full Body Matress Model 81-A5000
445
81 × 36 inches
12 (5.5) NA
SKED
450
84 × 36 inches
18 (8.1) NA
PVC-coated polyesther mesh
Low-density easy glide polyethylene SSP HD Rescue Stretcher5
445
77 × 12 inches
8.9 (4)
Polyethylene Cordura nylon sheeting
Troll Evac II Body Splint
575
79 × 26 inches
12 (5.5) Polyolefin
Nylon 6.0 finished coated
Vertical: 5800 lbs (R)3
Y, Yes; N, no; NA, not applicable; NN, not needed; NR, not rated; NP, not published; 1 = low, unlikely; 10 = high, very likely. 1The weight of the ISS basket alone is 22 lbs; complete is 40 lbs (shell = 7 lbs; frame = 22 lbs; bed insert, lifting straps, restraint system, belts, and buckles = 11 lbs). 2The welded lift points on the Troll Alpine Stretcher are rated at 6000 lbs each. 3Strength rating is for bridle only. 4A KED, Oregon Spine Splint, or similar short spine board device is recommended for spinal immobilization. 5Smith Safety Products (SSP) adds an external polyethylene sheet to their "HD" (320) model to upgrade it to the "USAR" (321) model, which is less likely to snag obstacles than is the "HD" model. 6The rated strength listed is the tensile strength of the 44-mm flat web handles on the Troll Evac II Body Splint.
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Chapter 27 - Aeromedical Transport James P. Bagian Robert C. Allen
Rapid provision of appropriate definitive care to acutely ill and injured patients is a major goal of all emergency medical services (EMS) systems throughout the world. The ability to rapidly transport and initiate treatment of severely ill or traumatized patients is important in decreasing morbidity and mortality. This is particularly germane to wilderness and environmental emergencies, where medical resources are scarce, transport times to definitive care facilities are often prolonged, and terrain and weather conditions are inherently difficult. Aeromedical transport crews can deliver emergency medical care at the scene, and the time to definitive care can be greatly decreased. This maximizes the patient's chance for a successful recovery.
AEROMEDICAL EVOLUTION Rapid evacuation of trauma victims from an injury scene to the location of definitive care is a modern concept with roots in antiquity. The New Testament documented an early instance of prehospital care and transport: "A certain Samaritan . . . went to him and bound up his wounds, pouring oil and wine, and set him on his own beast and brought him to an inn, and took care of him."[78] The greatest impetuses to the advancement of emergency care and transportation have been epidemics and wars.[61] Before the classical Greco-Roman period, injured soldiers were often left on the battlefield to die. Later, Homer described the use of chariots to evacuate fallen warriors during the Trojan War.[48] Napoleon's forces devised horse-drawn carriages, or ambulance volantes, for the same purpose.[52] The North American Indians devised the travois, a litter that could be pulled by a person or animal to transport ill or injured persons. [59] The U.S. Army began a similar practice during the Seminole War of 1835–1842 and used it again in the Civil War. Major Jonathan Letterman established the process of rapidly clearing wounded soldiers to a point behind the battle line where they could be further triaged to an expectant area for persons with mortal wounds, a local treatment area for the "walking wounded," or a hospital if definitive care was feasible. The central concept was efficient access to surgery for the victim of trauma. These developments were soon followed by the invention of flying machines. In France, Richet had prophesied the potentials of air transport in 1869. [61] This was before the first balloon airlift. The prophesy was validated the following year during the Franco-Prussian War when the first documented aeromedical evacuations took place. During the Prussian siege of Paris, 160 wounded soldiers were evacuated and transported by hot air balloon over enemy lines.[80] In the United States, air evacuation took place soon after the Wright brothers flew in 1903.[39] Grossman and Rhoades presented their idea of air transport of patients to the War Department in 1910, but the government refused to fund them. It was not until World War I that the U.S. military began to utilize aircraft to carry injured soldiers, and this occurred only rarely. However, the French transported patients as early as 1912 aboard Dorland ARII fighters converted to carry litters, despite the government's objection to the concept of aeromedical transport: "Are there not enough dead in France today without killing the wounded in airplanes?"[39] The United States began utilizing its first dedicated air ambulances in 1920, using the deHavilland DH-4A, followed by the Cox-Klemin XA-I. World War II saw the widespread application of fixed-wing aircraft for evacuation. More than 1.4 million were transported from front-line hospitals to tertiary care facilities, with only 46 deaths en route.[86] During this time the concept of medical care during transport was implemented. In November 1942 the War Department began to train flight surgeons, flight nurses, and enlisted medical personnel for aeromedical transport.[39] Also during 1942, Igor Sikorsky produced a rotor-wing aircraft, called a "helicopter," which the army configured with external litters. It was used in an air evacuation for the first time in 1944 in Burma.[36] Helicopters did not enjoy widespread use until more reliable machines became available. The Sikorsky S-51 and later the Bell 47-B were deployed over the rugged terrain and uncertain roads of Korea with great success to provide wide-scale evacuation of wounded soldiers to Mobile Army Surgical Hospital (MASH) units. Although only 11 dedicated "Medevac" helicopters were used, more than 17,700 casualties were evacuated. For the first time, injury victims could travel directly from the point of injury to definitive surgical care. This set the stage for the Army helicopter evacuation ("Dust Off") operations in Vietnam in 1962. With the
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TABLE 27-1 -- Mortality Rates and Evacuation Times During Major Wars EVACUATION TIME (HR) MORTALITY RATE (%)
CONFLICT World War I
18
18
World War II
4–6
3.3
Korea
2–4
2.4
Vietnam
1–2
1.8
From Stewart RD: Trauma Q, May 1985, p 1. Bell UH-IA Iroquois ("Huey") under the leadership of Major Charles Kelly, the Army's 57th Medical Detachment became known for the courage and hard work of flight crews, who flew despite darkness, adverse weather, and enemy fire. Later, the turbine-powered Bell model UH-1H was used to evacuate up to nine patients at a time by hoist from above a dense jungle canopy. By 1967, about 94,000 injured men had been evacuated. [69] As air evacuation matured, the time from wound to definitive care declined from 18 hours in World War I to between 1 and 2 hours in Vietnam.[88] Although medical advances have contributed to improved survival, battlefield mortality has steadily declined from 18% in World War I to 1.8% in Vietnam, perhaps more because of rapid aeromedical transport to definitive care ( Table 27-1 ). Unfortunately, emergency medical care for civilians greatly lagged behind the developments in the military. In the late 1960s, rescue efforts were more organized, skilled, and rapidly performed for a man shot in the Vietnam conflict than for a civilian injured on U.S. highways.[61] Civilian ambulances were said to be no faster than taxis.[77] Civilian transport began to change dramatically in the United States in 1966 when the National Academy of Sciences-National Research Council put forth the white paper Accidental Death and Disability. The Neglected Disease of Modern Society (U.S. Department of Health, Education and Welfare). This document was the impetus for improving EMS systems through the country, and soon the civilian sector began to emulate the military model. Outside the United States, Germany and Switzerland had developed a network of helicopter and fixed-wing air evacuation and transport services that continue to provide rapid access to care from even the most remote areas.[38] The first U.S. civilian aeromedical program was begun in 1969 as a joint effort between the Maryland State Police and the University of Maryland Center for the Study of Trauma (now the Maryland Institute for Emergency Medical Service Systems). Certain hospitals were designated as trauma centers, and victims of highway and other trauma were flown by police pilot-paramedic teams in a primary response role at the accident scene. Since 1970 the service has flown more than 199,000 missions.[82] With the development of faster and more powerful helicopters, reconfiguration of fixed-wing aircraft for aeromedical needs, enhanced knowledge of aeromedical physiology, and experience accumulated through more than 50 years of transport experience, the acceptance, utilization, and success of aeromedical transport are universal. The role of aeromedical transport in the wilderness setting continues to evolve as its importance in providing rapid emergency medical care to sick and injured patients is recognized.
TYPES OF AEROMEDICAL TRANSPORT PROGRAMS Hospital-Based Programs The most ubiquitous type of program is hospital based. Helicopter service is often provided in primary (to the accident scene) and secondary (to the community hospital emergency department) response roles. In addition, many hospitals provide fixed-wing transport in a secondary response role for long-distance transports or when transport by helicopter is impractical. According to the Association of Air Medical Services, in early 1994 there were more than 175 hospital-or health care provider-affiliated and 20 freestanding rotor-wing transport programs in the United States. These services transported more than 172,000 patients in 1993. Nationally, approximately 70% of all flights are interfacility transports, and 30% are flights from the scene.[63] In a hospital-based transport program the hospital frequently leases the helicopter from a vendor, who also supplies the pilots, maintenance, and fuel. The hospital has the responsibility for providing the medical crew and determining the configuration of the crew. In addition, the program directors are responsible for medical control and quality improvement. The hospital may choose to own the aircraft and contract with a vendor for operations or employ its own pilots and mechanics. In most cases the helicopter resides on a helipad atop or near the hospital, and the crew, which may consist of a specially trained flight nurse, flight paramedic, and physician, is quartered in the hospital ready for immediate launch (see Flight Crew). Non-Hospital-Based Programs Non-hospital-based service is provided by an entity that may be supported by a consortium of hospitals, or it may be an independent corporation, ambulance service, or aviation fixed-base operator (FBO). The aircraft may be owned or leased by the entity or by an aviation contractor. Although this is not a common model for
642
helicopter services in the United States, many fixed-wing services operate in this manner. A corporate airplane may be provided on demand for use in an air ambulance mode with its interior reconfigured, or a dedicated airplane may be provided with a custom-made air-ambulance interior configuration, usually under a Supplemental Type Certificate (STC). Public Safety, Police, or State Services The aircraft (usually a helicopter) may be owned and operated by a governmental agency such as the state highway patrol and operated under part 135 of the Federal Aviation Regulations (FAR). As in the Maryland model, flight personnel typically include police pilots and emergency medical technician-paramedics. Military Assistance to Safety and Traffic Program The Military Assistance to Safety and Traffic (MAST) program was established to supplement the civilian EMS systems. Under this program, air medical evacuation services are supplied by active-duty military medical units to the extent that their training budgets allow, provided they can use actual patient transports instead of training exercises. The MAST mission is "secondary"; it is available only when its personnel and equipment are not being used in support of the unit's primary mission. MAST may be requested by the local EMS or disaster management agency. Typical aircraft include the Bell UH-1 and Sikorsky UH-60 (Black-hawk). The medical crew usually consists of medical corpsmen. The MAST program may not compete with similar civilian services. Other Military Resources The U.S. Air Force provides aeromedical transport in support of U.S. military disaster conditions. This service can be requested through the Rescue Command Center at Langley Air Force Base in Virginia. Other available resources include the Air National Guard and the U.S. Coast Guard. Many states have organizations (e.g., California Department of Forestry) that may be called on to assist in search and rescue (SAR) operations in preparation for aeromedical transport. Many other countries have analogous units; the Israeli Air Force, for example, operates a squadron that provides civilian and military rescue and evacuation services.
PATIENT MISSION TYPES Primary Response In a primary response role the aeromedical transport service responds to an accident scene or field location, usually at the request of police, fire, or local EMS personnel, and serves as the initial and sole mechanism of transport to the hospital. In this instance the aeromedical crew may function as "first responders." Helicopters are most suited to a primary response role. The required response times must be short (less than 10 minutes from call to take-off); thus the flight crew must be stationed at or near the launch site 24 hours a day. The service radius ("stage length") is short (typically less than 50 miles), and crews need to be experienced in techniques for landing in proximity to obstacles, under poor conditions, and on uncertain surfaces. In prehospital situations, patients' conditions vary widely, and often, little or no assessment or stabilization is performed before arrival of the flight crew. Medical personnel must possess a high degree of training and experience and should possess at a minimum emergency medical technician (EMT) skills required for patient extrication and stabilization at the scene. Secondary Response In the secondary response role a patient has already been transported by other means to a hospital where some degree of stabilization may have occurred. The aeromedical service transports the patient in the early stages of care from the emergency department of a hospital to a facility better equipped to offer definitive care. Response times required for this type of mission must be competitive with one-way ground transport times. Stage lengths are short to intermediate (150 miles). The transport vehicle is typically a helicopter, although in some remote and wilderness areas, fixed-wing services are also suited to this role. Flight crews used in a secondary response vary depending on the needs of the patient (see Medical Mission Types). The responding aeromedical service typically consists of flight nurses, paramedics, and in some cases flight physicians. Tertiary Response In a tertiary response an inpatient who requires specialized services unavailable at the current facility or who requests relocation is transported to a new facility. Tertiary transports may involve helicopters or fixed-wing aircraft, depending on the level of urgency, stage length, and the cost of transport. Commercial entities throughout the world specialize in this type of service.
MEDICAL MISSION TYPES The needs of different patient types may be categorized by medical problem; this in turn dictates the requirements of the aeromedical transport service. In most hospital-based helicopter programs the majority of patients transported are categorized as adult trauma, cardiac, or medical noncardiac. A number of programs offer or specialize in pediatric, neonatal, perinatal, and organ transplant services, for which specialized crews and equipment may be required. In
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addition, aeromedical transport programs that provide SAR operations require specialized equipment and training. Trauma Patients Trauma patients transported in the primary or secondary response modes may account for 20% to 60% of a hospital-based helicopter service's transport activity, depending on the hospital's function and capability as a trauma center and the relationship between the aeromedical service and the community EMS and public safety network. A study of one urban setting noted that 20% of helicopter missions were to injury scenes, which were located at a mean distance of 14.4 miles from the hospital. Of patients transported, 19% had penetrating trauma, and 81% blunt trauma (66% from motor vehicle accidents). The most common organ system injuries involved the head (65%), extremities (39%), chest (31%), and abdomen (27%). The overall mortality of transported patients was 24%. The most common procedures required at the scene were endotracheal (ET) intubation (41%) and cardiopulmonary resuscitation (CPR) (18.7%). The most common life-threatening conditions were cardiac arrest (18.7%), airway obstruction (5.1%), cardiac tamponade (3.2%), and tension pneumothorax (1.7%).[33] A multicenter study of blunt trauma victims transported by helicopter aeromedical services from both urban and rural environments found a mean trauma score of 13 (of 16), mean age of 29 years, and overall mortality rate of 15%.[8] These and other studies indicate the need for skilled crews in the transport of trauma patients.[91] Medical personnel must have the ability to assess the patient adequately to detect frequent in-flight complications and to intervene with appropriate procedures, including intravenous (IV) cannulation, ET intubation, CPR, chest decompression, and at times a surgical airway ( Box 27-1 ). In wilderness areas the flight crew must be skilled at victim extrication and operating in rugged terrain. They must be familiar with standard trauma care and the range of clinical entities most frequently seen in the wilderness setting. In addition, because resources may be limited and backup unavailable, they may be required to function semiautonomously. For this reason, protocols and standing orders are valuable. Most important are training, skill, and judgment. Patients with Cardiac Disease Patients with most cardiac disease most often are transported in a secondary or tertiary response role, by either helicopter or fixed-wing aircraft. They typically account for 20% to 50% of an aeromedical service's transport activity. The conditions of these patients are often medically complex. Technologically sophisticated treatment modalities may include antiarrhythmics, vasopressors, inotropes, vasodilators, thrombolytic agents, cardiac monitoring, arterial and central venous pressure monitoring, pacemakers, implantable defibrillators, and intraaortic balloon counterpulsation devices.[23] [30] [37] [50] The flight crew must have sophisticated knowledge, expertise, and experience and may include a cardiac critical care nurse and a physician.
Box 27-1. TRAUMA CARE ABOARD EMERGENCY MEDICAL SERVICES HELICOPTERS
MECHANISM OF INJURY Motor vehicle accident Fall Industrial or agricultural accident Gunshot or stab wound Burn Sporting accident Drowning Hypothermia
PROCEDURES PERFORMED BY FLIGHT CREW Endotracheal intubation Cardiopulmonary resuscitation Intravenous lines Central venous access Extrication and splinting Bladder catheterization Nasogastric tube insertion Venous cutdown Tube thoracostomy Cricothyrotomy Pericardiocentesis Antishock garment application
Patients with Medical, Noncardiac Conditions Patients with medical, noncardiac conditions, like those with cardiac disease, are most often transported in the secondary or tertiary response mode by either helicopter or fixed-wing aircraft. This group consists largely of patients with acute neurologic disease or shock or who require assisted ventilation. [41] The spectrum of potential in-flight challenges includes cardiovascular problems, arrhythmias, hypotension, respiratory difficulties requiring acute airway management, seizures, and alterations in level of consciousness. The flight team must be able to manage an airway and operate a ventilator. Additional considerations relate to the cabin environment and need for pressurization if hypoxemia is present, if barotrauma is likely, or if trapped gas exists, as well as the need to predict the requirement for and manage finite oxygen resources in flight.
644
Pediatric Patients Pediatric patients may have traumatic or medical conditions.[9] [44] In a study of 636 pediatric patients transported by air in the Salt Lake City area, 57.5% were transported by helicopter and 37.5% by fixed-wing aircraft, with a mean stage length of 207 miles (helicopter, 82 miles; fixed-wing, 452 miles). Less than 1% of flights were from the scene. The patient age ranged from 3 weeks to 16 years, with 45% less than 1 year old. Trauma was the most common diagnosis (15.3% head injury, 9.3% multiple injuries), followed by neurologic illness (24.2%), respiratory failure or infection (20.1%), gastrointestinal or genitourinary problems (10.2%), metabolic disease (9.2%), cardiovascular disease (6%), and general pediatric surgical problems (5.7%). The overall mortality was 7%.[60] Many of the considerations for pediatric transport are similar to those for adults, especially with older children. Infants may require an incubator, however, and flight crews must be experienced in caring for infants and children. Specifically, knowledge of pediatric advanced cardiac life support skills, including pediatric drug dosages, airway sizes, and fluid management, is essential. Perinatal Patients The need for expedient evaluation, preparation, and transport of the obstetric-gynecologic patient is increasing. Types of problems include ectopic pregnancy, pelvic inflammatory disease, toxic shock syndrome, abnormal fetal presentation, multiple gestation, diabetes in pregnancy, placenta previa, abruptio placentae, disseminated intravascular coagulation, preeclampsia-eclampsia, and preterm labor. The decision to transport patients in advanced preterm labor should be based on such factors as distance between hospitals, time required to cover the distance, personnel available for the transport, gestational age, and speed with which labor has progressed. The flight crew must be knowledgeable about these problems and comfortable with their treatment so as to ensure a favorable outcome for both mother and child. Neonates Neonates have unique anatomy and physiology, and the diseases that affect them require specific knowledge and skills by those involved in their transport. Specific issues include newborn assessment, including assignment of an Apgar score, airway clearance, temperature, homeostasis, and familiarity with neonatal resuscitation.[3] Access to references concerning neonatal emergency drug dosages should be available.[2] [72] The ability to perform umbilical vein catheterization is an important skill for any member of the transport team involved in neonatal care. In addition, knowledge of fluid, electrolyte, and glucose requirements is essential.[53] The flight crew involved in the transport of a neonate often includes a neonatal nurse and a neonatologist. Search and Rescue
Wilderness search and rescue is a unique aspect of aeromedical care and transport that requires significant training and expertise. Most dedicated aeromedical aircraft in the United States are not well suited for SAR operations (see Aircraft for Search and Rescue). Most standard aeromedical crews are not trained in SAR techniques. Many aeromedical helicopters and some fixed-wing aircraft become involved in SAR activities, however, so it is important to be familiar with SAR techniques. In addition, outside the United States, persons providing aeromedical transport are frequently involved in SAR activities (see Chapter 25 ). The keys to a successful SAR operation include proper communications, transport, evacuation, and medical treatment, in the setting of favorable weather conditions and topography. The helicopter, equipped with a hoist and winch, is one of the most effective means of providing SAR in the wilderness setting and is essential in mountainous regions. A long delay between the time of the accident and the call for assistance, combined with a serous injury, adversely affects patient outcome. Helicopters are helpful in various SAR activities, including low-altitude search activity, search area evaluation, and movement of supplies and equipment. They may be the only means of extrication and rescue from the scene. Fixed-wing aircraft are also useful for search and can provide secondary transport, especially when long distances are involved. The U.S. Air Force routinely uses helicopters and fixed-wing aircraft for long-distance SAR operations. Fixed-wing aircraft often arrive at the scene first and may deploy pararescuemen by parachute. If the rescue site is over water, the aircraft may also deploy an inflatable boat with motor and rescue equipment. The pararescuemen and their survivors are then recovered by surface vessels or by rescue helicopters that have been refueled aerially in order to reach the rescue site ( Figure 27-1 ). This capability permits the rapid deployment of rescuers while allowing the most expeditious recovery of survivors and their delivery to definitive care. Theses services are on alert for all space shuttle launches to provide SAR support in the event of a mishap. In the United Kingdom the Royal Air Force operates a helicopter SAR service that flew 1490 missions from 1980 to 1989, almost all of which involved vacationers along the coasts or in the mountains.[55] The Danish helicopter rescue service was founded in 1966 and uses a Sikorsky (S-61) helicopter. Since 1973 its crew has included a physician trained in aerospace medicine and helicopter transport. From 1973 to 1989 it flew 5733
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Figure 27-1 MH-60G Pave Hawk hoisting a pararescueman during a search and rescue exercise. A variant of the UH-60 Blackhawk, the Pave Hawk is flown by U.S. Air Force rescue squadrons. Modifications include forward-looking infrared equipment, night-vision-compatible cockpit lighting, terrain and navigation radar, air refueling probe, auxiliary fuel tanks, and hoist. (Courtesy U.S. Air Force.)
missions, 2075 of which involved direct medical intervention. The most frequent problems were abdominal trauma and cardiopulmonary diseases.[95] In the high Alps, more than 90% of all rescues are performed using helicopters (3000 per year).[4] Of these, 5% are combined rescues; that is, the helicopter carries the rescuers below cloud level, near the site of the accident. Only 5% of mountain rescues are purely ground rescues, mainly necessitated by visibility.[76] Currently a network of SAR systems extends throughout the Alps. In some countries (France, Italy, Germany, Austria, and Spain), air rescues are managed partially or totally by the army or the state. The aircraft most often used for this purpose are the Alouette III, Lama, Ecureil (French), Bolkow 105, 117 (German), Augusta AK 117 (Italian), and Bell (United States). In Switzerland the rescue system in remote terrain is managed by the Swiss Alpine Club and three air rescue companies, Swiss Air Rescue (REGA), Air Glaciers, and Air Zermatt. Switzerland may be unique in that its 18 strategically placed helicopter rescue bases allow an aircraft to reach any accident scene within 15 minutes of take-off. Since the foundation of REGA in 1952, more than 150,000 patients have been transported by either fixed-wing aircraft or helicopter. Up to 8000 patients (5500 from accident scenes) are transported by helicopter every year. Twenty percent of these rescues require a winch, with one third of all winch operations occurring in accident sites that are difficult to reach.[28] More than 75% of all persons rescued by winch were thought to have injuries requiring physician assistance at the scene. Eighty percent of all
Figure 27-2 Helicopter rescue in extremely difficult terrain. (Courtesy P. Bärtsch, MD, and the Swiss Alpine Club.)
Swiss air rescue missions are physician assisted, and 20% have a paramedic in charge. All the physicians and rescue crews are physically fit and trained in alpine techniques, since two thirds of all rescue missions performed from 1990 to 1993 were in topographically remote and difficult terrain ( Figure 27-2 ). Difficult helicopter SAR operations are those that involve low visibility, strong winds, night missions, high-angle rescues, and long-line hoist operations (extension of the hoist cable up to 120 m [394 feet]). In addition, in mountainous regions, power cables and transport cables present a considerable risk. In all cases the rescue risks to the flight crew (as well as to the patient) must be weighed against the degree of injury and risk of further morbidity. The U.S. Air Force, Army, Navy, and Coast Guard equip and train groups to operate in these hostile rescue environments. Helicopters are frequently equipped with precision navigation systems and night vision, forward-looking infrared (FLIR), and thermal imaging equipment. The intense training and specialized equipment permit rescue operations under much more demanding conditions than those encountered by civilian services. Of the military services, only the U.S. Coast Guard has a primary mission of civilian SAR; Army, Navy, or Air Force groups may be requested to assist in civilian rescues in areas where they are available. An increasing number of people participate in alpine sports, including mountain climbing, downhill skiing, mountain biking, and paragliding.[30] A typical representation of the type of mountaineering accidents experienced
646
in the Swiss Alps is shown in Table 27-2 . In addition to SAR in mountainous regions, aeromedical rescue presents great challenges to the medical and flight crews involved in rescues from sea and white water, floods, vertical rock faces, and avalanches. Medical treatment of the survivors should begin immediately at the site of the accident unless
ACTIVITY Delta gliding Paragliding Off-slope skiing
TABLE 27-2 -- Mountaineering Accidents in the Swiss Alps, 1992 (N = 1845 Persons) NUMBER OF PATIENTS RESCUED 18 196 35
Ski touring
238
Mixed climbing
456
Rock climbing
178
Hiking
723
From Dürrer B, Hassler R, Mosimann U: Mountaineering accidents in the Swiss Alps and rescue activities of the Swiss Alpine Club, 1992.
Figure 27-3 A, Jungle penetrator used as a hoist device on most military rescue helicopters. The streamlined shape allows it to slip through dense tree canopies to reach the ground. A foam flotation collar can be attached, making the penetrator buoyant. B, Jungle penetrator rigged for hoist. The seats are flipped down, and the safety straps are pulled out from their stowed position and passed over the head and under the arms of the victim, who then straddles one of the seat paddles. Although the penetrator has three seats, usually only one or two personnel are hoisted at a time. (Courtesy Robert C. Allen.)
weather conditions are deteriorating or the scene is inherently unsafe. If a hoist extraction is needed, the patient with potential multisystem trauma should be evacuated by a rescue net or basket (Stokes) litter with careful spinal immobilization. A tag line attached to the litter prevents spinning during hoist operations. The tag line should be attached with a weak link so that the tag line will break away if the litter becomes uncontrollable. Persons with minimal or isolated injuries may be hoisted by a jungle penetrator ( Figure 27-3 ), rescue basket, or other dedicated hoist device. If a hoist device is not available, the victim may be hoisted by climbing harnesses or rescue belts. [27] The climbing harness or belt should be carefully inspected to make sure that it has not been damaged in the mishap, that it will withstand the strain of the hoist operation, and that it can be safely attached to the hoist cable. The extent of medical treatment rendered on site before extraction depends on many factors, including the victim's condition, scene safety, medical supplies available, medical skill of the rescuers, weather conditions, aircraft loiter time, and flight time to definitive care.
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Good communication between the flight crew and the rescue team is essential to the decision process. Aeromedical crews involved in mountain rescue need to have a thorough understanding of the unique medical problems frequently found in high-altitude rescue situations.
AEROMEDICAL AIRCRAFT Many different types of aircraft can be adapted to the air ambulance role. Each type has its strengths and weaknesses. On the other hand, not all aircraft are well suited for SAR in wilderness areas. Matching the physical and flight characteristics of the aircraft to the needs of the mission is vital. In many circumstances, compromises must be made because of aircraft availability. Rescuers must consider the physical characteristics of the aircraft when caring for a victim in flight. Cabin Space Cabin space should be considered not only in terms of total interior volume in cubic feet, but also with regard to floor space, headroom, and the ergonomics of cabin layout. Ample headroom should be available for the patient to lie comfortably on a secured stretcher and for access by two crew members to all parts of the body. Specifically, access to the head is needed for intubation, the chest for CPR, and the extremities for monitoring perfusion. Some helicopters, such as the Aerospatiale AStar/TwinStar or the MBB BO-105, provide ample upper body access but only limited lower body access while in flight. The relationship of flight crew members when seated (and secured by seat belts) in proximity to the patient is important. The ideal configuration places one medical crew member at the patient's head for airway management and verbal interaction and one at the patient's side to monitor vital signs and perform necessary non-airway-related procedures. This arrangement is typified by the MBB BK-117 helicopter ( Figure 27-4 ). Although some rotor-wing aircraft, such as the BK, are theoretically capable of transporting two patients, this greatly increases demands on the flight crew and the aircraft and diminishes access to both patients. Policies and procedures regarding two-patient transport in these aircraft should be carefully considered. In some large helicopters, such as the CH-46, CH-47 or MH-53, there is enough room to work on multiple patients. Even on relatively large (by civilian standards) military helicopters, however, such as the Coast Guard HH-60J Jayhawk ( Figure 27-5 ), space for patient care can be at a premium. Cabin space can be more generous in fixed-wing aircraft. Cabin-class airplanes, such as the Beech King Air and Piper Cheyenne III, provide an aisle and capability to carry more than one patient and additional crew or family members. Access for Patient Loading The cargo door should be wide enough that the patient's stretcher can be maneuvered into the aircraft without undue tilting, and it should be positioned comfortably near stretcher height to obviate the need for strenuous lifting during ground loading. Standard door configurations on many aircraft do not meet these needs. The "clamshell" doors on an MBB BK-117 helicopter and the oversized cargo door on a Gulfstream Commander 1000 work well for patient loading ( Figure 27-6 ). Useful Load One of the most important considerations for a given patient transport is the aircraft's useful load. This difference
Figure 27-4 Stanford LifeFlight MBB BK-117. (Courtesy Geralyn Martinez.)
Figure 27-5 U.S. Coast Guard HH-60J Jayhawk helicopter in low hover over water, preparing to lower hoist cable to the rescue swimmer. Note the extensive spray under the aircraft. The Jayhawk, a variant of the UH-60 Blackhawk, is a medium-range helicopter used for search and rescue, drug interdiction, and maritime law enforcement. (Courtesy US Coast Guard.)
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between the maximum take-off weight and the basic empty weight is a reflection of the load-carrying capability. In most EMS helicopters the useful load ranges between 1500 and 2800 pounds. On-board avionics, medical equipment, fuel, and crew weights must be
Figure 27-6 MBB BK-117 with rear clamshell doors open. (Courtesy Susan Lockman, Stanford Lifeflight.)
Figure 27-7 Weight calculation aboard aircraft.
subtracted from this value to yield the maximum allowable patient weight ( Figure 27-7 ). Fuel weighs 6 pounds per gallon; a twin-engine helicopter may burn 70 gallons per hour (420 pounds per hour), requiring it to carry 600 pounds or more fuel for a 30-minute-radius flight (with 30-minute reserve). Thus it becomes evident that a flight crew of three weighing a total of 500 pounds with a full load of fuel, oxygen, and medical gear may not have the capability to carry even a small patient, especially on a hot day when the helicopter's performance (lift) is reduced. This consideration can become critical on flights from the accident scene, where terrain obstacles may require vertical take-off and climb-out, demanding maximum helicopter performance. Density altitude (a factor of the air temperature and the pressure altitude) is critical in the performance of helicopters in mountain regions. High altitude combined with hot weather can seriously degrade the performance of even the most powerful helicopters. Weight and Balance Not only must the weight of the loaded aircraft remain at or below the maximum allowed take-off weight for that aircraft, but the center of gravity (CG) must lie within fore and aft limits established by the manufacturer. Each loading configuration places the CG in a unique position, which must be calculated by the pilot before flight, or the flight characteristics may be adversely affected, compromising safety. This consideration may dictate where certain pieces of medical equipment, such as oxygen bottles, may be placed or where heavier crew members must sit.
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On flights from the accident scene the patient's weight is approximated before departure. With pressure to hasten departure, accurate weight and balance calculations are difficult. Thus the aircraft used must have enough margin in the CG envelope that CG limits are not easily exceeded for the given mission profile. Cruise Speed One of the most basic reasons for transporting a patient by air is to take advantage of the greater speed of aircraft compared with ground vehicles. This allows the patient earlier arrival at the destination and minimizes time spent out of the hospital. Not only do aircraft have a speed advantage, but they can travel in a straight line from origin to destination without the curves and deviations present in surface travel. For an aircraft to compete with a ground vehicle in speed in a primary or secondary response mode, it must be at least twice as fast as an ambulance, since the helicopter must fly round trip (outbound to destination and inbound with patient) in the time that the ambulance would travel one way. This is possible with most EMS helicopters, unless (1) the referral location has no suitable landing area (necessitating a time-consuming transit of crew and stretcher to and from the location), (2) ground "packaging" times for the flight crew with the patient are excessive, or (3) an ambulance has a clear, straight highway as a means of alternative transport. Most EMS helicopters are capable of attaining 120 to 150 mph over the ground, although a headwind or tail-wind may hinder or improve these figures ( Table 27-3 ). Piston twin-engine aircraft have a cruise speed range of 220 to 275 mph, turboprop aircraft of 300 to 385 mph, and jets of 400 to 535 mph or more.[22] [70]
TABLE 27-3 -- Helicopters Frequently Used for Aeromedical Transport CRUISE SPEED (MPH) ENGINE(S) SHP USEFUL LOAD (LB) SERVICE CEILING (FT)
HELICOPTER
RANGE (MILES)*
Bell 206L-3
130
SE-T
650
1950
20,000
325
AStar 350D
140
SE-T
615
1868
15,000
379
TwinStar 355F1
147
TE-T
420 each
2391
13,120
368
MBB BO-105 CBS
145
TE-T
420 each
2732
17,000
334
Agusata 109A II
163
TE-T
420 each
2605
15,000
359
Bell 222UT
152
TE-T
684 each
3376
15,800
380
MBB BK-117
160
TE-T
650 each
2645
17,000
368
Sikorsky S-76
167
TE-T
650 each
4700
15,000
550
Dauphin 2
161
TE-T
700 each
4118
15,000
564
Data from Collins RL et al: Flying 1985 annual & buyer's guide, New York, 1985, Ziff-Davis; and 1987 hospital aviation directory, Hosp Aviat 6(4):8, 1987. SE-T, Single engine, turbine; TE-T, twin engine, turbine; SHP, shaft horsepower. *Range includes fuel for warmup, taxi, climb, and 30-minute reserve.
Range Aircraft range is limited by the amount of fuel, which is a function of fuel tank capacity and useful load. In most cases a trade-off is made between payload and fuel; the more weight in fuel, the less weight in passengers (or patients). The maximum time aloft can be calculated by dividing usable fuel on board by rate of fuel burn per hour at cruise speed. Multiplying maximum time aloft by cruise speed yields the maximum range. The Federal Aviation Administration (FAA), under FAR part 91.23, requires that a 45-minute fuel reserve remain at the conclusion of all flights conducted under instrument flight rules (IFR), and a 30-minute reserve under visual flight rules (VFR). Most EMS helicopters operate under VFR, whereas most fixed-wing operations are IFR. Because helicopters typically fly to and from a point at which refueling is not available, round-trip fuel must be carried; this effectively limits the customary radius of operation to approximately half the range (less required reserves). Although it is possible to refuel en route to an airport, this adds to the flight time. Therefore helicopters typically operate within a radius of 150 miles or less, unless the transport is one-way outbound or unless refueling at the destination is feasible. Fixed-wing aircraft operate from airport to airport; thus the radius of operation is closer to the maximum range with reserves. Many fixed-wing aircraft are capable of ranges in excess of 1000 miles, with some jets able to travel more than 2000 miles. Pressurization The partial pressure of oxygen in the atmosphere declines with increasing altitude so that at 5486 m (18,000 feet) it is one-half that at sea level. Part 91.32 of FAR requires the use of supplemental oxygen for the pilot at flight altitudes above 3810 m (12,500 feet) for longer
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AIRCRAFT
CRUISE SPEED (MPH)
TABLE 27-4 -- Fixed-Wing Aircraft Used for Aeromedical Transport CABIN ENGINES USEFUL LOAD (LB)* SERVICE CELING (FT)
RANGE (MILES)†
TAKE-OFF (FT)‡
Seneca III
221
NP
TE-P
1921
25,000
721
1250
Baron 58TC
277
NP
TE-P
2447
25,000
1150
2700
Cessna 402C
245
NP
TE-P
2774
26,900
1164
2200
Navaho 350
250
NP
TE-P
2533
24,000
1200
2200
Cessna 414
258
P
TE-P
2386
30,800
1300
2600
Cessna 421
277
P
TE-P
2807
30,200
1522
—
Cessna 441
330
P
TE-T
4124
35,000
2195
—
Cheyenne II
293
P
TE-T
4053
31,000
1275
2500
Cheyenne III
347
P
TE-T
4448
35,000
1789
3200
MU-2
317
P
TE-T
3975
27,300
1412
—
King Air F90
309
P
TE-T
4383
31,000
1315
2900
Commader 1000
323
P
TE-T
3965
30,750
2149
Citation I
410
P
TE-J
5222
41,000
1500
3000
Lear 25D
509
P
TE-J
7150
51,000
1600
4000
Data from Collins RL et al: Flying 1985 annual & buyers guide, New York, 1985, Ziff-Davis; 1987 hospital aviation directory, Hosp Aviat 6(4):8, 1987; and McNeil EL: Airborne care of the ill and injured, New York, 1983, Springer-Verlag. NP, Nonpressurized; P, pressurized; TE-P, twin-engine, piston; TE-T, twin-engine, turboprop; TE-J, twin-engine, turbojet/turbofan. *Useful load excluding avionics, fuel, passengers. †Range estimated at cruise speed, less 45-minute reserve. ‡Approximate nonbalance-field take-off length.
than 30 minutes.[31] Above 4267 m (14,000 feet), supplemental oxygen must be used by the pilot and all minimum required flight crew at all times. Technically a medical flight crew member is not a required minimum crew member for the operation of the aircraft; neither is the copilot of an aircraft operated under FAR part 135 and certified for single-pilot operations (as with most aeromedical aircraft). Thus the medical crew member is not required to wear supplemental oxygen, although doing so would be prudent, especially for smokers. At altitudes greater than 4572 m (15,000 feet), in addition to the above requirements, each occupant must be provided with supplemental oxygen (although there is no legal requirement to use it). The effects of hypoxia with increases in altitude are more pronounced in patients with lung disease and preexisting hypoxia; this necessitates supplemental oxygen at much lower altitudes. Supplemental oxygen at night will enhance night vision even at altitudes below 3810 m and should be considered for the flight crew, based on operational requirements. To eliminate the need to provide supplemental oxygen, pressurization is available in many larger, fixed-wing aircraft ( Table 27-4 ). A pressurized aircraft is able to pump air into the cabin to maintain a pressure differential between the cabin and outside air, generally 4 to 8 pounds per square inch (PSI). This allows the cabin atmosphere to be maintained at or below the equivalent of a 2438-m (8000-foot) altitude, despite actual altitudes of 9144 m (30,000 feet) or higher.[62] Pressurization obviates the need for supplemental oxygen for crew members and nonpatient passengers, but passengers with lung disease may still require it. Also, by limiting the drop in cabin pressure that occurs with altitude, changes in trapped gas volumes, such as in ET tube cuffs, air splints, and the gastrointestinal tract, can be decreased or eliminated. Special categories of patients include those with dysbarism. Exposure to increased altitude, with its concomitant decrease in ambient pressure, should be avoided. If possible, sea-level ambient pressure should be maintained when transporting these patients. On the other hand, helicopters are nonpressurized and generally fly at lower altitudes where altitude-related hypoxia is unlikely. One exception occurs in mountainous regions where altitudes required to rescue victims or cross mountain passes may exceed 3658 m (12,000 feet). Reasons for transporting patients at higher altitudes include terrain avoidance, the need to surmount adverse weather (which usually occurs within 6096 m [20,000 feet] above ground), and greater speed and fuel efficiency at higher altitudes. Service Ceiling The service ceiling is the maximum altitude at which an aircraft can still maintain a rate of climb of 30.5 m (100 feet) per minute. This ceiling is important in predicting an aircraft's ability to climb above adverse terrain and weather and in taking advantage of favorable winds aloft to maximize ground speed. In the western
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United States, mountainous areas require flight at least 610 m (2000 feet) above the highest terrain along the route of flight, which means a 3658- to 4877-m (12,000to 16,000-foot) service ceiling. These altitudes restrict most helicopters and require use of supplemental oxygen in nonpressurized airplanes. Flight operations that typically require flight at these altitudes should have access to aircraft with sufficiently high service ceilings and pressurization. Runway Length Although not a factor in helicopter operations, runway length restricts certain fixed-wing aircraft from landing. Most airports in rural areas have runway lengths between 610 and 1220 m (2000 and 4000 feet). Higher-performance airplanes usually have progressively longer runway requirements and may be unable to land and take off safely on these strips. Thus, when transport from a rural location with a short runway is requested, it is important to determine the capability of the aircraft being used. Piston twin-engine aircraft can usually operate safely from a 762- to 914-m (2500- to 3000-foot) strip but may have difficulty with 610 m (2000 feet); turboprop airplanes require 762 to 1067 m (2500 to 3500 feet); and jets usually require runway lengths of 1220 m (4000 feet) or more.[62] The take-off roll for airplanes increases with increasing temperature and airport altitude; on a hot day, many airplanes may be incapable of taking off from a short runway if heavily loaded. In winter conditions, operating on icy runways may pose a safety hazard for braking. Turboprop airplanes and jets have a reverse thrust mode that can slow the aircraft on rollout without braking. Weather Operations Adverse weather conditions that may affect a given flight include restrictions in visibility resulting from precipitation, fog, haze, or clouds, as well as airframe icing, turbulence, and wind shear. Flight during instrument meteorologic conditions (IMC) requires adherence to IFR, whereas visual meteorologic conditions (VMC) allow alternative use of VFR. VMC for airplanes are defined as visibility of at least 3 miles and ceiling of at least 305 m (1000 feet) (departing from an airport in controlled airspace).[31] The ability to fly IFR not only improves the likelihood that the mission can be undertaken and completed safely should clouds or adverse weather be present but also enhances the ability of the air traffic control center to follow the flight and properly separate aircraft. IFR capability has drawbacks. Sophisticated and expensive equipment and training are required. Virtually all fixed-wing aircraft are capable of IFR operations, but most EMS helicopters are not. IFR operations are usually conducted from airport to airport (where an instrument approach is available), but most helicopters travel to and from nonairport points without an instrument approach. The percentage of actual missions canceled or aborted because of IMC is small in most rotor-wing programs. One study determined that inadvertent excursions into IMC occurred about 1.3 times per pilot per year, and the anticipated percentage of operations that would be conducted IFR, if it were available, was 9.4%.[68] For most hospital-based programs the cost of upgrading to a more expensive IFR-equipped helicopter (especially if a copilot is necessary for IFR certification), plus the added expense of maintaining pilot IFR proficiency, would be prohibitive. As a rule, military helicopters fly with a pilot and copilot and are usually capable of flying in IFR conditions, although IMC are far from ideal for SAR operations. Performance Closely related to aircraft speed is its ability to climb, expressed in feet per minute (fpm). Known as performance, this ability dictates the type of aircraft used for a given aeromedical transport mission (see Table 27-2 ). The greater the performance (a complex function of power, weight, wing, propeller, and air density characteristics), the better is the aircraft's ability to outclimb adverse weather or to avoid rising terrain or obstacles. Helicopters are unique in their ability to hover above the ground effect, that is, to climb vertically out of the supporting cushion of air produced by the rotor wash. Helicopters perform better when they have a running start, building up forward speed while still in the cushion of ground effect until translational lift is developed. Translational lift results from the forward to backward flow of air over the rotor blades. A helicopter's ability to climb vertically out of ground effect is limited by horsepower and weight. On a hot day at high altitude, performance may be insufficient to take off vertically. [46] This must be considered when selecting a landing site away from an airport. If a confined space surrounded by obstacles is selected, a vertical take-off may be required.[18] Fixed-wing aeromedical aircraft are virtually all twin engine not only for enhanced speed, performance, and cabin space but also for the necessary redundancy of systems required for IFR operations under FAR part 135. If one engine fails, a second is available to allow flight to be maintained; however, if failure occurs during take-off, single-engine climb performance may not be adequate to provide lift. This fact may be critical if insufficient altitude has been gained to allow a return to the airport before obstructions are encountered. Therefore single-engine climb performance for various types of aircraft must be considered, especially if operating out of high-altitude airports, in hot weather, or in mountainous regions (see Table 27-4 ). In general, single-engine climb performance is about 200 to 290 fpm
652
Figure 27-8 A, U.S. Coast Guard C-130 Hercules aircraft. This long-range aircraft is used for ice patrol, fisheries management, and search and rescue. B, Coast Guard HH-65 Dolphin helicopter. This short-range light-lift helicopter is used for near-shore search and rescue, maritime fisheries enforcement, and law enforcement. (Courtesy US Coast Guard.)
in piston twins, 600 to 900 fpm for turboprops, and 1000 to 2000 fpm for jets. [62] The airplane with the best single-engine climb performance will provide the greatest margin of safety, but the cost of equipment, pilot training, and adequate runways will be high.
Aircraft for Search and Rescue Search and rescue is a special type of aeromedical transport that demands aircraft uniquely suited to this role. The aircraft should have good visibility to the sides and below, the ability to fly slowly and to hover, the ability to land away from an airport, and adequate performance in high-density altitude conditions. In addition, certain extrication situations require the capability to hoist victims from rugged or hostile terrain. Helicopters are the aircraft of choice for many SAR missions ( Figure 27-8 ). Few hospital-based EMS helicopters are configured for hoist operations, and hospital flight crews are typically not trained in SAR techniques. The SAR mission differs from other types of medical missions in its requirement for low-level flight over potentially hostile terrain, its use of flight crews for visual surveillance for survivors or wreckage, the need for a prolonged hover if hoist operations occur, and the need for flight crew training in wilderness survival principles if a mishap occurs. Experience and training in these activities are essential for safety. In general, military helicopters and their crews are better equipped and trained to carry out SAR operations. For example, U.S. Coast Guard and U.S. Air Force helicopters have radio locating equipment to pinpoint emergency location transponders (ELTs), also known as emergency position-reporting beacons (EPRBs); possess night vision and FLIR cameras to maximize the probability of visually locating a survivor; and have hoists that enable them to extract survivors from areas where landing is not an option. Flight crews on these missions must be specially trained in the use of rescue equipment and must possess the appropriate medical qualifications and experience to deal properly with atypical EMS situations. U.S. Navy and U.S. Coast Guard rescue swimmers and U.S. Air Force pararescuemen are trained to enter the water or proceed on land to aid in the recovery of survivors. Navy and Coast Guard rescue swimmers receive basic medical training; pararescuemen are trained to the EMT-paramedic level and are given additional training in long-term care of trauma victims. Special hazards exist in mountainous areas. High-density altitudes may limit an aircraft's performance, but local weather patterns may be erratic. On the leeward side of mountains or ridges, severe downdrafts may prevent a helicopter from hovering out of ground effect. The landing site selected should be free of terrain obstacles and should allow for a long, shallow approach and departure. Open areas away from the leeward side of mountains or ridges are preferable. SAR aircraft may not routinely carry the same medical equipment (e.g., ventilators, pacemakers, and defibrillators) as the typical EMS helicopter. Therefore care should be taken to verify that the medical equipment carried on a SAR aircraft is adequate for the intended mission (see Chapter 25 ). Pilot Requirements Helicopter EMS are usually VFR operations, and the FAA has established minimum requirements for pilot experience. FAR part 135.243 specifies that the pilot in command of a helicopter carrying passengers for hire must have at least 500 hours of flight time, including at least 100 hours of cross-country time with 25 hours at night. Fixed-wing services are typically IFR operations, and pilots must have at least 1200 hours of flight time, including 500 cross-country, 100 night, and 75 hours of
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actual or simulated instrument time. They must also be instrument rated and possess a commercial certificate. Most EMS helicopter pilots have much more experience than the minimum requirements; one survey found 59% had more than 4000 hours and none fewer than 2000 hours.[32] The pilot in command is solely responsible for the safety of all passengers and must decide whether to accept or decline a mission. For this reason the pilot is often not told the nature of the medical mission until a decision to go is made. This decision should be based on the destination, weather conditions, environmental circumstances, and estimated time at the scene, airport, or destination facility. No mention of patient type or severity should be made to the pilot before the launch decision is made so that this decision is objective. The pilot has the final say on all decisions related to safety of flight. Communications Helicopter EMS units must have the capability to communicate on very-high-frequency (VHF) airbands assigned for air traffic control, flight service, and local airport Unicom. In addition, the ability to communicate with ground EMS and public safety via VHF and ultra-high-frequency (UHF) airbands is essential. Air use frequencies are accessible through standard aircraft communications transceivers, but EMS communications require additional radio equipment designed for this purpose. Additional needs include communication with the helicopter's base station, either on a locally assigned public-use frequency or a Federal Communications Commission (FCC)-assigned discrete frequency in the VHF airband. Another means of communication is aircraft 800-MHz radiotelephones that can access the surface telephone network. Communication over air-band frequencies requires strict adherence to FAA communications guidelines and a radiotelephone operator permit from the FCC.[26] Medical Equipment and In-Flight Monitoring On-board medical supplies and equipment are typically tailored to the needs of a specific transport program and include medications, airway and ventilation supplies, dressings and bandages, IV fluids, immobilization devices, military antishock trousers (MAST), and stretchers.[73] The U.S. Department of Transportation (DOT), in conjunction with the American Medical Association (AMA), has published guidelines for on-board equipment for air ambulance operation ( Box 27-2 ).[92] Power Most aircraft systems operate from 14 or 28 volts of direct-current (DC) power supplied by an engine-driven alternator or generator. This is not adequate to operate most medical devices, which require 110 to 120 volts of alternate-current (AC) power. Such devices cannot be used without an internal battery of sufficient charge to provide power for the duration of the mission, or unless a 110- to 120-volt AC power source is available from a power inverter, which must be installed under an STC. Power inverters are common components of EMS helicopters and dedicated fixed-wing aircraft that have been retrofit with a custom-made air ambulance cabin configuration, but they may not be a standard component in fixed-wing aircraft that support a dual role and use an interchangeable corporate configuration. Stretcher The patient stretcher must be secured to the aircraft according to the requirements of FAR part 23.561 or 25.561 for seats: 3.0 g's upward (2.0 g's, part 25), 9.0 g's forward, and 1.5 g's sideways. For helicopters the requirements are 1.5 g's upward, 4.0 g's forward, and 2.0 g's sideways. Special configurations, especially those incorporating oxygen bottles and metal framework, may require an STC. Other guidelines (recommendations only) for stretcher configurations are for clear view and access to the patients with at least 30 inches of headroom and at least 12 inches of aisle beside the head. The stretcher should be at least 19 inches wide by 73 inches long.[92] If the patient is positioned with head forward, the acceleration that occurs during take-off of a fixed-wing aircraft may cause venous pooling in the lower extremities and transient hypotension. To prevent this, the patient can be positioned with feet forward. Climate Control The aircraft must be capable of maintaining a comfortable interior environment; about 24° C (75° F) is recommended. During summer months the extensive glass area on a helicopter can produce a greenhouse effect, which may necessitate air conditioning for the comfort of both crew and patient. Lighting Lighting should be available to enable the crew to attend to the patient's needs but not interfere with cockpit operations. Curtains or other physical barriers may satisfy this need. Suction Suction is a requirement for ambulance operations in most states and should be available at all times during aeromedical transport. Integral suction as a custom retrofit system or a portable battery-powered device can be used. Oxygen
In general, enough oxygen should be provided for the flight, plus a 45-minute reserve (IFR; 30 minutes VFR).
654
655
656
In addition, oxygen should be carried to allow for ground handling time at either end. The amount of oxygen required can be obtained by multiplying the desired flow rate in liters per minute (L/min) by the total duration of transport and patient loading and unloading. Table 27-5 lists the capacities of various types of oxygen tanks and their respective weights. Some portable ventilators have a gas-driven logic circuit that requires additional air or oxygen. Electrically powered ventilators have a lower requirement for oxygen but carry the additional need for a power inverter. Most patients are transported with oxygen supplied by nasal cannulae (1 to 6 L/min). A single E-sized oxygen cylinder is adequate for short flights, although backup cylinders are usually carried. Patients intubated and maintained on 100% oxygen, as well as those ventilated on long flights, will exceed the capacity of an E cylinder quickly; several E cylinders or an H cylinder will be required. Box 27-2. U.S. DEPARTMENT OF TRANSPORTATION-AMERICAN MEDICAL ASSOCIATION GUIDELINES FOR ON-BOARD MEDICAL EQUIPMENT FOR AEROMEDICAL TRANSPORT
BASIC MEDICAL EQUIPMENT RECOMMENDED FOR EACH FLIGHT 1/patient Litter or stretcher with approved restraints 2/patient Sheets 2/patient Blankets 1/patient Pillow with cover impervious to moisture 1/patient Pillowcase 1 set
Spare sheets and pillowcase (if weight and space allow)
1 unit
Medical oxygen with manual control; adjustable flowmeter with gauge (0 to 15 L/min); attachment for humidification (NOTE: The oxygen unit must be attached to the aircraft in an approved manner. The amount of oxygen to be carried is determined by multiplying the prescribed flow rate times the length of time the patient must be on oxygen and adding a 45-minute reserve. The minimum amount of oxygen carried should be enough to supply one patient for 1 hour at 10 L/min. It may be necessary to carry a portable oxygen unit if oxygen is not available for patient transfer at some point in the flight.)
2 each
Oxygen masks in adult, child, and infant sizes
6
Connecting tubes
1
Oxygen key
1 unit
Portable suction with connecting tubes
2 each
Suction catheters (various sizes)
2
Tonsil suction tips
1 unit
Squeeze bag-valve-mask unit capable of receiving oxygen through an inlet, and delivering 80% to 100% oxygen through the mask; with masks in adult, child, and infant sizes (bags in adult and small child/infant sizes)
1 unit
Oxygen-powered, manually triggered breathing device (100-L/min flow rate)
1
Blood pressure cuff, sphygmomanometer
1
Stethoscope (NOTE: To record blood pressure readings, a Doppler or electronic stethoscope may be required if noise or vibration levels are high. An electronic unit must not cause electromagnetic interference on aircraft equipment.)
2 each
Oropharyngeal airways in adult, child, and infant sizes
1
Emesis basin
1
Urinal or bedpan or both
1/patient Sound suppressors 1
Pneumatic antishock trousers with pressure relief valve
2
Cervical collars
2
20-gallon trash bags
1 box
Zipper-lock plastic bags or similar product
1
Flashlight, 2 D batteries or equivalent with spare batteries and bulb
2
Locking hooks (or other positive locking device for intravenous fluid containers)
1 qt
Drinking water
12
Paper cups
DRESSINGS AND SUPPLIES KIT, DESIGNED TO BE CARRIED ON EACH FLIGHT 4
Cardboard or air splints or equivalent in arm and leg sizes
12
Tongue depressors
2
Mouth gags or padded tongue depressors
1
Bandage scissors
4
Tourniquets
1 each
Rolls of adhesive tape, ½, 1, 2, 3 inch
1 each
Rolls of paper tape, various sizes
4
Kling bandages or equivalent
1
3-inch elastic bandage
1
4-inch elastic bandage
4
Kerlix rolls or equivalent
2 pairs
Sterile gloves
3
Petrolatum gauze
1 box
Adhesive bandages
6
Disposable surgical face masks
2 each
Syringes, 3, 5, and 10 ml (TB and insulin)
3 each
Needles, 18, 20, and 22 gauge
3 each
Needles, 19, 21 gauge, scalp/vein
2
Surgical dressings
24
Sterile gauze pads
6
Nonsterile gauze pads
2
Triangle bandages
2
Wrist restraints
2
Eye covers
1 roll
Aluminum foil, sterilized and wrapped
1
Large safety pin
2
Clinical thermometers
4
Airsick bags
12
Waterless towelettes
1 box
Tissues
MEDICATION AND INTRAVENOUS KIT, DESIGNED TO BE CARRIED ON EACH FLIGHT 2
Epinephrine HCl, 1:1000, 1 ml, prefilled syringe
2
Epinephrine HCl, 1:10,000, 10 ml, prefilled syringe with intracardiac needle
2
Aminophylline inj., 500 mg in 2-ml ampules
4
Atropine sulfate, 0.5 mg in 5-ml prefilled syringe
2
Diphenhydramine HCl, 50 mg/ml, 1-ml prefilled syringe
2
Dextrose, 25 g/50 ml, prefilled syringe
2
Intravenous injection sets with microdripper
2
Lidocaine HCl, 2 g/10 ml, prefilled syringe
3
Lidocaine HCl, 20 mg/ml, 5-ml prefilled syringe
6
Naloxone HCl, 0.4 mg/ml, 1-ml ampules
1
Nitroglycerin, 0.4 mg, sublingual tablets, 100
2
Digoxin inj., 0.5 mg/2 ml, ampules
4
Furosemide, 10 mg/ml, 2-ml ampules
2
Chlorpromazine HCl, 25 mg/ml, 1-ml ampules
6
Sodium bicarbonate inj., 3.75 mg/50 ml, prefilled syringe
2
Morphine sulfate, 15 mg/ml, prefilled syringe
1
Hydrocortisone sodium succinate, 100 mg/vial
1
Methylprednisolone sodium succinate, 1000 mg/vial
1
Plasma protein fraction, 250 ml with infusion set
2
Sterile water for injection, 20 ml
3
Diazepam, 5 mg/ml, 2-ml prefilled syringe
6
Alcohol swabs
1
Phenylephrine HCl, 0.25%, nasal spray
2
Ammonia inhalant solution, 0.5-ml ampule
2
Isoproterenol HCl, 1:5000, 1-ml ampules
1
Tourniquet
1
0.9% sodium chloride inj., 500-ml bag
1
0.9% sodium chloride inj., 250-ml bag
1
Lactated Ringer's inj., 250-ml bag
1
Lactated Ringer's inj., 500-ml bag
2
Lactated Ringer's inj., 1000-ml bag
3
Needles, 15 gauge, 1 ½ inch
1
Dextrose, 5% in water, 250 ml
1
Dextrose, 5% in water, 500 ml
1
Dextrose, 5% in normal saline, 250 ml
1
Dextrose, 5% in normal saline, 500 ml
1
Pressure pack or infusion pump
1 each
Drip tubing, regular and pediatric
2
Armboards
6
Alcohol wipes
1
Clean hemostat
1 each
Sterile hemostat, curved and straight
1
Nasogastric tube, 14 gauge
2
Sterile normal saline for injection, 20 ml
2 pair
Sterile gloves
1
Knife handle
1
Subclavian set
1
No. 15 blade
1
Intravenous infusion cuff
1
Intravenous infusion cuff
1 each
Rolls of tape, 1 and 2 inch
AIRWAY MANAGEMENT KIT, DESIGNED TO BE CARRIED ON EACH FLIGHT 1
Laryngoscope with curved and straight blades in various sizes; spare batteries and bulb
As required
Adapters for attaching endotracheal tubes to oxygen, etc.
1
Rubber-shod forceps
1
Magill forceps
1
Esophageal obturator airway with gastric suction capability
1
McSwain dart or Heimlich valve
1
Syringe, 60 ml
1
Needle, 14 gauge
1
Syringe, 10 ml
1 each
Rolls of adhesive tape, 1 and 2 inch
1
Viscous lidocaine HCl, 2%
1 tube
Surgical lubricant
BURN KIT, TO BE CARRIED WHEN REQUIRED 3
Normal saline, 1 ml in plastic container
1
Sterile burn sheet, 57 × 80 inch
5 packs
Xeroform gauze, 5 × 9 inch
1
Irrigating syringe, 50 ml
2 pairs
Sterile gloves
4
Kerlix rolls
2 packs
Fluffy gauze
POISON DRUG OVERDOSE KIT, TO BE CARRIED WHEN REQUIRED 1
Irrigation tray
1
Surgical stomach tube for lavage
1 each
Specimen bottles for urine, gastric, and miscellaneous
2 each
Stomach tubes, 14, 16, and 18 Fr
1
Rubber stomach tube, no. 20
1 tube
Lubricant
1 box
Glucagon, 1 unit
2
Ipecac Syrup, 30 ml
1
Physostigmine salicylate, 1 mg/ml, 2-ml ampules
1
Pralidoxime chloride, 1-g kit
1
Activated charcoal, 10 g
OBSTETRIC KIT, TO BE CARRIED WHEN REQUIRED 1
Disposable obstetric pack with sheets, cord clamps, DeLee suction, plastic bag, silver swaddler, sterile gloves
2
Oxytocin, 10 units/ml, 1-ml ampule
1
Episiotomy scissors
1
Ring forceps
PEDIATRIC KIT, TO BE CARRIED WHEN REQUIRED AND ALWAYS WITH OBSTETRIC KIT 1
Pediatric laryngoscope handle with blades
1 each
Pediatric endotracheal tubes with stylette, 2.5, 3, 3.5, and 4 Fr
1
Pediatric Magill forceps
2
Bulb syringes
2
DeLee suction
2
Pediatric drip intravenous tubing
1 each
Feeding tubes, 3.5, 5, and 8 Fr
1
Pediatric blood pressure cuff, sphygmomanometer
ADDITIONAL EQUIPMENT FOR TRAUMA PATIENTS, TO BE CARRIED WHEN REQUIRED 1
Scoop stretcher
1
Long backboard
1
Foley catheter set
1
Femur traction splint
1
Suture kit
ADDITIONAL EQUIPMENT FOR CARDIAC PATIENT, TO BE CARRIED WHEN REQUIRED 1 unit
Cardiac monitor with strip chart recorder
1 each
Spare ECG electrode for each lead
1
Spare roll of ECG recording paper
1 unit
Defibrillator with four pads and conductive gel (defibrillator may come as a unit with the cardiac monitor)
1
Rubber mat or other means of electrically isolating the patient from the aircraft
1
Cardiac board
ADDITIONAL EQUIPMENT FOR SPECIFIC PATIENTS, TO BE CARRIED WHEN REQUIRED 1 unit
Respirator capable of continous ventilation, with ventilator, tubing, exhaled volume measuring device, set of tracheostomy endotracheal adaptors
1 unit
Incubator, with all equipment suitable for neonatal care
Modified from US Department of Transportation, National Highway Traffic Safety Administration; American Medical Association Commission on Emergency Medical Services: Air ambulance guidelines, Washington, DC, 1981, The Department. Inj., Intramuscular injection; Fr, French; ECG, electrocardiogram.
Ventilators On short flights, most patients can be bag ventilated manually, with the addition of a positive end-expiratory pressure (PEEP) valve as needed. Manual ventilation has drawbacks. Minute ventilation can rarely be precisely controlled, leading either to respiratory acidosis or more often to alkalosis. The patient's tidal volume limits may be exceeded, with resultant pulmonary barotrauma. More important, the medical attendant will be completely occupied with ventilation and is TABLE 27-5 -- Oxygen Tank Specifications ENDURANCE† (HR ) CYLINDER SIZE
CAPACITY* (L)
WEIGHT (lb)
AT 2 L/min
AT 10 L/min
D
11
356 2
1
G
32
1200 10
2
Q
70
2320 19.3
3.8
150
6900 57.5
11.5
H and Q
From National EMS Pilot's Association: Hosp Aviat 5(6):17, 1986. †Estimated endurance; actual values may vary. *At 21° C (70° F), 14.7 PSI. Capacity varies with ambient conditions.
thus unavailable to perform other tasks. This takes on added importance if complex infusions are being administered or in-flight complications occur. The likelihood that manual ventilation will be unsatisfactory increases with the duration of transport, medical complexity of the patient, and severity of underlying lung disease. Compact ventilators are available for use in the aeromedical transport environment.[12] The simplest are pressure ventilators with a timing valve mechanism that will deliver a predicted minute ventilation at a given rate and tidal volume adjustable to patient size. These require that the patient have normal airway compliance. If airway resistance increases, smaller tidal volumes will result, and tidal volumes usually cannot be varied independently from rate. Volume-cycled ventilators
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are superior and available in configurations in which tidal volume and rate can be varied independently. Oxygen bottles, a 50-PSI regulator, high-pressure gas lines, a patient breathing circuit, and source of humidification need to be present. As mentioned, ET tube cuffs need to be appropriately monitored during flight to prevent overinflation resulting from decreased ambient pressure. Infusion Devices Several methods of IV infusion delivery are available in the aeromedical setting: gravity-feed microdrip or macrodrip tubing with the drip rate manually adjusted, gravity-feed automatic infusion regulators with a closed-loop drip-monitoring feedback mechanism controlling drip rate, and infusion pumps. If a pump is used over moderate or long transport distances, the internal battery power may be inadequate, necessitating an external source of power, usually an AC power inverter. With infusions that must be carefully maintained, an infusion pump is preferable. With frequent patient movement and manipulation, tubing can bend and kink, altering resistance to fluid flow. Air trapped in tubing (or in glass IV bottles) can expand with changes in altitude and increase or decrease the infusion pressure. Thus a reliable servocontrolled infusion system provides a margin of safety. Monitor-Defibrillator Combination monitor-defibrillators operate from internal batteries when 110 to 120 volts AC is not available. Other monitors capable of pressure monitoring from arterial lines or pulmonary artery catheters may be used, but these may have limited usefulness on flights of short duration, during which vibration and motion (turbulence) can introduce artifact and erroneous readings, as may occur aboard a helicopter. These devices may find a greater role with dedicated fixed-wing aircraft that frequently transport critically ill patients over long distances. Noninvasive blood pressure measurement is reasonably accurate in most patients, although these devices may have insufficient sensitivity.[57] Potential hazards of defibrillation while airborne remain a concern, although trials support its safety.[23] [43] Caution is still advised, and care should be taken to ensure that crew and aircraft systems are isolated from potential electrical contact (see Common Aeromedical Transport Problems). The pilot should be notified before defibrillation. It is unlikely that defibrillation will cause a problem with the aircraft, but if in a critical phase of flight (e.g., take-off, landing), the pilot may delay the shock until the critical phase of flight is accomplished. Oximetry Pulse oximetry is often indicated for optimal patient care. Pulse oximeters use a colorimetric method, with placement of a soft probe over a fingertip, in a thin skinfold such as an earlobe, or against the conjunctiva.[1] [84] They may be extremely useful in aeromedical transport, during which other methods to detect changes in respiratory status are difficult. Mechanical Resuscitators Cardiac arrest resuscitation while airborne in a small cabin is difficult and physically demanding. In most instances a standard medical crew of two will be completely occupied in performing chest compressions and ensuring ventilation. Additional tasks may be impossible. Therefore a mechanical resuscitator may be used to prevent fatigue and free crew members for other tasks.[67] Mechanical resuscitators are gas-powered devices capable of providing ventilation and chest compressions automatically. Some models provide only chest compressions.
FLIGHT CREW Crew Configuration One of the continuing controversies in aeromedical transport involves crew composition ( Table 27-6 ). The ideal crew composition varies considerably with the mission profile. When the aircraft is involved in a primary response to the accident scene, inclusion of an EMT may be beneficial. The transport of patients whose illness or injuries are complex or whose clinical conditions are extremely unstable may benefit from the presence of a physician. All aeromedical transport programs include one or more of the following providers in the transport medical crew. Emergency Medical Technician-Paramedic EMTs are increasingly a part of the aeromedical flight team. In 1993, 71% of rotor-wing transport programs reported using an EMT-paramedic (EMT-P) as a member of the flight team, vs. 44% in 1988.[15] Paramedics vary in their level of training depending on the state in which they work but usually follow DOT guidelines, which include three levels of certification. EMT-basic provides basic ambulance, rescue, and first-aid skills. EMT-intermediate may include IV and intubation skills. The EMT-paramedic level involves such skills as intubation, IV techniques, medication administration, defibrillation, and arrhythmia recognition and treatment. For an aeromedical flight team member, additional training relating to the aeromedical environment is desirable.[81] [92] EMTs can be of particular value in operations that necessitate frequent interaction with ground EMS. In some regions, helicopter EMS service is integrated into the regional primary response network so that they arrive at the accident scene before ground units, and flight team members experienced in scene assessment and victim extrication are essential.
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TABLE 27-6 -- Medical Attendants in Aeromedical Transport, 1988–1993 PERCENTAGES 1988 1990 1991 1992 1993 HELICOPTER Medical crew One attendant
8
3
3
2
2
Two attendants
92
97
97
98
98
RN/paramedic
44
54
53
57
71
RN/RN
15
11
11
19
21
RN/physician
10
12
11
10
3
RN/other
17
15
20
7
2
Other
14
8
5
7
3
8 hours
2
2
4
6
3
12 hours
62
68
70
82
63
24 hours
18
16
15
11
10
12 and 24 hours
9
9
5
0
19
Other
9
5
6
1
5
One attendant
17
17
10
4
5
Two attendants
83
83
90
96
95
RN/paramedic
41
38
36
54
59
RN/RN
17
15
25
18
24
5
3
2
0
6
RN/other
22
35
32
18
9
Other
15
9
5
10
2
8 hours
—
3
2
2
8
12 hours
46
43
50
47
46
24 hours
14
14
14
19
8
Other
40
40
34
32
38
Crew configuration
Regular-duty shift length
FIXED-WING AIRCRAFT Medical crew
Crew configuration
RN/physician
Regular-duty shift length
From Cady G: Air Med J 12:308, 1993. RN, Registered nurse.
Flight Nurse At least one flight nurse is part of almost all aeromedical transport programs; in 1993, 21% of rotor-wing programs reported using two flight nurses as the sole team members.[15] Critical care or emergency nursing experience is usually a prerequisite, with additional training that includes patient assessment, advanced cardiac life support (ACLS), a trauma life support course, prehospital care skills, certain procedures such as ET intubation, advanced IV cannulation techniques, and in some cases, needle thoracotomy, venous cutdown, cricothyrotomy, and other specialized patient care activities. The flight nurse often is also a certified EMT.
Flight Physician The experience and training of physicians involved in aeromedical transport depend on their role. Those who function as the on-line medical control physician communicate via radio or 800-MHz radiotelephone with the flight crew, monitors care, and gives necessary orders. In the United States, physicians fly as a component of the flight team in a minority of aeromedical transport programs; in 1993, only 3% of all rotor-wing transport programs reported the routine use of a physician, vs. 10% in 1988.[15] In helicopter EMS operations an emergency physician or trauma surgeon may be appropriate, whereas with fixed-wing transport of intensive care unit (ICU) patients an intensivist may be of value. Physicians functioning in this role must have a current level of skill and expertise sufficient to address a wide range of clinical problems. They must also possess additional training relative to the airborne environment, including flight physiology, aircraft operations, and prehospital care ( Box 27-3 ). Most important, they must function in this role with sufficient frequency so as to maintain their skills and remain safe and comfortable within the aeromedical setting. In doing so, they become an asset to the flight team rather than a distraction or liability. Studies during the late 1980s and early 1990s attempted to determine whether a physician crew member has an effect on the outcome of patients transported by helicopter.* Some studies concluded that a physician crew member had a positive impact on patient outcome, whereas others found no difference in outcome between similar cohorts of patients transported by flight crews with two nurses or a nurse and a paramedic. The cost of using a physician crew member is substantially higher than that of a nurse-nurse or nurse-paramedic crew configuration. Some argue that this higher cost would be offset by the decrease in hospital stay or lost person-years that would occur if a physician were a standard member of the flight crew. With advanced training in critical procedures and treatment protocols combined with on-line medical direction, a nonphysician flight crew usually functions as well as a crew that includes a physician. No objective evidence supports the benefit of a physician as a standard flight crew member. Crew Member Stress By its nature, aeromedical transport involves moving a gravely ill patient into an adverse environment with *References [ 5]
[ 6] [ 14] [ 40] [ 42] [ 75] [ 83] [ 85]
.
659
limited resources. Under these conditions a medical crew of only two or three persons must perform complex tasks, solve difficult problems, and make life-or-death decisions. They must perform in a physically confining space that may be uncomfortable, and they must do so under time pressure and with little or no physical assistance. In some cases, rescuers' lives may be at risk. This scenario occurs in few other arenas of civilian medical care. Box 27-3. SPECIALIZED TRAINING FOR AEROMEDICAL TRANSPORT Aviation physiology Atmospheric pressure changes with altitude Gas expansion with altitude Changes in partial pressure of oxygen with altitude Effects of motion and acceleration Effects of noise and vibration Changes in temperature and humidity Aircraft safety Aircraft systems and equipment operations In-flight emergency procedures Survival techniques Patient extrication and immobilization Patient loading and handling aboard an aircraft Patient care techniques in the aeromedical environment Respiratory support and ventilation aboard the aircraft Pertinent Federal Aviation Administration regulations and procedures Familiarity with the local EMS system Radio communications skills and techniques Hazardous materials response procedures Record keeping and documentation in aeromedical transport Preflight, in-flight, and postflight procedures Clinical procedures Cardiopulmonary resuscitation aboard the aircraft Defibrillation aboard the aircraft Intravenous cannulation Endotracheal intubation Tube thoracostomy Needle thoracotomy Cricothyrotomy Central vein catheterization Pericardiocentesis
Cricothyrotomy Central vein catheterization Pericardiocentesis Nasogastric tube insertion Bladder catheterization Antishock trouser application Interosseous line placement Umbilical vein catheterization
"Stress" describes an array of adverse physiologic and psychologic reactions that occur when a person perceives a threat to existence. Although stress may not diminish performance, it may be responsible for errors, faulty judgment, and uneven manual skill performance. It may also affect the physical and psychologic health and satisfaction of the flight crew member.[16] When measured during patient flights, the level of anxiety among aeromedical crew members was significantly higher than during a baseline period on the ground.[87] Factors that correlate with high in-flight anxiety levels include adverse weather conditions (e.g., low ceilings, high winds), severity of the patient's medical condition, complexity of illness or injuries, and the crew member's fatigue. Efforts should be made to minimize stress among crew members. This includes frequent and adequate training; continuing education and feedback; adequate medical backup, including on-line medical direction, written protocols, and treatment guidelines that can aid in difficult decisions; a supportive rather than an intimidating or critical quality assurance program; adequate rest; and safe weather minimums. Both routine mission debriefing and critical incident stress debriefing (CISD) should be an integral part of all transport programs.[64] [65]
FLIGHT PHYSIOLOGY Aeromedical care is different from ground-based care not only because of special equipment and the space-limited environment, but also because of the hostile physical milieu. Hypoxia and Altitude The earth is blanketed by a sea of air. The troposphere lies in the first 9144 to 18,288 m (30,000 to 60,000 feet) and contains atmospheric moisture. Vertical convection currents, as well as a temperature decline with increasing altitude at a lapse rate of 2° C per 305 m (3.6° F per 1000 feet), occur here. Virtually all atmospheric weather occurs in this layer. Above this level lies the stratosphere, extending from 18,288 to 30,480 m (60,000 to 100,000 feet), where temperature remains relatively constant and no moisture or vertical convection currents exist. Air exerts pressure on everything it contacts in an amount equal to the weight of the column of air above the point of reference. At sea level the atmospheric pressure is 14.7 PSI or 760 mm Hg. As the person ascends, a progressively smaller air mass remains to exert weight, and the pressure diminishes. At 5486 m (18,000 feet) the atmospheric pressure is one half of that at sea level, and at 8534 m (28,000 feet) it is one third as great
660
Figure 27-9 A, Atmospheric pressure vs. altitude. B, Alveolar (PAO2 ) and arterial (PaO2 ) oxygen tensions vs. altitude.
GAS
TABLE 27-7 -- Composition of Air PERCENT
Nitrogen
78.09
Oxygen
20.95
Carbon dioxide
0.03
Other gases
0.07
Water vapor
1–5 at sea level
From Del Vecchio RJ: Physiologic aspects of flight, Oakdale, NY, 1977, Dowling College Press. ( Figure 27-9 ). Similarly, under the weight of air, individual molecules tend to compact, so the density of air is also greatest at the surface and diminishes with increasing altitude. These phenomena underlie most of the important physiologic consequences of flight. Air is composed of several gases, of which oxygen makes up approximately 21%, an amount that is relatively constant despite increasing altitude ( Table 27-7 ).[25] [73] Henry's law states that the quantity of gas that goes into solution depends on the partial pressure of that gas (and its solubility characteristics) as exerted at the air-water interface. The partial pressure of oxygen in alveolar air (PAO2 ) is determined by multiplying the fractional composition of oxygen in inspired air (FiO2 ) by the atmospheric pressure (barometric pressure, PB ) after the opposing vapor pressure of water (PW , 47 mm Hg) has been subtracted. This is the basis of the alveolar air equation, as follows: PAO2 = FiO2 × (PB - PW ) - PCO2 /R
where PCO2 is the arterial carbon dioxide tension and R is the respiratory quotient (approximately 0.8). Arterial oxygen tension (PaO2 ) in normal individuals is within 10 to 15 mm Hg of the P AO 2 . With lung disease characterized by ventilation-perfusion mismatch, intrapulmonic shunting, or severe diffusion defects, the alveolar-arterial (A-a) oxygen gradient is much larger, and higher amounts of inspired oxygen are required to produce sufficient oxygenation of arterial blood. The atmospheric PO2 , PAO2 , and the PaO2 all decline with altitude ( Figure 27-9 ). To some extent, PaO2 can be maintained through hyperventilation as PCO2 is reduced, but eventually PaO2 will decline below 60% and hemoglobin will begin to desaturate greatly. It is important during aeromedical transport to maintain hemoglobin saturation at or above 90%. Knowledge of the patient's preflight PaO2 will enable a calculation of the patient's A-a oxygen gradient, which can then be subtracted from the PAO2 calculated for the anticipated en route altitude (or cabin altitude in a pressurized craft) to yield the expected en route PAO2 . Nomograms can be devised for this purpose ( Figure 27-10 ). If the en route expected PaO2 is unacceptably low, supplemental oxygen is required. The FiO2 required to maintain the PAO2 at a given level can be calculated from the alveolar air equation as follows: FiO2 = (PAO2 + PCO2 /R)/(PB - PW )
Or, if PCO2 = 40, R = 0.8, and PW = 47 mm Hg, then: FiO2 = (PAO2 + 50)/(PB - 47)
This allows PAO2 to be determined by adding the PaO2 desired (the minimum acceptable is 60 mm Hg) to the known A-a oxygen gradient (calculated from the preflight blood gas). PB can be estimated over the first 15,000 feet (4572 m) of ambient or cabin altitude as follows: PB = 760 - (23 × Alt)
where Alt is the altitude above sea level in thousands of feet. Transport cabin environments rarely exceed
661
Figure 27-10 Arterial oxygen tension (PaO2 ) at altitude vs. PaO2 at sea level. Locate the sea-level Pa O2 on the x axis and intersect with the cruise altitude (on the diagonal). Read across to find the PaO2 at altitude (y axis).
these altitudes, since pressurized craft are usually capable of maintaining cabin pressure equal to 8000 feet (2438 m) or below at normal cruising altitudes. Nonpressurized craft must provide supplemental oxygen above 15,000 feet. Even a modest increase in FiO2 is usually enough to maintain oxygenation under these circumstances, unless a severe A-a oxygen gradient exists, in which case the addition PEEP may be necessary. The previous equation would predict that a PaO2 of 80 mm Hg at sea level on 40% oxygen would require that an FiO2 of 50% at 8000 feet be maintained. An oximeter can simplify monitoring of oxygenation; as altitude increases, a fall in oxygen saturation can be treated with increases in FiO2 . Effects of Pressure Changes Trapped Gas.
Boyle's law states that the volume of a gas varies inversely with pressure. This means that trapped gases expand as an aircraft ascends to higher altitude (and lower pressure) and contract as it descends. The volume change can be determined from the following equation: P1 × V1 = P2 × V2
Clinically, this is manifested by such alterations as expansion or contraction of air splints or MAST pants, changes in ET tube cuff size, expansion of bowel gas in cases of intestinal obstruction or ileus, expansion of
TRAPPED GAS LOCATION
TABLE 27-8 -- Clinical Manifestations of Trapped Gas Expansion CLINICAL MANIFESTATIONS
Intestinal lumen
Abdominal pain, distention
Pleural space
Pneumothorax, tension pneumothorax
Subcutaneous
Subcutaneous emphysema
Paranasal sinuses
Facial pain
Middle ear
Ear pain
Dental root
Tooth pain
Blood
Air embolism, decompression sickness
Air splints, antishock trousers
Compartment syndrome, ischemia
IV bottle and tubing
Fow rate increase
Blood pressure cuff
Tourniquet effect
Endotracheal tube cuff
Air leak, hypoventilation
pneumothorax air space, and expansion of air trapped in IV lines (or glass IV bottles) ( Table 27-8 ). Certain precautions must be taken, such as the use of plastic IV bags and frequent monitoring of pressure cuffs. Dysbarism.
Decompression sickness occurs mainly in scuba divers that ascend too soon after a dive. Too rapid a decrease in ambient pressure allows nitrogen bubbles to form in the microcirculation, which may lead to ischemia and tissue damage (see Chapter 57 ). Care must be taken in the transport of an ill or injured diver to allow a surface interval of at least 12 hours before transport. An alternative is to attain at least a level D (PADI) dive stage, with a cabin altitude not to exceed 2438 m (8000 feet). If an individual must be transported abruptly after submersion, the transport must be conducted at the lowest possible safe altitude in a pressurized aircraft, to reduce the risk of decompression illness. Motion and Acceleration Aircraft not only move through space in a rectilinear fashion, which cannot be detected by human senses in the absence of visual cues, but also rotate about three axes: longitudinal (roll), vertical (yaw), and horizontal (pitch) ( Figure 27-11 ). Motions about these axes are sensed by the semicircular canals located in the inner ear. Sensations from these organs are useful as an adjunct to visual cues. However, they may quickly lead to spatial disorientation, a phenomenon often experienced by individuals traveling in a turbulent environment without a visual frame of reference. For example, when an aircraft enters a bank to the right, the sensation may be initially correctly interpreted. However, after rollout of the stationary bank to a neutral position, a sensation of
662
Figure 27-11 Axes of movement in aviation.
rolling into a left bank may be sensed. If uncorrected, apprehension may follow. The best remedy for this effect is to maintain a visual reference to the correct position. Vestibular stimuli, especially in turbulence with limited or no visual frame of reference, may result in motion sickness, manifested most often as nausea or vomiting. Affecting both patients and flight crews, motion sickness can be counteracted with antiemetics such as antihistamines (e.g., dimenhydrinate, 50 mg orally) or phenothiazines (e.g., prochlorperazine, 10 mg orally); however, these may produce sedation and are potentially hazardous in flight. Transdermal scopolamine patches applied behind the ear have been used as effective prophylaxis for nausea and vomiting during flight. Noise and Vibration Noise and vibration are components of all aircraft environments, especially helicopters. The most obvious impact of noise is on communications within the cabin, particularly with the patient, who is least likely to have a headset and access to the aircraft's intercom. In addition, the patient's breath sounds are difficult if not impossible to hear, and thus other means to identify changes in respiratory status, such as pulse oximetry, must be employed. Headsets are essential for effective communication among flight crew members aboard a helicopter, although they are usually unnecessary aboard larger fixed-wing aircraft. Noise may lead to permanent defects in auditory acuity if exposure is prolonged or recurrent. Veteran pilots demonstrate 10- to 20-dB reductions in
high-frequency auditory acuity. Noise and vibration may also lead to stress and fatigue.
COMMON AEROMEDICAL TRANSPORT PROBLEMS Pretransport Preparation Once the decision is made to transport a patient by air and the appropriate aeromedical service is contacted, preparations must be made to ensure patient safety and comfort and to aid the flight crew in patient care. A study of the causes of ground delays in a rural inter-hospital helicopter transport program found that on arrival of the flight team, 31% of patients required minor interventions (insertion of IV line or nasogastric tube, blood transfusion, bladder catheterization, MAST application) before take-off, and 33% required major interventions (ET intubation, tube thoracostomy, central venous access).[54] When no intervention was required, the mean ground time was 31.2 minutes, compared
663
with 57.4 minutes when one or more major interventions were required. Box 27-4. PRETRANSPORT PREPARATIONS
SCENE RESPONSE Airway secured Stabilization on a rigid spine board with cervical immobilization device, neck rolls, and tape Two large-bore intravenous lines Antishock garment applied Landing zone selected and secured
INTERHOSPITAL TRANSPORT Airway secured Stabilization on a rigid spine board with cervical immobilization device, neck rolls, and tape Two large-bore intravenous lines Tube thoracostomy for pneumo/hemothorax Bladder catheterization (if not contraindicated) Nasogastric catheterization (if not contraindicated) Lactated Ringer's solution hanging Typed and cross-matched blood if available Extremity fractures splinted (traction splinting for femur fractures) Copies of all available emergency department records and laboratory results, including a description of the mechanism of injury
To minimize delays, pretransport preparations should be made for victims of acute trauma ( Box 27-4 ). Patient Comfort Motion, vibration, noise, temperature variations, dry air, changes in atmospheric pressure, confinement to a limited position or backboard, and fear of flying may cause patient discomfort. Patient Movement Patient handling and movement can contribute to morbidity and mortality in unstable patients.[93] All transported patients should be adequately secured to the stretcher with safety straps to prevent sudden shifting of position or movement of a secured fracture. During transport from the ground to the aircraft cabin, attempts should be made to limit sudden pitching of the stretcher. DOT guidelines recommend design of cabin access such that no more than 30 degrees of roll and 45 degrees of pitch may occur to the patient-occupied stretcher during loading.[62] The stretcher, in turn, should be adequately attached to the floor. Motion sickness in the patient may be treated with an antiemetic such as promethazine (25 mg orally, intravenously, or intramuscularly) or prochlorperazine (5 to 10 mg orally, intravenously, or intramuscularly). Scopolamine disks are useful for prolonged flight and do not require parenteral or oral administration, although their antiemetic effects are not always uniform and may not occur until 4 to 6 hours after application. They may be best used to decrease motion sickness in the flight crew. Noise Noise can be avoided with hearing protectors, which are devices similar to headphones but without internal speakers. Inexpensive hearing protectors are available as deformable foam ear plugs. In some cases, headphones may be used in an awake patient if the crew wants the patient to communicate on the intercom system. Eye Protection When a patient is loaded on or off a helicopter with the rotors turning, the patient's eyes must be protected. Serious eye injuries can result from debris blown into the air. Lightweight sky diver goggles ("boogie goggles") are effective and inexpensive. The eyes must be protected even if the patient is unconscious. Taping temporary
patches over the eyes is also effective. Respiratory Distress Patients with respiratory disease or distress should have immediately treatable conditions addressed before take-off. ET intubation is essential if airway patency is threatened or if adequate oxygenation cannot be maintained with supplemental oxygen. It is better to err on the side of caution when making a decision about a patient's airway. During flight it is easier to treat restlessness in an intubated patient than airway obstruction or apnea in a nonintubated patient. Nearly all patients should receive supplemental oxygen. FiO2 should be increased with increasing cabin altitude to maintain a stable PO2 ( Figure 27-12 ). When oxygen saturation monitoring is unavailable and pretransport arterial oxygen content unknown, 100% oxygen may be administered throughout the flight to ensure adequate oxygenation. Patients with chronic lung disease who are prone to hypercapnia may have a deterioration in condition if the hypoxic drive is eliminated. In these patients the least oxygen necessary to maintain saturation above 90% is advisable; this amount may be estimated in advance or calculated from the alveolar air equation. Close in-flight monitoring is essential. Finally, altitude changes may affect ET cuff volume, so cuff pressure must be checked frequently. Cardiopulmonary Resuscitation and Cardiac Defibrillation CPR in an aircraft is difficult. The rescuers must perform several tasks simultaneously while ventilating the lungs or compressing the chest, all in a physically confining space. The crew must be familiar with modifications
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Figure 27-12 Fraction of inspired oxygen required to maintain oxygen tension at 90 mm Hg (varying with altitude).
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in technique.[45] As previously mentioned, there should be no concern with airborne defibrillation if all electronic navigational equipment on the aircraft has a common ground, as mandated by the FAA standards. Despite cramped quarters and sensitive electrical equipment, defibrillation can be safely performed in all types of aircraft currently used for emergency transport utilizing standard precautions routinely used during defibrillation on the ground. [23] [94] In the interest of safety, however, it is best to notify the pilot before performing defibrillation. Patient Combativeness Patients may be combative to the point that they pose a threat to the safety of the flight and crew. An uncontrollable patient may cause sudden shifts in aircraft balance or may strike a crew member or important flight instruments or equipment. Such patients should be properly restrained in advance. If sedation is necessary, a careful neurologic examination documented beforehand is essential. Useful agents include diazepam (5 to 20 mg intravenously) or shorter-acting agents, such as midazolam (2 to 10 mg intravenously or intramuscularly.) Paralyzing agents, such as pancuronium, vecuronium, and succinylcholine, have the advantage of not altering the sensorium, but they require airway control with ET intubation.[90] In addition, it is necessary to sedate a patient who is paralyzed to facilitate intubation and transport. Endotracheal Intubation ET intubation may be difficult to perform while airborne, especially in a confining cabin, and should be done before departure if possible. This is especially true in trauma victims with head injuries and in burn victims who have carbonaceous sputum or hoarseness. Special techniques are available to supplement standard methods of intubation, including a lighted stylet, ET tubes with controllable tips, and digital intubation. Sedation or pharmacologic paralysis may be necessary. Of 106 aeromedical transport programs in the United States that reported using neuromuscular blocking agents, 39 use them to facilitate intubations, and 67 use them once a patient is intubated to manage combativeness and ensure airway patency.[79] Induction of paralysis before intubation in the aeromedical setting is controversial. One study reported a 96.6% success rate using succinylcholine to facilitate intubation, with 3.4% of patients requiring an emergency surgical airway.[66] Besides the need for surgical airway if intubation is unsuccessful, concerns exist about cervical spine manipulation during intubation in the paralyzed patient, unrecognized esophageal intubation in a nonbreathing patient, and the relative contraindications to the use of succinylcholine in certain patients. As shorter-acting nondepolarizing paralytic agents (e.g., mivacurium) are developed, this adjunct to airway and combativeness control in the aeromedical setting will be studied further.[51] In some flight programs, nonphysician crew members are taught to perform emergency cricothyrotomy. Although occasionally lifesaving, this procedure is often difficult to perform and should be undertaken only as a final method to secure an emergency airway. Thrombolysis The air transport of patients with acute myocardial infarction often involves thrombolytic therapy. Because bleeding is a major adverse effect of thrombolytic agents, one study investigated whether air transport resulted in a higher incidence of bleeding complications compared with a similar cohort of patients given thrombolytic drugs who were transported by ground ambulance. The study concluded that helicopter transport of patients with acute myocardial infarction after initiation of thrombolysis is comparatively safe and without a clinically significant increase in bleeding complications.[34] Flight Safety Because aeromedical transport involves medical care delivered in a hostile environment, the patient and crew are at risk of injury or death in the event of a mishap. Flight crew training must emphasize safety. The pilot is ultimately responsible for the safety of the aircraft's occupants and is trained not only to operate the aircraft skillfully and safely, but also to provide necessary safety instructions and guidance to crew members and passengers. Safely practices vary depending on the type of aircraft but include common guidelines. Approaching the Aircraft.
Helicopters with turning rotor blades must be approached only from the front and sides and only while under pilot observation ( Figure 27-13 ). The tail rotor must be given wide berth, especially on helicopters with rear doors. It is advisable to station a crew member in a safe position to direct approaching individuals away from the tail rotor. Shutting down the helicopter's engines completely, when the situation allows, is prudent before patient loading and unloading. Approaching in a crouched position minimizes the risk of contact with the rotor blades should a sudden gust of wind or movement of the aircraft cause them to dip. Loose clothing and debris should be secured ( Box 27-5 ). Fixed-wing aircraft should be approached with similar precautions regarding propellers. This is especially important in aircraft with access doors in front of the wing and engine nacelles. Engine shutdown on the side of entry enhances safety of loading and unloading.
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Figure 27-13 Helicopter safety. A, Safe approach zones. B, The proper way to approach or depart a helicopter. Safety Belt Use.
The use of safety belts (preferably with shoulder harnesses, especially in helicopters) is an important safety measure. Certain patient care activities (e.g., ET intubation, CPR), however, may be impossible to perform with safety belts secured. The design and selection of aircraft and interior configurations should allow maximal access to the patient with the crew members properly restrained. Throughout the flight the crew members and patient should remain restrained as much as possible in smooth air and at all times in rough air. Movement inside the cabin affects aircraft balance. An aircraft loaded near its aft CG limit may exceed its limits if a crew member moves to a new position within the cabin. Changes in position should be preceded by consultation with the pilot. Light aircraft are sensitive to turbulent air, and appropriate precautions must be taken to avoid being injured from sudden motion. Proper Use of Aircraft Equipment.
Crew members must be familiar with all aircraft equipment they may be required to operate in flight or in an emergency. This includes all aircraft doors, fire extinguisher, communications equipment, oxygen equipment, and electrical outlets. In addition, the crew must be familiar with emergency shutdown procedures. Finally, before takeoff, door security must be confirmed by a crew member familiar with the operation of the door.
Box 27-5. HELICOPTER SAFETY
DO: Approach and depart downhill. Use crouched position. Approach after visual contact and approval from pilot. Await direction of flight crew. Approach from the front or the sides. Secure area first of people and then of loose debris.
DON'T: Approach or depart uphill. Use tall intravenous poles or other objects. Use loose sheets or clothing. Smoke tobacco within 50 feet. Run near the aircraft. Drive a vehicle within 30 feet. Shine headlights or flashlights toward the aircraft.
In-Flight Obstacle Reporting.
An extra pair of eyes can be invaluable to a pilot in a busy airspace or on a scene approach complicated by trees and electrical or phone wires. Primarily important in VFR conditions, assistance with obstacle identification can enhance the safety of the mission; however, flight should not occur under conditions in which obstacle reporting by a crew member is essential to safety, since the person must then divide attention between patient care and obstacle reporting. Ground Coordination and Control.
Enthusiastic rescue personnel or curious onlookers may approach the aircraft in a hazardous manner. Flight crew members must be able to communicate with ground units during the landing phase to ensure adequate scene preparation; they may be required to perform crowd control while on the ground. This requires directing individuals away from the rotor blades, propellers, or other hazardous equipment at the scene. If loading or unloading the patient while the rotors or propellers are still turning ("hot loading" or "hot off-loading") is necessary, special precautions must be undertaken for ground crews, the flight crew, and the patient. Emergency Procedures.
All crew members should memorize and routinely practice emergency procedures.
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These procedures should address in-flight fires, electrical failures, loss of pressurization, engine failure, emergency landing with and without power, precautionary landing away from an airport, and other in-flight emergencies. Survival.
An emergency or precautionary landing away from an airport necessitates survival before rescue arrives. Under adverse environmental conditions and with injured victims, survival may depend on specific actions by the crew. The crew should be proficient in emergency egress from the aircraft, including escape after crashes and water landings, especially in helicopters. After water landings, helicopters usually roll inverted and sink rapidly. Helicopter "dunker" training is required for all military helicopter crews. The crews are strapped into a simulated helicopter fuselage and lowered rapidly into a pool, simulating a semicontrolled water landing. The fuselage then rolls inverted and the crew must open emergency exits and egress the simulator. This type of training has been shown to save lives in helicopter water crashes. All crew members should be trained in the use of emergency signaling devices, such as ELTs, flares, signal fires, and ground emergency signals. Survival skills should
be taught to all crew members, including advanced first aid, building emergency shelters, fire starting, and obtaining water and food from the environment. Aeromedical Accidents.
Attention continues to focus on EMS helicopter accidents. Statistics from 1986 estimated a rotor-wing accident rate of 17.65 with 5.88 fatalities per 100,000 transports.[35] Aviation accident rates are typically reported in relation to flight hours. EMS fatalities therefore amounted to 6.0 per 100,000 flight hours, compared with 3.3 for the helicopter industry in general. The EMS rate subsequently declined, however, with 3.0 accidents per 100,000 transports reported in 1991 ( Figure 27-14 ).[74] [88]
From 64% to 84% of EMS accidents result from pilot error, approximately 23% from mechanical causes, and 3% from unknown causes.[19] Of accidents caused by pilot error, adverse weather was a contributing factor in 67% ( Table 27-9 ).[17] In all, two thirds of fatal weather-related accidents occur at night, and 86% of all fatal accidents occur at night or in marginal weather conditions ( Table 27-10 ). [20] Only 35% to 40% of all EMS helicopter flights occur at night. The most common phase of flight for weather-related accidents was en route (86%), with 14% occurring on departure and none on approach ( Table 27-11 ). Only 5% of fatal EMS helicopter accidents occur in flights to or from the scene, although such flights account for 24% of EMS helicopter missions. [21] When scene-related accidents occur, they result in fatalities 9% and injuries 35% of the time, suggesting a low-energy impact vs. an en route crash. Causal factors related to scene accidents include wire and obstacle strikes (70%),
Figure 27-14 Aeromedical helicopter accident rate, 1972 to 1991. (From Preston N: J Air Med Transport 11:14, 1992.)
TABLE 27-9 -- Major and Primary Causes and Severity of Aeromedical Accidents, 1972 to 1989 PERCENTAGES 1972–1985 1987–1988 1989 MAJOR CAUSES Weather
30
30
17
Engine failure
18
9
0
Obstacle strike
18
10
33
9
20
17
25
40
33
Pilot error
64
60
83
Mechanical failure
30
30
0
6
10
17
Fatal
36
50
67
Injury
28
30
17
Damage only
36
20
17
Control loss Other PRIMARY CAUSE
Unknown ACCIDENT SEVERITY
From Collett HM: J Air Med Transport 9(2):12, 1990.
TABLE 27-10 -- Effect of Weather on Accident Seriousness SEVERITY OF ACCIDENT
WEATHER RELATED
PERCENTAGE
Fatal
14/21
67
Injury
3/17
18
Damage only
1/32
3
From Collett HM: Hosp Aviat 5(11):15, 1986.
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TABLE 27-11 -- Environment of Fatal Accidents VISIBILITY
ACCIDENTS PERCENT
Day visual meteorologic conditions
3
14
Night visual meteorologic conditions
4
19
Day marginal
4
19
Night marginal
10
48
TOTAL
21
100
From Collett HM: Hosp Aviat 5(11):15, 1986. loss of control (18%), and mechanical failure (12%). The landing phase is involved in scene-related accidents in 41% of cases, whereas the take-off phase is involved in 59%. Because 40% of scene-related accidents occur at night and approximately 40% of helicopter EMS flights occur at night, scene accidents do not appear more hazardous at night than in the day. Single-engine helicopters have more often been involved in engine failure accidents (77%) than have twin-engine craft (the two types are approximately equal in number in the EMS industry). Recommendations for enhancing safety include instituting stringent guidelines to limit flights at night or in adverse weather, increasing pilot proficiency training, and reducing pilot fatigue and workload factors. Decisions on the appropriateness of air transport regarding utilization and weather should be based on general protocols that are not subject to the emotional turmoil of a medical crisis.[10] The trend in the industry has been toward twin-engine helicopters for an increased margin of safety from engine failure accidents. In addition, for dedicated EMS helicopter flights, a statistically strong relationship exists between the ability to fly under IFR and a lower accident rate.[56] The Association of Air Medical Services considered the question of whether all helicopters should be required to have IFR capability when it published its voluntary standards for rotor- and fixed-wing aircraft. This was not mandated because of the tremendous expense and because many programs were unlikely to comply.[58]
Ground to Air Signaling.
It is best to have radio communication between the ground party and the helicopter crew. This may not be possible, however, and hand signals may be needed to communicate. Standard hand signals are used by military rescue personnel for communication between a deployed rescue swimmer and the helicopter ( Table 27-12 ). These same signals can be used while on land. To acknowledge the signals, the hoist operator gives a thumbs up or the pilot flashes the rotating beacon.
INTENTION
TABLE 27-12 -- Swimmer to Helicopter and Ground to Air Signals ACTION
Deploy medical kit
Arms above head, wrists crossed
Situation OK
Thumbs up
Lower rescue cable with rescue device attached
Arm extended over head, fist clenched
Lower rescue cable without rescue device attached
Climbing-rope motion with hands
Helicopter move in/out
Wave in/out with both hands
Cease operations
Slashing motion across throat
Deploy litter
Hands cupped, then arms outstretched
Personnel secured, raise cable
Vigorously shake hoist cable or thumb up; vigorous up motion with arm
Team recall
Circle arm over head with fingers skyward
Landing Zone Operations.
The ideal helicopter landing zone is a wide, flat, clear area with no obstacles in the approach or departure end. Vertical landings and take-offs can be done, but it is safer for the helicopter to make a gradual descent while flying forward. Higher altitudes and higher temperatures require larger landing zones. The center of the landing zone can be marked with V, with the apex pointing into the prevailing wind. Any obstacles can be marked with brightly colored, properly secured clothing. The size of the landing zone depends on the weather conditions, type of helicopter involved, altitude, temperature, and types of obstacles in the area. Small helicopters such as the Jet Ranger can usually land safely in a 60 × 60-foot landing zone. Larger helicopters such as the Bell 412 require a 120 × 120-foot zone.[95] Large military helicopters may require even greater landing zones. In general, pilots prefer the largest, flattest piece of ground they can find. The condition of the ground (e.g., loose snow, dust, gravel) should be communicated to the pilot before the final approach. Before the helicopter lands, all loose clothing and equipment should be secured. During approach, no personnel or vehicles should move on or near the landing zone. Once the helicopter is on the ground, it must be approached only from the front and side, and then only while under direct observation of the pilot. The aft portion of the aircraft and areas around the tail rotor must
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be avoided at all times. Some helicopters (e.g., BK-117) have rear doors for loading and unloading patients, and ground personnel should wait for directions from the crew before approaching the rear area. If the ground is uneven or slopes, all personnel should approach and depart from the helicopter on the downslope side. It is safest to load the patient into the helicopter with the engines off and the rotors stopped ("cold load"). If the patient must be loaded with the engines on and blades turning ("hot load"), eye and ear protection should be worn by all personnel approaching the helicopter, including the patient. A safety person should be assigned to prevent anyone from inadvertently walking toward the tail rotor. Once the patient is loaded, all personnel should leave the landing zone, take cover, and stay in place until the helicopter has departed. It is best to be off to the side, not directly in the take-off path. Hoist Operations.
If the helicopter is not able to land and has a rescue hoist installed, hoist operations may be the only means of evacuating the patient. In most circumstances a helicopter crew member rides the hoist down to the site to rig the survivor into the rescue device and to oversee the hoist operation, using the following guidelines: Do not touch the hoist, rescue device, or cable until after it has touched the ground (or water). Helicopters can build up a very powerful static electricity charge that will be grounded through whatever the hoist touches first. This has been known to knock rescuers and survivors off their feet. Once the rescue device and cable have touched the ground, put the patient into the rescue device, taking care to keep the hoist cable clear of all personnel. Do not allow the hoist cable to loop around any personnel or around the rescue device, since serious injury is possible when the cable slack is taken up. Make sure that the patient is properly secured in the rescue device, with all safety straps tightened. When the patient is secured, move away from the rescue device and signal "up cable." If the rescue device is a basket (Stokes) litter, use a tag line with a properly installed weak link to prevent the litter from spinning during the hoist. Night Operations.
Night helicopter rescue operations are considerably more dangerous than daylight operations. In most cases it is best to delay helicopter insertion or extraction operations until daylight. If this is not possible, however, night missions can be done safely with careful planning and coordination between the helicopter and ground party. The same rules of daylight helicopter operations apply to night operations, but with extra care taken to ensure that all personnel understand their roles. In night operations it is virtually mandatory to have radio communications between the ground and the helicopter. "No-comm" night operations should only be attempted by personnel specially trained and experienced in these techniques. The landing zone should be clearly marked and the pilot allowed to make the approach. All personnel should stay clear of the landing zone until the pilot has made a safe landing. Personnel approaching the landing zone should have a small light or reflective material attached to their outer clothing so they can be clearly seen. The minimum number of people should approach the helicopter, and a safety observer is mandatory to keep the ground team together and clear of the tail rotor and rotor blades. The landing zone should be as large as possible, preferably at least 50% larger than a daylight landing zone. Any obstacles should be clearly marked with light-colored streamers, small lights, or even light-colored clothing. The landing zone can be illuminated with flashlights at the corners, with another flashlight at the center point. These flashlights should be pointed at the ground, not into the air; flashlights pointed at the helicopter during landing and take-off may distract or momentarily blind the crew. If flashlights are not available, small fires can be used to illuminate the edges of the landing zone, although the helicopter can scatter burning embers for many meters. If crew members are using night vision equipment, lights must never be flashed at the helicopter. Even the amount of white light from a small flashlight may be sufficient to overload the night vision equipment, functionally blinding the crew.
Dispatch and Communications.
The dispatch center is the focal point for communications during aeromedical transport operations. Dispatchers receive incoming requests for service; obtain necessary information relative to the launch decision: coordinate the interaction between essential parties; "scramble" the flight crew; assemble and maintain necessary information regarding destination, weather, local telephone numbers, and frequencies; follow the progress of the flight; input data into the system database; and communicate with ground EMS units and hospitals. Communication may occur through a combination of methods: land telephone lines into a dispatch switchboard, hospital-EMS net transceiver, discrete frequency transceiver (communications with aircraft), or walkie-talkie radios. Familiarity with the EMS system and EMS communications is essential for successful dispatch. Flight following is an important part of aeromedical safety and involves tracking the position of the aircraft during a mission by plotting the location according to reports from the pilot at 10- to 15 minute intervals. If an accident or in-flight emergency occurs, the dispatcher
670
is soon aware and can initiate SAR to a precise location, which enhances the chances of survival.
APPROPRIATE USE OF AEROMEDICAL SERVICES Aeromedical transport combines skilled treatment and stabilization capability with rapid access to definitive care, but not without risk, and at high cost ($1 to $2 million per year for a program, or about $2000 per transported patient, which is approximately 400% higher than ground transport).[13] However, the comparative risk of aeromedical transport must be placed in perspective against the risk of patient death from nonreferral or from less timely ground transport with limited medical capability en route. Although not proved, advanced provider skill levels during prehospital care are considered beneficial, especially in severely ill or injured patients.[49] In rural and wilderness environments, advanced life support (ALS) services may be made more readily available by EMS helicopters. This is especially true in areas that are difficult or impossible to reach by ground. The speed of access to definitive care is another consideration in choosing the mode of transport. In isolated rural or wilderness locations, a helicopter may be the only means of expedient access. Prolonged victim extrication allows time for a helicopter to arrive at the scene, decreasing total transport time and thereby increasing the advantage of helicopter transport. Patient comfort also must be considered, especially on long transports over rough roads. Although a helicopter moves in three dimensions, fore and aft acceleration is usually steady, without the starting and stopping motions present during ground transport. However, helicopters typically travel within 914 m (3000 feet) of the ground's surface and are more subject to turbulence than are high-flying fixed-wing aircraft. Whether aeromedical transport reduces mortality when compared with ground transport has not been determined definitively. An uncontrolled national multicenter study of trauma patients transported by helicopter showed a 21% reduction in mortality from that expected based on predictions from the Trauma Score-Injury Severity Score (TRISS) methodology and national normative trauma outcome data.[8] A similar study using the TRISS methodology compared actual mortality with helicopter vs. ground transport and showed a 52% reduction from expected mortality when patients were transported by air, vs. no reduction in expected mortality when transport occurred by ground.[7] Another study using TRISS methodology found a benefit of aeromedical transport only in patients with severe trauma (a probability of survival less than 90%).[11] In 1990 the Association of Air Medical Services (AAMS) issued a position paper on the appropriate use of emergency air medical services. In 1992 these recommendations were accepted by the California Medicaid provider as reasonable criteria for the use of air medical transport. In a review of 558 consecutive patient transports, 98% had met at least one of the AAMS criteria.[71] The risk of aeromedical transport can be placed in perspective if the overall risk of death using ground transport, estimated from the trauma score, is compared with the risk when patients are transported by air. Assuming a reduction in risk of between 21% and 52% when transport is by air, the additional risk of death from crashes (6 per 100,000 transports, or 0.006 per transport) is negligible in comparison to the benefits. This is probably true, however, only for patients with moderate to severe, but nonmortal, injuries (i.e., trauma scores between 5 and 14). Those having minor injuries, with near 100% likelihood of survival, are unlikely to gain additional benefit; those having mortal injuries, with little hope of survival, are unlikely to be saved by any means attempted or employed. The decision to transport a patient by air requires judgment and a realistic appraisal of the risks. A patient should be transported by air only if he or she is so ill that transport is necessary; if ground transport is unavailable, delayed, or unable to reach the patient; or if aeromedical transport would reduce the risk of death by permitting more rapid access to definitive care, providing greater medical skill en route, or both.
SUMMARY It has been estimated that since aircraft took to the sky to assist in the emergency transport of sick and injured patients, more than 1 million have been transported over 100 million miles. With a conservative estimate of mortality reduction of even 10%, close to 100,000 patients may owe their lives to the speed and skill provided by aeromedical transport teams.[47] DISCLAIMER The opinions expressed in this chapter are those of the authors and do not necessarily represent the opinion or endorsement of the Department of Veterans Affairs, the Department of Defense, or the United States Air Force.
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Chapter 28 - Wilderness Survival Warren D. Bowman
This chapter examines the human body's requirements for homeostasis and how they can be satisfied in a wilderness environment where little oxygen, food, or water may be available and where extremes of heat or cold may exist. The requirements are similar whether the individual becomes lost with few resources during a simple day hike or whether injury occurs or severe environmental conditions develop during a well-planned wilderness expedition. Although improvisation and living off the land are mentioned, anticipation, prevention, and especially preplanning are much more important and form the core of this discussion. As an example taken from Antarctic exploration, Roald Amundson's style of thorough preparation and the use of well-tested equipment should be emulated rather than Robert Scott's intuitive and untested approach.[12] The outcome of an encounter with severe environmental stress varies with the type, magnitude, and duration of the stress and with the stressed subject's resources. These resources include the state of acclimatization; physical integrity, particularly conditioning and the presence of illness or injury; experience; equipment and the ability to improvise intelligently; and such intangibles as "backcountry common sense" and the will to survive. The recommendations in this chapter are based on personal experience, the opinions of survival experts, research, and analysis of actual survival situations. General principles are emphasized, but "tricks of the trade" may hold the key to life or death. Unfortunately, most of the lay literature emphasizes tales of misfortune, hazardous adventures, and mindless bravado in the face of unnecessary hardships brought on by errors of the participants, while great deeds go unrecorded or forgotten because the experience and competence of the adventurers kept catastrophic, "newsworthy" experiences to a minimum. In the words of Corneille, "To vanquish without risk is to triumph without glory."[6] Increased leisure time and growing interest in outdoor activities place more people into settings where survival situations may develop. The cross-country skier, winter mountaineer, and winter camper may be exposed to extremes of cold and storms. The expeditionary mountaineer may explore regions where winter exists year-round and where ambient oxygen is low. The desert traveler may be exposed to extremes of heat and the tropical traveler to extremes of both heat and humidity. Passengers in aircraft, seacraft, or land vehicles may be stranded in almost any type of environment. A common thread in the development of life- or limb-threatening emergencies is the insistence on traveling during storms and other stressful environmental conditions, when more prudent persons would stay put in a comfortable bivouac. Excuses for this include reaching a predetermined but not essential goal on time so that others will not worry. Physicians who participate in wilderness recreation or treat adventurers need to be aware of the physiologic and psychologic impacts of environmental stress and how related deleterious effects can be prevented and treated. The knowledgeable traveler should plan for unexpected situations using preventive aspects of survival. This includes being familiar with weather forecasts, strategizing worst-case scenarios, carrying emergency items, avoiding solo travel in isolated areas, and leaving notice of the projected route and expected time of return. With good planning, deteriorating weather or an injury-forced bivouac becomes more of an inconvenience than a life-threatening ordeal. However, chance plays a part in survival. Serious but unforeseen hazards can occur, or environmental stresses can be so severe that survival is impossible regardless of preparations. Anyone who ventures into wilderness must accept the possibility, however remote, of death or serious injury. For survival the body requires a constant supply of oxygen, a core temperature regulated within relatively narrow limits (about 24° to 42° C [75° to 107° F]), water, food, and self-confidence, faith, and will to live. For comfort and optimum performance, body temperature must be close to normal, and the body must be rested, well nourished, in top physical condition, and free from disease and injury. The most immediate of these requirements are maintenance of body integrity (through accident prevention) and regulation of body temperature. Dehydration, starvation, and exhaustion make temperature maintenance more difficult and interfere with the rational thought and agility required to prevent accidents. Insufficient oxygen becomes a contributing factor at extreme altitude or in such mishaps as suffocation caused by avalanche burial or carbon monoxide (CO) poisoning from cooking in an unventilated shelter. Abundant food and water are of little value to a hypothermic person with insufficient clothing and shelter or to the victim of heatstroke, even though lack of food and water eventually weaken and
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kill an otherwise healthy individual. Lack of self-confidence, faith, and the will to live may cause an attitude of panic and defeatism that prevents a person from taking timely survival actions, such as conserving energy, preparing shelter, or lighting a fire. Poor physical conditioning or the presence of illness or injury may interfere with the body's ability to produce heat by shivering or to lose heat by sweating and increasing skin perfusion, which can hamper wood gathering, shelter building, and other necessary actions.[4] The most important organ for survival is the human brain, since voluntary actions such as preparedness, regulation of energy expenditure, adjustment of clothing, and seeking shelter are more important than involuntary mechanisms of adaptation to environmental stress.
OXYGEN As a human ascends from sea level, the body is subjected to increasing cold, decreasing oxygen, increasing solar radiation, and decreasing atmospheric pressure. For every 305 m (1000 feet) of altitude gain, the ambient temperature drops by about 2.2° C (4° F), the barometric pressure drops by about 20 mm Hg (0.1 mb/m), and the amount of ultraviolet (UV) radiation increases by about 5%. The percentage of oxygen in the atmosphere remains constant, but the partial pressure of oxygen diminishes with altitude so that at 3077 m (10,000 feet) it is only two-thirds that at sea level and at 5488 m (18,000 feet) only half.[3] During acute exposure to high altitude the effects of hypoxia initially can cause fatigue, weakness, headache, anorexia, nausea, vomiting, dyspnea on exertion, insomnia, and Cheyne-Stokes respirations (see Chapter 1 ). These symptoms are probably present to some degree in everyone who goes rapidly from sea level to 2462 m (8000 feet) or above. The clinical effects of hypoxia are often difficult to distinguish from those of cold, high winds, dehydration, and exhaustion. Serious degrees of acute mountain sickness (AMS) are unusual below 3692 to 4308 m (12,000 to 14,000 feet) but have been reported in trekkers as low as 2308 m (7500 feet). In Yellowstone National Park, mild AMS is not infrequently seen in visitors at just over 1829 m (6000 feet). At any height, oxygen in ambient air may be prevented from reaching the cellular level because of interruption of normal transport pathways, generally by illness or injury. Examples of this in the wilderness include the following[4] : 1. Insufficient oxygen in inspired air in avalanche burial, near drowning, or living in a poorly ventilated snow cave 2. Upper airway obstruction from a facial injury, blockage by the tongue in an unresponsive patient, or aspiration of foreign material 3. Interference with proper lung function caused by pneumonia, pulmonary edema, pulmonary hemorrhage, pulmonary contusion, atelectasis, hemothorax, pneumothorax, or chest wall injury 4. Circulatory insufficiency caused by myocardial infarction, pericardial tamponade, shock, or pulmonary embolism 5. Interference with ventilatory control after injury to the respiratory center or hyperviscosity-induced cerebral infarction 6. Interference with the oxygen-carrying capacity of the blood from anemia or CO poisoning The emergency and definitive treatments of such conditions follow standard techniques detailed elsewhere in this book and include the administration of oxygen, if available. CO poisoning is probably a greater hazard than is generally appreciated. Many famous polar explorers, including Byrd, Andree, and Stefannson, were killed by or had narrow escapes from the effects of stoves operated in tightly enclosed living areas.[20]
REGULATION OF BODY TEMPERATURE Humans are called homeotherms because as warm-blooded animals they maintain a body temperature that varies within very narrow limits despite changes in environmental temperature. In poikilotherms, or coldblooded animals, body temperature varies with that of the environment. Homeothermy is necessary to support the enzyme systems of the human body, which function best at 37° to 37.5° C (98.6° to 100° F). The human body can be viewed as a heat-generating and heat-dissipating machine where internal temperature is the net result of opposing mechanisms that tend to increase or decrease body heat production, increase or decrease body heat loss, and increase or decrease addition of heat from the outside. Through these mechanisms the internal body temperature usually can be regulated successfully despite ambient temperatures that vary more than 55° C (100° F) from the coldest to the hottest seasons in temperate climates. Basal body heat production occurs at about 50 kcal/m2 /hr. This can be increased by muscular activity (involuntary [shivering] and voluntary), eating, inflammation and infection (fever), and in response to cold exposure. Shivering can increase heat production up to 5 times the basal rate and vigorous exercise up to 10 times. Cold exposure increases hunger, the secretion of epinephrine, norepinephrine, and thyroxine, and semiconscious activity such as foot stamping and dancing in place. Eating provides not only needed calories but also the temporary increase in basal metabolic rate that occurs during digestion alone (specific dynamic action, or SDA). The SDA of protein is five to seven times higher than that of fat and carbohydrate and lasts longer. However, the onset of the SDA is much faster with carbohydrate than with protein or fat. Therefore the person who is cold inside a sleeping bag at bedtime should eat carbohydrate, and to stay warm all night, protein.
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Figure 28-1 Line chart showing windchill and state of comfort under varying conditions of temperature and wind velocity. The numbers along the left margin of the diagonal center block refer to the windchill factor, that is, that rate of cooling in kilocalories per square meter per hour of an unclad, inactive body exposed to specific temperatures and wind velocities. Windchill factors above 1400 are most hazardous.
In hot weather, body heat production can be decreased by slowing muscular activity and avoiding foods with a high SDA. In cold weather, heat can be added to the body by close exposure to a fire or other heat source, such as sunlight, and by ingesting hot food and drink. In hot weather, external heat addition can be decreased by staying in the shade, wearing clothing that blocks the sun's rays, and avoiding hot objects and hot food and drink. The body loses heat to the environment by conduction, convection, evaporation, radiation, and respiration. It may gain heat from the environment by the same mechanisms (except for evaporation). The relative importance of these mechanisms depends on temperature, humidity, wind velocity, cloud cover, insulation, contact with hot or cold objects, sweating, and muscular exercise. With a resting body in still air at 21° C (70° F), radiation, conduction, and convection account for 70% of total heat loss, evaporation for 27%, and urination, defecation, and respiration for only 3%. During work, however, evaporation may account for up to 85% of heat loss.[4] It is useful to think of the body as composed of a core (heart, lungs, liver, adrenal glands, central nervous system, and other vital organs) and a shell (skin, muscles, and extremities). Most of the adjustments in response to cold or heat exposure occur in the shell. They are designed to maintain a relatively constant core temperature; in below-freezing weather, these adjustments may predispose parts of the shell to frostbite and other types of localized cold injury. The importance of avoiding travel and seeking shelter during storms and extreme cold cannot be overemphasized. The additive chilling effect of wind when added to cold is impressive. Windchill charts ( Figure 28-1 ) show the relationship between actual temperature,
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FABRIC
TABLE 28-1 -- Fiber Characteristics of Natural and Synthetic Fibers SPECIFIC GRAVITY (RATIO TO THERMAL CONDUCTANCE† (cal/m2 EVAPORATIVE WATER) ABILITY‡ ) *
WICKING ABILITY
MOISTURE REGAIN§
Wool
1.32
2.1
Low
Moderate
17
Cotton
1.54
6.1
Low
High
7.9
Nylon
1.14
2.4
High
Low
4
Polyester
1.38
2.4
High
Low
1
Acrylic
1.15
2.4
High
High
1
Polypropylene
0.91
1.2
High
High
5
Modified from Davis AK: Nordic skiing—a scientific approach, Minneapolis, 1980, University of Minnesota. *The lower the specific gravity, the better the insulating ability. †The lower the thermal conductance, the slower the flow of heat from the body. ‡The higher the evaporative ability, the shorter the amount of time a fiber will be wet, that is, in a reduced insulative state. §Moisture regain is the amount of moisture a fiber can absorb before feeling wet.
wind velocity, and "effective" temperature at the body surface. "Windchill" refers to the rate of cooling; the actual temperature reached is no lower than it would be if wind were absent (unless evaporation of liquid is occurring from the body surface). The increase in heat loss as the wind rises is not linear; rather, it is roughly proportional to the square root of the wind speed. At moderate ambient temperatures the body's core temperature is kept stable by constant small adjustments in metabolic rate, muscular activity, sweating, and skin circulation. When the body is chilled, automatic and semiautomatic mechanisms increase internal heat production by slightly increasing the metabolic rate, by shivering, and by semiconscious activities (e.g., foot stamping) and reduce heat loss by diminishing sweat production and shell circulation. The person has a strong urge to curl up in a ball, thereby reducing the body's surface area. At the same time the brain tells the body to decrease heat loss by adding insulation and wind protection, to seek shelter, and to increase heat gain by increasing muscular activity, building a fire, seeking sunlight, and eating.[4] When the body overheats, these actions are reversed. The body increases heat loss by increasing circulation to the skin and extremities and increasing sweating. These mechanisms require more water, which stimulates the thirst response. Heat production is decreased because of a feeling of sluggishness and languor, leading to a reduction in physical activity and in the amount of heat produced by muscles. The brain tells the body to decrease heat gain and increase heat loss by providing shelter from the sun, removing clothing, and fanning oneself.
COLD WEATHER SURVIVAL Body temperature in a cold environment is maintained by decreasing heat loss, increasing internal body heat production, and adding heat from the outside. The most efficient of these methods is conservation of body heat by decreasing heat loss, generally by using clothing and shelter. Decreasing Heat Loss Heat loss from conduction and convection can be prevented by interposing substances of low thermal conductivity, such as clothing made of good insulating materials, between the body and outside air. Clothing creates a microclimate of warmed, still air next to the skin surface. Clothing's value depends on how well it traps air, the thickness of the air layer, and whether these qualities are reduced by wetting ( Table 28-1 ). Traditional insulating materials are wool, down, foam, and older synthetics such as Orlon, Dacron, and polyester. Wool retains warmth when wet because of moderately low wicking action and a unique ability to suspend water vapor within its fibers without affecting its low thermal conductance. It can absorb a considerable amount of water without feeling wet but is heavier than synthetics, itchy, and more difficult to dry. Its toughness and durability, however, make it a good choice for garments subject to hard wear, such as trousers, mittens, and socks. Cotton, particularly denim and corduroy, is a poor insulator. It dries slowly because of low evaporative ability; high thermal conductance is further increased by wetting. Cotton has no place in the backcountry in cold weather. Orlon, acrylic, and polyester were developed to duplicate the properties of wool without wool's higher cost. They traditionally have been used in hats, sweaters, and long underwear. They are almost as warm and not as itchy as wool, and they evaporate moisture better. A number of newer fabrics are woven from fibers that have lower thermal conductance, greater insulating ability, and better wicking action
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than traditional fibers. Examples include polypropylene and treated polyesters, such as Capilene, Thermax, and Thermastat. Polyester is also made into pile and fleece, which are light, dry easily, trap air well, and stay warm when wet because the fibers do not absorb water. Examples are Polartec, Borglite, Polarplus, and Synchilla. Fibers used as fillers in quilted garments include hollow synthetic fibers designed on the principle of reindeer hair, such as Hollofil II and Quallofil. Microfibers that provide good insulating ability with less bulk include Thinsulate, Thermoloft, and Thermolite. One of the newest microfibers, Microloft, is supposed to be warmer than down at the same weight. New synthetics come on the market frequently—consult trade journals and "gear" issues of outdoor magazines. The "layer principle" of clothing is effective in preventing overheating and chilling. Multiple layers of clothing provide multiple layers of microclimate. Layers are added as necessary to prevent chilling or subtracted to prevent excessive perspiration. Since water conducts heat 25 to 32 times faster than air at the same temperature, clothing wetted by perspiration or water may cause rapid heat loss from conduction and evaporation. The need to add or subtract layers should be anticipated before chilling or heavy perspiring occur. Clothing should be easily adjustable, sweaters should be of the zipper or cardigan type, and outer layers should be cut full enough to allow expansion of inner layers to their full thicknesses. Zippers in the axillary and lateral thigh areas are useful for ventilation. Loss of heat from convection can be prevented by wearing windproof outer garments of nylon, tightly woven cotton-nylon blends, or water-resistant laminates such as Gore-Tex. Typical examples include a parka with hood and a pair of windproof pants (regular or bib style) or ski warm-up pants. The loss of heat from infrared radiation can also be prevented by insulation, emphasizing proper covering for body parts with a large surface area/volume ratio. The uncovered head can dissipate up to 70% of total body heat production at an ambient temperature of -16° C (5° F), partly because the body does not reduce blood supply to the head and neck as it does to the extremities in cold weather. High heat loss through radiation during cold nights can be decreased by sleeping in a tent or under a tarp instead of in the open. Coverage for the head, ears, hands, and feet should not restrict circulation. Developed initially for skiers, the "neck warmer," or "neck gaiter," can be pulled up over the back of the head to form a hood or up over the lower face to form a mask. Heat loss from the respiratory tract can be diminished by avoiding overexertion and overheating with excessively heavy breathing. When it is extremely cold, inspired air can be warmed by pulling the parka hood out in front of the face to form a "frost tunnel." Heat loss from conduction occurs by direct contact with a colder object. Sitting on a pack, foam pad, log, or other object of lower heat conductivity is preferable to sitting in the snow or on a cold rock. At low temperatures, bare skin freezes to metal. This can be avoided by wearing light gloves when handling metal objects. Gasoline or other liquids with freezing points lower than that of water can cause frostbite if accidentally poured on the skin at low temperatures. During bivouacs in snow shelters, contact with the snow can be avoided by using a foam pad or improvising a mattress of evergreen boughs, grass, or dry leaves. In cold or windy weather an injured person needs windproof insulating material under as well as over and around the body. Heat loss from conduction and evaporation can be lessened by avoiding wetting and by changing to dry clothes or drying out quickly when wet. Ideally, outer clothing should be windproof, should not collect snow, and should shed water but not be waterproof, since waterproof garments prevent evaporation of sweat. Newer fabrics, such as Gore-Tex, are suited for this and for outermost layers. Dressing for Cold Weather Anyone who ventures outdoors in cold weather should have enough clothing, either on the body or in the backpack, for the most extreme environmental conditions likely to be experienced. First Layer LONG UNDERWEAR.
Wool is still an excellent choice for long underwear but is expensive and may be difficult to find. Merino wool is less itchy. Polypropylene, acrylic, and the newer polyesters may be preferable because of their lower cost, good insulating ability, and good evaporative ability (see Table 28-1 ). Again, fabrics containing cotton should be avoided. Synthetics tend to retain body odor more than wool after washing. SOCKS.
One or two pairs of moderate to heavy wool or wool/nylon blend socks are excellent, preferably with an additional pair of light polypropylene socks worn underneath next to the skin. At least one spare pair of the wool socks should be carried. THIN GLOVES (GLOVE LINERS).
Light polypropylene, wool, silk, or fingerless wool or pile gloves are useful for moderately cold conditions or when finger dexterity is required, as in adjusting ski bindings. Polyester/Lycra gloves provide a tighter but more stretchable fit to enhance fine finger movements. Second Layer SHIRT.
Shirts should be made of light, soft wool or a suitable synthetic such as acrylic and should have long
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sleeves. Large breast pockets with buttons or Velcro are handy to carry items such as sunglasses and a compass. Shirts should open completely in front or at least have a half-zipper. A turtleneck feature protects the neck, as do neck warmers and mufflers, which can be pulled up to protect the lower face. PANTS.
Wool or pile pants are best and should have pockets that are easily accessible for hand warming. Pile pants should have reinforcements at the knees and buttocks and a zipper or Velcro fly for males. Full or partial lateral leg zippers are convenient. FOOT GEAR.
The type of boot chosen depends on the type of activity and the expected environmental temperatures. For moderate temperatures, sturdy leather climbing boots made of full-thickness leather, 6 to 8 inches in height with rubber lug soles and roomy enough to accommodate the desired numbers of socks, are ideal. Boots made of leather and fabric such as Gore-Tex are lighter and suited for trail hiking but are not as durable for rough terrain. Boots must be long enough so that the toes do not strike the front of the boot during downhill walking. They should be laced firmly enough that the heel does not move up and down, but not so tightly that circulation is restricted and the toes cannot be wiggled easily. For colder temperatures, double boots are preferable. These can be all-leather boots or can have outer shells of plastic or nylon with inner boots of felt or foam. All-leather versions are becoming difficult to obtain. The Canadian type of shoe-pak (e.g., Sorel) with a removable inner felt liner is a good choice for light snowshoeing and other nontechnical outdoor activities in the cold. Special double ski boots are available for ski touring, Telemark skiing, and ski mountaineering, depending on whether three-pin or mountaineering ski bindings are used. HAT.
Hats should be of the stocking variety, made of wool, pile, Orlon, polypropylene, or wool-polypropylene, and large enough to cover the ears. A small bill feature is desirable to shade the eyes. "Bomber" caps with bills and pull-down earflaps and "Andean" caps with ear coverings are popular. Some arrangement should be provided to protect the face from cold wind, as with a balaclava configuration or a separate face mask. A useful combination is a ski hat with a neck warmer that can be pulled up to cover most of the lower face. Third Layer PARKA.
The parka can be a standard ski or mountain parka filled with down, Dacron, Quallofil, Thinsulate, or other lofting material. A more versatile combination is two separate garments: a pile jacket plus a Gore-Tex shell. For snow camping a pile jacket with a thin outer layer of nylon (three-season, squall, or warm-up jacket) may be preferred because, unlike an uncovered pile jacket, it does not collect snow when worn without the shell. The shell should have a hood with a drawstring, a two-way zipper with an overlying weather flap closed with snaps or Velcro, a cloth flap to protect the chin from the metal zipper pull, armpit and/or lateral chest zippers for ventilation, and at least four outer pockets plus one or two inside pockets to contain frequently needed items (e.g., gloves, compass, map, sunglasses, neck warmer). Outer pockets should be located where they can be reached while wearing a backpack with a fastened waist belt. The shell should be fingertip length unless bibs are worn. Pockets with horizontal openings may close with Velcro, but those with vertical openings should close with zippers. Because the parka is anchored by the shoulders, when using one hand it is generally easier to pull a vertical zipper down than up. In some brands of parkas, vertical zippers are pulled down to close the pockets; in other brands they are pulled up. I prefer the down type because the danger of losing pocket contents from difficulty closing a zipper is worse than any delay from difficulty opening a zipper. For ventilation, there should be zippered openings at the armpits. These should be large enough so the parka can be converted into a vestlike garment during warm conditions by inserting the wearer's arms through the openings and tucking the sleeves inside the parka. Since these zippers usually perform more easily when pulled from the distal to the proximal direction, this direction should close them, since increasing wind protection is usually more urgent than decreasing it (freezing is more dangerous than sweating). WIND PANTS.
These should be light and water repellent; Gore-Tex is a good choice. Long, zippered side openings are useful to permit donning pants without removing boots, as well as for ventilation and access to inner pants pockets. HAND GEAR.
One of the more serious and still unsolved cold weather problems is how to keep fingers warm while leaving them unhampered enough to do work. Mittens are warmer than gloves since fingers that touch each other warm each other, but even thin mittens do not allow delicate finger movements. An important part of the cold finger solution is to prevent core cooling and compensatory extremity vasoconstriction by addressing core temperature stabilization through exercise, eating, and wearing enough layers on the trunk.
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A common strategy is to wear a pair of thin gloves of polypropylene, silk, thin wool, or polyester-Lycra inside a wool or pile mitten covered with a windproof and water-resistant glove shell. For delicate finger work, the gloved hand is removed from the mitten, the work done as fast as possible, and the hand returned to the mitten. However, since insulating materials insulate in both directions, when inside a warm mitten, cold fingers wearing gloves will not rewarm as fast as cold, bare fingers. Therefore another solution is to use bare fingers, which will perform faster than gloved fingers, returning them to warm mittens periodically until the task is done. This is not practical, however, when working with metal in very cold weather. Another approach is to keep a pair of gloves warm in a pocket and put them on after removing the hands from mittens. Polyester-Lycra gloves are easier to don than many other types of thin gloves. Excellent three-layer mitten sets include windproof shells with leather palms and two sets of removable pile mittens, at least one of which is fastened with Velcro. Another good system is a thin glove liner inside a heavy wool (Dachstein, ragg, or wool-polypropylene) mitten inside a Gore-Tex shell. An option that gives more finger dexterity in moderately cold conditions is a polypropylene glove liner inside a fingerless wool glove inside a shell. However, more layers result in more difficulty working with the hands. Shells should have easily accessible "nose warmers" of pile or mouton on the backs, should be long enough to cover the wrists, and should have palms of soft leather or sticky fabric for securely holding ice axes and ski poles. GAITERS AND OVERBOOTS.
Gaiters, which are long nylon tubes that cover the lower leg and upper part of the boot, are designed to keep snow, sand, and gravel out of boots and socks. They extend upward to just below the knee, open at the side or in front with a zipper or Velcro, and have a strap that fits under the boot sole to keep them snug on the boots and a drawstring at the top to hold them up. Gaiters with a front opening closed by a wide Velcro strap are easiest to don and doff. Shorter versions that extend to just above the ankle are adequate for summer mountaineering and may be preferable for cross-country skiers who need access for tightening boot buckles before descents.
High-altitude mountaineering requires special insulated overboots or lined gaiters. Fourth Layer.
The previous three layers are usually worn on the body. A fourth layer should be easily available in the pack. This should include quilted or pile pants and jacket (or vest). RAIN GEAR.
In moderate climates or in spring conditions when rain and wet snow may be encountered, outer garments of Gore-Tex or similar material should be used. For maritime climates and during seasons of heavy rain, it may be better to have two separate sets of outer garments: a light, thin, windproof nylon jacket and pants and a waterproof (coated nylon) jacket and pants. Vapor Barrier Systems.
Waterproof garments and sleeping bag liners close to the skin can prevent saturation of outer clothing and sleeping bags with sweat and the resulting reduction in insulating value. Sweating is reduced, and body water requirements are decreased. Vapor barriers seem to work better in very cold weather than at moderate temperatures. A light garment of polypropylene or similar material should be worn next to the skin, with the waterproof garment over this. Persons with hyperhidrosis and those who dislike clammy skin may object to a vapor barrier system. Shelter Everyone who spends time in the wilderness should practice the construction of several types of emergency survival shelters. The function of a shelter is to provide an extension of the microclimate of still, warm air furnished by clothing and to contain heat generated by the body, a fire, or other heat source. A properly designed shelter should permit easy and rapid construction with simple tools and should give good protection from wind, rain, and snowfall. The type and size of shelter depend on the presence or absence of snow and its depth, on natural features of the landscape, and on whether firewood or a stove and fuel are available. If external heat cannot be provided, a shelter must be small and windproof to preserve body heat. Small trees, branches, thick grass, leaf piles, small caves, and snow holes under downed trees or dense evergreens can be used. If possible, a shelter should be constructed in the timber to provide protection from the wind and access to firewood. Generally, shelters partway up the side of a ridge are warmer than those in a valley, since cold air tends to collect in valleys and basins during the night. Exposed, windy ridges above the timberline are cold. Areas exposed to flooding (drainages, dry river beds), rockfalls, or avalanches and under dead trees or limbs should be avoided. If open water is available, the camp may be located nearby, although in nonsurvival conditions, camps should be at least 200 feet from bodies of water. To avoid drifting snow, tents and shelters should be located with the entrance at right angles to the prevailing winds.
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SUBSTANCE
TABLE 28-2 -- Thermal Conductivity of Various Substances CONDUCTIVITY TEMPERATURE MEASURED (° C)
Air
0.006
0
Down
0.01
20
Polyester (hollow)
0.016
Polyester (solid)
0.019
Snow (old)
0.115
0
Cork
0.128
30
Sawdust
0.14
30
Wool felt
0.149
40
Cardboard
0.5
20
Wood
0.8
20
Dry sand
0.93
20
Water
1.4
12
Brick
1.5
20
Concrete
2.2
20
Ice
5.7
0
*
*Conductivity is the quantity of heat in gram calories transmitted per second through a plate of material 1 cm thick and 1 cm 2 in area when the temperature difference between the sides of the plate is 1° C.
Figure 28-2 Natural shelter.
Snow is a good insulator ( Table 28-2 ). Its heat conductivity is 1/10,000 that of copper and somewhat better than wool felt, so snow shelters may be warmer than other types of constructed shelters as long as the inhabitants remain dry. Contact with the snow or cold ground is avoided by using a foam pad, dry leaves, grass, or (in survival conditions only) a bed of evergreen boughs. Natural Shelters.
Caves and alcoves under overhangs are good shelters and can be improved by building wind walls with rocks, snow blocks, or brush. A fire should be built in such a way that heat reflects onto the occupant. The fire should be 5 to 6 feet from the back of the shelter, with a reflector wall of logs or stones on the opposite side of the fire; the occupant should sit between the fire and the back of the shelter ( Figure 28-2 ). In deep snow, large fallen logs and bent-over evergreens frequently have hollows under them that can be used as small caves. Cone-shaped depressions around the trunks of evergreens ("tree wells") can be improved by digging them out and roofing them over with evergreen branches or a tarp. A fire built to one side of such a shelter will reflect its heat off the snow toward the occupant. Ventilation must be adequate,
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and the fire should not be positioned under snow-laden branches. Constructed Shelters.
When no snow is available, shelters can be built of small trees, branches, brush, and boughs. A tarp can be rigged into a lean-to shelter. In cold weather the most satisfactory form is a lean-to with two sides closed with brush, a fire at the open front, and a wall of logs or stones on the far side of the fire to reflect heat into the lean-to's interior ( Figure 28-3 ). Walls or roofs of brush, branches, or broad leaves should be thatched (i.e., each layer should overlap the one below it). Snow Shelters.
If snow shelters become too warm, the walls will be wet and the roof will drip. A useful rule of thumb is that persons inside a snow shelter should be able to see their breath at all times.[24] SNOW TRENCHES.
A snow trench is the easiest and quickest survival snow shelter and the one least likely to make the diggers wet. It can be dug in most areas that are flat or on slight to moderate inclines as long as the snow is 3 feet or deeper or can be piled to that depth. A 4 × 6-foot trench can be dug in 20 minutes, one end roofed over with a tarp or boughs, and a fire built at the opposite end ( Figure 28-4 ). If a large tarp and a stove are available, a trench can be dug that is as comfortable as a snow cave and will hold two or three people. The object is to keep the maximal amount of snow around and over the trench. The trench is dug as narrow as possible at the surface while still providing sufficient room to shovel; a suitable size for the top is 4 feet wide and 8 feet long. It is undercut at the back and sides so that the bottom is 6 to 7 feet wide and 9 to 10 feet long ( Figure 28-5 ). A narrow entrance
Figure 28-3 Lean-to shelter. Sides should be closed with brush or snow and a fire built in front.
helps contain heat and can be closed with a small plastic sheet or a pack. Four or more skis or small tree trunks are laid from side to side over the top of the trench, with ski poles or branches interwoven at right angles. A tarp is then laid on top of these and snow piled around its edges to hold it down. In very cold weather the entire tarp can be covered by a layer of snow; at least 8 inches is needed for proper insulation. When the entrance is closed, a small stove and the occupants' body heat will raise the interior temperature to -4° to -1° C (25° to 30° F). Higher temperatures should be avoided so that clothing and bedding will not become wet from melting snow. Above the timberline in deep, wind-packed snow, a similar trench can be roofed with snow blocks that are laid horizontally, set as an A-frame, or laid on skis ( Figure 28-6 ). Chinks between the blocks are caulked with snow. SNOW CAVES.
Although a small snow cave large enough for one person can be dug with a ski or cooking pot, it is much better to have a shovel. Two shovels are best: a medium-sized general-purpose aluminum scoop
Figure 28-4 Emergency snow trench. A, Pit is dug and overlaid with skis and poles. B, Tarp is placed over the skis and secured with snow and heavy objects.
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Figure 28-5 A, Three-person snow trench. B, Completed trench the morning after a heavy snowfall.
shovel and a small, straight shovel (French type) to use while excavating the interior of the cave. The site is a large snow drift such as found on the lee side of a small hill. Areas in avalanche zones are avoided (see Chapter 2 ). The entrance is dug just large enough to crawl through and is angled upward toward the sleeping chamber ( Figure 28-7, A ), which should be large enough for a stove and two occupants lying side by side. After the entrance is dug with the scoop shovel, the digger crawls inside, lies supine, and uses the straight shovel to excavate the chamber until room is sufficient to move around and use the larger scoop shovel. A ventilation hole as large as a ski pole basket is cut in the roof over the cooking area. A cave large enough for two persons takes several hours to dig. Pine branches or other natural material are used to cover the floor if a sleeping pad is not available. Since the diggers tend to become wet, water-resistant or waterproof jackets 683
Figure 28-6 A, Above-timberline snow trench. B, Completed snow trench the morning after a heavy snowfall.
and pants should be worn. A faster method is to excavate a large entrance so there is more room to dig, then partly fill in the entrance hole with snow blocks cut with a shovel or snow saw ( Figure 28-7,B and C ). SNOW DOMES.
When the ground is flat or the snow cover is shallow, snow can be piled into a large dome 6 to 7 feet high and left to harden for a few hours ( Figure 28-8 ). A low entrance is dug on one side, and from there the interior is carved out to make a dome-shaped room large enough to sleep three people. A ventilation hole is cut in the roof over the stove. IGLOOS.
Igloos are the most comfortable arctic shelters but require time, experience, and some engineering skill. They are not recommended for the novice but may be worth the effort if the party will be stranded for any length of time. Igloos require one or ideally two
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Figure 28-7 A, Snow cave entrance. B, Snow cave partly closed with snow blocks. C, Interior of snow cave.
snow saws and snow of the proper consistency. Windblown snow in a treeless area is best; otherwise a large area of snow can be stamped well and left to harden over several hours. To mark the diameter of the igloo, a ski pole is held by the handle and the body turned so that the pole basket makes a large circle. This will outline the
Figure 28-8 A, Preparing a snow dome. B, Completed snow done.
base of an igloo suitable for three people. Cutting some of the snow blocks from inside this circle will lower the floor so that fewer blocks are required for the dome. At least two persons are needed, one to cut and carry the blocks and the other inside the igloo to lay the blocks. The blocks should be about 18 inches wide, 30 inches long, and 8 inches thick. They are laid in a circle leaning in about 20 to 30 degrees toward the center of the igloo, with the sides trimmed for a snug fit. The tops of the first few blocks in the first circle are beveled so that a continuous line of blocks is laid, with the first few blocks of each succeeding circle cocked upward ( Figure 28-9 ). A common error is not to lean the blocks inward enough, resulting in an open tower instead of a dome. Gaps are caulked with snow. The dome should be 5 to 6 feet high inside and can be closed with a single capstone of snow. The entrance is dug as a tunnel under rather than through the edge of the igloo, preventing warm air from escaping. Tents and Bivouac Sacs.
Tents are generally comfortable and dry but in very cold weather are not as warm as snow shelters. They are preferable to snow shelters at mild temperatures, during damp snow conditions at temperatures above freezing, or when the snow cover is minimal. Bivouac sacs are carried by climbers on
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Figure 28-9 A to C, Stages of igloo construction. D, Building an igloo, southeast ridge of Mt. Foraker. E, Double igloo for a party of five.
long alpine-style climbs or for emergencies. They are usually made of Gore-Tex or waterproof fabric and hold one or two persons. Many modern packs have extensions, so when used with a cagoule or anorak (roomy, knee-length, hooded pullover garment), they form an acceptable bivouac sac. Increasing Internal Body Heat Production Internal body heat production can be increased voluntarily by raising the level of muscular activity and by eating. To obtain maximal heat production from exercise, the body should be well fed and in peak physical condition. This is particularly important for persons with sedentary jobs who participate in vigorous outdoor sports and for rescue personnel who may be subject to severe, unplanned, and prolonged physical stress. A suitable physical conditioning program should develop both aerobic and motor fitness. The goal of aerobic exercise is efficient extraction of oxygen from alveolar air. This is best developed by rhythmic endurance exercises such as running, cross-country skiing, cycling, swimming, and using exercise bicycles and Nordic skiing simulators. The most effective activities are those that exercise lower and upper extremities simultaneously. Exercise should be vigorous enough to produce a heart rate of 75% of the age-related maximum (0.75 × [220 minus the participant's age]) for at least 15 minutes 4 days a week. Motor fitness, which includes strength, power, balance, agility, and flexibility, is developed by vigorous competitive team sports, selected calisthenics, and weight-lifting exercises. Providing External Heat: Fire Building The ability to build a fire under adverse conditions is an essential skill that should be practiced by persons
686
Figure 28-10 Stages of building a fire. A, Select a spot out of the wind. Start by placing tinder, such as small, dry evergreen twigs, in a lean-to fashion against a larger branch. B, Add a layer of kindling (larger dry branches and split sticks) over the tinder, being sure that air can reach each piece. C, Insert a lighted match, candle, or cigarette lighter into the base of the lean-to. D and E, Add larger pieces of kindling and fuel (large sticks and pieces of split wood) as the fire catches well. Keep the fire small so that you can get close to it.
who engage in outdoor activities ( Figure 28-10 ). Necessary equipment includes a sturdy knife, a candle, and waterproof matches. In addition, a tube of chemical fire starter (available in most outdoor stores) is highly recommended, especially for wet climates. To burn, a fire needs air, but not too much air. The fire site should be out of the wind behind a rock or log or in a snow pit. If the fire is built on bare ground, all flammable material such as moss and grass should be cleaned off by scraping the ground surface down to mineral soil over an area at least 3 feet in diameter. If snow is too deep to be removed down to bare ground, the fire should be built on a platform of green logs. Building a fire requires three types of combustible material: tinder, kindling, and fuel. Tinder is any type of finely divided, high flammable material. It must be dry. Examples include grass and leaves, inner bark of birch trees, shavings from dry sticks, cotton balls, small sticks, and fine grades of steel wool. The most readily available natural material is the small dry twigs found on the lower, dead branches of evergreens. If the outer wood of small branches is wet, it can be shaved off, or the branches can be split lengthwise into several thinner lengths with a sturdy knife to expose the dry core. The tinder is arranged in lean-to form by placing it against a larger branch, smallest sticks on the bottom and larger ones on top, separated just enough so that
687
air can reach each piece. To conserve matches, one match should be used to light a candle or segment of fire starter, which in turn lights the tinder. The flame should be placed under the middle of the lean-to of tinder so that lower, smaller pieces will set fire to higher, larger pieces. Kindling is larger material, usually larger pieces of dead branches and large branches that have been split lengthwise with a knife. Once the tinder is burning well, these larger pieces of dry wood are added. Fuel is the largest material, usually branches and sections of dead tree trunks several inches or more in diameter. These should be split if an ax is available. Standing dead wood is preferable to wood lying on the ground, and wood that has lost its bark to wood with bark, because both will be drier and less rotten than their alternatives. Fuel is added after the kindling is burning well. Several times more fuel than the predicted need should be collected. When dead branches are gathered, only those that snap loudly when broken off should be selected. If no ax or saw is available, the fire can be built next to a large, downed log, which may catch and burn for several days. Long, dead sections of trees can be shortened by laying them across a fire so that when they burn through, two shorter sections result. Fires generally should be kept small, both to conserve wood and to allow them to be approached more closely. The wood supply should be protected from rain and snow. A fire can be started without matches by using an automobile cigarette lighter or batteries and steel wood. A "wire" can be made by twisting and pulling out a fine-grade (e.g., 4-0) steel wool. This will catch fire if the ends are touched to the positive and negative terminals of two fresh C or D batteries in tandem. A fire starter can be made by stripping the insulation from the middle of a wire and wrapping the bare portion 7 to 10 times around a dry stick. If the two ends of the wire are touched to the terminals of an automobile battery, the wire will become red hot and the stick will ignite (the wire should be long enough that the flame is not close to the battery, where it could ignite hydrogen gas produced by the battery). When scraped hard with a file or knife blade, commercial "metal matches" made of magnesium will produce showers of sparks that will ignite tinder such as fine steel wool, cotton, or small dry shavings. Food* For optimum performance, the human body requires a daily supply of calories, carbohydrate, protein, fat, minerals, and vitamins. Carbohydrates supply calories and are essential for replacement of muscle glycogen. If diet is inadequate, body carbohydrate and fat stores and finally tissue protein will be depleted to provide calories for heat and energy. Carbohydrate in the form of liver and muscle glycogen is used up first, then fat is used at a steady rate until gone. Protein is used rapidly at first, then more slowly, and finally rapidly again just before death. [9] A moderately active 70-kg (154-pound) male normally requires the food equivalent of 2800 kcal/day, but if exercising in cold weather, he may require more than twice this amount. Protein intake should be at least 65 g/day, and carbohydrates should make up 60% to 70% of the diet. Although most persons in a survival situation worry more about food than anything else, food is usually less important than shelter or water because a person can survive for weeks without food, even in cold weather. Enough water must be available, however, and energy expenditure must be kept to a minimum. Most wilderness parties carry adequate supplies of food; problems arise if food is exhausted, lost, or contaminated. Bare ridges, high mountains above timberline, and dense evergreen forests are difficult places to find wild food, even in summer. Success is more likely on river and stream banks, on lake shores, in margins of forests, and in natural clearings. Since in most cases the amount of wild food found by an untrained individual will not provide enough calories to replenish the energy expended in searching for it, it is important always to carry extra food for emergencies. The following general rules about wilderness edibles have many exceptions, so no unfamiliar wild food should be eaten except in extreme circumstances (see Chapter 48 and Chapter 49 ): 1. All wild foods except fruits and berries should be cooked. This will make them more palatable, more digestible, and safer to eat. 2. Persons who spend time outdoors should know the edible plants and animals of familiar areas. Similar species are often found in similar though unfamiliar areas. 3. Plants to avoid include mushrooms and other fungi, buttercups, plants with umbrella-shaped flowers, wild beans and peas, all unknown berries except blue and black ones, all bulbs except those with an onion odor, and all plants with milky or colored sap or shiny leaves. Compound berries (e.g., raspberries, blackberries, thimbleberries, salmonberries) are safe to eat. 4. No one should eat large quantities of a strange plant food without first tasting it. A. Touch the plant's sap or juice to the inner forearm or tip of the tongue. B. If no ill effects occur, boil plant parts in two 5-minute changes of water. Place 1 teaspoon of the resulting material in the mouth for 5 minutes, and chew but do not swallow it. If a *References [ 2]
[ 7] [ 16] [ 17] [ 19] [ 22] [ 23] [ 26]
.
688
burning, nauseating, or bitter taste results, immediately spit if out. If no unpleasant effect occurs, swallow it and wait 8 hours. C. If no ill effects (e.g., nausea, cramps, or diarrhea) occur after 8 hours, eat 2 tablespoons and wait an additional 8 hours. D. If no ill effects occur at the end of this period, consider the plant edible. 5. All land mammals, birds, and birds' eggs can be eaten. The entire carcass, both fat and lean, should be eaten, except for canine, seal, and polar bear livers. Crustaceans below the high-tide mark, mollusks, insects, reptiles, and some amphibians can be eaten. Salamanders and frogs should be skinned; toads should be avoided altogether. Fish, crustaceans, and mollusks should be eaten promptly because they spoil quickly. Fish and meat can be preserved by drying. Black mussels, mollusks with cone-shaped shells, Pacific reef fish, "puffers," fish eggs or entrails, and any fish that looks "ugly" should be avoided (see Chapter 54 ). Any fish with an unpleasant odor, pale slimy gills, flabby skin, flesh that remains pitted when pressed on, or sunken eyes should be avoided, as well as all aquatic life during a red tide. 6. Edible parts of wild plants may include roots, leaves (especially young leaves), stems (usually require peeling), shoots, buds, grass seeds, inner bark (aspen, cottonwood, birch, willow, lodgepole pine, Scotch pine), nuts, and berries (except as noted in 3).
Figure 28-11 Snare loop. A, Simple snare loop. B, Locking device for a wire snare loop. Animal Food.
Mammals and birds can be trapped, snared, or shot. Some, such as spruce hens and porcupines, can be clubbed. Fish can be hooked, speared, or trapped. To secure this type of food, however, the hunter must locate the prey. On land this is done by searching for signs such as trails, droppings, burrows, dens, and bedding areas.
Carnivore dung usually contains hair and bone; herbivore dung has indigestible plant parts. Trails lead to feeding and watering places. Successful hunting requires patience, skill at stalking, and knowledge of animal behavior. The best times to hunt are at dawn and dusk as animals are moving to or from their bedding areas. Small animals can be snared or trapped. Snares should be baited or located on a game trail at a place where the animal has no choice but to enter the snare. This can be a naturally narrow or a prepared area. The mouths of dens and burrows are good places to set snares. Gloves should be worn during snare construction to minimize human scent. Snare loops can be made from any type of bare wire or improvised from strips of green bark, cord, shoelaces, or clothing strips. Light, strong wire such as 28-gauge piano wire is best. A small loop is tied at one end of the wire, and the main loop is made by feeding the other end through the small loop ( Figure 28-11, A ). The main loop is adjusted to catch the animal around the neck and to fit the expected size of the prey (e.g., three fingers in width for squirrels, fist sized for rabbits). Snares using loops are effective because the animal almost always lunges forward, tightening the loop around its neck. A locking device should be included to prevent the wire loop from loosening after the animal is trapped ( Figure 28-11, B ). Snares should be set at midday when animals are bedded down. The trapper approaches the area at a 90-degree angle to the trail, sets the snare, and backs away, keeping downwind from the animal's expected location and not walking on the game trail. Natural surroundings should be disturbed as little as possible. Snares and traps should be checked twice daily. In general, one animal is caught for every 15 snares set. Many different types of traps have been invented; most include a trigger arrangement that is baited or located so that it releases when disturbed by the animal's movement. Trigger release allows a counterweight to pin the animal or a bent sapling to straighten and hoist it off the ground ( Figure 28-12 ).
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Figure 28-12 A, Figure-4 deadfall. B, Twitch-up snare.
Figure 28-13 A, Split-shaft fish spear. B, Fish trap.
Birds can be caught with snares or baited fishhooks. Fish can be taken with hook and line, traps, and spears. Emergency survival kits should contain several hooks and a long length of line. Insects, smaller fish, worms, shellfish, or meat can be used as bait, or lures can be improvised from pieces of brightly colored cloth, feathers, or bits of shiny metal. In open streams the best places to fish are pools below falls and behind rocks. Locating fish is more difficult in the winter, when they retreat into the deep parts of lakes. Holes can be cut in the ice of frozen lakes. The best time to fish is early morning or dusk. An effective fish spear is the split-shaft type ( Figure 28-13, A ), which has two toothed jaws held apart by an easily dislodged trigger. A spear works best if it is used to pin a fish against the bottom or bank so the fish can be grasped with the hands before it works loose. In streams, fish traps can be made by using rocks or vertical willow branches to build an enclosure with a funnel-shaped opening, the narrow end extends
690
well into the enclosure ( Figure 28-13,B ). The trap should be located so that the water current drives fish into the wide end of the funnel. Another type of trap can be made by tying the neck and sleeves of a T-shirt closed, placing the shirt with the tail propped open in the water at the downstream end of a pool where fish have been seen, and chasing the fish into the shirt. Another way to catch large fish (at least 10 inches long) is by "tickling."[17] [23] This involves crawling slowly upstream along a stream bank, feeling underneath the bank and under nearby logs for fish. They are usually found lying still with their heads pointed upstream. If a fish is felt, the person moves the hand slowly forward, grasps the fish at the gills, and flips it onto the bank. Tickling fish and constructing and using fish traps are difficult in winter. Plant Food.
Edible plants ( Figure 28-14 ) are common in mountain meadows and even in forests, although considerable energy may be needed to dig up or gather plant material. This is especially true during the winter months, when gathering roots and berries may require
Figure 28-14 Edible wild plants. A, Pine cone. B, Acorns. C, Wild onion. D, Dandelion.
removing snow from large areas and digging in frozen ground. Tender new needles of pines and other conifers are edible, although not very tasty. Pine nuts are found in pine cones, which can be picked from trees. All pine nuts are edible and high in caloric value but are so small in some species that it is impractical to gather them. The gatherer should look for unopened cones, scorch them over a fire, and split them by pounding with a rock. The nuts are removed and roasted. Acorns are another good source of food; they should be boiled for an hour with three changes of water to remove the bitter tannic acid. Cattails and arrowheads can be found in low-lying, marshy areas and lake shores. In spring the sheathed top spike of the cattail can be boiled and eaten and the sprouts eaten raw. Pollen from the blooming flower spike can be used as flour. Although fibrous, the roots contain much starchy material and can be boiled or roasted. Arrowhead tubers are boiled or roasted for 30 minutes and eaten after peeling. Dandelions, woolly louseworts, wild onions, elk thistle, and bistort can sometimes be found under the snow in mountain meadows. The roots of all these
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plants are edible and nourishing but should be boiled. Many bulbs are poisonous, however, and only those with an onion odor should be eaten. The young leaves and shoots of ferns can be boiled and eaten, and the leaves of mountain sorrel can be eaten raw. Wild rose hips are edible. Elk thistle stems are edible if peeled and boiled. Young dandelion roots and leaves can be eaten; older ones should be boiled in several changes of water to remove the bitter taste. The inner bark of aspen, cottonwood,
Figure 28-14 E, Elk thistle. F, Fern. G, Arrowhead. H, Bistort. I, Cattail.
birch, willow, lodgepole pine, and Scotch pine is edible.
Berries, such as huckleberries, raspberries, crowberries, cranberries, bearberries (Kinnikinnick), salmon-berries, and thimbleberries can sometimes be found under or over the snow and are edible ( Figure 28-15 ). Certain types of lichen can be eaten. Iceland moss should be boiled for an hour, reindeer moss boiled or roasted, and rock tripe dried and then boiled.
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Figure 28-15a Edible berries. A, Blueberry. B, Blackberry. C, Cranberry. Cooking.
As noted, all wild foods except fruits and berries should be cooked. Cooked food is usually more appetizing, easier to chew, more digestible, and safer because cooking destroys microorganisms. Hot food also helps maintain morale. A large metal container, preferably a pot with a bale (see Appendix A ), is indispensable to heat water and other liquids. Since cooking over a fire will cover the outside with soot, a stuff sack is useful to store the pot. Since it can tip over easily, the pot should not be placed directly on burning wood but on two firm rocks or green logs with fire in between. Rocks from a stream or dry wash should not be placed near a fire, since steam from internal moisture can cause an explosion. A pot can also be hung over the fire on a sturdy green stick, one end of which is supported by a forked stick driven into the ground and the other end anchored by rocks. Most types of wild food can be cooked successfully by boiling, and the cooking water retains the food's fat and natural juices. This water should be consumed as well.
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Figure 28-15b D, Crowberry. E, Bearberry. F, Salmonberry.
Meat and fish can be roasted on a spit made from a green tree branch or can be fastened to a flat rock or the flat surface of a split log tipped on edge to face the fire. Water Water constitutes about 60% of the body weight of an average young adult male; the value for a female is slightly lower. The percentage of water tends to decrease with age. In a sedentary adult, normal daily water loss includes about 1400 ml of urine, 800 ml through the skin and lungs, and 100 ml in the stool, for a total of 2300 ml daily. Since about 800 ml of water per day is contained in food and 300 ml produced by metabolism, a minimum daily intake of 1200 ml is necessary in a temperate climate at sea level to avoid dehydration.[9] In a hot dry climate, at high altitude, or with exertion, insensible losses and sweating increase considerably, so fluid intake should be increased proportionally. Monitoring urine output determines whether intake is adequate; 1 to 1.5 L of light-colored urine should be excreted per day. Adding fruit flavors and making hot drinks improve the palatability of water. Electrolyte drinks and salt tablets are generally unnecessary in cold weather, since the electrolytes lost in sweat are easily replaced by a normal diet. When water supplies are limited, overexertion is avoided and sweat "rationed." Almost all surface water should be considered contaminated by animal or human wastes, with the possible exception of small streams descending from
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Figure 28-16 A, Emergency snowshoe. B, Detail of snowshoe binding.
untracked snowfields or high, uninhabited areas. At altitudes below 5488 m (18,000 feet), simply bringing water to a boil will kill Giardia cysts and most harmful bacteria and viruses. Water can also be disinfected by filtration or addition of chemicals (see Chapter 51 ). At subfreezing temperatures and in locations above the snow line where liquid water is difficult to find, snow or ice must be melted to obtain water. This requires a metal pot (which should be included in every survival kit), fire-starting equipment, and wood for fuel. The time and effort required and decreased thirst in cold weather favor development of dehydration under survival conditions. Whenever open water is encountered, individuals should drink their fill of disinfected water, then top off all canteens. Each evening, enough snow is melted to provide water for supper plus a full canteen, which is placed in the bottom of the sleeping bag to keep it from freezing and is ready for use during the night or for making breakfast in the morning. Before leaving camp in the morning, melted snow provides everyone with at least a full canteen for the day. Melting ice or hard snow is more efficient than melting light, powdery snow. To avoid scorching the pot, the snow is melted slowly, or water is heated in the bottom of the pot before adding snow. On warmer sunny days, snow can be spread on a dark plastic sheet to melt. Emergency Snow Travel Travel in deep snow is almost impossible without skis or snowshoes. Even though travel may be unwise for other reasons, wilderness foot travelers in both subarctic and temperate latitudes should know how to improvise snowshoes from natural materials in case they are stranded by a late- or early-season snowstorm. Emergency snowshoes ( Figure 28-16,A ) can be made from poles that are 6 feet long, ¾ to 1 inch thick at the base, and ¼ inch thick at the tip, and sticks ¾ inch thick and 10 inches long.[2] Twelve long poles and 12 short sticks are needed. For each snowshoe, six long poles are placed side by side on the ground, and the middle point of the poles is marked. One short stick is lashed crosswise to the tail (base) of the poles, and three short sticks are lashed side by side just forward of the midpoint of the poles where the toe of the boot will rest. Two sticks are lashed where the heel of the boot will strike the snowshoe. The tips of the six poles are tied together. Each binding ( Figure 28-16, B ) is made of a continuous length (about 6 feet) of nylon cord, preferably braided, since it will eventually fray. The midpoint of the cord is positioned at the back of the boot above the bulge of the heel. Each end of the cord is run under the three side-by-side short sticks at the side of the boot, then up and across the boot toe so that it crosses the other end on top of the toe, forming an X. Then each end is looped around the cord running along the opposite side of the boot, and the ends are brought around the back of the boot heel. The cord is pulled tight around the boot, and the ends are tied together at the lateral side of the heel. On walking the tip of the snowshoe should rise, the boot heel should rise, and the boot sole should remain on the snowshoe.
Snow travelers should avoid stepping close to trees (because of funnel-shaped "tree wells" around tree trunks), large rocks (because of weak snow or moats around them), and overhanging stream banks. The person who falls into a stream or lake should roll repeatedly
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in powdery snow to wick the water from clothing, brushing the snow off each time. A fire completes the drying process.[2] Stalled or Wrecked Vehicles Persons stranded in automobiles or downed airplanes can survive using the equipment in the vehicles. Survivors should stay with the vehicle rather than go for help, since a vehicle is much more visible to rescuers than is a person. Floor mats and upholstery can be used for insulation, but it is much better to have a vehicle survival kit containing extra clothing and blankets (see Appendix D ). Automobiles.[25]
In cold weather, drivers should keep their vehicles in the best possible mechanical condition, using winter-grade oil, the proper amount of radiator antifreeze, deicer fluid for the fuel tank, and windshield antifreeze for the cleaning fluid. Windshield wiper blades that are becoming worn should be replaced. A combination snow brush and ice scraper should be available, and a can of deicer is useful on frozen door locks and wiper blades. Snow tires, preferably studded (illegal in some states), are desirable, but chains should be carried as well. All-wheel drive or four-wheel drive is optimal, and front-wheel drive superior to rear-wheel drive. The battery should be kept charged, the exhaust system free of leaks, and the gas tank full (drive on the upper half of your tank). A cell phone or citizen's band radio is useful. The marooned driver should tie a brightly colored piece of cloth to the antenna and at night should leave the inside dome light on to be seen by snowplow drivers and rescuers (headlights use too much current). If necessary for heat, the motor and heater can be run for 2 minutes each hour (after checking to see if the exhaust pipe is free of snow). To avoid CO poisoning, a downwind window is cracked 1 to 2 inches. Reusable CO detectors are available and can be carried in the survival kit. One or two large candles should be carried to provide heat and light if the gasoline supply runs out. Two candles can raise the interior temperature well above freezing. Airplanes.
Airplane fuselages are poorly insulated. Unless a stove is available, survivors are usually better off constructing a shelter than can be heated with a fire (as described earlier), outside but near the aircraft. Batteries and cigarette lighters can be used as fire starters. Oil and gasoline can be used as fuel if poured over a container full of dirt or sand.
HOT WEATHER SURVIVAL Environmental conditions predisposing to serious heat stress can be found in most temperate zone regions during the summer months and in the tropics year-round. The amount of heat stress is proportional to both temperature and relative humidity; thus a tropical jungle environment with a relatively lower temperature and higher humidity can be as dangerous as a drier desert environment with a relatively higher temperature. Serious heat illness occurs when endogenous heat production plus exogenous heat gain forces the core temperature to dangerous levels (more than 40° to 46° C [104° to 105° F]) despite the body's cooling mechanisms. These mechanisms include involuntary cutaneous vasodilation, sweating, and voluntary mechanisms, such as seeking shelter from the sun, avoiding excess insulation and heat-producing physical activity, and replacing lost fluids and electrolytes (see Chapter 10 ). The body adapts better to heat and altitude than to cold. It acclimatizes to heat by increasing the blood volume, dilating skin blood vessels, and improving cardiac efficiency so as to carry more heat from the body core to the shell. The process of acclimatization takes about 10 days, during which the subject starts to perspire at a lower temperature, the volume of perspiration increases, and the perspiration contains fewer electrolytes. The following discussion emphasizes survival in a desert environment (see also Chapter 29 ). Practical Methods for Adjusting to Hot Weather [4] Heat loss by conduction, convection, and radiation can be increased by exposing the maximum amount of skin to the circulating air. This should be done only when in the shade; when in the sun, skin should be completely protected by clothing. Wearing clothing when exposed to hot sun also reduces water loss by reducing sweating. Because heat loss and sweating may be impaired by sunscreens, a good compromise is to cover the face and hands with a sunscreen having a high sun protection factor (SPF) number and to wear a long-sleeved shirt and long trousers of tightly woven, loose-fitting, light-colored (preferably white) cotton. Avoid T-shirts, which have an SPF of only 5 to 9. Special clothing with an SPF of 30 or greater is available (e.g., Solumbra). If desired, ventilation holes can be cut at the axillae and groin. Hydration is maintained by drinking adequate fluids, some of which can contain electrolyte supplements. Optimal hydration maintains blood volume and shell circulation and supports the sweating mechanism. Enough water must be carried or be available in the field. Water bottles should be wrapped with clothing to insulate them and buried in the backpack. The layer principle of clothing is recommended in the desert as well as in cold weather. Layers can be taken off during the heat of the day and added at night when the dry desert air cools rapidly. Since high winds and sandstorms occur frequently in desert areas, a
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wind-resistant parka and pants are desirable; since rains occasionally occur as well, the garments should also be water repellent. Because of its high thermal conductivity, poor insulating ability, and good wicking ability, cotton—which is avoided in cold weather—is the fabric of choice for hot weather clothing. Clothing should be loose to promote air circulation. Before exposure to prolonged or strenuous hot weather exertion, individuals should allow time for acclimatization. Heat gain from the environment can be minimized by using clothing to protect the head and body from the direct rays of the sun. A hat with a wide brim or a Foreign Legion-style cap with a neck protector and ventilation holes in the crown is recommended. A neck protector can be improvised from a large bandana by placing it on the head with the point just above the forehead, bringing the two tails around in front of the ears, tying them under the chin, and then replacing the hat. Travelers should seek shelter during the hottest part of the day. Caves and overhangs can be used, but gulleys and other dry watercourses should be avoided because of the danger of flash floods. A sun shelter can be made by suspending a tarp from brush or cacti or by laying the tarp on a framework of poles. Travelers who become stranded in a vehicle should lie under it. Because desert air is much cooler a foot above or a few inches below the ground surface, the desert traveler should lie on a platform or in a scooped-out depression rather than directly on the ground. Direct contact with the hot ground and other hot objects, particularly hot metal, should be avoided. Sturdy hiking or climbing boots should be worn to protect the feet, not only from the hot ground but also from sharp rocks, the spines of cacti, and snakes. Gaiters should be worn or improvised from strips of cloth to keep sand and insects out of boots and socks. The hands should be protected with leather gloves. Rest periods should be taken in the shade rather than in the direct sun. High-quality sunglasses should be used to protect the eyes; if necessary, sunglasses can be improvised from a piece of cardboard or wood with a narrow slit cut for each eye. Body heat production can be minimized by avoiding muscular exertion during periods of high heat and humidity. Persons should travel only early in the morning, late in the evening, or at night. Desert Survival* About 20% of the earth's land surface is made up of desert. Desert areas average less than 25.4 cm (10 inches) of rainfall annually. Deserts range from barren sand or gravel plains without a living plant for a hundred miles to areas of grass and thorny bushes than can support camels and goats. Despite lack of moisture, many plants and animals have adapted to the hot, arid environment and are able to thrive in many deserts. Deserts heat up rapidly during the day, but because of low humidity and the low specific heat of the ground, they cool rapidly at night. Daily temperature ranges may be as great as 55° C (100° F).[26] These temperature changes produce alternate expansion and contraction of rocks, causing them to break up into smaller and smaller fragments and eventually to form gravel or sand. Lack of rainfall reduces the eroding effect of water, so wind and wind-borne sand are the most important agents of erosion. When the rare rains occur, water tends to run off rather than sink into the ground, and flash floods may occur; dry watercourses (arroyos, wadis, dry washes) are familiar features. Sudden weather changes are common; desert travelers in the fall, winter, and spring should be prepared for cold as well as hot weather. Dust storms and strong solar glare can be hazardous. Southerly deserts may be hot year-round, whereas northern ones may have four recognizable seasons. Desert temperatures as hot as 134.4°F in the Sahara at Azizia and 134°F in Death Valley, California, have been recorded. [16] At such temperatures, the ground can become so hot that feet may be burned through shoes, and serious burns can result from touching exposed metal. Desert plants have developed special characteristics that enable them to conserve water and survive long periods of drought. Some have extensive root systems that quickly absorb rainfall moisture, and others have exceptionally long roots that reach down to the water table. Many plants are dormant during the hottest season; others have thick external coverings that resist evaporative losses. Some are able to store water during wet seasons to allow survival through dry periods. Desert animals forage and hunt during the cool of the evening and night, resting in cool places during the day. Food.
Natural food is difficult to obtain in true deserts but is less important than water. A survivor can live several weeks without food if water is available. More natural food is available in the deserts of the American Southwest than in Old World deserts, such as the Sahara and Gobi ( Figure 28-17 ). No plant with milky juice should be eaten. All cactus fruits are edible, and the leaves of flat-leafed cacti (e.g., prickly pear) can be peeled and eaten, preferably after boiling. Wild cherries, wild celery, wild currants, wild onions, acacia beans, and piñon nuts are found in some areas. Grass seeds and the soft part of grass stalks are edible. Kangaroo rats, jerboas, rabbits, prairie dogs, lizards, tortoises, snakes, and insects, particularly locusts, *References [ 2]
[ 9] [ 16] [ 19] [ 22] [ 23]
.
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Figure 28-17 Edible desert plants and animals. A, Mesquite bean. B, Prickly pear. C, Snake. D, Desert tortoise. E, Lizard. F, Kangaroo rat. G, Jackrabbit.
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TABLE 28-3 -- Expected Days of Survival at Various Environmental Temperatures and with Varying Amounts of Available Water (Not Available) From Adolph et al: Physiology of man, New York, 1947, Interscience. are all edible. Small mammals and birds can be trapped or snared as described previously. If firearms are available, larger animals such as antelope, deer, foxes, and badgers can be procured and leftover meat dried in the sun.[16] [22] [23] If water is limited, however, it is wise to base the diet on carbohydrate rather than protein, since more water is required to excrete the waste products of protein in the urine. Water.
There is no substitute for water in the desert, although a person can prolong life in a survival situation by decreasing water loss. Waterholes and oases are rare in deserts. They occasionally may be located by watching the behavior of animals and birds, which travel toward water at dawn and dusk. Animal trails tend to lead to water and may be joined by other trails and become wider as they approach it. Birds may circle before landing at a waterhole, especially in the morning. A pool of water with no animal tracks or droppings may be poisonous. Muddy and dirty water should be filtered through cloth, and all water should be treated chemically or by filtration or boiling before drinking (see Chapter 51 ). Persons should not drink urine or water from a vehicle radiator (which contains glycols). Table 28-3 (Table Not Available) shows the expected days of survival in the desert in relation to the amount of water available. A useful device for producing potable water is a solar still ( Figure 28-18 ). The materials needed include a 6 × 6-foot piece of sturdy, clear plastic sheeting (preferably reinforced with duct tape in the center), a shovel, a 6- to 8-foot piece of surgical tubing, a 1-quart plastic bowl, duct tape, and a knife. A cone-shaped hole about 3 ½ feet in diameter and 18 to 20 inches deep should be dug in a low area where water would stand the longest after a rain. With the surgical tubing taped securely to its bottom, the bowl is placed in the center of the hole. The plastic sheet is positioned loosely on top of the hole and weighted with a fist-sized rock in the center so that it sags into a cone whose apex is just above the bowl. Crushed desert vegetation is placed inside the hole to provide additional moisture, preferably barrel and saguaro cactus parts. Unknown or possibly poisonous plants are avoided. Dirt and rocks are piled around the rim on top of the plastic sheet to seal the edges of the hole. Urine can be placed inside the hole in an open container. Contaminated surface water can also be purified inside a solar still, but water from a vehicle radiator should not be used because the glycols will distill along with the water. The still is not opened once it starts operating. It will produce 1 pint to 1 quart of water per 24 hours without added urine or vegetation and up to 4 quarts with it. The surgical tubing is used to suck water from the bowl periodically as it collects. If vegetation is plentiful, another type of solar still can be made from a large, clear plastic bag.[21] On a slope, a hole several feet in diameter is dug with a craterlike rim surrounded by a moat that drains downhill into a small hole. The bag is centered on the large hole with its edges over the moat and its mouth downhill at the small hole. An upright stick is placed
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Figure 28-18 Solar still.
inside the bag in the middle and clean rocks along the crater rim inside the bag to keep the bag anchored and ballooned out. Duct tape reinforces the bag where the stick tents it. After the bag is filled with vegetation, its mouth is tied shut. The vegetation should not touch the sides of the bag or spill into the part of the bag that is over the moat. The warmth of the sun causes water to evaporate from the vegetation and condense on the inside of the bag, run down into the part of the bag that is over the moat, run downhill toward the mouth of the bag, and collect in the part of the bag's neck that is in the small hole. Survivors open the mouth of the bag and pour out the water as needed.
NAVIGATION Even if in a familiar area, backcountry travelers should always to carry a compass, map, and altimeter. Prior training and experience in map reading and compass use are necessary.[13] The best type of compass for the layperson is the Swedish Silva compass, designed to be used in the sport of orienteering. The compass is always followed even if at odds with "gut feelings" about direction. Topographic maps are available at most outdoor stores in both the 7.5- and 15-minute series. Global positioning system (GPS) units are small, electronic devices that can plot a traveler's position by receiving signals from satellites. Although very useful, especially in poor visibility, they are expensive and battery dependent, require at least three satellites in the unobstructed sky above, and need experience to translate their output into a position on a map.[5] The backcountry traveler should be expert with map and compass before considering a GPS unit. Travelers who lose or forget their compass should still be able to find directions (see Chapter 73 ). At night, north can be found by identifying the Big Dipper (Northern Hemisphere only) and following the "pointers" (farthest stars on the bowl of the dipper) to the North Star (Polaris), the most distal star in the handle of the Little Dipper, which is located about halfway between the Big Dipper and the -shaped constellation Cassiopeia. On a sunny day a nondigital watch set to standard time can be used to find direction. When the hour hand is pointed toward the sun, south will be one-half of the shorter of the two distances between the hour hand and 12 o'clock.
WEATHER FORECASTING[5]
[ 11] [ 15] [ 18] [ 27]
Travelers entering the backcountry must check expected weather conditions. Modern weather forecasting, because of radar, satellite technology, and other advanced techniques, is accurate but not infallible. Local and national radio and television networks broadcast local and regional reports hourly. The Weather Channel has multiday forecasts and is also available on the Internet at www.weather.com. The best source of up-to-date local weather information is the National Weather Service, which broadcasts
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24 hours a day at frequencies from 162.400 to 162.550 MHz on very-high frequency (VHF) FM. Multichannel radios with a weather band receive these frequencies, and inexpensive, lightweight radios receive only these frequencies. When evaluating avalanche conditions, travelers must know the weather conditions over the previous few days as well. The U.S. Forest Service provides information on avalanche conditions in many mountainous areas, especially in western states (see Chapter 2 ). Since weather information from outside sources is usually impossible to access in a wilderness environment, the wilderness traveler should be able to predict weather to some extent. This requires a knowledge of both local weather patterns and basic meteorology, particularly the significance of cloud patterns, wind directions, barometric pressure changes, and temperature changes. Backcountry weather forecasting is an inexact science, however. In Michael Hodgson's words, "Predictions relative to weather are only educated guesses, never statements of fact. Always be prepared for the worst."[11] The major factors that influence weather are solar radiation, the components of the atmosphere (especially water vapor), topography, physical properties of large water bodies and land masses, and the effects of the earth's daily and yearly rotation on the amount of solar radiation that reaches each part of the earth. The earth's atmosphere is constantly in motion. The primary motion is basically circular, involving vertical upward motion as air is heated at the equator, then horizontal motion of this warm air toward the poles where it cools, descends, and moves back toward the equator to replace heated, upward-moving air. If the earth did not rotate, this circular motion would be in a north-south direction. The earth's rotation, however, causes the direction of movement to be deflected to the right (in the Northern Hemisphere), so the movement becomes more west to east (Coriolis effect) in the temperate zone (area between Tropic of Cancer and Arctic Circle). Because the earth's surface is covered unevenly by land masses, water bodies, and polar ice, and because these regions are heated irregularly as the earth rotates on its axis, systems of moving cold and warm air masses are formed. Cold, moist air masses tend to form over cold (polar) seas and warm, moist air masses over warm seas. Cold, dry air masses tend to form over cold (polar) land and warm, dry air masses over warm land. The polar regions have large, stable areas of cold, high-pressure air (polar highs), and the equatorial regions (between 10 degrees south and north of the equator) have a large area of stable, warm, moist, and low-pressure air (doldrums). Atmospheric pressure in air masses depends on their temperature: higher in cold air masses and lower in warm air masses. Winds are caused by air moving from a high-pressure to a low-pressure area; the greater the pressure difference, the higher the wind speed. Each air mass, which may cover hundreds to thousands of square miles of the earth's surface, is nearly homogenous for temperature and humidity. In the northern temperate zone, air masses generally move from west to east; in North America, exceptions include cold, relatively dry air masses that move south from northern Canada in the winter and warm, moist air masses that move north from the Gulf of Mexico in the summer. Cold air masses move faster than warm air masses (25 to 35 mph vs. 10 to 20 mph). The boundaries between air masses are called fronts. Frontal air is generally unstable and frequently an area of violent weather. A cold front is an area where heavy, cold air is displacing lighter warm air, frequently by coursing under it. A warm front is an area where lighter, warm air is replacing a retreating mass of heavier, cold air. Warm, low-pressure air masses are called lows, or cyclones; cold, high-pressure ones are called highs, or anticyclones. Since air flows from areas of high pressure to areas of low pressure, lows are characterized by winds blowing from their edges toward their centers and highs by winds blowing from their centers toward their edges. The Coriolis effect causes winds in the Northern Hemisphere to move in a clockwise direction from the center to the periphery in a high and in a counterclockwise direction from the periphery to the center in a low. Understanding these principles can help the traveler interpret shifting wind directions as highs and lows pass. Weather within an air mass is controlled by its moisture content, the relationship between land surface and air mass temperatures, and terrain features such as up or down slopes. Precipitation can occur in either a high or a low but is more common in a low. The amount of moisture in a mass of air can be described as the air's relative humidity, or the amount of water vapor in the air compared with the amount it could hold at its current temperature without condensation occurring. Warm air can hold more water vapor than can cold air. The term dew point refers to the temperature at which the relative humidity becomes 100% and the water vapor in air starts to condense. Since the temperature drops about 2.2° C (4° F) for every 305 m (1000 feet) of ascent (1.6° C [3° F] if moist, 3° C [5.5° F] if dry), rising air cools and descending air warms. Water vapor in rising air will condense when the air cools to its dew point, producing fog, clouds, and precipitation. The wilderness traveler should be able to identify the different types of clouds and know their significance. Clouds are divided into four types based on
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Figure 28-19 Different types of clouds. (Modified from Woodmencey J: Reading weather, Helena, Mont, 1998, Falcon.)
level, form, and association with precipitation ( Figure 28-19 and Figure 20 Figure 20 ). The highest clouds are cirrus clouds, which develop above 6000 m (20,000 feet). These ice-crystal clouds frequently appear thin, veil-like, and delicate. The feathery ones are called "mare's tails." The sun shines brightly through cirrus clouds. Middle-level clouds (2000 to 6000 m [6500 to 20,000 feet]) have the prefix alto- (e.g., altocumulus). Low-level clouds (2000 m or below) have the prefix strato- or suffix -stratus (e.g., stratocumulus, nimbostratus). These terms are also used to indicate clouds in sheets or layers at high altitudes (e.g., altostratus, cirrostratus). Clouds of high vertical development (500 to 18,200 m [1600 to 60,000 feet]) are the larger types of cumulus clouds frequently associated with heavy precipitation. Developing ones that ascend to 9100 m (30,000 feet) are called cumulus congestus with billowing tops resembling cauliflowers. The largest ones rise to 18,200 m (60,000 feet) or above, are called cumulonimbus, and have anvil-shaped tops. Both types have darkening bases. Because of these clouds' height, precipitation falls long distances through supercooled water droplets. Depending on conditions, hail, soft hail (graupel), or huge snowflakes may result. The prefix nimbo- or suffix -nimbus indicates that a cloud is associated with precipitation. The term cumulus refers to any clouds that present as large or small groups of separate fluffy masses (e.g., cirrocumulus, altocumulus, cumulus fractus, depending on their altitude). Cumulus humilis refers to the middle-level, white, cottony clouds with white bases seen in fair weather. In the inland parts of North America, the worse winter weather (blizzards) is associated with moving masses of warm air (lows) and the worst summer weather (severe
thunderstorms) with rising masses of warm air and moving masses of cold air (highs). There are two types of thunderstorms, both associated with cumulonimbus clouds (thunderheads). Frontal thunderstorms result when an arriving cold front slides under a warm air mass. Air mass thunderstorms consist of two subtypes. Orographic thunderstorms result when moist air is forced up over a mountain range, causing thunderstorms on the windward side. Convective thunderstorms result from rising vertical currents of air caused by heating of ground or water by solar radiation. These are the typical afternoon or early-evening thunderstorms, which may be accompanied by tornadoes when severe. An advancing warm front bringing precipitation has a predictable series of lowering, darkening cloud formations: scattered cirrus, sheets of cirrostratus, sheets of altostratus, then nimbostratus. Precipitation can begin with the appearance of either altostratus or nimbostratus clouds. The combination of cirrus clouds followed by cirrostratus and altostratus clouds usually predicts precipitation within 24 to 48 hours. Cumulus congestus and especially cumulonimbus clouds indicate thunderstorms. The wilderness traveler can anticipate weather to a limited extent by using a thermometer and altimeter (or barometer), noting the wind direction, and identifying clouds. Some digital watches have altimeter and barometer features. Both measure air pressure, but the altimeter registers higher as altitude increases (pressure drops) and the barometer registers higher as pressure rises. While traveling in mountains, barometer and altimeter readings will change as altitude changes, regardless of a low or high pressure area. In the evening, however, the movable arrow on an anaeroid altimeter can be set or the altitude (or barometric pressure) recorded. The next morning the evening reading is compared with the morning reading. Most severe winter storms are accompanied by an altimeter rise of 150 to 240 m (500 to 800 feet). A rapid altimeter rise (barometer drop) may signify high winds or a short severe storm and a slow steady altimeter rise (barometer drop) a long storm. A rapid altimeter drop (barometer rise) may also mean high winds. Measuring and recording the air temperature several times daily (remembering that normal temperature drops with increased altitude) can confirm an advancing
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Figure 28-20 A and B, Cirrus. C, Altocumulus lenticularis. D and E, Altostratus. F, Altocumulus. G, Nimbostratus. H, Cumulus humilis.
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Figure 28-20 I, Cumulus congestus. J, Cumulonimbus.
low or high when coordinated with other observations. If a low is moving directly toward you, the wind will shift so that it is blowing from the southeast or south (Northern Hemisphere). If the wind comes from the southwest or west, the low is passing north of you; if from the northeast or east, it is passing south of you. An easy way to check this is to stand with your back to the wind. The low-pressure area will be in front of you and to your left.[5] As a front passes, the wind will gradually shift 180 degrees. The shores of large bodies of water have characteristic wind patterns because of the difference in warming and cooling rates of water and land. As the land warms, breezes begin to blow from water to shore in the morning. As the land cools, breezes begin to blow from land to water in the evening. Since cloud patterns are always changing, they must be observed at regular intervals throughout each day in order to develop the ability to predict their meanings with any confidence. Mountain Weather Mountain weather is more unpredictable than weather in lower, flatter country. Winds frequently blow up and down mountain valleys regardless of their orientation because of the funnel effect of the valley and temperature differentials caused by solar radiation. The funnel effect may also cause heavy snowfalls at passes or the higher ends of valleys. On a sunny day the sun warms mountaintops and high slopes first, the warm air rises, and winds blow up the slope. In the evening, the tops and high slopes cool first, the cool air descends, and winds blow down the slope. Glaciers and large snowfields produce significant cool, down-slope winds. Except on the clearest days, mountaintops may have clouds over them or nearby because of up-slope winds that carry moist air high enough to reach its dew point. In the summer, mountains warm up during the morning and early afternoon, creating cumulus congestus and cumulonimbus clouds that produce thunderstorms, lightning, and hail. Therefore the standard recommendation for summer climbers is to arise early and reach the summit before noon. Lightning usually precedes rain in a thunderstorm and can strike up to 5 miles away from the storm. Distance is estimated by counting the seconds between the lightning flash and the first noise of thunder; 5 seconds equals 1 mile (see Chapter 3 ). Precipitation is frequently heavy on the windward side of large mountain ranges; the leeward sides are usually much drier and in low areas may be desert. Stationary lens-shaped clouds (altocumulus lenticularis) are frequently seen near mountaintops in windy weather and signify high winds at the summits. High winds also produce long snow plumes from summits and ridges. The summit wind speed will be about twice the valley wind speed.[27] Winds blowing at right angles to a mountain range tend to concentrate at any gaps or passes in the range, creating high winds due to the Venturi effect. Warm winds on down slopes in the winter (Chinook or foehn winds) are produced when cool, dense air blowing over mountaintops loses its moisture as precipitation on the windward side; the drier air then warms rapidly as it descends on the lee side. These warm winds can melt snow rapidly. Weather is more stable at certain times of the year than others, but the times vary by geographic area. For example, in the northern Rocky Mountains the best times to hike or climb in the summer are the last week of July, all of August, and the first week in September. The best time to ski, tour, or climb in the winter is February. In Alaska the best climbing weather in winter is during February and in spring and summer from April through June. In the Himalaya and Karakorum Mountains, the best climbing weather is immediately before and after the summer monsoon (a seasonal, northward flow of warm, moist air from the Indian Ocean).
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The principal value of understanding weather signs is in predicting severe, life-threatening storms and providing adequate time to seek shelter or the option to stay put rather than try for a summit. Travel in severe weather, especially above timberline, should never be undertaken casually. Summary of Backcountry Weather Forecasting 1. Blue sky, a few cirrus or cumulus humilis clouds, cold temperatures, low to medium winds, and a steady or dropping altimeter are predictors of good weather. 2. A lowering cloud pattern (cirrus followed by cirrostratus, altostratus, and nimbostratus), rising temperatures, wind freshening and shifting to blow from the southeast or south, and an altimeter rise of 152 to 244 m (500 to 800 feet) indicate a possibly severe winter storm. 3. Building cumulus congestus clouds changing to cumulonimbus clouds indicate probable thunderstorms and possible hail. A thunderstorm is frequently heralded by a rush of cold air (cold front). 4. Signs that a severe winter storm is abating include clouds thinning, cloud bases rising, temperature falling, altimeter dropping, and winds shifting to blow from the
north or northwest.
SANITATION Adherence to proper habits of cleanliness and sanitation is as important in the wilderness as at home.[4] The hands are washed with biodegradable soap after urinating and defecating, before cooking and eating, and before dressing open wounds. If soap is unavailable, snow or the cleanest available plain water is used. Dishes and pots are washed with hot water, avoiding soap. Waste water is scattered over a wide area and never dumped into a body of water. Bathing and washing clothes should be done at least 60 m (200 feet) from bodies of water, using water in a container. Gloves, preferably rubber (impermeable) ones, are worn when handling moist animal or human tissues. Campers should dig and defecate in a "cathole" at least 8 inches deep, 6 inches wide, downhill, and at least 60 m from camp, water sources, or snow to be melted for water, covering feces completely with dirt. No camp should be within 60 m of a lake or stream, which is 70 to 80 normal steps for most adults. Travelers should urinate on rocks or dirt, not on green plants. When sleeping in a tent or snow shelter, a 500-ml wide-mouth polyethylene bottle can be used as a urinal to avoid going outside, especially at night. Special funnels to use with the bottle are available for women.
PSYCHOLOGIC ASPECTS OF SURVIVAL Dealing with the psychologic aspects of survival is as important as confronting physical and environmental factors. As mentioned previously, the dangerous mindset that keeps a person continuing on a hazardous course, such as completing a climb or reaching a distant campsite despite conditions that would make a more prudent person bivouac or turn back,[8] is a recurring scenerio. In a survival emergency, a person with adequate oxygen, a stable body temperature, shelter, water, and food may still die if unable to withstand the psychologic stress. Conversely, persons have survived amazing hardships with little more than a strong determination to live. Individual reactions, however, cannot be predicted in advance. Groups faced with unexpected emergencies testify that courage and leadership appear in unexpected places. If persons possess the necessary skills and have at least a minimum of survival equipment (see appendix to this chapter), the odds are strongly in their favor. Medical personnel have the advantage of being trained to suppress panic. Fear and surrender are normal reactions that must be opposed by whatever psychologic tools are available. In some cases, religious faith or the desire to rejoin loved ones have been credited with survival. Anxieties that paralyze action include fear (of the unknown, being alone, wild animals, darkness, weakness, personal failure, discomfort, suffering, and death) and panic. Panic, the uncontrolled urge to run away from the situation, interferes with good judgment, resulting in inappropriate actions, such as abandoning weaker companions, dividing the party, and discarding vital survival equipment. Useless flight saps available energy, leads to exhaustion, and hastens death. Other psychologic reactions include apathy and the normal desires to be comfortable and to avoid pain.[23] Apathy is giving up, a state of indifference, mental numbness, surrender, and unwillingness to perform necessary tasks. The person shows resignation, quietness, lack of communication, loss of appetite, fatigue, drowsiness, and withdrawal. Apathy in one's self is overcome by faith in abilities and equipment and belief in survival and the possibility of rescue. Apathy in others is combated by communicating plans and positive feelings about resources and outcomes to them, and including all group members in planning and survival activities. Comfort is not essential to survival. Severe discomfort from injuries, illnesses, thirst, hunger, excessive heat or cold, sleep deprivation, and/or exhaustion is inevitable in a survival situation and must be tolerated in order to live. There are many accounts of adventurers who have survived many days with severe injuries
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such as open fractures because of the will to live, or who have dragged themselves for miles despite multiple injuries to find help. Providing an ill or injured party member with psychologic support is important. This includes appearing calm, unhurried, and deliberate yourself while trying to encourage optimism, patience, and cooperation. A person with a minor injury or illness should be encouraged to self-evacuate, accompanied by at least one healthy party member. When a person with a severe injury or illness needs to be evacuated, the party must decide whether to use the resources at hand or to send for help. The decision will depend on the weather, party size, training, available equipment, distance, type of terrain involved, type of injury or illness, victim's condition, and availability of local search and rescue groups, helicopters, and other assistance. Unless the weather is excellent, the party strong and well equipped, the route short and easy, and the victim comfortable and stable, the best course of action generally is to make a comfortable camp and send the strongest party members for help. A written note should include each victim's name, gender, age, type of injury or illness, current condition, and emergency care; the party's resources and location (preferably map coordinates); and names, addresses, and telephone numbers of relatives. The victim who must be left alone should have an adequate supply of food, fuel, and water. As soon as you realize that you are lost, stop, sit down in a sheltered place, calmly go over the situation, and make an inventory of your survival equipment and other resources. If it is cold or becoming dark, start a fire and eat if you have food. Take out your map or draw a sketch of your route and location based on natural features. Unless you know your location and can reach safety before dark, prepare a camp and wait until morning. Do not allow yourself to be influenced by a desire to keep others from worrying or the need to be at work or keep an appointment. Your life is more important than anyone else's peace of mind.[10] If you are alone and unquestionably lost, and especially if injured, you must decide whether to wait for rescue or attempt to walk out under your own power. Almost always, it is better to use the time to prepare a snug shelter and conserve strength if rescue is possible. If you decide to leave, mark the site with a cairn or bright-colored material such as surveyor's tape, leave a note at the site with information about your condition, equipment, and direction of travel, and then mark your trail. These actions will aid rescuers and enable you to return to the site if necessary. Travel should never be attempted in severe weather, desert daytime heat, or deep snow without snowshoes or skis. If no chance of rescue exists, prepare as best possible, wait for good weather, and then travel in the most logical direction.
SIGNALING Besides radios, cell phones, and other electronic equipment, signaling devices are either auditory or visual. Three of anything is a universal distress signal: three whistle blasts, three shots, three fires, or three columns of smoke. The most effective auditory device is a whistle. Blowing a whistle is less tiring than shouting, and the distinctive sound can be heard farther than a human voice. An effective visual ground-to-air signal device is a glass signal mirror, which can be seen up to 10 miles away but requires sunlight. Smoke is easily seen by day and a fire or flashlight by night. On a cloudy day, black smoke is more visible than white; the reverse is true on a sunny day. Black smoke can be produced by burning parts of a vehicle, such as rubber or oil, and white smoke by adding green leaves or a small amount of water to the fire. Ground signals (e.g., SOS, HELP) should be as large as possible—at least 3 feet wide and 18 feet long—and should contain straight lines and square corners, which are not found in nature. They can be tramped out in dirt or on grass or can be made from brush or logs. In snow the depressions can be filled with vegetation to increase contrast. Many pilots do not know the traditional 18 international ground-to-air emergency signals, which have been replaced with the following five simple signals adopted by the International Convention on Civil Aviation[23] : V I require assistance X I require medical assistance N No Y Yes ? Am proceeding in this direction
Air-to-ground signals include the following: Message received and understood: rock plane from side to side. Message received but not understood: make a complete right-hand circle.
When using cell phones, radios, and other electronic devices, persons should move out of valleys and gulleys to higher elevations if possible. Operational pay phones in campgrounds closed for the season or other facilities can be used to call for help. Most will allow 911 or another emergency number to be dialed without payment, but carrying the right change and memorizing your telephone credit card number are recommended.
PROTECTION FROM WILD ANIMALS Although persons in a survival situation often worry about wild animal attacks, these are rare. Many wild animals flee when confronted with a shouting, moving human. Exceptions include polar bears, grizzly bears,
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moose, bison, cougars, jaguars, wild pigs, elephants, lions, tigers, water buffalo, leopards, wolverines, females with young (e.g., bears, moose, elk, deer), rabid mammals, and feral dogs and cats (see Chapter 41 , Chapter 42 , Chapter 43 ). Polar bears, some grizzly and black bears, the great cats, and crocodiles may hunt humans as food. Venomous snakes, insects, arachnids (e.g., scorpions and ticks), and marine animals are also a concern (see Chapter 33 , Chapter 34 , Chapter 35 , Chapter 36 , Chapter 37 , Chapter 38 , Chapter 39 , and Chapter 60 , Chapter 61 , Chapter 62 ). The only effective weapon against large mammals and reptiles is a high-powered rifle, although pepper spray may discourage an attacking bear. Improvised weapons such as a spear tipped with a hunting knife, are useless. Food should not be kept in a shelter or backpack during the night. All food should be placed in a nylon bag and hung between two trees on a high line. Above the timberline, small rodents such as mice may gnaw holes in expensive tents to reach food inside, so all food should be bagged and hung on a line between two high boulders. In desert and other snake or scorpion country, travelers should avoid walking barefoot, especially at night, and should not place hands, feet, or other body parts in uninspected places. Desert campers should carry tents with floors and tightly zipped doors. Those sleeping outside should shake out clothing, footgear, and bedding before using them. In warm weather, insect repellent should be carried and used liberally.
HOW TO PREPARE FOR A POSSIBLE SURVIVAL SITUATION Basic survival equipment and skills for those interested in wilderness travel should include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.
Practice physical conditioning and healthful habits. Avoid alcohol, tobacco, and "recreational" drugs. Develop the ability to swim well. Learn how to use a map and compass and find directions without a compass. Be able to build a fire under adverse conditions. Have a working knowledge of local weather patterns and be able to use an altimeter, thermometer, cloud forms, and wind directions to predict storms. Avoid exposure to meteorologic hazards, such as blizzards and lightning strikes. Be familiar with the special medical problems of the type of wilderness involved. For example, for cold weather and high-altitude travel, be familiar with the prevention, diagnosis, and treatment of hypothermia, frostbite, and altitude illnesses. Travel in the desert and tropics requires familiarity with tropical infections, snakebites, tropical skin diseases, and heat illness. Understand basic principles of prehospital emergency care and the improvisation of splints and bandages. Carry a survival kit containing equipment appropriate for the topography, climate, and season (see appendices to this chapter). Be able to construct appropriate types of survival shelters. Acquire a working knowledge of the characteristics of natural hazards and how to predict and avoid them. These include forest fire, lightning strike, avalanche, rockfall, cornice fall, flash flood, white water, deadfall, storms of various kinds, and the hazardous animals and plants of the area of travel. Read and analyze accounts of survival experiences (see Suggested Readings). [1] [12] [14] Be aware of the psychologic aspects of a survival situation and of errors in judgment that can lead to a survival emergency. Know the edible plants and animals of the area of projected travel, as well as the poisonous or venomous species. Basic hunting, trapping, and fishing skills are valuable. Never travel alone. Always let responsible persons know your destination and expected time of return, and do not fail to notify these persons of your return to avoid unnecessary rescue attempts. After you leave, avoid changing destination and time plans except in unusual circumstances. Failure to follow these guidelines has led to many unsuccessful searches.
References 1.
Accidents in North American mountaineering, Golden, Colo, American Alpine Club, and Banff, Alpine Club of Canada (published yearly).
2.
Aircrew survival, Washington, DC, 1996, Department of the Air Force, US Government Printing Office.
3.
Bowman WD: Winter first aid manual, ed 4, Denver, 1984, National Ski Patrol System.
4.
Bowman WD: Outdoor emergency care, ed 3, Denver, 1998, National Ski Patrol System.
5.
Clark R et al: Mountain travel and rescue, a manual for basic and advanced mountaineering courses, Denver, 1995, National Ski Patrol System.
6.
Corneille P: Le Cid, Act II, Scene 2, 1636.
7.
Craighead FC Jr, Craighead JJ (revised by Smith RE, Jarvis DS): How to survive on land and sea, ed 4, Annapolis, Md, 1984, US Naval Institute.
8.
Fear G: Surviving the unexpected wilderness emergency, Tacoma, Wash, 1979, Survival Education Association.
9.
Guyton AC, Hall JE: Textbook of medical physiology, ed 9, Philadelphia, 1996, WB Saunders.
10.
Harris B: A handbook for wilderness survival, New York, 1996, Evans.
11.
Hodgson M: The basic essentials of weather forecasting, Merrillville, Ind, 1992, ICS Books.
12.
Huntford R: The last place on earth, New York, 1986, Atheneum.
13.
Kjellstrom B: Be expert with map and compass, New York, 1994, MacMillan.
14.
Logan N, Atkins D: The snowy torrents: avalanche accidents in the United States 1980–1986, Denver, 1996, Colorado Geological Survey.
15.
Ludlum DM: The Audubon Society field guide to North American weather, New York, 1991, Alfred A. Knopf.
16.
Nesbitt PH, Pond AW, Allen WH: The survival book, New York, 1959, Funk & Wagnalls.
17.
Patterson CE: Surviving in the wilds, Toronto, 1979, Personal Library Publishers.
18.
Reifsnyder W: Weathering the wilderness, the Sierra Club guide to practical meteorology, San Francisco, 1980, Sierra Club Books.
19.
Shanks B: Wilderness survival, New York, 1987, Universe Books.
20.
Stefansson V: Unsolved mysteries of the Arctic, New York, 1938, Macmillan.
21.
Stoffel R, Lavalla R: Survival sense for pilots and passengers, Olympia, Wash, 1980, Emergency Response Institute.
22.
Survival, Field Manual 21–76, Washington, DC, 1986, Department of the Army, US Government Printing Office.
23.
Survival training, Washington, DC, 1985, Department of the Air Force, US Government Printing Office.
24.
Wilkinson E: Snow caves for fun and survival, ed 2, Boulder, Colo, 1992, Johnson.
25.
Winter wheeling in Wyoming, Cheyenne, 1998, Wyoming Department of Transportation.
26.
Wiseman J: The SAS survival handbook, London, 1996, HarperCollins.
27.
Woodmencey J: Reading weather, Helena, Mont, 1998, Falcon.
Suggested Readings Auerbach PS: Medicine for the outdoors, ed 3, New York, 1999, The Lyons Press. Clifford H: The falling season, New York, 1995, HarperCollins. Kochanski M: Bushcraft: outdoor skills and wilderness survival, Vancouver, 1987, Lone Pine. Krakauer J: Into thin air, New York, 1997, Villard. Lansing A: Endurance, New York, 1976, Avon. MacInnes H: The price of adventure: mountain rescue stories from four continents, Seattle, 1978, The Mountaineers. MacInnes H: High drama: mountain rescue stories from four continents, Seattle, 1980, The Mountaineers. Olson LD: Outdoor survival skills, ed 6, Chicago, 1997, Chicago Review Press. Parr P: Mountain high mountain rescue, Golden, Colo, 1987, Fulcrum. Randall G: Cold comfort: keeping warm in the outdoors, New York, 1987, Lyons Books. Riles MJ: Don't get snowed: a guide to mountain travel, Matteson, Ill, 1977, Greatlakes Living Press. Rutstrum C: Paradise below zero, New York, 1974, Collier Books. Simpson J: Touching the void, New York, 1988, HarperCollins. Waterman J: Surviving Denali: a study of accidents on Mount McKinley, 1910–1982, New York, 1983, American Alpine Club. Waterman J: Surviving Denali: a study of accidents on Mount McKinley 1903–1990, ed 2, New York, 1991, AAC Press. Whittlesey LH: Death in Yellowstone: accidents and foolhardiness in the first national park, Boulder, Colo., 1995, Rinehart. Wilkinson E: Snow caves for fun and survival, Denver, 1986, Windsong Press.
APPENDIX A Everyone should develop the habit of carrying at least a Swiss Army knife and matches in a waterproof container when away from paved roads.
Sample Basic Wilderness Survival Kit This kit is carried in a small backpack, with a capacity of 3200 to 4000 cubic inches. Shelter-building equipment: Plastic or nylon tarp (not a "space blanket") ? inch braided nylon cord, 50 to 100 feet Folding saw Fire-building equipment: Waterproof matches Candle Fire starter (substitute: camera film) Sharp, sturdy hunting knife (e.g., folding Buck knife with 4-inch blade) Signaling equipment: Pencil and small notebook Whistle Card with ground-to-air signals
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Two sets of correct change for pay phone Signal mirror, preferably glass with sighting device Flashlight (or preferably headlamp), with spare batteries and bulb Other: Compass Map Nondigital watch Metal pot with bale and sack to store it Metal cup with handle Spoon Toilet paper Sunburn cream Lip balm with high SPF number Spare socks (used as spare mittens in emergency) Emergency food First-aid kit Sunglasses Canteen (full) Water disinfection equipment: chemicals or filter Insect repellent (in season) Repair kit, adapted to type of travel (e.g., ski, snowshoe, kayak): Leatherman type of tool (or Swiss Army knife) small pliers with wire-cutting feature, small crescent wrench Small screwdriver with multiple tips Picture wire Fiberglass tape Duct tape Steel wool for shimming Assorted nuts, bolts, and screws
Additional considerations: Altimeter Thermometer (plastic alcohol type clipped to loop on outside of pack) Spare eyeglasses Swiss Army knife with scissors Fishhooks and line No. 28 piano wire for snares Cellular telephone (if service available) GPS locator .22-caliber rifle and ammunition Surveyor's tape Cigarette lighter
APPENDIX B
Sample Winter Survival Kit Basic survival items from Appendix A Spare clothing for severe weather: at least four layers total, including spare mittens Snow shovel: small grain-scoop type with detachable handle Optional items: Piece of Ensolite or Therm-a-Rest mattress Sleeping bag Gore-Tex bivouac sac Stove and fuel Light ax Snow saw
APPENDIX C
Sample Desert Survival Kit Basic survival items from Appendix A Fold-up steel shovel with short handle Items for construction of four solar stills: Four sheets of clear plastic, 6 × 6 feet, reinforced in center by cross of duct tape Four pieces of surgical tubing, 6 to 8 feet long Four 1-quart plastic bowls 5-gallon water jug, full 1-liter wide-mouth bottle for use as urinal Spare sunglasses Heavy leather gloves Citizen's band radio Light rifle or target pistol with ammunition
APPENDIX D
Vehicle Cold Weather Survival Kit (see Chapter 69 ) Sleeping bag or two blankets for each occupant Extra winter clothing, including boots, for each occupant Emergency food Waterproof matches Long-burning candles, at least two First-aid kit Spare doses of personal medications, if any Swiss Army knife Three coffee cans with lids, for toilet Toilet paper Citizen's band radio or cell phone Flashlight with extra batteries and bulb Battery booster cables Extra quart of oil (place some in hubcap and burn for emergency smoke signal) Tire chains Snow shovel Tow chain, at least 20 feet long Small sack of sand Two plastic water jugs, full Tool kit Gas line deicer Flagging, such as surveyor's tape (tie to top of radio antenna for signal)
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Signal flares Long rope (e.g., clothesline) to act as safety rope if you leave car in blizzard Carbon monoxide detector Ax Folding saw Full tank of gas
APPENDIX E
Minimal Equipment for Survival First-Aid Kit (see Chapter 69 ) Cravats, at least two Rubber gloves Roll of 3-inch Kling (self-adhering roller bandage) Roll of 2-inch adhesive tape (waterproof preferred) 2-inch rubberized bandage (Ace or Coban) Small prepackaged bandage strips Nonadhering sterile gauze pads Sterile compresses 20-ml syringe and needle or splash shield for irrigating wounds Steel sewing needle (can be part of sewing kit) Single-edged razor blade Thermometer (low readings for cold environments) Nonprescription analgesic of choice (e.g., acetaminophen, ibuprofen) Prescription analgesic of choice (e.g., APAP with codeine, 30 mg; APAP with propoxyphene, 100 mg) Diphenhydramine, 25- or 50-mg capsules Small bottle or package of swabs of povidone-iodine solution 10% Duct tape, fiberglass strapping tape (for improvising litters and splints; carried in repair kit); other splinting materials can usually be improvised using ski poles, ice axes, hammers, branches, and parts of backpacks or vehicles Splinter forceps Persons who are taking regular medications, such as asthmatics and diabetics, should carry emergency supplies of their medicines in addition to regular supplies; anyone who has had an anaphylactic reaction should carry an emergency epinephrine kit (EpiPen or Ana-Kit) Physicians may take additional items, such as injectable epinephrine, an injectable narcotic, and skin glue Other considerations (for longer trips): Drug for nausea and vomiting (e.g., prochlorperazine or promethazine suppositories) Drug for diarrhea (e.g., loperamide) All-purpose antibiotic (e.g., ciprofloxacin) Topical ophthalmic ointment (e.g., gentamicin)
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Chapter 29 - Jungle Travel and Survival John B. Walden
Persons who venture into the tropical rainforest step into an exotic and mysterious environment that can be unforgiving. Preparedness makes the difference between misery and pleasure.
TROPICAL ENVIRONMENT In these forests lies a virtually limitless supply of excitement, joy and wonder to be encountered in new illuminations on the constructs and workings of life on earth.[23] Tropical rainforests, located between the Tropic of Cancer (23°27' N latitude) and the Tropic of Capricorn (23°27' S latitude), are regions with at least 4 inches of precipitation per month and a mean annual monthly temperature exceeding 24° C (75° F) without any occurrence of frost.[10] Facts and figures fail to capture the essence of tropical rainforests and their extraordinary biologic diversity. Seen from the air, the forest stretches from horizon to horizon in a vast green carpet. In season the crowns of trees in full blossom dot the landscape with vivid splashes of red, orange, and yellow. Sizable streams may be hidden beneath the emerald canopy. Rivers, usually muddy yellow or black, snake through the forest; early-morning or late-afternoon sun transforms these braided rivers into glistening, mirrorlike strands of liquid silver. Observed from the forest floor, the jungle is entrancing. In virgin, deep forest, all is muted and shadowy save for random shafts of light that stream down to spotlight labyrinths of oddly shaped branches and spectacularly colored flowers. Shrubs and herbaceous plants are scarce in forest away from the flood plain, so it is relatively easy to walk undisturbed. The dimness is occasionally disrupted by areas bathed in bright light from larger holes in the canopy caused by a recently fallen tree, sandy beach, or cutting and burning by humans. It is in these sunlit areas that the traveler encounters the lush and nearly impenetrable wall of foliage portrayed in adventure films. The tidy "textbook" division of vegetation into distinct tiers is somewhat arbitrary and not easily confirmed, even by experts.[27] In addition to upland terra firme forests, lowland forests remain submerged for several months each year. Such forests, or várzeas, make up only a small percentage of forested land but are infinitely more fertile than their nonflooding and nutrient-poor counterparts. Despite environmental differences within the jungle, the basics of travel remain the same.
TRIP PREPARATION Reading National Geographic[3] and Wilson[35] [36] provide an excellent introduction to people, places, and biodiversity issues. The Emerald Realm[10] is a superb overview of the world's tropical forests. The references at the end of this chapter offer insights into the complex inner workings of the moist tropical forest.[1] [26] [27] The books by Kritcher[20] and Forsyth et al[14] are especially helpful. Trips into the rainforest should be scheduled for the dry season, because trails are more serviceable for trekking at that time. Information on weather patterns can be obtained from agencies of national governments, anthropologists, missionaries, and the excellent series World Survey of Climatology. [31] Attitude In selecting participants, experienced expedition leaders look for a sense of humor; the ability to see the bright side in difficult times may be an asset more valuable than physical conditioning. Houston[18] and others have discussed the role of humor as a predictor of success. Erb[11] [12] noted that successful or failed participation in wilderness ventures also is a significant predictor. A number of expedition leaders privately note that two individuals who have a sexual relationship often form a team within a team, to the detriment of the expedition as a whole. Conditioning Indigenous peoples in jungle regions are almost always slender. After trekking with large numbers of non-indigenous men and women in equatorial regions, I have observed that overweight or powerfully built individuals, particularly men, seem to fare the worst, especially with heat-related illness. Achieving an ideal weight is beneficial on the trail. Although being in good shape is sensible, a person need not be an elite athlete to trek through the jungle and enjoy the experience. Good leg strength, acquired by training with stair-climbing exercise machines, offers appropriate preparation. To keep up with native porters and guides, the prospective expedition member should practice hiking
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at a fast pace. Once in the jungle, travelers should imitate the energy-saving, fluid rhythm of local inhabitants. Because trekkers frequently encounter single-log bridges, a well-developed sense of balance is desirable. Walking on the rails of train tracks or on curbs may help in preparation. To adapt to the specific situations, trekkers should go to the woodlands and practice walking on logs. Head stability is important. Equilibrium can be enhanced by avoiding brisk head movements and by employing the "gaze-anchoring" technique of tightrope walkers. The person fixes the gaze on a spot near the end of the log and does not stare down at the spot just ahead of the feet. [2] [6] Special cleats (Covell) should be considered for crossing log bridges that are high off the ground, long, and slippery. The cleats can be snapped on quickly before crossing a log bridge and promptly snapped off at the other end. IMMUNIZATIONS Travelers to rainforest regions should protect against the following diseases by vaccination or with prophylactic medications: 1. 2. 3. 4. 5. 6. 7. 8.
Diphtheria, tetanus Hepatitis A, hepatitis B Measles, mumps, rubella Polio Rabies Typhoid Yellow fever (in certain regions of tropical Africa and South America) Malaria
Malaria is prevalent throughout the tropics. Before travel to malarious areas, appropriate prophylaxis is needed. Updated information on the risk of malaria in various regions may be obtained through the International Travelers' Hot Line service at the Centers for Disease Control and Prevention (877-FYI-TRIP, www.cdc.gov). The Medical Letter on Drugs and Therapeutics issue on parasitic diseases, published every 2 years, is an excellent source for current recommendations on preventing and treating malaria (see Chapter 66 ). Persons traveling into remote regions of Amazonia where Indian groups live in isolation should receive yearly influenza vaccinations to reduce the likelihood of inadvertently transmitting disease to these high-risk native inhabitants. Protection against meningococcal disease should be considered where circumstances warrant. Medical Kit The Wilderness Medical Society points out that it is inappropriate to pack medications and equipment when no team member has the knowledge or experience to use them safely.[19] The following items for a basic medical kit ( Box 29-1 ) are adequate for personal use in the rainforest setting (see Chapter 69 ): 1. Bismuth subsalicylate (Pepto-Bismol tablets) is an effective over-the-counter preparation for preventing and treating common traveler's diarrhea. It also is useful for heartburn and indigestion. Pepto-Bismol tends to turn the tongue and stools black. 2. Diphenhydramine hydrochloride (Benadryl, 50-mg capsules) is safe and effective as an antihistamine, for motion sickness, and as a nighttime sleep aid. 3. Ciprofloxacin hydrochloride (Cipro, 500-mg tablets) is highly active against the important bacterial causes of enteritis, including Escherichia coli, Vibrio cholerae, Salmonella, Shigella, Campylobacter jejuni, Aeromonas, and Yersinia enterocolitica. 4. Clotrimazole and betamethasone dipropionate (Lotrisone) cream has antifungal properties and a steroid for rashes. 5. Epinephrine autoinjector (EpiPen/EpiPen Jr.) provides for emergency treatment of severe allergic reactions to insect stings, foods, or drugs. 6. Ibuprofen (600-mg tablets) is a good choice for mild to moderate pain from such problems as menstrual cramps, rheumatoid arthritis, and osteoarthritis. It also lowers elevated body temperature caused by common infectious diseases. 7. Ketorolac (Toradol, 60-mg for injection) provides good short-term relief for moderate to severe pain. It is preferred over narcotics only because it is less likely to cause problems with customs officers and police. 8. Lidocaine hydrochloride may be required as a local anesthetic agent for relief of the excruciating 711
pain resulting from stingray envenomation and conga ant or caterpillar stings. It should be infiltrated into and around the wound area using a dental aspirating syringe and 25-gauge needle. Lidocaine carpules (used by dentists) are protected and easy to carry and use in the rainforest.[16] 9. Metronidazole (250-mg tablets) is excellent for treating giardiasis, acute amebic dysentery, and Trichomonas vaginitis. 10. Mupirocin (Bactroban) ointment 2% should be immediately applied to burns, abrasions, lacerations, and ruptured blisters, which can rapidly become infected in
the tropics. 11. Permethrin 5% cream and 1% shampoo should be applied before returning home by travelers who have been in close contact with heavily infested tribal peoples. Many natives, especially in the tropics of Central and South American, are infested with scabies and head lice. 12. The SAM splint is lightweight, waterproof, reusable, and not affected by temperature extremes. 13. Sulfacetamide sodium (Sodium Sulamyd) ophthalmic solution 10% is excellent for treating conjunctivitis, corneal ulcers, or other superficial ocular infections. 14. Sunscreen is essential in open areas such as rivers or jungle clearings. Sunscreens designated "waterproof" retain their full sun protection factor (SPF) rating for longer periods during sweating or water immersion than do products designated "water resistant." Opaque formulations are excellent for the nose, lips, and ears. Visitors to the tropics should wear lightweight, long-sleeved shirts and a wide-brimmed hat when exposed to the sun for prolonged periods (see Chapter 14 ). 15. Tramadol hydrochloride (Ultram, 50 mg tablets) is used for moderate to severe pain.
Box 29-1. MEDICAL KIT FOR JUNGLE TRAVEL Bismuth subsalicylate tablets (48) Diphenhydramine hydrochloride 25- or 50-mg capsules (15) Ciprofloxacin hydrochloride 500-mg tablets (20) Clotrimazole and betamethasone dipropionate cream (60 g) Epinephrine autoinjector (2) Ibuprofen 200- or 600-mg tablets (30) Ketorolac 60-mg single-dose syringe (2) Lidocaine hydrochloride carpules (3) Metronidazole 250-mg tablets (21) Mupirocin ointment 2% (30 g) Permethrin 5% cream (60 g) Permethrin 1% shampoo (2 oz) SAM splint (1) Sulfacetamide sodium ophthalmic solution 10% (15 ml) Sunscreen (4 oz) (2) Tramadol hydrochloride 50-mg tablets (20)
Box 29-2. GEAR FOR JUNGLE TRAVEL Trail shoes (1 pair) Camp boots (1 pair) Covell cleats Socks (3 pairs) Hat (1) Pullover garment (1) Shirts Long sleeved (2) Short sleeved (2) Pants (2 pairs) Undergarments Underpants (3) Sports bra (2) Poncho (1) Flannel sheet Hammock or Therm-a-Rest Mosquito net Backpack for porter Personal backpack Antifogging solution for eyeglasses Batteries Binoculars Camera equipment and film Campsuds Candles Cup/plate Ear plugs Fishing supplies Garbage bags 30-gallon size (4) 13-gallon size (4) Headlamp Inflatable cushion Insect repellent Laminated map(s) Machete Waterproof matches/cigarette lighter Pen Toilet paper Leatherman pocket survival tool Poly bottles (2) Razor/battery-operated shaver Spoon Sport sponge Sunglasses Umbrella Whistle Zipper-lock bags Gallon size (5) Quart size (5)
Zipper-lock bags Gallon size (5) Quart size (5) Pint size (5)
Common sense dictates supplementary items. Women on long trips might add miconazole vaginal suppositories to treat yeast infections; older men might take a 16 French catheter and sterile lubricating jelly for dealing with problems from prostatic hypertrophy. The fingers may swell rapidly during vigorous activity in the rainforest. To eliminate the possible need for emergency removal, all rings should be removed before jungle trekking. Gear The goal is to travel as light as possible. The more stuff that is packed, the greater is the likelihood of breakdowns, complications, and misery. The items mentioned have withstood the test of time over years of long-distance tropical trekking ( Box 29-2 ).
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Gear must hold up under difficult jungle travel conditions that include heat, wetness, and mud. No line of advertised gear is ideally suited for the traveler in the tropics. In the United States, L.L. Bean, Inc. (www.llbean.com) and Recreational Equipment, Inc. (REI) (www.rei.com) are good sources for equipment that is usually satisfactory for the tropics (see Chapter 69 ). Footwear.
Since feet absorb more punishment than any other part of the body, suitable footwear is the most important item of gear. This is one area where a person absolutely must not carry inferior equipment. If the feet cannot go, nothing can go. Military-style "jungle boots" are unsuitable for serious, long-distance trekking. After an hour of hard walking through streams and muddy trails, blisters will form on every surface of the foot and the skin will peel off in sheets, bringing a jungle trip to a premature end. Furthermore, safely crossing log bridges and mossy, slime-covered river rocks is almost impossible in these boots. Two pair of shoes are needed: one suitable for the wet, slippery conditions imposed by the trail and another that meets the need for dryness and comfort in camp. TRAIL SHOES.
The following features are desirable in trail shoes: 1. Uppers that hit just above or just below the ankles. Some people choose a high-cut design, reasoning that the extra height gives some added snake protection. 2. Extra protection over the big toe. Rubber or leather toecaps prevent the big toe from being severely battered and bruised. 3. Moderately deep-tread outsoles. Traction on rugged and muddy terrain is important. Running shoes with hard, "high-impact" soles should not be worn because they become slippery on wet logs or river rocks. 4. Quick drying time. Uppers of Cordura nylon and split leather, in addition to resisting abrasion and being aerated, dry rapidly in the sun. Even though hiking shoes usually become soaked within minutes on the trail, it is a psychologic boost to start each day with dry shoes. Since jungle travelers can be in waist-high water while on the trail, waterproof shoes with Gore-Tex liners are not essential. 5. Snagproof design. Shoes or boots with "quick-lace" steel hooks should be avoided; vines and weeds become tangled around the metal hooks, causing the wearer to stumble and pulling the laces untied. Shoelaces should always be double knotted. 6. Light weight 7. Well broken in CAMP BOOTS.
Footwear needs are different in camp where the trekker wants dry feet. Shoes, although excellent for the trail, are not suited for camp. A boot that comes to midcalf keeps mud off the feet and pants. Rubber remains an excellent material for keeping water away from the feet. Rubber lug soles provide traction. When rubber-soled boots are worn, however, extreme caution is needed when crossing bridges and walking on rocks. Camp boots should be light weight, since they must be carried in a pack on the trail. Discount stores usually carry lightweight, lug-soled rubber boots that meet the criteria for jungle camp boots. OTHER OPTIONS.
The lightweight, comfortable, mesh/neoprene fabric "water" shoes popular for beach and sailboarding activities may have a place on river trips when substantial time will be spent in dugout canoes or rubber rafts. Thongs and open-toe sandals are fine for most towns and cities in the tropics, but in certain jungle regions such as the Amazon Basin, exposed feet invite hordes of biting insects. The jungle traveler must never go barefoot. Plant spines and glass can puncture the feet, and larvae of ubiquitous parasites such as hookworm and Strongyloides can enter through the skin. The burrowing jigger flea, Tunga penetrans, is a serious pest and can be avoided by wearing shoes. SOCKS.
Cotton or thin synthetic socks should be worn in the jungle to decrease the risk of blisters from wet trail shoes, to reduce insect bites (particularly from no-see-ums), and to lessen the risk of lacerations from sawgrass. Clothing.
In many countries military green or camouflage-style clothing is strictly contraindicated. This is particularly true in military dictatorships or in remote border regions. To be mistaken for a guerilla or foreign infiltrator by the military, police, or security (undercover) forces can lead to harassment, detention, or worse. HAT.
For protection from radiant heat and objects falling in the forest, the traveler should wear a lightweight, light-colored hat that has a medium or wide brim. It need not be waterproof but should be made of material that can be wadded up. A useful feature is a fastener on each side to snap the brim up for traveling on the trail. A pith helmet, widely regarded as affectatious, is fine for open savanna and river trips, but on the trail, branches make it impractical. PULLOVER.
Drenching rain may leave a person feeling chilled and uncomfortable, particularly when traveling mainly by canoe or raft. Chilling generally is not a
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problem when hiking on the trail so long as the person keeps moving. A Dacron polyester fleece pullover such as L.L. Bean's Polarlite Pullover, REI's Polarlite Sweater,
or a Patagonia pullover will keep a person warm. Wet garments should be wrung out so that they continue to offer thermal protection. Professional white-water boatmen working in tropical regions generally pack a polyester outerwear garment. SHIRTS.
Two light-colored, ultralightweight, long-sleeved cotton shirts should be taken. At the end of the day, the trail shirt should be washed and rinsed so that it will be ready, although perhaps still damp, the next morning. The second shirt can be used in camp or as a spare for the trail. Expensive synthetic shirts guaranteed to wick away moisture are poor jungle trail shirts, and make the person sweaty and sticky. In camp, if no-see-ums and mosquitoes are few, a lightweight, short-sleeved cotton shirt is practical. Two should be packed. A four-pocket style called the guayabera, favored by men throughout Latin America and the Caribbean, is ideal. La Casa de Las Guayaberas (Naroca Plaza, 5840 SW 8th St., Miami, FL 33144; 305-266-9683; fax 305-267-1687) has an exceptional selection of short- and long-sleeved guayaberas; be sure to specify 100% cotton. PANTS.
Two pairs of ultralightweight, light-colored cotton pants are needed. One pair is worn on the trail during the entire trip. Trail pants should be washed often. The other pair is worn around camp and in towns along the way. Jeans become waterlogged as soon as they become wet and are totally unsuitable for tropical trekking. Although synthetic shirts are unsuitable, nylon Supplex pants can substitute for cotton on the trail. Mangrove Sanded Supplex pants (Sportif, 800-776-7843) hold up well, are quick drying, have a built-in mesh brief, and meet criteria for comfort on the trail. Pants with zip-off legs to create instant shorts should be avoided. UNDERGARMENTS.
Underpants and sport bras should be made of cotton. PONCHO.
An ultrathin waterproof poncho is useful on rafting or canoe trips and in villages but is worthless on the trail. Bedding FLANNEL SHEET.
Tropical rainforests become uncomfortably cold between midnight and sunrise. A cotton sheet does not provide enough warmth, a blanket is too heavy, and a summer-weight sleeping bag retains too much body heat. A flannel sheet sewn together like a mummy bag (40 × 90 inches), but without a taper, provides suitable warmth either in a hammock or on a pad. Many inhabitants of the tropical forests sleep with their feet near a fire that is tended throughout the night. They have learned that the chill of damp, cool jungle nights can be lessened as long as the feet stay warm. Also, disposable "warm packs" can be wrapped within a sock. HAMMOCK.
Soft cloth hammocks are too bulky and heavy for trips and begin to smell after a few days. Fishnet cotton hammocks tend to fall apart within hours or days. The so-called camping tent-hammocks or military tent-hammocks are usually bulky, heavy, impossible to sling properly, extremely uncomfortable, hot, unstable, and never able to keep the rain out in a heavy tropical downpour. The nylon Double Hammock sold by Wal-Mart (Model EZ-190 by E-Z Sales Manufacturing, 1432 West 166 St., Gardena, CA 90247) has proved nearly ideal for jungle travel. It is compact, lightweight, durable, and reasonably comfortable. It cannot rot or absorb odors. For easier handling, the ski rope tie-end lines that are sold with the Double Hammock should be replaced with ?-inch double-braided rope. THERM-A-REST.
The Therm-a-Rest foam pad is the choice of expedition organizers throughout the world. It combines the insulating qualities of foam and the cushioning of an air mattress, rolls up to a compact size, and inflates on its own when the valve is opened. The traveler who will be sleeping on a pad should pack a 1 ½ × 2 ½-yard plastic ground sheet. The sheet should not be placed directly on the jungle floor, where stinging insects and snakes abound. It should be used only in a hut or on an elevated platform. The ground sheet may also be beneficial for temporary rain protection and for keeping bow spray off a person or gear during water travel. MOSQUITO NETTING.
A mosquito net designed for use with a hammock is basically a rectangular box that is open at the bottom with sleeves at each end panel for the passage of the ropes by which the hammock is slung. Such nets are difficult to find outside the tropics. Fortunately, a serviceable mosquito net can easily be made from "no-see-um netting" (available by request from REI). Backpacks.
A sturdy, well-designed backpack should be used to carry gear. Reflective material should be sewn onto the back of each backpack. Iron Horse Safety Specialists (800-323-5889, fax 214-340-7775, e-mail
[email protected]) sells red-orange reflective material for daytime visibility and reflective silver for nighttime reflectivity. On serious jungle treks, porters are present. This frees expedition members to carry much lighter loads.
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BACKPACK FOR PORTER.
An internal-frame backpack of 3000 to 4000 cubic inch capacity is a good size. It should have external pockets for quick access to liter-sized water bottles. Indigenous peoples are accustomed to carrying packs and hauling loads with a strap, known as a tumpline, slung over the forehead or chest. Many natives, including Amazonian Indians, dislike using the shoulder straps that come as standard equipment on backpacks. Given enough straps, almost any native porter can quickly rig a satisfactory tumpline on a backpack. PERSONAL PACK.
A daypack of 1200 to 2000 cubic inch capacity is useful for carrying a camera, snack food, and other gear that must be kept handy. A waterproof liner will keep perspiration from wicking into the bag and wetting everything inside. The pack should have two outside pockets for quick access to liter-sized water bottles. PACK FOR RIVER TRIPS.
A durable, waterproof "dry" bag, used by river runners, is worth considering, especially if the trip will involve spending days or weeks at a time in dugout canoes or rubber rafts. Most of these packs, however, cannot stand up to the demands of long-distance overland trekking. The straps tend to be uncomfortable and frequently rip
out on the trail. Other Useful Items ANTIFOGGING SOLUTION FOR EYEGLASSES.
Antifog solution, available from dive shops, reduces humidity-induced fogging of glasses. BATTERIES.
Alkaline batteries should be brought from home. Batteries sold in Third World nations do not last long and often leak. BINOCULARS.
The traveler who is an avid bird watcher or enjoys watching butterflies or seeking out orchids high on distant limbs will want to pack a pair of binoculars that are lightweight, compact, shockproof, and waterproof or water resistant. CAMERA EQUIPMENT.
Older-style cameras with mechanical shutters are reliable in regions of high humidity. Film with an ISO of 200 is ideal for use in the low-light conditions of the jungle and much preferred over slower film. CAMERA CASE OR BAG.
Hard-bodied Pelican cases are waterproof and virtually indestructible. The silver-gray color cuts down on heat absorption and is preferred in hot climates. The cases are ideal for rafting or canoe trips but bulky for trekking. On the trail, waterproof "dry" bags protect equipment. CAMP SOAP.
A biodegradable soap should be used. The soap Campsuds works in hot, cold, fresh, or salt water and cleans dishes, clothing, hair, and skin. CANDLES.
Electricity tends to fail at unpredictable times in small towns and even in cities in Third World countries. Travelers should carry dripless candles, but spring-loaded candle lanterns should be avoided. CUP AND PLATE.
A large Lexan polycarbonate cup is unbreakable, does not retain taste or odor, and serves the role of cup, bowl, and plate. Travelers who want an actual plate should buy one made of indestructible Melamine. EAR PLUGS.
Travel in the tropics often involves flying in incredibly loud helicopters, cargo planes, or short takeoff and landing (STOL) aircraft. Sponge ear plugs that roll up and fit in the ear canal offer inexpensive, effective protection against hearing damage. FISHING SUPPLIES.
For additional "food insurance" the jungle traveler should carry 75 feet of 20-pound-test fishing line, a 12-inch steel leader with swivel, and a few hooks. Breakdown travel rods and spincast reels should be considered for sport fishing or adding fresh meat to the daily provisions. Throughout the tropics, most species of fish find Rat-L-Trap lures, particularly the chrome and blue combination, irresistible. GARBAGE BAGS.
Four 30-gallon capacity and four 13-gallon capacity large plastic garbage bags can hold clothes, bedding, and other items that must stay absolutely dry and can keep dirty boots isolated from clean items in the backpack. HEADLAMP.
Battery-operated headlamps offer hands-free convenience at night for reading or going to the latrine. They should shine at least 10 hours on a set of batteries. INFLATABLE CUSHION OR PILLOW.
A small, durable, cloth-covered inflatable cushion is recommended for sitting in a dugout canoe or aluminum boat. INSECT REPELLENT.
To repel mosquitoes, flies, ticks, chiggers, fleas, and gnats (but not no-see-ums), insect repellent should contain 15% to 30% diethyl-toluamide (DEET). Formulations should not contain higher than 30% DEET, often called "jungle juice." These may pose health hazards (see Chapter 32 ). Technique is critical when applying insect repellent. Before dressing, the person should spray the ankles, lower legs, and waist. After the socks are put on, a band should be sprayed around the top; a band should also be sprayed around both pant legs to midcalf. A light spray to the shirt, front and back, may also help. The
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hands should be sprayed, rubbed vigorously, and run through the hair. Some repellent should be dabbed on the face, neck, and ears, carefully avoiding the eyes; contact lens wearers should be especially vigilant when applying insect repellent. No-see-ums, which are tiny gnats that abound throughout the tropics of the Americas, are the most common source of insect annoyance in many regions. They are active at sunset and attack humans emerging from jungle streams. No-see-ums cannot bite through even the thinnest cloth and are usually inhibited by Skin So Soft (SSS, Avon). (SSS is not effective against ticks, fleas, flies, and chiggers and offers little protection against mosquitoes.) SSS should be applied liberally and often to the wrists, knuckles, bare ankles, face, ears, and scalp. Men with full beards seem to be especially troubled by tiny gnats and may benefit by applying small amounts of SSS to the beard area. LAMINATED MAP.
Accurate maps exist for most regions on earth. From the best map available, travelers should laminate photocopied portions that are relevant to a particular itinerary (see Rescue Strategies).
MACHETE.
A machete is the single essential tool for jungle survival and for the many tasks in camp and on the trail that require steel with a sharp edge. It is hazardous to use a machete in the rain or when cutting wet grass, however, since the weapon may fly out of the hand. Also, when cutting brush, the person often encounters sawgrass. The resulting skin lacerations, which are not noticed at the first because sawgrass is razor sharp, may take a week or two to heal. Because of the risks involved, an experienced individual should be in charge of transporting and using the machete. MATCHES OR CIGARETTE LIGHTER.
Waterproof, windproof Hurricane Matches light when damp and stay lit for several seconds even in the strongest wind. Many jungle travelers prefer a butane cigarette lighter. ORGANIZER BAGS.
See-through organizer bags help reduce clutter and minimize the risk of misplacing small items. PEN.
The Fisher Space Pen (Fisher Pressurized Pen, 711 Yucca St., Boulder City, NV 89005) writes upside down without pumping, under water and over grease, and in hot and cold temperature extremes. It has an estimated shelf life of over 100 years. POCKET TOOL.
A favorite pocket tool for the outdoors enthusiast is the Swiss Army knife. The Leatherman Super Tool is recommended for jungle travel and survival and features needle-nosed pliers and 12 locking implements. POLY BOTTLES.
Essential gear includes two quart- or liter-sized wide-mouth water bottles made of high-density polyethylene or Lexan polycarbonate. A 2-ounce, heavy-duty poly bottle comes in handy for carrying a salt and pepper mixture to add flavor to boiled plantains and yucca. RAZOR OR BATTERY-OPERATED SHAVER.
Both men and women should carry lightweight disposable razors. Most men find that lightweight, AA battery-operated shavers give two shaves a day for up to 2 weeks before requiring a change of batteries. SPOON.
Knife-spoon-fork sets are unnecessary. With a knife blade, a good tablespoon made of either Lexan polycarbonate or stainless steel is sufficient for eating. SPORT SPONGE.
A camp towel, made of microporous material, is lightweight, compact, and superabsorbent; it replaces the cotton towel. With the Cascade Designs Pack Towel or similar brand, the body and even hair can be dried much more quickly than with a traditional towel. SUNGLASSES.
Sunglasses should be polarized with full ultraviolet light protection. Many travelers prefer sunglasses with red-tinted lenses. Because red is the complement of green, these lenses make the jungle foliage stand out intensely and sharply, with enhanced contrast and depth of field. Retainers hold eyeglasses securely during vigorous activity. TOILET PAPER.
American toilet paper is much softer than that purchased in Third World countries. The traveler should never wipe with jungle leaves. UMBRELLA.
A collapsible umbrella is useful in tropical cities and in remote villages when walking from hut to hut. It also offers excellent protection from the sun on canoe or raft trips. The umbrella should be reflective silver, not heat-absorbing black. WHISTLE.
A high-quality plastic whistle can be used to signal in case someone strays off the path. ZIPPER-LOCK BAGS.
Heavy-duty zipper-lock freezer bags are excellent for organizing medicines, toiletries, and other small objects. Bring five each of the gallon, quart, and pint sizes.
COPING WITH THE JUNGLE ENVIRONMENT A visit to the rainforests of the New World tropics can be either a sublime experience or a hellish ordeal.[14] Wetness The superhumid lowland rainforest receives up to 400 inches of rain a year; in contrast, Indiana averages
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about 40 inches. In the higher elevation cloud forest, dense cloud cover throughout the year is accompanied by constant mist or drizzle. In such heat and high humidity, people become mentally fatigued as a result of being constantly wet. Fortunately, travelers can use basic strategies for coping with the physical and psychologic burden of wetness. Wetness is as much a state of mind as a physical condition. Dryness while trekking or working during the day is not a requisite for physical or mental health. Wetness does not equate with illness, significant discomfort, or dampened spirits. People can tolerate being wet throughout much of the day if they know that they have a dry change of clothes to wear in camp and that they will be dry at night. In addition to the psychologic benefits, being dry at night means that maceration is less likely to develop in intertriginous areas. Bedding and clothing can be protected from moisture by careful wrapping in plastic garbage bags. Despite all efforts, however, certain "dry" items eventually become damp or accidentally soaked. Wet articles should be spread out on shrubs and bushes. They will dry within 2 hours in full sun. Myiasis caused by the tumbu fly, Cordylobia anthropophaga, of sub-Saharan Africa can be avoided by hanging clothing to dry in bright sunlight, never on the ground. Clothing dried over a wood fire absorbs odors that do not wash out. Health Issues Health Risks.
The subject of the tropics causes many people to think about tropical diseases such as filariasis and animals such as the candirú (see later discussion). Malaria, hepatitis, and motor vehicle accidents are the three leading health problems in most tropical regions. Tropical travelers who venture off the path may be exposed to bodily harm and serious diseases, such as leishmaniasis, onchocerciasis, and Chagas' disease. Bouts of diarrhea or other annoyances will likely occur, regardless of the extent of precautions taken, but death is unlikely. Duration of Travel and Emotional Response.
Cashel et al[5] examined the mood pattern of participants on a wilderness course and noted a high level of confusion, fatigue, anger, depression and tension on day 4. After 2 to 3 weeks of travel in remote areas, the general health of expedition participants deteriorates as a result of insect bites, falls, and noxious plants. Inexperienced trekkers may quickly tire of unfamiliar food and miss usual comforts. Experienced leaders therefore prefer to limit expeditions to 3 weeks. Preventing Heat-Related Illness.
The following guidelines may help prevent heat-related illness (see Chapter 10 and Chapter 11 ). 1. Before undertaking long-distance trekking in the tropics, acclimatize by spending at least 5 days in a hot, humid environment and engaging in moderate daily exercise. This acclimatization will be lost within a week if not maintained.[15] 2. Avoid alcohol and certain drugs. Medications such as ß-blockers, anticholinergics, and diuretics increase the likelihood of heat-related illness and should be avoided if possible. 3. Wear ultralightweight, light-colored, and loose-fitting cotton clothing and a wide-brimmed hat. 4. Whenever possible, have a native porter carry all gear. 5. Maintain adequate hydration. Before setting off on the trail, drink a liter of disinfected water. A half hour later, drink a second liter. One hour after the second liter, drink a third, then consume approximately 1 L every 2 to 4 hours while on the trail. Heat cramps, often severe, tend to occur when large amounts of water are ingested without adequate salt replacement. Oral rehydration salts (ORS), in premeasured packets added to a liter of disinfected water, provide an ideal balance for replacing lost electrolytes. Trekkers should drink at least 1 L of water containing ORS before setting out on the trail and a second liter after especially strenuous days. ORS packets are distributed by the World Health Organization and UNICEF but are difficult to obtain commercially overseas. In the United States, oral rehydration therapy packets may be obtained from Cera Products (888-237-2598) and Jianas Brothers (816-241-2880). Sport beverages, such as Gatorade, help maintain adequate electrolyte balance but not as well as ORS. Salt tablets are not recommended because they are gastric irritants and may even delay acclimatization because of aldosterone suppression. [15] Unexpected Isolation Various factors contribute to unexpected isolation in the jungle, such as inclement weather, mechanical problems, or political turmoil that shuts down public transportation. Many people respond with anger and irritability, which can be devastating to group dynamics. Travelers should accept the situation and use the additional time to appreciate the tropical forest, take photographs, or read paperback books. It helps to shift out of gear mentally and allow the intellectual machinery to idle. Nearly everyone has the experience of driving for hours and arriving at a destination with virtually no recollection of the trip. The same can be accomplished in the village setting, lying around on a hammock. The hours and days pass surprisingly quickly, akin to cruising in a sailboat with no engine. The person learns patience and develops an appreciation that the rhythms of nature are not governed by the ticking of a clock. Unexpected isolation allows many visitors to experience the biospheric cadence.
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Figure 29-1 Construction of mosquito netting for use with a hammock: sleeve hole = 88 inches in circumference; small hole = 18 inches in circumference; smallest holes (for supporting sticks) = 4 inches in circumference.
Camp Life
Shelter.
Natives rarely spend the night in makeshift shelters, and it is usually best to use existing dwellings for a hammock or sleeping pad. Common courtesy governs their placement or sleeping pad inside the hut of a native. Travelers should ask about taboo spots before bedding down. When huts are not available for use, a tarpaulin provides satisfactory shelter from the rain. Rip-stop polyethylene tarps (8 × 10 feet) are lightweight and waterproof. Coated nylon tarps are also acceptable but must be sealed with a product such as Seam Grip. Figure 29-1 illustrates a typical method of erecting a tarp. First, a thick line is run between two trees 7 to 8 feet off the ground and cinched tight. The long axis of the tarp is centered over the rope, and a rope attached to the middle grommet on each end is tied to the tree. The corner grommets are tied to available trees, bushes, or strong clumps of grass; a tie-down in the middle on each side is also helpful. The sides of the roof should be made high enough to enter and exit conveniently but not so high that driving rain can come in at an angle. Once the tarp is up, the hammock ropes are run through the sleeves of the mosquito net. Then the hammock is slung. It should be suspended high enough that it will not sag to the ground during the night as it naturally gives under an adult's weight. Next, the mosquito net is suspended. The ropes running from tree to tarp, from tree to mosquito net, and from tree to hammock should be sprayed with DEET-containing insect repellent to keep ants and other pests from using the ropes as trails. Finally, a few broad leaves (banana leaves or heliconia) folded at the spine are draped over the bare rope extending from the tree to the tarp to keep rain from running down the tarp and hammock ropes. Knowledge of two knots is needed for slinging a hammock. These knots always hold and always come undone quickly without jamming. The half hitch is used to tie the hammock to a horizontal beam, as follows ( Figure 29-2 ): 1. Pass the working end of the rope around the object to which it is to be secured. 2. Pass the working end of the rope around again without crossing over itself. 718
3. Bring the end over and around the standing part and through the loop that has just been created. You have just made a half hitch. 4. Make a second half hitch below the first half hitch. 5. Pull tight.
Figure 29-2 Half hitch knot.
The camel hitch is used to tie the hammock to a vertical post secure, as follows ( Figure 29-3 ): 1. 2. 3. 4.
Make three turns around the vertical pole. Bring the working end up and over the turns. Make a turn at the top and pass the end back under itself. Make a second turn at the top and pass the end back under itself.
Weather conditions can change in minutes, and travelers must be prepared with adequate shelter. The use of a tent as shelter in the tropical rainforest is not recommended. Food.
Solitary travelers or small groups usually do not need to pack large amounts of food. Edibles are always available in areas inhabited by friendly natives. As a general rule, food is safe to eat if it is peeled, cooked, or boiled.
Figure 29-3 Camel hitch.
Figure 29-4 The palm grub is a favorite delicacy.
Travelers in the tropics must be open to eating local food. Most creatures are edible, such as boiled caiman (alligator), cooked capybara (a 50-kg rodent), or roasted palm grubs (larvae of Rhynchophorus). Raw palm grubs, up to 5 inches long, are tasty and a favorite of Amazonian Indians ( Figure 29-4 ). They are eaten by slashing open the thin integument with the thumbnail, extracting and discarding the intestinal tract, placing the opened skin to the mouth, and sucking out the turgid contents. In addition to palm grubs, more than 20 species of edible insects, including ants and termites, are collected year-round by the people of Amazonia. [9] Large hairy spiders 10 inches in diameter, Theraphosa leblondi, are often roasted on an open fire. After the barbed hairs are singed off, the spider is placed in the embers; it has a shrimplike taste. Indians of the Americas have perfected the art of smoking fish and meat so that they remain safe to eat for long periods. It is common to see huge hunks of tapir meat or slabs of 100-pound catfish resting on racks, coal black from the smoking process. The tropics have an abundance of flora as food. The yard-long heart of palm is cool and delicious when
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eaten in its raw state or may be included in a soup spiced with tropical herbs. Familiar tropical fruits include papaya, mango, pineapple, and passion fruit (Passiflora). Many New World fruits have no name in English and generally have not found their way into the world market, such as chirimoya, guanabana, pitahayas, naranjilla, uchuva, tamarillo, zapote, sapotilla, and badea.[22] [25] [34] The boiled fruit of the peach palm, Bactries gasipaes, is nutritious and flavorful. The banana and its cousin, the plantain, provide a large percentage of the total caloric intake of natives in the American and African tropics. Curiously, in many native villages it is difficult to find the sweet, finger-length bananas and the common yellow bananas exported from tropical countries. The green plantain features prominently
in the daily fare of inhabitants of the tropics. The plantain has little taste and is exceptionally dry. Yucca (manioc or cassava), Manihot esculenta, is a staple source of carbohydrate nutrition throughout the Americans and much of tropical Africa. The two kinds of yucca, "sweet" and "bitter," are the same species but differ in their distribution and amount of a poisonous constituent, a cyanogenic glycoside, in the root.[30] Sweet and bitter yucca cannot be easily distinguished; one must know which variety was planted. Sweet yucca, common in the eastern lowlands of the Andean countries of Colombia, Ecuador, and Peru, is eaten after the bark containing the toxic substance is peeled off and the root boiled. In bitter yucca the poison is more concentrated and distributed throughout the root, so it must be extracted before consumption. Amerindians use an apparatus called the tipití to express the poisonous juice from the peeled and grated flour of manioc roots. Travelers in a large group should carry dried, packaged foods, since the host village might not be able to provide sufficient foodstuffs or travelers might pass through isolated and uninhabited regions. Packaged foods should also be carried by travelers in regions where natives are unfriendly. Dried instant food only needs water to make a meal. A few selections should be tried before a large supply for field use is ordered. It is not necessary to add hot water to all packaged foods; adding disinfected, ambient-temperature water produces acceptable results for most foods. Drawbacks to prepackaged foods include expense, space, and disposing of the empty foil packages. I carry the following supplemental food items for 2- to 3-week treks into remote but inhabited jungle regions: one 2-ounce heavy-duty poly bottle filled with salt and pepper mixed half and half, a few pounds of rice, a tin of long-keeping butter (or oil) for cooking the rice, a few tins of tuna or sardines packed in tropical hot sauce, and several Power-Gel energy packets for trail snacks. Hard caramels can be given to porters after long or difficult passages. Potable Water.
Potable Aqua (tetraglycine hydroperiodide 16.7%) tablets are recommended for disinfecting water because they are easy to use and have proved effective in killing bacteria, viruses, and most parasite cysts (see Chapter 51 ). Water filters are not recommended for purifying jungle water; they clog with silt and must be cleaned frequently. If a water filter is used, it should be fitted with a good pre-filter to catch the excess silt. Jungle Hazards The following hazards are common in the wilderness jungle setting or thought to be common. Other chapters provide additional insights and viewpoints, particularly with respect to treatment. Arthropods ANTS.
The conga ant, Paraponera clavata, 1 to 1 ½ inches long, is the terror of the American tropics. The bite of these large black ants can produce intense pain and fever for up to 24 hours, which provides the Spanish name veinte-cuatro (twenty-four). Fortunately, they are conspicuous because their large, shiny black bodies tend to stand out against foliage. Special caution is needed when ducking under or climbing over trees, where ants are often found. A conga bite requires strong pain medication and perhaps the injection of lidocaine at the bite site. Travelers should avoid touching trees and bushes. Many plants in the tropics provide a home and food for ants, which provide aggressive defense of the plants. Fire ants are common throughout the tropics and subtropics. Their bite causes discomfort but not excruciating pain. Characteristic pustular lesions in crops often result from fire ant stings. CHIGGERS.
Chiggers, a form of mite, are a problem throughout equatorial regions. Whereas temperate-climate chiggers may cause mild discomfort for a few days, the tropical chigger sets up an inflammatory and allergic reaction that often persists for weeks. In the South American tropics, chiggers are found in grassy fields, such as jungle airstrips and yards around mission compounds. Walking through chigger-infested areas without protection could leave a person covered with chigger bites. After a few days the victim begins to itch mildly. As the days pass, the itching intensifies, seems to come in waves, and may change its focus. Prevention is the best treatment. Areas known to be infested with chiggers should be avoided when possible. Spraying shoes or boots and lower pant legs with repellent containing DEET is highly effective. Pretreatment of clothing with permethrin has been recommended. Travelers in the American tropics should never walk through grassy areas in shorts.
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JIGGER FLEA.
Tunga penetrans, the jigger flea or chigoe, originally found in South and Central America, has now spread to East and West Africa and India. The fertilized female flea enters the feet through cracks in the soles, between the toes, and around the toenails. The female swells to the size of a pea and may be readily identified as a white papule with a central pit, through which the female extrudes excrement and eggs. When eggs are ripe for release, intense itching causes scratching that helps release large numbers of flea eggs. Incomplete removal of the jigger frequently results in complications caused by secondary infection. A simple extraction technique virtually eliminates complications. Open the skin over the nest of eggs with a surgical blade. Fold back the flaps, remove the easily identified egg sac, and with tweezers, remove the head of the female flea, which can be seen once the egg sac has been removed. Wash the area with hydrogen peroxide.[16] MYIASIS.
Myiasis (skin infestation by fly larvae) is common in many regions of sub-Saharan Africa (the tumbu fly, Cordylobia anthropophaga) and Central and South America (the human botfly, Dermatobia hominis). The victim finds an itchy swelling that slowly enlarges into a lesion with a single breathing pore from which bubbles clear or slightly bloody drainage. Later, movement is felt under the skin as the developing larva wriggles around. Removing the larvae before they emerge on their own is generally advised. Surgical excision, however, should be undertaken with caution because accidental rupture of the larval tegument can lead to secondary infections. Various methods to close off the breathing pore so the larva will emerge on its own include application of bacon fat, meat, chewing gum, or petroleum jelly. SCORPIONS AND SPIDERS.
Stinging scorpions and venomous spiders are common throughout the tropics and provide another reason to exercise caution before sitting down or placing a hand on logs, bushes, or the ground. VENOMOUS MOTHS, BUTTERFLIES, AND CATERPILLARS.
The larvae and adults of a number of moths (genus Hylesia) and butterflies bear venomous hairs that may cause skin eruptions. A rash may result from direct contact with the adults or larvae or by windblown hairs. Direct contact with certain Amazonian caterpillars can cause disabling pain. In the Amazon tropics, noxious smoke from burning garbage (e.g., plastic wrappers) may cause tree-dwelling caterpillars to loosen their hold on overhead branches and rain down on unwary campers.
Treatment of lepidoptera envenomation may require injection of lidocaine at the site of intense pain and administration of analgesics, antihistamines, and corticosteroids ( Chapter 36 and Chapter 37 ). Moth hairs may be removed with sticky lint removers used for clothing. WASP AND BEE STINGS.
Sudden, intense pain from the sting of certain species of tropical wasps and bees can be so severe that it knocks the victim to the ground as though hit with an electric shock. Perfumes and brightly colored or flower-patterned clothing should be avoided.[19] Bird watchers should not venture too close to the hanging nests of yellow-rumped caciques and oropendolas, because wasps are invariably associated with these nests. Fish STINGRAY.
The stingray, a flattened, cartilaginous cousin of the shark, may be encountered buried just beneath the surface of the bottom ooze in tropical rivers and streams throughout the Amazon Basin, Africa, and Indo-China. Rays inflict injury by lashing upward with the caudal appendage, driving one or more retroser-rated venomous spines deep into the victim's foot, ankle, or lower leg. This produces agonizing pain, often accompanied by headache, vomiting, and shortness of breath. After the initial phase of envenomation, tissue necrosis may develop. Wearing shoes or boots when wading in water does not always prevent a stingray from jabbing its barb into the foot or leg. Prevention lies in shuffling the feet along the bottom so that the ray will have enough warning to glide away safely (see Chapter 60 ). ELECTRIC EEL.
The so-called electric eel (actually an eel-shaped fish) is encountered from Guatemala to the La Plata River in South America and is especially common in the Amazon region. A person can drown after being stunned by a jolt from this fish. Electric eels are said to prefer deep water. Inhabitants of regions heavily infested with eels report a slight tingling sensation when one is close. No practical way exists to prevent these shocks. CANDIRÚ.
The candirú is a toothpick-sized parasitic catfish that inhabits Amazonian waters and may invade the urethra of urinating humans. Orifice penetration by the wily candirú can be prevented by wearing a tight bathing suit and not urinating underwater. Native methods of dislodging these fish from the urethra include drinking a tea made from the green fruit of the jugua tree, Genipa americana L. Vitamin C (2 to 5g) may serve the same purpose[4] (see Chapter 62 ). PIRANHA.
Although no human deaths have been documented, piranha have nipped off the fingertips of canoeists dangling their hands in the water. Mammals
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BATS.
Vampire bats are found throughout Mexico, Central America, and South America, especially in areas that have large cattle ranches. Sleeping humans are unaware of the presence of a feeding bat; the phlebotomy is painless. Both vampire and fruit bats carry rabies. Sleeping under mosquito netting prevents bat bites. The risk of rabies can be reduced by prophylactic human diploid cell rabies vaccine. DOGS.
Most native groups keep dogs for hunting. Populations with a history of recent tribal warfare often keep packs of dogs close by as an early warning system. These semiwild dogs should be treated with caution; threatening them may cause immediate attack, since they are not easily intimidated. When approaching huts or villages, the traveler should allow porters to deal with the dogs first. Dogs intent on biting often adopt particular behavior patterns. The dog protecting its territory crouches low, straightens its back and tail, emits a deep guttural growl, and stares fixedly at a specific part of the person's anatomy. Such behavior indicates imminent attack and a sharp blow to the nose may be necessary. Freezing in place may prevent an attack, and direct eye contact should be avoided. JAGUARS.
Jaguar attacks are rare. Recommendations are based on advice for avoiding a cougar attack. Increase your apparent size by raising your arms above the head and waving an object such as a backpack or stick, or opening a jacket. Yell, shout, whistle, or speak loudly and forcefully in a low, deep tone of voice. Back away slowly; do not turn your back and run. [8] Reptiles SNAKES.
Snakebites are rare; 450,000 hours of field work at sites in Costa Rican rainforests were documented without a single snakebite.[7] Most poisonous snakes tend to blend into their surroundings, and nonnatives rarely see them. The most effective protection is putting a jungle-reared guide in front on the trail. Natives almost always spot a poisonous snake and can quickly dispatch it. Snakes are often encountered along the shoreline of rivers and small streams. Particular caution is needed when hiking in such areas or when disembarking from a canoe or rubber raft. In the forest the hiker should always step onto a log and then step away from it. The log should not be straddled; snakes often are encountered where the log makes contact with the jungle floor. Since many venomous snakes in the tropics are heat seeking and hunt at night, caution is needed. Anacondas (water boas) feature in the folklore of all native cultures in the regions of Amazonia where these enormous snakes (up to 30 feet long) live. These non-poisonous
Figure 29-5 Needle-sharp spines ring the peach palm.
snakes kill by looping coils around prey and then tightening the coils, suffocating the victim. Anecdotal reports of anacondas attacking and swallowing humans, particularly children and women bathing at the edge of jungle streams, are unconfirmed.
ALLIGATORS AND CROCODILES.
Although they appear torpid lying in the sun, alligators and crocodiles can move amazingly fast. Humans cannot outswim or outrun a charging crocodile. Bites should be treated with thorough cleaning of the wound, surgical debridement if necessary, tetanus prophylaxis, and an appropriate antibiotic. A study of the oral flora of 10 alligators captured in Louisiana revealed various aerobic and anaerobic organisms responsive to trimethoprim-sulfamethoxazole.[13] Plants ARMED OR SPINE-BEARING PLANTS.
Spine-bearing trees abound in forested areas of the tropics. The peach palm (Bactris gasipaes), a tall, slender palm whose heart and fruit mesocarp are prized by natives, is found from Nicaragua to Bolivia. The trunk of this tree is ringed with needle-sharp spines ( Figure 29-5 ). Peach palms often grow alongside trails. Contact with this palm can result in penetration of spines deep into the flesh. Spines that enter a joint space may require surgical extraction. Secondary infection and inflammation often occur. HALLUCINOGENIC PLANTS.
Jungle-dwelling tribes throughout Central and South America use hallucinogenic plants. Powerful drugs, such as ayahuasca (Banisteriopsis), Brugmansia, the virola snuffs, and yopo (A. peregrina), are used by shamans seeking the truth. [28] [29] [30] These powerful intoxicants should be avoided. SAWGRASS.
In many regions of the tropics, sawgrass is an ever-present nuisance. This scalpel-like blades of this
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Figure 29-6 Poison-dart frog.
grass can slice into exposed skin. Even when treated with antibiotic ointment, the lacerations often take 1 to 2 weeks to heal. Hikers should avoid sawgrass; special care is needed when working with a machete. Miscellaneous Hazards POISON-DART FROGS.
Poison-dart frogs, tiny, brilliantly colored species in the genus Dendrobates, may be encountered in Central America and Northern South America ( Figure 29-6 ). Phyllobates terribilis secretes a toxin from its skin so powerful that a lethal dose could be absorbed if enough secretion entered an open wound. It is wise to avoid all contact with brilliantly colored frogs, caterpillars, and snakes. FALLING TREES.
Tropical trees do not have deep roots and often fall in relatively modest winds. In many regions of the world, risk of snakebite is significantly lower than the risk of injury or death from falling trees. In the forest, hammocks should be slung away from large trees. Travelers setting up camp should always look up at the branches of any trees near camp; although the base of the tree may appear sound, higher areas may be rotted. FORDING RIVERS.
The hiker should never attempt to cross a fast-flowing or deep river with a pack on his back. Regaining footing in a rapidly moving current can be difficult. Unless experienced in crossing such streams, the traveler should take the hand of a native guide or porter. LOG BRIDGES.
On frequently used trails, natives generally place a single log across creeks, ravines, and swampy areas. These log bridges may be up to 20 feet high and 75 feet long. Good balance is essential. Because a backpack impairs balance, a porter should carry it across. MERCURY CONTAMINATION.
Travelers to the Amazon Basin should be aware of the serious, widespread contamination of waterways by mercury that gold miners (garimpeiros) use to process their ore. Although most manufacturers of portable water treatment and filtration systems do not specifically claim to remove mercury, any activated carbon system should reduce the risk. The manufacturers of SafeWater Anywhere, (www.safewateranywhere.com), a 1-L squeeze-bottle filter, cite 99.25% mercury removal. Travelers should exercise caution in choosing rivulets as a source of potable water in areas where mercury contamination is known or suspected. RISING RIVERS.
Streams, particularly narrow ones bounded by vertical banks, can rise 20 feet in a few hours as a result of intense rains. Camp should not be set up on an island or beach in a small canyon during the rainy season. A cloudburst in the headwaters can send a wall of water rushing downstream, even though it may be a clear, moonlit night at the campsite. Traveling with Children in the Tropics The following guidelines should be considered when trekking with children in the tropical forest: 1. Do not attempt a daylong hike. Unlike indigenous children, others cannot hike all day in the humid tropical forest. Preadolescents should hike only 1 to 2 hours; for children aged 12 to 16 can hike 2 to 3 hours. Do not subject a child to jungle trail conditions unless the child has had extensive experience hiking in temperate climates. 2. Do not attempt difficult or dangerous trails. 3. Avoid trekking during the rainy season. 4. Keep the child well hydrated. 5. Provide proper footwear (running or hiking sneaker-type shoes or boots with an adequate tread). Avoid leather boots. 6. Keep the child ahead of you and behind a native guide. Children should not be out of sight on the trail. 7. When wading across rivers, have an adult native guide hold the child's hand. 8. Always have children wear a properly sized life vest while rafting, taking canoe trips, or crossing deep, swift, or wide rivers. 9. Do not allow a child to carry any equipment in a daypack other than 2-L bottles of drinking water.
10. Ensure that routine vaccinations are up to date. Special vaccinations, such as yellow fever and typhoid should be considered for certain jungle areas. Hepatitis A vaccine is recommended. Antimalarials are indicated. Any child who plans to visit the tropics should be a strong swimmer. Many natives begin swimming in infancy
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and are accustomed to deep or rapidly flowing water that would be extremely hazardous to visiting children. Swimming holes are often located in the swift-flowing outer loop of jungle rivers, where depths may reach 6 feet or more within a yard of the shoreline.
SURVIVAL Every year, inexperienced people enter the jungle and become lost. After a person ventures only a mere few yards into the forest, especially jungle that has been cleared and is now a tangle of secondary growth, everything begins to look the same. To avoid becoming lost, travelers should always have an experienced guide when traversing unfamiliar territory. Tribal peoples of the world's tropical forests have an uncanny ability to find their way and arrive at the desired destination, even after days of travel. They can always find food and water and, if necessary, rapidly construct a shelter or a weapon. Occasionally, travelers are left behind on the trail by indigenous guides. Unintentional desertion occurs when trekkers hire natives who have had no experience with neophytes. Realizing that their charges cannot keep up on the trail, the guides run ahead and sit down to rest, not knowing that others cannot navigate the trail alone. Travelers who want to avoid being left behind on the trail should hire a guide who is experienced in traveling with nonnatives. Suitable guides and porters can usually be identified with the help of a village leader, local school teacher, village health worker, missionary, or anthropologist. Rescue Strategies For individuals in a jungle survival situation, lifesaving items include a large-scale map, a global positioning system (GPS) unit, some form of electronic voice communication, and a machete. Topographic maps are available from numerous international and national mapping agencies. Satellite images with extraordinary resolution are available from Space Imaging (1-800-232-9037) or the U.S. Geological Survey (Eros Data Center 47914, 252 ND St., Sioux Falls, SD 57198-0001; 1-800-252-4547; edcwww.cr.usgs.gov). Small, lightweight GPS units display precise latitude, longitude, and altitude. Such information is extremely useful for navigation and for communicating one's location to rescue aircraft. Newer units quickly lock onto satellites and are more likely to work under the jungle canopy. Canoeists, rafters, or trekkers contemplating an expedition into largely uninhabited and unexplored regions should consider buying a compact emergency position-indicating radio beacon (EPIRB). The 406 MHz EPIRB units offer a reliable method of alerting various rescue services via a global satellite system. These units should be activated only in a true emergency when lives are at risk. Hand-held satellite phones are available for worldwide communication. Although currently expensive to purchase and operate, their potential to provide rescuers with precise GPS location makes these lightweight phones worthy of serious consideration for inclusion for wilderness travel. Lightweight, hand-held, very-high-frequency (VHF) aircraft transceivers are excellent for emergency communications. Visitors to remote areas should know the radio frequencies used by rescue aircraft. VHF transceivers are line-of-sight instruments, so they are most useful when aircraft are overhead without objects, such as trees or mountains, between the hand-held unit and the aircraft. In many regions of the world the Mission Aviation Fellowship (MAF) provides air service to remote airstrips in small villages. If assistance is needed, a hand-held radio transmitter can be used to call an MAF short take-off and landing (STOL) aircraft. Bush pilots appreciate having information on the condition of seldom-used airstrips. A crude but acceptable device can be constructed to measure airstrip hardness ( Figure 29-7 ). Cut a pole exactly 2 inches in diameter and approximately 6 feet long. Starting exactly 6 inches from one end, taper that end to a point. Lash a cross-member on the pole, and have a person weighing approximately 170 pounds stand with assistance on the cross-member. Make a map of the strip, noting the depth to which the pointed end of the pole sinks into the earth at several dozen sites. Communicate this information to the pilot by radio. If the pole goes in only 2 inches in most areas, the strip is considered ideal; 2 to 4 inches is marginal; penetration beyond 4 inches indicates that the airstrip is unsuitable for landing and take-off. If rescue is not feasible, the traveler should continually move downstream at a fast pace. Inhabited areas usually have a trail running alongside a stream. The trail may veer away from the stream where natives have cut a path to connect two villages. Marking the trail every 10 yards with a machete makes it easier to return to the starting point. To avoid confusion, the traveler should mark trees only on one side of the trail. Where human paths are in frequent use, identifying a trail is fairly easy. Seldom-used trails or any trail traversed during times of optimal plant growth may be extremely difficult for the nonnative to identify and follow. Even under adverse circumstances, however, there are clues to trail identification. Paradoxically, concentrating only on the actual foot path will almost certainly cause you to lose sight of the trail. Think of the jungle trail not as a track on the ground but as the intestinal lumen of "some gigantic leafy creature,"[17] with vertical margins, often an overhead horizontal boundary, and sometimes a visible path beneath the
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Figure 29-7 A, Young man sharpening a stick to a point. B, Lashing a cross-member to a pole. C, Standing on the pole to take measurements of the depth of penetration into the airstrip.
Figure 29-8 Log flotation device. A, Two lightweight logs are tied together. B, Device in action.
feet. Diagonally sliced saplings or neatly severed branches indicate someone has used a machete. There is a particular reflectivity off the ground where humans have trod; this reflectivity is the best way to follow a trail at night. These trail-finding clues are often so subtle that you may sense the trail rather than see it. Game trails meander and are narrower than human trails. In the jungle setting, navigation with a compass for a distance of more than 200 yards is fraught with hazard. Travelers should not attempt to cut overland if lost, inexperienced, or on their own unless a significant landmark is visible or sounds of humans or domesticated animals, indicating a settlement, are clearly heard. A raft may be constructed by lashing logs together with rope or tough, pliable jungle vines. Balsa trees (Ochroma pyramidale), encountered throughout much of Amazonia, make the best rafts. Balsa is often found growing alongside rivers and has the following characteristics: tall, columnar trunk with branches and leaves bunched at the top, which gives the tree a "skinny" look; beige or gray-beige trunk; bark that is smooth but tends to flake, giving it a mottled appearance; and broadly heart-shaped, more or less three-lobed leaves. The key feature of balsa wood is its remarkably light weight. Bamboo also can be used to construct a first-class raft. A log flotation device may be constructed by tying together two balsa logs or other lightweight wood placed 2 feet apart ( Figure 29-8 ).[32]
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A "brush" raft may be made by placing buoyant vegetation within clothing or a poncho. Dry leaf litter ("duff") or plants such as water hyacinth may be used.[32] Food Food is readily available in inhabited regions. Even abandoned villages yield enough fruit and vegetables on which to survive. Throughout the tropical world, bananas and the large plantain "cooking banana" are ubiquitous. Root crops such as taro, yams, and yucca should be sought. Yucca roots should be shredded or pounded and then boiled to release their toxic compounds. As an extra precaution, the wet pulp should be flattened into a "pancake" and cooked on a grate to eliminate any remaining volatile hydrogen cyanide gas. All land crabs, mammals, birds, freshwater fish, turtles, snakes, and lizards are edible but should be cooked first to eliminate parasites. It is virtually impossible to kill game without firearms. In inexperienced hands, traps and snares are not effective. Much better results are obtained from fishing (see Chapter 28 ). Water Water may be made safe by boiling or using chemical disinfectants, such as Potable Aqua tablets. Drinkable water may be found in lianas, often called "water vines," throughout jungle regions. Vines that contain water are fairly easy to identify because they tend to resemble the "grapevines" of North American forests and have rough, scaly bark. These vines may be several inches thick and contain surprising amounts of clear water. Vines that do not contain drinkable water tend to have smoother bark and, when cut, exude sticky, milky liquid. Travelers should not drink from vines that contain milky, latex-like sap; this substance is poisonous. Maximal amounts of water are collected from water-bearing vines if the first cut is high on the vine and the second cut is lower on the vine near the ground. When the water stops flowing from the cut section, cutting approximately 6 inches from the opposite end will start the flow again. Water may be trapped within sections of certain types of green bamboo. Bamboo that contains water makes a sloshing sound when shaken. Water also may be obtained from green bamboo stalks by bending a stalk over, tying it down, and cutting off the top. Water dripping from the severed tip can be collected in a container during the night ( Figure 29-9 ). [32] Large amounts of water can be found in the voluminous natural cisterns formed by the cuplike interiors of epiphytes (air plants), such as bromeliads. The water should be strained through a cloth.[32]
Figure 29-9 Bamboo can be a source of water.
Water may be collected from a banana or plantain plant by cutting the plant approximately 1 foot above the ground and scooping out the center of the stump into a bowl shape. The hollow thus formed fills immediately with water. The first two fillings have a bitter taste and should be dipped out. The third and subsequent fillings are drinkable. A banana plant can furnish water in this fashion for several days ( Figure 29-10 ).[32] In coastal regions, unripe (green) coconuts provide adequate supplies of refreshing milk. The milk of mature coconuts has a laxative effect and should be avoided. Shelter Abandoned, temporary shelters previously constructed by natives on hunting expeditions seem to attract particularly aggressive, large biting spiders and stinging ants. Also, venomous snakes may be attracted to rodents residing in these abandoned shelters. It is often preferable to take the extra time to set up a new camp than to risk encountering venomous insects, arachnids, and snakes. In an emergency a proper shelter can be constructed using only plant materials. Figure 29-11 illustrates the basics of constructing a sleeping platform and lean-to. A shingled covering can be made quickly and easily from long, broad banana or heliconia leaves. Tropical palms provide a more substantial roof but require more time and skill in construction. After selecting a suitable ground-hugging species or chopping down a slender tall palm (palm trees with spines often provide the best fronds), each frond is separated into halves by grasping
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Figure 29-10 Water collected from a banana plant.
it at the distal end, separating the leaves as though parting hair down the middle, and splitting the frond in two with a quick jerk ( Figure 29-12 ). The halves should be overlapped like shingles and secured to the roof framework. It is much easier to construct an adequate shelter using a tarpaulin (see Camp Life). Psychology of Survival Travelers reared on movies and novels depicting the horrors of the Amazon may have irrational fears of being lost or stranded in the jungle. Visible daytime threats worsen with the onset of darkness, when perception becomes distorted. Travelers incapacitated by fear may throw away survival items or may flee from rescuers. Strategies that can increase travelers' confidence in survival include the following: 1. Previous jungle experience. It is helpful to begin tropical excursions in the structured setting of small-group travel. Ecotours, particularly in Costa Rica and Ecuador, offer a combination of rainforest trekking and cross-cultural experience. 2. Survival manuals. Military experts and others provide insights from decades of experience.[32] [33] 3. Information on the tropical rainforest. Familiarity with exotic plants and animals lessens the likelihood of fear while increasing awareness of potential utility in a survival situation. The anthropological literature is replete with first-person accounts by anthropologists who have lived under trying circumstances with minimally contacted tribal populations throughout the tropics. 4. Classic accounts of adventure and survival. The Adventure Library (800-754-8229) offers an excellent series of survival epics.[21] 5. Courses in wilderness-oriented skills. The National Outdoor Leadership School (NOLS, 307-332-5300, www.nols.edu) teaches wilderness-oriented skills and leadership in a core curriculum stressing safety and judgment, leadership and team work, outdoor skills, and environmental studies. 6. Traveling with a machete, the one indispensable tool. A map, compass and a GPS unit are other recommended items. 7. Taking stock. The traveler facing a wilderness crisis assess a situation analytically and rationally before planning the course of action. Having survival skills is
important; having the will to survive is essential. [33]
Figure 29-11 Sleeping platform.
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Figure 29-12 Indian splitting a frond to make a covering for a lean-to.
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Wilson EO: Threats to biodiversity, Sci Am 261:108, 1989.
36.
Wilson EO: The diversity of life, New York, 1993, Norton.
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Chapter 30 - White-Water Medicine and Rescue Eric A. Weiss
Rivers have what man most respects and longs for in his own life and thought—a capacity for renewal and replenishment, continual energy, creativity, cleansing. John M. Kauffman, Flow East
Rafting, canoeing, and kayaking have become the third largest outdoor recreation industry in the United States.[34] Over 19 million people canoe and kayak each year, and more than 57 million enjoy rafting.[6] Combined participation in river sports is growing at a rate of 15% annually.[35] [43] Kayaks and rafts are also used by law enforcement officers, park rangers, and game wardens to patrol and manage their territories.[29] New equipment designs have opened up more difficult rivers for exploration and commercial recreation. It is not surprising that the number of river-related accidents and deaths has also increased dramatically. The American Canoe Association reports that approximately 130 white-water fatalities occur each year.[43] This chapter examines the unique and dynamic hazards associated with rivers and white-water paddling. Safety equipment, accident prevention, common injuries, environmental hazards, medical management, and swift water rescue are also reviewed.
HISTORICAL PERSPECTIVE White-water boating as a recreational activity began in the United States in earnest during the late nineteenth century when adventurers attempted to emulate Major Wesley Powell's Colorado River expedition by rowing boats down many of the West's large rivers.[24] These heavy wooden boats were replaced by inflatable rafts after World War II, when surplus neoprene assault boats and life rafts became available for civilian use.[3] In 1966, fewer than 500 people boated the Colorado River through the Grand Canyon in an entire year. Recently, the figure exceeded 500 per day.[24] Rafting did not become popular in the eastern United States until the early 1960s. In 1968, commercially guided raft trips were offered for the first time on the New River in West Virginia.[45] The Chattooga River in Georgia attracted many rafters after the movie Deliverance was filmed there in 1971. The Youghiogheny River in Pennsylvania and the South Fork of the American River in northern California have become the two most heavily rafted rivers in the country. Technologic advances have revolutionized river running. Electronically welded plastic has largely replaced rubber as the primary material used in raft construction, making the vessels lighter, stronger, and easier to repair. Self-bailing rafts, introduced in 1983, are now ubiquitous and provide greater maneuverability, allowing rafters to run rivers previously considered too difficult and dangerous. Unfortunately, greater mobility has been paralleled by an increase in the number of accidents occurring far from medical care. A major innovation in kayaking was the development of the plastic kayak, first manufactured in 1972 by the Holloform Company ( Figure 30-1 ).[45] Kayaks had been previously constructed from resinous materials, such as fiberglass and Kevlar, which were more fragile and less likely to "broach," or wrap around rocks. Paddlers were reluctant to run steep, rocky rivers for fear of breaking their boats. Most recreational white-water kayaks are now made of molded polyethylene plastic, which does not break apart and has the potential to fold when broached or pinned, trapping the paddler. Kayakers with "indestructible" boats are pushing the limits of navigable rivers. Even Niagara Falls has been successfully run by a kayaker! The enormous popularity of rafting and kayaking has led to exponential growth of professional guide services. In 1990, 35 million people were taken down U.S. rivers by commercial companies.[43] Faced with increased competition, guide services have been leading inexperienced clients with little formal training and few practical skills into difficult and dangerous rivers ( Figure 30-2 ). In the summer of 1988, five U.S. executives died after their raft flipped on the Chilco River in British Columbia. One of the survivors was reported to have said, "We looked at white water as sort of a roller coaster ride."[41]
MORBIDITY AND MORTALITY There is a paucity of data that document the relative risk of white-water-related activities. In Colorado, fewer people die while engaged in rafting, canoeing, and kayaking than in climbing, bicycling, and skiing. Figures compiled by the Colorado Department of Public Health and Environment showed that 69 people died in climbing or hiking accidents, 36 while bicycling and 32 while snow skiing during a 3-year period ending in 1995. Rafting, canoeing, and kayaking incidents, by comparison, resulted in 19 fatalities ( Table 30-1 ).
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Figure 30-1 River rescue. The plastic kayak has revolutionized white-water sports. (Courtesy Paul Auerbach, MD.)
Figure 30-2 Class V commercial rafting on the Chattooga River, Georgia. (Courtesy Robert Harrison, Whetstone Photography.)
A retrospective analysis of injury reports submitted by commercial rafting outfitters to the West Virginia Division of Natural Resources from 1995–1997 revealed a total of 200 injuries with a resulting overall injury incidence rate of 0.263 per 1000 rafters. The average age of injured persons was 33.14 years, 53.3% were male, and 59.8% had previous rafting experience.[47]
ACTIVITY
TABLE 30-1 -- Recreational Fatalities in Colorado, 1993–1995 (252 deaths were the result of recreational activities) RANK FATALITIES
Climbing/hiking
1
69
Bicycling
2
36
Snow skiing
3
32
Swimming
4
25
Canoeing/kayaking/rafting
5
19
Horseback riding
6
18
Boating/water skiing
7
13
Fishing
8
11
Hunting
9
6
Data from Colorado Department of Public Health and Environment.
The body parts most frequently injured during rafting mishaps are the face (33.3%), including the eye (12.1%), mouth (6.6%), other facial parts (5.1%), nose (4.5%), and teeth (4.0%), followed by the knee (15.3%), arm/wrist/hand (11.6%), and other parts of the leg, hip, or foot (10.5%). The most common injury types are lacerations (32.5%), sprains/strains (23.2%), fractures (14.9%), contusions/bruises (9.8%), and dislocations (8.2%). Most injuries occur in the raft as a result of collisions among passengers, being struck by a paddle or other equipment, or entanglement of extremities in parts of the raft.[47] Because most injuries occur in the raft and involve the face, accident-preventive measures include attaching face protection to paddling helmets and carrying fewer passengers per raft.
EQUIPMENT The dynamic and unpredictable nature of rivers can turn any mishap into a tragedy. For this reason, the initial mission of white-water medicine is to emphasize safety and accident prevention. According to the U.S. Coast Guard's boating accident statistics, the most common factor contributing to white-water-related deaths is failure to wear a personal flotation device (PFD, or life jacket).[43] Exposure to cold river water can stimulate respiratory and cardiovascular reflexes, making it difficult for a swimmer to keep his or her head above water (maintain freeboard) (see Chapter 8 ). [25] The Coast Guard is charged with regulating and testing life jackets and classifies PFDs into five types. Of these, only two types are commonly used in white-water sports. The type III PFD, a vest-type jacket favored by most paddlers, permits greater mobility and comfort. The Coast Guard requires that type III PFDs have a minimum of 15 ½ pounds of flotation (lift). Because most
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adults effectively weigh between 10 and 12 pounds in the water, this allows at least 3 ½ pounds of effective required buoyancy. Type V PFDs are used by commercial outfitters because they provide greater flotation and are constructed asymmetrically with over half of the jacket's flotation distributed in the front. This is supposed to turn an unconscious wearer face up. Although this may be true in calm water, it does not work reliably in swift water. A PFD should fit snugly and not ride up over the head when a person is in the water. Because even a well-fitting life jacket can be pulled off by turbulent water, some manufacturers now include crotch straps as an added safety feature. Testifying before a congressional subcommittee, the president of the National Transportation Safety Association cited the Chilco River accident to support his contention that crotch straps be made mandatory on all white water-use life jackets. Several survivors reported that their life jackets rode up over their heads and did not keep their faces above water. Life jackets with built-in rescue harnesses, pioneered by the Europeans, are now widely available in the United States. A typical harness system uses seat-belt webbing threaded through a metal retainer, then run into a plastic cam-lock buckle with a toggle. The toggle allows the user to find the buckle in white water. To release the system, the user pulls the toggle, opening the buckle and allowing the webbing to slip through the retainer and release. A D-ring mounted on the back of the jacket provides a point for clipping in a rope ( Figure 30-3 ). This quick-release belt allows the wearer to attempt a strong swimmer rescue but also to get free of the tethering line quickly in an emergency. Beyond flotation, life jackets have other benefits that make them highly useful in wilderness settings. Their insulating properties help prevent hypothermia. The closed-cell foam flotation material acts as thoracic padding during falls on slippery rocks or when swimming rapids after exiting the craft. Life jackets also make excellent improvised splints; they can be fashioned into cervical collars, cylindrical knee braces ( Figure 30-4 ), or padded ankle stirrups. The American Whitewater Affiliation (AWA) safety code recommends the use of helmets at all times in kayaks and canoes, and in rafts and other craft when attempting rapids of class IV or greater difficulty. Surveys have shown that head trauma after capsizing comprises 10% to 17% of all kayaking accidents.[29] [44] Another vital piece of safety equipment is a rope, which should be readily accessible and secured in a manner that facilitates rapid deployment and prevents entanglement. Throw ropes for river use should float, have a certain amount of dynamic stretch, and not absorb water. Self-contained throw bags have virtually replaced
Figure 30-3 A, Life jacket with built-in rescue harness. B and C, A quick-release buckle allows the wearer to release the tether when necessary. It is essential for swiftwater use.
coiled ropes for river use and generally hold about 50 to 75 feet of ?-inch polypropylene rope inside a nylon stuff sack. Newer styles can be attached to life jackets for rapid access. They can also be thrown to rescuers by a paddler who is pinned or broached. Commercial outfitters and 732
Figure 30-4 A paddler wearing a type III life jacket around his knee as an improvised knee immobilizer to help stabilize a sprained knee.
large groups of rafters should carry at least one 300-footlong static rope to be used for Telfar lowers, Tyroleans, and other rescue situations where mechanical advantages are used. Knives should be readily accessible. Fixed blades are preferable to folding ones unless the folded blade can be opened easily with one hand. Double-edged blades can cut in two directions and thus require minimal handling in precarious situations. Some modern knives designed for kayakers feature serrated edges that can cut through plastic boats during entrapment. Whistles should be worn so paddlers can alert others that an accident has occurred. Paddlers are often spread out over the course of a rapid, and yelling over the roar of the water is usually a frustrating and fruitless endeavor. Placing adequate barriers between the human body and the environment is of paramount importance in aquatic sports. Functional, insulated clothing should be considered a mandatory safety item to prevent hypothermia. Cotton is a poor choice for river wear; it loses all of its insulating properties when wet and dries slowly. Newer synthetics such as polypropylene and polyester pile absorb no more than 1% of their weight in water and maintain thermal insulating qualities when wet.[27] When combined with a nylon or Gore-Tex paddling jacket, a synthetic underlayer provides effective protection from cold and wind. Wet suits, previously considered to be optimal garments for paddlers in extreme conditions, are stiff and somewhat constricting.[1] The dry suit, with tight-fitting latex seals at the wrist, ankle, and neck, is the new "gold standard" for cold water boating. By sealing water out and preventing evaporative heat loss, the dry suit can keep a paddler warm even during winter conditions. [17] Overheating is occasionally a problem with dry suits. Recently a dry suit contributed to profound and unexpected hyperthermia in a kayaker who had suffered a submersion injury in cold water.[4]
RIVER HAZARDS The International Scale of River Difficulty grades rivers and rapids into classes I to VI. An American version of this rating has been adopted by the AWA for most U.S. rivers ( Box 30-1 ).[42] Some western rivers use the Grand Canyon System, which rates rapids on a scale from 1 to 10. Neither scale is a truly objective standard; individual and regional variations are common, and the margin of difficulty for a particular rapid may differ significantly for kayaks and rafts. Unfortunately, important safety parameters, such as water temperature, remoteness, and evacuation potential, are not taken into consideration. The difficulty of a river generally increases with the volume of flow and the average gradient. The volume of water in a river is usually expressed as a measure of cubic feet per second (cfs). It is the amount of water moving past a certain point during a given period of time. The volume of a river can be determined by multiplying the width by the depth times the speed of the current. As the water level rises, its speed and power increase exponentially, raising the difficulty of most rapids.[3] Occasionally, however, a rapid becomes easier as the added water submerges hazardous obstacles. Gradient is the amount of drop between two points and is expressed as feet per mile. The steeper the gradient, the faster the water moves. Not all water flows downstream. The most common upstream flow is an eddy, which is created when water flows around an obstacle. The water piles up higher than the river level on the upstream side of the obstacle, while the water on the downstream side is lower. Water flows around the obstacle then back toward it to fill in the low spot. The line between the upstream and downstream current is the eddy line. Eddies are one of the most important features of the river for boat maneuvering and rescue. Exiting the main current by pulling into an eddy allows the paddler to stop the descent and safely scout the next rapid. It also provides a location for a paddler to set up rescue for his or her companion upstream. Hydraulics, also known as holes, reversals, rollers, suck-holes, and pour-overs, are the most common hazards in rivers. A hydraulic is created when water flows over an obstacle, causing a depression that produces a relative vacuum within which the downstream water recirculates ( Figure 30-5 ). The water below a hydraulic is typically very aerated and presents a white, foamy appearance. Rafts and kayaks can be turned upside down by the force of a hydraulic, and if the reversal currents are strong enough, crafts and people can become trapped in the recirculating flow. When proceeding into a rapid that contains a hazardous hydraulic,
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Figure 30-5 Recirculating currents created by a hydraulic. Water and "swimmers" are released downstream beneath the surface.
one of the group should preset a rope below the hole to facilitate rescue. Box 30-1. AMERICAN VERSION OF THE INTERNATIONAL SCALE OF RIVER DIFFICULTY CLASS I: EASY Fast-moving water with riffles and small waves. Few obstructions, all obvious and easily avoided with little training. Risk to swimmers is slight; self-rescue is easy. CLASS II: NOVICE Straightforward rapids with wide, clear channels that are evident without scouting. Occasional maneuvering may be required, but rocks and medium-sized waves are easily avoided by trained paddlers. Swimmers are seldom injured, and group assistance, although helpful, is seldom needed. CLASS III: INTERMEDIATE Rapids with moderate, irregular waves that may be difficult to avoid and can swamp an open canoe. Complex maneuvers in fast current and good boat control in tight passages or around ledges are often required; large waves or strainers may be present but are easily avoided. Strong eddies and powerful current effects can be found, particularly on large-volume rivers. Scouting is advisable for inexperienced parties. Injuries while swimming are rare; self-rescue is usually easy, but group assistance may be required to avoid long swims. CLASS IV: ADVANCED Intense and powerful but predictable rapids requiring precise boat handling in turbulent water. The advanced river may feature large, unavoidable waves and holes or constricted passages that demand fast maneuvers under pressure. A fast, reliable eddy turn may be needed to initiate maneuvers, scout rapids, or rest. Rapids may require "must" moves above dangerous hazards. Scouting is necessary the first time down. Risk of injury to swimmers is moderate to high, and water conditions may make self-rescue difficult. Group assistance for rescue is often essential but requires practiced skills. A strong Eskimo roll is highly recommended. CLASS V: EXPERT Extremely long, obstructed, or violent rapids that expose a paddler to above-average danger. Drops may contain large, unavoidable waves and holes or steep, congested chutes with complex, demanding routes. Rapids may continue for long distances between pools, demanding a high level of fitness. Eddies may be small, turbulent, or difficult to reach. At the high end of the scale, several of these factors may be combined. Scouting is mandatory but often difficult. Swims are dangerous and rescue is difficult, even for experts. A very reliable Eskimo roll, proper equipment, extensive experience, and practiced rescue skills are essential for survival. CLASS VI: EXTREME Class VI runs exemplify the extremes of difficulty, unpredictability, and danger. The consequences of errors are very severe, and rescue may be impossible. For teams of experts only, at favorable water levels, after close inspection and taking all precautions. This class does not represent drops believed to be unrunnable but may include rapids that are only occasionally run.
From Safety code of the American Whitewater Affiliation, Phoenicia, NY, 1989, American Whitewater Affiliation.
Hydraulics release water downstream from beneath the surface. This may be the only avenue of escape for a swimmer. Escape from a strong hydraulic may require a person to stay submerged and to resist the urge to return immediately to the surface. Surfacing too early can result in recirculation. Fortunately, most hydraulics eventually release people regardless of what action they take.
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Novice paddlers often misjudge the force of hydraulics. It is not the height of the drop that generates the recirculating power but rather the shape and angle of the obstruction, combined with water volume and adjacent eddy currents. A "smiling" hydraulic has its outer edges curving downstream, so that the recirculating water feeds out into the main current and is thus easier to escape. In a "frowning" hydraulic, the outer edges curve back upstream into the center of the hydraulic, making escape much more difficult. Low-head dams or weirs from massive hydraulics with enormous recirculating potential. Unlike natural hydraulics, these human-made structures form hydraulics all the way across the river, leaving no escape routes. In the Binghamton Dam disaster of 1975, a 13 ½-foot Boston whaler with a 20-horsepower engine was pulled into a
hydraulic while attempting a rescue, resulting in the deaths of three firefighters. [39] Undercut rocks are boulders or ledges that have been eroded just beneath the water surface. These usually occur on geologically older rivers. They can be difficult to recognize and pose significant risks for entrapment and drowning, even in class II rapids. The potential for entrapment can also occur when swimmers attempt to stand up and walk in swift-moving currents. A foot can become wedged in an undercut rock or between rocks beneath the surface, causing the victim to lose his or her balance and fall face down into the river ( Figure 30-6, A ). With the foot entrapped,
Figure 30-6 A, Attempting to stand up in shallow water can produce foot entrapment in an undercut rock. B, Proper way to swim while in a rapid.
the victim cannot regain an upright or even face-up position. This type of mishap has caused drownings in water less than 3 feet deep. A swimmer in a rapid should assume a supine position, with feet at the surface and pointed downstream to serve as shock absorbers. This position minimizes the potential for both foot entrapment and head and neck trauma ( Figure 30-6, B ). Strainers are obstacles, such as fallen trees, bridge debris, or driftwood lodged between rocks or jutting out from the shore, that allow water to pass through (sieve effect) while trapping the swimmer or boater. Flooded rivers, a favorite of expert boaters, often develop many new strainers as riverbank debris is washed into the flow. In the summer of 1987, five paddlers drowned when their raft struck a large strainer on Canada's Ellaho River.[41] Negotiating a strainer requires special tactics. The safest option for the swimmer is to swim aggressively into the strainer head first rather than feet first, and then attempt to climb over the debris ( Figure 30-7, A ). Approaching a strainer feet first may lead to underwater entrapment ( Figure 30-7, B ). Human-made hazards can also pose a threat to river runners. Bridge pilings, submerged automobiles, dams, and low-hanging power lines can pin or injure boaters. A broach occurs when a boat wraps sideways around an obstacle or when both bow and stern become stuck on separate obstacles simultaneously. Common obstacles
Figure 30-7 A, Proper approach to a strainer. B, Incorrect approach to a strainer.
735
include boulders, trees, bridge pilings, and ledges protruding from canyon walls. Drowning can occur if the paddler leans upstream away from the obstacle and flips upside down while still broached or if the boat collapses and entraps the victim ( Figure 30-8 ).
Figure 30-8 Broach.
Figure 30-9 1, Vertical pin. 2, Pitchpole pin.
A vertical pin happens when a kayaker plunges over a drop and the end of the boat becomes trapped between rocks beneath the surface. The force of the water can fold a plastic kayak over on itself, trapping the occupant upside down beneath the surface ( Figure 30-9 ). A survey of 365 members of the AWA revealed that 33% of serious kayaking incidents and 41% of open canoeing mishaps involved either pinning or broaching ( Table 30-2 ).[44] In a separate survey of 500 paddlers between 1989 and 1993, 42% of kayaking fatalities resulted from vertical pins, broaches, or entrapments in strainers. Kayak construction can have important safety implications in both broach and pin situations. The force of the current against the deck of the boat or back of the paddler can make it impossible for the victim to extract his or her legs and escape. Boat makers have developed kayaks with larger cockpits that make it easier to raise the knees out and escape the craft. Transverse bulk-head-type
INCIDENT
TABLE 30-2 -- Serious White-Water-Related Incidents NUMBER PERCENTAGE OF ACCIDENTS
Vertical pin entrapment
18
8
Broach entrapment
46
21
Rock sieve entrapment
16
7
Undercut rock entrapment
23
10
Recirculation in hydraulic
47
21
Long swim
42
19
From Wallace D: AWA J 3:27, 1991.
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Figure 30-10 Safety Deck system, which offers an emergency exit for a kayaker in distress.
foot braces have replaced pedal-type braces to prevent the kayaker from being shoved forward in the boat. This feature ensures the escape potential offered by larger cockpits. One of the compromises of the larger cockpit, however, is that the sprayskirt is more likely to come off in turbulent water. Another safety feature, the Safety Deck System (Outdoor Safety Systems, Princeton, NJ), uses a manually releasable foredeck section that can be jettisoned by the paddler for emergency exit ( Figure 30-10 ). During normal use, this deckplate is securely fastened to the boat and does not alter its shape or performance. The Safety Deck System has been tested extensively with positive results, but unfortunately its cost has precluded commercial development.
SUBMERSION ACCIDENTS Almost all fatalities on rivers result from submersion. Each year the River Safety Task Force of the American Canoe Association compiles accounts of drownings and other accidents. Every 3 years it publishes the River Safety Report, which chronicles and analyzes these accidents.[39] [40] [41] [43] Most submersion fatalities occur after paddlers unexpectedly swim from their boats or become trapped in them underwater. The exact cause of drowning often remains unclear and is inexplicably blamed on immersion hypothermia. Although hypothermia induces impaired judgment and coordination and may be an important contributing factor, immersion hypothermia is probably never the sole cause of death.[46] Studies by Hayward and others have shown that seminude subjects are able to maintain normal core temperatures for 15 to 20 minutes in 10° C (50° F) water.[19] [20] Continuous immersion for up to 1 hour would be required to produce profound hypothermia.[20] Cold water immersion precipitates drowning by three other mechanisms. Sudden cold water immersion produces profound cardiovascular and respiratory responses. Reflex sympathetic output can markedly increase blood pressure and heart rate, resulting in lethal arrhythmias.[16] [25] [26] An immediate and involuntary gasp occurs after cold water immersion. This is followed by hyperventilation.[8] Pulmonary ventilation increases up to fivefold because of increased tidal volume and respiratory rate.[38] The initial gasp can result in aspiration of water and laryngospasm. Hyperventilation produces respiratory alkalosis with resultant muscle tetany and cerebral hypoperfusion.[8] This response can increase the risk of drowning in a person struggling to maintain an airway freeboard in rough water. The respiratory stimulation produced by cold water immersion significantly decreases breath-holding duration.[21] This fact has enormous implications for kayakers who must hold their breath while attempting to roll up a boat after flipping upside down. This probably accounts for the unexplained swims by expert kayakers who sometimes fail to right themselves after flipping in cold water. Peripheral cold water-induced vasoconstriction exacerbates rapid cooling of muscles and nerves in the extremities, resulting in loss of strength and coordination.[38] The ability to swim, maintain freeboard, avoid obstacles, and climb from the river may be greatly impaired.[28] Even when the air temperature is warm, paddlers running cold water rivers should wear sufficiently insulated clothing. The combination of hyperventilation and muscle dysfunction can be lethal for a swimmer in rough water. A PFD helps but does not prevent even small waves from submerging a swimmer's head.[15] These dangers make imperative the need to preset safety systems in significant rapids and rescue swimmers first. Unfortunately, paddlers have drowned when their companions chased after equipment, assuming that the swimmer could climb out of the river without assistance.[40] [42] Safety kayaks with enhanced buoyancy are recommended on commercial raft trips, since they provide additional flotation for clients who fall overboard. Although some maintain that the respiratory and cardiovascular reflexes can be abolished by repeated exposure of the face to cold water, there are currently no scientific data to support this theory of acclimatization.
TRAUMA A survey of commercial raft clients revealed that the most common significant injury was a sprained or fractured ankle.[45] Ironically, these injuries usually occur out of the water when persons walk on loose, wet, and slippery rocks during scouting and portaging or when entering
737
or leaving the river. Ankle and other lower extremity injuries also occur on the river when rafters are tossed onto each other in rapids. Kayakers are prone to ankle injuries from forced dorsiflexion or inversion when the bow of the boat hits an obstruction. The feet are held against the narrow horizontal braces while the heels are pushed underneath, or the entire ankle is inverted. European- and some American-designed kayaks with bulkhead foot braces have reduced this problem. Management of foot and ankle injuries should begin with ice, elevation, and compression to reduce swelling. Cold river water is usually substituted for ice. Compression wrapping is important after icing to prevent swelling from reflex vasodilation. Splinting is important to reduce pain and edema and to limit exacerbation of the injury during evacuation. Pneumatic splints, still carried by many raft companies, provide adequate support and compression but are prone to overinflation when heated by the sun. Zippers often malfunction when they rust or jam with sand. Neurovascular integrity must be checked frequently with an air splint. Ankle splints can be improvised from life jackets, kayak float bags, articles of clothing, or a SAM splint. Strains are common in white-water sports. Researchers at Dalhousie University in Halifax, Nova Scotia, analyzed dynamic electromyographic potentials of the various muscle groups used in kayaking and then correlated them with videotaped sequences.[32] Muscles used most often in kayaking that are prone to strain injury are shoulder extensors (latissimus dorsi, teres major, pectoralis major), medial scapula rotators (rhomboideus major and minor, pectoralis minor), lateral scapula rotators (pectoralis minor, serratus anterior), shoulder flexors and horizontal adductors (anterior deltoideus, pectoralis major, coracobrachialis), elbow extensors (triceps), and spine erector muscles. Any training program for kayakers needs to emphasize conditioning of these muscle groups. Back strain afflicts rafters, kayakers, and canoers. Rafters are prone to back injuries while portaging, pushing stuck rafts off rocks, and carrying the crafts to and from the river. Raft guides are notorious for suffering back strain when pulling capsized customers, who often weigh more than they do, back into the rafts. Kayakers and canoers injure their backs lifting water-laden boats and loading their crafts onto automobile roofs. Sitting for prolonged periods with legs extended and minimal back support leads to muscle fatigue in kayakers, compounding the potential for injury. Repetitive dorsiflexion of the wrist required to operate an offset (feathered) kayak paddle produces tendinitis and synovitis.[31] A paddle constructed with a 75- to 80-degree offset instead of the traditional 90 degrees can reduce wrist stress. Aspirin or nonsteroidal TABLE 30-3 -- Common White-Water-Related Injuries, 1980–1991 (N = 85) NUMBER PERCENTAGE OF INJURIES
INJURY TYPE Shoulder dislocation
14
16.5
Near drowning
11
12.9
Fractures
15
17.6
Head and neck
6
7
Hypothermia
4
4.7
Leg injuries
11
12.9
Lacerations
9
10.5
Fatalities
7
8.2
From Wallace D: AWA J 3:27, 1991.
Figure 30-11 High brace maneuver.
antiinflammatory agents ingested 30 minutes before paddling, combined with ice application afterward, may be beneficial. Wrist supports provide limited relief. The injury most often associated with kayaking is anterior shoulder dislocation. Various surveys have placed its incidence in kayakers at 10% to 16%, making it the second most common white-water-related injury ( Table 30-3 ). [5] [30] [44] [45] The maneuver most notorious for precipitating this injury is the high brace. Often used while supporting the kayaker in a hydraulic, surfing on a wave, or rolling the kayak upright after a flip, the high brace entails abduction of the humerus, with external rotation of the glenohumeral joint ( Figure 30-11 ). If the arm becomes extended behind the midline plane of the body by the force of the current, the triad of abduction, external rotation, and extension of the shoulder can stretch or rupture the glenoid labrum and capsule, resulting in anterior subluxation or dislocation.[37] The paddle acts as a lever to increase the force on the glenohumeral joint.
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To minimize the risk of shoulder dislocation, the preferred method of bracing is the "low brace," in which the arm is held in internal rotation and close to the body (adduction). Although initially awkward for the novice paddler, this bracing maneuver is inherently stronger and more versatile because it allows backpaddling out of a hydraulic. Exercises that strengthen the rotator cuff and deltoideus, triceps, and pectoralis muscles reinforce the glenohumeral joint. The paddler with a dislocation is usually aware that something has gone wrong and holds the extremity away from the body, unable to bring the arm across the chest.[37] The shoulder may appear square because of anterior, medial, and inferior displacement of the humeral head into a subcoracoid position. Although on-scene reduction of shoulder dislocations is controversial, immediate relief of pain, curtailment of ongoing injury, and subsequent ability to function more actively in evacuation are strong reasons to do it. Several techniques have been advocated for reduction.[36] The key element is rapid initiation, since the longer a shoulder remains dislocated, the more difficult the eventual reduction becomes. Relocation is often delayed because river corridors rarely afford rapid access to a flat and comfortable area upon which to place a victim in the supine or prone position, a requirement for most techniques. For river and other wilderness settings, reduction is facilitated by using a technique in which the victim is standing or sitting ( Figure 30-12 ). As soon as the diagnosis is made, the victim bends forward at the waist while the rescuer supports the chest with one hand. With the other hand, the rescuer grabs the victim's wrist and applies steady downward traction and external rotation. While maintaining traction, the rescuer can slowly flex the shoulder by moving it in a cephalad direction until reduction is obtained. If two rescuers are available, one should support the victim at the chest while the other pulls countertraction and flexion at the arm. Scapular manipulation
by adducting the inferior tip using thumb pressure and stabilizing the superior aspect of the scapula with the cephalad hand may augment reduction ( Figure 30-13 ).[33] [36]
Shoulder reduction can also be done while the victim is sitting. Grab the victim's forearm close to his or her elbow with both hands and, with the elbow bent at 90 degrees, pull steady downward traction on the arm. After about a minute of sustained traction, slowly raise the entire arm upward until reduction is complete. Gingerly rotating the forearm outward while pulling traction may facilitate reduction. If a second rescuer is present, scapular manipulation can be performed simultaneously as described above. Another relocation technique uses the victim's life jacket to allow one rescuer to apply both controlled traction and countertraction.[11] This technique requires
Figure 30-12 Weiss technique for shoulder relocation with the victim standing. A, The rescuer supports the victim's chest with one hand and pulls down and forward (B) with the other hand.
that the victim be supine, with room for the rescuer to sit adjacent to the dislocated shoulder. The rescuer then slides his or her foot and leg through the life jacket's arm opening, under the neck, and out through the jacket's head opening. The rescuer's leg functions as a head rest, while the foot braced against the opposite shoulder strap of the life jacket provides countertraction. Holding the forearm of the affected side with the elbow bent at 90 degrees, the rescuer slowly leans back to apply traction while the leg exerts countertraction. The life jacket allows countertraction force to be distributed across the victim's 739
Figure 30-13 If two rescuers are available, scapular rotation to assist shoulder relocation can be performed while the second rescuer pulls the arm down and forward. The inferior top of the scapula is pushed medially.
Figure 30-14 Using a life jacket to assist in countertraction for shoulder relocation.
chest. External and internal rotation can be applied to the humerus during traction to facilitate reduction ( Figure 30-14 ). One should always monitor circulation and motorsensory function to the wrist and hand before and after attempting a shoulder reduction. To prevent a recurrent
Figure 30-15 Shoulder harness for support after shoulder dislocation.
dislocation, the kayaker's arm should be splinted across the chest with a sling or swath or by safety pinning the sleeve of the arm across the chest. If circumstances preclude exiting the river without further kayaking, the shoulder can be partially stabilized by wrapping an elastic or neoprene wrap around the torso and involved arm to limit abduction and external rotation ( Figure 30-15 ). Head, facial, and dental trauma are more common in kayakers and decked canoeists than in rafters because of the potential for flipping upside down while still in the craft. Minor abrasions, lacerations, and contusions are common; serious head injury with loss of consciousness is rare. Head and facial trauma can be minimized by wearing a protective helmet and tucking forward, instead of leaning backward, while rolling. Spine fractures have been reported in kayakers and canoers.[40] [41] [43] Cervical spine injuries have occurred in kayakers in conjunction with head trauma sustained after flipping upside down. Vertical compression fractures of the thoracolumbar spine have occurred from
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axial loading when a kayaker landed flat after paddling over a waterfall. One kayaker was rendered paraplegic after landing on his back on rocks while attempting to negotiate a waterfall.[43] Fortunately, his companions recognized the injury and kept him supported on minicell blocks from their kayaks until a backboard could be obtained. Significant visceral and musculoskeletal injury can occur when a swimmer is sandwiched between a downstream boulder or obstruction and the upstream craft that has been exited. Swimmers should always stay upstream of their craft. Many kayakers suffer abrasions and contusions to the fingers and knuckles while hanging upside down after flipping. Oar frames, oars, paddles, and the metal ammunition boxes used to keep supplies dry can all inflict injury when rafts are capsized or paddlers are tossed about in turbulent water. Blisters on the hands are a frequently reported problem in paddling surveys.[45] Kayakers develop them at the metacarpophalangeal (MCP) joint of the thumb along the ulnar aspect. Common sites of blister formation in rafters and canoeists are the proximal palmar surfaces of the MCP joints. Taping and moleskin application reduce the incidence of this potentially incapacitating problem.
INFECTIONS Blisters, abrasions, and lacerations are always at increased risk for infection in an aquatic environment. Maceration from prolonged immersion in water and exposure to atypical pathogens are contributing factors. An outbreak of Staphylococcus aureus skin infections among raft guides in Georgia and South Carolina nearly led to the demise of two rafting companies.[10] Sharp grommets on the thwarts of the rafts had caused repeated lower extremity abrasions. The causative organism was cultured from rafts up to 48 hours after use. Daily raft disinfection enabled the companies to remain in operation. Otitis externa (swimmer's ear) is a common problem among paddlers. Water exposure to the ear canal macerates the epithelium and elevates the normally acidic pH of the canal, predisposing the ear to infection.[12] The bacteria most commonly cultured are Pseudomonas aeruginosa, Proteus vulgaris, and Staphylococcus species. [12] [23] Antibiotic eardrops with or without hydrocortisone are widely available and very useful. Irrigation of the canal with commercially available solutions containing acetic acid and alcohol helps prevent infection by lowering the pH and drying the canal.[23] The drops should be applied after each outing (see Chapter 63 ). Recent publicity given to water contamination by Giardia lamblia has been reinforced by statistics from the Centers for Disease Control and Prevention, which report
Figure 30-16 Giardia lamblia trophozoite seen by methylene blue wet mount staining under oil (1000×). The finding of cysts or trophozoites in a patient with diarrhea is sufficient to make a tentative diagnosis of giardiasis.
Giardia organisms to be the most common pathogenic intestinal parasite in the United States (see Chapter 51 and Chapter 52 ). Giardia cysts abound in mountain streams and rivers once considered to be sources of pristine water ( Figure 30-16 ). They persist in very cold water and have no detectable taste or smell. Rivers are contaminated by animals that defecate in or near the water. Studies by the Wild Animal Disease Center at Colorado State University, Ft. Collins, Colorado, have identified more than 30 animal species as Giardia carriers. Paddlers who travel to foreign countries should seek information on local endemic diseases and relevant prophylactic measures. White-water rafting and kayaking in Third World countries subject paddlers to unusual aquatic-related infections. This is exemplified by a report of schistosomiasis in rafters returning from Ethiopia.[22] Schistosomiasis is endemic in large areas of Africa, South America, and the Caribbean and is transmitted to humans who swim or come into contact with fresh water containing the larval stage. Paddlers who return from endemic regions should be screened with serologic testing, since up to 50% of infections are asymptomatic.[31] Malaria has been reported in rafters returning from New Guinea, and both leptospirosis and hepatitis have stricken kayakers venturing to Costa Rica. [2] In the United States, pulmonary blastomycosis was reported among canoeists in Wisconsin.[7]
ENVIRONMENTAL HAZARDS Although hypothermia is rarely the cause of death among white-water paddlers, hypothermia-induced impairment of judgment and coordination is a significant contributing factor in many fatalities and accidents.[18] [28] [39] [40] [41] The paddling season usually begins in
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early spring when air temperatures are cool and snow melt-swollen rivers run extremely cold. Paddlers with rusty skills are more prone to frequent swims and the effects of cold water immersion. Many rivers, especially in the western United States, are controlled by dams that release water from far beneath the surface and thus remain cold year round. Placing adequate barriers between the human body and the environment and carrying adequate food and waterproof matches are of paramount importance. Another common environmental affliction suffered by paddlers is rhus dermatitis from poison oak or poison ivy. Most cases occur during spring paddling when the vines are potent but the characteristic leaves have not yet appeared. Barrier creams such as StokoGard Outdoor Cream and Tecnu Ivy Shield can be used by individuals highly sensitive to the plants. After plant contact occurs, the oil may be removed from the skin by washing within 30 minutes.[13] A commercial product, Tecnu Oak and Ivy Cleanser, can remove oil from the skin for up to 8 hours after exposure. Any solvent may help remove some of the urushiol oil from the skin. Gasoline, paint thinner, acetone, and rubbing alcohol have all been reported to be effective. Unfortunately, these products can also be irritating to the skin Treatment of rhus dermatitis consists of oral antihistamines and systemic corticosteroids. A 2-week course is needed to prevent recurrence of the rash (see Chapter 47 ).[13] Sunburn and the effects of chronic exposure to solar radiation are compounded by water's ability to reflect up to 100% of ultraviolet radiation (UVR), depending on the time of day. Sand can reflect up to 17% of harmful UVR. Most rivers are situated in mountains, where UVR increases 4% to 5% with each additional 305 m (1000 feet) of altitude.[9] Sunscreens must be applied frequently because they are prone to wash off in the water. Zinc oxide and other barrier creams are more resistant to water and are preferable on areas of intense exposure, such as the nose and lips. Paddlers with fair skin should consider using gloves to protect the hands from UVR exposure. Eye protection from UVR is often overlooked or avoided by paddlers because sunglasses frequently fog while on the river. Application of Dawn dishwashing soap to the lenses prevents fogging for up to 30 minutes. Polarizing lenses reduce glare off the water, but the polarizing feature does not in and of itself filter UVR and infrared radiation. Venomous snakes, especially pit vipers, along with scorpions, spiders, and fire ants, are frequently encountered by river enthusiasts and should be considered potential hazards. Paddlers should know appropriate first-aid measures for envenomations. Paddlers commonly consume wild foliage, which may produce severe illness. In one published report, six rafters were poisoned and one of them died after eating water hemlock, Cicuta douglaslii.[31]
SWIFT WATER RESCUE Time is the most important factor in river rescue and often precludes the use of technical rope-based systems. Experience and an understanding of river dynamics are essential. The most common rescue scenario involves a swimmer who has exited the craft. The victim may be moving downstream at 5 to 10 miles per hour in the middle of a large river. Since the dynamic nature of swift water does not often allow time for a shore-based rescue system to be established, many white-water rescues are made from a raft, canoe, or kayak. Rafts should stay close together in rapids to render mutual aid. Throw bags can be used directly from the raft to rescue swimmers, or the victim may often be reached with an outstretched arm and a paddle. A swimmer should be pulled back into the raft by grabbing the shoulder straps on his or her life jacket and then leaning backward into the raft to pull the person in. The swimmer can assist by pulling up on the frame, D-ring, or hand line as he or she is being pulled in. Kayaks can be used to rescue swimmers in midcurrent. The kayak is also an excellent platform to provide additional flotation for a swimmer who is trying to maintain freeboard in rough water. The most common method of rescuing swimmers with kayaks is to have them grab the bow or stern "grab loop" of the boat and then tow them to safety. The loop is usually sized so that it is easy to grab yet will not admit an adult-sized hand. The swimmer can also grab onto the back of the cockpit rim and pull his or her torso onto the back deck. This gets the swimmer out of the cold water and reduces the likelihood of injury from rocks. Boogie Boards originally developed for use in the ocean surf have been modified for rescue use on rivers. Rescue Boards are larger and come with two sets of handles—one for the rescuer and one for the victim. The boards add a substantial amount of flotation to a rescue swimmer and, when used with swim fins, can provide a maneuverable platform for reaching and picking up a victim. The latest craft to be adapted to swift-water rescue is the personal watercraft, or Jet Ski. Introduced in 1987, these machines have become increasingly popular with professional rescue agencies. Since they lack an exposed propeller, personal watercraft are safe for swimmers and can negotiate shallow rivers. They can be maneuvered upstream in rapids, and turn within a short radius. Newer versions, adapted for rescue, can tow a backboard or litter device behind them and are quite stable. Rescue from entrapment requires a higher level of skill and often presents greater potential risk to the
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Figure 30-17 Strong swimmer rescue.
rescuer. The method used depends on whether the victim can maintain adequate freeboard. If the entrapment site is accessible, direct contact with the victim is quickest and most effective. A rescuer may wade to the entrapment site or reach it by boat if there is a stable site to exit the craft. When wading, the rescuer should use a paddle for support. Start by facing upstream, with legs slightly wider than shoulder width. Reach out, turn the paddle blade parallel to the current, and plunge it into the water. Just before the blade hits bottom, turn it sideways to the current. The force of the onrushing water will pin it to the bottom. The paddle and your two legs form a tripod, which is more stable than your legs alone. Move slowly across the current, facing upstream, moving only one of these three points at a time. The river downstream should be scouted for hazards before entering and, if possible, a rope thrower should be stationed downstream in the event the rescuer loses footing. A strong swimmer rescue is the next quickest method but entails significant risk to the rescuer ( Figure 30-17 ). The rescuer is tethered to a rope that provides added stability against the force of the current. If a quick-release harness is not available, a loose loop of rope can be passed under the rescuer's armpits. A tag line rescue should be considered if the victim cannot be reached directly. A tag line is a rope stretched across the river downstream that is then brought upstream to the victim ( Figure 30-18 ). Getting the line across the river sometimes constitutes an insurmountable obstacle. If the river is narrow, it may be possible to throw the line across. Otherwise, it can be ferried across by a boat or team of swimmers. During a ferry, as much of the rope as possible should be kept out of the water to avoid drag.
Figure 30-18 Tag line.
Figure 30-19 Two throw bags connected with a carabiner to make a tag line.
There are two types of tag lines ( Figure 30-19 ). A floating tag line has a life jacket or some other flotation device attached to the middle to keep the rope on the surface, which helps support the victim. A snag tag is a weighted line submerged and walked upstream to
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Figure 30-20 Submerged snag tag.
snare a foot or other body part that has been trapped under the surface. A snag tag can be made by joining together two throw bags filled with rocks ( Figure 30-20 ).
References 1.
Allan JR, Elliot DH, Hayes PA: The thermal performance of partial coverage wet suits, Aviat Space Environ Med 57:1056, 1986.
2.
Backer H: Malaria in returned travelers, Wilderness Med 4:11, 1987.
3.
Bechdel L, Ray S: River rescue, Boston, 1989, Appalachian Mountain Club Books.
4.
Brody AJ, Mitchell C, Springer M: Submersion injury complicated by hyperthermia in a kayaker wearing a dry suit, J Wilderness Med 4:198, 1993.
5.
Burrell CL, Burrell R: Injuries in whitewater paddling, Physician Sports Med 10:119, 1982.
6.
Canoe Magazine, Canoe America Associates, Kirkland, Wash, Dec 1993.
7.
Centers for Disease Control: Blastomycosis in canoeists—Wisconsin, MMWR 29:450, 1979.
8.
Cooper KE, Martins S, Riben P: Respiratory and other responses of subjects immersed in cold water, J Appl Physiol 40:903, 1976.
9.
Daniels F: Physical factors in sun exposure, Arch Dermatol 85:98, 1962.
10.
Decker MD et al: An outbreak of staphylococcal skin infections among river rafting guides, Am J Epidemiol 124:969, 1986.
11.
Dutkly P: A simple method of treating shoulder dislocations for the whitewater enthusiast, Wilderness Med 5:9, 1988.
12.
Ellison RT III, Zimner SH: Infectious disease emergencies. In Kravis TC et al, editors: Emergency medicine: a comprehensive review, ed 3, New York 1993, Raven Press.
13.
Epstein WL: Plant-induced dermatitis, Ann Emerg Med 16:950, 1987.
14.
Fraser RE: Paddling precautions advised, Physician Sports Med 10:16, 1982.
Girten TR, Wehr SE: An evaluation of the high-water performance characteristics of personal flotation devices, USCG Report, USCG-M-84-1 (167/4), Springfield, Va, 1984, National Technical Information Service. 15.
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Golden FS, Golden C: Problems of immersion, Br J Hosp Med 45:371, 1980.
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Goldman RF et al: Wet versus dry suit approaches to water immersion protective clothing, Aviat Space Environ Med 37:485, 1966.
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Harwett RM, Bijlani MG: The involvement of cold water in recreational boating fatalities. I, Accid Anal Prevent 14:147, 1982.
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Hayward JS: The physiology of immersion hypothermia. In Pozos RS, Wittmers LE, editors: The nature and treatment of hypothermia, Minneapolis, 1983, University of Minnesota Press.
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Hayward JS, Eckerson JD: Physiological responses and survival time prediction for humans in ice water, Aviat Space Environ Med 55:206, 1984.
21.
Hayward JS et al: Temperature effect on the human dive response in relation to coldwater near drowning, J Appl Physiol 56:202, 1984.
22.
Istre GR et al: Acute schistosomiasis among Americans rafting the Omo River, Ethiopia, JAMA 251:508, 1984.
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Jenkins BH: Treatment of otitis externa and swimmer's ear, JAMA 175:402, 1961.
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Jennings AK: Whitewater, wildwater, Royal Oak Press, 1981, West Virginia.
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Keatinge WR, Evans M: The respiratory and cardiovascular response to immersion in coldwater, Q J Exp Physiol 46:83, 1961.
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Keatinge WR, Hayward MG: Sudden death in coldwater and ventricular arrhythmia, J Forensic Sci 16:459, 1981.
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Keatinge WR et al: The effects of work and clothing on the maintenance of the body temperature in water, Q J Exp Physiol 46:69, 1961.
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Keatinge WR et al: Sudden failure of swimming in coldwater, BMJ 1:480, 1969.
29.
Kizer KW: Medical aspects of whitewater kayaking, Physician Sports Med 15:128, 1987.
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Kizer KW: Medical problems in whitewater sports, Clin Sports Med 6:663, 1987.
31.
Kizer KW: Whitewater medicine, Emerg Med Clin North Am 29:91, 1987.
32.
Mayer PJ: Helping your patients avert canoe and kayak injuries, J Musculoskel Med 4:31, 1987.
33.
McNamara RM: Reduction of anterior shoulder dislocations by scapular manipulation, Ann Emerg Med 21:1140, 1993.
34.
National Sporting Goods Association survey, Bellevue, Wash, 1989, GMA Research.
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Participation in sports activities by selected characteristics: 1990, Mount Prospect, Ill, 1990, National Sporting Goods Association.
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Reibel GD, McCabe J: Anterior shoulder dislocation: a review of reduction techniques, Am J Emerg Med 9:180, 1991.
37.
Serra JB: Management of trauma in the wilderness environment, Emerg Med Clin North Am 2:3, 1984.
38.
Steinman AM, Hayward JS: Coldwater immersion. In Auerbach PS, Geehr EC, editors: Management of wilderness and environmental emergencies, St Louis, 1989, Mosby.
39.
Walbridge CW, editor: Best of the river safety task force newsletter, 1976–1982, Lorton, Va, 1983, American Canoe Association.
40.
Walbridge CW, editor: River safety report, 1982–1985, Lorton, Va, 1986, American Canoe Association.
41.
Walbridge CW, editor: River safety report, 1986–1988, Lorton, Va, 1989, American Canoe Association.
42.
Walbridge CW, editor: Safety code of the American Whitewater Affiliation, Phoenicia, NY, 1989, American Whitewater Affiliation.
43.
Walbridge CW, editor: River safety report, 1989–1991, Lorton, Va, 1992, American Canoe Association.
44.
Wallace D: Scary numbers and statistics—results of AWA close calls and serious injuries survey, AWA J 3–4:27, 1991.
45.
Weiss EA: Whitewater medicine, J Wilderness Med 2:245, 1991.
46.
Whisman SA, Hollenhorst SJ: Injuries in commercial whitewater rafting, Clin J Sport Med 9:18, 1999.
47.
Wilkerson JA, Bangs CC, Haward JS: Hypothermia, frostbite and other cold injuries, Seattle, 1986, The Mountaineers.
APPENDIX: White-Water First-Aid Kits The following variables should be considered when designing a white-water first-aid kit: remoteness and accessibility of the river, Third World travel conditions, the number of people the kit will need to support, preexisting medical conditions; and space and weight restrictions. When assembling a kit, the following components are generally recommended for rafting and kayaking: Rafting Kit Waterproof dry bag or Pelican box Cardiopulmonary resuscitation mouth shield (CPR-Microshield) Hypothermia/hyperthermia thermometer Bandage scissors Fine-point tweezers or forceps Temporary dental filling (Cavit) Glutose paste Irrigation syringe with 18-gauge catheter Povidone-iodine solution 3M surgical stapler (1 stapler holds 25 staples) Dermabond tissue glue Wound closure strips (Steri-Strips) Tincture of benzoin Polysporin ointment Moleskin Latex or non-latex (hypoallergenic) gloves Antiseptic towelettes Safety pins Waterproof matches Accident report form and pencil Large garbage bag 4 × 4-inch sterile dressings 8 × 10-inch trauma pad or Bloodstopper dressing Eye pads Nonadherent dressing (Xeroform or Aquaphor) Triangular bandage 3-inch conforming gauze bandage 3-inch elastic bandage with Velcro closure 1-inch × 10-yard surgical tape Duct tape (can be wrapped around the paddle shaft) Strip and knuckle bandages Cotton-tipped applicators Aloe vera gel Diphenhydramine capsules Cortisone cream Acetaminophen tablets Ibuprofen tablets Eardrops Prophylactic eardrops (mixture of rubbing alcohol and white vinegar) Treatment eardrops (Cortisporin Otic Suspension) Epinephrine injectable or EpiPen Prochlorperazine suppository Diazepam or midazolam
Oxycodone Oxymetazoline (Afrin) nasal spray Antibiotics (trimethoprim/sulfamethoxazole, ciprofloxacin, cephalexin)
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Sunscreen (sun protection factor [SPF] 15 or higher) Insect repellent Iodine tablets Tampons Tea bags
Kayaking Kit Waterproof dry bag or small Pelican box Cardiopulmonary resuscitation mouth shield Hypothermia/hyperthermia thermometer Scissors Fine-point tweezers or forceps Small surgical stapler (3M) or Dermabond Glue Wound closure strips Tincture of benzoin Polysporin ointment Latex or non-latex (hypoallergenic) gloves Antiseptic towelettes Safety pins Waterproof matches Accident report form and pencil 3 × 3-inch sterile dressings Nonadherent dressings 2-inch conforming gauze bandage Duct tape Strip and knuckle bandages Cotton-tipped applicators Diphenhydramine Acetaminophen Ibuprofen Prophylactic eardrops Epinephrine Prochlorperazine suppository Diazepam or midazolam Oxycodone Sunscreen Insect repellent Iodine tablets
APPENDIX: Universal River Signals Stop: Potential hazard ahead. Wait for "all clear" signal before proceeding. Form a horizontal bar with your outstretched arms. Those seeing the signal should pass it back to others in the party. ( Figure 30-21 .) Help/Emergency: Assist the signaler as quickly as possible. Give three long blasts on a whistle while waving a paddle over your head. ( Figure 30-22 .) All Clear: Come ahead (in the absence of other directions, proceed down the center). Form a vertical bar with your paddle or one arm held high above your head. Paddle blade should be turned flat for maximum visibility. To signal direction or a preferred course through a rapid around an obstruction, lower the previously vertical "all clear" by 45 degrees toward
Figure 30-21 Stop signal.
Figure 30-22 Help/emergency signal.
Figure 30-23 All clear signal.
the side of the river with the preferred route. Never point toward the obstacle you wish to avoid. ( Figure 30-23 .)
APPENDIX: Organizations American Canoe Association (ACA) 7432 Alban Station Boulevard Suite B-226 Springfield, VA 22150-2311 American Whitewater Affiliation (AWA) P.O. Box 85 Phoenicia, NY 12464 Chinook Medical Gear P.O. Box 1736 Edwards Business Center B11 Edwards, CO 81632
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Rescue 3 P.O. Box 4686 Sonora, CA 95370 Safety Deck System Outdoor Safety Systems 140 Quaker Road Princeton, NJ 08540 National Organization for River Sports Box 6847 Colorado Springs, CO 80904
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Chapter 31 - Cave Rescue Steve Hudson Loui H. Clem
A cave can be one of the most hostile environments a rescuer can enter. Not only must a cave rescuer be adept at managing the unique challenges of functioning in the cave environment, he or she must also manage a unique set of rescue problems relating to rescuer safety, equipment, logistics, access and extrication, and mission support. A cave rescue should never be undertaken without qualified cave rescuers on scene. In addition, the incident commander must be familiar with or seek the advice of someone who is familiar with the unique challenges of the cave environment. The time to learn about caving is not as a medic on a cave rescue. If there is any chance that you will encounter a cave rescue as part of your profession or avocation, time spent familiarizing yourself with caves and caving techniques may be lifesaving.
ENVIRONMENT Any natural opening in the earth large enough to enter is considered a cave. Human-made mines and tunnels are not caves. Although these often seem similar to caves, their entry often requires special skills and equipment different from those for caves. Caves take many forms, including sinkholes, cracks, sumps, siphons, springs, pits, and caverns. Caves are formidable places, dark and dangerous. Running, seeping, or standing water originally formed most caves, so water is a major part of many cave environments. As caves become less active hydrologically, they may dry up. Some caves are so dry that dust induces respiratory problems in visitors. Temperature extremes are likely. Caves tend to be at the mean ground temperature of the area. For the most part, U.S. continental caves run from cool to cold. Very warm climates sport warm caves, whereas alpine mountain caves measure close to freezing temperatures and may even contain ice. Tropical and desert caves can be so hot that cavers must wear lightweight garments to explore, but more common is the problem of hypothermia from sitting around underground waiting for the next assignment or struggling in cold and wet passages. It is not uncommon to be supine or prone in 4-inch deep, 13° C (55° F) water with one's back pressed against cold rock, facing a stiff breeze. Caves can be fragile, often heavily decorated with mineral formations that have formed over thousands of years. Cavers try to protect these formations whenever possible by avoiding walking on or touching delicate areas or otherwise altering the cave. Even the natural oils rubbed off of human hands can alter growth of an active formation. The caver's motto, "leave nothing but footprints, take nothing but pictures, and kill nothing but time," extends to rescue operations. Everything brought in must be packed out at the end of the operation. An abandoned flashlight battery can leach its chemicals and poison the cave-adapted life-forms found in a cave passage.
PERSONAL SAFETY Whether entering a cave for exploration or for rescue purposes, personal gear requirements are tailored to caving. Clothing should be appropriate to the environment. Caves can be wet, dry, dusty, cold, warm, or a combination of these. Wind can exist in passages because of temperature and pressure differentials between the cave and the outside air, and chill factor becomes a significant consideration. Undergarments should provide the necessary thermal layers, while outerwear provides a protective barrier against the elements. A mountaineering type of helmet, with a nonelastic "three point" chin strap that keeps it planted properly on the head, is a must. The helmet protects against impact with the hard and often sharp rock of cave ceilings and walls in tight or low passages and offers rockfall protection. It is also a convenient mounting platform for the required light source. It takes only one episode of trying to navigate in the complete darkness underground to understand why no fewer than three light sources should be carried by each person in a cave. Rescuers underground without functioning lights become other subjects to be rescued. Electric lights are preferred, but carbide lamps may also be used. At least two of these lights should be helmet mountable for hands-free operation, each with sufficient "burn time" capacity or spare batteries to travel in and out of the cave. If carbide lamps are used, care should be taken when working close to victims because it is easy in tight spots to forget that the light on your head is an open flame that can quickly burn anything with which it comes in contact. For this reason, most cave rescuers prefer electric lights. Many cavers find gloves useful for both thermal insulation and protection against sharp rocks and sticky
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mud. If the cave has vertical components, leather-palmed gloves are necessary for rope work. Cave mud is slippery and adheres to everything. It makes walking and scrambling through a cave dangerous. Lug sole boots provide the best traction, and stiff leather uppers help protect feet against sharp rocks. For small passages or "crawlways," a set of durable kneepads is a wise adjunct. As in any remote environment, the caver should be self-sufficient and able to care for at least himself for an extended period. This requires replacement batteries or carbide, fresh water for drinking, food for energy, a basic first-aid kit, and extra insulation, such as extra thermal layers and a hat that can be worn under the helmet. Cavers often store a folded trash bag in the suspension of their helmets, to be used as an emergency shelter from wind and water, among other possibilities. An additional challenge for the extended cave visit is the requirement to pack out whatever is packed in, including human waste. Strong, leak-proof plastic containers are useful for that purpose. Use a small, durable pack to carry extra gear. Carry what is needed and no more. Keep in mind that the pack will be alternately carried, pulled, pushed, and dragged through cave passages of different sizes, so things such as straps and external attachments will become an impediment to maneuverability. Not all caves have vertical drops, but for those that do—or when in doubt—carry a lightweight seat and chest harness, rack or figure-8 descender, and an ascending system. One or two 20-foot sections of 1-inch tubular webbing come in handy for an extra step-up or to construct a quick belay or hand line.
EQUIPMENT The amount of equipment used during a cave rescue is prodigious. Each person entering the cave must have at least the minimum complement of personal gear. Ropes and hardware are utilized nearly as quickly as they can be produced; items that are difficult to find, such as hard-wired field-phones or cave radio systems, become necessities. Ropes used underground are usually of the static kernmantle variety. The tougher the sheath, the better the rope. Adequate carabiners, anchor materials, and other hardware should be available for rigging. If multiple locations must be rigged for raising, lowering, or traversing, the best possible scenario is to have enough gear to rig each site individually. Having to derig a system, sort the gear, carry it past the proceeding litter, and rerig another system can be time consuming and a recipe for disaster. Even a small cave might require multiple sites rigged for safe patient extrication. Prebagged packages of gear for specific common rigging tasks are often useful. Include anchor webbing, ample carabiners, pulleys, prussiks, belay devices, lowering devices, and rope grabs as required to set up one site per bag. Although most cave evacuations require litter transport, evaluate the situation carefully to determine whether a litter is really necessary. A properly stabilized "walking wounded" caver can be helped out of a cave in short time and with little manpower. Put that same person into a litter, and the number of rescuers and hours to the hospital goes up exponentially! If litter transport is deemed necessary, the next difficult decision is which litter (or litters) to use. On any given evacuation, this selection requires a fine balance of requirements. Maneuvering a bulky litter through narrow cave passages can be a challenging proposition. In larger caves, or where a vertical raise is required, basket litters are the best choice. Plastic-bottomed versions are preferable over steel and mesh versions, allowing the option of dragging the litter where necessary. In tighter caves, drag-sheet types of litters, such as the wraparound Sked, provide low-profile advantages but are less comfortable and protective for the victim. Occasionally, a cave is so restrictive that even the length of such a litter is problematic, and a short board, such as a KED or OSS, is the only alternative. It is not unheard of to begin the carry in a tight section of a cave using a OSS, add a Sked once the passage opens up a bit, drop the Sked into a full basket litter for ease of carrying in a large walking passage, then drop all the way back to the OSS to negotiate a tight entrance passage. When choosing a litter and victim packaging, take comfort into account. Although rescuers are working up a sweat, the victim lying in the litter can be extremely cold. Thermal layers are a necessity and include a sleeping bag, vapor barrier, and moisture barrier to keep the victim dry. The victim should have adequate head and face protection and, if the environment will become vertical at any point, a harness. Anticipate transport time; evacuation can take days, so extra warmth and padding may be needed. A reasonable first-aid kit should contain writing materials for recording victim condition, basic medications, airway management tools, bandages, cervical collars, and splints. Sealing each item in plastic helps keep out cave grit, and the entire kit can be packaged in a largemouth bottle or other watertight, durable container. Because of extended times involved in reporting caving accidents and responding to and accessing injured cavers, most victims are either very stable or dead. The upshot is that advanced life support (ALS) skills and equipment are generally not required. Dragging a defibrillator into the cave with your first-aid kit is for the most part unjustified. This is fortunate, since the effect of cave mud and water would render all but the sturdiest military models ineffective. Newer semiautomatic defibrillators may fare better.
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The cave environment is no more friendly to even simple interventions such as intravenous (IV) infusions. In most cases, hanging a gravity-operated IV is not an option, so positive pressure infusion methods must be used. Further, consideration must be given to methods for keeping the insertion point clean, and care taken not to interrupt flow while negotiating tight passageways.
LOGISTICS Logistics of an underground rescue are complicated at best and a nightmare if not managed well. Lack of easy communication, limited access, extended time, and difficulty in obtaining rest for teams all contribute to complexity. Communication is essential to keep rescuers from becoming lost, to issue instructions, and to distribute nutrition. Various hard-wired field-phone systems are available for use in cave rescue, but generally only well-established teams have access to these. A relatively new development is the availability of special low-frequency cave radios that can transmit voice through dense rock and soil. Without such systems, message runners are indispensable. A group of swift, agile, safe, and well-trained cavers—and a method for keeping them rested and nourished—is invaluable. A team of rescuers sent into a known location can take hours or most of a day to reach the victim. It is logistically impractical for these rescuers to carry sleeping bags and food to allow rest and recovery before starting their work assignment. Keeping rescuers rested, fed, watered, and warm many hours away through a challenging cave rescue requires an incident management team that can predict the needs of the underground workers hours before they themselves realize the need. Whether or not a communication system is available, establishment of a control point at or near the cave entrance(s) is critical. Entrance control should be established as soon as rescuers arrive at the cave. All personnel and equipment entering or leaving the cave should be recorded into a log kept by entrance control. This log becomes invaluable hours later to determine when teams should be replaced, if someone is still in the cave, and who carried in what piece of missing vital gear. The Incident Command System (see Chapter 24 ), or a modified version of it, provides the best framework for managing cave rescue personnel, by performing required functions while maintaining a reasonable span of control. Generally, the functions required on a cave rescue are similar to those required on any other rescue, although the specific means of accomplishing the functions will vary. There should always be one person in command of an operation. This is the foundation of creating accountability and organization, which are the keys to efficiency and safety. The incident commander assesses the incident, activates resources, determines the strategy, and approves the plan for the operation. Other functions vital to success are planning, operations, logistics, and finance. The incident commander may have one or more people to assist, or he or she may be responsible for several of these functions. Someone must plan strategies, supervise the operation, take care of the physical needs of the rescuers and the required equipment, and track the resources used.
CAVE ACCESS Gaining access to the caver victim is a matter of overcoming an array of obstructions inherent in the cave. Merely to move a few hundred feet through a cave might require rappelling, crawling on one's belly, and squeezing through cracks in the rocks while dragging equipment, climbing over large rocks, swimming, and slithering through mud. The total darkness of a cave is confining to some, and even this simple matter can quickly become a major obstacle. Noncaver responders may have psychologic inhibitions, such as fear of the dark or confined spaces. In no case should a rescuer ever be pushed beyond his or her comfort level in accessing a victim. Claustrophobia can cause panic and severe dysfunctional behavior. Other factors inherent to the cave include temperature variables, wetness, and restrictive cave passages. Certain large or weak personnel and/or bulky and heavy equipment might be physically incapable of getting through these tight spaces. If the cave rescue requires raising or lowering a victim, or traversing the victim over horizontal rope lines, persons skilled in cave rigging should be responsible for building the systems. Rigging in caves is an art because of anchoring difficulties, directional changes, tight squeezes, and minimal working surface. Details on cave rigging and professional training can be acquired through the National Cave Rescue Commission, a nonprofit organization that teaches courses in cave rescue techniques and management. Many vertical drops in caves are overhung at the top, preventing the caver access to a wall while descending and ascending the rope. In cases where the roped drop has the rope running against a wall, it can be advantageous to place anchors at points throughout the length of the drop. This "rebelay" method allows multiple people to ascend/descend simultaneously, lessens rope wear points, and provides the added safety of having a shorter rope length to protect for each anchor. Practice at crossing rebelays is essential before attempting to enter a cave thus rigged. The caver must be able to essentially transfer from one free-hanging rope to another while hanging in midair. This is easy to do with the correct
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equipment setup and practice but not so easy when the technique is tried for the first time underground on the way to a medical emergency. Usually, single rope techniques are used, especially where a free-hanging drop is involved. This means that just one rope is put over the side for the rescuer to ascend or descend. The use of an additional belay line not only requires additional personnel but might prove more hazardous if the two lines become entangled. In the United States, the most common cave ascending systems are the Mitchell system and various renditions of the ropewalker system. These are both efficient means of ascending and can easily be mastered with practice. The frog system, popular in other countries, requires more climbing effort but is easier to use when ascending past rebelays in the system. It is imperative that an ascending system be fitted to the user. Some rigs work better for tall, lean frames, and others work best for heavier body types. All rescue personnel entering a vertical cave should have their own personally fitted rope climbing system and must have practiced climbing in that system in a safe practice area. Large holes or boulder slopes inside the cave may best be negotiated by using a highline traverse. Highlines often require great amounts of time to set up properly but can shave away hours of litter movement time by passing above difficult cave terrain that otherwise would present many challenges for a litter carried by hand. Use of a highline is most practical when it is known in advance that there will be sufficient time for rigging. The decision to take the time to rig a traverse should be made based on these three factors: the time it will take to move the victim to the obstacle you want to be traversed, the time necessary to rig the highline, and the time that will be saved by using the highline to move the victim over the obstacle.
HAZARDOUS ATMOSPHERES One often-overlooked hazard to cavers is the ambient atmosphere. Most caves in the United States breathe naturally either from changes in barometric pressure or from the chimney effect of multiple entrances. Some caves have small rooms that have so little airflow that a few cavers can quickly consume most of the oxygen. Buildup of gases CO, CO2 , methane, and/or hydrogen sulfide is not uncommon in caves. Instances of gasoline seeping into caves from underground storage tanks have been recorded. If poor air quality is suspected, use of an air monitoring device is essential. It is possible to enter a cave containing high levels of unhealthy gases, but only with appropriate caution. In such cases, it is advisable to solicit participation of the local hazardous materials emergency response team. With the assistance of a hazardous materials or confined space rescue team, "bad air" in caves can be mitigated in several ways. One way is to release compressed air into the cave, forcing good air in and bad air out. Success of this method is limited, and because of the massive amounts of air in a cave, this method is slow at best. If this method is used, entrants should carry an air monitor, since "pockets" of bad air may remain trapped in parts of the cave. Another option is to release oxygen into the cave. Although this can speed the air exchange process somewhat, it has its own disadvantages. In addition to being difficult to accomplish, it is possible to elevate the oxygen level in the cave to that of deleterious combustion. Exhaust fans offer a reasonable method, although care must be taken to prevent generator exhaust from entering the cave. If necessary, rescuers can be equipped for entry with surface-supplied air with bail-out bottles, self-contained breathing apparatus, or rebreathers. Each of these has advantages and disadvantages, but all are difficult to manage in the cave environment and thus should be avoided if possible. Pre-event training and practice in the safe use of any of this equipment is imperative before entering an atmosphere that is hazardous for breathing. Other airborne hazards, such as histoplasmosis and rabies, are not detectable by air monitor. If these hazards are suspected, no rescuer should enter the environment without an appropriate filter mask and other personal protective equipment. Water and caves are usually closely associated. Created by water, caves are a natural deposit for overflow or drainage from a variety of sources. Many caves can flood with little or no warning, and a recreational caver or rescuer caught in a flooding cave is in mortal danger. Flooding is usually associated with heavy rains, which can cause diffuse seepage over a large area of the cave or a high flow into sinkholes. Occasionally, sinking streams can carry floodwater. In some parts of the world, entire rivers disappear underground, flow through caves, and resurface miles away. A flood crest from many miles upstream can pass through these caves without warning. Flood-prone caves are generally identifiable by their makeup. Cave walls coated with thick mud can be an indication that flooding is not unusual in that section of the cave, and extra caution is warranted. Bedrock cave walls with gravel deposits at key points in the cave, and debris lodged in the ceiling can also be warning signs. Becoming trapped in a flooding cave is not desirable, but it is survivable. If possible, find a high point in a wide passage, downstream of any major constriction, and wait out the flood. It is also possible, with enough advance warning, to remove a sediment dam downstream that may otherwise cause water to back up into your "safety zone." It is seldom wise to attempt to swim, either upstream or down.
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For a rescuer called to assist cavers trapped in a flooded cave, entering the torrent is not wise. If the location of the trapped victims is known, it may be possible to use (or make) another entrance from which to evacuate them. If entry through the main entrance is necessary, it is imperative that the water level be controlled before entry. Methods of accomplishing this goal vary depending on the situation. Often, it may be enough to simply wait out the flood and let the water level subside naturally. If the water level is still on the rise, however, or if the source remains constant, additional measures may be warranted. Keep in mind that water is a powerful force, and any plan should be engineered by professionals. One of the simplest diversion methods is to broaden the flood crest so that less of it flows into the cave. Water can be diverted using sandbags, hay bales, or dirt or by digging channels. If this is not possible or feasible, one may be able to lower the water level by digging through debris downstream, thereby expediting the exit. Pumping is also an option, although the hazards inherent in this method should be evaluated closely beforehand. Entering a flooded cave with scuba equipment is a dangerous, last-resort method that should only be attempted by certified cave divers. A scuba entry may be justified if cavers are known to have been entrapped for an extended period of time, if there is a known medical emergency, or if the cave is completely flooded. In these cases, it may be advisable for certified cave divers to enter and assess the condition of entrapped persons, transport survival supplies, or provide medical assistance. Only in the most dire circumstance is it justified to attempt to transport a victim through a flooded passage. At a minimum, a scuba entry requires two to three divers, as well as a backup diver. Diving is gear intensive and requires an air compressor, extra tanks, 110-volt electricity to charge dive lights, underwater communications equipment, waterproof bags, full face masks for subjects, water rescue suits, underwater strobe lights, transport cases, and surface personnel to assist with transporting equipment.
VICTIM CARE As with many remote accidents, the time it takes to report, respond to, and access a caving accident usually means that the victim, if alive, is relatively stable. Although this generalization has exceptions, the treatment issues faced by most rescuers are related to extended transportation times. Data obtained in American Caving Accidents indicate that the leading cause of caving injury is falls, and that hypothermia, fractures, and head injuries top the list of complaints. Unfortunately, spinal injury is invariably present, and this can compound the transportation challenge. The approach to medical care should be similar to any other medical situation, with one notable difference: the victim has suffered an acute injury but will be confined for transport for an extended period. Care, then, will be a combination of acute emergency responses adapted for a victim who is, for all practical purposes, bedridden. Once the victim has been stabilized and packaged, the assessment process should continue throughout the evacuation. It is best if one medical person can stay with and monitor the victim throughout the evacuation. Hypovolemia is a common complaint, so establishing an IV early in the intervention can be useful. Take measures to ensure that rescuers will be able to maintain IV access and manage the supplies throughout the evacuation, and infuse only fluids not contraindicated by head or other injury. If the victim is alert and oriented, fluid administration will increase the need to urinate, so take this into consideration. As best as possible, maintain communication with the victim, encouraging him or her to flex muscles to maintain good circulation. Allow the victim to assist in care as much as possible. Availability of ALS and drug therapy is useful on extended transports, so it is helpful to have strong rapport with the local medical authorities should complex treatment become necessary.
CONCLUSION Never underestimate a cave rescue. Caves are unique environments, and entry should not be attempted without appropriate technical training and preparation. The advantage to any rescue group of establishing a good working relationship with local cavers cannot be overemphasized. These are the persons with knowledge of the caves; with the training, equipment, and experience to handle the obstacles and the environment; and who already feel at ease underground. They could prove to be your most valuable resource for a successful cave rescue. Many cavers have taken extensive training in cave rescue techniques and are members of organized cave and cliff rescue teams. The first step to finding cavers is to contact a local chapter, or "grotto," of the National Speleological Society, the largest cave exploration, education and science-oriented organization in the United States. Contact them at: National Speleological Society 2813 Cave Avenue Huntsville, AL 35810
[email protected] http://www.caves.org/
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Given the unique underground environmental and topographic conditions, nothing can replace formal training in cave rescue techniques and specific cave rescue problems and solutions. Persons interested in enhancing their training should get in touch with the National Cave Rescue Commission (NCRC). The NCRC conducts week-long cave rescue seminars and weekend orientations across the United States. Contact them at the address above as the National Cave Rescue Commission of the National Speleological Society or at: http://www.caves.org/io/ncrc/
Suggested Readings Hudson S, editor: Manual of U.S. cave rescue techniques, ed 2, Huntsville, Ala, 1988, National Speleological Society. Putnam W, editor: American caving accidents, published annually, Huntsville, Ala, National Speleological Society.
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Part 6 - Insects, Animals, and Zoonoses
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Chapter 32 - Protection from Blood-Feeding Arthropods Mark S. Fradin
BLOOD-FEEDING ARTHROPODS Of all the hazards, large and small, that may befall the outdoor enthusiast, perhaps the most vexatious comes from the smallest perils—blood-feeding arthropods. Mosquitoes, flies, fleas, mites, midges, chiggers, and ticks all readily bite humans. The resulting bites may, at best, result only in minor annoyance; at worst, arthropod bites may transmit to humans multiple bacterial, viral, protozoan, parasitic, and rickettsial infections ( Box 32-1 ). Mosquito-transmitted diseases alone will be responsible for the deaths of one out of every 17 people currently alive.[108] This chapter reviews the arthropod species that bite humans and discusses various options for personal protection against nefarious insects. Mosquitoes (Family Culicidae) Mosquitoes are responsible for more insect bites than any other blood-sucking organism. Mosquitoes are found all over the world, except in Antarctica. These two-winged insects belong to the order Diptera. There are 170 species of mosquitoes in North America and more than 3000 species worldwide. Anopheline, or malaria-transmitting, mosquitoes can be distinguished by their resting position on the skin, characteristically appearing with the bodies raised high, almost as if standing on their heads. Most other species, in contrast, rest with their bodies parallel to the skin surface ( Figure 32-1, A ). Mosquitoes vector more diseases to humans than do any other blood-feeding arthropod. Mosquitoes transmit malaria to 300 to 500 million people each year, resulting in as many as 3 million deaths per year.[99] They vector multiple arboviruses to humans, including several forms of encephalitis, epidemic polyarthritis, yellow fever, and dengue fever (see Chapter 66 ). Mosquitoes also transmit the larval form of the nematode that causes lymphatic filariasis. Only female mosquitoes bite, requiring a blood-protein meal for egg production. Male mosquitoes feed solely on plant juices and flower nectar. Mosquitoes feed every 3 to 4 days, consuming up to their own weight in blood with each feeding. Certain species of mosquitoes prefer to feed at twilight or nighttime; others (such as the aggressive Asian tiger mosquito, Aedes albopictus) bite mostly during the day. Some mosquito species are zoophilic (preferring to feed on animals, including birds, reptiles, mammals, and amphibians), whereas others are anthropophilic (preferring human blood). Members of the genera Anopheles, Culex, and Aedes are the most common biters of humans. In some mosquitoes, seasonal switching of hosts provides a mechanism for transmitting disease from animal to human. Mosquitoes rely on visual, thermal, and olfactory stimuli to help them locate a blood meal.[5] [6] [12] [18] [38] [49] For mosquitoes that feed during the daytime, host movement and dark-colored clothing may initiate orientation towards an individual. Visual stimuli appear to be important for in-flight orientation, particularly over long ranges, whereas olfactory stimuli become more important as a mosquito nears its host. Carbon dioxide and lactic acid are the best-studied attractants. Carbon dioxide serves as a long-range attractant, luring mosquitoes at distances of up to 36 m (118 feet).[36] [37] [102] At close range, skin warmth and moisture serve as attractants.[5] [12] Volatile compounds, derived from sebum, eccrine and apocrine sweat, and/or the cutaneous microflora bacterial action on these secretions, may also act as chemoattractants. [55] [69] [95] Floral fragrances found in perfumes, lotions, soaps, and hair-care products can also lure mosquitoes.[30] There can be significant variability in the attractiveness of different individuals to the same or different species of mosquitoes.[15] [50] Men tend to be bitten more readily than women, and adults are more likely to be bitten than children.[50] [73] Heavyset people are more likely to attract mosquitoes, perhaps because of their greater relative heat or carbon dioxide output. [83] During the day, mosquitoes tend to rest in cool, dark areas, such as on dense vegetation, or in hollow logs, tree stumps, animal burrows, and caves. To complete their life cycle, mosquitoes also require standing water, which may be found in tree holes, woodland pools, marshes, or puddles. To minimize the chances of being bitten by mosquitoes, campsites should ideally be situated as far away from these sites as possible. Blackflies (Family Simuliidae) At 2 to 5 mm in length, blackflies[3] [8] [21] [39] [48] ( Figure 32-1, B ) are smaller than mosquitoes. They have short antennae, stout humpbacked bodies, and broad wings. Blackflies are found worldwide. The adults are most prevalent in late spring and early summer and are most likely encountered
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near fast-running, clear rivers or streams, which they require to complete their life cycle. Unlike most mosquitoes, blackflies tend to bite during the daytime. They primarily use visual cues to locate a host. Dark moving objects are particularly attractive, but carbon dioxide and body warmth also serve as attractants. Only the female bites, taking up to 5 minutes to feed. Blackflies may be present in swarms, inflicting numerous bites on their victims.
Box 32-1. DISEASES TRANSMITTED TO HUMANS BY BITING ARTHROPODS
MOSQUITOES Eastern equine encephalitis* Western equine encephalitis* St. Louis encephalitis* La Crosse encephalitis* Japanese encephalitis Venezuelan equine encephalitis Malaria Yellow fever Dengue fever Bancroftian filariasis Epidemic polyarthritis (Ross River virus) Chikungunya fever Rift Valley fever
TICKS Lyme disease* Rocky Mountain spotted fever* Colorado tick fever* Relapsing fever* Ehrlichiosis* Babesiosis* Tularemia* Tick paralysis* Tick typhus
FLIES Tularemia* Leishmaniasis* African trypanosomiasis (sleeping sickness) Onchocerciasis Bartonellosis Loa loa
CHIGGER MITES Scrub typhus (tsutsugamushi fever) Rickettsial pox*
FLEAS Plague* Murine (endemic) typhus
LICE Epidemic typhus Relapsing fever
KISSING BUGS American trypanosomiasis (Chagas' disease)
KISSING BUGS American trypanosomiasis (Chagas' disease)
*May be found in the United States.
Blackflies are attracted to the eyes, nostrils, and ears
Figure 32-1 Blood-feeding arthropods. A, Mosquito: Culex and Anopheles. B, Blackfly. C, Biting midge.
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Figure 32-1 D, Tabanid fly. E, Sand fly. F, Tsetse fly. G, Stable fly. H, Kissing bug. I, Flea. J, Chigger mite. K, Hard tick. L, Soft tick.
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of their hosts. They often crawl under clothing or into the hair to feed. The insect's mouthparts are used to tear the skin surface, producing a pool of blood from which the fly feeds. Blood loss from the bite site often persists after the blackfly has departed. The resulting intensely pruritic, painful, and edematous papules are typically slow to heal. Rare systemic reactions, including fever, urticaria, anaphylaxis, and even death, have been reported after blackfly bites. Although these flies are not known to transmit disease to humans in North America, in the tropics, blackflies are vectors of the parasite Onchocerca volvulus, which causes river blindness. Midges (Family Ceratopogonidae) Also known as no-see-ums, sand gnats, sand fleas, and flying teeth, biting midges [3] [8] [21] [39] [48] are small (less than 2 mm), slender flies with narrow wings ( Figure 32-1, C ). Their small size makes them difficult to see, and they can pass readily through common window screens. Biting midges may be found worldwide. They breed most commonly in salt marshes but may also be found in freshwater wetlands. Despite their inconspicuous size, female midges are aggressive biters, frequently attacking in swarms and inflicting multiple painful and pruritic bites within minutes. Midges often crawl into the hair before biting. Depending on the species, midges may bite during the day or at nighttime. Their activity is greatest during calm weather, declining as wind speed increases. Biting midges are not known to transmit disease in North America. Tabanids (Family Tabanidae) The family Tabanidae ( Figure 32-1, D ) includes horse-flies, deerflies, greenheads, and yellow flies.[3] [8] [21] [39] [48] These insects are relatively large (10 to 20 mm) robust fliers, with numerous species worldwide. Tabanids breed in aquatic or semiaquatic environments, with a life cycle of over a year. They are able to fly for miles and rely primarily on vision to locate a host by movement. These flies are most active on warm, overcast days. Only the females bite, using scissorlike mouthparts to create within the skin a bleeding slash, which is slow to heal. Despite their size, these flies usually bite painlessly, but the resulting reaction can include intense itching, secondary infection, and, rarely, systemic reactions, such as urticaria or anaphylaxis. Since the adult fly usually only lives about a month, and only one generation emerges per year, the potential season for being bitten is fortunately relatively short. In the United States, deerflies have been shown to be capable of transmitting tularemia to humans; in Africa, the deerfly may vector the filarial parasitic worm, Loa loa. Sand Flies (Family Psychodidae) Sand flies[3] [8] [21] [25] [39] [48] are tiny (2 to 3 mm), hairy, and longlegged flies, with multisegmented antennae and a characteristic -shape to the wings when at rest ( Figure 32-1, E ). Only female sand flies are blood-feeders, feeding mostly during calm, windless nights, and resting during the day in animal burrows, tree holes, or caves. Most sand fly bites tend to occur on the face and neck. In tropical and subtropical climates, sand flies have been shown to vector multiple cutaneous, mucocutaneous, and systemic diseases, including bartonellosis and three forms of leishmaniasis. The only sand fly-transmitted disease in the United States has been cutaneous leishmaniasis, reported in Texas. Tsetse Flies (Family Glossinidae) Tsetse flies[3] [8] [21] [39] [48] are found only in tropical Africa. They are 7 to 14 mm long, yellowish-brown, with wings that fold over their backs, giving them the appearance of honeybees at rest ( Figure 32-1, F ). Both genders bite, feeding in daytime on a wide variety of mammals, including humans. Tsetse flies seem to rely primarily on vision and movement to identify their hosts. Their bites may cause petechiae or pruritic wheals. Tsetse flies vector African trypanosomiasis (sleeping sickness). Stable Flies (Family Muscidae) Stable flies[39] [48] resemble common houseflies and are most often encountered in coastal areas. Unlike a housefly, which rests with its body parallel to the surface, a stable fly rests with its head held higher than its posterior ( Figure 32-1, G ). Both male and female stable flies are vicious daytime biters, requiring a blood meal every 48 hours to survive. If disturbed, they will attempt to feed multiple times, preferring to bite the lower extremities. Horses and cattle are the preferred hosts, but hungry stable flies will readily bite humans. These flies have knifelike mouthparts that they use to puncture flesh before pumping up the blood. Stable flies breed in decaying vegetation and in herbivore manure and are frequently found congregated on sunny walls. Stable fly bites are generally self-limited. They are not known to transmit disease to humans. Kissing Bugs (Family Reduviidae) Kissing bugs[3] [8] [21] [26] [39] [48] (assassin bugs) are large (10 to 30 mm in length) insects with cone-shaped heads, overlapping wings, and an alternating pattern of orange and dark brown stripes on the lateral abdomen ( Figure 32-1, H ). Kissing bugs get their name from a tendency to bite around the human mouth, but they may also bite other parts of the body. Both male and female reduviids bite, requiring a blood meal to mature through five nymphal growth stages. Reduviids are nocturnal feeders, attracted to their hosts by warmth, carbon dioxide, and odor. During the day, they rest in trees or indoors in crevices of house walls and ceilings. Kissing
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bug bites are initially painless, but frequent exposure to the bites can produce erythema, edema, and pruritus at the bite sites. More importantly, kissing bugs are the vector for Trypanosoma cruzi, the causative agent of Chagas' disease, which has been reported in Central and South America, as well as in the southwestern United States.
Fleas (Family Pulicidae) Adult fleas[3] [8] [21] [39] [48] are small (2 to 6 mm), wingless insects, with three pairs of powerful legs that enable them to jump distances of up to 30 cm ( Figure 32-1, I ). Hungry fleas of both genders feed on the nearest warm-blooded animal, without clear host preference. Fleas usually move around, probing and biting several times, resulting in grouped lesions of pruritic papules. Fleas are capable of transmitting sylvatic plague and murine typhus. Chigger Mites (Family Trombiculidae) Trombiculid mites[3] [8] [21] [39] [48] ( Figure 32-1, J ) may be found worldwide. Commonly known as chiggers, redbugs, or harvest mites, these reddish-yellow insects are readily encountered in damp, grassy, and wooded areas, especially along the margins of forests, where they may number in the thousands. Only the tiny (less than 0.2 mm) larval stages are parasitic, feeding on mammals, birds, reptiles, and amphibians. Chiggers are most active in the summer and early autumn. They usually infest humans by crawling up the shoes and legs, preferring to attach to skin at areas where the clothing fits tightly, such as at the top of socks or around the elastic edges of underwear. Chiggers do not burrow into the skin or actively suck blood. Rather, they pierce skin with their mouthparts and secrete a proteolytic salivary fluid that dissolves host tissue, which they, in turn, suck up. If undisturbed, chiggers may feed for several days before dropping off. In humans, this rarely occurs because the larvae usually cause enough irritation that they are dislodged by scratching. The host response to chigger bites is brisk, often leading to intensely pruritic, bright red 1to 2-cm nodules. In Asia, chiggers may serve as vectors of scrub typhus. Rickettsial pox is also transmitted by a mite bite. Ticks (Families Ixodidae and Argasidae) (See Chapter 33 ) Ticks[3] [8] [21] [39] [48] [105] are classified as hard ticks (family Ixodidae) and soft ticks (family Argasidae) ( Figure 32-1, K and L ). Hard ticks are so named because of the presence of a sclerotized plate, or scutum, that covers part of the body. Both types of ticks may be found worldwide, but hard ticks are more commonly encountered in North America. Hard ticks are usually found in weedy or shrubbed areas, along trails, and at forest boundaries, where mammalian hosts, such as deer, are plentiful. Soft ticks are more resistant to desiccation than are hard ticks. Soft ticks thrive in hot and dry climates and are commonly found in animal burrows or caves. Both genders are bloodsuckers. Soft ticks are nocturnal and feed rapidly, in just a few minutes. Hard ticks most commonly feed during the day and may feed on a single host for days. Ticks are unable to fly or jump. Hard ticks climb vegetation and "quest," waiting passively for hours or days, forelegs outstretched, until they detect the vibration or carbon dioxide plume of a passing host. When they encounter fur or skin, they climb onto the host and then crawl around in search of an appropriate location on which to attach and feed. The attachment bite is usually painless. People in suspected tick habitats should check clothing frequently for the presence of ticks. If multiple ticks are seen on clothing, they are most easily removed by trapping them on a piece of cellophane tape, or by rolling a sticky tape-type lint remover across them; hundreds of small ticks can be easily removed by this method. Attached ticks are more difficult to remove. Tick mouthparts are barbed, and some species of tick also secrete a cement that firmly anchors the tick into the skin. Erythema, pruritus, and edema are commonly seen at the site of a tick bite. Improper partial removal of the mouthparts may initiate a long-lasting foreign body reaction, leading to secondarily infected lesions that are slow to heal, or granuloma formation that may persist for months. (For a discussion of the best method for tick removal, see Chapter 33 .) After the tick is removed, the bite site should be cleansed with soap and water, or an antiseptic, and hands should be washed. It may be prudent to save the tick, in case later identification becomes necessary. Prompt removal of attached ticks will greatly reduce the likelihood of disease transmission. Laboratory studies of attachment times for Borrelia burgdorferi (Lyme disease)-infected ticks showed that transmission of the spirochete rarely occurred if the tick was attached for less than 48 hours.[79] [80] [81] [82] [104] [105] In the United States, soft ticks of the genus Ornithodoros are capable of transmitting to humans the Borrelia spirochete that causes relapsing fever. Three genera of the hard ticks Ixodidae transmit disease to man: Ixodes (which vectors Lyme disease, babesiosis, and tick paralysis), Dermacentor (vectors tularemia, Rocky Mountain spotted fever, ehrlichiosis, Colorado tick fever, and tick paralysis), and Amblyomma (vectors tularemia, ehrlichiosis, and tick paralysis).[71] [105] Larval, nymph, and adult ticks may all transmit disease during feeding. Transovarial transmission also enables female ticks to directly infect their offspring.
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Box 32-2. MANUFACTURERS OF PROTECTIVE CLOTHING, PROTECTIVE SHELTERS, AND INSECT NETS PROTECTIVE CLOTHING (includes hooded jackets, pants, headnets, ankle guards, gaiters, and mittens) Bug Baffler, Inc. P.O. Box 444 Goffstown, NH 03045 (888) 774-7391 Insect Out P.O. Box 49643 Colorado Springs, CO 80919 (888) 488-0285 BugOut Outdoor Wear, Inc. P.O. Box 185 Centerville, IA 52544 (515) 437-1936 Skeeta P.O. Box 72103 Fairbanks, AK 99707 (907) 479-9389 The Original Bug Shirt Company 908 Niagara Falls Blvd., #467 North Tonawanda, NY 14120 (800) 998-9096 Shannon Outdoor's Bug Tamer 1210-A Peachtree Street Louisville, GA 30434 (800) 852-8058 PROTECTIVE SHELTERS AND INSECT NETS Long Road Travel Supplies 111 Avenida Drive Berkeley, CA 94708 (800) 359-6040 Wisconsin Pharmacal Co. 1 Repel Road Jackson, WI 53037 (800) 558-6614 Travel Medicine, Inc. 369 Pleasant Street Northampton, MA 01060 (800) 872-8633
PERSONAL PROTECTION Personal protection against insect bites may be achieved in three ways: avoiding infested habitats, using protective clothing and/or shelters, and applying insect repellents. Habitat Avoidance Avoiding infested habitats reduces the risk of being bitten. Mosquitoes and other nocturnal bloodsuckers are particularly active at dusk, making this a good time to be indoors. To avoid the usual resting places of biting arthropods, campgrounds should ideally be situated in areas that are high, dry, and open, as free from vegetation as possible. Attempts should be made to avoid unnecessary use of lights, which attract multiple insects. Physical Protection Physical barriers can be extremely effective in preventing insect bites, by blocking arthropods' access to the skin. Long-sleeved shirts, socks, long pants, and a hat will protect all but the face, neck, and hands. Tucking pants into the socks or boots makes it much more difficult for ticks or chigger mites to gain access to the skin. Light-colored clothing is preferable, since it makes it easier to spot ticks and is less attractive to mosquitoes and biting flies. Ticks will find it more difficult to cling to smooth, closely-woven fabrics (e.g., nylon).[98] Loose-fitting clothing, made out of tightly woven fabric, with a tucked-in T-shirt undergarment is particularly effective at reducing bites on the upper body. A light-colored, full-brimmed hat will protect the head and neck. Deerflies tend to land on the hat instead of the head, and blackflies and biting midges are less likely to crawl to the shaded skin beneath a hat brim. Mesh garments or garments made of tightly woven material are available to protect against insect bites. Head nets, hooded jackets, pants, and mittens are available from a number of manufacturers in a wide range of sizes and styles ( Box 32-2 ). Mesh garments are usually made of either polyester or nylon and, depending on the manufacturer, are available in either white or dark colors. With a mesh size of less than 0.3 mm, many of these garments are woven tightly enough to exclude even biting midges and ticks. As with any clothing, bending or crouching may still pull the garments close enough to the skin surface to enable insects to bite through. One manufacturer (Shannon Outdoors, Louisville, Ga.) addresses this potential problem with a double-layered mesh that reportedly prevents mosquito penetration. Although mesh garments are effective barriers against insects, some people may find them uncomfortable during vigorous activity or in hot weather.
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Figure 32-2 A to C, Protective shelters. D, Bed nets. (A, C, and D courtesy Wisconsin Pharmacal Co.; B courtesy Long Road Travel Supplies.)
Lightweight insect nets and mesh shelters are available to protect travelers sleeping indoors or in the wilderness ( Figure 32-2 ). The effectiveness of insect nets or shelters may be enhanced by lightly spraying them with a permethrin-based contact insecticide, which provides weeks of efficacy after a single application. Repellents For many people, applying an insect repellent may be the most effective and easiest way to prevent arthropod bites. The quest to develop the "perfect" insect repellent has been an ongoing scientific goal for years and has yet to be achieved. The ideal agent would repel multiple species of biting arthropods, remain effective for at least 8 hours, cause no irritation to skin or mucous membranes, possess no systemic toxicity, be resistant to abrasion and wash-off, and be greaseless and odorless. No presently available insect repellent meets all of these criteria. Efforts to find such a compound have been hampered by the multiplicity of variables that affect the inherent repellency of any chemical. Repellents do not all share a single mode of action, and different species of insects may react differently to the same repellent.[88] To be effective as an insect repellent, a chemical must be volatile enough to maintain an effective repellent vapor concentration at the skin surface but not evaporate so rapidly that it quickly loses its effectiveness. Multiple factors play a role in effectiveness, including concentration, frequency and uniformity of application, the user's activity level and overall attractiveness to bloodsucking arthropods, and the number and species of the organisms trying to bite. The effectiveness of any repellent is reduced by abrasion from clothing; evaporation and absorption from the skin surface; wash-off from sweat, rain, or water; and a windy environment. [34] [50] [51] [67] [68] [86] Each 10° C (18° F) increase in ambient temperature can lead to as much as 50% reduction in protection time.[51] Presently available insect repellents
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TABLE 32-1 -- DEET-Containing Insect Repellents MANUFACTURER/DISTRIBUTOR
PRODUCT NAME
FORM(S)
Sawyer Products Tampa, Fla. (800) 940-4464
DEET Plus
Lotion and pump spray
17.5
Sawyer Gold
Pump spray
17.5
Sawyer Controlled Release
Lotion
20
Sawyer Gold
Lotion
30
Sawyer Gold
Spray aerosol
38
Maxi-DEET
Pump spray
100
OFF! Skintastic Unscented
Pump spray
5
OFF! Skintastic Unscented
Pump spray
7
OFF! Skintastic Unscented
Lotion
7.5
OFF! Skintastic with Sunscreen (SPF 30)
Lotion
10
OFF! Unscented
Aerosol spray
15
Deep Woods OFF! with Sunscreen (SPF 15)
Lotion
20
Deep Woods OFF! Unscented
Aerosol spray
25
Deep Woods OFF! for Sportsmen
Aerosol spray
30
Deep Woods OFF! for Sportsmen
Pump spray
S.C. Johnson Wax Racine, Wisc. (800) 558-5566
% DEET
100
Tender Corporation Littleton, NH (800) 258-4696
Ben's Backyard
Lotion and pump spray
24
Ben's Wilderness
Aerosol
27
Ben's Max 100
Lotion and pump spray
Travel Medicine, Inc. Northampton, Mass. (800) 872-8633
Ultrathon
Cream
United Industries Corp. St. Louis, Mo. (800) 767-9927
Cutter Just For Kids
Pump spray
7
Cutter Skinsations with Sunscreen (SPF 15)
Lotion
7
Cutter Skinsations
Aerosol and pump spray
7
Cutter Skinsations
Gel; towelettes
7
Cutter Unscented
Aerosol spray
10
Cutter Backwoods Unscented
Aerosol and pump spray
23
Cutter Outdoorsman Unscented
Aerosol; lotion; solid stick
30
Repel Insect Repellent
Gel
Repel Family Formula
Pump spray
18
Repel Sportsmen Formula
Pump spray
18
Repel Sportsmen Formula
Lotion
20
Repel Family Formula
Aerosol
23
Repel Sportsmen Formula
Aerosol
29
Repel Classic Sportsmen Formula
Aerosol
40
Repel 100
Pump spray
Wisconsin Pharmacal Co. Jackson, Wisc. (800) 558-6614
100 35
7
100
NOTE:
Some manufacturers give only the concentration of the m-isomer; others list total concentrations of all DEET isomers. Technical grade 100% DEET is 95% m-isomer and 5% other isomers. do not "cloak" the user in a chemical veil of protection; any untreated exposed skin can be readily bitten by hungry arthropods.[67] CHEMICAL DEET.
N,N-diethyl-3-methylbenzamide (previously called N,N-diethyl-m-toluamide), or DEET, remains the gold standard of presently available insect repellents. DEET has been registered for use by the general public since 1957. It is a broad-spectrum repellent, effective against many species of crawling and flying insects, including mosquitoes, biting flies, midges, chiggers, fleas, and ticks. The United States Environmental Protection Agency (EPA) estimates that about 30% of the U.S. population uses a DEET-based product every year; worldwide use exceeds 200 million people annually. [112] [114] Decades of empirical testing of more than 20,000 other compounds has not led to the release of a superior repellent.[17] [47] [53] [84] [91] [111] DEET may be applied directly to skin, clothing, mesh insect nets or shelters, window screens, tents, or sleeping bags. Care should be taken to avoid inadvertent contact with plastics (such as wrist watch crystals and glasses frames), rayon, spandex, leather, or painted and varnished surfaces, since DEET may damage these. DEET does not damage natural fibers, such as wool and cotton. In the United States, DEET is sold in concentrations from 5% to 100% in multiple formulations, including lotions, solutions, gels, sprays, and impregnated towelettes and wristbands ( Table 32-1 ). As a general rule,
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higher concentrations of DEET will provide longer-lasting protection. For most uses, however, there is no need to use the highest concentrations of DEET. Products with 10% to 35% DEET provide adequate protection under most conditions. In fact, most manufacturers, responding to consumer demand, have recently begun to offer a greater variety of low-concentration DEET products. The American Academy of Pediatrics currently recommends that DEET-containing repellents used on children contain no more than 10% DEET.[35] [100] Persons adverse to applying DEET directly to their skin may get long-lasting repellency by applying DEET only to their clothing. DEET-treated garments, stored in a plastic bag between wearings, maintain their repellency for several weeks.[15] Products with a DEET concentration over 35% are probably best reserved for circumstances in which the wearer will be in an environment with a very high density of insects (e.g., a rain forest), where there is a high risk of disease transmission from insect bites, or under circumstances in which there may be rapid loss of repellent from the skin surface, such as under conditions of high temperature and humidity or rain. Under these circumstances, reapplication of the repellent will likely be necessary to maintain its effectiveness. Two companies (3M, Minneapolis, Minn., and Sawyer Products, Tampa, Fla.) manufacturer extended-release formulations of DEET that make it possible to deliver long-lasting protection without relying on high concentrations of DEET. 3M's product, Ultrathon, was developed for the U.S. military and is currently exclusively sold to the public through Travel Medicine, Inc. (Northampton, Mass.; 800-872-8633). This acrylate polymer DEET formulation, when tested under multiple different environmental/climatic field conditions, was as effective as 75% DEET, providing up to 12 hours of greater than 95% protection against mosquito bites.[2] [41] [54] [72] [94] [96] Sawyer Products' controlled-release 20% DEET lotion traps the chemical in a protein particle that slowly releases it to the skin surface, providing repellency equivalent to a standard 50% DEET preparation, lasting about 5 hours.[28] Preliminary data suggest that about 50% less of this encapsulated DEET is absorbed when compared with a 20% ethanol-based preparation of DEET.[27] Given its use by millions of people worldwide for 40 years, DEET continues to show a remarkable safety profile. In 1980, as part of the EPA Registration Standard for DEET,[112] over 30 additional animal studies were conducted to assess acute, chronic, and subchronic toxicity; mutagenicity; oncogenicity; and developmental, reproductive, and neurologic toxicity. The results of these studies neither led to any product changes to comply with current EPA safety standards nor indicated any new toxicities under normal usage. The EPA's Reregistration Eligibility Decision (RED),[114] released in 1998, confirmed that the Agency believes that "normal use of DEET does not present a health concern to the general U.S. population." Case reports of potential DEET toxicity exist in the medical literature and are fully reviewed by Fradin.[32] Fewer than 40 cases of significant toxicity from DEET exposure have been documented in the medical literature over the last four decades; over three quarters of these resolved without sequelae. Many of these cases involved long-term, excessive, or inappropriate use of DEET repellents; the details of exposure were frequently poorly documented, making causal relationships difficult to establish. These cases have not shown a correlation between concentration of the DEET product used and the risk of toxicity. The reports of DEET toxicity that raise the greatest concern involve 14 cases of encephalopathy, 13 in children under age 8 years old.[20] [24] [32] [44] [45] [64] [75] [76] [120] Three of these children died, one of whom had ornithine carbamoyl transferase deficiency, which might have predisposed her to DEET-induced toxicity.[44] [45] The other children recovered without sequelae. The EPA's analysis of these cases concluded that they "do not support a direct link between exposure to DEET and seizure incidence."[114] Animal studies in rats and mice show that DEET is not a selective neurotoxin.[75] [89] [112] Even if a link between DEET use and seizures does exist, the observed risk, based on DEET usage patterns, would be less than one per 100 million users.[114] The EPA has issued guidelines to ensure safe use of DEET-based repellents.[114] Careful product choice (most often of a DEET concentration of 35% or less), judicious use, and common-sense application will greatly reduce the possibility of toxicity. Conservative use of low-concentration DEET products is most appropriate when applying repellents to children. Guidelines for properly applying insect repellents are given in Box 32-3 . Questions regarding the safety of DEET may be addressed to the EPA-sponsored National Pesticide Telecommunications Network, available each day from 6:30 AM to 4:30 PM Pacific Standard Time at (800) 858-7378 or via their website at http://ace.orst.edu/info/nptn/.
SKIN-SO-SOFT PRODUCTS.
Skin-So-Soft Bath Oil (Avon, New York, N.Y.) received considerable media attention several years ago when it was reported by some consumers to be effective as a mosquito repellent. When tested under laboratory conditions against Aedes aegypti mosquitoes, Skin-So-Soft Bath Oil's effective half-life was found to be 0.51 hours.[87] In one study against Aedes albopictus, Skin-So-Soft Oil provided 0.64 hours of protection from bites and was 10 times less effective than 12.5% DEET. [96] Skin-So-Soft Oil has been found to be somewhat effective against biting midges, but this effect is felt to be a result of its trapping the insects in an
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oily film on the skin surface.[66] It has been proposed that the limited mosquito repellent effect of Skin-So-Soft Oil could be due to its fragrance or to the presence of diisopropyl adipate and benzophenone in the formulation, both of which have some repellent activity.[10] [53] Box 32-3. GUIDELINES FOR SAFE AND EFFECTIVE USE OF INSECT REPELLENTS For casual use, choose a repellent with 10% to 35% DEET. Repellents with 10% DEET or less are most appropriate for use on children. Use just enough repellent to lightly cover the exposed skin; do not saturate the skin. Repellents should be applied only to exposed skin and/or clothing. Do not use under clothing. To apply to the face, dispense into palms, rub hands together, and then apply thin layer to face. Young children should not apply repellents themselves. Avoid contact with eyes and mouth. Do not apply to children's hands to prevent possible subsequent contact with mucous membranes. After applying, wipe repellent from the palmar surfaces to prevent inadvertent contact with eyes, mouth, and genitals. Never use repellents over cuts; wounds; or inflamed, irritated, or eczematous skin. Do not inhale aerosol formulations or get them in eyes. Do not apply when near food. Frequent reapplication is rarely necessary, unless the repellent seems to have lost its effectiveness. Reapplication may be necessary in very hot, wet environments because of rapid loss of repellent from the skin surface. Once inside, wash off treated areas with soap and water. Washing the repellent from the skin surface is particularly important under circumstances in which a repellent is likely to be applied for several consecutive days. If you suspect you are having a reaction to an insect repellent, discontinue its use, wash the treated skin, and consult a physician.
Adapted from United States Environmental Protection Agency, Office of Pesticide Programs, Prevention, Pesticides and Toxic Substances Division: Reregistration Eligibility Decision (RED): DEET (EPA-738-F-95-010), Washington, DC, 1998, EPA.
Avon Products, Inc. makes no claims about its bath oil being an effective repellent. They currently manufacturer Skin-So-Soft Bug Guard, which contains 0.10% oil of citronella as the active ingredient. In July 1999, Avon introduced a new chemical-based insect repellent to the U.S. market, IR3535, or ethyl-3-(N-butylacetamido) propionate, which can be found in Skin-So-Soft Bug Guard Plus. The limited data presently available to the public on this repellent show that, although it is more effective than most botanical-based repellents, it does not match the overall efficacy of DEET.[22] Botanical Repellents.
Thousands of plants have been tested as sources of insect repellents. Although none of the plant-derived chemicals tested to date demonstrate the broad effectiveness and duration of DEET, a few show repellent activity. Plants with essential oils that have been reported to possess repellent activity include citronella, cedar, verbena, pennyroyal, geranium, lavender, pine, cajeput, cinnamon, rosemary, basil, thyme, allspice, garlic, and peppermint.[7] [16] [23] [40] [53] [85] Unlike DEET-based repellents, botanical repellents have been relatively poorly studied. When tested, most of these essential oils tended to show short-lasting protection, lasting minutes to 2 hours. A summary of readily-available plant-derived insect repellents is shown in Table 32-2 . CITRONELLA.
Oil of citronella was initially registered as an insect repellent by the EPA in 1948. It is the most common active ingredient found in "natural" or "herbal" insect repellents presently marketed in the United States. Originally extracted from the grass plant Cymbopogon nardus, oil of citronella has a lemony scent. Conflicting data exist on the efficacy of citronella-based products, varying greatly depending on the study methodology, location, and species of biting insect tested. One citronella-based repellent was found to provide no repellency when tested in the laboratory against Aedes aegypti mosquitoes.[10] However, a field study of the same product showed an average of 88% repellency over a 2-hour exposure. The product's effectiveness was greatest within the first 40 minutes after application and then decreased with time over the remainder of the test period.[107] All Terrain Co. (Encinitas, Calif.; 800-246-7328) produces a citronella-based lotion in which the essential oil has been encapsulated into a beeswax matrix, which slowly releases it to the skin surface, prolonging its efficacy. In laboratory testing against Aedes aegypti, this product provided complete protection for the first 2 hours, and 77% protection 4 hours after application.[43] In general, studies show that citronella-based repellents are less effective than DEET repellents. Citronella provides a shorter protection time, which may be partially overcome by frequent reapplication of the repellent. In 1997, after analyzing available data on the repellent effect of citronella, the EPA concluded that citronella-based insect repellents must contain the following statement on their labels: "For maximum repellent effectiveness of this product, repeat applications at one hour intervals."[113] Citronella candles have been promoted as an effective way to repel mosquitoes from one's local environment. One study compared the efficacy of commercially
available 3% citronella candles, 5% citronella incense, and plain candles to prevent bites by Aedes species mosquitoes under field conditions. [62] Subjects
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TABLE 32-2 -- Botanical Insect Repellents MANUFACTURER
PRODUCT NAME
FORM(S)
ACTIVE INGREDIENT
Avon Corp. New York, NY (800) 367-2866
Skin-So-Soft: Moisturizing Suncare Plus SPF 15 and 30
Lotion
Citronella oil 0.05%
Bug Guard ± SPF 15
Pump spray
Citronella oil 0.1%
Bug Guard Moisturizing
Lotion and towelettes
Citronella oil 0.1%
Verdant Brands, Inc. Bloomington, Ind. (800) 643-8457
Blocker
Lotion, oil, and pump spray
Soybean oil 2%
Quantum, Inc. Eugene, Ore. (800) 448-1448
Buzz Away
Towelette and pump spray
Citronella oil 5%; oils of cedarwood, peppermint, eucalyptus, lemongrass
Buzz Away, SPF 15
Lotion
Tender Corp. Littleton, NH (800) 258-4696
Natrapel
Lotion and pump spray
Citronella 10%
All Terrain Co. Encinitas, Calif. (800) 246-7328
Herbal Armor
Lotion
Herbal Armor SPF 15
Lotion
Citronella oil 12%, peppermint oil 2.5%, cedar oil 2%, lemongrass oil 1%, geranium oil 0.05%, in a slow-release encapsulated formula
Herbal Armor
Pump spray
Green Ban Norway, Iowa (319) 446-7495
Green Ban For People: Regular
Oil
Citronella oil 5%, peppermint oil 1%
Double Strength
Oil
Citronella oil 10%, peppermint oil 2%
near the citronella candles had 42% fewer bites than controls who had no protection (a statistically significant difference). However, burning ordinary candles reduced the number of bites by 23%. There was no difference in efficacy between citronella incense and plain candles. The ability of plain candles to decrease biting may be due to their serving as a "decoy" source of warmth, moisture, and carbon dioxide. The citrosa plant (Pelargonium citrosum "Van Leenii") has been marketed as being able to repel mosquitoes through the continuous release of citronella oils. Unfortunately, when tested, these plants offer no protection against bites.[11] [70] BLOCKER.
Blocker is a "natural" repellent that was released to the U.S. market in 1997. Blocker combines soybean oil, geranium oil, and coconut oil in a formulation that has been available in Europe for several years.[115] Studies conducted at the University of Guelph, Guelph, Ontario, Canada, showed that this product was capable of providing over 97% protection against Aedes species mosquitoes under field conditions, even after 3 ½ hours of application. During the same time period, a 6.65% DEET-based spray afforded 86% protection, whereas Avon's Skin-So-Soft citronella-based repellent gave only 40% protection.[59] A second study showed that Blocker provided a mean of 200 ± 30 (SD) minutes of complete protection from mosquito bites.[60] Blocker also provided about 10 hours of protection against biting blackflies; in the same test, 20% DEET only gave 6 ½ hours of complete protection.[61] EUCALYPTUS.
A derivative (p-menthane-3,8-diol, or PMD) isolated from oil of the lemon eucalyptus plant has shown promise as an effective "natural" repellent.[16] This repellent has been very popular in China for years and is currently available in Europe under the brand name Mosi-guard. In field tests against anopheline mosquitoes, PMD showed repellency comparable with 50% DEET.[109] PMD required more frequent reapplication than DEET to maintain its potency but was significantly more effective than 50% citronella oil.[13] [110] Release of PMD-based repellents awaits final EPA approval in the United States. Efficacy of DEET vs. Botanical Repellents.
Limited data are available from studies that directly compare plant-derived repellents with DEET-based products. Available data proving the efficacy of "natural" repellents are often sparse, and there is no uniformly accepted standard for testing these products. As a result, different studies often yield varied results, depending on how and where the tests were conducted. In general, when compared with "natural" products, DEET-based repellents
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Figure 32-3 Average protection times—DEET vs. botanical repellents. A, DEET 6.65%; B, DEET 4.75%, C, soybean oil 2%, geranium oil, coconut oil; D, citronella oil 0.1%; E, citronella oil 5%, cedarwood oil, eucalyptus oil, peppermint oil; F, prickly pear extract 40%; G, citronella oil 0.05%; H, DEET 9.5%, impregnated into a wristband.
demonstrate longer-lasting effectiveness. In a laboratory study against Aedes aegypti mosquitoes, two commercially available "natural" repellents containing citronella (and other plant-derived essential oils) demonstrated no repellent effect, even when applied at twice the concentration that would typically be expected to be used.[10] In the same study, DEET-based repellents (at various concentrations) provided at least 2 hours of protection.[10] Another study comparing "natural" repellents with low-strength DEET products, conducted under carefully controlled laboratory conditions with caged mosquitoes, demonstrated a dramatic difference in effectiveness between several currently marketed insect repellents. Low-concentration DEET lotions (under 7%) consistently proved to be more effective than any of the tested "natural" repellents in their ability to prevent mosquito bites[19] ( Figure 32-3 ). Alternative Repellents.
There has always been great interest in finding an oral insect repellent. Oral repellents would be convenient and would eliminate the need to apply creams to the skin or put on protective clothing. Unfortunately, no effective oral repellent has been discovered. For decades, lay literature has made the claim that Vitamin B1 (thiamine) works as a systemic mosquito repellent. When subjected to scientific scrutiny, however, thiamine has unanimously been found not to have a repellent effect on mosquitoes.[52] [117] The U.S. Food and Drug Administration (FDA), prompted by misleading consumer advertising, issued the following statement in 1983: "There is a lack of adequate data to establish the effectiveness of thiamine or any other ingredient for OTC (over the counter) internal use as an insect repellent. Labeling claims for OTC orally administered insect repellent drug products are either false, misleading, or unsupported by scientific data."[29] Tests of over 100 ingested drugs, including other vitamins, failed to reveal any that worked well against mosquitoes.[106] Ingested garlic has also never proven to be an effective deterrent. Insecticides
Permethrin.
Pyrethrum is a powerful, rapidly acting insecticide, originally derived from the crushed dried flowers of the daisy Chrysanthemum cinerariifolium.[9] Permethrin is a human-made synthetic pyrethroid. It does not repel insects but instead works as a contact insecticide, causing nervous system toxicity, leading to death, or "knockdown," of the insect. The chemical is effective against mosquitoes, flies, ticks, fleas, lice, and chiggers. Permethrin has low mammalian toxicity, is poorly absorbed by the skin, and is rapidly metabolized by skin and blood esterases.[46] [119] Permethrin should be applied directly to clothing or to other fabrics (tent walls[90] or mosquito nets[63] ) and not to skin. Permethrins are nonstaining, nearly odorless, resistant to degradation by heat or sun, and will maintain their effectiveness for at least 2 weeks, through several launderings.[92] [97] The combination of permethrin-treated clothing and skin application of a DEET-based repellent creates a formidable barrier against biting insects.[42] [54] [101] In an Alaskan field trial against mosquitoes, subjects wearing permethrin-treated uniforms and a polymer-based 35% DEET product had greater than 99.9% protection (1 bite/hr) over 8 hours; unprotected subjects were bitten an average of 1188 bites/hr.[58] Permethrin-sprayed clothing also proved very effective against ticks. One hundred percent of Dermacentor occidentalis ticks (which carry Rocky Mountain spotted fever) died within 3 hours of touching permethrin-treated cloth.[56] Permethrin-sprayed pants and jackets also provided 100% protection from all three life stages of Ixodes dammini ticks, the vector of Lyme disease.[98] In contrast, DEET alone (applied to the skin) provided 85% repellency at the time of application; this protection deteriorated to 55% repellency at 6 hours, when tested against the Lone Star tick Amblyomma americanum. [103] Ixodes scapularis ticks, which may transmit Lyme disease, also seem to be less sensitive to the repellent effect of DEET.[93] Permethrin-based insecticides available in the United States are listed in Table 32-3 . To apply to clothing, spray each side of the fabric (outdoors) for 30 to 45 seconds, just enough to moisten it. Allow the fabric to dry for 2 to 4 hours before wearing it. Permethrin solution is also available for soak-treating large items, such as mesh bed nets. Reducing Local Mosquito Populations Consumers may still find advertisements for small ultrasonic electronic devices that are meant to be carried on the body and claim to repulse mosquitoes by emitting
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MANUFACTURER
TABLE 32-3 -- Permethrin Insecticides PRODUCT NAME
FORM(S)
ACTIVE INGREDIENT
Duranon
Aerosol and pump sprays
Permethrin 0.5%
Perma-Kill
Liquid concentrate
Permethrin 13.3%
Sawyer Products Tampa, Fla. (800) 940-4464
Permethrin Tick Repellent
Aerosol and pump sprays
Permethrin 0.5%
United Industries Corp. St. Louis, Mo. (800) 767-9927
Cutter Outdoorsman Gear Guard
Aerosol spray
Permethrin 0.5%
Wisconsin Pharmacal Co. Jackson, Wisc. (800) 558-6614
Repel Permanone
Aerosol spray
Permethrin 0.5%
Coulston Products Easton, Penn. (610) 253-0167
"repellent" sounds, such as that of a dragonfly (claimed to be the "natural enemy" of the mosquito), male mosquito, or bat. Multiple studies, conducted both in the field and laboratory, show that these devices do not work.[4] [14] [31] [57] Likewise, mass-marketed backyard bug "zappers," which use ultraviolet light to lure and electrocute insects, are also ineffective: mosquitoes continue to be more attracted to humans than to the devices.[74] One backyard study showed that of the insects killed by these devices, only 0.13% were female (biting) mosquitoes.[33] An estimated 71 to 350 billion beneficial insects may be killed annually in the United States by these devices. [33] Newer technologies, utilizing more specific bait, such as a warm, moist plume of carbon dioxide, as well as other known chemical attractants, may prove to be more successful in luring and selectively killing biting insects. Pyrethrin-containing "yard foggers" set off before an outdoor event can temporarily reduce the number of biting arthropods in a local environment. These products should be applied before any food is brought outside and should be kept away from animals or fish ponds. Burning coils that contain natural pyrethrins or synthetic pyrethroids (such as d-allethrin or d-transallethrin) can also temporarily reduce local populations of biting insects.[65] [118] Some concerns have been raised about the long-term cumulative safety of using these coils in an indoor environment.[1] [78] Wood smoke from campfires can also reduce the likelihood of being bitten by mosquitoes. The smoke's ability to repel insects may vary depending on the type of wood or vegetation burned.[77] [116] Integrated Approach to Personal Protection An integrated approach to personal protection is the most effective way to prevent arthropod bites, regardless of where one is in the world and which species of insects may be attacking. Maximum protection is best achieved through avoiding infested habitats and using protective clothing, topical insect repellents, and permethrin-treated garments. When appropriate, mesh bed nets or tents should be used to prevent nocturnal insect bites. DEET-containing insect repellents are the most effective products currently on the market, providing broad-spectrum, long-lasting repellency against multiple arthropod species. Insect repellents alone, however, should not be relied on to provide complete protection. Mosquitoes, for example, can find and bite any untreated skin and may even bite through thin clothing. Deerflies, biting midges, and some blackflies prefer to bite around the head and will readily crawl into the hair to bite where there is no protection. Wearing protective clothing, including a hat, will reduce the chances of being bitten. Treating one's clothes and hat with permethrin will maximize their effectiveness, by causing "knockdown" of any insect that crawls or lands on the treated clothing. To prevent chiggers or ticks from crawling up the legs, pants should also be tucked into the boots or stockings. The U.S. military relies on this integrated approach to protect troops deployed in areas where arthropods constitute either a significant nuisance or medical risk. The Department of Defense's Insect Repellent System consists of DEET applied to exposed areas of skin, and permethrin-treated uniforms, worn with the pant legs tucked into boots, and the undershirt tucked into the pant's waistband. This system has been proven to dramatically reduce the likelihood of being bitten by insects. Persons traveling to parts of the world where insect-borne disease is a potential threat will be best able to protect themselves if they learn about indigenous insects. Protective clothing, mesh insect tents or bedding, insect repellent, and permethrin spray should be carried. Travelers would be wise to check the most current Centers for Disease Control and Prevention (CDC) recommendations about traveling to countries where immunizations (e.g., against yellow fever) or antibiotic prophylaxis (e.g., against malaria) should be undertaken before departure.
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The CDC maintains these recommendations on its website at www.cdc.gov/travel/index.htm, or by telephone at (888) 232-3228. An excellent summary of information on issues relating to travel health can also be found at www.tripprep.com. This website culls its information daily from the CDC, the Morbidity and Mortality Weekly Report, the World Health Organization, and the U.S. State Department.
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Chapter 33 - Tick-Borne Diseases Douglas A. Gentile Jason E. Lang
Ticks are familiar pests to those who frequent wilderness or rural areas. They inhabit forests, marshes, deserts, steppes, mountains, and high meadows and have few natural enemies. Most feed on an extremely wide range of hosts, including humans. Ticks are most noted for their high nuisance potential, but they are also efficient vectors for a large number of zoonoses. In fact, ticks transmit a greater variety of infectious agents than any other group of arthropods and run a close second to mosquitoes as vectors of human disease worldwide.[142] In the United States, ticks outrank even mosquitoes as vectors, and tick-borne illnesses constitute an important infectious disease problem, particularly in wilderness and other outdoor recreational areas. Ticks belong to the class Arachnida, which also includes spiders and scorpions, and they are closely related to mites. Taxonomists divide ticks into two major families: Ixodidae (hard ticks) and Argasidae (soft ticks). Argasid ticks are covered with a leathery integument, and the capitulum (head) is subterminal and not visible from above. Ixodid ticks possess a hard, shield-like scutum, which covers the entire dorsal surface in males but only the anteromedial portion in females ( Figure 33-1 ). The head of ixodid ticks is anterior and visible from above. Hard ticks have three feeding stages: larva, nymph, and adult. If molting through all stages occurs on the same host, the tick is referred to as a one-host tick. Most Ixodidae are three-host ticks, with each stage feeding on a different host. Hard ticks feed on mammals, reptiles, and birds, and virtually all feed slowly over the course of days. Most take a single adult blood meal, and engorgement with blood is a prerequisite to egg laying. Females may ingest more than 50 times their body weight in blood and other fluids. Ixodid ticks transmit all the major tick-borne diseases in North America, with the exception of relapsing fever. A typical ixodid life cycle is illustrated by Dermacentor andersoni, a major vector for Rocky Mountain spotted fever. The tick hatches as a six-legged larva and actively attaches to a small mammal, often a rodent. After feeding for 3 to 5 days, it drops off and molts to the eight-legged nymph. The nymph hibernates in soil, becoming active again in the spring. After feeding for 4 to 9 days on a larger animal, it again drops off and undergoes a second molt to the adult stage. The mature tick attaches to a third host, on which mating may occur. As with many ticks, D. andersoni is capable of surviving for extended periods (more than a year in adults) without a blood meal. Whereas ixodid ticks are wide ranging, most argasids are nidicolous, or nest loving. Nymph and adult Argasidae generally inhabit the host lair, hiding in cracks and crevices when not feeding. They usually have several nymphal stages (instars), with each stage taking a blood meal. Adults may take several blood meals, feeding rapidly over hours when the host returns. Although some ticks are host specific, most are opportunists feeding on a variety of hosts. Appendages on the capitulum, the chelicerae, function as piercing and tearing structures, enabling the entire capitulum to be inserted into the host's integument ( Figure 33-2 ). Retrose teeth on the chelicerae help anchor the tick to the host; many ixodid species also secrete a cementlike substance that seals the wound and further secures the attached tick. Salivary glands secrete an anticoagulant, allowing the tick to ingest the host's blood easily.
Tick Envenomation Ticks cause human disease either by transmitting microorganisms or by secreting toxins or venoms. The nature of most tick toxins is poorly understood. Many appear to be secreted by the tick salivary glands. Some stimulate potent host immune responses; others appear to have direct tissue toxicity. Clinical effects range from localized reactions to anaphylaxis, paralysis, and death.[16] Local reactions vary from formation of a small pruritic nodule to development of extensive areas of ulceration, erythema, and induration. Lesions may be accompanied by fever, chills, and malaise unrelated to infection. The severity of the reaction varies with both host susceptibility and tick species. A granuloma histologically resembling a lymphoma may develop at the site of a tick bite as long as 6 weeks after the tick is removed.[124] The lesion is believed to be caused by a salivary toxin. Treatment is surgical excision. Pajaroello Tick Bites According to local folklore of southern California and Mexico, the bite of the pajaroello tick Ornithodoros coriaceus is more feared than the bite of a rattlesnake. In fact, pajaroello bites usually result in a 10 to 30 mm erythematous papule with minimal associated pain and itching. The papule gradually resolves over 3 to 4
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Figure 33-1 Female and male Dermacentor andersoni, the tick that causes Rocky Mountain spotted fever.
Figure 33-2 Tick anatomy. A, Dorsal aspect. B, Ventral surface.
771
weeks. Severe local and systemic reactions have been reported but are rare and probably occur in persons sensitized by previous bites. Local erythema, pain, and edema develop rapidly, followed by tissue necrosis and ulceration. Fever, chills, rigors, and hypotension occur rarely. Severe reactions are probably caused by sensitization to a salivary toxin.[94] [114] Treatment of pajaroello bites includes wound disinfection and administration of tetanus toxoid. The rare severe allergic reaction may require epinephrine, antihistamines, and corticosteroids. When tissue necrosis occurs, excision and primary closure should be considered.
TICK PARALYSIS As early as 1912, Todd[336] recognized that paralysis occurred in humans and animals after the bite of certain tick species. Tick paralysis has been observed only sporadically in humans since that time but has occasionally constituted a serious veterinary problem.[230] Also known as tick toxicosis, tick paralysis is an acute, ascending, flaccid motor paralysis that can appear similar to Guillan-Barré syndrome, botulism, and myasthenia gravis. Although uncommon, familiarity with the clinical features of the disease is important, since prompt diagnosis and removal of the tick are curative. Tick paralysis has been reported worldwide, but most human cases occur in North America and Australia.[292] [360] Forty-three species of ticks, both Ixodidae (hard ticks) and Argasidae (soft ticks), have been reported to cause tick paralysis.[55] Human cases in North America are usually caused by D. andersoni or less often D. variabilis, although Amblyomma americanum ( Figure 33-3 ), A. maculatum, and Ixodes scapularis have also been implicated.[131] The Pacific Northwest and Rocky Mountain areas account for most cases. In Australia, Ixodes holocyclus is primarily associated with the disease, although I. cornuatus has been implicated.[132] [135]
Figure 33-3 Lone star tick (Amblyomma americanum), implicated in cases of tick paralysis in North America. (Courtesy Sherman Minton, MD.)
Tick paralysis occurs during the spring and summer months (April to June) when nymphs and mature wood ticks are feeding. Children are affected more often than adults, with most cases reported among girls less than 10 years of age. Girls are affected twice as often as boys, probably because ticks on the female scalp are hidden in longer hair.[1] Men account for most of the adult cases, presumably because of increased occupational and recreational exposure to tick habitats. Tick paralysis in humans develops 5 to 6 days after an adult female tick attaches, usually to the head or neck (male ticks do not cause paralysis). Initially the victim may be restless and irritable and may complain of paresthesias in the hands and feet. Over the ensuing 24 to 48 hours, an ascending, symmetric, and flaccid paralysis develops with loss of deep tendon reflexes. Weakness usually is initially greater in the lower extremities; within 1 to 2 days, severe generalized weakness may develop, accompanied by bulbar and respiratory paralysis. Some victims develop cerebellar dysfunction with incoordination and ataxia.[1] [130] Facial paralysis as an isolated finding has occurred in patients with ticks embedded behind the ear.[226] In uncomplicated cases, fever and chills are absent, and the white blood cell (WBC) count and cerebrospinal fluid (CSF) analyses remain normal. Resolution of paralysis on tick removal establishes the diagnosis. Laboratory aids to diagnosis are not available. In North America, recovery is rapid after removal of the tick, with most victims showing improvement within hours and complete resolution within several days. Undiagnosed, however, tick paralysis may be fatal; mortality in children was 12% in a large Canadian series.[271] Case reports of Australian tick paralysis suggest that it may be more severe than its North American counterpart. Victims often appear more acutely ill. Paralysis may continue to progress for 48 hours after tick removal, and recovery may be prolonged.[16] [17] [226] A recent report of six cases in children in Australia however, found little difference in the course between Australian and North American patients.[132] A neurotoxic venom secreted from the tick salivary glands during a blood meal causes the paralysis. The venom's mechanism of action appears to produce a conduction block in the peripheral branches of motor neurons, diminishing acetylcholine release at the neuromuscular junction.[130] [215] Electrophysiologic measurements in humans consistently demonstrate slower motor conduction and reduction in muscle action potential amplitude.[81] [212] [330] Additionally, the neurotoxin may increase the stimulatory current potential necessary to elicit a response at the motor end plate.[165] A central effect of the toxin has been postulated to explain the cerebellar dysfunction observed in some patients.
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After removal of the tick, treatment is supportive. Tick antivenom from hyperimmunized dogs has been developed for Australian tick paralysis and may be beneficial in victims with severe disease, although they have a high incidence of acute allergy and serum sickness.[132] [226] The most important aspect of treatment is to consider tick paralysis in any victim with ascending paralysis, then search for and remove the concealed tick.
TICKS AS VECTORS Ticks transmit a wide variety of infectious agents, all of which cause zoonoses. Ticks may act either as amplifiers or as reservoirs for a given agent.[143] In the agent-tick amplifier system the reservoir for the agent is a vertebrate. An immature tick ingests the microorganism while feeding on an infected vertebrate or while feeding concurrently on a vertebrate host with an infected tick. The pathogen replicates in the tick and is passed transstadially, from larval to nymphal to adult stage. The maturing tick transmits the agent to other vertebrate hosts when it feeds. A key epidemiologic feature of this system, transstadial survival of microorganisms, is common in argasid and ixodid ticks but rare in hematophagous insects. This important difference primarily results from the relatively insignificant anatomic changes that occur in the tick during molting.[143] In the agent-tick reservoir system, the microorganism is passed transovarially from one generation of ticks to the next. The agent replicates within the tick TABLE 33-1 -- Major Tick-Borne Diseases in the United States MAJOR VECTORS GEOGRAPHIC DISTRIBUTION
DISEASE
ORGANISM
Lyme disease
Borrelia burgdorferi
Ixodes scapularis, I. pacificus
Coastal mid-Atlantic, northern West Coast, Wisconsin, Minnesota
Rocky Mountain spotted fever
Rickettsia rickettsii
Dermacentor andersoni, D. variabilis
South-central states, coastal southern states
Relapsing fever
Borrelia hermsii, B. turicatae, B. parkeri
Ornithodoros hermsi, O. turicata, O. parkeri
Worldwide, most often rural western states
Colorado tick fever
Orbivirus
D. andersoni
Rocky Mountain states, California, Oregon
Ehrlichiosis
Ehrlichia chaffeensis
Ixodes scapularis?
Coastal mid-Atlantic states, northern West Coast, Wisconsin, Minnesota
Amblyomma americanum?
South-central states, coastal southern states
Babesiosis
Babesia microti
Ixodes scapularis
Coastal southern New England and mid-Atlantic states
Tularemia
Francisella tularensis
A. americanum
South-central states, Montana, South Dakota
and depends solely on the tick population for survival. The agent may also replicate within the vertebrate host of the tick, allowing amplification of the cycle, thereby increasing the density and prevalence of the microorganism. Table 33-1 lists the major tick-borne diseases in the United States, where Lyme disease, babesiosis, and ehrlichiosis have only recently been recognized. Lyme disease and babesiosis constitute important infectious disease problems in endemic areas, and Lyme disease is now the most common tick-borne illness in the United States and throughout the world. Tularemia and Rocky Mountain spotted fever are observed throughout the United States and continue to produce significant morbidity and mortality. Tick-borne relapsing fever and Colorado tick fever occur in the western states and are particularly likely to affect campers, hikers, hunters, and others who frequent wilderness areas. Borrelia Infections Borreliae are bacteria belonging to the order Spirochaetales, which also includes the treponemes and leptospires. Borrelia species can be stained with aniline dyes, including routine blood stains such as Wright and Giemsa; this feature allows easy differentiation from the other two genera. [288] Borreliae are helical, actively motile spirochetes, usually 10 to 20 µm long, with three to 10 spirals.[102] Strains cannot be differentiated on the basis of morphology but are classified according to specificity of the tick-spirochete relationship, the range of animals susceptible to infection, and cross-immunity.[19]
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Human Borrelia infections occur worldwide, with the possible exception of parts of the southwestern Pacific.[102] All are transmitted by hematophagous arthropods. Borrelia recurrentis causes an epidemic form of relapsing fever that is transmitted by the human body louse Pediculus humanus. A group of closely related Borrelia species causes tick-borne or endemic relapsing fever. A third borrelial disease was recognized in 1982 with the identification of B. burgdorferi as the etiologic agent of Lyme disease. Lyme Disease.
An epidemic form of oligoarticular arthritis, originally diagnosed as juvenile rheumatoid arthritis, was recognized in 1975 in the area around Lyme, Connecticut.[308] Subsequent clinical observations revealed a complex, multisystem disorder with dermatologic, cardiac, and neurologic complications. The new disorder was termed Lyme disease. The rural setting in which most cases occurred, the close geographic and seasonal clustering of cases, and the clinical response to penicillin suggested an arthropod-borne infection. The presence of a distinctive erythematous skin lesion, erythema migrans, preceding the arthritis pointed to a tick vector.[300] Erythema migrans had been observed in Europe since 1910, where it was associated with the bite of the sheep tick Ixodes ricinus.[5] Epidemiologic evidence implicated the deer tick Ixodes scapularis (dammini) as the likely vector of Lyme disease. In 1982, Burgdorfer and associates[44] isolated a treponeme-like spirochete, Borrelia burgdorferi, from the midgut of I. scapularis ticks collected from a known endemic focus of Lyme disease. [28] Subsequently, sera from nine patients clinically diagnosed with Lyme disease yielded high antibody titers to the spirochetes by indirect immunofluorescence.[2] Isolation of B. burgdorferi from the blood, CSF, and skin lesions of affected patients finally confirmed the spirochetal etiology of Lyme disease.[26] [29] [311] EPIDEMIOLOGY.
Lyme disease accounts for more than 90% of all reported vector-borne illnesses in the United States. In 1996 a record 16,461 cases were reported from 45 states, resulting in an overall national incidence of 6.2 per 100,000 population, with 91% of cases in eight states[59] ( Box 33-1 ). Nantucket County, Massachusetts, reported the highest county-specific incidence nationally with 1247.5 cases per 100,000. The highest proportion of cases occurred in the age groups 0 to 14 years (3784, or 23%) and 40 to 79 (7694, or 47%), with males making up 53% of the gender-reported cases. About 80% of cases occur from May to August, with peak incidence in July. A cross-sectional survey of 1200 physicians in Maryland revealed that Lyme disease may be greatly under-reported, with less than 10% of cases meeting the Centers for Disease Control and Prevention (CDC) diagnostic criteria.[51] [66] CDC criteria for Lyme disease include presence of an erythema migrans rash 5 cm or greater in diameter or laboratory confirmation of infection with evidence of at least one manifestation of musculoskeletal, neurologic, or cardiovascular disease. Campbell and associates[51] also found several fold underreporting using a nine-component deterministic model. The principal vectors of Lyme disease are several closely related ticks of the genus Ixodes. The deer tick I. scapularis (dammini) is the best documented vector; its geographic distribution correlates with endemic foci of Lyme disease in the northeastern and Midwestern United States.[272] [312] [351] The range of I. scapularis extends from the northeastern United States to the southeastern states. The northern form of I. scapularis was originally thought to be a separate species and was named Ixodes dammini. Subsequent studies demonstrated mating compatibility and genetic similarity, however, and the two forms are now considered to be the same
species.[19] The southern form of I. scapularis appears to be responsible for Lyme disease cases in the southeastern United States.[43] [232] Northern I. scapularis larvae, abundant in late summer and fall, and nymphs, numerous in spring and summer, are aggressive and parasitize a number of vertebrate species.[43] The preferred host is the deer mouse Peromyscus leucopus, which serves as an important reservoir for B. burgdorferi. [33] [289] [297] Transovarial transmission in ticks occurs but appears to be unusual.[40] Adult I. scapularis ticks, abundant in spring and fall, have a narrow host range, feeding primarily on deer, which are key hosts in the life cycle of the tick ( Figure 33-4 ). The high incidence of Lyme disease in the northeastern United States has been linked to increases in the deer population.[316] [363] In some focal endemic areas, up to 60% of I. scapularis ticks are infected with B. burgdorferi, and tick populations may be high, even on well-kept lawns. [95] A third endemic focus in the United States has been identified on the West Coast (California and Oregon),
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Figure 33-4 Life cycle of Ixodes scapularis. The cycle of ixodid ticks typically spans 2 years and includes three blood meals in the spring. The adult female tick releases her eggs, which hatch as six-legged larvae; during the summer, the larvae take a blood meal that lasts approximately 2 days. Larval ticks then enter a dormant phase with cooler fall weather. The ticks then molt in the spring, entering the second phase of their life cycle as eight-legged nymphal ticks. In the late spring or summer, nymphal ticks take a blood meal that typically lasts for 2 to 3 days. The nymphal ticks then molt as eight-legged adults in the fall. The adults mate on white-tailed deer; after mating the male dies, but the female takes one more blood meal before she lays her eggs and dies. (Modified from Habicht et al: Sci Am 257:78, 1987.)
where the vector is the western black-legged tick Ixodes pacificus, another member of the I. ricinus complex. The zoonotic transmission cycle for I. pacificus differs from I. scapularis, as evidenced by only 1.5% of I. pacificus surveyed in northern California and southwestern Oregon being infected with B. burgdorferi, a fraction too small to maintain an animal reservoir.[45] In addition, the major hosts for immature I. pacificus are species of lizards, which are not competent hosts for B. burgdorferi. [175] Instead, the enzootic cycle is maintained by a second tick, Ixodes neotomae, which does not bite humans.[18] Up to 15% of I. neotomae ticks are infected with B. burgdorferi, which is enough to maintain endemic disease. The primary host for I. neotomae is Neotoma fuscipes, the dusky-footed wood rat, which is a competent reservoir for B. burgdorferi. [37] Larval I. pacificus ticks feed on a variety of vertebrates and become infected when they feed on N. fuscipes. Transmission to humans may then occur from an infected nymph or adult. Box 33-1. INCIDENCE OF LYME DISEASE, 1996 (RATE PER 100,000 POPULATION)
Connecticut
94.8
Rhode Island
53.9
New York
29.2
New Jersey
27.4
Delaware
23.9
Pennsylvania
23.3
Maryland
8.8
Wisconsin
7.7
Cases of Lyme disease in states outside the range of I. scapularis and I. pacificus suggest that additional vectors are involved. Ticks from five genera (Amblyomma, Dermacentor, Haemaphysalis, Ixodes, Rhipicephalus) and other arthropods, such as mosquitoes, horseflies, and deerflies, are naturally infected with B. burgdorferi, but only members of the I. ricinus complex appear to be competent vectors for the disease.[172] [186] [214] [232] Investigators have found an uncultivable spirochete in Amblyomma americanum ticks, leading to speculation that a related borrelial species is causing a Lyme disease-like illnesses in the southeastern and south-central United States. Lyme disease or similar syndromes also occur in Europe, Asia, and Australia. Garin and Bujadoux[116] in France recognized as early as 1922 that neurologic abnormalities occasionally followed erythema migrans. This symptom complex has been described variously as Bannwarth's syndrome, tick-borne meningopolyneuritis, and meningopolyneuritis. The neurologic features include intense radicular pains, chronic lymphocytic meningitis, and peripheral nervous system involvement, particularly facial palsies. The full description of Lyme disease in the United States has led to the recognition of other erythema migrans-associated manifestations (arthritis and cardiac symptoms) in Europe.[121] [261] [353] Patients with these European diseases (arthritis, carditis, meningoradiculitis) demonstrate increased antibody titers against B. burgdorferi. [156] [269] [321] The established vector for European erythema migrans, I. ricinus, is closely related to the common vectors for Lyme disease in the United States, I. scapularis and I. pacificus, and the major reservoirs in Europe are species of rodents. [197] Areas of central Europe recently reported that more than 40% of I. ricinus ticks are infected by B. burgdorferi.[323] B. burgdorferi isolated from I. ricinus shows minor differences from U.S. strains in morphology, outer surface proteins, plasmids, and deoxyribonucleic acid (DNA) homology.[2] [260] [298] As a result, B. burgdorferi is now divided
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Figure 33-5 (Figure Not Available) Time course and frequency of symptoms. Approximately 50% of victims report recent tick bite. The initial stage I symptoms occur in approximately 70% to 80% of infected individuals. Weeks after the initial tick bite the skin, nervous system, and joints are most often affected as the spirochete spreads hematogenously. Stage II symptoms typically begin 4 to 10 weeks after the initial infection and occur in approximately 50% of untreated patients. Stage III typically starts much later, often 1 ½ to 2 years and rarely more than 5 years after initial infection. (Modified from Schmid GP: Rev Infect Dis 11(suppl 6):51460, 1989.)
into three strains: B. burgdorferi sensu stricto, Borrelia afzelli, and B. garinii.[323] North American isolates are limited to B. burgdorferi sensu stricto, but all three strains are found in Europe. These strain variations likely account for differences in clinical manifestations and serologic response between North American and European cases. Lyme disease cases have also been reported from China, Japan, and Russia, where the principal vector is Ixodes persulcatus, and from Australia in the Hunter Valley[320] and along the New South Wales coast.[198] No ticks of the I. ricinus complex have been found in Australia, suggesting that other vectors are likely to be identified. Spirochetal development in most ticks is limited to the midgut, but the organisms disseminate during feeding and appear in saliva, providing the likely mechanism for disease transmission.[33] [253] This phenomenon also explains the relationship between duration of tick feeding and B. burgdorferi transmission. In one study, nymphal I. scapularis transmitted B. burgdorferi to one of 14 rodents exposed for 24 hours, five of 14 rodents exposed for 48 hours, and 13 of 14 rodents exposed for 72 hours.[233] A study of persons with tick bites investigated disease progression, as diagnosed by development of erythema migrans, seroconversion on enzyme immunoassay (EIA) and immunoblot, or both. Using the established scutal index to determine length of tick engorgement, investigators found that female and nymph ticks attached
for greater than 72 hours were much more likely to induce Lyme disease than ticks attached less than 72 hours.[287] Although all three stages of the tick may bite humans, the nymph is primarily responsible for transmission of Lyme disease.[312] The small size of nymphs accounts for only 30% of patients with Lyme disease recalling a tick bite.
Box 33-2. LYME DISEASE: STAGE I Incubation: 7–10 days (range, 3–32 days) Duration: 28 days (range, 1–14 months)
SYMPTOMS (INCIDENCE) Erythema migrans (60%–89%) Mild lymphadenopathy (23%) Low-grade fever (19%–39%) Mild fatigue and malaise (54%) Neck stiffness (35%) Mild arthralgia and myalgia (44%)
CLINICAL MANIFESTATIONS.
Lyme disease is multisystemic and multiphasic. It can be divided into three stages based on chronologic relation to the original tick bite, with different clinical manifestations at each stage (Figure 33-5 (Figure Not Available) ). The disorder usually begins as a localized infection with erythema migrans and associated symptoms (stage I; Box 33-2 ).[120] [218] Within days to weeks, spirochetes may disseminate through blood or lymph, and neurologic, cardiac, or joint abnormalities may develop (stage II). Finally, chronic, persistent infection (stage III) of the joints, nervous system, skin, or eyes may occur months to years after the onset of Lyme disease. Clinical expression, however, may vary greatly. Incomplete disease presentations occur, and virtually any clinical feature may be present in isolation or recur at intervals, complicating clinical diagnosis. Although the exact roles of the infecting spirochete, spirochetal antigens, and host immune responses are unclear, tissue invasion and persistence of infection probably cause many later manifestations of Lyme disease. This concept is supported by the isolation of
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Figure 33-6 Erythema migrans rash of Lyme disease in a pregnant female. (Paul Auerbach, MD.)
B. burgdorferi from blood, skin lesions (erythema migrans), and CSF.[28] [311] The organism has also been identified in the eye,[314] myocardium,[190] and synovium.[285] Patients at all stages of disease respond to appropriate antimicrobial therapy, and early treatment generally leads to an excellent long-term prognosis. Stage I: early localized.
Erythema migrans is the most characteristic clinical manifestation of Lyme disease ( Figure 33-6 ). An average of 7 to 10 days (range, 3 to 32 days) after inoculation from a tick bite, B. burgdorferi spreads locally in the skin, producing an expanding, annular, and erythematous lesion. Initially a central red macule or papule forms at the site. As the lesion expands, partial central clearing may be seen, particularly in larger lesions, whereas the outer borders remain bright red. The borders are usually flat but may be raised and indurated. The center of some early lesions becomes intensely red and indurated or may even become vesicular or necrotic. In some cases, multiple red rings form within the outside margin, or the central area turns blue before clearing. The lesion often reaches a diameter of 15 cm (range, 3 to 68 cm), increasing in size as much as 1 centimeter per day. Erythema migrans may appear anywhere on the body. In cases with a single erythema migrans lesion, the most common sites include the head and neck region (26%), extremities (25%), back (24%), abdomen (9%), axilla (8%), groin (5%), and chest (3%).[120] Erythema migrans is usually warm to the touch and often described by the patient as burning, but occasionally as itching or painful. Constitutional symptoms may accompany erythema migrans but are usually mild and consist of regional lymphadenopathy, fever, and malaise. Fever is usually low grade but can reach 40° C (104° F) and is more common in children than adults. Lymphadenopathy is typically localized, related to the erythema migrans lesion, but can be generalized. Erythema migrans fades after an average of 3 to 4 weeks (range, 1 to 14 weeks) without treatment; with antibiotics the lesion resolves after several days. Recurrent lesions may develop 1 to 14 months after the initial lesion in victims who do not receive antibiotic therapy, appearing as erythema migrans, secondary lesions, or both. Rarely, evanescent small red circles and blotches may develop. Patients treated with appropriate antibiotics rarely have recurrent skin lesions.[310] Retrospective reviews typically note erythema migrans in 60% to 80% of patients with Lyme disease, but a prospective longitudinal cohort study of more than 200 children and an adult prospective population-based study reported erythema migrans in almost 90% of patients.[52] [120] [295] It is important to differentiate erythema migrans from local tick bite reactions, insect and spider bites, tinea, cellulitis, and plant dermatitis. Unfortunately, only a minority of victims recall a tick bite. Annular erythematous lesions occurring hours after a tick bite represent hypersensitivity reactions, not erythema migrans. In addition, a rash that resolves in 48 hours is unlikely to be Lyme disease. Biopsy of erythema migrans shows dermal and epidermal involvement at the center, but only dermal changes in the periphery, which are findings suggestive of an arthropod bite.[310] Although erythema migrans is highly suggestive of Lyme disease, it is not pathognomonic. A study of rashes in the southern United States that clinically resembled erythema migrans found little association serologically or microbiologically with Borrelia burgdorferi infection. Many of these rashes were associated with bites from the Amblyomma americanum tick, which have recently been found to be infected by Borrelia lonestarii sp nov. Currently, no known association exists among A. americanum, B. lonestarii, and a Lyme disease-like illness.[50] Stage II: early disseminated.
Within days or weeks after infection, the B. burgdorferi may spread from the skin to other organs through the blood or lymph. During this stage, spirochetes can be recovered from the blood. B. burgdorferi probably spreads initially to all organs, but like its spirochetal cousin Treponema pallidum (syphilis), it appears to sequester in
certain niches.[298] During the hematogenous spread of early disseminated disease, the most common manifestation seen is multiple erythema migrans. These annular secondary skin lesions develop in 20% to 50% of patients in the United States. The secondary lesions are generally smaller, migrate less, and lack indurated centers. They may be located anywhere except the palms
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and soles. Ten to fifteen percent of patients have more than 20 such lesions; rarely the lesions exceed 100 in number. Blistering and mucosal involvement do not occur; this is an important feature in differentiating the lesions from erythema multiforme. Other skin manifestations include a malar rash (10% to 15%) and rarely urticaria. [310] Constitutional symptoms typically accompany stage II Lyme disease. Malaise and fatigue are most common, may be severe, and are usually constant throughout the duration of the illness. Often a low-grade and intermittent fever accompanies stage II. In children, temperature elevations may be constant and can reach 40° C. Tender regional lymphadenopathy in the distribution of erythema migrans or the posterior cervical chains is common, and generalized lymphadenopathy and splenomegaly may occur.[310] Nausea, vomiting, and sore throat have also been reported. Prominent respiratory and gastrointestinal manifestations should suggest an alternative diagnosis or coinfection. Symptoms of meningeal irritation predominate in some patients. Severe headaches are typically intermittent and localized. Stiff neck with extreme forward flexion occurs, but Kernig's and Brudzinski's signs are negative. Some patients have evidence of mild encephalopathy with somnolence, insomnia, memory disturbances, emotional lability, dizziness, poor balance, or clumsiness. Dysesthesias, most often of the scalp, may be particularly bothersome. Musculoskeletal complaints are common. Arthralgias, myalgias, and pain in tendons, bursae, or bones are typically migratory, sometimes lasting only hours in one location. Patients may complain of generalized stiffness or severe cramping pain, particularly in the calves, thighs, and back. Frank arthritis is uncommon in the first several weeks of illness.[310] In 10% of patients, symptoms of hepatitis (e.g., anorexia, weight loss, nausea, vomiting, right upper quadrant pain), hepatomegaly, and generalized abdominal pain occur. Anicteric hepatic symptoms usually resolve in less than 1 week but may persist intermittently for several weeks. Respiratory symptoms are generally minor. Conjunctivitis occurs in 10% to 15% of patients.[310] During this phase of the illness, Lyme disease might easily be confused with a viral or collagen vascular disease, especially with no preceding skin rash. A distinguishing feature of Lyme disease is that early signs and symptoms are intermittent and rapidly changing. Such a pattern in a victim from an endemic area should suggest Lyme disease. After dissemination, B. burgdorferi typically produces sequestered infection, most often of the nervous system, heart, and joints. Neurologic manifestations develop in 10% to 40% of patients with erythema migrans who are not treated with appropriate antibiotics.[70] [225] Symptoms begin an average of 4 weeks (range, 0 to 10 weeks) after the onset of erythema migrans, usually after a latent period. However, neurologic signs and symptoms may be the presenting manifestations of Lyme disease. In untreated persons, symptoms usually resolve after several months (median duration, 30 weeks).[225] Meningoencephalitis is the most common neurologic presentation. Headache, typically fluctuating in intensity, is the predominant symptom. Subtle symptoms of encephalitis include sleep disturbances, poor concentration, memory loss, irritability, emotional lability, and confusional state. Unlike stage I disease, CSF examination in stage II often shows pleocytosis with an average of 100 cells/mm3 , predominantly lymphocytic, usually with elevated protein level but with normal glucose level and opening pressure.[225] Behavioral or mood disturbances are the second most common symptom reported in children and adolescents with neurologic Lyme disease. Symptoms include fatigue, difficulty concentrating in school, oppositional behavior, irritability, and anxiety.[23] Despite normal intellects, children with neurologic Lyme disease shows impaired auditory and visual sequential processing. [32] Facial nerve palsy develops in 11% of Lyme disease patients and 50% of those with Lyme disease meningitis. It may occur as an isolated finding. Facial paralysis in Lyme disease is similar to Bell's palsy, except that it is bilateral in 25% of cases. When bilateral, facial paralysis develops sequentially, with the opposite side presenting days to weeks after initial involvement. Duration of facial paralysis is from weeks to months, and 99% of patients have nearly complete return of function even if left untreated.[62] [227] Involvement of other cranial nerves is unusual. The third common neurologic manifestation of Lyme disease is radiculoneuritis, including thoracic sensory radiculitis, motor radiculoneuritis in extremities, brachial plexitis, mononeuritis, and mononeuritis multiplex. This syndrome generally presents either as a painful limb, with stabbing, shooting, or burning pains, paresthesias, weakness, and fasciculations, or as an acutely herniated disk. The outcome is generally complete recovery, although a few patients have had residual weakness.[225] Radiculopathy and peripheral neuropathy are uncommon in children with Lyme disease. [31] The triad of meningitis, cranial neuritis, and radiculoneuritis presents a unique clinical picture. However, any neurologic manifestation of Lyme disease may occur alone and may be the presenting manifestation. Other neurologic abnormalities described in association with Lyme disease include chorea, cerebellar ataxia, myelitis, dementia, pseudotumor cerebri, and optic atrophy.[248] [250] [267]
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Cardiac abnormalities develop in 4% to 10% of patients with untreated Lyme disease.[256] [309] The onset ranges from 3 to 21 weeks after the tick bite. The most common abnormality is fluctuating atrioventricular block, including first-degree, Wenckebach, or complete heart block. More than 80% of patients with documented Lyme carditis have abnormalities of the conduction system.[223] [309] Progression to symptomatic complete heart block may require a temporary transvenous pacemaker. Patients typically report dizziness, palpitations, dyspnea, chest pain, and syncope. Hospitalization with continuous cardiac monitoring is advisable for patients with a second-degree or complete atrioventricular block, as well as for those with first-degree block if the PR interval exceeds 300 milliseconds. Electrophysiologic studies indicate that the block is at the level of the atrioventricular node. The block does not respond to atropine, suggesting a direct effect on the node.[223] [256] Evidence for more diffuse cardiac involvement, most often electrocardiographic (ECG) changes compatible with myopericarditis, is found in about one half of patients with carditis. Radionuclide angiography may show left ventricular dysfunction in some patients, which is seldom clinically significant. Cardiomegaly rarely occurs in U.S. patients, although dilated cardiomyopathy is often reported from Europe. [286] [294] Valvular involvement is generally not a feature. At least one death has been linked to cardiac involvement,[190] but abnormalities usually resolve completely, often within 1 to 2 weeks.[309] Severe cardiac complications have been described in pediatric patients but are relatively rare.[120] In approximately 60% of untreated persons with erythema migrans, arthritis develops an average of 4 weeks and up to 2 years after onset of illness. The typical pattern is brief, recurrent episodes of asymmetric, oligoarticular swelling and pain in large joints, separated by longer periods of complete remission. Arthritis may be monarticular or migratory, usually one joint at a time, in as many as 10 different joints. Arthritis in a single joint is usually of short duration (median, 8 days) but may persist for months. The knee is most often affected, followed by the shoulder, elbow, temporomandibular joint, ankle, wrist, hip, and small joints of the hands and feet.[362] Many regard the rheumatologic findings of Lyme disease as primarily a North American phenomenon.[298] [324] Frank arthritis with joint swelling usually does not begin until months after onset of illness, and other than the knee, joint swelling is unusual. Inflamed knees are typically more warm and swollen than red or painful. Baker's cysts may develop and rupture, simulating thrombophlebitis. A majority of patients have repeated attacks, averaging three recurrences, which become less frequent and less severe over time.[302] In children, arthritis may be more delayed, developing an average of 4.3 months (range, 2 days to 20 months) after onset of illness. Children also often have complete resolution between recurrences, whereas adults more often have chronic effusions and morning stiffness between episodes. In a prospective study of patients with Lyme arthritis confirmed by CDC criteria, 90% had arthritis in at least one knee.[119] Half the children had only a single episode of arthritis, and half had recurring joint involvement. Most children did well regardless of whether they received antibiotic treatment.
Synovial fluid in Lyme disease is inflammatory, with a median WBC count of 25,000/mm3 , predominantly polymorphonuclear leukocytes. Higher counts may simulate septic arthritis.[146] Complement level is generally greater than one-third that of serum, and protein level ranges from 3 to 8 g/dl. Synovial biopsy reveals hypertrophy, vascular proliferation, and a mononuclear cell infiltrate.[307] Although B. burgdorferi DNA can be detected by polymerase chain reaction (PCR) in the synovial fluid of up to 85% of untreated patients with Lyme arthritis, the organism is rarely cultured successfully from joint fluid.[221] [307] After treatment with antibiotics, B. burgdorferi DNA can no longer be detected in synovial fluid. Other reported manifestations of stage II Lyme disease occur much less frequently. Conjunctivitis can be a transient, early ophthalmologic manifestation in disseminated disease. In one patient, iritis progressed to panophthalmitis and unilateral blindness, with spirochetes isolated in the vitreous debris.[310] Other findings associated with B. burgdorferi infection include adult respiratory distress syndrome (ARDS),[163] myositis,[12] and osteomyelitis.[146] A solitary borrelial lymphocytoma may develop in patients with Lyme disease from Europe (approximately 1% of cases); it occurs rarely in patients in the United States. This tumorlike nodule is associated with B. afzelli and B. garinii and is characterized histologically by a dense polyclonal lymphocytic infiltrate with germinal centers in the dermis or cutis. Clinically it presents as a red to dark-blue-red nodule a few centimeters in diameter, most often on the earlobe in children and the nipple in adults. The lesion is often painful or itchy. Onset ranges from 1 to 6 months (mean 1.8 months) after a tick bite. Untreated, borrelial lymphocytoma may persist for many months, but it usually disappears within a few weeks after antibiotic therapy. [325] In one study the lesion resolved after 6 weeks in 86% of patients after treatment with antibiotics.[326] Patients with borrelial lymphocytoma are likely to have systemic disease and should be evaluated for neurologic and cardiac involvement. Stage III: late disease.
Late or persistent infection usually begins a year or more after the onset of erythema
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migrans, although patients may present with stage III disease as the initial manifestation of Lyme disease. The skin, joints, and nervous system are most often affected. Chronic arthralgias and oligoarthritis develop in about 50% of untreated patients.[306] In about 10% of adult patients with arthritis the knees or other large joints become chronically involved, as seen radiographically. Juxtaarticular osteoporosis, cartilage loss, cortical or marginal bone erosions, and joint effusions may be seen. Features of degenerative arthritis, cartilage loss, subarticular sclerosis, and osteophytosis are found less often.[175] Patients usually do not have continual joint inflammation for more than several years, and recurrences tend to become progressively milder.[303] Rheumatoid and antinuclear antibodies are generally absent,[307] although the incidence of B cell alloantigens DR2 and DR4 appears to be increased in patients with chronic Lyme arthritis.[301] The chronic form is unusual in children.[119] Patients with Lyme disease may develop persistent nervous system involvement months to years after becoming infected. Several distinct but often overlapping syndromes have been described. The best established syndrome is a severe, progressive encephalomyelitis characterized clinically by spastic paraparesis, cerebellar ataxia, cognitive impairment, bladder dysfunction, transverse myelitis, hemiparesis, and cranial neuropathy, particularly of the seventh and eighth cranial nerves.[3] CSF examination typically shows a lymphocytic pleocytosis and intrathecal production of anti-B. burgdorferi antibody. Magnetic resonance imaging of the brain may show abnormalities of the white matter. Among seropositive persons, boys seem to develop neurologic symptoms more than girls. Chronic involvement of the peripheral nervous system also occurs in Lyme disease. Patients may have painless distal paresthesias or painful radiculopathy. The distal paresthesias are generally intermittent, are often symmetric, and involve the legs more frequently than the upper extremities. Radicular pain is more frequently asymmetric and may involve the cervical, thoracic, or lumbosacral segments, often in combination. The pain is typically spinal with radiation into the affected limbs or trunk.[179] Nerve conduction and electromyographic studies suggest a mild axonal polyneuropathy with reductions in motor or sensory nerve conduction velocities and denervation of spinal and limb muscles.[180] The underlying pathophysiologic mechanism appears to be mononeuritis multiplex. [105] Rarely, patients with neuroborreliosis may have strokes, seizures, or severe dementia.[97] Several syndromes have also been described in which the association with infection by B. burgdorferi is less certain. Some patients with serologic evidence of infection develop mild encephalopathy with memory difficulties, depression, mood swings, language disturbances, and fatigue. These patients may or may not have increased intrathecal production of antibodies to B. burgdorferi, although some do show improvement with antibiotic treatment.[179] The syndromes termed postborreliosis disorders are more problematic. After treatment for Lyme disease, many patients note persistent fatigue, sleep disorders, depression, or cognitive difficulties. The cause is unknown, and patients do not respond to antibiotics.[105] Acrodermatitis chronica atrophicans is the best example of prolonged latency followed by persistent infection in Lyme disease. Observed primarily in Europe where the causative organism is B. afzelli, the dermatitis may develop years after the onset of illness.[216] [298] It begins with an inflammatory phase with bluish red discoloration, often at the site of a previous erythema migrans lesion, preferentially involving the extensor surfaces of the extremities. The inflammatory phase may persist for years or decades, with gradual conversion to atrophy of the skin.[11] After initial hyperpigmentation, hypopigmentation develops, and eventually the skin becomes frail. One third of patients have an associated (usually sensory) polyneuropathy. Other, unusual late manifestations of Lyme disease include recurrent hepatitis, myositis, eosinophilic lymphadenitis, and ARDS. Several patients with a history of Lyme disease developed a keratitis similar to syphilitic keratitis years after their initial infection.[298] Late Lyme disease occurs infrequently in children.[370] The roles of persistent infection with B. burgdorferi immune mechanisms in late Lyme disease remain unclear. PCR studies show B. burgdorferi in joint fluid and CSF of untreated patients with late Lyme disease. After antibiotic therapy, PCR studies may be negative, although inflammation persists within involved joints, especially in patients with HLA-DR4 B-cell alloantigens.[221] Immune mechanisms may also play a role in chronic neurologic disease. LYME DISEASE DURING PREGNANCY.
Lyme disease during pregnancy historically has been of considerable concern because other spirochetes, the treponemes, cause significant congenital infection. The risk of fetal and postnatal complications of Lyme disease during pregnancy require further study, but human transplacental transmission of B. burgdorferi has been documented.[184] [193] [268] [354] In each case the infant was either stillborn or died shortly after birth; one mother had been treated with oral penicillin for Lyme disease early in pregnancy.[354] However, fetal infection appears to be rare. In a report of 19 pregnancies complicated by Lyme disease, five had an adverse outcome, although several were minor with no permanent sequelae, and no two outcomes were the same. B. burgdorferi infection was not documented in any fetus or neonate, and disease exposure earlier in pregnancy was not associated with
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increased adverse outcome.[193] Serologic surveys in endemic areas also suggest a low but real risk of fetal transmission. One survey of 2014 pregnant women in Westchester County, New York, showed 0.7% seropositivity, with no significant difference in obstetric outcomes between seropositive and seronegative mothers.[327] In a second report comparing serologic status, 8% of neonates from endemic areas were seropositive for B. burgdorferi from cord blood sampling, compared with only 0.8% in infants from nonendemic regions. All neonates with positive serology showed an immunoglobulin (IgG) response, but none had elevated B. burgdorferi IgM antibodies. Neonates from the endemic region had fewer malformations but a significantly increased rate of cardiac malformations compared with the non-endemic group.[361] Despite the increase in Lyme disease, the risk of adverse outcome during pregnancy remains low. No clear association exists between Lyme disease and congenital anomalies, and no distinct pattern of teratogenicity has been identified. The risk of transplacental transmission appears minimal, and currently, no published data support a congenital Lyme disease syndrome. Despite the relatively low risk, women who acquire Lyme disease during pregnancy should be treated promptly with antibiotics. A 1996 prospective study of 58 pregnant women with erythema migrans given oral or intravenous (IV) penicillin or ceftriaxone reported only seven adverse outcomes, unrelated and none clearly associated with Lyme disease.[188] Although no randomized trials have compared oral with parenteral therapy during pregnancy, the American College of Obstetrics and Gynecology (ACOG) recommends oral penicillin or amoxicillin for three weeks in patients with early localized disease or those with recent deer tick bites. For patients with severe acute disease, neurologic sequelae, or chronic disseminated disease, the ACOG recommends IV therapy with penicillin.[8] Others also recommend IV penicillin, 20 million units/day in divided doses for 10 to 14 days.[354] In patients allergic to penicillin, erythromycin (500 mg four times daily) is an alternative. Ceftriaxone
has also been recommended.[216] Pregnant or lactating women should not receive tetracyclines. DIAGNOSIS.
The diagnosis of early Lyme disease is best made using careful consideration of clinical and epidemiologic data. According to the CDC surveillance criteria, the clinical diagnosis includes exposure to an endemic region by a patient presenting with erythema migrans and accompanying generalized symptoms. Diagnosis with early disease does not require laboratory confirmation. However, incomplete cases without erythema migrans may prove difficult to diagnose, presenting as a viral-like illness.[99] Arthritis or neurologic involvement may develop months after the cutaneous eruption, which the patient may not remember. Most patients do not recall a tick bite. The confirmation of late disease requires clinical evidence of disseminated disease plus laboratory evidence of infection. Routine laboratory studies add little to the early diagnosis of Lyme disease and should not be used as a screening tool in healthy persons. Most patients have a mildly elevated erythrocyte sedimentation rate (ESR), gamma-glutamyltransferase (GGT), aspartate transaminase (AST, SGOT), and alanine transaminase (ALT, SGPT), and decreased absolute WBC count. Some patients have mild anemia. Immunoglobulins A and G are usually normal, whereas IgM may be elevated, especially in severe and neurologic or arthritic disease. Positive culture for B. burgdorferi is the best laboratory evidence of causality but is difficult to obtain. Skin culture may be useful in patients in whom primary erythema migrans lesions are suspected. Saline lavage-needle aspiration and 2-mm punch biopsy of the leading edge of a suspected erythema migrans lesion obtain spirochetes in 29% and 60% of samples, respectively. [371] In specialized laboratories, the success rate of skin biopsy may be as high as 80%.[29] Biopsy from other areas is typically unsuccessful. Other tests to detect B. burgdorferi infection lack sensitivity or are primarily research tools. Direct visualization techniques have yields too low to be clinically useful and are difficult to distinguish from elastin tissue fibers, procollagen fibers, and other artifacts.[279] Urine antigen testing lacks sensitivity. PCR technology amplifies genomic and nongenomic gene sequences of B. burgdorferi from tissue samples and can be used as a surrogate to culture. DNA sequences can be detected in blood, urine, CSF, skin, and synovial fluid of patients with Lyme disease. PCR testing is promising but is not standardized and has large interlaboratory variability. Accordingly, routine use of PCR is not currently recommended for the diagnosis of Lyme disease. This leaves detecting indirect evidence of infection—antibodies to B. burgdorferi—as the only practical laboratory aid to diagnosis. Unfortunately, antibody response to B. burgdorferi develops slowly. Serologic studies are usually negative in the first 3 to 6 weeks of illness, particularly in patients with limited manifestations. However, patients with complicated Lyme disease (neurologic, cardiac, or joint involvement) or those in remission typically have elevated specific antibody titers.[206] [279] IgM antibody titers generally peak between the third and sixth weeks after the onset of illness; IgG antibody titers rise slowly and are highest weeks to months later when arthritis is present. Early treatment with antibiotics may blunt or completely suppress antibody formation. Both IgM and IgG antibodies may persist for months or years after clinical resolution, even after treatment with appropriate antibiotics.[98] Also, patients with early disseminated
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Lyme disease (carditis, meningitis, neuropathy) may be seronegative. Current methods for detecting antibodies to B. burgdorferi include indirect immunofluorescent assay (IFA), enzyme-linked immunosorbent assay (ELISA), and Western blot or immunoblot. In most laboratories, ELISA appears to be the test of choice for evaluation of suspected Lyme disease (89% sensitivity, 72% specificity), although IFA can be comparable when performed by experienced technicians.[125] [340] Western blot is often used as the second test in a two-test protocol to increase the specificity of serologic testing by demonstrating the presence of antibodies to epitopes that are unique to B. burgdorferi.[85] Western blot's particular usefulness lies in identifying false-positive results. Because a positive ELISA result is usually statistically defined as a value two standard deviations above the mean, approximately 5% of the normal population will have a "false-positive" result. Consequently, according to the CDC national consensus panel, positive results from serologic testing are significant only if both ELISA and Western blot are positive. False-positive results are also common in patients with other treponemal diseases (syphilis, yaws, and pinta), leptospirosis, relapsing fever, viral infections (varicella), and autoimmune diseases such as systemic lupus erythematosus (SLE).[206] Patients with Lyme disease, however, do not have positive Venereal Disease Research Laboratories (VDRL) tests. In addition, antibodies directed toward oral flora may cross-react, causing false-positive results.[206] [252] The importance of appreciating the limitations of serologic testing cannot be overstated. Considerable caution must be exercised in interpreting test results. In one study, only 23% of patients referred to the Lyme Disease Clinic at New England Medical Center had active Lyme disease, and a majority of those without Lyme disease had been treated inappropriately with antibiotics.[304] In this study, the most common reason for lack of response to antibiotics was misdiagnosis. The limitations of laboratory testing in Lyme disease include lack of sensitivity and specificity of serologic tests and considerable interlaboratory and intralaboratory variability in test results.[274] The persistence of antibodies in patients with past or asymptomatic infection with B. burgdorferi also complicates serologic testing. If another illness develops, as occurred in 20% of patients referred to the New England Medical Center clinic, it may be incorrectly attributed to Lyme disease. This is particularly problematic in patients with nonspecific symptoms of chronic fatigue or fibromyalgia, in whom the predictive value of a positive ELISA is low. The overdiagnosis of Lyme disease has significant health system and patient care implications. In a study of 209 individuals referred to a university-based Lyme disease clinic with a diagnosis of the disease, only 21% met criteria for active Lyme disease, 60% had no evidence of current or previous infection, and 19% had evidence of previous but not active disease. The 79% of patients without active Lyme disease displayed significant anxiety and stress related to their diagnosis of Lyme disease, used considerable health care resources, and had frequent adverse antibiotic reactions. [249] Diagnosis of Lyme disease requires careful consideration of epidemiologic and clinical information, supplemented by serologic testing when appropriate. For greatest cost-effectiveness, testing by serologic means should be guided by a patient's pretest likelihood of disease, taking into account exposure history, endemicity, and clinical signs and symptoms. Only 1.2% of tick bites in endemic regions result in erythema migrans.[340] For patients in nonendemic areas and with nonspecific symptoms, the pretest probability of Lyme disease is low, and these patients should not be referred for laboratory testing. Likewise, even patients from endemic areas who only present with nonspecific symptoms (e.g., fatigue, headache, myalgias, arthralgias, palpitations) have a low pretest probability and should not be referred for serologic testing. Serologic testing is most useful in patients with an intermediate pretest probability of having Lyme disease (20% to 80%). Serologic testing should be done in a reference laboratory and confirmed with a Western blot. In patients from endemic areas who have erythema migrans, serologic tests are not indicated because the pretest probability of Lyme disease is very high; a negative serologic test is likely to be a false negative. Many patients with localized Lyme disease have not developed antibodies at the time of testing, especially if drawn within 2 weeks of symptom onset. These patients should be assumed to have Lyme disease, whether or not serologic tests are positive, and treated empirically. Convalescent titers are not helpful, since early antibiotic treatment may prevent seroconversion. Uncertainty about a lesion being erythema migrans demands careful observation. A lesion that resolves in 1 to 2 days, that does not expand centrifugally, or that is less than 5 cm in diameter is unlikely to be erythema migrans.[118] If Lyme probability appears intermediate after considering the factors of exposure, tick history, and clinical manifestations, the two-step ELISA and Western blot testing is recommended. Most patients with symptoms of early disseminated or late Lyme disease have positive serologic tests. If clinical and epidemiologic data strongly support the diagnosis of Lyme disease, however, antibiotic treatment is appropriate even with negative findings, since some patients will not have seroconverted. Although patients with symptoms of central nervous system (CNS) involvement often undergo CSF testing for B. burgdorferi antibodies, this is not always necessary.[118] The CDC surveillance criteria require diagnostic levels of IgM or IgG antibodies to B. burgdorferi in serum or CSF.
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Because almost all neuroborreliosis patients have positive serum serologies, CSF testing is not required to diagnose Lyme disease. As noted, a positive test does not establish the diagnosis of Lyme disease but merely indicates that infection has likely occurred in the past. Because immunoglobulins can persist in the serum for years after clinical improvement, serology testing has no role in measuring treatment response. The sensitivity and specificity of T-cell recognition of B. burgdorferi antigens are controversial.[298] [340] In patients with isolated nonspecific symptoms such as chronic fatigue, transient musculoskeletal pain, or difficulty concentrating, Lyme serologic tests should not be performed. These symptoms are rarely if ever the sole manifestation of Lyme disease. The pretest probability of Lyme disease in this situation is so low that a positive test is likely to be a false positive.
TREATMENT.
Most manifestations of Lyme disease will resolve without treatment; however, appropriate antibiotic therapy hastens resolution in all stages of disease and prevents later complications.[264] [312] B. burgdorferi is highly sensitive to tetracycline, aminopenicillins, ceftriaxone, and imipenem, both in vitro and in vivo.[151] [152] [153] Alternative antimicrobials include penicillin (unlike Treponema pallidum, however, B. burgdorferi is only moderately susceptible), oxacillin, chloramphenicol, macrolides, and several newer oral cephalosporins. Both cefixime and cefuroxime appear to have equal efficacy to standard therapy.[6] [153] Cefuroxime axetil and possibly azithromycin have been found comparable with doxycycline in a clinical trial in patients with early Lyme disease.[183] [217] [299] Erythromycin also has good in vitro activity but is not as effective as amoxicillin or doxycycline in vivo. Aminoglycosides, sulfa drugs, first-generation cephalosporins, quinolones, and rifampin have little activity against B. burgdorferi. Table 33-2 outlines the current approach to antimicrobial therapy in Lyme disease. In stage I Lyme disease, amoxicillin and doxycycline are the drugs of choice. Amoxicillin is safe in pediatric and pregnant patients. The recommended duration of therapy is at least 14 days and up to 4 weeks if symptoms persist or recur. Because B. burgdorferi is very slow growing, prolonged antibiotic exposure may be necessary to kill the organism.[6] Also, some treatment failures have occurred with shorter courses of therapy, so many clinicians recommend at least 21 days of therapy. Choosing an antimicrobial agent for early Lyme disease also depends on attainable CSF levels, since B. burgdorferi can invade the CNS early in the course of infection, even in the absence of specific neurologic symptoms.[182] Although some clinicians have used probenecid to increase serum levels of amoxicillin, probenecid may block the entry of beta-lactam antibiotics into brain parenchyma and thus should not be routinely administered.[368] Oral penicillin and erythromycin are not recommended because they are less effective at preventing late complications (myocarditis, arthritis, meningoencephalitis) than amoxicillin and doxycycline.[310] Within the first 24 hours of therapy, 15% of patients develop a Jarisch-Herxheimer reaction (JHR), with worsening fever, rash, malaise, and arthralgias. [216] [217] [312] Treatment for JHR is symptomatic with nonsteroidal antiinflammatory drugs (NSAIDs), and symptoms rarely continue beyond 24 hours from the time of antibiotic administration. Antimicrobials should not be discontinued. Treatment of early disseminated Lyme disease should be based on the severity of disease. Patients with mild disease, such as facial nerve palsy with normal CSF, first-degree heart block with a PR interval less than 0.30 second, multiple erythema migrans lesions, or early arthritis, can be treated with any of the oral regimens for 3 weeks. In a trial of patients with early disseminated borreliosis without meningitis, a 21-day course of oral doxycycline was equal in efficacy to 14 days of parenteral ceftriaxone.[75] Patients with severe disease (evidence of meningoencephalitis or more severe heart block) should be treated with parenteral antibiotics. IV penicillin (meningitis dosage), ceftriaxone (2 g every 24 hours for 2 to 4 weeks), and cefotaxime are all effective in treating CNS involvement (meningitis, cranial neuritis, or radiculoneuritis) in Lyme disease.[8] [230] [303] Ceftriaxone was more effective in some studies than penicillin, and the once-daily dose schedule makes outpatient treatment feasible. [73] [74] Meningitic symptoms usually resolve with therapy in 1 week, although complete recovery of motor deficits may require 7 to 8 weeks.[306] No controlled studies have compared oral vs. parenteral therapy for Lyme carditis, and cardiac manifestations of Lyme disease usually resolve within 1 to 2 weeks, even without antibiotic treatment.[8] However, B. burgdorferi can directly invade the myocardium and produce a cardiomyopathy.[294] Other manifestations of disseminated infection also occur in patients with cardiac involvement. [239] For these reasons, patients with evidence of cardiac involvement more severe than a first-degree heart block should be treated with IV antibiotics for at least 2 weeks. Such patients should also be admitted for telemetry and possible temporary pacemaker placement if complete heart block develops. Optimal therapy for Lyme arthritis remains controversial. Several oral and parenteral regimens have been used successfully. A reasonable approach for patients without evidence of neurologic involvement is to use an oral regimen initially.[308] Four to eight weeks of oral antimicrobial therapy is recommended for acute, intermittent, or chronic arthritis. Generally these patients do well, but treatment failures occur.[69] If an adequate clinical
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DRUG
DOSE
TABLE 33-2 -- Antimicrobial Recommendations for Lyme Disease DURATION
EARLY LOCALIZED DISEASE Adults Tetracycline
250 mg po qid
14–28 days
Doxycycline
100 mg po bid
14–28 days
Amoxicillin
500 mg po tid
14–28 days
Cefuroxime
500 mg po tid
14–28 days
Amoxicillin
50 mg/kg/day po tid
14–28 days
Doxycycline (over 8 yr)
100 mg po bid
14–28 days
Erythromycin
30–50 mg/kg/day po qid
14–28 days
Tetracycline (over 8 yr)
250 mg po qid
14–28 days
Cefuroxime axetil
30–40 mg/kg/day po bid
14–28 days
Children
EARLY DISSEMINATED AND LATE DISEASES* LATE DISSEMINATED NEUROLOGIC DISEASE† Adults Ceftriaxone
2 g/day IV qd
14–28 days
Cefotaxime
2 g/day IV q8h
14–28 days
Penicillin G
20 million IU/day IV q4h
14–28 days
Ceftriaxone
75–100 mg/kg/day IV qd
14–28 days (max, 2 g/day)
Cefotaxime
90–180 mg/kg/day IV q8h
14–28 days
Penicillin G
300,000 U/kg/day IV q4h
14–28 days (max, 20 million U/day)
Amoxicillin
500 mg po qid
28 days
Doxycycline
100 mg po bid
28 days
Ceftriaxone
75–100 mg/kg/day IV qd
14 days
Amoxicillin
50 mg/kg/day po tid
28 days
Ceftriaxone
2 g/day IV qd
14 days
Children
LATE DISSEMINATED ARTHRITIS Adults
Children
DISSEMINATED DISEASE AND CARDITIS Adults Doxycycline
100 mg po bid
21–28 days‡
Amoxicillin
500 mg po q8h
21–28 days‡
Ceftriaxone
2 g/day IV qd
14–28 days§
Ceftriaxone
75–100 mg/kg IV/IM qd
14–21 days (max, 2 g/day)
Penicillin G
300,000 U/kg/day IV q4h
14–21 days (max, 20 million U/day)
Children
po, Orally; IV, intravenously; IM, intramuscularly; bid, twice a day; tid, three times a day; qid, four times a day; qd, every day; q4h or, q8h, every 4 or 8 hours. *For multiple erythema migrans, use treatment for early localized disease for at least 21 days. For isolated facial palsy, use treatment for early localized disease for at least 21 to 28 days. †Neurologic involvement limited to an isolated facial palsy should be treated as early disease. ‡For mild cardiac involvement, i.e., first degree atrioventricular block with PR interval less than 0.30 second. §For second- or third-degree heart block, although no evidence indicates that intravenous is better than oral regimens.
response is not obtained, a parenteral regimen can be tried. Clinicians should keep in mind, however, that the response to antibiotics may not occur for 3 months or longer after completion of therapy.[239] Treatment can be augmented with NSAIDs.[216] In chronic infection (stage III) the outcome after antibiotic treatment is usually favorable, but incomplete resolution is common.[179] In cases of chronic neuroborreliosis, treatment should consist of at least 28 days of IV antibiotics.[74] [181] Some experts now advise continuation
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of treatment for an additional month for late Lyme disease manifestations that do not completely respond to an initial 4-week regimen. In 23 patients with late disease, ceftriaxone had better efficacy than IV penicillin.[74] One case report suggests ß-lactam resistance as a possible cause for suboptimal resolution of disease with penicillin treatment.[117] ASYMPTOMATIC TICK BITES.
Patients with asymptomatic tick bites frequently present for care. In one survey, physicians in Maryland reported seeing 11 times as many patients seeking help after "tick bites" than true diagnosed cases of Lyme disease.[66] Three randomized, placebo-controlled studies have addressed antibiotic prophylaxis for tick bites.[7] [65] [277] Patients in the placebo groups developed Lyme disease or seroconversion 1% to 3.4% of the time, despite 15% to 30% of ticks being infected. No patients in the treatment groups developed Lyme disease. A meta-analysis of the three studies concluded that there was no significant difference between the groups and that routine prophylaxis of tick bites is not warranted, even in endemic areas.[352] Many physicians do not adhere to this recommendation. Maryland physicians ordered serologic testing in two thirds of patients with asymptomatic tick bite and treated more than half with prophylactic antibiotics.[109] The major area of concern appears to be patients with tick bites who become infected but do not develop erythema migrans (when the disease is easily treated) then develop the late and more serious manifestations of Lyme disease. However, the risk of serious late sequelae in untreated patients with a tick bite is extremely low. First, less than 5 % of those bitten by the I. scapularis tick in endemic areas become infected. Second, most patients with an identified tick bite remove the tick before it has been attached for the 36 to 48 hours required to transmit an infectious inoculum of B. burgdorferi. Finally, 80% to 90% of the few patients who do become infected will develop erythema migrans, which is easily treated. Physicians should weigh a number of factors related to the likelihood of disease acquisition in deciding whether to treat asymptomatic tick bites with antibiotics. Those factors include species and stage of the offending tick, duration of attachment, geography, and patient factors such as pregnancy. If a decision is made to treat, the literature supports using a 10-day course of amoxicillin or doxycycline. VACCINE.
The high incidence of Lyme disease and the potential for long-term morbidity have led investigators to focus increasing effort on developing an effective vaccine. Two large trials of vaccines against the outer surface protein A (Osp A) of B. burgdorferi have been completed. Efficacy was 49% to 68% after the second dose, increasing to 76% to 92% after three doses. [279] [317] Both vaccines were administered in three doses at 0, 1, and 12 months. The vaccines appear to work by neutralizing spirochetes in the midgut of the biting tick during engorgement but before transmission of the organism.[115] [281] One of the vaccines, LymeRix, has received Food and Drug Administration (FDA) approval. The vaccine is recommended for individuals 15 to 65 years of age living in highly endemic areas or those in intermediate areas with extensive work outside in forested, grassy areas. The Osp A vaccine caused few complications in either trial or in earlier safety trials; the most common side effects were localized pain and tenderness. [160] However, these first generation vaccines are not without problems. Because the vaccines are not 100% effective, vaccinated patients can still contract Lyme disease. In recent trials, antibody levels appear to decrease rapidly after vaccination, suggesting the need for boosters to maintain immunity. [115] Follow-up studies are required to determine long-range efficacy beyond 20 months, and new vaccine schedules must be devised with the goal of achieving full immunization within one Lyme disease season. The current vaccines are not approved for children under age 15, despite children representing almost one fourth of Lyme disease cases.[194] In addition, because antibodies to B. burgdorferi proteins react in vitro with cardiac and skeletal muscle proteins, neuronal tissue, hepatocytes, and synovial cells, the FDA advisory committee has urged caution in using the Osp A vaccine in persons with arthritis. Finally, the Osp A vaccines result in a positive ELISA result but a negative Western blot.[369] This may lead to confusion if clinicians follow the recommended two-step testing protocol. Inactivated whole-cell vaccines are effective in laboratory animals and are available for use in dogs. Delays in use of whole-cell vaccines for humans stem from concern that molecular mimicry of whole-cell proteins may lead to immune cross-reactivity and chronic inflammatory conditions. Relapsing Fever.
Relapsing fever is an acute borrelial disease characterized by recurrent paroxysms of fever separated by afebrile periods. It occurs in both endemic and epidemic forms ( Table 33-3 ). The endemic or sporadic form occurs worldwide and is caused by a group of closely related Borrelia species. Argasid ticks belonging to the genus Ornithodoros and wild rodents both serve as reservoir hosts, but the tick serves as the main vector. [338] The epidemic form of relapsing fever is transmitted by the human body louse; it has not been reported in the United States in recent years. The Ornithodoros ticks that transmit tick-borne relapsing fever (TBRF) act as both vectors and reservoirs for Borrelia organisms. Transovarial transmission allows all developmental stages to be potentially infective. The
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ARTHROPOD VECTOR
TABLE 33-3 -- Tick-Borne Relapsing Fever Borreliae BORRELIA SPECIES GEOGRAPHIC DISTRIBUTION
Ornithodoros hermsii
B. hermsii
Western United States and Canada
O. turicata
B. turicatae
Southwestern United States and Mexico
O. parkeri
B. parkeri
Western United States and Mexico
O. moubata
B. duttonii
Tropical Africa
O. tholozani
B. persica
Central Asia, Middle East, Greece
O. tartakovskyi
B. latyschevi
Iran, Central Asia
O. erraticus
B. crocidurae
Russia, Middle East, East Africa, Turkey
O. graingeri
B. graingeri
Kenya
O. talaje
B. mozzottii
Mexico, Central America
O. rudis
B. venezuelensis
Central and South America
O. asperus
B. caucasica
Iraq, Russia
O. marocianus
B. hispanica
Northern Africa, southern Europe
ticks generally feed at night and attach themselves to the host for a short time, usually less than 1 hour. The bite is seldom painful and frequently goes unrecognized. The ticks are extremely resilient and may survive for years between feedings. Ticks ingest Borrelia organisms while feeding on an infected vertebrate, most often a rodent. Borreliae enter the tick hemocele and then spread to other tick tissues, including the salivary glands, coxal organs, and reproductive organs. The coxal organs in argasid ticks are specialized tissues for excretion of excess fluids and solutes accumulated during feeding. In some Ornithodoros species, the coxal fluid is released near the mouthparts during feeding, allowing transmission of spirochetes to vertebrate hosts. Transmission may also occur through saliva or regurgitated gut contents. [19] Borreliae remain infective within ticks for many months.[288] A high degree of specificity exists between the major strains of relapsing fever Borrelia and associated tick vectors. For instance, the three Borrelia species found in the United States—B. hermsii, B. turicatae, and B. parkeri—show complete specificity for their respective vectors, which are O. hermsi, O. turicata, and O. parkeri. B. hermsii can be transmitted only by O. hermsi, not by O. turicata or O. parkeri. This specificity is used extensively in classification of Borrelia species.[76] EPIDEMIOLOGY.
Ornithodoros ticks generally inhabit rodent burrows and nests, cracks and crevices in human and animal habitats, caves, and similar locations. Habits and patterns of infection vary between tick species. In parts of Africa, ticks live in the dust and cracks of earthen-floored huts, and sporadic cases are seen throughout the year. In the Middle East, Mexico, and southwestern United States, ticks live in the guano of cave floors, and human infection is often associated with visiting or camping in caves. The majority of cases of TBRF in the United States are attributed to B. hermsii. Its vector, O. hermsii, inhabits the coniferous forest biome of the western United States and Canada, where it lives in remains of dead trees and burrows inhabited by mice, rats, and chipmunks. Ticks are carried by rodents into poorly maintained cabins and huts; lodging in such shelters by hikers and hunters is a major factor in acquiring relapsing fever.[104] [144] Occasional cases are also caused by O. turicata (transmitting B. turicatae) in Texas (associated with travel into caves) and adjacent areas of the Southwest; O. parkeri (transmitting B. parkeri) rarely bites humans.[143] TBRF is found throughout most of the world, although endemic areas include Colorado,[90] [144] California,[90] the Pacific Northwest,[104] southern British Columbia, plateau regions of Central and South America, central Asia, Mediterranean countries, and most of Africa. In California, where reporting of relapsing fever is encouraged, two to 12 cases are reported per year. [90] Large outbreaks have been reported from Spokane County, Washington,[333] Colorado,[338] and the north rim area of the Grand Canyon.[53] Between 1985 and 1996, the 285 cases of TBRF reported in the United States occurred in California, Colorado, Idaho, Texas, Washington, Arizona, New Mexico, Nevada, Oregon, Utah, and Wyoming.[338] TBRF is more common in men, presumably because of increased exposure to tick vectors, and occurs primarily during summer months. TBRF is rarely fatal in adults, but in infants less than 1 year of age, case fatality rates may be 20% or higher.[176] [288] CLINICAL MANIFESTATIONS.
The characteristic clinical feature of TBRF is abrupt onset of fever lasting about 3 days (range, 12 hours to 17 days), an afebrile period of variable duration, and then relapse with return of fever and other clinical manifestations. The initial febrile period terminates with rapid defervescence or a "crisis," accompanied by drenching sweats and intense thirst. Febrile periods in TBRF are associated with bacteremia. Resolution of fever occurs when the host develops an adequate antibody response to the spirochete. During
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afebrile periods the spirochete remains "hidden" in organ tissue and undergoes antigenic conversion to a new serotype. Relapse occurs when the new serotype causes bacteremia. After being bitten by an infected tick, victims may develop a pruritic eschar at the site of the tick bite, but the lesion is usually absent by the onset of clinical symptoms. After an incubation period of approximately 7 days, victims develop fever, frequently accompanied by shaking chills, severe headache, myalgias, arthralgias, upper abdominal pain, photophobia, cough, nausea, and vomiting. The temperature is usually greater than 39° C (102.2° F), and patients may manifest extreme muscular weakness and lethargy. Splenomegaly develops in approximately 40% and hepatomegaly in 18% of TBRF patients. From 10% to 40% have neurologic involvement, approaching the incidence seen in Lyme disease. The most common neurologic complications are meningismus and facial nerve palsy.[48] Facial palsy, when present, typically occurs after the second febrile episode and usually resolves within 2 to 9 weeks with or without treatment. Other reported neurologic complications include neuropsychiatric disturbances, encephalitis, peripheral neuropathy, myelitis, and pathologic reflexes. Iritis or iridocyclitis occurs in up to 15% of untreated cases, typically occurring later in the fever course. Formation of adhesions between the iris and anterior lens capsule frequently leads to visual defects. A rash, ranging from a macular eruption to petechiae and erythema multiforme, develops in 25% to 30% of patients.[288] Mortality rates have been as high as 40% in some epidemics of louse-borne relapsing fever,[280] but TBRF is generally self-limited, although clinical features may be severe and prolonged. Neurologic complications generally resolve spontaneously, but severe depression may persist for months. Hemorrhagic complications, pneumonia, ARDS, hepatosplenomegaly, petechiae, or myocarditis may develop rarely.[77] [104] [357] Relapsing fever in pregnancy results in a high incidence of spontaneous abortion,[288] premature birth, and perinatal morbidity. [156] Fetal death is probably caused by direct placental invasion by spirochetes, resulting in thrombocytopenia and retroplacental hemorrhage. [297] Prior studies have linked pregnancy with a more serious maternal disease course.[132] [205] [206] A more recent case-control study, however, found no significant difference in pregnant women's mortality or complications.[155] Infection in the neonatal period usually occurs by placental transmission and presents as overwhelming sepsis with very high mortality.[372] ANTIGENIC VARIATION.
The phenomenon of relapse in TBRF is caused by the ability of borreliae to undergo antigenic variation in an infected host. The organisms are capable of spontaneous conversion to many serotypes. Clinically, defervescence occurs when the dominant serotype is eradicated by interaction with host antibody. Spirochetemia probably persists at undetectable levels during the afebrile period and consists of mixed serotypes. Relapse occurs when a variant population reaches detectable levels. Antigenic variation is under complex genetic control and does not appear to require contact of the organism with host antibody.[17] [322] DIAGNOSIS.
The clinical diagnosis of TBRF requires thorough knowledge of the epidemiology of the disease and a high index of suspicion. TBRF is uncommon and occurs only sporadically. A history of recent exposure to old cabins, caves, or any rodent-friendly environment suggests the diagnosis. Routine laboratory tests are of little value. The WBC count is usually normal but may be increased or decreased. A left shift is often present. Thrombocytopenia is common but non-specific. The CSF is often abnormal, with a lymphocytic pleocytosis (typically 10 to 2000 cells/mm3 ), usually with a normal glucose and elevated protein. A false-positive serologic test for syphilis (Wassermann) occurs in about 5% of cases. [288] The diagnosis of relapsing fever is confirmed by demonstrating spirochetes on peripheral blood smears. A routine peripheral blood smear (Wright-Giemsa stain) from a febrile patient is initially positive in 70% of cases.[288] The diagnostic yield can be increased by examining thick smears and by staining with acridine orange using
fluorescence microscopy.[275] Inoculating laboratory animals (rats, mice) with blood and examining blood smears from the animals will also increase the diagnostic yield. The visual yield of spirochetes in peripheral blood smears diminishes with each successive febrile sampling. B. hermsii can be cultured in BSK-II medium, with the yield increasing in acutely febrile patients. Serologic tests are difficult to perform and are not yet practical utility.[338] TBRF is probably underrecognized and underreported and has been misdiagnosed as Lyme disease.[88] TREATMENT.
Tetracycline and erythromycin are both effective in treating relapsing fever. A single oral dose of 500 mg of either drug is effective in louse-borne relapsing fever.[47] However, a 7- to 10-day course (500 mg orally four times a day) is generally recommended in tick-borne disease.[143] [288] For children less than 9 years of age, erythromycin is recommended (30–50 mg/kg/day in four divided doses), with the first dose given intravenously. The borreliae are also sensitive to penicillin and chloramphenicol, but treatment failures have been reported with penicillin.[47] Animal studies have shown that early treatment with a ß-lactam antibiotic within 24 hours of onset of spirochetemia decreases CNS involvement.[48]
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TABLE 33-4 -- Human Rickettsial Diseases ORGANISM ARTHROPOD VECTOR
GEOGRAPHIC DISTRIBUTION
Murine typhus
Rickettsia mooseri (typhi)
Flea
Worldwide
Epidemic typhus
R. prowazekii
Body louse
Worldwide
Scrub typhus
R. tsutsugamushi
Chigger
Asia, Australia
Rocky Mountain spotted fever
R. rickettsii
Ticks
Western Hemisphere
Eastern spotted fevers
R. conorii
Ticks
Eastern Hemisphere
DISEASE TYPHUS GROUP
SPOTTED FEVER GROUP
R. sibirica R. australis Rickettsial pox
R. akari
Mites
United States, Russia
Q fever
Coxiella burnetii
Ticks
Worldwide
Trench fever
Rochalimaea quintana
Body louse
Africa, Mexico
Ehrlichia
E. sennetsu
Ticks
Japan
E. canis
Worldwide
JHR often occurs after the first dose of antibiotics. In one series, 54% of patients developed a JHR.[88] It is often severe and may be fatal. The reaction begins with a rise in body temperature and exacerbation of existing signs and symptoms; vasodilation and a fall in blood pressure follow. This complex reaction is mediated in part by products of mononuclear leukocytes. The leukocytes are stimulated by increased contact with antibiotic-altered spirochetes. Neither endotoxin nor complement appears to be necessary in the pathogenesis of JHR.[46] JHR typically occurs within a few hours of initial antibiotic dosing and cannot be prevented by prior steroid treatment. Waiting to begin treatment until the patient is afebrile does not prevent JHR.[144] Pretreatment with acetaminophen and hydrocortisone results in only a mild reduction of hypotension and does not prevent rigors.[47] Patients who are receiving the initial dose of antibiotics for relapsing fever should receive an IV infusion of isotonic saline in anticipation of a possible JHR. This is generally sufficient to counteract the hypotension. Lower initial doses of tetracycline or erythromycin may reduce the frequency of JHR.[144] Tick-Borne Rickettsial Diseases Bacteria of the family Rickettsiaceae are small, fastidious intracellular parasites with gram-negative bacterium-like cell walls, typical prokaryotic DNA arrangement, and considerable independent metabolic activity. The six major antigenic groups cause a variety of human diseases worldwide ( Table 33-4 ). Three are potentially transmissible to humans by ticks: spotted fever group (SFG) diseases, Q fever, and Ehrlichia infections. Organisms from the genus Rickettsia cause the various spotted fevers. Coxiella burnetii is the etiologic agent of Q fever. Ehrlichia are intraleukocytic Rickettsiaceae that infect humans and a variety of wild and domestic animals. Spotted Fever Group Diseases.
Rickettsia of the SFG share intracellular growth characteristics and a group-specific antigen. They are distributed worldwide and, with the exception of Rickettsia akari (rickettsial pox), are transmitted by the bite of ixodid ticks ( Table 33-5 ). Ticks serve as the natural hosts, reservoirs, and vectors for the rickettsiae.[200] The organisms replicate freely within the tick host and are passed transovarially and transstadially. Amplification of the cycle occurs when uninfected ticks feed on an infected vertebrate host or concurrently with an infected tick. In most natural vertebrate hosts the SFG rickettsiae induce an inapparent infection with transient rickettsemia. Human infection occurs through accidental intrusion into the natural cycle of infection or when ticks are transferred into human environments. Humans are incidental and "dead-end" hosts not involved in sustaining the life cycle of the organism. PATHOGENESIS.
The tick-borne SFG diseases share a similar pathogenesis. The usual route of infection is by direct inoculation through the skin through the bite of a tick vector. Infection may also develop after contamination of broken skin with infected tick parts or feces, after blood transfusion from an infected donor, [356] or through aerosol transmission among laboratory personnel working with pathogenic rickettsiae.[224] Local proliferation of rickettsiae probably occurs at the site of the tick bite, and a primary lesion or eschar frequently develops. Regional lymphadenitis may develop
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TABLE 33-5 -- Spotted Fever Group Diseases MAJOR VECTOR GEOGRAPHIC DISTRIBUTION
DISEASE
ETIOLOGIC AGENT
Rocky Mountain spotted fever
Rickettsia rickettsii Dermacentor andersoni, D. variabilis Western
PRIMARY LESION
USUAL SEVERITY
None
Moderate-severe
Often present
Mild
Hemisphere North Asian tick typhus
R. sibirica
Dermacentor, Haemaphysalis
Europe to Russian Far East
Mediterranean spotted fever
R. conorii
Rhipicephalus sanguineus, Haemaphysalis
Mediterranean littoral, South Africa, Kenya, India
Often present
Moderate
Queensland tick typhus
R. australis
Ixodes holocyclus
Australia
Often present
Mild
in the distribution of the eschar, suggesting early lymphatic spread. Rickettsemia is typically present at the onset of clinical illness and persists throughout the febrile period.[364] The SFG diseases are characterized by disseminated vasculitic lesions.[347] The rickettsiae invade, proliferate within, and ultimately destroy capillary and precapillary endothelial cells. In Rocky Mountain spotted fever (RMSF) the organisms spread into larger arterioles and arteries and invade medial smooth muscle cells. Medial necrosis and destruction of the vascular wall may follow. At sites of endothelial cell damage, a perivascular inflammatory response ensues, and platelet and fibrin thrombi tend to form and occlude the vessel lumen. In severe cases, vascular thrombi lead to necrosis of peripheral parts, including fingers, toes, the external ear, and scrotum. Antibodies develop 5 to 7 days after the onset of illness but do not appear to play a significant role in the pathogenesis of the vasculitis.[366] Immunity develops with clinical recovery, tends to be long lasting, and appears to involve both antibody- and cell-mediated mechanisms. CLINICAL MANIFESTATIONS AND DIAGNOSIS.
The SFG diseases display similar clinical manifestations, including fever, chills, headache, and myalgias. Three to 5 days after the onset of illness a characteristic maculopapular rash develops on the ankles, feet, wrists, and hands, then spreads centripetally to involve the entire body, including the palms and soles. With the exception of RMSF, the SFG diseases are generally mild, self-limited illnesses, with deaths seen primarily in elderly or debilitated patients. Untreated RMSF, however, may be severe, with a mortality rate approaching 30%.[40] Early diagnosis and treatment virtually eliminate mortality and reduce morbidity in SFG diseases. At the onset of illness, however, signs and symptoms are frequently nonspecific, leading to diagnostic confusion with viral or other infectious diseases.[158] Rash, the most characteristic feature of the illness, may develop late or, rarely, not at all. Identification of the eschar is helpful, but its presence is variable, and it is always absent in RMSF. Only 60% to 70% of patients recall a tick bite. Laboratory data (e.g., hyponatremia, thrombocytopenia) may provide clues to the diagnosis but are nonspecific. Serologic evidence of infection develops late in the illness. Early diagnosis therefore is based primarily on clinical evidence and relies on the ability to correlate clinical signs and symptoms with epidemiologic features. Rickettsial infection is confirmed by identification of rickettsiae in tissues (not widely available), by isolation of rickettsiae from infected blood or tissues (difficult and hazardous to laboratory personnel), or by demonstration of antibody rise in paired sera. The widely used Weil-Felix test is based on the unique sharing of polysaccharide antigens between certain Proteus strains (OX-19, OX-2) and the SFG rickettsiae. This agglutination test lacks both sensitivity and specificity, however, and should be abandoned if other serologic methods are available. Newer and more sensitive serologic methods include complement fixation, microimmunofluorescence, IFA tests, microagglutination, indirect hemagglutination, and ELISA.[63] [157] [231] TREATMENT.
Early treatment of the spotted fevers is the most important factor in speeding convalescence and reducing mortality. Antibiotic therapy begun early in the course results in rapid resolution of clinical abnormalities. Tetracycline and chloramphenicol are both very effective, although neither drug is rickettsicidal. The antibiotics inhibit the rickettsiae until an adequate immune response by the patient eradicates the infection. Tetracycline is given orally at a dosage of 25 to 50 mg/kg/day in four divided doses (2 g/day in adults); the dose of chloramphenicol is 50 and 75 mg/kg/day for adults and children, respectively. Appropriate IV doses of both drugs may be substituted. Penicillins, streptomycin, and sulfonamides are ineffective. Treatment
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should be continued until the patient is afebrile for 48 hours, or for a minimum of 5 to 7 days. Relapses are uncommon but may be treated with the same drug when they occur.[366] ROCKY MOUNTAIN SPOTTED FEVER
Epidemiology.
RMSF is the most common fatal tickborne disease in the United States.[67] It was first recognized in the northwestern United States in the latter part of the eighteenth century and may have been prevalent even earlier in Native Americans of that region. It has since been identified throughout the Western Hemisphere. Human infections have been reported from all 48 contiguous states except Maine. The disease is also seen in Canada, Mexico, and parts of Central and South America. A major shift in the demographics of RMSF occurred during the twentieth century. Before 1930 most cases were reported from the Rocky Mountains region of the western United States; in recent years more than 90% of cases have been reported from southern and eastern states. Reported cases in the mountain states have actually decreased more than tenfold, with only 2% of cases between 1981 and 1991 occurring in the Rocky Mountain States.[199] "Rocky Mountain" spotted fever has thus become somewhat of a misnomer. In the early 1970s a marked increase in the reported cases of RMSF was seen in the United States, reaching a peak in 1981 of 1192 cases, for an incidence rate of 0.51 cases per 100,000 population. Reported cases have gradually declined since that time, more recently ranging from 600 to 1200 cases reported each year.[60] Most of this decline has occurred in the South Atlantic states, although they still account for a majority of the cases reported each year. States with the most cases in 1991, for example, were North Carolina (159 cases), Oklahoma (71), Tennessee (58), and Georgia (41).[58] The changes in the incidence and endemicity of RMSF have been attributed to cyclic changes in tick populations, changes in the virulence of infecting rickettsiae, and the process of suburbanization.[27] [137] [199] A convincing explanation, however, is still lacking. RMSF is caused by the gram-negative intracellular bacterium Rickettsia rickettsii. The epidemiology of RMSF is determined by the seasonal and geographic distribution of R. rickettsii-infected ticks. Many species of ixodid ticks have been implicated as vectors of the disease, [40] [173] [199] but the most important species in the United States are Dermacentor variabilis, the American dog tick, and Dermacentor andersoni, the wood tick. Ticks of the Dermacentor genus are quite hearty, often living up to 5 years and displaying resilience to desiccation, cold, and starvation. Ticks transmitting RMSF outside the United States include Rhipicephalus sanguineus in Mexico and Amblyomma cajennense in Central and South America. D. andersoni is the principal acarine host of R. rickettsii in the western United States and Canada. It feeds on virtually any available warm-blooded animal. D. variabilis is the primary host in the eastern United States and Canada. The domestic dog is the major host of adult D. variabilis, but the tick will feed on a variety of large and medium-sized animals. Nymphal and larval D. variabilis feed on various mice, voles, and rabbits. Serosurveys have indicated that a broad range of vertebrate hosts are infected with R. rickettsii, although not all sustain rickettsemia of sufficient magnitude to transmit the infection to feeding ticks. R. rickettsii occurrence in the United States does not depend on the presence of any given order of mammal.[199] Domestic dogs become infected with R. rickettsii and may become acutely ill with fever and rash. Dogs probably do not play an important role in the amplification cycle of RMSF but may be important in transporting infected ticks close to humans.[128] Several studies have shown an association between domestic dogs and RMSF.[41] [128] [196] An infected tick may detach from a dog and complete its engorgement on a human, thereby transmitting R. rickettsii. Alternatively, infection through abraded skin or conjunctivae may occur during manual deticking of dogs.[349] Transmission by a tick vector delimits the clinical epidemiology of RMSF. It is a seasonal disease occurring when ticks are active; 95% of U.S. cases occur between April 1 and September 30, with most in May, June, and July. Exposure to wooded areas or areas of high grass increase the risk of disease. In southern states the season is longer with more winter cases, although sporadic cases can occur even in cold climates. RMSF also tends to be focally endemic, with a high proportion of cases occurring in small, circumscribed areas. This may be the clinical expression of "islands" of infected ticks.[196] It is more common in males (60%) and young people (50% less than 20 years of age), who are more likely to be exposed to tick habitats.[332] [334] The demographic group with the highest incidence of RMSF is 5- to 9-year-old children in the mid-Atlantic and southern United States.[60] [70] Other factors influencing human transmission include the duration of tick attachment and the prevalence of R. rickettsii in ticks. Transmission from the tick salivary glands may occur in as short as 6 to 10 hours of tick attachment, although some cases require more than 24 hours. Only a small percentage of ticks, even in highly
endemic areas, are infected by Rickettsia. The chance of exposure to R. rickettsii from a tick bite ranges from 1 in 2123 in North Carolina to less than 1 in 1500 in Ohio. Clinical manifestations.
RMSF ranges from mild, even subclinical illness to fulminant disease, with vascular collapse and death occurring within 3 to 6 days of onset.
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CLINICAL FINDING
TABLE 33-6 -- Clinical Findings in Rocky Mountain Spotted Fever PERCENT OF CASES
Fever
99
Headache
80–90
Any rash
85–90
Myalgias
70–85
Petechial rash
45–60
Nausea and vomiting
56–60
Abdominal pain
34–50
Conjunctivitis
30
Stupor
21–37
Diarrhea
19–20
Edema
18
Meningismus
17–18
Splenomegaly
14–29
Hepatomegaly
12–15
Pneumonitis
13–17
Coma
10
Jaundice
8–9
Seizures
8
Clinical manifestations reflect the pathogenesis of the infecting rickettsia. Infection typically is through the skin, with spread occurring primarily by blood and lymphatic channels. The rickettsial species attaches to and invades vascular endothelial and smooth muscle cells using surface exposed protein and rickettsial phospholipase. The rickettsial species multiply intracellularly, becoming cytopathic. Vascular injury often ensues, with activation of clotting factors, extravasation of intravascular fluid, and impaired perfusion. Vascular permeability is elevated, with resultant edema, hypovolemia, and hypoalbuminemia. The incubation period ranges from 2 to 14 days (7-day mean onset); severe disease is associated with a shorter incubation period. Typically the victim has sudden onset of fever and chills, with or without headache, and myalgias. The classic triad of fever, rash, and history of tick exposure is present in only 3% to 18% of persons at the initial physician visit.[162] The fever is usually high, greater than 39° C (102.2° F) in two–thirds of patients in the first 3 days of illness, and myalgias and headache may be severe. The most characteristic feature, the rash, usually develops 2 to 5 days after the onset of illness. Other signs and symptoms, including abdominal pain, vomiting, diarrhea, confusion, conjunctivitis, and peripheral edema, are common ( Table 33-6 ). A history of tick exposure is present in 85% of confirmed cases. [334] The rash in RMSF results from injury to dermal capillaries and small blood vessels. It typically develops first on the wrists, hands, ankles, and feet 2 to 3 days after disease onset. The rash then spreads rapidly and centripetally to cover most of the body, including the palms, soles, and face. Initially the lesions are pink macules, 2 to 5 mm in diameter, that readily blanch with pressure. After 2 to 3 days the lesions become fixed, darker red, papular, and finally petechial. The hemorrhagic lesions may coalesce to form large areas of ecchymoses. Necrosis may develop, especially in areas supplied by terminal arteries, such as fingers, toes, nose, ears, and genitalia. Involvement of the scrotum or vulva is a diagnostic clue.[83] In its classic form, the rash occurring during the summer months in an endemic area is almost pathognomonic for RMSF. Unfortunately, it is often absent on initial patient presentation, making diagnosis more difficult. The rash is delayed in approximately 10% of patients,[138] with younger patients generally displaying the rash earlier in the disease course. In an additional 10% to 15% of laboratory-confirmed cases of RMSF, no rash is noted ("spotless" fever).[107] [137] [139] In other patients the rash is evanescent, occurring only with fever spikes. One report indicates a possible actinic nature to the RMSF rash, worsening in sun-exposed areas.[20] Neurologic involvement in RMSF ranges from mild headache to serious focal or generalized disorders of cerebral function. Headache is very common. Meningismus occasionally develops but does not correlate well with CSF findings, which may be normal or may show modest protein elevation and pleocytosis of both lymphocytes and polymorphonuclear cells (usually 8 to 35 cells/mm3 ). Cerebral vasculitis may manifest with focal neurologic deficits, which are quite variable but usually transient. Seizures may develop during the acute phase of the illness but rarely persist.[125] Lethargy and confusion are common and may progress to stupor or profound coma. Generalized cerebral dysfunction may be secondary to vasculitic lesions, especially in the reticular network of the brainstem, or to toxicity from severe rickettsial infection (fever, hypotension, hyponatremia, and thrombocytopenia with intracranial hemorrhage). Children with RMSF who develop coma have an increased risk of subsequent behavioral disturbances and learning disabilities. One case report describes Guillain-Barré syndrome as a complication of acute RMSF.[22] [129] [207] [338] Myocarditis is frequently found at necropsy in fatal RMSF; however, the clinical significance of the cardiac involvement is unclear. Pathologic study shows a patchy, interstitial, mononuclear infiltrate that appears to coincide with the distribution of rickettsiae in myocardial capillaries, venules, and arterioles. [348] Abnormal left ventricular function can frequently be demonstrated echocardiographically in hospitalized patients.[103] [191] Overt clinical manifestations of left ventricular dysfunction are uncommon, however, and hypotension and pulmonary edema are generally attributable to noncardiogenic causes. Cardiac enlargement rarely may be seen on chest radiographs.[177] [192] ECG abnormalities include nonspecific ST-T changes, conduction abnormalities
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(primarily first-degree atrioventricular block), and arrhythmias (paroxysmal atrial tachycardia, nodal tachycardia, and atrial fibrillation).[192] Most patients have complete resolution of cardiac abnormalities with clinical improvement, but persistent echocardiographic abnormalities have been noted.[191] Infection of the pulmonary microcirculation by R. rickettsii results in interstitial pneumonitis and increased pulmonary vascular permeability. Although pulmonary involvement is not usually a prominent aspect of RMSF, a significant number of patients complain of cough, chest pain, dyspnea, or coryza.[49] Patchy infiltrates may occasionally be seen on chest radiographs, and noncardiogenic pulmonary edema may develop in severe cases, with potential progression to ARDS.[82] [177] [262] Gastrointestinal symptoms are common in RMSF and are prominent complaints in some patients. At autopsy, rickettsial vascular lesions are found throughout the gastrointestinal tract and pancreas, although actual necrosis appears to be a rare event.[240] Occasionally, RMSF presents as an acute abdomen, suggesting appendicitis or cholecystitis.[350] In the kidneys a focal perivascular interstitial nephritis is concentrated near the corticomedullary junction. Clinically, however, significant renal involvement is usually caused by prerenal azotemia or acute tubular necrosis after a hypotensive episode.[329] Monarticular arthritis in the acute phase of RMSF has been reported.[329] The major complications of RMSF result from direct vasculitic injury. In late stages of the disease, diffuse vasculitic lesions cause increased systemic capillary permeability, leading to hypovolemia and vascular collapse. Disseminated intravascular coagulation (DIC), acute renal failure, metabolic acidosis, and cardiorespiratory dysfunction may ensue and often presage death. Endothelial leukocyte adhesion molecules and cytokines are thought to play an important role in the pathogenesis of
fulminant RMSF. Long-term sequelae include paraparesis; hearing loss; peripheral neuropathy; bladder and bowel incontinence; cerebellar, vestibular, and motor dysfunction; language disorders; and disability from limb amputation. When death results, it typically occurs after delayed treatment and 8 to 15 days following symptom onset. The exception is with fulminant RMSF, in which death occurs in less than 5 days, with hemolysis the most likely pathogenic cause. Risk factors associated with mortality include elevated serum creatinine, increased AST, increased bilirubin, hyponatremia, thrombocytopenia, and advanced age.[64] Diagnosis.
Before antimicrobials were available, RMSF was frequently a fatal disease. Even with effective antibiotic agents the mortality rate remains approximately 5%.[106] [138] Patients older than 30 years, males, and nonwhites are at higher risk.[106] [137] [138] Elderly patients appear more likely to have a severe course of illness and to have atypical features, including delayed or absent rash.[139] [213] In susceptible individuals, such as those with glucose-6-phosphate dehydrogenase (G6PD) deficiency, RMSF may be fulminant and rapidly fatal.[346]
Box 33-3. LABORATORY FEATURES OF ROCKY MOUNTAIN SPOTTED FEVER Normal leukocyte count Left shift, toxic granulations, Döhle's bodies Thrombocytopenia Hyponatremia Cerebrospinal fluid pleocytosis Increased serum transaminase levels Increased serum creatinine levels
The most significant factor in deaths from RMSF is a delay in diagnosis and in starting appropriate antibiotic therapy. Before antibiotics the mortality rate (1939 to 1945) was 23%, compared with 5.2% between 1981 and 1992. Patients who receive antibiotic treatment after 5 days of illness may die from advanced disease. Unfortunately, early diagnosis in RMSF is often difficult. The classic triad of rash, fever, and tick bite is actually rare during the first 3 days of illness, [139] and confirmatory laboratory evidence is usually lacking early in the disease. Factors leading to a delay in diagnosis include absence or late appearance of the rash, lack of a history of tick bite or tick exposure, and nonspecific or unexpected initial symptoms leading to an incorrect initial diagnosis. RMSF rarely is diagnosed by culture results, making historic data and clinical findings imperative. RMSF should be suspected and antibiotic treatment strongly considered in any patient who resides in or has recently visited an endemic area during the summer months and who has fever, headache, and myalgias even in the absence of a rash. Symptoms referable to the pulmonary, gastrointestinal, and central nervous systems often occur in RMSF and should not delay diagnosis. The differential diagnosis of RMSF is extensive and includes meningococcemia, thrombotic thrombocytopenic purpura, immune complex vasculitis, ehrlichiosis, mononucleosis, measles, enteroviral infections, leptospirosis, and murine typhus. Meningococcemia may be impossible to differentiate initially, but chloramphenicol is effective therapy for both diseases. The rash of atypical measles may mimic that of RMSF.[220] Gastrointestinal infection, respiratory infection (pneumonia, bronchitis), acute abdomen, and meningitis/encephalomyelitis are often misdiagnosed. Routine laboratory values are nonspecific and provide limited clues to diagnosis, especially early in the course of illness, when serum antibodies are rarely detectable ( Box 33-3 ). Thrombocytopenia has been reported in more than 50% of patients in some series, [346]
792
although the actual incidence may be closer to 35%.[137] [139] Hyponatremia is also common and is probably a result of antidiuretic hormone (ADH) secretion in response to intravascular volume depletion.[98] Other laboratory abnormalities include anemia, azotemia, hypoalbuminemia, CSF pleocytosis with monocytic predominance, increased creatine kinase, and elevated bilirubin and AST/ALT levels. Peripheral WBC count is usually normal. Box 33-4. LABORATORY DIAGNOSTIC TESTING FOR ROCKY MOUNTAIN SPOTTED FEVER
SEROLOGIC DIAGNOSIS Latex agglutination assay Indirect immunofluorescence assay
SKIN BIOPSY-RELATED DIAGNOSIS Polymerase chain reaction Direct immunofluorescence antibody staining Immunoperoxidase staining
Laboratory confirmation of RMSF has generally relied on serologic techniques detecting antibody increases in paired sera ( Box 33-4 ). Even with the most sensitive tests, antibody rises are not seen until 5 to 10 days after the onset of symptoms, negating serologies at initial presentation. Early antibiotic therapy may delay titers even longer.[231] Serologic diagnosis requires a fourfold increase in titer between acute and convalescent sera, which does not typically occur until 6 to 10 days after symptom onset.[342] The Weil-Felix test is neither sensitive nor specific for RMSF and should not be used if other tests are available. The complement fixation test is widely available but also lacks sensitivity.[231] False-positive results can occur during pregnancy with latex agglutination assays.[355] The most sensitive and specific serologic tests currently in use appear to be the IFA and indirect hemagglutination tests.[157] The most promising method for early laboratory diagnosis of RMSF is immunofluorescent identification of R. rickettsii in biopsy specimens of the skin rash. Rickettsiae have been identified as early as the fourth day of illness with this method.[367] Sensitivity is 70% to 90%, with a specificity of 100%.[237] Serologic confirmation of RMSF
requires a fourfold rise in antibody titers by indirect immunofluorescence or a single titer greater than 64. Treatment.
Mortality is largely eliminated in RMSF by early treatment with tetracycline or chloramphenicol. Patients treated within 4 days of symptom onset are three times less likely to die than those treated later.[70] Treatment should continue for at least 5 to 7 days or until the patient is afebrile for more than 2 days. IV therapy is required only if the patient cannot tolerate oral intake. Treatment with doxycycline may be preferable to chloramphenicol because tetracyclines may be associated with a higher survival rate.[334] Although tetracycline can cause teeth staining in children, the risk is related to cumulative dose. A single course of therapy for RMSF is unlikely to stain teeth. Potential complications of chloramphenicol include bone marrow suppression, aplastic anemia, and gray syndrome. Rickettsiae are sensitive to fluoroquinolones, which remain a potential option even if human data are lacking. Mediterranean spotted fever (R. coronii) has been successfully treated with fluoroquinolones.[24] In dogs, tetracycline, chloramphenicol, and enrofloxacin all appear to have equal efficacy in treating RMSF. [35] In severe cases, supportive therapy is also essential to a favorable outcome. Fluid replacement is critical in the hypotensive patient but must be monitored closely because of the risk of fluid extravasation through damaged vessels. Measurement of pulmonary capillary wedge pressures with a Swan-Ganz catheter may be necessary, especially if pulmonary edema develops. Use of corticosteroids has not been adequately evaluated but may be beneficial in patients with widespread vasculitis or encephalitis. [201] [366] Prophylactic antibiotics after a tick bite are not recommended because of the low incidence of infection and risk of adverse reactions. Routinely testing ticks for rickettsial antigen is not beneficial.[263] Although none currently exists, promising vaccines are in development. EASTERN SPOTTED FEVER.
Three other SFG diseases are transmitted to humans by tick bite: Mediterranean spotted fever (MSF), North Asian tick typhus, and Queensland tick typhus. The three diseases closely resemble one another and have many similarities to RMSF. Generally, the course of illness in all three is milder than in RMSF, although complications and death may occur in susceptible patients. The diseases are characterized by abrupt onset of fever, headache, and malaise after a short incubation period (5 to 7 days). Unlike in RMSF, a primary lesion (eschar, tache noire) is often present at the site of the tick bite and may be associated with regional lymphadenitis. The lesion is classically a small ulcer, 2 to 5 mm in diameter, with a black center and red areola. A rash that varies from maculopapular to petechial usually develops 3 to 5 days after the onset of illness. Untreated, the fever and other symptoms resolve after several days to 2 weeks. Treatment with tetracycline or chloramphenicol significantly shortens the course of illness and, if instituted early, prevents complications. MSF is caused by Rickettsia conorii and has been described under various names, often reflecting its geographic occurrence: Marseilles fever, South African tick
793
bite fever, Kenya tick bite fever, India tick typhus, and boutonneuse fever. As the names indicate, MSF is endemic in areas bordering the Mediterranean Sea, as well as parts of Africa and India. The major vector of MSF in the Mediterranean countries is the dog tick Rhipicephalus sanguineus. Several tick species have been implicated as vectors in other areas: Haemaphysalis leachi (Kenya, South Africa), Rhipicephalus simus, Dermacentor reticulatus, and Ixodes hexagonus. [101] All stages of R. sanguineus occasionally attach to humans, and dogs may be important in transporting the ticks close to humans.[339] As with other SFG diseases, MSF occurs during the warm weather months. Seasonal occurrence, geographic location, and the presence of a tache noire (noted in 50% to 75% of cases) are the most helpful criteria for early diagnosis. [211] [244] Although the disease is usually mild in children and young adults, a malignant form resembling severe RMSF has been described.[243] [345] The elderly, alcoholics, and patients with G6PD deficiency appear particularly at risk.[147] [153] The diagnosis can be confirmed by specific serologic testing or by immunofluorescent demonstration of R. conorii in cutaneous lesions. [242] North Asian tick typhus or Siberian tick typhus is endemic throughout Siberia, from European Russia to the Soviet Far East. It is seen primarily in agricultural areas and is closely associated with steppe landscapes.[41] The causative organism, Rickettsia siberica, is transmitted to humans by several species of Dermacentor and Haemaphysalis ticks. In the natural cycle, adult ticks feed on large wild and domestic animals, especially cattle and dogs. As for other SFG rickettsiae, humans are accidental and dead-end hosts. Queensland tick typhus is caused by Rickettsia australis. It is endemic to southern and northern Queensland, and the major vector is the scrub tick, Ixodes holocyclus. [41] Both Queensland tick typhus and North Asian tick typhus are benign illnesses of mild to moderate severity with typical rickettsial manifestations: fever, headache, variable appearance of an eschar at the site of the tick bite, and a rash. SFG rickettsiosis also occurs in Japan, where the causative agent appears to be a distinct serotype of SFG rickettsiae.[331] Q FEVER.
Q fever is a worldwide zoonosis affecting both wild and domestic animals. It was first described in 1937 as an occupational disease of abattoir workers and dairy farmers in Australia.[78] Aerosol spread of Coxiella burnetii, the causative organism, is the usual mode of transmission to humans. Sexual transmission has been implicated but not proved.[171] Although ticks may become infected with C. burnetii after feeding on an infected vertebrate, tick-borne transmission to humans appears to be very rare. Fewer than 10 cases of Q fever per year are reported in the United States. Serosurveys have shown widespread prevalence, suggesting frequent asymptomatic infection or underdiagnosis and underreporting.[134] [280] The most common clinical presentation of Q fever is an influenza-like illness with fever, headache, myalgias, and pneumonitis. Abnormal liver function tests, jaundice, and hepatomegaly may be seen. Glomerulonephritis has been reported with both acute Q fever and endocarditis-associated chronic infection. [166] C. burnetii infection during pregnancy, although not known to be teratogenic, can create placental insufficiency resulting in premature delivery or even intrauterine death.[113] [241] A severe case of acute cerebellitis with tonsillar herniation was recently reported.[265] In most victims the illness resolves spontaneously within 2 to 4 weeks of onset, with treatment hastening the resolution. Q fever may also be a chronic infection, with or without a history of an acute episode. Granulomatous hepatitis and culture-negative endocarditis are the chronic forms of the disease. Endocarditis, fatal in 25% to 60% of patients, can affect native and prosthetic valves (underlying valvular disease is almost invariably present), although it has a predilection for the aortic valve.[123] Infections of aneurysms and vascular prostheses have also been described.[110] A post-Q fever syndrome involving fatigue, myalgia, arthralgia, night sweats, sleep disturbances, and mood alterations has been described and may occur in 20% to 42% of proven cases.[14] [228] Diagnosis of Q fever depends primarily on serologic testing. Two specific complement-fixing antibodies (phase 1 and phase 2) develop after infection with C. burnetii. In patients with acute Q fever, phase 2 antibody is usually detectable by the second week of illness; phase 1 is not detectable. The finding of phase 1 antibody indicates chronic infection. IgA subclasses (IgA1 seen in acute and chronic disease, IgA2 seen only in chronic disease) may also help detect chronic vs. acute infection. Only patients with endocarditis were found to have IgA2 antibodies to phase II antigens.[49] For the acute phase, tetracycline 500 mg orally four times a day will hasten resolution. Treatment of chronic Q fever is not always successful. Patients probably need to be treated with tetracycline for at least 12 months.[7] Some recommend adding another drug, such as lincomycin or cotrimoxazole, but with unproven efficacy.[112] [341] Patients with endocarditis typically receive treatment with tetracycline and quinolone for at least 4 years, although new research supports shortened treatment with doxycycline and hydroxychloroquine.[245] A vaccine has been used to prevent infection in high-risk abattoir workers. Prevention through avoidance of potentially infectious animal tissues, especially raw milk and products of conception, should be followed.
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TABLE 33-7 -- Human Forms of Ehrlichiosis
GRANULOCYTIC
MONOCYTIC
Infecting organism
Ehrlichia equi-like agent
Ehrlichia chaffeensis
Tick vector
Ixodes scapularis
Amblyomma americanum, Dermacentor variabilis
Geographic distribution
Northeast, Midwest
South-central states, Southeast
EHRLICHIA INFECTIONS.
Ehrlichia is a genus in the Rickettsiaceae family. Ehrlichiae are pleomorphic, gram-negative, obligatory intracellular pathogens that cause disease in humans and animals throughout the world. Their life cycle takes place primarily within the cytoplasm of circulating WBCs or platelets. Ehrlichiae can be divided into at least three genogroups based on 16S ribosomal ribonucleic acid (rRNA) gene sequences, but they are clinically classified more often by target cell specificity. Two forms of ehrlichiosis occur in humans: human monocytic ehrlichiosis (HME) and human granulocytic ehrlichiosis (HGE) ( Table 33-7 ). HME is caused by the Ehrlichia chaffeensis, which attacks mononuclear phagocytes. The Lone Star tick (Amblyomma americanum) is the primary vector of E. chaffeensis, and HME occurs predominantly in the south-central and eastern United States. Serologically and morphologically, E. chaffeensis appears to be closely related to Ehrlichia canis, which causes an illness in dogs.[185] HGE is caused by an agent similar to Ehrlichia equi, infects neutrophils, and is likely transmitted by Ixodes scapularis and Dermacentor variabilis ticks.[87] [222] HGE occurs primarily in the upper Midwestern and northeastern United States. The agent causing HGE is closely related serologically, morphologically, and by genomic sequencing to both Ehrlichia phagocytophila and E. equi, which are pathogenic to dogs, horses, sheep, goats, and deer. HME has been reported in more than 30 states since 1986. Most cases occur in the south-central and southern Atlantic states (Oklahoma, Missouri, Virginia, Georgia), principally in areas where RMSF also occurs.[199] In one study, 68% of HME patients reported a tick bite, and 83% reported tick exposure in the 7 to 21 days before disease onset.[108] A recent analysis of ticks in northern California found that more than 13% of Ixodes ticks and 20% of D. variabilis ticks were infected with E. chaffeensis.[167] Most HGE cases occur in Minnesota and Wisconsin, with fewer cases in the southern New England states. Among HGE patients, 6% report tick bites, and almost all report exposure to ticks before illness. The reservoir hosts for E. equi-like agents are thought to be wild rodents, deer, and sheep.[15] In field studies a high proportion of I. scapularis in endemic areas are infected with the ehrlichiosis-causing agent.[266] Although most cases of ehrlichiosis are sporadic, reports exist of Army reservist and retirement community outbreaks.[229] [293] Patients with ehrlichiosis tend to be older than patients with RMSF, with a slight male predominance. More than 70% of cases occur between May and July. Human ehrlichiosis has a broad clinical spectrum ranging from subclinical infection to a mild viral-like illness to a life-threatening disease. Because of the shared tick vector and increased seroprevalence of HGE in patients with Lyme disease, confusion surrounds the clinicopathologic spectrum of the disease. As with Borrelia and Babesia organisms, the vector tick must remain attached for more than 36 hours for effective transmission of Ehrlichia organisms. After an average incubation period of 7 days (range, 1 to 21 days), high fever, headache, chills or rigors, malaise, myalgia, and anorexia typically develop. Leukopenia, thrombocytopenia, and elevated liver enzymes may also be present. A rash, usually macular or papular but occasionally petechial or erythematous, develops in 20% to 40% of patients a median of 8 days after the onset of illness.[149] The rash appears to be more common in children than adults and involves the palms or soles in fewer than 10% of cases.[21] Severe and even fatal complications develop in some patients, usually in elderly or immunocompromised patients or in settings of delayed diagnosis or treatment.[87] Respiratory complications may be relatively common; cough, pulmonary infiltrates, dyspnea, and respiratory failure have all been reported. Other serious complications include encephalopathy, meningoencephalitis, shock, opportunistic infections, gastrointestinal hemorrhage, and renal failure. Immunocompromised patients are a high risk for death. In HME, bone marrow and hepatic granulomas and multiorgan perivascular lymphohistiocytic infiltrates have been observed. In HGE, Ehrlichia-mediated defects in host defense and immune suppression have resulted in opportunistic fungal and viral infections. [344] The most common CNS manifestation that predicts CSF abnormality is altered mental status. In one study of 15 patients with altered sensorium who underwent CSF testing, eight had abnormalities, including elevated lymphocytes (up to 1000 cells/µl) and protein in the CSF. In a review of 21 additional cases with CNS manifestations, 13 of 21 patients had abnormal CSF findings. Fourteen patients underwent brain computed tomography, revealing no abnormalities. Four of the 21 patients with CNS symptoms died.[246] HGE is clinically similar to HME, although only 8% of HGE patients develop rash.[86] Elevated serum creatinine
795
and transaminases, along with thrombocytopenia, occur in most patients. These abnormalities are usually mild and of short duration.[93] As with RMSF, the diagnosis of ehrlichiosis depends on clinical findings. Serologic tests can be used to confirm the diagnosis. Indirect IFA testing against E. chaffeensis is now available from the CDC, and Western blot can be used to confirm seropositive specimens.[187] Antibody levels rise rapidly during the first 3 weeks and peak after approximately 6 weeks. Controlled trials of antibiotic therapy have not been conducted for ehrlichiosis, although tetracycline (or doxycycline) appears to be effective. In vitro studies show antibiotic susceptibility to rifampin, quinolones, and doxycycline. [164] Chloramphenicol has been used to treat ehrlichiosis, but treatment failures have been reported, and E. chaffeensis is resistant to chloramphenicol in vitro.[36] Rifampin is bactericidal against E. chaffeensis in vitro, however clinical experience is limited. Recently, a pregnant HGE patient was treated successfully with rifampin.[39] Currently, tetracycline (doxycycline) should be considered the drug of choice for ehrlichiosis. The optimal dosage and duration of treatment need more investigation, but current recommendations are for oral or IV doxycycline (100 mg twice daily for adults, 3 mg/kg/day in two divided doses for children) for a minimum of 5 to 7 days. Dosing should be minimized as much as possible with children to prevent staining teeth. Because ehrlichiosis is potentially life threatening (2% mortality rate for HME, 7% to 10% for HGE), empiric treatment should be instituted before laboratory confirmation.[343] Tick-Borne Viral Diseases Ticks transmit a wide variety of viruses to humans. As with other tick-borne diseases, the viral illnesses are zoonotic. Ticks ingest the organisms while feeding on a viremic host; the virus replicates within the tick and is passed transstadially. Transovarial transmission has been documented for tick-borne encephalitis virus and Crimean-Congo hemorrhagic fever virus; the role of transovarial passage in maintaining these viruses in nature is unknown.[143] Amplification occurs when the infected tick feeds on an uninfected vertebrate. Humans usually are accidentally infected after intrusion into the natural tick-vertebrate cycle. Tick-borne viruses cause clinical syndromes in humans that can be classified into four broad groups: influenza-like febrile illness with malaise, headache, myalgias, and arthralgias; febrile illness with hemorrhagic complications; febrile illness associated with meningoencephalitis; and subclinical or very mild illness. A specific virus may produce any or all of these syndromes depending on the virulence of the organism, host susceptibility, and the stage of the illness. For example, Colorado tick fever (CTF) virus usually causes an influenza-like febrile illness, but in susceptible hosts it may produce meningoencephalitis or rarely a hemorrhagic diathesis. Diagnosis of tick-borne viral diseases requires clinical acumen and interpretation of epidemiologic and clinical information. Isolation of the virus, usually by intracerebral inoculation in suckling mice, or demonstration of a rise in antibody titers in the victim confirms the diagnosis. As with most viral diseases, treatment is primarily supportive. Only CTF occurs with any frequency in the United States. Table 33-8 lists other tick-borne viruses. Colorado Tick Fever.
Colorado tick fever (CTF) is an acute self-limited febrile illness caused by a small, 12-segmented RNA virus of the family Reoviridae and genus Coltivirus. The Salmon River virus, a related but antigenically distinct virus isolated from a patient with likely CTF, is a new putative coltivirus. The distribution of CTF includes the western United States and Canada, specifically the Rocky Mountains, Black Hills, Sierra Nevadas, and coastal range of California, corresponding largely to the range of the Rocky Mountain wood tick, Dermacentor andersoni. Distribution exists at altitudes of 1219 to 2048 m (4000 to 10,000 feet), typically among pine-juniper-sagebrush vegetation. The natural reservoir normally depends on the small mammal-tick cycle but also involves small mammals in California outside the known range of D. andersoni, suggesting that other tick species are capable of transmitting the virus.[174]
CTF virus is maintained in its natural cycle by transmission between ticks and rodents.[202] Larval stages of D. andersoni ingest the virus while feeding on a viremic rodent host and pass it transstadially from larva to nymph to adult. Hibernating nymphs and adults carry the virus through the winter. Infected ticks emerge in the spring and feed on susceptible animals, renewing the cycle. Nymphal and adult ticks may also acquire the virus by feeding on viremic hosts. The virus does not appear to cause disease in its natural hosts; humans are incidental and dead-end hosts, usually infected by adult ticks. Transmission occurs between March and September with a peak between April and June. Risk factors include exposure to outdoor vegetation and often involve camping, hiking, and fishing. Ticks may be carried home on clothing or equipment, leading to infection. CTF is usually a benign, self-limited febrile illness that is difficult to distinguish from many other agents, especially Rickettsia rickettsii. More than 200 cases of CTF are reported annually in the United States, but the actual incidence is probably much higher; many cases are not brought to medical attention or are diagnosed simply as a viral illness. It is a seasonal disease occurring from late March to early October, with a peak incidence
796
VIRUS
TAXONOMIC GROUP
TABLE 33-8 -- Tick-Borne Viral Diseases MAJOR VECTOR ANIMAL GEOGRAPHIC HUMAN ILLNESS HOSTS DISTRIBUTION
Colorado tick fever
Reoviridae, genus Orbivirus
Dermacentor andersoni
Rodents, other small mammals
Mountain highland areas of western United States and Canada
Kemerovo
Reoviridae, genus Orbivirus
Ixodes ricinus, I. persulcatus
Domestic and wild mammals, birds
Powassan encephalitis
I. marxi, I. cookei
Louping ill
FREQUENCY OF RECOGNIZED DISEASE
RISK FACTORS
Biphasic FI, ME especially in children, in prolonged viremia
Sporadic, common in endemic areas
Occupational and recreational pursuits in mountain areas
Siberia, Czech and Slovak Republics
Mild FI, occasional ME, not fatal
Sporadic, rare
Occupational and recreational pursuits in forested areas
Small mammals
Northern United States, Canada
FI, ME: possible sequelae and death especially in young
Sporadic, rare
Rural areas, pets?
I. ricinus
Goats, sheep, cattle, small mammals
Central and eastern Biphasic ME Europe
Sporadic, common in endemic areas
Agricultural and forestry workers, drinking goat's milk
Russian spring-summer encephalitis
I. ricinus, I. persulcatus
Goats, sheep, cattle, small mammals
Siberia
Biphasic ME, possibly severe, with 20% mortality
Sporadic, common in endemic areas
Agricultural and forestry workers
Kyasanur Forest disease
Haemaaphysalis spinigera
Monkeys, small mammals
Southern India
FI, ME, possible hemorrhagic complications
Sporadic, epidemics occur
Residence in or travel to endemic areas
Omsk hemorrhagic fever
Dermacentor pictus?
Muskrats
Western Siberia
FI, hemorrhagic complications
Rare
Direct contact with muskrats
Crimean-Congo hemorrhagic fever
Hyalomma marginatum, H. anatolicum, others
Domestic and wild mammals
Southern Russia, Middle East, India, Pakistan, central Africa
FI, petechial-ecchymotic Sporadic, rash, hemorrhage, epidemics occur 3%–30% mortality
Agricultural workers
TICK-BORNE ENCEPHALITIS COMPLEX
Dugbe
Bunyaviridae, genus Nairovirus
Ixodid species
Cattle
Nigeria, Central African Republic
Acute FI
Rare, primarily children
Herding or caring for livestock
Bhanja
Probably Bunyaviridae
Ixodid species
Domestic and wild mammals
Yugoslavia, Italy, Kenya, Nigeria, India
FI, ME
Rare
Agricultural workers
Thogoto
Possibly Orthomyxoviridae
Ixodid species
Ruminants
Egypt, Kenya, Nigeria
FI, ME, optic neuritis
Rare
Herding or caring for livestock
Quaranfil
Unclassified
Argas arboreus
Pigeons, wild birds
Africa, Iran, Afghanistan
FI
Rare
Residence in endemic areas
FI, Febrile illness; ME, meningoencephalitis.
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in May and June. All age groups are susceptible to CTF, but it occurs most often in young men, reflecting their greater recreational and occupational activities in outdoor mountain areas. A history of tick exposure can be obtained in approximately 90% of patients with CTF; the usual time between the tick bite and the onset of symptoms is 3 to 6 days (range, 0 to 14 days).[127] [291] CTF usually begins with the abrupt onset of fever. Most victims experience severe headaches, myalgias, and lethargy; complaints of photophobia, ocular pain, anorexia, nausea and vomiting, and abdominal pain are common. A macular or maculopapular rash is reported in 5% to 12% of patients but is not a prominent feature. The most characteristic feature of the illness is a biphasic or "saddle-backed" temperature pattern. Victims initially experience 2 to 3 days of fever, followed by a 1- to 2-day remission and then an additional 2 to 3 days of fever. This pattern is helpful when present but cannot confirm the diagnosis, since it is observed in only about 50% of patients.[127] [291] CTF is usually mild, but severe complications can occur, particularly in children under age 10. Meningoencephalitis has been described in several children. [54] [84] [282] [291] Two children developed a hemorrhagic diathesis and died.[127] Other unusual complications associated with CTF include pericarditis,[1] [141] myocarditis,[92] hepatitis,[178] epididymoorchitis,[128] and pneumonitis.[127] Information on CTF contracted during pregnancy is inconclusive, but of five cases reported, one terminated in a spontaneous abortion and in another a live-born infant had multiple congenital anomalies.[210] CTF virus is teratogenic in mice.[136] Nearly half the patients with CTF require 3 weeks or longer to recover fully from the illness. The most common persistent symptoms are malaise and weakness. Prolonged symptoms occur most frequently in patients over age 30. [127] Treatment of CTF is supportive; infection generally confers lifelong immunity. CTF virus circulates free in the plasma and bone marrow of infected patients until the end of the first week of illness, when it is neutralized by antibodies. In the bone marrow the virus infects erythrocyte precursors and persists within mature erythrocytes, where it is protected from antibodies. This allows viremia to persist for a
prolonged period, even when clinical recovery is complete. Infective virus can be recovered from the blood for a month or longer in nearly 50% of patients. [127] Persistent viremia in blood donors poses a risk to recipients of blood transfusions; transfusion-acquired infection has been reported.[58] Other hemopoietic cells may also be affected in CTF. Leukopenia involving both granulocytes and lymphocytes is common and may be helpful diagnostically, although one third of patients have normal WBC counts.[130] Thrombocytopenia may also develop; anemia associated with the virus is rare. Traditionally, serologic analysis provided little firm evidence of CTF infection during the acute phase because of the delay in appearance of various antibodies. Recently, diagnosis during the acute phase using reverse-transcriptase PCR has been reported, making this method a promising tool for early detection and treatment.[13] [149] Isolation of CTF virus from blood or CSF by inoculating suckling mice or cell cultures confirms the diagnosis and has been reported as the most reliable technique.[38] A fluorescent conjugate prepared against CTF viral antigen can be used to stain erythrocyte smears, but the test lacks sensitivity.[127] Serologic tests (neutralizing antibody, complement fixation, IFA) are available, but titers rise slowly, and these are traditionally not diagnostic during the clinical illness. Improvements in early serologic testing are ongoing, with recent reports of IgM detection against synthetic viral peptides and Western blot analysis, facilitating easier diagnosis during the acute phase of illness. Babesiosis Babesia species, as with malarial organisms, are pleomorphic intraerythrocytic protozoan parasites. More than 70 distinct species have been described from various vertebrate hosts.[254] Some of the most important species include B. bigemina, B. bovis, and B. divergens (all in cattle); B. caballi and B. equi (horses); B. canis (dogs); and B. microti (rodents). Babesiae are transmitted to vertebrates primarily through the bite of ixodid ticks. Epidemiology.
Babesiosis has long been recognized as an important veterinary disease, receiving biblical reference as the "divine murrain" infecting the cattle of the pharaoh Ramses II (Exodus 9:3). Various epidemics of cattle fever have been documented throughout history.[34] Human disease was originally reported in 1957 in a splenectomized man in Yugoslavia.[283] Five cases of human infection with bovine Babesia (B. bovis, B. divergens) were reported from Europe between 1957 and 1976; two cases of babesiosis of unknown species were reported from California in 1968 and 1981; a human case of B. gibsoni infection was reported in California in 1993; and a single B. caucasia infection was reported from Russia in 1978.[148] [254] [255] These cases were widely separated geographically, and all occurred in splenectomized individuals. Since 1970 the incidence of human babesiosis has accelerated, primarily because of an outbreak of B. microti infections in the northeastern United States. The first case was recognized in a patient with an intact spleen in 1969 on Nantucket Island, Massachusetts.[358] Since then, more than 450 confirmed cases have occurred in the United States.[71] [203] B. microti is endemic to the coastal regions of southern New England, where the principal vector is the northern deer tick Ixodes scapularis.
798
Most cases are contracted on Cape Cod and the offshore islands of Massachusetts (Nantucket, Martha's Vineyard), New York (Shelter Island, Long Island), and Rhode Island (Block Island).[71] Cases have also been reported from Wisconsin and Minnesota, a known focus of I. scapularis. [319] The high incidence of B. microti infection is caused by its ability to produce disease in individuals with intact spleens. A new strain of B. microti called WA-1, thought to be spread by Ixodes pacificus, has been isolated from an immunocompetent patient with an intact spleen in Washington State.[238] The ecology of B. microti parallels that of Borrelia burgdorferi, the agent of Lyme disease. The major vector in both diseases is I. scapularis. White-footed mice (Peromyscus leucopus) constitute the major reservoir for B. microti. Larval or nymphal ticks ingest the parasite during a blood meal from an infected rodent. Babesiae replicate within the tick and are passed transstadially. Amplification of the cycle occurs when the infected tick transmits the organism to a vertebrate host during the next blood meal. White-tailed deer (Odocoileus virginianus) are the principal hosts for adult ticks; larvae and nymphs feed on deer, mice, and other small mammals.[290] Human babesiosis occurs when humans accidentally intrude on the natural cycle and are bitten by an infected tick. As in other tick-borne diseases, the peak incidence is during the warm weather months from May to September, when ticks are actively feeding. The majority of infections with B. microti are asymptomatic. Recent serologic testing shows that although seroconvergence has increased greatly over the past 30 years, it stabilized in the 1990s. An epidemiologic survey of 136 cases in New York showed that the most important risk factors for severe babesial disease are advanced age, asplenia, and immunodeficiency. Babesial infection appears to be as prevalent in children as in adults, however, the intensity of disease greatly increases over age 40. In one study, 23% of patients with babesiosis had concurrent Lyme disease infection. [203] Case reports have also shown multiple coinfection involving borreliosis, ehrlichiosis, and babesiosis,[209] with more severe symptoms in coinfected individuals compared to single organism infection. [169] Prolonged, subclinical infection creates the potential for transmission of B. microti through blood donation. More than 26 cases of babesiosis acquired by transfusion have been reported.[79] [173] [189] [284] [365] Seroprevalence surveys in endemic regions show donor exposure rates of 3% or greater.[80] Currently, control of transfusion-related infection is limited to identifying donors at high risk of exposure (from endemic regions, history of tick bites, seasonal exposure to tick-favorable landscapes). This strategy may become less effective as tick-endemic areas expand. Transfusion Figure 33-7 (Figure Not Available) Babesia life cycle. Within a tick, Babesia parasites infect gut cells, undergo asexual division, and eventually migrate to the salivary glands. The organism is introduced into a human when the infected tick takes in a blood meal. Transmission usually involves the nymphal tick, but the duration of attachment required for transmission of Babesia species is not known. Babesia species can be transmitted to humans concomitantly with Borrelia burgdorferi. (Modified from Boustani MR, Gelfand JA: Clin Infect Dis 22:612, 1996.)
has also reportedly transmitted new species of Babesia, causing significant disease in immunocompetent individuals.[141] Pathogenesis.
Babesiae are transmitted from wild and domestic animal reservoirs to humans by Ixodes ticks. The life cycle of I. scapularis, the tick responsible for transmission of B. microti to humans from rodents, spans 2 years, beginning in the spring with the hatching of the larval form. In the late spring and summer months the larvae feed on a variety of hosts and acquire babesial infection. Typically, larvae become infected from their preferred host, leucopus. Ingested Babesiae reach the gut of the feeding tick, where they reproduce sexually. The newly formed zygote eventually spreads throughout the body of the tick. After reaching the salivary glands, the babesial sporoblasts remain dormant until the next spring when the tick larva molts to a nymph. The nymph then seeks a blood meal, infecting a new host (rodents or humans). In endemic areas, as many as 60% of white-footed mice are infected by late summer. The nymph I. scapularis is the primary vector of human babesiosis, but adult ticks can also transmit the disease. After inoculation by a tick bite, Babesia sporozoites rapidly invade erythrocytes, where they differentiate into merozoites. Great pleomorphism is displayed,[214] but ring-shaped and ameboid trophozoites are the predominant form. Multiplication occurs by asexual asynchronous budding. After the parasite multiplies, the infected erythrocyte ruptures, freeing the organisms to invade other red blood cells (RBCs); severe hemolytic anemia may ensue (Figure 33-7 (Figure Not Available) ).
799
Infection with B. microti reduces the malleability of erythrocytes, causing microvascular stasis and decreased RBC life span. Electron microscopy has shown extensive RBC wall damage, including protrusions, perforations, and extrusions in the cell membrane. Asplenia or steroid therapy can worsen the disease and prolong parasitemia. An intact spleen preferentially destroys infected RBCs because of their decreased malleability. Prolonged parasitemia is common in babesiosis.[257] B. microti may persist for as long as 4 months in an otherwise healthy patient.[358] Parasitemia may remain after clinical recovery or may develop in asymptomatic individuals. An intact spleen is important in resistance to Babesia organisms. Although the presence of a spleen is not protective against B. microti, the disease is often more severe in splenectomized patients. Age is also an important factor in susceptibility to babesiosis. Children and young adults usually have subclinical or mild, self-limited infections, whereas older adults are more likely to have severe, clinically apparent disease.[25] [258] Chronic medical disorders may be an additional risk factor for severe babesiosis.[26]
Clinical Manifestations.
Acute B. microti infection is characterized by the gradual onset of malaise, anorexia, and fatigue, followed within several days to a week by fever, sweats, and myalgias. Other, less common symptoms include headache, nausea and vomiting, depression, abdominal pain, and dark urine. In a review of 17 patients with babesiosis, 52.9% presented with temperature greater than 38.3° C (101° F), and four of the nine had morning fever spikes; eight had relative bradycardia.[161] Incubation is 1 to 4 weeks after a tick bite or 6 to 9 weeks after transmission by blood transfusion. Most victims do not recall a tick bite, and rash is not a feature of the illness. If rash resembling erythema migrans appears, Lyme disease coinfection should be considered. Physical examination is usually normal, except for fever (steady or intermittent) and mild splenomegaly in some patients. Petechiae and ecchymosis may rarely occur. Laboratory evaluation reveals a mild to moderate hemolytic anemia; normal to slightly reduced WBC counts; and in some patients, mild to moderate thrombocytopenia. Serum lactate dehydrogenase (LDH) and bilirubin levels are mildly elevated in most patients, reflecting the hemolytic anemia. [126] [257] AST and ASL may be elevated, and urine may show proteinuria and hemoglobinuria. In one series, 13 of 17 patients (76.5%) had lymphopenia, and five (29.4%) had rouleau formation in the peripheral blood smear.[161] A review of 139 hospitalized patients with babesiosis in New York from 1982 to 1993 looked at common signs and symptoms and the prognostic factors associated with poor outcome.[359] Of the 139 patients, 9 (6.5%) died, 35 (25.2%) were admitted to the intensive care unit, and 35 (25.2%) required more than 14 days of hospitalization. In these patients with severe disease the mean age was 62.5 years, and 62% were male. The most common symptoms were fatigue, malaise, weakness (91%); fever (91%); shaking chills (77%); and diaphoresis (69%). Prognostic indicators for severe outcome included high alkaline phosphatase, male gender, and elevated WBC count. Only 12% of patients with severe disease had a history of splenectomy, and only 2% had received a prior blood transfusion. Although most patients with normal splenic function recover without specific therapy, prolonged fatigue and malaise are common.[257] Splenectomized persons generally have more severe clinical disease with higher levels of parasitemia and more severe hemolytic anemia.[258] Elderly persons, immunocompromised patients, and those with human immunodeficiency virus (HIV) also are at higher risk for severe infection. Pulmonary edema has been reported.[34] Typically, the level of parasitemia ranges from 1% to 10%. In Europe, babesiosis results from infection with B. divergens or B. bovis and has been reported only in splenectomized patients. The illness is characterized by high fever, chills, headache, and severe hemolytic anemia, often resulting in hemoglobinuria, jaundice, and renal insufficiency. Major findings on physical examination include fever, hepatomegaly, jaundice, and hypotension. More than half of the reported cases have been fatal. [255] Only one case of human babesiosis during pregnancy has been reported to date.[247] The patient recovered without specific therapy, and the neonate did not develop babesiosis. Cases of intrauterine infection in animals, however, have been reported. Diagnosis.
Babesiosis should be considered in any person with an unexplained febrile illness who has lived in or traveled to an endemic region in the midsummer months, especially with a history of a tick bite or tick exposure. The diagnosis of babesiosis can be confirmed by identifying the intraerythrocytic parasites on Giemsa-stained blood smears. Persons with intact spleens usually have low levels of parasitemia (less than 5% parasites), and examination of repeated smears may be necessary.[126] [257] The predominant forms of B. microti closely resemble the small rings of Plasmodium species. A later tetrad form may be seen and is positive morphologic evidence of babesiosis. Differentiating Babesia from Plasmodium may be difficult but is
800
possible by noting the absence of pigment deposits in erythrocytes parasitized with the older stages of Plasmodium species ( Box 33-5 ). Box 33-5. LABORATORY DIAGNOSIS OF BABESIOSIS Peripheral blood smear (Wright or Giemsa staining) showing intraerythrocytic Babesia Polymerase chain reaction Indirect immunofluorescent assay Intraperitoneal inoculation of splenectomized hamsters
When organisms cannot be detected on blood smears, the diagnosis can made by intraperitoneal inoculation of the patient's blood into splenectomized hamsters. Serologic studies may also be helpful in confirming the diagnosis[259] but are performed in only a few laboratories. A titer greater than 1:64 on IFA testing is considered consistent with seropositivity, and a titer greater than 1:256 is diagnostic of acute infection. No test for circulating Babesia antigen is available. PCR testing for Babesia can be as sensitive and specific as standard testing and may be reproducible enough for routine use in diagnosis of acute babesiosis.[168] Treatment and Prevention.
Chemotherapy for B. microti infection consists of a combination of clindamycin and quinine and should reserved for patients with severe disease or those with asplenia, immunosuppression, or elderly status. [72] The clindamycin dose for adults is 1.2 g intravenously twice daily or 600 mg orally three times daily for 7 days. Children should receive three oral doses of clindamycin for 7 days (20 to 40 mg/kg/day). The quinine dose for adults is 650 mg orally three times daily and for children is 25 mg/kg/day in three divided doses, each for 7 days. Parasites are eradicated from the blood with this therapy, although treatment failures have been reported.[278] [284] Recently, azithromycin was used as a successful alternative to clindamycin in one treatment failure.[278] In seriously ill patients with high levels of parasitemia, exchange transfusion may also produce rapid clinical improvement.[147] [328] Patients with mild clinical disease typically recover without specific anti-Babesia chemotherapy, although few patients have been followed longitudinally. A recent prospective study showed that parasitemia lasted for a mean of 82 days in 24 asymptomatic subjects not treated with the standard regimen.[170] Even those receiving clindamycin and quinine had delayed resolution of parasitemia, however, and 9 of 22 subjects had significant side effects from standard therapy. Exchange transfusion with clindamycin/quinine therapy has proved to be effective in three cases of B. divergens infection.[34] Avoidance of ticks is the only currently effective method of preventing babesiosis. Splenectomized patients should probably be advised to avoid visiting areas endemic for babesiosis.
TICK-BITE PREVENTION AND PROPHYLAXIS Prevention of tick-borne diseases is directed toward preventing tick bites. Avoidance of areas (nearby water supply, dense ground cover) supporting the reservoir species, often the white-footed mouse in the northeastern United States, will decrease tick exposure.[273] Protective clothing (long pants cinched at the ankles or tucked into boots or socks) should be worn when in tick-infested areas. Spraying clothes with an insect repellent may provide an additional barrier against ticks. Most repellents contain diethyltoluamide (DEET), which repels ticks but does not kill them. Permanone is an aerosol spray tick repellent for use on clothing. Its active ingredient, permethrin, kills ticks on contact. Field tests have shown Permanone to be 90% to 100% effective in preventing tick bites. Permethrins have very low toxicity in mammals. Close inspection of all parts of the body at least twice daily should be done when traveling in tick-infested areas. Adult ixodid ticks are generally on the body for 1 or 2 hours before attaching. Even after a tick attaches, disease transmission may be prevented by prompt removal. Proper removal of the tick is important, since infection may be acquired by careless handling of infected ticks, even without a bite. The tick should be grasped as close to the skin surface as possible with blunt curved forceps, tweezers, or protected fingers. The tick should be pulled out with steady pressure, taking care not to crush or squeeze the body, since expressed fluid may contain infective agents. After the tick is removed, the bite site should be disinfected. Traditional methods of tick removal, such as applying fingernail polish, isopropyl alcohol, or a hot match head, do not effect tick detachment and may induce the tick to salivate or regurgitate into the wound.[219] -shaped devices are available that slide between the tick and the skin so that the tick can be lifted from its attachment. In general, prophylactic antibiotics are not recommended for tick bites. Clinical trials of antibiotic prophylaxis for RMSF and Lyme disease demonstrate that the risk of infection in a patient who seeks medical treatment for a tick bite is very low. In most areas of the United States the chances are small that a tick harbors an infectious agent. Even if the tick is infected, the agent probably will not be transmitted if the tick is found and removed promptly. Together, these facts suggest that the risk/benefit ratio of an adverse reaction to the antibiotic vs. disease prevention will be high.
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Chapter 34 - Spider Bites Leslie V. Boyer Jude T. McNally Greta J. Binford
INTRODUCTION TO SPIDERS The spiders number approximately 34,000 described species and are found in all habitats except for the open sea.[37] [59] [206] They are carnivorous predators with important ecologic roles in most terrestrial ecosystems. Many are capable of wind-borne dispersal (ballooning), which has led to colonization of even the most isolated land masses on earth. As with ticks, mites, scorpions, and other arachnids, spiders have a body consisting of an abdomen and an unsegmented cephalothorax (prosoma) with chelicerate jaws, pedipalps, and four pairs of legs ( Figure 34-1 ). They are distinct from other arachnids in having loss of abdominal segmentation, and male pedipalpal tarsi are modified as secondary genitalia.[253] In addition, spiders have venom that is produced in a gland in the anterior prosoma and delivered through a cheliceral fang. On the abdomen, they have silk-producing glands and a set of spinnerets. The primary function of venom in spiders is prey capture or, rarely, defense. Venoms are complex mixtures of neurotoxic and proteolytic peptides, proteins, and biogenic amines.[1] [15] [102] [185] [253] Most of these toxins are target specific, acting selectively on arthropods, vertebrates, or other groups, including some with mammalian-specific activity.[1] [120] [202] Venom composition varies widely across spider species, and variation may exist within species between sexes and among geographically isolated populations.[184] Venom potency also varies within individuals both seasonally and developmentally. Despite this tremendous venom diversity, only a few dozen spider species are considered harmful to people because (1) most others have an insufficient quantity of venom, (2) the toxins do not affect mammals, or (3) the fangs cannot penetrate human skin. In a few species, although laboratory evidence suggests potential mammalian toxicity, human envenomations have not been reported, perhaps because of the rarity of encounters between spiders and humans in some habitats. Table 34-1 lists an assortment of spider families, including those with species that have been reported to bite humans. All spiders are carnivorous and have the challenge of capturing live prey. Prey capture is a multistep process in which spiders must find prey, ensnare it, immobilize it, and digest it externally before the liquefied meal can be consumed. This process and the role of venom are very diverse. The neurotoxins in spider venom are primarily used for prey immobilization. Venoms of a few spiders are known to have some proteolytic components that likely begin the process of external digestion. The bulk of digestion, however, results from digestive enzymes that are ejected from the mouth, a distinctly separate opening from the venom duct (Figure 34-2 (Figure Not Available) ). Occasionally, spider digestate may infect wounds created by spider bites, which affects the clinical appearance, although no direct evidence substantiates this suspicion. In addition to venom, some theraphosids (tarantulas) produce urticating hairs that irritate skin or mucous membranes of animals or humans. Exposure may result from direct contact with the spider or its web or from proximity to airborne hairs launched by an aggravated individual.
GENERAL ASSESSMENT AND TREATMENT OF SPIDER BITES Awareness of the differential diagnosis is crucial for management of any patient presenting for evaluation of "spider bite," because the offending creature is rarely observed and identified. In general, it is outside of normal biologic activity for spiders to bite humans, except in defense. A defensive bite risks the spider's life and tends to occur only when its life is threatened by being crushed. Thus true spider bites are much less common than insect bites or cutaneous infections. Furthermore, no pathognomonic clinical signs prove the diagnosis without retrieval and identification of a spider that was seen actually biting.[236] Diagnosis of arachnidism without direct evidence can lead to inappropriate treatment and the lack of consideration of more severe underlying medical issues.[145] [148] [151] [228] Therefore the medical history, physical examination, and laboratory evaluation must often consider an alternative etiology. Treatment plans should include careful follow-up and patient counseling to take into consideration any uncertainties in the final diagnosis. The differential diagnosis of a local lesion may include fungal, bacterial, and viral infection, especially herpes simplex and zoster; the vesiculobullous diseases; arthropod-borne infectious diseases (e.g., Lyme disease); other bites and stings; foreign body reactions; and systemic conditions that predispose to focal skin
808
Figure 34-1 External anatomy of an araneomorph spider. A, Dorsal. B, Ventral (legs omitted). Figure 34-2 (Figure Not Available) Longitudinal section of the prosoma. E, Endosternite; Eso, esophagus; P, pharynx; SEG, supraesophageal ganglion; S, sucking stomach; SUB, subesophageal ganglion. (Modified from Foelix RF: Biology of spiders, ed 2, Oxford, UK, 1996, Oxford University Press.)
809
TABLE 34-1 -- SPIDERS OF CLINICAL INTEREST SCIENTIFIC NAME (NUMBER OF GENERA AND SPECIES): GEOGRAPHIC RANGE CLINICAL REMARKS COMMON NAME
TAXONOMIC REFERENCES [59] [208]
Phylum Arthropoda, Class Arachnida, Order Aranea (3 Suborders, Worldwide 105 families, 3067 genera, approx. 34,000 species): Spiders No species believed clinically relevant
[209] [212]
Suborder Mesothelae (1 family, 2 genera, 40 species)
Asia (part)
Suborder Mygalomorphae (15 families, 260 genera, 2200 species): Mygales
Worldwide
[218]
Theraphosidae (86 genera, 800 species): tarantulas and baboon spiders
Worldwide
[218]
Aphonopelma (Rheochostica): tarantula
New World
Rheochostica henzi (previously Dugesiella henzi): tarantula
New World
Mygalarachne (previously Sericopelma)
CLINICAL REFERENCES
Minor local reaction; urticating hairs
[299]
[213] [218]
[218]
Minor local reaction
[218]
Pterinochilus: tarantula
Africa
Minor local reaction
[218]
Pamphobaetus: tarantula
Brazil
Minor local reaction
[218]
Avicularia: tarantula
New World
Minor local reaction
[218]
Lasiodora: tarantula
Brazil
Minor local reaction
[218]
Grammostola cala: Chilean rose tarantula
New World
Minor local reaction; urticating hairs
[218]
Acanthoscurria: tarantula
New World
Minor local reaction; urticating hairs
[218]
Euathlus (previously Brachypelma): tarantula
New World
Minor local reaction; urticating hairs
[218] [248]
Harpactirella lightfooti: baboon spider or bobbejaan-spinnekop
Africa
Poecilothuria: tarantula
Australia
Selenocosmia
East Indies, India, Australia
[218]
Phormictopus
South America, Caribbean
[218]
Lampropelma: tarantula
Asia, India
Minor local reaction
[218]
Haplopelma minax: Thailand black tarantula
Asia, India
Urticating hairs
[218]
[218]
Minor local reaction
Hexathelidae (11 genera, 74 species): funnel-web mygalomorphs
[36] [61]
[42] [122] [195]
[218]
[36]
[218]
Atrax
Eastern Australia
Atrax robustus: Sydney funnel-web spider
Eastern Australia
[115] [218]
Local pain; severe neurotoxicity
[115] [218]
[90] [91] [126] [262] [263] [271] [303] [305]
[115] [218]
Hadronyche (Atrax)
Eastern Australia
H. formidabilis: northern funnel-web spider
Eastern Australia
Local pain; severe neurotoxicity
[115] [218]
[11] [118]
H. versutus: Australian Blue Mountains funnel-web spider
Eastern Australia
Local pain; severe neurotoxicity
[115] [218]
[11]
H. infensus
Eastern Australia
Local pain; severe neurotoxicity
[115] [218]
[11] [299]
H. cereberus
Southeastern Australia
Local pain; severe neurotoxicity
[115] [218]
Dipluridae (17 genera, 157 species): funnel-web mygalomorphs
Worldwide
Trechona venosa
South America
Idiopidae (18 genera, 267 species): front-eyed trapdoor spiders
Pantropical, India
Aganippe subtristis
Australia
Arabantis
Australia
Mysgolas (previously Dyarcyops, Hermea)
Australia, New Zealand
Ctenizidae (10 genera, 116 species): trapdoor spiders
Worldwide, except South America
[67] [218]
Bothriocyrtum
North America
[218]
Ummidia
North, Central America
[218]
Actinopididae (3 genera, 41 species): trapdoor spiders
Australia, Central and South America
[218]
Missulena bradleyi: mouse spider
Australia
[218]
Mammalian toxin; no human reports Minor local reaction
[218]
[170]
[218]
[299]
[218] [218]
Minor local reaction
Mammalian toxin; one case of systemic effects
[218]
[218]
[267]
Suborder Araneomorphae (90 families, 2700 genera, 32,000 species): true spiders Filistatidae (12 genera, 87 species)
Worldwide
[156]
Sicariidae (2 genera, 129 species): recluse, brown, or fiddle spiders
Worldwide
[156] [210]
Loxosceles: recluse, brown, or fiddle spiders
New World, Mediterranean, Africa
[105]
[10] [20]
L. reclusa: brown recluse spider
North America (central, southeast)
Local necrosis; systemic syndrome
[105]
[111] [214] [292]
L. arizonica: Arizona brown spider
North America (southwest)
Local necrosis; systemic syndrome
[105]
L. rufescens
Worldwide
[105] [156]
L. intermedia
Brazil
[40]
L. gaucho
Brazil
[40]
L. spinulosa
South Africa
L. laeta: corner spider or spider behind the pictures
South America, Australia, Painful local lesion; Finland systemic syndrome
[105] [156]
L. parrami
South Africa
[193]
Sicarius: six-eyed crab spiders
Neotropics, South Africa
Dysderidae (20 genera, 371 species): giant-fanged, six-eyed spiders
Worldwide
[68]
Dysdera
Worldwide
[68]
Desidae (28 genera, 200 species): long-jawed intertidal spiders
Worldwide
[230]
Badumna insignis: black house spider
Australia, New Guinea
Zodariidae (350 species): hunting spiders
Worldwide
Supunna picta
Australia
Filistata
Local necrosis; DIC
Local pain, rarely necrosis
[196] [197] [198]
[117]
Minor local reaction [166]
Nephila: golden-silk spiders
Pantropical
[163]
Argyronetidae (1 genus, 1 species): water spiders
Europe
[230]
Argyrontea aquatica
Europe
[230]
Gnaphosidae (111 genera, 2156 species): ground and mouse spiders
Worldwide
[209]
Herpyllus ecclesiasticus: parson spider
North America
Drassodes
Worldwide
[207]
Lamponidae (1 genus, 50 species): white-tailed spiders
Australia, Tasmania, New Zealand
[209]
Lampona cylindrata: white-tailed spiders
Australia, New Zealand
Miturgidae (23 genera): forest floor and cave spiders
Worldwide
Miturga
Australia, New Zealand
Minor local reaction; rarely necrotic
Heteropodidae (82 genera, 850 species): giant crab, huntsman, and large, wandering crab spiders
[172] [298] [300]
[38]
Tetragnathidae (50 genera, 900 species): long-jawed orb-weaving Worldwide spiders
Minor local reaction; brief systemic effects
[10]
[127]
[209]
[173]
[114] [300]
[92]
Palystes natalius: lizard-eating spider
South Africa
Minor local reaction
Heteropoda
Worldwide
Isopeda
Australia, New Guinea, East Indies
Minor local reaction
Olios
America, Australia
Local pain, brief nausea
Delena cancerides: social huntsman spider
Australia
Minor local reaction
Oxyopidae (9 genera, 400 species): lynx spiders
Worldwide
Peucetia viridans: Green lynx spider
North and Central America, West Indies
Salticidae (475 genera, 4500 species): jumping spiders
Worldwide
Breda jovialis
Australia
[64]
[195] [200]
[298]
[232]
[298]
[76]
Minor local reaction
Minor local reaction
[39]
[123]
[80] [216]
[299]
Phidippus
New World
Local pain, minor ulceration
[234]
Holoplatys
Australia
Minor local reaction, itch, headache
[299]
Mopsus
Australia
Thiodina
America
Opisthoncus
Australia
Thomisidae (160 genera, 1960 species): crab spiders
Worldwide
[74] [246]
Misumenoides
Americas
[246]
Ctenidae (37 genera, 472 species): wandering spiders
Worldwide
Phoneutria: armed spiders
South America
P. nigriventer: Brazilian armed spider
Brazil, Paraguay
Elassoctenus harpax
Australia
Cupiennius
South and Central America, West Indies
[175]
Lycosidae (76 genera, 2196 species): wolf spiders
Worldwide
[76] [313]
Lycosa: wolf spiders
Worldwide
Local pain
L. raptoria
South America
Local pain
L. tarentula: "tarantula"
Palearctic
Subject of folklore
L. godeffroyi
Australia
Local pain
[308]
Minor local reaction
Local pain; systemic neurotoxin
[299]
[82]
[122] [170]
[47] [226]
[313]
L. erythrognatha Clubionidae (25 genera, 590 species): sac, running spiders, and two-clawed hunting spiders
Worldwide
Cheiracanthium: sac and running spiders
Worldwide
C. mildei
Holarctic
C. punctorium
Europe
Minor local reaction; fever
[258]
[32] [180] [181]
C. japonicum
Japan, China
Minor local reaction; brief systemic illness
[312]
[203]
C. longimanus
Australia
Minor local reaction; brief systemic illness
[32]
C. lawrencei
Africa
Local necrosis; systemic syndrome
[196] [197]
C. mordax
Australia
Minor local reaction, brief systemic illness
[32]
C. inclusum
America
Local pain, nausea
Corinnidae (51 genera, 659 species): sac spiders
Worldwide
Trachelas Supunna picta
Queensland
Tengellidae (5 genera, 18 species): running spiders
New World
Liocranoides
Appalachia, California
Agelenidae (41 genera, 600 species): grass and funnel-web spiders
Worldwide
Tegenaria agrestis: hobo or northwestern brown spider
Europe, America (Pacific Northwest)
Agelenopsis aperta: grass spider or funnel-web spider
Southwest United States, Mexico
[75]
[75]
[75]
[32]
[211] [311]
Minor local reaction
[211]
Minor local reaction
[65]
[205] [281]
[230]
Local necrosis; systemic syndrome
[231]
[2] [285] [289]
[53]
[290]
Zoridae (12 genera) Diallomus
Australia
Superfamily Orbicularia (13 families, 10,300 species) Theridiidae (62 genera, 2000 species) comb-footed spiders
Worldwide
Latrodectus: widow spiders
Worldwide
L. mactans: black widow spider
[311] [158] [164]
[300]
North America
[164] [168]
[82]
L. mactans hasselti: redbacked spider
Australia
[278]
[97] [140] [272]
L. hesperus: black widow spider
North America
L. tredecimguttatus
Mediterranean
[168]
L. pallidus
Libya to Russia
[168]
L. indistinctus: black button spider
Africa
L. geometricus: brown button spider
Worldwide
[168]
Steatoda
Worldwide
[159]
S. paykulliana: false black widow spider
Europe, Mediterranean
[167]
S. nobilis
England
Local pain; mild systemic effects
[294]
S. foravae: false button spider
Southern Africa
Minor local reaction
[190]
Achaeranea tepidariorum
Worldwide
Trivial local reaction
Araneidae (155 genera, 2600 species): orb-weaving spiders
Worldwide
Argiope: argiopes
Worldwide
A. argentata
America
A. trifasciata
Worldwide
Local pain; systemic neurotoxicity
[56] [179]
[188] [188]
[160]
[110]
Local pain; vesicle
[165] [165]
Araneus: cross, garden, and shamrock spiders
Worldwide
Eriophora biapicata
Australia
Neoscona: orb-weaving spiders
Worldwide
Phonognatha graeffei
Australia
[161] [162]
Minor local reaction [30]
Trivial local reaction
DIC, Disseminated intravascular coagulation. lesions (e.g., diabetes mellitus, leukemia, lupus erythematosus). "First-aid" interventions by the patient may mask an otherwise benign process by superimposition of trauma, burns, or chemical irritation. Systemic signs and symptoms may require differentiation from the effects of snake or scorpion neurotoxin, pesticide toxicity, sepsis, meningitis, hemolytic anemia, or acute abdomen, depending on the circumstances. The medical history should include details of the bite circumstances, to demonstrate consistency with expected spider habitat and behavior. This includes location indoors or outside, time of day or night, and human activity at the time of injury. The victim should attempt to recall the appearance of the involved arthropod; if it was believed killed through garments or bedclothes, an attempt should be made to retrieve its remains. Crushed spider parts can be examined and identified by arachnologists or entomologists at many universities and museums. Until identified, spiders may be preserved in 70% to 80% ethanol. The evolution of subsequent wound and systemic symptoms should be noted, along with modifiers, including home treatment and underlying health of the patient. If the local geography lacks species consistent with the suspected pathophysiology, the recent travel history of household contacts should be considered. Physical examination includes particular attention to the bite site, as well as general assessment for systemic effects. Local findings of importance include anatomic location (spiders are more likely to bite defensively at sites where clothing binds tightly; thin skin is more readily envenomed than callous skin) and number of separate lesions (multiple bites suggest parasitic insect bite rather than spider bite). Central punctae, vesicles, or erosions should be noted, as well as the pattern of peripheral changes, including erythema, pallor, hemorrhage, induration, tenderness or anesthesia, and local lymphatic involvement. Systemic findings, depending on the species involved, may include changes in vital signs, diaphoresis, generalized rash, facial edema, gastrointestinal distress, muscle fasciculations, spasm or tenderness, or altered mental status. The laboratory evaluation for envenomation is usually simple, seldom requiring more than complete blood count and urinalysis. Assessment for other elements of the differential diagnosis, however, may be much more elaborate. Depending on circumstances, this may include viral, bacterial, or fungal culture; Lyme disease titer; radiography of the abdomen or of the injured part; stool test for occult blood; electrocardiogram; or skin biopsy. General supportive measures are the mainstay of therapy for most spider bites. These include basic local hygiene, tetanus prophylaxis, analgesics, hydration, and surgical follow-up if indicated for debridement and management of extensive necrotic lesions. Corticosteroids are of unproven benefit and are generally not indicated. Antibiotics, although not of value for simple venom injury, are prescribed when bacterial cellulitis cannot be eliminated from the differential diagnosis. Specific measures, including antivenom, for treatment of envenomation by particular spider species are discussed later in this chapter.
GUIDE TO SPIDER DIVERSITY AND IDENTIFICATION This chapter provides more information on spider diversity than most reviews in order to (1) inform the reader of the immense diversity of spiders that are
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medically insignificant and thus emphasize the rarity of spiders known to cause medical problems; (2) emphasize the need for accurate species identification, particularly in reporting of cases for publication or teaching; and (3) facilitate accurate identification of spiders that are caught in the act of biting by directing professionals to proper identification keys. Table 34-1 includes species worldwide that are currently known or suspected to be medically noteworthy, even minimally, either through the effect of bites or urticating hairs. Geographic range and the most recent systematic work on each group are included. Box 34-1 lists genera of serious medical significance for each continent. For effective communication, groups of spiders must be recognized by the same name worldwide. This chapter uses the current official nomenclature. Box 34-1. CLINICALLY IMPORTANT SPIDER GENERA BY GEOGRAPHIC DISTRIBUTION
NORTH AMERICA Loxosceles Latrodectus Tegenaria
SOUTH AMERICA Loxosceles Latrodectus Phoneutria
AFRICA Loxosceles Latrodectus
EUROPE Latrodectus Loxosceles
AUSTRALIA Atrax Hadronyche (Atrax) Latrodectus
ASIA Latrodectus
Of the three spider suborders, two contain clinically significant species: Mygalomorphae and Araneomorphae. Mygalomorphs include the baboon spiders or tarantulas, trapdoor spiders, purse-web spiders, mygalomorph funnel-web spiders, and several other groups that lack common names. Most spiders are araneomorphs, including jumping spiders, orb-weaving spiders, widow spiders, and wolf spiders (see Table 34-1 ). The most conspicuous characteristics that distinguish these groups are the orientation of the chelicerae (jaws) and the number of book lungs. Spider fangs are located on the chelicerae, which open sideways in the Araneomorphae and move diagonally in the Mygalomorphae, requiring the latter to rear back for a downward, snakelike strike (Figure 34-3 (Figure Not Available) and Figure 34-4 ). Mygalomorphae have two pairs of book lungs, whereas most Araneomorphae have only one pair. Lung slits, which open into the book lungs, are easily visible in a ventral view of the anterior abdomen (see Figure 34-1 ). Characteristics that distinguish families, genera, and species include eye number Figure 34-3 (Figure Not Available) Movement of the chelicerae in mygalomorphs (A) and araneomorphs (B). (Modified from Foelix RF: Biology of spiders, ed 2, Oxford, UK, 1996, Oxford University Press.)
Figure 34-4 Fangs of mature male tarantula (Aphonopelma species). (Courtesy Michael Cardwell & Associates, 1992.)
and pattern, numbers of tarsal claws, and details of genitalic structure. Although many spider species are geographically localized (e.g., Atrax robustus in Australia, Phoneutria nigriventer in Brazil), some, such as the black widow (Latrodectus mactans), are found worldwide (see Table 34-1 ). Others, such as members of the Loxosceles genus, are widely distributed in more than one continent, and still others, such as Tegenaria agrestis, appear to have naturalized in specific geographic regions distant from their point of ecological origin. Because of the resulting worldwide species diversity and overlap, the remainder of this chapter is structured according to spider taxonomy rather than isolated species or geographic location.
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SUBORDER MYGALOMORPHAE Mygalomorphs make up less than 10% of all spider species. They are found worldwide, with greatest abundance and diversity in tropical regions. Tarantulas (Theraphosidae) are the most famous mygalomorphs and include the largest spiders known, reaching up to 10 cm in body length. Most mygalomorphs are smaller, some less than 1 mm in adult body length. Most live multiple years (some up to 20), and females continue to molt after reaching adulthood. They have diverse habits but typically live in silk-lined burrows or silken tubes. For the purpose of prey capture, mygalomorph silk is only slightly sticky relative to araneomorph silk and is generally used to trigger the presence of prey rather than to ensnare them. Once prey are detected, spiders run out of their retreat, seize prey in their jaws, and return to the retreat to feed. Individuals wander when dispersing, and males leave their retreats in search of females during mating season. Family Theraphosidae: Tarantulas and Baboon Spiders Theraphosidae is the largest mygalomorph family with respect to both numbers of species and sizes of the largest individuals ( Figure 34-5 ). Approximately 800 described species are found on all continents, with greatest abundance and diversity in tropical regions. They mature in 3 to 9 years and can live for 15 to 20 years. Individuals live in burrows, with trip-line threads extending from the entrance. These are sometimes located in abandoned rodent burrows or hollow trees. Theraphosids have dense tufts of specialized hairs on their tarsi (feet) that enable them to climb on smooth surfaces and may aid in prey capture. They have two tarsal claws, eight closely grouped eyes, and two pairs of spinnerets. Tarantulas may live for 1 to 25 years. As a group, they are found mainly in tropical and subtropical areas. Confusingly, "tarantula" was first applied to Lycosa tarentula, a species of European spider actually belonging to the wolf spider family, or Lycosidae, which are properly classified within the suborder Araneomorphae, described later in this chapter. In the United States the term tarantula usually refers only to the large spiders of the family Theraphosidae, suborder Mygalomorphae. Grammostola mollicoma is the largest tarantula known, with a body length of 7 to 10 cm and leg spread of 21 to 27 cm. [42] [104] Harpactirella lightfooti, the baboon spider or bobbejaan-spinnekop, is a mygalomorph spider found in South Africa. Body length is 3 cm; the cephalothorax is brown with a yellowish border. Venom.
Few tarantula venoms have been studied systematically. In the United States, Rheochostica henzi and
Figure 34-5 Theraphosidae. (Courtesy Gita Bodner.)
Figure 34-6 Mature female Aphonopelma iodium. (Courtesy Michael Cardwell & Associates, 1997.)
members of the genus Aphonopelma ( Figure 34-6 ) have venom containing hyaluronidase, nucleotides, and polyamines. [46] [54] [155] [239] [240] Polyamines are thought to act as neurotransmitters and increase venom effectiveness, particularly with respect to paralysis of insect prey.[253] Hyaluronidase is postulated to be a spreading factor, and the nucleotide adenosine triphosphate (ATP) potentiates the major effects of the venom on mice. Both venoms cause rapid, irreversible necrosis of skeletal muscle when injected intraperitoneally into mice.[204] Dugesiella (Rheochostica) venom was found to have a necrotoxin with several similarities to sea snake venoms.[155] In comparison, the venom of Scodra griseipes, an African tarantula, includes higher-molecular-weight (greater than 25,000 daltons) proteins and enzymes plus lower-weight polypeptides (4000 to 9000 daltons); the second group is believed to contain polypeptide neurotoxins.[52] S. griseipes venom toxins have a mammalian effect, but this species is not known to be clinically relevant. Recent work suggests that venom chemotaxonomy may be a useful method of nondestructive 816
species recognition, at least within the Brachypelma genus.[84] Urticating Hairs.
Several genera of tarantulas, including Haplopelma, Lasiodora, Grammostola, Acanthoscurria, and Brachypelma, possess urticating hairs irritative to skin and mucous membranes. These genera are located throughout the western hemisphere, with many species indigenous to the United States. When one of these spiders is threatened, it rubs its hind legs across the dorsal surface of its abdomen and flicks thousands of hairs toward the aggressor. These barbed hairs can penetrate human skin, causing edematous, pruritic papules. The itching may persist for weeks. There are four morphologic types of urticating hairs. Tarantulas within the United States possess only type I hairs, which do not penetrate the skin as deeply as type III hairs. Type II hairs are incorporated into the silk web retreat and not thrown off by the spider. Type III hairs can penetrate up to 2 mm into human skin; this is the type of hair most likely to cause inflammation. They are typically found on Mexican, Caribbean, and Central and South American species. Type IV hairs, which belong to the South American spider Grammostola, are able to cause inflammation of the respiratory tract in small mammals. Rats and mice have been reported to die of asphyxia within 2 hours after exposure to the hairs. [61] [299] Clinical Presentation.
Despite the presence in venom of components toxic to rodent nerves and skeletal muscle, most tarantula bites result in only mild to moderate local symptoms in humans. A few can cause more severe pain and swelling, numbness, or lymphangitis. Species of tarantula implicated as causes of human envenomation include those in genera Mygalarachne (formerly Sericopelma) of Panama, Pterinochilus of Africa, Aphonopelma of Mexico and the United States, Pamphobaeteus of South America, Euathlus of Costa Rica, Theraphosa of French Guyana, Grammostola of Colombia, Poecilothuria of India, Lampropelma of Thailand, Lasiodora of Brazil, and Avicularia of Central America and southwestern United States. Envenomation usually involves immediate pain at the bite site, occasionally followed by some redness and swelling and usually without necrosis or serious sequelae.* Although no fatalities have been reported, localized pain followed by emesis, weakness, and collapse has been noted after envenomation by Harpactirella lightfooti, the baboon spider of South Africa.[42] [122] [195] Urticating hairs may cause intense inflammation, which may remain pruritic for weeks. Individuals who handle tarantulas may unwittingly transfer urticating hairs from hand to eye, causing keratoconjunctivitis or ophthalmia nodosa. Keratoconjunctivitis has been described after handling of a Thailand black tarantula, Haplopelma minax. Fine intracorneal hairs were noted at examination, and inflammation settled quickly with topical corticosteroid treatment; at 36-month follow-up the eye was normal.[36] More severe ophthalmic complications occurred in two cases after handling of Chilean rose tarantulas, Grammostola cala. In these victims, initial findings were similar, with intracorneal hairs and keratoconjunctivitis, but progressive panuveitis followed, with corneal granulomas, iritis, cataract, vitritis, and chorioretinitis apparently related to migration of hairs through the media of the eye. The differences in outcome with exposure to the two species may result from differences in hair morphology,
which may also explain differences in other reports of ophthalmic injury from tarantula or caterpillar hair exposure.[36] Similar cases of ophthalmia nodosa have been described.[25] [154] Treatment.
Theraphosid bite management is symptomatic. Elevation and immobilization of the extremity and oral analgesics may help reduce pain. All bites should receive local wound care and appropriate tetanus prophylaxis. Urticating hairs can be removed from skin with repeated application and removal of sticky tape, followed by copious irrigation if necessary; exposed eyes should be irrigated primarily. Topical or systemic corticosteroids and oral antihistamines may also be useful for urticating hair reactions. Family Hexathelidae: Funnel-Web Mygalomorphs The family Hexathelidae includes 11 genera and approximately 74 species, which are currently known from the Old World and Chile.[218] The funnel webs that typify members of this group are silk-lined tubular retreats that extend into a protected space, such as a burrow in the ground or a hole in a tree. Sheets of silk radiate from the retreat and signal the presence of prey. These webs superficially resemble webs of araneomorph spiders in the family Agelenidae. Distinguishing characteristics of the spiders include a shiny carapace; long, spiny sensory hairs on the legs; and paired claws lacking claw tufts on the tips of the feet, with teeth lining the medial claw. Clinically significant hexathelid spiders are species of Atrax ( Figure 34-7 ) and Hadronyche. Technically, taxonomists now consider Atrax and Hadronyche species as members of only one genus. [218] To avoid confusion in the literature, species names still use either Atrax or Hadronyche, depending on their original names. We discuss these species as a cohesive taxonomic group. Among these, the species Atrax robustus is best known and most carefully studied. Atrax and Hadronyche species, all of which are believed to be dangerous, have *References [ 42]
[ 46] [ 54] [ 66] [ 104] [ 150] [ 239]
.
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Figure 34-7 Funnel-web spider (Atrax species) wearing a wedding ring. (Courtesy Sherman Minton, MD.)
been described in southern and southeastern Australia, Tasmania, Papua New Guinea, and the Solomon Islands. As a group, they prefer cool, moist coastal and mountainous regions.[116] [118] [249] Genus Atrax/Hadronyche BIOLOGY.
Funnel-web spiders have a glossy ebony cephalothorax and velvety black abdomen. The abdominal undersurface may have brushes of red hair. The fangs reach 4 to 5 mm in length and are capable of penetrating a fingernail or a chicken's skull, sometimes making removal of the spider difficult. Females are somewhat larger than males, with a body length of 4 cm. Mature males are more delicate, with a tibial spur on the second pair of legs and pointed pedipalps.[137] [242] Atrax robustus, the Sydney funnel-web spider, is limited to a 160 km range around the center of Sydney, Australia. The spider creates a tubular or funnel-shaped, silk-lined shallow burrow under rocks, logs, fences, stumps, or thick vegetation or around foundations of houses. Colonies of up to 150 spiders have been found. Females rarely roam far from their webs; males live a vagrant life after reaching maturity. Wandering males may enter houses or other areas of human habitation, especially during the summer months after a heavy rain. Its aggressive behavior and potent venom make the male Sydney funnel-web arachnid one of the most dangerous spiders in the world. It is responsible for all known fatal Atrax envenomations.* Hadronyche formidabilis, the northern funnel-web spider, is found in the central coastal region of New South Wales and the adjacent Blue Mountains. Its tree-dwelling habit was once thought to be unique, but it is now known that other species also live in trees. The webs may be camouflaged in rough-barked trees, such as melaleuca (paper bark), banksia, and eucalyptus.[118] VENOM.
Although many species have venom with significant in vitro toxicity, few have been implicated in human illness. The best described of these is A. robustus. Atrax venom causes widespread release of neurotransmitters.[79] [118] [125] [256] [263] This may occur by a direct action of the venom on nerve membranes, producing spontaneous action potentials and consequently provoking a global outpouring of transmitters that accounts for the neuromotor and autonomic stimulation seen clinically. Early efforts to purify the active component of Atrax venom resulted in reports of neurotoxins of various molecular weights purified from venom preparations in separate experiments.[261] These were termed Atraxotoxin (10,000 to 25,000 daltons, from milked venom),[118] robustoxin (4887 daltons, also from milked venom),[250] and atraxin (9800 daltons, from ground venom glands). [119] The relationships among these toxins are not clear, but atraxotoxin or atraxin may be a precursor of robustoxin. In addition to these components, Atrax venom contains various lower-molecular-weight compounds, including citric acid, lactic acid, phosphoric acid, glycerol, urea, glucose, gamma-aminolevulinic acid, glycine, spermidine, spermine, tyramine, octopamine, and 5-methoxytryptamine.[78] The best characterized of the toxins is robustoxin, whose 42-amino acid sequence was determined in 1985.[250] It is the sole lethal toxin that can be isolated by cation-exchange chromatography, and its effects in monkeys duplicate the effects of crude venom preparations. A 5 mg/kg intravenous (IV) dose of robustoxin to monkeys causes dyspnea, blood pressure fluctuations culminating in severe hypotension, lacrimation, salivation, skeletal muscle fasciculation, and death within 3 to 4 hours of administration.[191] Isolated human intercostal muscles were studied to determine the etiology of muscle fasciculations. Muscles treated with A. robustus venom developed marked contractions, which were abolished by d-tubocurarine.[48] Muscles treated with venom for more than an hour stopped contracting and could be stimulated only by increasing the stimulus duration. A. robustus venom has been shown to lack anticholinesterase activity.[260] Contractions are not a direct venom action on the muscle fiber, so acetylcholine appears to have been released from the presynaptic terminals.[96] Muscle fasciculations are apparently caused by abnormal repetitive firing of motor neurons. It was hypothesized that the venom changes the membrane's electric field, activating sodium channels without altering the transmembrane potential or damaging the neuronal membrane ultrastructurally.[79] [118] [256] Hypertension in Atrax toxicity may have several causes. Morgans and Carroll[186] [187] demonstrated direct alpha-adrenergic stimulation with vasoconstriction of isolated arterial preparations exposed to A. robustus *References [ 58]
[ 98] [ 118] [ 242] [ 275] [ 301]
.
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venom. In rabbit atria an initial decrease followed by an increase in cardiac inotropy and chronotropy may result from vagal acetylcholine and myocardial norepinephrine releases, respectively.[49] The combination of myocardial responses and peripheral vasoconstriction may explain the hypertensive response. Animal species vary in susceptibility to Atrax venom. Rabbits given 15 mg of crude venom intravenously and cane toads given 12 mg of female Atrax venom show no effects after envenomation. Primates, including humans, are among the most susceptible species. Newborn mice, also highly susceptible, have been used as an in vivo biologic assay for venom toxicity. [118] [265] Sutherland [267] found that a lethal dose of venom from a male A. robustus could be neutralized in newborn mice by
nonimmune sera from rabbits and other nonprimate vertebrates. Scheumack and co-workers [251] later demonstrated that the active fraction of nonimmune rabbit sera contained immunoglobulins G and M (IgG, IgM). In addition, venom potency varies with time of year, recent feeding history, maturation and gender of the individual spider.[12] Between 1956 and 1963, Wiener demonstrated significant differences in the venom of male and female Atrax spiders. Males had an average venom yield of 1.01 mg, less than the 1.84 average from females. On the other hand, guinea pig lethality was much greater after a bite by a male (75% to 90%) than by a female spider (20%). Weiner concluded that significant qualitative difference exists between the venoms of males and females. Monkeys, which have a pattern of envenomation similar to that in humans, provide a model in which Sutherland[265] [271] has described a biphasic clinical syndrome. Phase I begins minutes after venom injection, with local piloerection and muscle fasciculation. This extends proximally, becoming generalized over the next 10 to 20 minutes. After another 5 minutes, severe hypertension, tachycardia, hyperthermia, and coma with increased intracranial pressure may occur, followed by diaphoresis, salivation, lacrimation, diarrhea, sporadic apnea, borborygmi, and grotesque muscle writhing. Death may result from asphyxia caused by laryngeal spasm, combined with copious respiratory secretions, apnea, or pulmonary edema. Laboratory evaluation reveals metabolic acidosis and elevated plasma creatine phosphokinase. Phase II begins 1 to 2 hours after envenomation, as the phase I symptoms subside. The victim may return to consciousness and appear to recover. In severe cases, hypotension gradually worsens over 1 to 2 hours, with periods of apnea. Pulmonary edema and death may occur despite ventilatory support. CLINICAL PRESENTATION.
Up to 90% of Atrax bites may not result in significant envenomation.[299] Intense pain at the bite site may result from direct trauma as well as the venom's effect, but the bite does not provoke cutaneous necrosis. Wiener[303] studied the cutaneous effects of the venom on himself by injecting 0.5 mg intradermally. Local pain and a wheal surrounded by erythema lasted for 30 minutes, followed by localized sweating and piloerection. No systemic effects occurred. The earliest systemic signs and symptoms may include perioral tingling, nausea and vomiting, diaphoresis, salivation, lacrimation, and dyspnea. Pulmonary edema follows, along with a generalized central and peripheral neurologic syndrome that includes muscle fasciculations, tremor, spasms, weakness, and impaired consciousness. Death may occur secondary to pulmonary failure, hypotension, or cardiac arrest.[262] [299] Thirteen fatalities from A. robustus envenomation were recorded between 1927 and 1984. Children are particularly susceptible; those under 12 years may die within 4 hours of the bite.[91] [126] [268] Before the development of specific antivenom in 1980, severe envenomations resulted in a minimum 8-hour critical period, followed by a 9to 21-day hospital course.[90] [268] [271] No fatalities caused by H. formidabilis have been recorded, although, several severe envenomations have occurred.[118] Venoms of A. robustus, A. versutus, A. infensus, and A. formidabilis appear to have comparable vertebrate toxicity in vitro.[11] TREATMENT.
Immediate treatment after a bite is modeled after that for Australian snakebite and consists of four steps: (1) wrap the length of the bitten extremity with an elastic bandage, (2) splint to immobilize the extremity, (3) immobilize the victim, and (4) transport to the nearest hospital with the bandage in place.[201] [269] A human case report has illustrated the utility of this method, with occurrence, disappearance, recurrence, and reresolution of symptoms coinciding with compression wrap removal and replacement in a man bitten by a male A. robustus.[112] An experimental model in Macaca fascicularis monkeys has supported efficacy of the pressure immobilization technique.[264] [265] [273] Specific antivenom has been the mainstay of treatment for Atrax envenomation since 1981. The antivenom is a purified IgG product developed by Sutherland and associates[266] [274] at the Commonwealth Serum Laboratories by immunizing rabbits with a combination of male Atrax venom and Freund's adjuvant. The antivenom was demonstrated to neutralize Atrax venom in vitro and to reverse symptoms in monkeys before its introduction for human use. To date, it has been used with good effect in more than 40 humans bitten by Atrax and Hadronyche species.[71] [271] If a tourniquet or bandage is in place when the victim presents for hospital care, it should be removed in
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an intensive care setting, with careful observation for development or progression of symptoms. If systemic signs or symptoms occur, victims are usually treated with antivenom administration. Two ampules of antivenom (100 mg of purified IgG per ampule) are administered intravenously every 15 minutes until symptoms improve. Dosing is the same for children as for adults, and total doses of 2 to 8 ampules have been reported. During a 10-year period, antivenom was given to at least 40 persons, with no adverse effects or deaths reported.[271] In addition to antivenom administration, management is symptomatic and supportive. Oxygen, mechanical ventilation, and IV fluid support may be indicated in severe cases. Atropine (0.6 mg) may be used to lessen salivation and bronchorrhea. ß-Blockers may be indicated for severe hypertension and tachycardia. Other than antivenom, no consistently effective agent has been found to enhance survival after Atrax envenomation. Diazepam, atropine, and furosemide have been found to increase survival in monkeys, but this may not be the case in humans.[89] [118] Scheumack and colleagues[252] developed a toxoid from robustoxin by polymerization with glutaraldehyde. Immunization with the toxoid conferred protection against the lethal effects of 50 mg/kg Atrax venom in monkeys for at least 26 weeks after toxoid injection. Family Dipluridae: Funnel-Web Mygalomorphs Members of the family Dipluridae are found on all continents and are concentrated in tropical areas. Individuals build funnel webs similar to those of Hexathelidae. Diplurids are distinct from hexathelids in having posterior lateral spinnerets that are very long and widely separated. Most are 5 to 25 mm in length. Genus Trechona BIOLOGY.
Trechona venosa is a large South American funnel-web tarantula with neurotoxic venom potentially dangerous to humans. [42] [104] [122] As with all Trechona species, T. venosa is sedentary, living in holes or on plants in tropical forests along the Atlantic coast. The spider may be black or gray-brown with yellow stripes on the abdomen. Mature body length may be 3 to 4.5 cm, with 6- to 7-cm legs and 3- to 4-mm fangs. T. venosa is not found in Chile, but in this region it has been confused, particularly in venom studies, with a spider in the family Nemesiidae, Acanthogonatus subcalpeianus, which it resembles.[218] VENOM.
The venom of T. venosa is extremely toxic to rats, with an apparent action similar to that of Phoneutria species.[170] CLINICAL PRESENTATION.
No cases of human envenomation have been reported, although it is presumed that symptomatic envenomation by T. venosa is possible. TREATMENT.
Treatment is symptomatic and supportive.
SUBORDER ARANEOMORPHAE Enormous diversity is found within the group Araneomorphae, which contains 32,000 of the 34,000 currently described spider species.[59] Araneomorphs, or true spiders, are found throughout the world in all terrestrial (and a few aquatic) habitats. They show tremendous variability in size, appearance, and habit; however, no araneomorphs are as large as the largest tarantulas. Characteristics that distinguish araneomorphs include features of the spinnerets that enable them to produce extremely sticky silk. Also, all but a few groups have only one pair of book lungs. Most have eight eyes, but eye number varies from two to eight. Prey capture tactics usually determine where a spider will be found and are generally consistent within particular groups. Thus these tactics often provide conspicuous clues that help identify spiders. Family Sicariidae: Recluse Spiders Sicariidae includes two genera, Loxosceles and Sicarius, both of which are clinically important. The family falls within a larger group of families (Scytodoids) that all have only six eyes. In these two genera the eyes are in dyad pairs. The chelicerae are fused at the base, and the labium is fused to the sternum. Males have more slender abdomens and more prominent pedipalps than females. Previously, Loxosceles was placed in its own family, Loxoscelidae, but this was recently synonymized with Sicariidae.[210] Genus Loxosceles: Brown Spiders BIOLOGY.
Loxosceles, commonly known as brown or fiddle spiders, build small, irregular, and sticky webs in small areas, such as under rocks or wood or in human-made habitats. The genus contains more than 100 species, with centers of diversity in central America and Africa.[20] [77] [174] [238] [244] These spiders are 8 to 15 mm in adult body length, are light to dark brown, and have a dark, violin-shaped spot centered anterodorsally, such that the neck of the fiddle extends backward across the cephalothorax. The shape and darkness of the fiddle, relative lengths of the first two pairs of legs, and genitalia characteristics are features that help distinguish species[43] [133] [244] ( Figure 34-8 ). From the South American L. laeta to the South African L. spinulosa, these small arachnids have been associated with human pathologic conditions. Several species have been associated with necrotic arachnidism in the United States: L. reclusa (the true brown recluse
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Figure 34-8 Adult female desert violin spider (Loxosceles deserta). (Courtesy Michael Cardwell & Associates, 1994.)
Figure 34-9 Brown recluse spider (Loxosceles reclusa). (Courtesy Indiana University Medical Center.)
spider, Figure 34-9 ), L. rufescens, L. arizonica, and L. laeta. These spiders are native to all the southernmost states. In the Mississippi River valley, their territory extends as far north as southern Wisconsin. Species native to one region or habitat may adapt successfully to new locations after transport by humans.[197] [293] Brown spiders regularly roam in search of new web sites, and males wander in search of females. They are most active at night from spring through fall, emerging from woodpiles and rats' nests to hunt insects and other spiders. South African savanna species have been observed under stones and logs and in the tunnels of old termite nests; spelean species are found naturally in caves, but have also appeared in homes and export warehouses.[194] [196] [199] Brown spiders may infest homes, generally preferring warm, undisturbed environments such as vacant buildings and storage sheds. In Chile the tendency to inhabit human dwellings has earned L. laeta the names araña de los rincones (corner spider) and araña de detrás de los cuadros (spider behind the pictures).[245] Molts, or shed exoskeletons, may mark infested areas; the web may be limited to a small, flocculent structure alongside the egg sac. Females may live 1 to 3 years and longer in captivity. [104] [134] Naturally unaggressive toward humans, brown spiders are not prone to bite unless threatened or trapped against the skin. Bites typically follow retrieval of old bed sheets or jackets from storage. VENOM.
Fractionated Loxosceles venom contains at least eight or nine major protein bands and three or four minor bands identifiable by gel electrophoresis.[223] Hyaluronidase was first identified as a component by Wright and associates.[310] Hyaluronidase probably plays a facilitating role in lesion development, encouraging the spread of other venom components; however, it is not itself a cytotoxin. Hydrolytic enzyme activities include esterase,[310] alkaline phosphatase,[128] lipase,[142] and 5'-ribonucleotide phosphorylase,[103] but none of these alone appears to explain cytotoxicity. Sphingomyelinase D, a protein fraction of 32,000 dalton, appears to be the most important dermonecrotic factor in L. reclusa venom. This component is present in L. intermedia spiderlings starting with the third instar, with increasing activity throughout development until adulthood.[108] Injection of the purified fraction produces characteristic lesions in rabbits.[152] [280] A protein of similar molecular weight to sphingomyelinase D has been shown to have dermonecrotic activity in the venom of L. gaucho of Brazil,[21] and considerable homology has been noted among proteins derived from L. intermedia, L. laeta, L. gaucho, and L. reclusa.[22] Sphingomyelinase D is postulated to operate by a variety of mechanisms, including cell membrane binding and polymorphonuclear leukocyte neutrophil (PMN) chemotaxis. [100] [222] [254] Lesions are inhibited in rabbits by pretreatment with nitrogen mustard to deplete PMNs. Histologic studies suggest similarities between venom-induced lesions and those seen with the Arthus and Shwartzmann phenomena.[254] Some vertebrate species, such as rats and fish, are essentially unaffected by Loxosceles venom; others, such as rabbits, mice, and dogs, are highly susceptible to its effects.[243] Injected into humans, the venom is a hemolysin and cytotoxin, with enzymatic activities that may cause dermonecrosis and hemolysis. Pathogenesis of the human lesion is not well understood but depends on the functions of complement and PMNs.[17] [244] Venom from L. reclusa has a direct hemolytic effect on human erythrocytes; this process depends on the presence of serum components that include C-reactive protein and calcium.[135] [280] Platelet aggregation also is calcium dependent and is induced in vitro with sphingomyelinase D; this process may activate the prostaglandin cascade. Platelet aggregation appears to depend on serum amyloid protein, a serum glycoprotein of previously unknown significance.[99] [225] [280]
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Because Loxosceles venom provokes an immune response in experimental animals, efforts to develop diagnostic tests are based on antigen or antibody detection in human blood. In 1973, Berger and associates [29] reported an in vitro lymphocyte transformation assay for L. reclusa venom, which turned positive in the lymphocytes of exposed individuals within 4 to 6 weeks of initial exposure. This test may help to document prior exposure but not to diagnose envenomation at the time of the initial
bite. Barrett and co-workers[23] reported a passive hemagglutination inhibition test using rabbit antibody and human erythrocytes incubated in vitro with venom from L. reclusa. [23] Cardoso and associates, observing that efforts to detect antigen in human serum may fail because of insufficient antigenemia, have demonstrated the presence of L. gaucho venom in biopsy homogenate using enzyme-linked immunosorbent assay (ELISA). Barbaro and colleagues [21] demonstrated circulating IgG against L. gaucho venom in 4 of 20 patients, detectable between 9 and 120 days after the bite. Some of the variability in clinical presentation among victims of Loxosceles envenomation may be caused by differences in the venom of males and females. Female L. intermedia spiders produce a greater amount of more potent venom than males.[63] CLINICAL PRESENTATION.
Necrotic arachnidism, or loxoscelism in the case of bite by spiders of the genus Loxosceles, refers to the clinical syndrome that follows envenomation by a variety of spiders, for which L. reclusa, the brown recluse spider, is the prototype. The bites of these spiders often result in serious cutaneous injuries, with subsequent necrosis and tissue loss. Less often, severe systemic reactions may occur with hemolysis, coagulopathy, renal failure, and even death.[292] Reports of severe reaction to spider bites possibly attributable to brown spiders date to 1872, in a report of a 45-year-old Texas woman with a febrile illness accompanying a large necrotic lesion of her thigh.[50] In 1896, death from renal failure accompanying another bite in Texas was reported. [214] Spider bite was reported as a cause of blackwater fever (massive hemoglobinuria) in Tennessee in 1940.[111] The first documented case of loxoscelism (from L. rufescens) was reported by Schmaus[247] in Kansas in 1929. L. laeta was identified as the cause of similar lesions in South America in 1937, and L. reclusa was the cause of necrotic arachnidism in the Midwestern United States by 1958.[9] [10] Since then, numerous cases of cutaneous and more severe reactions have been attributed to spiders of the genus Loxosceles. The clinical spectrum of loxoscelism ranges from mild and transient skin irritation to severe local necrosis accompanied by dramatic hematologic and renal injury. Isolated cutaneous lesions are the most common
Figure 34-10 Brown recluse spider bite after 6 hours, with central hemorrhagic vesicle and gravitational spread of venom. (Courtesy Paul Auerbach, MD, and Riley Rees, MD.)
Figure 34-11 Brown recluse spider bite after 24 hours, with central ischemia and rapidly advancing cellulitis. (Courtesy Paul Auerbach, MD.)
presentation, and most bites may resolve spontaneously without the need for medical intervention.[28] [29] Many authors distinguish between simple local presentation and more severe systemic, or viscerocutaneous, loxoscelism. Local symptoms usually begin at the moment of the bite, with a sharp stinging sensation, although a victim may be unaware of having been bitten. Frequently the bite site corresponds to a portal of entry or a region of constriction of clothing, such as cuff, collar, waistband, or groin. The stinging usually subsides over 6 to 8 hours and is replaced by aching and pruritus as the lesion becomes ischemic from local vasospasm. The site then becomes edematous, with an erythematous halo surrounding an irregular violaceous center of "incipient necrosis" (actually hemorrhage and thrombosis).[44] [280] A white ring of vasospasm and ischemia may be discernible between the central lesion and the halo. Often the erythematous margin spreads irregularly in a gravitationally influenced pattern that leaves the original center eccentrically placed near the top of the lesion ( Figure 34-10 , Figure 34-11 , Figure 34-12 ). In more severe cases, serous or hemorrhagic bullae may arise at the center within 24 to 72 hours, and an eschar forms beneath. After 2 to 5 weeks this eschar sloughs, leaving an ulcer of
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Figure 34-12 Brown recluse spider bite after 48 hours, with incipient central necrosis.
variable size and depth through skin and adipose tissue, but sparing muscle.[130] Lesions involving adipose tissue may be extensive, perhaps from lipolytic action of the venom.[142] The ulcer may persist for many months, leaving a deep scar.[3] [235] [295] Local sequelae depend on the anatomic location. Persistent segmental cutaneous anesthesia has been attributed to nerve injury after a recluse bite on the side of the neck.[121] Epiglottic and periepiglottic swelling severe enough to require endotracheal intubation has been reported in a recluse bite involving a child's ear.[129] The bite of the somewhat larger South American spider L. laeta is reported to cause intense pain and extensive edema, with proportionately less necrosis than that caused by L. reclusa. The edema is notoriously prominent with facial bites and resolves over 2 to 4 weeks. [244] Systemic involvement is less common but may occur in combination with cutaneous injury from any Loxosceles species; it occurs more frequently in children but may be seen in adults.[215] [277] Systemic reaction may develop in cases with minor-appearing local findings, making diagnosis difficult.[280] When systemic involvement occurs, hemolytic anemia with hemoglobinuria is often the prominent feature, usually beginning within 24 hours of envenomation and resolving within 1 week.[81] During this time, measured hemoglobin may drop markedly, accompanied by jaundice and hemoglobinuria. The anemia is usually Coombs' test negative, but two cases of Coombs'-positive anemia have been reported. [292] Fever, chills, maculopapular rash, weakness, leukocytosis, arthralgias, nausea, vomiting, thrombocytopenia, disseminated intravascular coagulation (DIC), hemoglobinuria, proteinuria, renal failure, and even death have been reported.[33] [70] [106] [192] [292] The diagnosis of loxoscelism is based on spider observation and identification, typical history, and local and systemic signs. The differential diagnosis of the local injury includes bacterial and mycobacterial infection, herpes simplex, decubitus ulcer, burn, embolism, thrombosis, direct trauma, vasculitis, Lyme disease, and pyoderma gangrenosum.[5] [145] [217] [219] [270] A series of five proved or suspected L. reclusa bites to women in the second and third trimesters of pregnancy has been reported. Despite significant local injuries, rash, and microhematuria, no fetal injury was noted.[4] TREATMENT.
Treatment of loxoscelism depends on its severity. Cutaneous loxoscelism can usually be managed on an outpatient basis. Most mild cutaneous envenomations respond to application of local cold compresses,[147] elevation of the affected extremity, and loose immobilization of the part. Tetanus prophylaxis should be provided where indicated. Necrotic lesions may need debridement after erythema has subsided to define the margins of the central eschar. This usually involves significant debridement 1 or 2 weeks after the bite, with close follow-up for several weeks. In severe cases this can be followed with skin grafting or plastic surgery when the wound is stable. Severe necrotic or infected lesions may lead to hospitalization. Recently the use of dapsone has gained popularity for prevention of lesion progression in potentially necrotic wounds seen within 48 to 72 hours of a bite.[95] [101] Dapsone is a leukocyte inhibitor that in theory can minimize the local inflammatory component of cutaneous loxoscelism, thereby preventing or lessening subsequent skin necrosis. In 1983, King and Rees[146] reported the use of dapsone for envenomation in a human bitten by L. reclusa, based on a successful trial of dapsone pretreatment in guinea pigs injected with recluse venom. Since that time, no prospective, controlled human trial has proved dapsone efficacy, but a variety of case reports and series have supported its use in the treatment of potentially necrotic wounds treated in the first days after envenomation.[3] [26] [129] [171] [296] Typical dosage recommendations are for 50 to 100 mg orally, twice daily. Risks of dapsone therapy include hypersensitivity,[306] methemoglobinemia, and hemolysis in the presence of
glucose-6-phosphate dehydrogenase (G6PD) deficiency. Patients with systemic symptoms should be considered for admission when they have evidence of coagulopathy, hemolysis and hemoglobinuria, or rapid progression of other systemic signs. Care is mainly supportive, usually involving wound care, fluid management, presumptive treatment for bacterial superinfection, and occasionally, blood transfusion. Rarely, hemodialysis has been required for oliguric renal failure. [109] Discharge is appropriate when renal and hematologic status is stable. For patients with significant local or systemic signs or symptoms, laboratory evaluation should include peripheral blood cell count, basic coagulation screening, and urinalysis. Liver and renal function tests are indicated in severe poisonings. When use of dapsone is considered, a screening test for G6PD deficiency may be indicated. The frequency of follow-up testing depends on the course and severity of envenomation.
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Hospitalized patients may need close follow-up of anemia and renal function over several days. Corticosteroids have been injected either at the wound site or systemically,* but this remains of questionable benefit.[27] [221] Antihistamines may help control itching but do not change the lesion.[157] Some advocate early surgical excision of the wound site,[8] [16] [87] [132] but others have demonstrated that outcomes are better with early medical management in human patients,[69] [223] as well as in experimental animals.[221] Hyperbaric oxygen (HBO) treatment has been tried empirically in uncontrolled human trials, with reports of good outcome.[276] Comparison of HBO with no treatment in rabbits showed enhanced recovery at 24 days at the histologic level, but with no apparent clinical difference between the two groups.[259] Loxosceles-specific antivenom has been tried in both the United States and South America. In the early 1980s, Rees and colleagues[221] reported a protective effect of treatment with antivenom in rabbits before or up to 12 hours after envenomation. Small-vessel occlusion, leukocyte infiltration, and necrosis occurred but were diminished in antivenom recipients. Pretreatment in a separate study abolished symptoms of systemic loxoscelism.[220] In one study, 17 patients were separated randomly into dapsone, antivenom, and combination therapy groups; all patients received erythromycin. Individual results suggested that the antivenom was efficacious when given early, but the overall trial was inconclusive, indicating the need for further study.[224] Gomez and colleagues [107A] have studied the intradermal use of an anti-Loxosceles Fab-fragment in a rabbit model, suggesting therapeutic efficacy when the antivenom is injected up to 4 hours following envenomation. Currently, no Loxosceles antivenom is commercially available in the United States. In South America an antivenom to L. laeta was developed in 1954 by Vellard using immune serum of the donkey. Furlanetto developed L. laeta antivenom using immune serum of horses. Reports of the efficacy of systemically administered L. laeta antivenom are mixed.[244] An ELISA assay, developed for the detection of circulating venom antigen, has the potential to develop into a tool for clinicians and epidemiologists.[55] Genus Sicarius: Six-Eyed Crab Spiders BIOLOGY.
About 25 Sicarius species are known. Their range is limited to dry regions of South America and South Africa. Individuals live under stones or are sand dwellers. Some hide under sand and emerge to capture passing insects. Their bodies are flattened, and their legs are laterigrade, meaning the tips point anteriorly as in a crab. Adult body size ranges from 12 to 22 mm. VENOM.
The effects of venom of the South African crab spider Sicarius testaceus in a rabbit model demonstrated tissue necrosis and increased vascular permeability in the vicinity of the envenomation, as well as a dramatic decrease in platelet count. It is not clear whether this pattern is the same in humans.[283] CLINICAL PRESENTATION.
Sicarius species are occasionally implicated in human bites in South Africa. They tend to bite only when provoked and are rarely implicated in human poisonings, despite fairly high toxicity of the venom in laboratory animals. Envenomation reportedly can cause edema, erythema, and necrosis, occasionally associated with DIC.[196] [197] [198] TREATMENT.
Treatment of Sicarius envenomation is symptomatic and supportive. Family Desidae: Long-Jawed Intertidal Spiders Desidae has about 200 species that are distributed worldwide. Their chelicerae are often extended forward and have humps close to the prosomal attachment. Species range in body length from 4.5 to 12 mm. Most spiders in this family build small, irregular webs under rocks or logs. Some desids are closely associated with marine habitats, living in the intertidal zone. These spiders feed on marine animals and at high tide retreat into empty snail shells and worm tubes and seal off the entrance with silk. Others are found only on the water surface. Genus Badumna: Black House Spider BIOLOGY.
Badumna insignis (Ixeuticus robustus), or the black window spider, is a common Australian spider associated with a few human bite reports. This species is a nocturnal forager that builds tangled webs with silk retreats in and around human habitations.[299] VENOM.
Venom gland extract from B. insignis is reported to cause increased vascular permeability, as well as dose-dependent decreases in arterial pressure in rats, apparently from the presence of a serotonin-like substance in the venom.[149] Venom gland extract does not cause necrosis in cultured human or mouse skin.[14] CLINICAL PRESENTATION.
In one report, B. insignis caused local pain, itching, and swelling followed by regional lymph node tenderness and discoloration of the area around the bite. Over 2 weeks the lesion resolved, with some tissue necrosis and sloughing centrally.[172] In a series of five B. insignis bites, local lesions were painful but transient and unaccompanied by necrosis.[300] Systemic symptoms have rarely been reported, including nausea, vomiting, abdominal pain, pruritus, and painful knees.[299] *References [ 28]
[ 72] [ 73] [ 136] [ 139] [ 176] [ 214]
.
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TREATMENT.
Treatment of Badumna envenomation is symptomatic and supportive.
Family Zodariidae: Hunting Spiders Zodariids are a diverse group of hunting spiders. The estimated 350 species have a worldwide distribution but are primarily found in the tropics and subtropics. They are medium sized (3 to 15 mm), with the anterior spinnerets usually longer than the posterior structures. They hide under stones or burrow in pebbles or sand. Very few reports of documented human envenomation exist, although Supunna picta, a common leaf litter-dwelling spider of Australia, reportedly caused a transient erythematous rash and slight itch in a woman bitten at home. The lesion resolved uneventfully.[38] Family Gnaphosidae: Ground Spiders and Mouse Spiders Gnaphosids are common and found worldwide, with the highest densities in temperate areas. They are small to medium sized (2 to 14 mm) and usually dark in color (black, gray, or reddish brown). They have long, slightly flattened abdomens, and two of their spinnerets are conspicuous and cylindrical. Gnaphosids are nocturnal hunters, mostly on the ground, and during the day they retreat under rocks and stones or other tight quarters. Herpyllus ecclesiasticus, the parson spider, is distributed widely throughout the United States under rocks and rubbish and in houses. One case report of a bite by a H. ecclesiasticus described pruritus, arthralgia, malaise, and nausea beginning 1 hour after the bite. There was no necrosis.[173] [309] Treatment of bites is symptomatic and supportive. Family Lamponidae: White-Tailed Spiders Until recently the genus Lampona was placed in the family Gnaphosidae. The group was changed to family status because members do not share many of the characteristics that define Gnaphosidae.[209] Specialists believe that many undescribed genera in Australia belong to this group. Genus Lampona BIOLOGY.
Lampona cylindrata is a hunting spider with a distinctive cylindrical shape and white spot at the tip of the abdomen. They are often found indoors in Australia and New Zealand.[299] Individuals are wandering foragers that enter webs of other spiders and prey on them. VENOM.
The venom of L. cylindrata appears to increase vascular permeability in rats, perhaps from the release of endogenous bradykinin and prostaglandins.[149] Venom contains histamine and noradrenaline, both more highly concentrated in the venom of male spiders. [217A] CLINICAL PRESENTATION.
L. cylindrata was identified as the spider involved in a series of eight cases in Australia. Symptoms included a mild stinging sensation followed by 1 to 10 days of itching, redness, and swelling. In one case a small blister was present for a few hours; no necrosis was reported. The authors suspected that most L. cylindrata bites may be benign, despite earlier reports of ulceration after suspected L. cylindrata envenomations.[300] Gray [114] reported a case of more significant illness, with nausea, lethargy, and a small zone of necrosis after a known white-tailed spider bite. Although the vast majority of cases are relatively benign, significant skin necrosis occasionally may result from envenomation.[299] TREATMENT.
Treatment of Lampona envenomation is symptomatic and supportive. Family Heteropodidae: Crab Spiders and Hunting Spiders Biology.
Heteropodids, the "giant crab spiders," are distributed worldwide and are mostly tropical. They are large (10 to 40 mm) and resemble crabs, with the tips of all legs angling forward. They have flattened bodies and are capable of moving sideways. They have eight eyes in two straight rows. They are wandering hunters and typically nocturnal. In many places, they are welcome cohabitants with humans because they eat cockroaches. Palystes natalius, the lizard-eating spider, is one of the largest true spiders in South Africa. It has a brownish gray body with bright yellow and black striped legs. The female is larger than the male, with body length up to 4 cm. Venom.
Venom from the Australian heteropodid Isopeda montana has direct beta-adrenoreceptor action, and Delena cancerides, the social huntsman spider, appears to have both alpha- and beta-adrenoreceptor activity, although neither of these has been involved in recognized human envenomation. Both have been shown to increase vascular permeability in rats. [131] Clinical Presentation.
Only localized burning accompanied by slight swelling was noted after a female P. natalius bite to the left wrist. [195] [200] An Olios calligaster bite was followed by mild local symptoms, transient nausea, and faintness. Six bites by Isopeda species, predominantly I. pessleri, resulted in minimal local symptoms only. [300] Treatment.
Treatment of heteropodid bites is symptomatic and supportive.
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Figure 34-13 Green lynx spider (Peucetia viridans). (Courtesy Gita Bodner.)
Family Oxyopidae: Lynx Spiders Lynx spiders are found worldwide, with the greatest abundance in the tropics. They are small to medium sized (4 to 18 mm) and have a distinctive eye pattern, with six eyes in a hexagon and two smaller eyes below. Their abdomens are pointed posteriorly. They have long leg spines (macrosetae) that help detect motion through vibrations in the air. They are diurnal hunters with good vision and actively search for prey. Most are found on vegetation, and some are arboreal. Genus Peucetia
BIOLOGY.
Peucetia viridans, the green lynx spider of the United States and Mexico, is a diurnal hunting spider. P. viridans is translucent green, with red eyes and joints[123] ( Figure 34-13 ). VENOM.
Whole venom of P. viridans causes total and reversible block of non-N-methyl-D-aspartate receptor-mediated transmission in chick central nervous system.[138] CLINICAL PRESENTATION.
The bite results in a burning sensation, pruritus, erythema, and induration. TREATMENT.
Treatment of Peucetia bites is symptomatic and supportive. Family Salticidae: Jumping Spiders Salticidae is the largest family of spiders, with more than 5000 currently described species and many more yet to be described. They are distributed worldwide, with the highest densities in the tropics. Some have called them the "butterflies of the spider world" because most are brightly colored and some have iridescent scales. Some species mimic ants, beetles, pseudoscorpions, and bird droppings. Jumping spiders have excellent eyesight, with large, posteromedian eyes. They visually search for prey, then stalk and ambush with catlike movements. Males are often more brightly colored than females and perform elaborate courtship dances. They are always active during the day and are small, most less than 15 mm. Bites from spiders of the genus Phidippus, such as the jumping spider of the United States, can cause pain, erythema, pruritus, and sometimes minor ulceration. The swelling usually subsides within 2 days.[234] In Australia, local pain has been reported with the bite of spiders from genera Mopsus, Breda, Opisthoncus and Holoplatys. One patient bitten by a Holoplatys reported headache and vomiting.[299] Family Ctenidae: Wandering Spiders Ctenidae are mostly found in subtropical and tropical areas. They can be large spiders ranging from 4 to 40 mm. They hunt on the ground or on vegetation. They resemble and are closely related to wolf spiders but are distinguished by their eye arrangement (three rows: two eyes, then four, then two, the last two being the largest). They sometimes travel as stowaways on bananas. Genus Phoneutria: Banana Spiders (Armed Spiders) BIOLOGY.
The Phoneutria spiders of South America are large, nocturnal creatures notorious for their aggressive behavior and painful bite. The best known representative of the genus is Phoneutria nigriventer. It is known in Brazil as aranha armadeira, meaning "spider that assumes an armed display," because of its characteristic defensive-aggressive display.[242] P. nigriventer is the largest, most aggressive true spider found in South America, with an average body length of 35 mm, leg length of 45 to 60 mm, and fangs 4 to 5 mm in length for females. Males are slightly smaller.[241] The body is gray to brown gray with white marks forming a longitudinal band on the dorsal abdomen. A distinguishing characteristic is the red-brown brush of hairs around the chelicerae. P. nigriventer is mainly found in southern Brazil, Argentina, and Uruguay. Other species have been found in Bolivia and Colombia. The spiders do not construct a web, since they are nocturnal hunters, often traveling several hundred meters in search of prey. They may enter houses during this time, hiding in clothes in the light of day. According to Bucherl, 600 to 800 spider bites occur each year around the city of São Paulo alone.[41] VENOM.
Phoneutria venom is a complex mixture of histamine, serotonin, glutamic acid, aspartic acid, lysine, hyaluronidase, and other polypeptides. Histamine, serotonin, and incompletely characterized kallikreinkinin
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activating fractions contribute to local tissue swelling from the increased vascular permeability that may occur with envenomation.[6] [177] In addition, the venom contains at least six neurotoxic polypeptides, with molecular weights between 3500 and 8500.[62] The neurotoxic components include sodium channel poisons that appear to potentiate action potentials along axons, provoking erratic or rapid uncontrolled muscle twitches in invertebrates[83] as well as vertebrates.[7] [169] Microscopically, there is acute transient swelling of axons, particularly at the nodes of Ranvier, in a pattern similar to that caused by the venoms of scorpions Centruroides exilicauda and Leiurus quinquestriatus. The axons recover within a few hours of exposure, but return of nodal width to normal takes several days.[169] The effects of the venom have been studied in mice, rats, guinea pigs, rabbits, pigeons, and dogs. The venom has little or no effect on frogs and snakes, and it has four times greater toxicity in dogs than in mice. Rats and rabbits are very resistant to the venom's effects, but rabbit vascular smooth muscle contractions appear to be stimulated by a venom protein that acts independently of voltage-dependent sodium and calcium channels.[178] Dogs developed intense pain, manifested by yelping, followed by sneezing, lacrimation, mydriasis, hypersalivation, erection, ejaculation, and death after 200 mg/kg of venom was injected subcutaneously.[242] This is well within the dose that a single spider may inject. Electric stimulation yields an average of 1.6 to 3.2 mg of venom per spider.[41] CLINICAL PRESENTATION.
P. nigriventer venom acts on both the peripheral and the central nervous systems.[122] Although the majority of cases are clinically insignificant,[170] humans bitten by P. nigriventer may develop severe local pain that radiates up the extremity into the trunk, followed within 10 to 20 minutes by tachycardia, hypertension, hypothermia, profuse diaphoresis, salivation, vertigo, visual disturbances, nausea and vomiting, priapism, and occasionally death in 2 to 6 hours. Respiratory paralysis is generally the cause of death. Severe envenomation is more common among young children. Fatalities may occur in the debilitated or the young, but most people recover in 24 to 48 hours. Workers who handle bananas are frequently bitten because the spider hides in bunches of bananas. Bites have been reported in Switzerland and Argentina in produce workers inadvertently encountering these traveling spiders.[122] [241] [242] TREATMENT.
In most cases, symptomatic care is all that is necessary. Local pain control may be achieved by infiltration of local anesthetic near the bite site; this reportedly suffices for 95% of cases treated at the Hospital Vital Brasil. [170]
Figure 34-14 Wolf spider (Lycosa species). (Courtesy Arizona Poison & Drug Information Center, 1996.)
For more severe cases, a polyvalent antivenom (sero antiaracidico polivalente, Instituto Butantan) active against Phoneutria species is available in Brazil. Skin testing and antihistamine prophylaxis are recommended before its use. One to five ampules of antivenom are injected intramuscularly and/or intravenously, and clinical response is judged by the relief of pain or resolution of priapism. Opiates may potentiate the venom's effects on respiration and are generally not recommended in cases of systemic envenomation.[122] [241] [242] Family Lycosidae: Wolf Spiders Lycosidae are among the most common spiders. They are diverse, with more than 3000 species distributed worldwide. They are found from beaches to grassy fields and pastures. The Greek name lycosa (wolf) comes from the former belief that they hunted in packs.[60] [309] They range in size from 3 to 25 mm. Most species wander in active pursuit of prey, generally during the day. A few make deep burrows, and some even cover their burrows with doors. Most live on the ground, but some climb in vegetation. They have good vision, with conspicuously large, posteromedian eyes. Their eyes are arranged in three rows (four eyes, then two, then two). To attract mates, males wave their legs and sometimes stridulate to make sound. The female carries the egg sac attached to her spinnerets. When the young hatch, they climb on their mother's abdomen for transport. They have three claws on their tarsi. Genus Lycosa: Wolf Spiders BIOLOGY.
Lycosa is a large and widespread genus of wolf spiders ( Figure 34-14 ). It includes various middle-sized to large spiders with mildly cytotoxic venom capable of provoking transient inflammation in humans. The most famous wolf spider species is Lycosa tarentula, to which "tarantula" was first applied. Its bite was once
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believed to cause "tarantism," a syndrome of stupor, the desire to dance, and sometimes death, but this historic syndrome is now attributed to Latrodectus tridecimguttatus (neither a wolf spider nor a tarantula), and the wolf spider bite is now known to cause little more than stinging pain. The South American Lycosa raptoria has been reputed to be more dangerous than other wolf spiders, provoking necrosis at the site of envenomation. It now appears that this was also based on a misunderstanding. Necrotic arachnidism in South America is now attributed mainly to Loxosceles species. VENOM.
Lycosid venom is thought to be primarily cytotoxic, without hemolytic or anticoagulant activity.[309] Although scientific reports of necrosis are lacking after envenomation by the Australian wolf spider L. godeffroyi, media reports suggest that bites may lead to necrosis. Atkinson and Wright[13] have demonstrated that the raw venom of L. godeffroyi causes a strong inflammatory response and cutaneous necrosis when injected into mice. They further hypothesized that this action may result from contamination of the venom with digestive juices, since electrically collected raw venom caused necrosis, whereas venom gland extract did not.[14] CLINICAL PRESENTATION.
A series of 515 cases of confirmed Lycosa bites in Brazil showed that most occur between the hours of 6 AM and 6 PM, at a fairly consistent rate year-round. The most common bite sites were feet (40%) and hands (39%). The most common signs and symptoms were all local, with pain in 83%, swelling in 19%, and erythema in 14%. No local necrosis was described.[226] In the United States five cases of Lycosidae bites have been documented. One resulted in skin necrosis at the bite site, probably from the combined results of envenomation and infection.[47] TREATMENT.
Although South American antivenom active against Lycosa venom was available in the past, it was used in only one case of 515 reviewed by Ribeiro and associates.[226] Since 1985 the polyvalent Butantan Institute spider antivenom has not included the antilycosid fraction.[170] Most Lycosa cases can be managed with tetanus immunization and ice or oral analgesics; occasionally, local anesthetic block has been used for pain management.[226] Family Clubionidae: Sac Spiders and Two-Clawed Hunting Spiders Clubionids are common and distributed worldwide with the highest diversity of species in the neotropics. They are small to medium sized (2 to 15 mm) and are usually light brown to yellowish in color. They hunt nocturnally and make resting tubes in rolled
Figure 34-15 Cheiracanthium inclusum. (Courtesy Sherman Minton, MD.)
leaves or under rocks or stones, where they retreat during the day. Genus Cheiracanthium: Running Spiders and Sac Spiders BIOLOGY.
The genus Cheiracanthium as a whole has no distinctive marks or patterns.[110] [309] Members may be pale yellow, brown, green, or olive. The dorsal abdomen may have a median longitudinal stripe. Body size ranges from 7 to 15 mm, with a total diameter of 3 cm, including long, slender legs. In the United States, C. inclusum is the only indigenous species ( Figure 34-15 ). C. diversum is widely found in the Pacific islands. It was transported into Hawaii from Australia approximately 50 years ago. C. mildei was introduced from Europe and is now found from New England to Alabama to Utah. It is a common biting spider in Boston; it is most abundant in autumn, when most bites occur.[257] The South African sac spider C. lawrencei is a common nocturnal house spider that forages at night and may become trapped in bedding.[196] During the day these spiders hide in the concavities of leaves, curtains, or windowsills, encased in a silk sac. They are fast moving and aggressive when threatened.[198] VENOM.
Research on Cheiracanthium venom is limited. About 75% of guinea pigs bitten by C. mildei for the first time developed a wheal within 5 minutes, with 60% developing an eschar within 1 day.[257] Fractionation of dissected venom gland extracts from C. japonicum resulted in five fractions with lethal activity in mice. These were considered neurotoxic based on symptoms of dyspnea, flaccid paralysis, and death after intraperitoneal injection. [203] CLINICAL PRESENTATION.
Spiders belonging to the genus Cheiracanthium have a documented history of human envenomation since the eighteenth century. Species are
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known for their tenacious, painful bite. A pruritic, erythematous wheal appears within 30 minutes. Nausea, abdominal cramps, headache, and local necrosis have been reported. In 1901, Kobert described local swelling, erythema, pain, and fever after the author's third C. punctorium envenomation. [32] Maretic[180] [181] described local redness, pain, and edema but no necrosis after C. punctorium envenomation. In another case, C. inclusum caused local pain that radiated from the forearm bite site up the arm, associated with nausea. No other signs developed.[32] The Australian species C. mordax and C. longimanus caused local swelling, erythema, and pain associated with malaise, headache, dizziness, and nausea. Symptoms receded within 36 hours after treatment with antihistamines and local anesthetics.[32] Ori[203] found similar signs and symptoms after envenomation by C. japonicum. In South Africa, most C. lawrencei bites occur at night during sleep.[196] Paired bite marks 6 mm apart are evident within the first few hours. Local edema and erythema may be slight. By the third day the marks may become necrotic, with more edema, erythema, and pain; headache and fever may accompany this stage. The small ulcer begins to heal 7 to 10 days after the bite.[197] TREATMENT.
The lesion usually heals without problems, provided secondary infections are avoided. Treatment is supportive, consisting of cool compresses, elevation, immobilization, analgesics, and tetanus prophylaxis. Family Corinnidae: Sac Spiders Corinnids are ground-dwelling spiders primarily found in tropical regions. They were previously placed in the family Clubionidae and have similar habits. Spiders of the Trachelas genus are often encountered in houses in late summer and fall. T. volutus and several other Trachelas species reportedly cause mild local reactions without necrosis. Bites are painful initially and may swell. No systemic effects have been reported.[205] [281] Treatment is symptomatic and supportive. Family Agelenidae: Hobo, Grass, and Funnel-Web Spiders The 600 species of Agelenidae are mainly found in temperate regions of the Northern Hemisphere. They are medium-sized spiders, ranging from 8 to 15 mm in body length. Individuals build sheet webs that lead to a long funnel, which the spider uses as a retreat. When prey contacts the web, the spider runs out, bites it, and carries it back into the funnel. The large and conspicuous webs of these spiders often are long lasting, with spiders adding silk to make the sheet larger as the individual grows. Males may be found searching for females. Genus Tegenaria: Hobo Spiders BIOLOGY.
Tegenaria agrestis is commonly called the hobo spider or Northwestern brown spider. It is a 10- to 15-mm, light-brown spider with a yellowish green tint and chevrons on the dorsal abdomen. Individuals typically build funnel webs in disturbed habitats such as abandoned woodlots or along railroad tracks, with a hidden retreat beneath wood, rocks, or debris and silk extending beyond the cover. Spiders mature to adulthood in midsummer and mate and lay eggs in July through September. Adult males live for 1 year, then senesce and die at the end of the mating season. Adult females live for 2 years, so adults are present throughout the year. T. agrestis spiders are common and widespread natives of Europe and western central Asia.[124] This species was probably introduced in a seaport near Seattle in the early 1900s and was first formally identified in the 1930s.[85] [86] It has since expanded its range to British Columbia, Alaska, Oregon, Idaho, Montana, and Utah.[18] [227] [297] By the 1960s, individuals were often collected in and around human habitations in the Pacific Northwest. VENOM.
The venom of T. agrestis has become of interest in the last 15 years because of reports suggesting that their bites result in necrotic lesions. T. agrestis venom chemistry is not well characterized, and no necrotoxic component has been identified. Johnson and colleagues[141] identified potent insect-specific neurotoxic peptides and mammalian-specific peptides (5000 and 9000 daltons) that were lethal to mice at high dosage. Experimental envenomation of rabbits by live male spiders has resulted in extensive cutaneous injury and clear evidence of systemic poisoning. Local erythema appeared and faded within the first day; discolored patches were visible by day 4 and sloughed by day 6. Autopsy revealed petechial hemorrhages on the surfaces of the lungs, liver, and kidneys.[285] Since the early 1980s medically significant bites in the Pacific Northwest have been attributed to T. agrestis.[2] [286] [288] [289] In Europe, no medical problems have been associated with bites from these spiders. [32] [42] [57] Venom chemistry of American spiders is not different from venoms of English spiders, so the cause of the alleged difference in medical significance is currently under investigation.[35] Bites of males from the Pacific Northwest have more severe necrotic effects on mammalian tissues than bites from females.[285] Necrotic lesions have been attributed to this species all during the year, with a trend toward increased severity in the winter months.[289]
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Figure 34-16 Agelenopsis aperta. (Courtesy Eileen Hebets.) CLINICAL PRESENTATION.
T. agrestis has been implicated in several cases of necrotic arachnidism similar to that seen in Loxosceles envenomation. Systemic effects reported include headache, visual disturbances, hallucinations, weakness, and lethargy. Hemorrhagic complications have been reported in experimental animals. In general, direct observations are scarce of T. agrestis biting people, who then develop necrotic lesions.[2] According to Vest,[285] [289] who studied 22 cases of "highly probable" T. agrestis envenomation, the local lesion followed a pattern reminiscent of loxoscelism. The initial lesion appeared as a small reddened induration, often surrounded by a large zone of erythema. Vesicles occurred within 36 hours, then burst; marked necrosis developed in 50% of cases. The most common symptoms included headache, weakness, and lethargy.[287] TREATMENT.
No studies have investigated treatment for envenomation by Tegenaria species. As with mild cases of loxoscelism, patients should be treated supportively, with tetanus prophylaxis, careful wound debridement as needed, and observation. Genus Agelenopsis: Grass Spiders and Funnel-Web Spiders BIOLOGY.
Agelenopsis aperta is common in and restricted to the deserts of the southwestern United States, ranging from California to East Texas ( Figure 34-16 ). They build large, conspicuous sheet webs, with retreats under rocks and logs or in tufts of grass. Adults are 13 mm in body length. VENOM.
The venom of this species is among the best known of all spiders in terms of biochemical composition and neurophysiologic activity of the individual components. Its clinical relevance in humans, however, has only recently been recognized. Nineteen toxins have been characterized in A. aperta venom, with three distinct classes that act synergistically to subdue insect prey rapidly and irreversibly.[202] The µ-agatoxins modify sodium channel kinetics, increasing neurotransmitter release generally; the ?-agatoxins block presynaptic, voltage-sensitive calcium channels; and the a-agatoxins are a family of low-molecular-weight acylpolyamines that block glutamate-sensitive receptor channels in insect muscle. The coexistence of toxins with different mechanisms of neurotoxicity appears to confer a synergistic action to the overall venom effect in insect prey. The ?-agatoxins range in target specificity from invertebrates to mammals.[284] CLINICAL PRESENTATION.
Two cases of envenomation by A. aperta have been reported in southern California. A 9-year-old boy developed a tender but nonnecrotic bite site, followed by a 2-day systemic syndrome that included headache, nausea, disorientation, pallor, and unsteady gait. A 54-year-old man developed a painful, indurated lesion that persisted for a week; he had no systemic symptoms. [290] TREATMENT.
Treatment of Agelenopsis envenomation is symptomatic and supportive. Family Theridiidae: Comb-Footed Spiders The family Theridiidae, sometimes called cobweb or comb-footed spiders, is speciose, diverse, and distributed worldwide. The spiders are small to medium sized (1 to 14 mm, usually less than 8 mm) and often have globose abdomens. They make irregular, tangly webs in which the spider hangs upside down. The silk is very sticky, easily entangling prey. Spiders throw silk over ensnared prey using a tiny comb at the end of the fourth leg. They then envenom prey and suck them dry through a small hole in the exoskeleton, since they have no cheliceral teeth for chewing. Genus Latrodectus: Widow Spiders BIOLOGY.
Latrodectus (Latin for "robber-biter") species are among the largest theridiids. Females are 12 to 16 mm in body length. Males are much smaller, with longer legs relative to their body size. Individuals build typical theridiid cobwebs with very strong strands of silk. Arthropods are the most common prey, but widows also kill and consume vertebrates (e.g., small lizards and snakes). The folkloric belief that widow females kill and consume their mates does happen, although not as a rule. The 8- to 10-mm female black widow is shiny black with a characteristic red hourglass marking on the ventral abdomen. Species are distinguished based on hourglass shape and dorsal color patterns. Males are lighter in color, with white and gray markings and a faint
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Figure 34-17 Adult female Latrodectus mactans with fresh egg case. (Courtesy Michael Cardwell & Associates, 1999.)
Figure 34-18 Mature female brown widow spider (Latrodectus geometricus). (Courtesy Michael Cardwell & Associates, 1999.)
hourglass. This feature becomes more prominent with maturity. The female spins an irregular web in sheltered corners of fields, gardens, and vineyards and under stones, logs, and vegetation. Uncommon in occupied dwellings, the spiders may be plentiful in barns, garages, trash heaps, and outbuildings. A few Latrodectus species (e.g., L. variolus) are arboreal. The web's tattered "cobweb" appearance may belie an ongoing state of occupation, particularly during the daytime, when the spider is out of sight. The female seldom ventures far from the web, in which she suspends an ovoid or tear-shaped, whitish egg case. Latrodectus spiders are worldwide in distribution, most plentiful in temperate and subtropical regions, and most abundant during summer.[32] Latrodectus mactans mactans, the black widow, is cosmopolitan and occurs in every state except Alaska ( Figure 34-17 ). In North America, species include L. geometricus (the brown widow, Figure 34-18 ), L. bishopi (the red-legged
Figure 34-19 Mature female western black widow (Latrodectus hesperus). (Courtesy Michael Cardwell & Associates, 1993.)
Figure 34-20 Red-backed spider (Latrodectus mactans hasselti). (Courtesy Sherman Minton, MD.)
widow), L. variolus, and L. hesperus ( Figure 34-19 ). Species known to envenom humans are endemic to Australia (L. m. hasselti, Figure 34-20 ) and to Europe and South America (L. tredecimguttatus). Related species are found in Asia and the Middle East (L. pallidus) and in Africa (L. indistinctus). The species L. tredecimguttatus is most important in the Mediterranean region, the Middle East, and parts of Russia, where it is sometimes referred to as L. lugubris. It may have red or orange spots or may be pure black and is known as kara kurt (Russian for black wolf). L. indistinctus, the black button spider of South Africa, has a narrow or broken red dorsal band or may be black. The red-backed spider (L. m. hasselti) is medically important in Australia, New Zealand, and southern Asia. It has a dorsal red band similar to that of L. indistinctus, and the female also has a ventral red hourglass reminiscent of L. m. mactans. L. geometricus is brown with black, red, and yellow markings and is
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common in southern Africa and warmer parts of the Americas. Widow spiders tend to bite defensively when accidentally crushed. In the Mediterranean basin, southern Russia, and South Africa, bites are associated with grain harvesting and threshing and with grape picking. In the United States, most bites occur in rural and suburban areas of southern and western states, with no special age, gender, or occupational predilection. In regions where outdoor privies are in common use, human envenomations are likely to involve the buttocks or genital area.[34] [107] [180] [307] Outbreaks of latrodectism may occur locally in epidemic fashion, lasting several years, and depend on changes in spider predator and parasite balance and on occupational variations in human-spider contact. Apparent outbreaks may also result from sudden increases in publicity and reporting.[31] [143] VENOM.
Unlike many other arthropod venoms, that of the widow spiders appears to lack locally active toxins capable of provoking inflammation. The venom contains several toxic components, including a potent mammalian neurotoxin, a-latrotoxin, which induces neurotransmitter release from nerve terminals. In 1964, Frontali and Grasso[93] demonstrated three electrophoretically and toxicologically distinct fractions of Latrodectus venom. In 1976, Frontali and associates [94] further purified and defined these fractions, encountering one major constituent (the B5 fraction, later renamed a-latrotoxin) with significant toxicity in mice and frogs (other fractions have effects more specific to insect physiology). Alpha-latrotoxin, a protein mix with an average molecular weight of 130,000, caused profound depletion of presynaptic vesicles with swelling of the presynaptic terminal at frog neuromuscular junctions; complete blockade of neuromuscular transmission followed within 1 hour. The toxin binds irreversibly with the lipid bilayer of the cell membrane, producing cation-selective channels and interfering with endocytosis of vesicle membranes.[51] [88] The mechanism of action is not fully understood, but multivalent cations, including calcium, may enter the presynaptic nerve terminal through these channels, interfering with calcium-dependent intracellular processes. [113] [185] These effects appear to be specific to presynaptic nerves but independent of the transmitter involved. Acetylcholine, noradrenaline, dopamine, glutamate, and enkephalin systems are all susceptible to the toxin.[229] Grishin[120] has described the venom of L. tredecimguttatus, which has a family of seven protein toxins of high molecular weight. These all cause massive neurotransmitter release from presynaptic endings. They differ from each other in the specificity of the target animal. Alpha-latrotoxin acts selectively on vertebrate nerve endings; five latroinsectotoxins act on insects, and one toxin is specific for crustaceans. These large molecules have several functional domains responsible for ionophoric and secretogenic actions. Amino acid sequence analysis of precursor toxins reveals high levels of sequence identity between the different latrotoxins. It also reveals a series of ankyrin-like repeats that might be the structural basis of the interactions between the toxins and the membranes.[120] L. indistinctus and L. geometricus also contain a-latrotoxin, the former with a greater venom yield per spider.[189] CLINICAL PRESENTATION.
Latrodectism, the syndrome often resulting from Latrodectus envenomation, is best known for widespread, sustained muscle spasm rather than for local tissue injury. Although long-term outcomes are usually excellent, victims may have significant hypertension, autonomic and central nervous system dysfunction, and abdominal pain severe enough to be mistaken for acute abdomen. The initial bite may be sharply painful, but many bites are not recognized initially, so diagnosis is often presumptive and based on local and systemic signs. Local reaction is typically trivial, with only a tiny papule or punctum visible on examination. The surrounding skin may be slightly erythematous and indurated. In most cases, symptoms do not progress beyond this point. In one Australian series, 76% of victims presenting to a hospital for care had local symptoms only.[140] In some cases, however, neuromuscular symptoms can become dramatic within 30 to 60 minutes as involuntary spasm and rigidity affect the large muscle groups of the abdomen, limbs, and lower back. Rhabdomyolysis has rarely been reported. [97] A predominantly abdominal presentation may closely mimic an acute abdomen. Associated signs include fasciculations, weakness, ptosis, priapism, thready pulse, fever, salivation, diaphoresis, vomiting, and bronchorrhea. Pulmonary edema has been described in Europe[183] and South Africa.[153] [291] Respiratory muscle weakness combined with pain may lead to respiratory arrest. Hypertension with or without seizures may complicate management in elderly or previously hypertensive individuals. Isolated (normotensive) seizures do not appear to be a feature of latrodectism. Intractable crying may be the predominant feature in neonates. [45] Pregnancy may be complicated by uterine contractions and premature delivery.[20] [133] [182] [231] [237] A characteristic pattern of facial swelling, known as Latrodectus facies, may occur hours after the bite and is sometimes mistaken for an allergy to drugs used in treatment. The usual course of an envenomation is to achieve complete recovery after a few days, although pain may last a week or more. The clinical picture of Latrodectus poisoning is similar around the world. In the 1980s in California the most common site of envenomation referred to a toxicology
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service was the lower extremity (48%), followed by upper extremity (28%), trunk (18%), and head or neck (5%). The most common systemic symptom was abdominal or back pain (58%), followed by extremity pain (38%), hypertension (29%), and diaphoresis (22%). [56] In Australia a 1961 survey showed 37% of victims were bitten on the upper extremities, 27% on the lower extremity, 22% on the buttock or penis, 17% on the trunk, and 4% on the head or neck.[304] A 1978 report showed a decline in incidence of genital and buttock involvement (9.7%), perhaps related to a decrease in the use of outdoor lavatories.[275] Australian envenomations showed a similar pattern of pain and diaphoresis, with more prominent local inflammation and lymphadenopathy and less hypertension than reported in the United States. In South Africa, envenomation by L. geometricus results primarily in local pain, whereas L. indistinctus provokes a syndrome of generalized pain, diaphoresis, and muscle rigidity similar to that seen in the United States.[188] Victims bitten by L. tredecimguttatus may have spasm of facial muscles, swollen eyelids, lacrimation, and photophobia, more often resulting in recognized Latrodectus facies. A rash may appear 2 to 11 days after envenomation.[179] TREATMENT.
Although the worst pain usually occurs during the first 8 to 12 hours after a bite, symptoms may remain severe for several days. All symptomatic children, pregnant women, and patients with a history of hypertension should be admitted to the hospital. Discharge is usually possible within 1 to 3 days, when hypertension and muscle spasm have subsided. A patient with a satisfactory response to antivenom may be sent home after several hours' observation. Care of the local site includes routine cleansing, intermittent application of ice, and tetanus prophylaxis. Severe pain and muscle spasm usually respond to IV narcotics or benzodiazepines. Careful observation of respiratory status is vital when either or both of these are used. Calcium gluconate infusion, advocated in the past, has proved only minimally useful and is no longer recommended. Hypertension may be treated with an infusion of sodium nitroprusside or nifedipine if the patient does not respond to pain control with narcotics or antivenom. Antivenom active against Latrodectus venom is available in the United States from Merck and Co.; in Australia from Commonwealth Serum Laboratories; and in South Africa from the South African Institute of Medical Research. Standards for Latrodectus antivenom use vary around the world, as do guidelines for its administration.[56] [188] [271] In general, antivenom should be used in cases involving respiratory arrest, seizures, uncontrolled hypertension, or pregnancy.[238] In less severe settings, its value must be weighed against the risks of acute hypersensitivity and delayed serum sickness. In Australia, 0.5% to 1% of cases result in anaphylaxis, and some patients develop serum sickness.[275] Death from anaphylaxis has been reported in the United States.[56] The usual therapeutic antivenom dose is one to three vials or ampules. Efficacy of antivenom is reported as satisfactory in 94% of patients in Australia,[298] with anecdotal reports of efficacy even weeks to months after envenomation.[19] Laboratory evaluation may include complete blood cell count, electrolytes, blood glucose, and urinalysis. Common findings include leukocytosis and albuminuria. In victims with severe muscle spasm, creatine phosphokinase levels may be elevated. Abdominal films and stool examination for occult blood, both of which should be normal after widow spider envenomation, may help with the differential diagnosis of abdominal pain. A pregnancy test should be done if indicated. No specific antigen or antibody detection technique is currently available for clinical diagnosis. Genus Steatoda: False Black Widow Spiders BIOLOGY.
Steatoda species are found worldwide. They are 3 to 8 mm in body length, smaller than Lactrodectus, and typically are dark brown, often with white markings on the
abdomen. They build tangly cobwebs and sit in crevices under stones, in tree bark, or in cracks of buildings near the web. Steatoda paykulliana of Europe, S. foravae of southern Africa, and S. grossa of the United States bear an external resemblance to members of the Latrodectus genus and therefore are referred to as false widow or button spiders. VENOM.
The crude venom of S. foravae contains a major polypeptide of the same molecular weight as a-latrotoxin and can elicit a comparable neurotransmitter release syndrome in mice. The median lethal dose, however, is significantly higher, and the relative potency in mice is 10 to 20 times less than for L. indistinctus.[190] CLINICAL PRESENTATION.
In humans, S. nobilis of southern England has caused brief local pain and slight swelling, followed by local sweating and piloerection, facial flushing, and feverishness.[294] One report of S. foravae bite in southern Africa showed minimal local inflammatory response without systemic toxicity.[190] In one Australian report a 2-year-old child bitten by a juvenile Steatoda (species unknown) developed lethargy, irritability, diaphoresis, and hypertension 22 hours after the bite. He improved gradually after administration of two ampules of red-backed spider (Latrodectus) antivenom.[255] TREATMENT.
In general, care is symptomatic and supportive. Similarities between the neurotoxins in
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Figure 34-21 Orb weaver (Argiope species). (Courtesy Eileen Hebets.)
Steatoda and Latrodectus venoms, however, suggest the use of Latrodectus antivenom in severely symptomatic cases. Family Araneidae: Orb-Weaving Spiders Members of the family Araneidae are familiar to most people because they are common and build conspicuous, mainly circular, two-dimensional orb webs in open places. This is an abundant family, with 4000 species described and distributed worldwide. Species range in adult body size from 2 to 28 mm and often have extreme size dimorphism, with males much smaller than females. They are extremely diverse in size, shape, web design, and prey capture tactics. They can be brightly colored, with typically ovoid abdomens and large chelicerae with several teeth. Although diverse and abundant, they are of minimal clinical concern. The venoms of many araneid spiders are known to have polyamine neurotoxins that postsynaptically block glutamate receptors in vertebrates.[144] These are currently known from species of Nephila, Argiope, Araneus, and Neoscona. Genus Argiope: Argiopes BIOLOGY.
Argiope aurantia, known as the golden orb weaver or black and yellow garden spider, is common in California, Oregon, and the eastern United States ( Figure 34-21 ). Other Argiope species are found throughout the United States, the Orient, and Australia.[104] It is a large, brightly colored spider with a large, symmetric orb web and a leg spread of up to 7.5 cm. VENOM.
Although Argiope venom appears to be cytotoxic in vivo, research indicates the venom has neurotoxic effects in vitro. Venom gland extracts from Argiope trifasciata are postsynaptic blockers of neuromuscular transmission at locust glutamate receptors. [282] CLINICAL PRESENTATION.
Bites may cause local pain and erythema. Bites by Argiope argentata reportedly cause local pain, erythema, and vesicle formation, which resolve within 24 hours except for the bite marks.[110] [309] TREATMENT.
Treatment is symptomatic and supportive.
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Chapter 35 - Scorpion Envenomation Jeffrey R. Suchard David A. Connor
INTRODUCTION Scorpion envenomation can result in distinct clinical syndromes. Most scorpion species' stings cause only local pain and inflammation that respond well to minimal supportive therapy and wound care. These scorpions pose no significant management issues and, with few exceptions, are not discussed here in further detail. The truly dangerous scorpions of the world, typified by Tityus species in the Caribbean region and in South America, Androctonus species and Buthus occitanus in North Africa, Leiurus quinquestriatus in the Near East, and Mesobuthus tamulus in India, cause an "autonomic storm" with prominent cardiopulmonary effects. A third clinical syndrome occurs from stings of Centruroides species in the southwestern United States and Mexico and from Parabuthus species in southern Africa. These produce prominent neurologic effects associated with excess cholinergic tone. Children are typically more severely affected than adults and often require prompt medical management to avoid morbidity and mortality. The ideal treatment of scorpion envenomation remains controversial, primarily because controlled clinical trials are lacking. Although anecdotal experience and comparisons of historic cohorts demonstrate a benefit from aggressive symptomatic and supportive care, the proper use of antivenins has not been fully resolved.
TAXONOMY AND ANATOMY Scorpions are grouped in the phylum Arthropoda ( Figure 35-1 ). Scorpions have a crablike or lobsterlike body shape with seven sets of paired appendages ( Figure 35-2 ): the chelicerae, the pedipalps (claws), four sets of legs, and the pectines (a pair of comblike structures on the ventral surface). The segmented tail curves upward dorsally, ending in a terminal bulbous segment called the telson, which contains paired venom glands and the stinger ( Figure 35-3 ). The presence and size of a subaculear tooth, a small tubercle near the base of the stinger, vary among species and stage of maturity. In the United States, a subaculear tooth on a small, slender scorpion usually indicates Centruroides exilicauda (C. sculpturatus) ( Figure 35-4 ).[40] [129] Many scorpion specimens reveal a broken stinger that does not penetrate human skin well.[132] Scorpions grasp prey in their pedipalps and then rapidly thrust the tail overhead to sting. The chelicerae tear the food apart. Scorpions feed primarily on ground-dwelling arthropods and small lizards. The scorpion consumes only the juices and liquefied tissues of its prey, discarding the solid parts. Scorpions envenom by stinging; although stings may be reported as bites,[12] [45] [124] true scorpion bites have not been documented and would be inconsequential if they did occur. A characteristic physical property of scorpions is that they fluoresce when illuminated by ultraviolet light, as from a "black light" or a medical Wood's lamp ( Figure 35-5 ). This property is used in collecting scorpions for breeding or venom harvesting and in providing pest control. The fluorescent pigment in scorpion cuticle is probably riboflavin.[97] Scorpions can sting multiple times; however, it appears that the first sting depletes or nearly depletes the telson of venom. A case series of three pairs of scorpion sting victims from India found that consecutive stings by Mesobuthus tamulus caused severe cardiovascular manifestations in the first victim but not in the second.[14] We have observed a similar difference in the severity of neurologic manifestations from consecutive Centruroides exilicauda stings in Arizona.
GEOGRAPHIC DISTRIBUTION Scorpions are widely distributed in regions within 50 degrees north and 50 degrees south of the equator[85] and are found on all continents[116] except Antarctica. Scorpions are characteristic of desert areas, semiarid grasslands, and the tropics but may also be found in temperate and subtropical regions.[73] [85] [97] [116] An estimated 5000 deaths from scorpion stings occur annually worldwide,[62] making scorpions second only to snakes as sources of fatal envenomation.[148] Estimates vary regarding the number of scorpion species. In 1985, Herschkovich et al[84] reported the existence of 500 scorpion species divided into six families. Russell[129] reported 500 to 800 species, others reported 650,[28] [36] [150] and Neale [116] estimated at least 700 species. More recent reports estimate 1000 species,[62] [132] and in 1998, Hutt and Houghton[85] reported 1400 scorpion species divided into nine families ( Figure 35-6 ). The Buthidae is the largest and the most dangerous family and, with few exceptions, contains the only species capable
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Figure 35-1 Organization of the phylum Arthropoda, showing the relationship of scorpions to spiders and more distantly related insects.
of producing clinically significant envenomations, through their neurotoxic venoms. [73] [85] [132] At least 30 species can inflict potentially fatal stings.[62] All genera commonly recognized as dangerous are buthid scorpions: Centruroides and Tityus in the Western Hemisphere, and Androctonus, Buthus, Mesobuthus, Leiurus, and Parabuthus in the Eastern Hemisphere.
VENOM Scorpion venoms are complex mixtures containing mucopolysaccharides, hyaluronidase, phospholipase, acetylcholinesterase, serotonin, histamine, protease inhibitors, histamine releasers, and neurotoxins.[41] [132] Neurotoxins are pharmacologically the most important venom constituents.[132] Centruroides exilicauda venom glands contain two types of columnar cells, one secreting mucus and another producing neurotoxins. This species' venom has no enzyme that causes tissue destruction, however, so local effects are minimal or absent.[40] The neurotoxins are single-chain, basic polypeptides of 60 to 70 amino acids, reticulated by four disulfide bridges. Each scorpion species' venom contains several neurotoxins, but they all share a similar structure and homologous sequences.[68] [132] In neuronal membranes, these toxins cause two effects with regard to fast sodium channels involved in action potential transmission: (1) incomplete inactivation of sodium channels during depolarization, resulting in a widening of the action potential, and (2) a slowly developing, inward sodium current after repolarization, leading to membrane hyperexcitability. The net result is repetitive firing of axons,[40] enhancing release of neurotransmitters (acetylcholine, norepinephrine, dopamine, glutamate, aspartate, ?-aminobutyric acid [GABA]) at synapses and at neuromuscular junctions.[53] [59] [128] [146] This is clinically demonstrated as excessive neuromuscular activity and autonomic dysfunction. Some scorpion
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Figure 35-2 Anatomy of a scorpion. (Redrawn from Keegan HL: Scorpions of medical importance, Oxford, Miss, 1980, University Press of Mississippi).
Figure 35-3 Electron micrograph of scorpion telson. B and C, Close-up images demonstrating stinger with paired venom pores.
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Figure 35-4 Centruroides exilicauda (C. sculpturatus), the bark scorpion of Arizona.
Figure 35-5 Scorpions fluoresce in ultraviolet light.
neurotoxins also have effects on calcium-activated potassium channels,[63] [127] chloride channels,[44] and L-type calcium channels.[9]
REGIONAL EPIDEMIOLOGY India Between 86 and 99 scorpion species, with at least 45 buthid species, are found in India. Only one species is regarded as dangerous: Mesobuthus tamulus, formerly known as Buthus tamulus, called the red scorpion.[43] [111] Heterometrus (formerly Palamnaeus) gravimanus, the black scorpion, is a larger species that does not cause systemic toxicity.[15] [148] Heterometrus bengalensis is common in eastern India. [94] M. tamulus is a particular problem in southern coastal India. Stings predominantly occur in April, May, and June at night among young farmers wearing minimal clothing.[15] [22] In many cases, stings occur at the tip of an extremity, with the only symptom being pain, which can be controlled with local anesthetic injections.[22] [42] Systemic toxicity occurs from release of catecholamines, with major morbidity and mortality resulting from cardiopulmonary toxicity.* The 30% fatality rates reported in the 1960s and 1970s are now 2% to 3% with treatment using vasodilators and calcium channel blockers.[17] [19] An 11.8% mortality rate, however, was found among 152 children admitted in Calcutta from 1985 to 1989, although treatment details were not reported.[28] Mesobuthus tamulus antivenin is produced for research purposes only. It is not commercially available and would not likely be available in the predominantly rural environment where most stings occur. Bawaskar and Bawaskar[13] [14] [15] [16] [17] [18] [19] [20] [21] [22] have developed treatment protocols recognizing the limited medical resources available for the majority of victims, including the potential risks of transporting unstable patients. They recommend oral prazosin and nifedipine for victims with adrenergic toxicity and intravenous (IV) nitroprusside for severe pulmonary edema. Iran Radmanesh[121] [122] has reported on scorpion envenomation in Khuzestan, a hot and humid province in southwest Iran. A specialized scorpion sting department was established in the provincial capital to study and treat this public health concern, since fatalities occur, especially among children in rural areas during the hot seasons. Over 6 months, 3217 patients were referred to the scorpion sting department, with 200 admitted and the remainder treated as outpatients. Three scorpion species were responsible for almost all cases: Androctonus crassicauda (41%) and Mesobuthus eupeus (45%) of the Buthidae and Hemiscorpion lepturus (13%) of the Scorpionidae.[121] Systemic envenomations by A. crassicauda, the Khuzestan black scorpion, resulted in prominent cholinergic signs, such as exocrine gland hypersecretion, urinary frequency and incontinence, and increased gastrointestinal (GI) motility. Adrenergic effects also occurred with lesser frequencies. Neurologic toxicity manifested as delirium, confusion, coma, restlessness, convulsions, localized muscle spasm near the sting site, opisthotonus, and paralysis. A polyvalent scorpion antivenin was ineffective in this series of A. crassicauda envenomations. [121] Hemiscorpion lepturus was responsible for 10% to 15% of stings during the hot season but caused almost all reported stings during winter. This scorpion has a cytotoxic venom, unlike the buthid neurotoxins. Most victims develop a 3- to 4-mm dark-blue macule surrounded by a 1- to 2-cm red halo within the first hour. The skin lesion may enlarge, become indurated and inflamed, and eventually necrose and slough. Serious skin lesions are associated with hemolysis and renal failure. Central nervous system (CNS) and cardiovascular *References [ 13]
[ 15] [ 19] [ 22] [ 28] [ 42]
.
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Figure 35-6 Families of the Scorpionida order. Buthidae family contributes the largest number of medically significant genera, as indicated by bold type.
844
Figure 35-7 Leiurus quinquestriatus, the yellow scorpion of North Africa and the Middle East. (Courtesy R. David Gaban.)
toxicity may be seen in severely envenomed patients. Ankylosis of the joints and psychologic sequelae have also been reported. Local authorities recommend surgical intervention for skin lesions, including prophylactic excision of the sting site, as well as supportive care for hemolysis and renal failure, No antivenin is available. [122] Fatal H. lepturus envenomation associated with renal failure has also been reported in Pakistan.[115] No prospective or controlled trials of excisional therapy for H. lepturus envenomation have been published, and routine or prophylactic surgical intervention is not recommended for envenomation by other scorpion species. Israel Leiurus quinquestriatus, known as the five-keeled gold scorpion or the yellow scorpion, is the most dangerous species found in Israel[31] [55] [84] [127] ( Figure 35-7 ). Other native species include Buthotus judaicus (the black scorpion), Androctonus crassicauda, A. bicolor, Nebo hierochonticus, Scorpio maurus, and Orthochirus innesi. [30] [31] [55] [138] More than 90% of all scorpions encountered in neighboring Jordan are either yellow or black scorpions (L. quinquestriatus or B. judaicus),[55] with the yellow being most common.[84] In the Negev desert, 95% of cases occur during the warmer months of April through October. Bedouin children are stung about 6 times more frequently than Jewish children, probably because of more time outdoors and lack of protective footwear. Males are affected 2.3 times more often than females, related to differences in gender roles, such as boys herding sheep or goats.[84] The reported mortality rate in children was 18% among Palestinians living on the West Bank in 1965, 3.7% among children in the Jerusalem area in 1991,[55] and 1.2% among children in the Negev area in 1985.[84] The L. quinquestriatus sting initially produces intense local pain, erythema, and edema, which can be followed by an outpouring of catecholamines and acetylcholine from nerve endings. Clinical signs of sympathetic overload predominate, with severe hypertension, tachyarrhythmias, and pulmonary edema. [1] [73] [74] [81] [123] Parasympathomimetic action of the venom may also cause bradyarrhythmias or atrioventricular block, usually preceding the sympathetic overload. Cardiomyopathy and myocardial damage with electrocardiographic (ECG) and serum marker (creatine kinase [CK], CK-MB, troponin) changes have been reported.[55] [73] [131] [136] Other common findings from severe stings include agitation, convulsions, encephalopathy, hypersalivation, diaphoresis, priapism, and pancreatitis.[2] [133] [134] Treatment recommendations differ, but all emphasize aggressive symptomatic and supportive care for severely envenomed patients. However, some authors propose the routine use of antivenin,[55] whereas others argue that serotherapy does not significantly alter outcome based on experimental pharmacokinetic data. [73] [74] [75] [81] Antivenin also had no demonstrable effect in one clinical series of Israeli patients.[135] Saudi Arabia At least 14 species of scorpions are found in Saudi Arabia; the two most common are Androctonus crassicauda, a black or dark-brown scorpion, and Leiurus quinquestriatus, a yellow scorpion associated with more stings.[7] [57] [90] [99] [116] Scorpion envenomation is responsible for 3% to 4% of all pediatric hospital admissions in northwestern Saudi Arabia from May to August, with few admitted in other seasons.[56] [57] The incidence of "scorpion sting syndrome" is 1.3 cases per 1000 emergency department patients; 76% of cases occurred between May and October, and 73% of stings occurred at night between 6 PM and 6 AM.[116] Many victims are children
playing barefooted outdoors or persons tending flocks of goats or sheep. Males are affected at least twice as often as females.[7] [56] [116] Mortality rates range from 2% to 5%.[7] [56] Antivenin is recommended and routinely administered for scorpion envenomation in Saudi Arabia.[7] [56] [57] [90] L. quinquestriatus envenomations are reviewed earlier. A. crassicauda stings are similar to those of the yellow scorpion, causing hypertension and CNS manifestations, but differ in other ways.[90] The pain from A. crassicauda sting has been reported as particularly severe. Generalized erythema was noted in 20% to 25% of children less than 5 years of age; this is not usually seen with other scorpion stings. The cause of this erythema is not clear, especially since elevated catecholamine levels after scorpion envenomation appear to be protective against allergic reaction. Cholinergic effects are seen less often with A. crassicauda stings. Scorpion envenomation became an issue to U.S. soldiers deployed during the Gulf War.[70] L. quinquestriatus and A. crassicauda were implicated in 57 scorpion
845
Figure 35-8 Androctonus australis, responsible for most severe scorpion envenomations in North Africa. (Courtesy R. David Gaban.)
stings over 4 months among 7000 troops of an armored cavalry division stationed in eastern Saudi Arabia. All patients with adequate data for further study recovered fully, usually with only supportive care in the field, probably reflecting that all were healthy adults. No antivenin was available. Typical signs and symptoms included local pain, tachycardia, hypertension, sweating, apprehension, headache, epigastric pain, nausea, restlessness, and local muscle cramping and paresthesias in lower extremity stings. Presumably, victims with only local pain failed to present to battalion aid stations, resulting in an apparently high incidence of systemic effects. Only two persons had significant presentations or subsequent complications. One victim had a clinical picture consistent with anaphylaxis and required intubation for respiratory support. The other victim developed a cutaneous ulcer that healed in 3 weeks with oral antibiotic therapy.[70] North Africa Scorpions are a common problem throughout North Africa. Hundreds of scorpion sting deaths occur annually in Algeria.[101] Libya reported 900 stings with seven fatalities per 100,000 population in 1979. [85] Most of the published North African scorpion research is from Tunisia, where 10 scorpion species are found, five of which are responsible for almost all stings.[69] Most stings are caused by Androctonus australis garzonii, Androctonus aeneas aeneas, and Buthus occitanus tunetanus. A. australis, known as the yellow scorpion, accounts for most severe envenomations ( Figure 35-8 ). A. aeneas is a dangerous black scorpion found only in the southern part of Tunisia. The next most common species are Scorpio maurus tunetanus and Euscorpius carpathicus sicanus, another black scorpion found only in the north; both are relatively harmless and have thin tails and thick claws. The more dangerous Tunisian scorpions
Figure 35-9 Androctonus amoreuxi, demonstrating the thin claws and thick tail characteristic of dangerous scorpion species. (Courtesy R. David Gaban.)
have long, thin claws and a thick tail[69] [96] ( Figure 35-9 ). Stings occur most often outdoors (92%) on the victim's extremities (95%) during the summer months. Eighty percent of all reported stings occur from July to September, with half of these in August.[69]
[96]
Between 30,000 and 45,000 scorpion stings are reported annually, correlating to an incidence of 4.5 to 20 stings per thousand inhabitants, depending on the location. About 2.5% of stings (900 to 1100 per year) result in systemic manifestations requiring hospital admission. The mortality rate ranges from 0.25% to 0.4%, which is about 10% of victims with systemic envenomations, or 35 to 105 deaths per year.[3] [69] [96] [97] [98] Two thirds of reported stings affect adults and older adolescents, but nearly all fatalities occur in younger children; the mortality rate for children is about 1%. [69] [96] The effects of Tunisian scorpion stings have been classified into four stages[69] and three grades[98] based on clinical severity. The first three stages or grades are essentially identical, and the fourth stage is the most severe form of grade III envenomation. The stages or grades do not necessarily reflect the natural time course of envenomation and are designated to aid risk evaluation and to direct treatment. Grade I envenomations have only local symptoms at the sting site. The most common complaint is intense burning pain. Paresthesias occur in 92% of victims. Mild systemic symptoms, such as irritability and restlessness, occur in 8% to 12% of victims. Local tissue alterations are rare. Grade I cases constitute 90% to 95% of all scorpion stings, and symptoms typically resolve in 3 to 8 hours. Grade II envenomations have local symptoms as in grade I, sometimes with local edema, associated with moderate systemic symptoms. Irritability (52%), restlessness (48%), tachycardia (34%), and moderate hyperthermia (27%) are characteristic features. Signs of excess cholinergic tone (e.g., diaphoresis, hypersalivation,
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Figure 35-10 Parabuthus transvaalicus, a dangerous scorpion of southern Africa. (Courtesy R. David Gaban.)
rhinorrhea, vomiting, diarrhea) are often found, as well as occasional dyspnea, gastric distention, and priapism. From 5% to 10% of stings present with grade II symptoms. The prognosis is favorable with return to baseline in 3 days, although 1% to 3% of patients initially classified as grade II progress to grade III. Grade III envenomations involve serious systemic complications, including cardiocirculatory shock, respiratory failure, pulmonary edema, hyperthermia, seizures, priapism, and coma. If the grading system is divided into four stages, the stage III victims have depressed level of consciousness, arterial hypertension, and tachycardia, usually occurring within 2 to 4 hours after the sting. ECG changes consistent with ischemia, respiratory failure, hyperglycemia, and an elevated white blood cell count are also seen. Stage IV signifies worsening neurotoxicity, heralded by profuse vomiting and associated with cardiovascular collapse, pulmonary edema, hyperthermia, seizures, and coma. Even patients with stage III envenomations have a favorable prognosis with appropriate care. Patients who recover will regain consciousness in several hours, and the ECG abnormalities will resolve in 2 to 4 days. All fatalities progress through stage IV, although recovery from stage IV can occur.[69] South Africa The majority of scorpion stings in South Africa, Zimbabwe, and neighboring countries do not cause systemic effects, although fatalities occasionally occur.[25] [26] [100] Scorpions found in southern Africa include the frequently dangerous Buthidae with thin pincers and thick tails ( Figure 35-10 ) and the relatively harmless Scorpionidae, Bothriuridae, and Ischnuridae with thick pincers and thin tails[26] [100] [110] ( Figure 35-11 ). Parabuthus species cause neuromuscular toxicity without the autonomic storm seen from the dangerous scorpions of northern Africa, the Mideast, and India.[25] [26] [110] At
Figure 35-11 Hadogenes troglodytes, an impressive-looking yet relatively harmless scorpion of southern Africa, has large claws and a thin tail. (Courtesy R. David Gaban.)
least 20 Parabuthus species are distributed throughout South Africa, Namibia, Botswana, Zimbabwe, and southern Mozambique.[110] Three other species can produce systemic effects but are not considered potentially fatal: Parabuthus mossambicensis, Uroleptes planimanus, and Opistophthalmus glabrifrons.[24] [25] Certain Parabuthus scorpions with large venom vesicles are capable of spraying venom when alarmed.[110] Stings typically occur in the early evening during the warmer months of October through April, with peak incidence in January and February.[25] [26] [110] Four children died in a series of 42 serious scorpion envenomations from South Africa. [110] No fatalities were noted among 244 patients (17 with severe systemic symptoms) in Zimbabwe.[26] In another study, however, five deaths occurred among 455 patients, with the fatalities in children less than 10 years old or adults over 55.[25] The overall case fatality rate from Parabuthus species ranges from 0.3% to 3%. [25] [26] Serious scorpion envenomation in southern Africa closely resembles that seen in the American Southwest from Centruroides exilicauda. [25] [26] [110] Immediate pain, local paresthesias, and hyperesthesia typically occur. Mild cases (60% of stings) are associated with only localized symptoms, moderate cases with three or fewer systemic features, and severe cases (10% to 30%) with more than three systemic signs or symptoms. The pain and paresthesias may generalize, sometimes within minutes in children and usually within 4 to 12 hours in adults. Of victims with severe envenomations, 75% have difficulty swallowing, myoclonic jerks, tongue fasciculations, hypersalivation, and profuse sweating; 50% have bilateral ptosis, slight local swelling, and difficulty urinating (33% with a palpably distended bladder). Children are typically affected more severely and are more likely to exhibit uncontrollable jerking, writhing, and thrashing movements characteristic of neurotoxic scorpion
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envenomation. Respiratory failure is the most common proximate cause of death. In untreated cases, urinary retention, ptosis, and sweating resolve in 2 days and dysphagia and hypersalivation in 4 days. After 1 week, 10% of victims still have muscle tremors and tongue fasciculations, and more than half still have localized pain at the sting site. Traditional herbal remedies are frequently used but have no apparent beneficial effect. In fact, rubbing the sting site, as commonly practiced with such herbal remedies, more than doubles the chance of developing a severe envenomation. Antivenin against Parabuthus transvaalicus is available commercially and recommended for victims with serious envenomations (see Figure 35-10 ). Brazil About 10,000 cases of scorpion envenomation are reported annually in Brazil,[109] with 80% occurring in southeastern regions.[117] Half the reported stings occur in the state of Minas Gerais,[109] although scorpions are also problematic in São Paulo and Bahia.[33] Most stings occur from December through February. [35] [61] Tityus serrulatus is the most prevalent species in Brazil and accounts for most fatal stings.[39] [109] Tityus bahiensis is the next most common species,[117] although severe envenomations are much more likely from T. serrulatus. [33] Equine antivenin for either T. serrulatus or both T. serrulatus and T. bahiensis is able to neutralize venom from all Brazilian scorpions studied. [117] Children are much more likely to have severe reactions.[61] In Minas Gerais, children less than 14 years of age accounted for 27% of scorpion envenomation admissions but for all cases of significant morbidity and mortality; 16% were treated in an intensive care unit (ICU) setting. Mortality was 3.5% in 1938[35] but with current treatment now ranges from 1% to 1.1% in children and is 0.28% overall. [61] [109] [126] Antivenin from a few manufacturers is available in Brazil and routinely used in severe envenomations.[33] [35] [61] [126] Trinidad Tityus trinitatis accounts for almost 90% of the scorpion population on Trinidad. Fatalities are rare but occur more often in children. Stings are more frequent in summer months.[11] Systemic effects of serious T. trinitatis envenomations include tachypnea, restlessness, vomiting, hypersalivation, cerebral edema, pulmonary edema, hypovolemic shock, seizures, and myocarditis.[41] The most striking clinical observation is the high incidence (up to 80%) of acute pancreatitis; scorpion stings are the most common cause of acute pancreatitis in Trinidad.[11] [65] Venezuela Tityus discrepans is the most common scorpion in Venezuela.[50] [54] The states of Monagas and Sucre in eastern
Figure 35-12 Centruroides limpidus, one of several closely related, dangerous Mexican scorpions. (Courtesy R. David Gaban.)
Venezuela are particularly endemic for scorpions.[50] A case series of 64 patients from the state of Merida in southwestern Venezuela classified scorpion envenomations by clinical criteria.[107] Whereas 27 patients had only local manifestations, the remainder had systemic effects of envenomation: 21 primarily had GI complaints, nine had neurologic symptoms and hypertension, and seven had severe envenomations with cardiac arrhythmias, pulmonary edema (five patients), and fatal cardiogenic shock (two patients). These last seven patients all received antivenin produced in Caracas. The survivors received antivenin within 5 hours, whereas the children who died received antivenin later than 5 hours after envenomation.[107] Mexico An estimated 200,000 scorpion stings occur annually in Mexico. [46] Of at least 134 native species, eight members of the Centruroides family are recognized as significantly dangerous ( Figure 35-12 ): C. elegans, C. infamatus infamatus, C. limpidus limpidus, C. limpidus tecomanus, C. noxius, C. pallidiceps, C. sculpturatus (exilicauda), and C. suffusus suffusus.[46] C. noxius has the most potent venom, [34] [102] but C. suffusus is usually cited as the most dangerous Mexican scorpion.[132] [150] Centruroides scorpions are relatively small and described as yellow, tan, or brown in color. Clavigero recognized as early as 1780 that "the venom of the small and yellow scorpions is more active than that of the big grey ones."[108] The 11 Mexican states on the Pacific coast are particularly endemic places for scorpions, with Colima, Nayarit, Guerrero, and Morelos having the highest mortality rates from scorpion envenomation.[46] [108] In the 1940s, 7.4 to 8.9 scorpion sting deaths occurred per 100,000 population. This rate decreased to 3.4 to 4.7 per 100,000 in 1957–1958. The great majority occurred in very young children. Approximately 10 times more deaths occurred from scorpions as from all reported snakebites. Most
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fatal cases occur in the summer months from April through July.[108] In the 1980s, 272 to 401 scorpion fatalities per year occurred nationwide, with respiratory failure as the proximate cause of death; this figure probably underestimates the true total by a factor of 2 to 3.[46] The following list of signs and symptoms has been reported with Mexican scorpion stings, although not all effects are necessarily seen in the same victim, and no apparent sequence of effects has been observed: hyperexcitability, restlessness, hyperthermia, tachypnea, dyspnea, tachycardia or bradycardia, diaphoresis, nausea, vomiting, gastric distention, diarrhea, lacrimation, nystagmus, mydriasis, photophobia, excessive salivation, nasal secretion, dysphagia with foreign body sensation, dysphonia, cough, bronchorrhea, pulmonary edema, arterial hypertension or hypotension, heart failure, shock, convulsions, ataxia, fasciculations, and coma.[46] Many of these effects appear to be caused by autonomic nervous system dysfunction, which can be seen from either neurotoxic or cardiotoxic scorpions. Unpublished verbal reports by physicians who have treated victims of scorpion envenomation in Mexico suggest that the clinical presentation is virtually identical to that caused by Centruroides exilicauda in the United States. The higher mortality from Mexican vs. American scorpion stings most likely results from differences in the human and scorpion population densities, in the ease of access to medical care (e.g., monitoring equipment, ICUs, and antivenin), and perhaps also to cultural differences in housing and protective clothing that promote human-scorpion interactions in Mexico.
Currently, a polyvalent antivenin protective against all native Centruroides species is produced by injecting horses with a mixture of macerated venom glands from the most important species (C. noxius, C. l. limpidus, C. l. tecomanus, and C. suffusus). Antivenin is recommended and often used in patients with systemic symptoms.[46] United States About 40 species of scorpions are found in the United States. [36] Only Centruroides exilicauda causes a significant number of systemic reactions and is known to be potentially fatal.[23] [36] [40] [129] [141] Approximately 30 Centruroides species are found distributed throughout the New World,[129] several of which are of medical importance and are mostly found in Mexico. Centruroides exilicauda (the currently preferred taxonomic designation) is also known as C. sculpturatus, or the bark scorpion, because of its preference to reside in or near trees. These scorpions also often hide under wood (old stumps, lumber piles, firewood, loose bark on fallen trees), in ground debris, or in crevices during the daytime. This is troublesome to humans, since the scorpions may hide in shoes, blankets, or clothing left on the floor during daylight hours, as well as under common ground cover and tents. C. exilicauda is found statewide in Arizona and also in some areas of Texas, New Mexico, northern Mexico, small areas of California, and near Lake Mead, Nevada. [40] The bark scorpion is relatively small, measuring up to 5 cm in length. Specimens are variously described as being a uniform yellow, brown, or tan; stripes are uncommon. The pincers (pedipalps) and tail are thin, giving the scorpion a streamlined appearance, in contrast to several of the larger but less dangerous scorpions with thick claws and tails. The presence of a subaculear tooth, a tubercle at the base of the stinger, is distinctive to C. exilicauda and is helpful in differentiating this neurotoxic scorpion from other species.[40] [141] The bark scorpion presents a significant public health problem in Arizona. About 10% of all calls received by the Samaritan Regional Poison Center in Phoenix are related to scorpion stings, the vast majority of which are known or highly suspected to have been caused by C. exilicauda; 6064 such calls were received in 1997, the most recent year with complete data available. The Arizona Poison and Drug Information Center in Tucson reported 2678 scorpion stings the same year. C. exilicauda was at one time the number-one killer among Arizona's venomous animals. From 1931 to 1940, more than 40 deaths were attributed to envenomation by this scorpion, mostly in young children and infants. The fatality rate fell dramatically between 1940 to 1970, probably because of improved pest control measures and advances in medical technology and supportive care. In 1972 these scorpion stings were still considered generally fatal to infants less than 1 year of age without treatment, extremely dangerous to older children, and occasionally fatal to adults with hypertension.[141] However, no death has been reported from scorpion envenomation in Arizona since 1968.[23] Because death can apparently be prevented with currently available supportive care, prior fatalities were probably caused by loss of upper airway and respiratory muscle control with the potential for aspiration, exacerbated by metabolic acidosis, hyperthermia, and rhabdomyolysis from excessive muscular activity.[40] Centruroides vittatus, the common striped scorpion, accounts for the most reported envenomations in the United States after C. exilicauda. C. vittatus has a black intraocular triangle and black stripes on the thorax. A review of 558 C. vittatus stings reported to Texas poison centers in 1997 found that 96% produced local symptoms of pain, bleeding, burning sensations, erythema, edema, hives, local paresthesias, and pruritus; systemic reactions occurred in 20% of victims. [142] The most common systemic features were paresthesias of the face, tongue, and perioral region, followed by dysgeusia, chills, sweating, dysphagia, fasciculations, nausea, and vomiting. C. vittatus is found primarily in the Southwest and Texas but also extends into southern Indiana and Illinois.[145]
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Figure 35-13 Hadrurus arizonensis, a "giant hairy scorpion" of the American Southwest. (Courtesy R. David Gaban.)
Hadrurus species are the longest and most heavily bodied scorpions native to North America and are known as "giant hairy scorpions" because of their size and conspicuous bristles ( Figure 35-13 ). They are native to Arizona, California, and parts of Utah, Nevada, Idaho, and Mexico. Vejovis species have a wide distribution from southern Canada, south through Wyoming, Colorado, and Texas, and west to California. Hypersalivation after Vejovis envenomation has been reported. Uroctonus species are found in mountain habitats from southern California to Oregon.[129] Isometrus maculatus is the only scorpion found in Hawaii[106] but is also found in southern Florida and California.[36] Envenomations cause mild systemic effects (myalgia and nausea), but no fatalities have been reported.[106] Diplocentrus species have been found in Florida, Texas, and California.[36] The Midwest and New England are not natural scorpion habitats, although three envenomations in Michigan were caused by scorpions unintentionally transported with personal belongings or with produce, two by Centruroides hentzi from Florida, and one by C. exilicauda from Arizona.[145] The Samaritan Regional Poison Center in Phoenix has also been consulted regarding stings from bark scorpion stowaways in the mail or personal belongings to Minnesota and Germany, respectively. Centruroides exilicauda Envenomation.
Stings from C. sculpturatus often produce significant neuromuscular effects without severe cardiopulmonary toxicity. Curry et al[40] reviewed clinical findings after C. exilicauda envenomation and proposed four clinical grades of envenomation to direct treatment ( Box 35-1 ). Grade I envenomation is characterized by local pain and paresthesias at the sting site. Usually, no local inflammation occurs, and the puncture wound is too small to be observed. If no scorpion was seen, the diagnosis may require historical or epidemiologic clues or other physical signs. The "tap test" has been recommended empirically in order to confirm a bark scorpion sting. With the patient looking away or otherwise distracted, gently tapping the sting site will greatly exacerbate the pain, a sign that does not occur with other envenomations.[40] [141]
Box 35-1. GRADES OF CENTRUROIDES EXILICAUDA ENVENOMATION I. Local pain and/or paresthesias at site of envenomation II. Pain and/or paresthesias remote from the site of the sting, in addition to local findings III. Cranial nerve dysfunction or somatic skeletal neuromuscular dysfunction 1. Cranial nerve dysfunction: blurred vision, wandering eye movements, hypersalivation, difficulty swallowing, tongue fasciculations, upper airway problems, slurred speech 2. Somatic skeletal neuromuscular dysfunction: jerking of the extremity(ies), restlessness, severe involuntary shaking and jerking that may be mistaken for a seizure IV. Cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction
Modified from Curry S et al: J Toxicol Clin Toxicol 21:417, 1983–1984.
Victims with grade II envenomations have local symptoms plus pain and paresthesias remote from the sting site. The more distant symptoms often radiate proximally up the affected extremity but may occur in even more remote sites (e.g., contralateral limbs) or as generalized paresthesias. Victims may complain of a "thick tongue" and "trouble swallowing" in the absence of objective motor abnormalities. Children and adults frequently rub their nose, eyes, and ears, and infants may present with unexplained crying.[40] Cranial nerve or somatic skeletal neuromuscular dysfunction is found in grade III envenomations. Cranial nerve dysfunction can be demonstrated as blurred vision, abnormal eye movements, slurred speech, tongue fasciculations, and hypersalivation. The combination of bulbar neuromuscular dysfunction and increased oral secretions may cause problems with airway maintenance. Abnormal eye movements most often are involuntary, conjugate, slow, and roving. Chaotic multidirectional conjugate saccades resembling opsoclonus and unsustained primary positional nystagmus may also be seen.[38] Many patients with abnormal eye movements prefer keeping their eyes closed. Somatic skeletal neuromuscular dysfunction can cause restlessness, fasciculations, alternating opisthotonos and emprosthotonos, and
shaking and jerking of the extremities that can be mistaken for a
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seizure. The abnormal skeletal muscle activity appears more undulating and writhing, however, than the tonic-clonic movements of generalized seizures. Also, unlike with seizures, the victim often remains awake and alert the entire time. Box 35-2. CENTRUROIDES EXILICAUDA ENVENOMATION, AS REPORTED BY AN INTENSIVE CARE SPECIALIST Arriving home in the early evening, I decided to go for a run. My running shoes were in the kitchen area, where I had left them the day before. As usual, I would wear my shoes without socks. As I put my left foot into the shoe, I felt an intense burning pain on the dorsum of my first toe. I pulled my foot out of the shoe and along with it came a 1 ½- to 2-inch, clear-brown scorpion. Having no idea what to do for a scorpion envenomation, I called the poison control center. I was informed that the systemic toxicity was usually mild for someone my age, and that if the pain was too severe, I should come in and be evaluated. As the minutes went by, I began to salivate and feel perioral paresthesias. As I walked, the paresthesias became more generalized, with a very noticeable paravertebral tingling with each step. After a few more minutes, I decided to call the poison control center to ask for advice. After dialing the number, I was unable to speak clearly because of severe dysarthria and excess salivation. The toe pain seemed to abate as other neurologic symptoms developed. Since I was unable to talk on the phone, and no neighbors were home to drive me to the hospital, I decided to drive myself. The normal 10-minute drive took 45 minutes. I had coordination difficulties with the gas pedal, clutch, and gear shifting. It was also nighttime, and I could not process the multiple visual inputs of car lights, street lights, and road lines in a way that would allow me to drive more than 5 to 10 miles per hour. I not only had to stop frequently and close my eyes for a few seconds but also had difficulty keeping the car in my driving lane. After arriving at the emergency department, I was ataxic, dysarthric, and drooling and had difficulty giving the admitting nurse a proper history. I'm certain that I was thought to be either mentally retarded or intoxicated. Examination by the ED physician revealed many abnormal cerebellar findings, continued salivation, inability to swallow liquids, continued symptomatic paresthesias, but no objective motor or sensory deficits. There were no physical signs of envenomation [at the sting site], but tapping the toe produced worsening pain. As my story became clearer to the ED physician, antivenom was ordered and administered. Within 20 minutes of finishing the infusion, all neurologic signs and symptoms were gone, except for toe pain. Personal account of Dr. Thomas Bajo, Phoenix, Arizona.
Grade IV envenomation is characterized by both cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction. On close examination, victims with skeletal muscle hyperactivity (at least grade III) usually also have cranial nerve dysfunction, meeting criteria for grade IV. In the most severe cases, stridor and wheezing occur, suggesting foreign body aspiration or reactive airways disease. Hyperthermia up to 40° C (104° F) probably results from excess motor activity. Respiratory failure, pulmonary edema, metabolic acidosis, sterile cerebrospinal fluid pleocytosis, rhabdomyolysis, coagulopathy, pancreatitis, and multisystem organ failure have also been reported in a few severely ill children.[23] After envenomation, symptoms may begin immediately and progress to maximum severity within 5 hours. Infants can reach grade IV in 15 to 30 minutes.[40] The symptoms abate at a rate that depends on age of the victim and grade of envenomation. Symptomatic improvement occurs within 9 to 30 hours without antivenin therapy.[32] [38] [40] [141] Pain and paresthesias are exceptions and have been known to persist for days to 2 weeks. Although adults appear to be envenomed more often, children are more likely to develop severe illness requiring intensive supportive care.[40] A review of 673 patients found that 67.8% of stings occurred in adults older than 20, with 14.9% in children younger than 11. Many more unreported envenomations probably occur in adults, placing the relative incidence for children even lower. Of the patients, 621 (92.3%) had symptoms of either grade I or II envenomations or were asymptomatic and thus required no specific therapy. Younger patients had a higher percentage of the more severe envenomations; 25.9% of children less than 6 years of age had grade III or IV envenomations, or 34% if asymptomatic patients (most likely never stung) are excluded. Only 6.1% of adults had grade III or IV envenomations. [40] Medically reliable descriptions of the victim's perspective of neurotoxic scorpion envenomation are rare, mostly because of the young age of those most severely affected ( Box 35-2 ). Other Countries In Spain from 1974 to 1978, 100 scorpion stings were reported, with most occurring in hot weather and 50%
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from Buthus species.[67] The poison control center in Marseilles, France, reported 976 scorpion stings from 1973 to 1994.[45] Local signs and symptoms predominated; only a few developed systemic toxicity (nausea, vomiting, tachycardia), and none developed neurotoxicity. Recommended treatment consists of administering analgesics and addressing tetanus immunization status, since hospitalization and antivenin are not necessary. Scorpions are also found throughout the eastern and tropical regions of Asia. Envenomation by Buthus martensii is a common medical problem in China.[147] This scorpion is also used in traditional Chinese medicine for its reputed effects of reversing circulatory failure. The black (Asian forest) scorpion Heterometrus longimanus is found in Indonesia, Malaysia, and the Philippines.[83] Australia is home to approximately 30 scorpion species.[140] Urodachus yaschenkoi stings reportedly can disable a young healthy victim for up to 24 hours, with prostration, pyrexia, and sweating. No neurotoxins were found in U. novahollandiae, the only Australian species that has had its venom studied.[140]
CLINICAL MANIFESTATIONS Cardiovascular Detailed descriptions of myocardial damage and other cardiovascular manifestations from the scorpions of Israel, India, Trinidad, Tunisia, and Brazil have been reported since the 1960s.[73] The overall incidence of heart failure or pulmonary edema is 7% to 32%, with shock reported in 7% to 38% and sudden cardiac death in 7% of victims. The cardiovascular effects of scorpion envenomation are complex and varied. Stimulation of the sympathetic and parasympathetic branches of the autonomic nervous system results in different clinical presentations that may change with time. Distinct syndromes may dominate the clinical picture in severe scorpion stings. Hypertension or hypotension can occur with or without pulmonary edema, and rhythm disturbances may consist of sinus bradycardia or tachycardia, premature depolarizations, supraventricular tachycardia, atrioventricular block, and ventricular tachycardia. [60] [74] A recent Indian study postulated that the cardiovascular effects follow a predictable pattern. [94] Stage I consists of vasoconstriction and hypertension. Stage II is characterized by left ventricular failure manifested as hypotension, with or without pulmonary edema depending on the patient's volume status. Stage III combines both left and right ventricular dysfunction, resulting in cardiogenic shock. A similar progression from a hyperdynamic and hypertensive phase to a hypokinetic, hypotensive phase with left ventricular dysfunction is also reported from Tunisia. [120] Transient parasympathetic effects may occur initially, resulting in bradycardia and hypotension, and are followed by sustained adrenergic hyperactivity.[17] Sinus tachycardia and hypertension are related to venom-induced catecholamine and angiotensin release.[17] [41] [76] [94] [99] Significant hypertension may be seen in up to 77% of patients with systemic envenomation, although a 17.5% to 30% incidence of hypertension is more common.[73] A loud protosystolic gallop, systolic parasternal lift, and transient apical murmur of papillary muscle dysfunction are associated with systemic hypertension.[17] [73] Myocarditis, with ECG changes and biochemical evidence of cardiac injury, is often reported. This myocardial damage is most likely caused by massive catecholamine discharge and sympathetic overstimulation, although direct venom cardiotoxicity has not yet been ruled out.* Many ECG changes consistent with myocardial ischemia and myocarditis have been found in persons stung by scorpions, including Q waves, ST-segment elevation or depression, peaked or inverted T waves, U waves, prolonged QTc intervals, and atrioventricular and bundle branch blocks.[15] [35] [73] [131] Most ECG abnormalities are transient, lasting only as long as the most severe clinical effects. Prolonged QTc intervals last for 48 to 72 hours, however, and T-wave inversions have persisted for 4 to 6 weeks.[14] Echocardiography has demonstrated left ventricular systolic dysfunction, which usually resolves by the next day.[99] Concurrent right ventricular dysfunction supports primary global scorpionic myocarditis rather than secondary myocardial ischemia from systemic hypertension.[120] Elevated serum levels of CK and CK-MB have been found in about one half of persons with systemic envenomation. Only about one half of those with elevated CK-MB levels also have ECG changes consistent with myocardial injury.[138] Concurrent CK, CK-MB, and troponin-I elevations have also been reported in a victim with transient bradycardia and second-degree (Mobitz type I) atrioventricular block. [131] Histologic examinations of cardiac tissue in fatal human cases have shown a mixed picture of toxic myocarditis and myocytolysis, with interstitial edema and hemorrhage, inflammatory cell infiltrates, focal necrotic foci, and fatty droplet deposition.[41] [73] Respiratory Effects Respiratory failure after scorpion envenomation has been attributed to direct CNS depression, hypertensive encephalopathy, upper airway obstruction, bronchospasm, impaired surfactant synthesis, and pulmonary edema (PE).[111] [134] [139] PE is the most severe respiratory feature in severe scorpion envenomation, occurring in 7% to 35% of victims and accounting for *References [ 17]
[ 41] [ 61] [ 73] [ 120] [ 136]
.
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about 25% of scorpion-related deaths.[1] [2] [123] The etiology and pathogenesis of PE from scorpion stings are not clear, and both cardiogenic and noncardiogenic factors have been implicated. Left ventricular systolic dysfunction may cause PE through venom-induced myocarditis and acutely increased afterload.[2] [4] [72] [123] Increased pulmonary capillary wedge pressures,[2] abnormal radionuclide scans,[123] and left ventricular dysfunction demonstrated by Doppler echocardiographic studies[1] support a cardiac origin of PE. Noncardiogenic causes for PE are less well documented but include shock, primary venom-induced lung injury, oxygen toxicity,[72] and the presence of various inflammatory mediators (interleukins, kinins, platelet activating factor).[4] Histologic and biochemical evidence of increased alveolocapillary membrane permeability has been demonstrated in animal studies and in a fatal human case of Tityus serrulatus envenomation.[5] Rabbit studies with Tityus discrepans venom found abundant intravascular microthrombi in lungs with PE, and heparin prevented the development of PE.[54] Such findings are atypical of noncardiogenic pulmonary edema, or adult respiratory distress syndrome (ARDS), and the researchers therefore suggest that scorpion venom respiratory distress syndrome (SVRDS) be recognized as a distinct clinical entity. Neurologic Effects Centruroides exilicauda (sculpturatus) stings produce significant neuromuscular effects, manifested by pain and paresthesias in lower grades of envenomation and by cranial nerve and somatic skeletal neuromuscular dysfunction in higher grades. These effects are caused by repetitive firing of neurons from venom-induced incomplete sodium channel inactivation.[40] Other scorpions may cause similar neurologic findings as part of their clinical picture. Centruroides vittatus causes neurotoxic symptoms in about 20% of victims.[142] Both local and diffuse paresthesias have been reported with Leiurus quinquestriatus stings.[31] Tityus serrulatus has caused unilateral facial paresthesias and fasciculations in the facial nerve distribution.[119] Neurologic signs are fairly common among patients with severe envenomations from scorpions categorized here as cardiotoxic. For purposes of discussion, scorpions may be divided into neurotoxic and cardiotoxic categories. In reality, all the scorpions that produce systemic effects are primarily neurotoxic. However, the neurotoxic effects from some species can induce massive release of endogenous catecholamines, causing prominent cardiopulmonary effects. Neurologic signs reported with cardiotoxic scorpions include paresthesias, tremors, shivering, agitation, hyperirritability, apprehension, restlessness, myoclonus, oculogyric crisis (opsoclonus?), convulsions, confusion, delirium, hyporeflexia, and coma.* In fatal human cases a preterminal encephalopathic phase is typical.[93] Intracranial pathology has been noted in several case reports of scorpion envenomation. Mesobuthus tamulus and Heterometrus swannerdani in India have been implicated in causing hemorrhagic strokes. In two cases, acute arterial hypertension may have ruptured intracranial blood vessels in the basal ganglia,[62] [124] although Heterometrus species do not cause systemic toxicity related to a catecholamine surge as does M. tamulus.[15] [148] A third case suggests that frontoparietal hemorrhage results from venom-induced vasculitis.[12] Two earlier cases of hemiplegia associated with scorpion stings in India were believed to result from cerebral thrombosis. [12] A 3-year-old boy stung by Nebo hierochonticus developed diffuse intracranial hemorrhages with cortical blindness and deafness, most likely related to disseminated intravascular coagulation (DIC).[8] A 13-year-old Israeli boy stung by L. quinquestriatus developed mutism and buccofacial apraxia with bilateral infarcts of the frontal opercular regions,[71] probably related to an episode of cardiogenic shock from ventricular tachycardia. Many persons with systemic scorpion envenomation exhibit anxiety and agitation, consistent with CNS excitation. Animal experiments have shown that intracerebroventricularly administered M. tamulus venom produces similar effects as yohimbine, a known anxiogenic agent.[27] Although in fatal cases of L. quinquestriatus envenomation, CNS manifestations always precede terminal hypotension and cardiac arrest, the venom crosses the blood-brain barrier poorly if at all,[88] [93] [125] so any encephalopathy would be secondary to peripheral effects. Others suggest that CNS manifestations of scorpion stings are caused by hypertensive encephalopathy or excessive levels of circulating catecholamines,[133] [134] not a direct venom effect. Hypoxia and pain may also contribute to agitation. Pancreatitis Scorpionic pancreatitis was reported by Waterman in 1938 from Tityus trinitatis stings and was found in 80% of patients studied by Bartholomew in 1970.[11] Most of these patients had epigastric abdominal pain radiating to the back starting within 5 hours of the sting and resolving within 24 hours. Some patients with
hyperamylasemia (38%) did not complain of abdominal pain, suggesting that the true incidence of pancreatitis may be significantly higher. Scorpion stings are the most common cause of acute pancreatitis in Trinidad.[11] Acute pancreatitis is the most common form of the disease, but edematous, hemorrhagic, and chronic relapsing pancreatitis may also occur.[65] Transient pancreatitis has also been reported from C. exilicauda[23] and in 93% of *References [ 22]
[ 33] [ 35] [ 55] [ 81] [ 98] [ 116] [ 122] [ 134]
.
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children envenomed by L. quinquestriatus.[137] The systemic severity of the envenomation or amount of abdominal pain does not appear to correlate with degree of elevation in serum amylase.[11] [137] Scorpion venom is known to be a potent secretagogue, stimulating exocrine secretion of the stomach,[144] salivary glands,[40] and pancreas. Enhanced release of proteolytic enzymes, accompanied by spasm of the sphincter of Oddi,[65] is hypothesized to cause acute scorpionic pancreatitis. Other Gastrointestinal Effects Nausea, vomiting, gastric distention, abdominal cramping, and occasional diarrhea are reported in victims with severe systemic symptoms.[46] [84] [99] [110] In Tunisia the onset of vomiting heralded worsening neurotoxicity and marked progression from stage III to stage IV envenomation.[69] Gastric distention associated with agitation and depressed level of consciousness place scorpion sting victims at increased risk for pulmonary aspiration of gastric contents. T. serrulatus venom increases the volume, acid output, and pepsin output of gastric juice in rats, probably mediated by release of acetylcholine and histamine. Serum gastrin levels are also elevated.[144] Pig studies with L. quinquestriatus venom found that despite an increase in oxygen transport and consumption, oxygen utilization in the GI tract was impaired.[139] Such impairment in oxygen utilization may occur in other tissues as well, contributing to metabolic acidosis in severe envenomations. Endocrine and Other Humoral Effects Scorpion envenomation has long been known to cause an "autonomic storm" with increased release of endogenous catecholamines, contributing to hypertension, tachycardia, and potentially fatal cardiopulmonary dysfunction. Envenomed patients with abnormal ECG tracings excrete elevated levels of free epinephrine, norepinephrine, and vanillylmandelic acid.[78] Elevated circulating catecholamine levels have also been reported.[5] Release of catecholamines may be caused by direct stimulation of postganglionic sympathetic neurons and the adrenal glands. Hypertension may also be caused by activation of the renin-angiotensin endocrine axis. Elevated levels of renin and aldosterone were found in victims stung by L. quinquestriatus. [80] Stings often induce hyperglycemia related to suppression of insulin secretion,[39] [111] in contrast to the enhanced secretion of the exocrine pancreas. Murthy and Hase [111] propose that this results in a syndrome of fuel-energy deficits related to inability to utilize existing metabolic substrates, exacerbating the cardiopulmonary insult. Insulin therapy has been found to reverse ECG changes, reduce angiotensin levels and circulating free fatty acids in experimental animals, and reverse hemodynamic changes and pulmonary edema in children stung by scorpions.[111] [113] M. tamulus venom lowers thyroxine and triiodothyronine levels in experimental myocarditis.[112] Kinins and other inflammatory mediators may play a role in the cardiovascular toxicity. T. serrulatus and C. exilicauda venoms potentiate the action of bradykinin by inhibiting angiotensin converting enzyme (ACE).[104] Animal experiments show reversal of venom-induced cardiovascular effects with aprotinin,[11] [58] [93] a kallikrein-kinin inhibitor, and icatibant,[58] a bradykinin antagonist, and augmentation of adverse effects with captopril,[10] an ACE inhibitor. Serum interleukin-6 (IL-6) levels were greatly elevated in 8 of 10 Israeli children, gradually decreasing toward normal over 24 hours.[138] High levels of circulating IL-1, IL-3, IL-6, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF) have also been found in a severely envenomed Brazilian patient.[4] Genitourinary Effects Priapism is frequently reported among male patients with systemic envenomation. Priapism results from enhanced parasympathetic tone and is often associated with vomiting and profuse sweating.[15] [16] The incidence of priapism ranges from 4% to 10%[3] [7] [121] up to 78% to 96%.[84] [135] In India, priapism, vomiting, and diaphoresis are considered premonitory diagnostic signs of severe M. tamulus envenomation. Priapism is reduced or absent within 6 hours of the sting even in severe cases, and the degree of priapism does not appear to correlate with the severity of envenomation.[15] In Tunisia, however, the incidence of priapism positively correlated with degree of severity.[98] Urinary retention is found in 33% of victims with systemic envenomation in southern Africa.[25] [26] [110] This finding, however, is not consistent with increased cholinergic tone, which should produce increased urination, as seen in other series.[7] A dorsal nerve block with 1% lidocaine was successful in treating severe local pain from a T. serrulatus sting to the penis.[118] Hematologic Effects Scorpion venoms are not generally noted to produce coagulopathies or other significant hematologic effects, although DIC has been reported.[7] [103] The occasional "defibrination syndrome" is seen more often in children, probably related to a higher relative dose, and can be experimentally reproduced in dogs. Platelet aggregation can be induced by catecholamines alone, and may therefore be an indirect effect of scorpion venom. Increased osmotic fragility of red blood cells has been demonstrated in some experimental models.[128] The only scorpion routinely implicated in dangerous hematologic effects is Hemiscorpion lepturus, which can cause severe hemolysis and consequent renal failure.[115] [122]
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Case reports from Saudi Arabia associate severe Nebo hierochonticus stings with DIC and intracranial hemorrhage.[7] [8] Neither species is from the Buthidae family. Immunologic Effects Scorpion toxins are antigenic and therefore capable of eliciting an immune response on reexposure. Positive skin prick and intradermal skin tests and radioallergosorbent assays have been found with the venom from C. vittatus[47] and Androctonus australis hector[101] in previously envenomed patients. Envenomation by C. exilicauda has produced an anaphylactic reaction, with urticaria, wheezing, and facial angioedema but without systemic neurotoxic findings, in an otherwise healthy adult patient previously stung by a scorpion.[149] Treatment with animal-derived antivenins places a person at risk for both immediate and delayed immunologic reactions. Since the treatment for hypersensitivity reactions includes epinephrine, and because many persons envenomed by cardiotoxic scorpions have elevated circulating catecholamines, such persons should be less likely to have anaphylactic reactions to antivenin. Brazilian patients stung by T. serrulatus were separated into groups with or without adrenergic manifestations. Both groups received antivenin.[6] The group with adrenergic toxicity developed significantly less signs and symptoms of early anaphylaxis (8% vs. 42.9%). Miscellaneous Systemic Effects Leukocytosis with white blood cell counts as high as 44,000/mm3 is common in persons with severe scorpion envenomation.[33] [35] [94] Mild to moderate hypokalemia was found in 13 of 17 patients with severe Tityus envenomations in Brazil[33] and eight patients with M. tamulus stings in India,[94] although elevated potassium and lowered sodium levels were found previously.[150] The same venom-induced metabolic changes that inhibit insulin release favor glycogenolysis and lipolysis, leading to elevated circulating levels of free fatty acids.[111] [112]
DIFFERENTIAL DIAGNOSIS Bites or stings from other arthropods should be considered in the differential diagnosis of scorpion envenomation. Pain at the site of Centruroides exilicauda sting may be similar to that from a black widow spider (Latrodectus species). However, severely ill victims of scorpion envenomation appear unable to lie still, whereas those with black widow spider bites can maintain a position for short periods before moving again to find a comfortable position. Black widow bite may produce hypertension, tachycardia, sweating, and other signs of adrenergic excess but does not produce the abnormal eye movements, fasciculations, and paresthesias found with scorpion sting or induce a positive tap test. Widow spider bites frequently produce a characteristic halo lesion at the site, whereas no lesion is usually visible after C. exilicauda sting. Many other arthropods can produce a small puncture wound accompanied by local tissue inflammation. This may be difficult to differentiate clinically from stings by scorpion species in the absence of cardiovascular or neurologic toxicity or without tentative visual identification of the arthropod involved. The tachycardia, respiratory distress, excessive secretions, and occasional wheezing that occur from C. exilicauda sting may be mistaken for asthma, airway obstruction with a foreign body, or poisoning with a cholinergic agent, such as an organophosphate insecticide. In the absence of the history of a scorpion sting, other disorders to be considered include CNS infection, tetanus, dystonic reaction, seizure, and intoxication with an anticholinergic, a sympathomimetic, phencyclidine, nicotine, or strychnine. Autonomic storm from a cardiotoxic scorpion sting may be confused with pheochromocytoma or a monoamine oxidase inhibitor-tyramine reaction. A victim of severe scorpion envenomation presenting late in the course may appear to have cardiac failure or sepsis. Toxicity from an illegal sympathomimetic is sometimes mistaken for envenomation by C. exilicauda. Young children from endemic areas presenting with unusual neurologic symptoms, such as agitation, choreiform or repetitive motion of the trunk and extremities, and abnormal eye movements, may be assumed to have been envenomed even without history of a sting or scorpion. [114] Occasionally the caregivers are aware of this potential for misdiagnosis and claim that their child was stung when they know or suspect that the child ingested methamphetamine. A case series of 18 inadvertent methamphetamine poisonings among children in central Arizona included three victims initially misdiagnosed with a scorpion sting and inappropriately treated with antivenin; one patient had an anaphylactic reaction.[95]
TREATMENT Ismail et al[93] summarized the current understanding of treating scorpion stings when noting, "It is strange that despite the long experience with scorpion envenomation, most of the treatment protocols advocated are based on isolated clinical observations, are sometimes controversial, and not instituted on rigid or strictly controlled animal or clinical studies.... Even in serotherapy, there are no quantitative studies regarding antivenom dosage, routes of administration, time-effectiveness relationship and titre of the antivenom used." Some treatment recommendations can be eliminated. A so-called lytic cocktail was once considered essential
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in treating Mesobuthus tamulus stings in India.[42] This mixture of pethidine (meperidine), chlorpromazine, and promethazine (equivalent to the DPT cocktail for pediatric sedation, which has fallen into disfavor in the United States) was claimed to induce "artificial hibernation" and improve outcome. Morbidity and mortality statistics, however, have not shown a difference between cohorts historically treated with the lytic cocktail and those not treated. Furthermore, any effect of such treatment would be sedation, which would increase the risk of airway difficulties. Some traditional herbal therapies involve rubbing the area near the sting site, which doubles the chance of developing a severe envenomation. [25] [26] Purported herbal therapies for scorpion stings have not been adequately tested and are probably of no benefit.[85] Other therapies no longer recommended include electric shock, barium, iodine, physostigmine, and snake or spider antivenin. [129] Although much controversy surrounds the proper treatment of scorpion envenomation, some consensus exists. Most victims, even those stung by potentially dangerous scorpions, demonstrate only local signs and symptoms and require only symptomatic outpatient treatment. It is prudent to observe such persons for several hours after the sting to ensure that progression to severe envenomation does not occur. For localized pain, many authorities recommend local anesthesia with lidocaine, bupivacaine, or dehydroemetine by infiltration or nerve block, such as a digital block for fingers or toes.* In southern Africa, Berman[25] [26] has reported successful treatment of poorly localized pain radiating up an extremity with an intracutaneous sterile water injection (ISWI), usually also with a local anesthetic infiltrated at the sting site. ISWI is performed by injecting small amounts (about 0.1 ml) of sterile water intradermally into points of maximal pain, producing up to 10 wheals. Pain relief is said to occur within 1 to 5 minutes, but pain may return in 4 to 12 hours and can be persistent. ISWI therapy cannot be generally recommended because it has not been tested in prospective or controlled trials or with scorpion stings elsewhere in the world. Scorpion stings are traumatic puncture wounds, and victims should be given appropriate wound care and tetanus prophylaxis if indicated. Victims with significant systemic scorpion envenomations should receive supportive and symptomatic care in a monitored hospital setting.[33] [56] [61] [77] [81] Many require admission to an ICU, although treatment should begin in the emergency department or outlying facility if available. Airway control must be addressed and continuous cardiovascular and respiratory monitoring instituted. Fluid resuscitation may be indicated secondary to fluid losses from vomiting, sweating, and increased insensible losses from hyperthermia. Both hyperthermia and hypothermia have been reported from scorpion stings, and both appear to worsen toxicity.[92] Hyperthermia usually resolves with standard acetaminophen doses, and hypothermia resolves with warm blankets. Pharmacologic Therapy Many drugs have been recommended in the treatment of scorpion envenomations, but few have been rigorously tested. Recommendations for atropine vary. Many victims exhibit signs of excess cholinergic tone, such as bradycardia, vomiting, sweating, and hypersalivation. If venom induces prominent adrenergic effects, the rescuer should not administer atropine.[18] [61] [81] Parasympathetic venom effects are usually transient and not life threatening, although atropine may be indicated for severe bradycardia. Also, in subsequent phases with more prominent adrenergic toxicity, atropine could worsen tachycardia and hypertension, leading to more severe cardiovascular effects. Atropine may be safe, however, for cholinergic effects from scorpions that do not cause prominent cardiotoxicity. Published cases from southern Africa[25] and anecdotal experience from Arizona suggest that atropine can reverse hypersalivation that interferes with airway control, which may obviate the need for intubation and decrease the risk of aspiration, although caution is still advised.[110] Protocols for the use of atropine and its optimal dosage have not been prospectively determined. The only therapy to date subjected to prospective, randomized, placebo-controlled human study has been antiinflammatory corticosteroids,[3] which showed no benefit. Treatment with corticosteroids has been regularly recommended and is still common in many countries. In Tunisia, 600 consecutive patients received either 50 mg/kg of hydrocortisone hemisuccinate or a placebo. No differences between the two groups were found in clinical severity (baseline and 4 hours after treatment), mortality, need for artificial ventilation, or duration of hospitalization.[3] Glucocorticoids and antihistamines are not recommended unless administered as treatment for allergic manifestations (e.g., anaphylaxis to antivenin).[26] [110] Vasodilator therapy has received much attention. Since excessive adrenergic tone appears to cause the most significant morbidity, vasodilators should block or reverse severe cardiopulmonary effects from scorpion envenomation. Prazosin is a selective a1 -adrenergic blocker, which is also thought to reverse the inhibition of insulin.[20] [21] In India an initial dose of 0.5 mg by mouth for adults and 0.25 mg for children is given to relieve hypertension and pulmonary edema. Repeat doses are given in 4 hours, then every 6 hours as needed for up to 24 hours. Sodium nitroprusside is *References [ 22]
[ 25] [ 26] [ 35] [ 86] [ 118]
.
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used in cases of life-threatening pulmonary edema.[22] Nifedipine, 5 to 10 mg "sublingually" by puncturing and swallowing the gelatin capsule, is also used in India along with the initial dose of prazosin. When this protocol was compared with "conventional treatment" (digoxin, furosemide, hydrocortisone, antihistamines, and atropine), the cohort treated with prazosin had significantly reduced morbidity and shortened recovery time.[21] [75] In Israel, hypertension from scorpion sting unresponsive to analgesics and sedatives has been treated with IV hydralazine or sublingual nifedipine, which are believed to reverse hypertensive encephalopathy. [133] A potential benefit of vasodilators over antivenin is the rapidity of onset.[75] Captopril has also been used to treat hypertension[94] but theoretically could worsen PE.[10] [22] [88] Insulin infusion has been used in India.[111] [113] Since scorpion venoms inhibit insulin secretion, this treatment may help reverse the consequent metabolic derangements. "Standard therapy" to which insulin infusions were added consisted of furosemide for elevated central venous pressures or PE, crystalloid for low central venous pressures, and hydrocortisone and dopamine for hypotension. Insulin was given in a glucose solution with 0.3 units regular insulin per gram of glucose, at a rate of 0.1 g glucose per kilogram body weight per hour. Six patients treated with insulin showed improvement in PE and hemodynamics, although furosemide and hydrocortisone appeared to offer little benefit.[111] Digoxin, diuretics, steroids, antihistamines, dopamine, dobutamine, and ß-adrenergic blockers have been used but are not generally recommended. Dantrolene, aminophylline, quinine, and aspirin are potential therapeutic adjuvants in scorpion envenomation.[22] [82] Antivenin Treatment recommendations seriously diverge regarding antivenin. (We use the term antivenin instead of antivenom, though either term is acceptable.) Most medical researchers believe that antivenin plays a crucial role in the treatment of seriously envenomed patients.* Proponents believe that (1) antivenin is the only specific therapy available against the primary physiologic insult and (2) it greatly improves outcome. Any previous disappointing experience with antivenin, they argue, probably results from inadequate dosing.[87] [88] Researchers from Israel and India do not recommend antivenin.[16] [81] [135] Opponents believe that (1) morbidity and mortality are not caused by the venom but by autopharmacologic agent release, which should not be reversed by antivenin therapy; (2) pharmacokinetic data do not support a role for antivenin; (3) antivenin has not improved outcome in Israeli studies; and (4) antivenin is often unavailable and would be prohibitively expensive in India, so other options must be chosen. Some suggest that commercial production of scorpion antivenin is needed in India.[148] Treatment without antivenin consists of managing serious cardiopulmonary and neurologic effects with pharmacologic agents and supportive care. Even when antivenin is administered by its proponents, adjunctive therapies to treat cardiac failure, PE, and other physiologic treatments are also used.
A major issue in the debate regarding the utility of antivenin is the pharmacokinetics of scorpion venom. Detectable circulating levels of venom support the use of antivenin to neutralize the toxins. Tityus serrulatus venom injected subcutaneously in rodents rapidly distributes to various tissues, with peak serum levels in 30 to 60 minutes.[125] [130] After 2 hours the venom decreased rapidly and was no longer detectable after 8 hours.[125] IV serotherapy therefore should be initiated as soon as possible, since it would become less effective when administered many hours after envenomation.[125] Ismail et al[88] [90] reported that scorpion venoms in animal experiments were rapidly absorbed and distributed to tissues but had more prolonged elimination phases. Scorpion venom has a half-life of 4.2 to 24 hours.[88] The authors concluded that although antivenin would theoretically be most efficacious if given immediately after envenomation, it is still indicated after a delay of several hours or more.[99] [130] Interestingly, Gueron et al[73] [81] reviewed these data and concluded instead that serotherapy would be ineffective and recommended against it. They suggested that the most severe cardiopulmonary effects would be present early and would not be reversed by antivenin given later. The clinical effects of scorpion envenomation are related to tissue concentrations of Androctonus amoreuxi venom in experimental animals,[89] although the slower distribution of antivenin to tissues suggests that it may be less effective when given after a significant delay. A series of 56 victims stung by T. serrulatus in Brazil correlated clinical severity to plasma venom concentrations. [48] IV antivenin lowers circulating levels of venom and presumably the clinical severity of envenomation; however, the effectiveness of antivenin on venom bound to other tissues has not been well defined. The role of serotherapy depends on the time to administration, becoming less effective with increasing delay.[96] [107] Since scorpion venom acts indirectly through the release of autopharmacologic substances, treatment with specific blockers may be more effective than antivenin in persons with delayed presentation.[89] Antivenin research is ongoing and may produce improved products in the future. Maximum neutralizing capacity of antivenin is obtained when soluble venom is used as the antigen rather than telson macerates and *References [ 2]
[ 32] [ 35] [ 40] [ 49] [ 60] [ 86] [ 110]
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ORGANIZATION
TABLE 35-1 -- Scorpion Antivenins PHONE NUMBER*
Institut Pasteur, Algiers, Algeria
[213] 2653497
Androctonus australis hector, Leiurus quinquestriatus, Buthus occitanus
Institut Pasteur, Casablanca, Morocco
[212] 2275778, [212] 2275206
Androctonus mauretanicus, B. occitanus, Scorpio maurus
Institut Pasteur, Tunis, Tunisia
[216] 283022-4, Telex: 14391 PATSU
A. australis, B. occitanus, Androctonus aeneas, L. quinquestriatus
The South African Institute for Medical Research, Johannesburg, South Africa
[27] 725-0511, Telex: 4-22211
Parabuthus transvaalicus, other Parabuthus species
Laboratorios BIOCLON S.A., Mexico City, Mexico (formerly MYN, Zapata, and Grupo Pharma)
[52] 592-87-70, [52] 561-12-11, [52] 592-88-93
Centruroides species
Gerencia General de Biologicos y Reactivos, Health Ministry, Mexico City, Mexico Instituto Butantan, São Paulo, Brazil
SPECIES COVERED
Centruroides species [55] 813 7222, [55] 815 1505, Telex: 11-83325-BUTA BR
Tityus serrulatus, T. bahiensis
Fundacao Ezequiel Dias, Belo Horizonte, Brazil
Fab2 fragment for Tityus species
Refik Saydam Central, Ankara, Turkey
Androctonus crassicauda, L. quinquestriatus, A. australis, B. occitanus
Twyford Pharmaceuticals GmbH, Ludwigshafen am Rhein, Germany
[49] (0621) 589-2688, [49] (0621) 589-2896, Telex: 464823
A. australis, B. occitanus, L. quinquestriatus, other Androctonus and Buthus species
Institut d'Etat des Serums et Vaccins, Tehran, Iran
[98] 02221-2005
A. crassicauda, Buthotus salcyi, Mesobuthus eupeus, Odontobuthus doriae, S. maurus
Central Research Institute, Kasauli, India (research only)
[91] C.R.I. 22
Mesobuthus tamulus, Palamnaeus species, Heterometrus species (possibly)
Lister Institute of Preventive Medicine, Elstree, Herts, United Kingdom (not in production)
[44] 081-954-6297
A. australis, B. occitanus, L. quinquestriatus, A. crassicauda
*Country code in brackets.
purified toxins.[34] Antibodies have been produced against nontoxic analogs of some scorpion neurotoxins,[52] nontoxic proteins found in scorpion venom,[37] [109] and neurotoxin amino acid sequences that are highly conserved among many species. [51] Fab antibody fragments have also been produced against scorpion venoms.[61] [102] These fragments induce a lower incidence of hypersensitivity reactions[61] and possess pharmacokinetic characteristics that make them more suitable than whole immunoglobulin G (IgG) antibodies.[91] Table 35-1 lists scorpion antivenins currently available worldwide.[8] [46] [126] [143] Centruroides exilicauda Envenomation Based on the experience of our medical toxicology group in Phoenix, Arizona since the mid-1970s and that of others treating Centruroides exilicauda envenomation, we favor the use of antivenin in severe envenomation. We routinely recommend and use antivenin in patients with respiratory compromise, as often seen in grade III or IV envenomation. Antivenin does not take precedence, however, over appropriate airway protection measures, including endotracheal intubation when indicated. Also, the presence of grade III or IV symptomatology is not an absolute indication for antivenin, and we have seen several victims (usually older children or adults) who met criteria for higher grades of envenomation but were alert with no respiratory distress. In several cases, atropine was the initial treatment given to some very young victims with hypersalivation significant enough to impact respiratory status. No significant adverse cardiovascular effects were noted, and atropine appeared to improve airway maintenance. No prospective studies of atropine in C. exilicauda envenomation have been published, so we cannot make a recommendation for or against its routine use. No widely recognized standard of care exists in the treatment of C. exilicauda envenomation in the United States. Some physicians in the Phoenix area routinely
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treat severely envenomed victims with only supportive and symptomatic care, usually in an ICU. The Arizona Poison and Drug Information Center based in Tucson also generally recommends supportive care without antivenin. For many years the recommended therapy for the neuromuscular hyperactivity seen in severe envenomations was large doses of barbiturates.[141] We believe that sedation with barbiturates, benzodiazepines, or other drugs in a person already with tenuous airway control unduly increases the risk for aspiration and respiratory failure; therefore these drugs should not be given unless the physician is prepared to intubate emergently and artificially ventilate the patient. A recent case series of patients treated with continuous IV infusions of midazolam was reported by physicians from Tucson, Arizona.[66] Among 33 patients treated in the ICU, the mean infusion time was 9.5 hours and the mean ICU stay was 15 hours, with 85% of patients discharged directly to their homes. Four patients with hypoxia responded to supplemental oxygen. The researchers concluded that continuous midazolam infusions were safe and effective. The neuromuscular hyperactivity of C. exilicauda envenomations, however, is not a centrally mediated phenomenon. CNS depressants may decrease motor agitation but only indirectly, whereas
antivenin directly treats the underlying cause. Regardless of the method, excessive motor activity should be controlled to avoid potential complications of hyperthermia, rhabdomyolysis, and metabolic acidosis. Antivenin typically works quickly, obviating the need for additional pharmacologic sedation to control hyperactivity. We administer parenteral analgesics for pain and benzodiazepines for agitation to patients not treated with antivenin in the ICU. The primary concern about using the currently available antivenin is hypersensitivity reactions. Both immediate (type I, or anaphylactic) and delayed (type III, or serum sickness) hypersensitivity reactions may occur. In 1999, Bond [32] reported no anaphylactic reactions to antivenin in 12 patients; 58% developed a delayed rash or serum sickness that resolved with oral antihistamines and corticosteroids. In 1994, Gateau et al[64] reported 145 cases of severe C. exilicauda envenomations treated with antivenin, with immediate hypersensitivity reactions in 8% generally characterized as mild; no follow-up for incidence of serum sickness was conducted. In 1999, LoVecchio et al[105] reported a prospective study of 116 patients treated with antivenin. Three patients (2.6%) who developed a rash during the antivenin infusion were treated with hydroxyzine, methylprednisolone, and epinephrine, and the infusions were completed at slower rates. An asthmatic patient who developed wheezing responded to treatment with an epinephrine infusion and an inhaled ß-agonist, and was admitted for observation. Nine other patients were admitted for oversedation from medications received before antivenin, to rule out aspiration, or for social reasons and all were discharged within 24 hours. During a 3-week follow-up period, 60 of the 99 patients (61%) developed serum sickness that responded to oral corticosteroids and antihistamines; mean duration of symptoms was 2.8 days with medication.
Box 35-3. RISKS AND BENEFITS OF CENTRUROIDES EXILICAUDA ANTIVENIN
SUPPORTIVE AND SYMPTOMATIC CARE Risks Typically requires admission to intensive care unit Symptoms may take many hours to days to resolve Potential overutilization of limited medical resources Increased hospitalization costs Potential for oversedation Aspiration Hypoxia Prolonged artificial ventilation Benefits Avoids risks of anaphylaxis and serum sickness
USING ANTIVENIN Risks Anaphylaxis: immediate hypersensitivity reaction Cardiopulmonary monitoring recommended Serum sickness: delayed hypersensitivity reaction Benefits Shorter hospital stay with discharge home likely within a few hours Rapid symptomatic improvement Avoids risks of oversedation
Intravenous antivenin results in rapid reversal of neurologic, respiratory, and cardiovascular toxicity in persons envenomed by C. exilicauda. Symptoms completely resolved within 1 to 3 hours in one study [32] ; 71% of patients in another study had resolution within 30 minutes.[64] Bond[32] summarized the potential benefits of antivenin administration as decreased time to resolution of symptoms, cost savings in the emergency department (vs. about $1000/day in ICU charges), and the avoidance of sedation, paralysis, and intubation risks. [32] We believe that the data support the safe use of IV antivenin for high-grade scorpion neurotoxicity, and that serious adverse effects are both uncommon and treatable ( Box 35-3 ). Other reasonable and informed physicians have concluded that since fatalities should not occur with appropriate supportive care, patients should not be subjected to any risk of antivenin anaphylaxis. In the United States, the only currently available scorpion antivenin is produced by the Antivenom Production Laboratory at Arizona State University.[32] [40] [64]
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This antivenin has been produced since 1965 by lyophilizing micron-filtered serum obtained from goats hypersensitized to C. exilicauda venom. It is also cross-reactive against at least two Mexican Centruroides species, C. limpidus and C. elegans.[29] Antivenin is produced in batches every 2 to 3 years and is supplied without charge to regional hospitals by Arizona State University. Because of the limited geographic area of its use, the antivenin has not been submitted for U.S. Food and Drug Administration approval, but it is used within the state by special action of the Arizona Board of Pharmacy. Some interest has been expressed by pharmaceutical companies regarding C. exilicauda antivenin, but no commercial preparation is currently available. Recommendations and Procedure.
Any of the following relative contraindications (roughly in decreasing order of importance) should suggest withholding animal-derived antivenin in favor of symptomatic and supportive care only: (1) prior administration of antivenin derived from the same species; (2) current ß-adrenergic blocker use; (3) history of asthma or atopy; (4) current ACE inhibitor use; and (5) history of allergy to the animal species from which the antivenin is derived, allergy to that animal's milk, or prior extensive exposure to the animal, especially its blood. The patient is placed on continuous ECG and pulse oximetry monitors. IV access is obtained, preferably with at least two IV lines. Equipment and medications for treating anaphylaxis and respiratory arrest are available. Specifically, we prepare an epinephrine drip, 1 mg in 250 ml of 5% dextrose in water (D5W) or normal saline (NS) on a primed IV line with a pump; IV methylprednisolone and hydroxyzine or diphenhydramine in the room are also made available. The lyophilized antivenin is reconstituted with as much sterile NS or D5W as fills the vial (about 10 ml), with gentle rocking to avoid foaming. The antivenin is then withdrawn from the vial and
dissolved in 50 ml of crystalloid (60 ml total) and placed on an IV pump. A skin test is then performed. Up to 0.02 ml of a 1:10 dilution of reconstituted antivenin is injected intradermally with a 27- or 30-gauge needle, the site marked with a pen, and the patient observed for at least 10 minutes for development of a wheal, rash, wheezing, or hemodynamic signs of anaphylaxis. The patient with a reaction is treated appropriately with the medications available. For C. exilicauda envenomation, a positive skin test contraindicates further antivenin therapy, and the patient is admitted for supportive care. Skin testing, however, does not always predict adverse reactions. One study showed a 96% sensitivity for mild immediate hypersensitivity reactions but only a 68% specificity.[64] The antivenin is initially administered at a very slow rate (5 ml/hr), which is doubled every 2 to 3 minutes as long as the patient tolerates the infusion (i.e., develops no signs of anaphylaxis), up to 150 ml/hr. Infusion of one vial by this method takes approximately 30 minutes, and most patients require only one vial of antivenin. The patient is observed for at least 1 hour after the initial antivenin infusion is complete before proceeding with additional antivenin, since most symptoms will resolve in this period. If the symptoms have resolved or regressed to a grade I or grade II envenomation and no complications (e.g., aspiration) are suspected, the patient is discharged. Since most patients treated with antivenin will develop a delayed hypersensitivity reaction, the patient and caregivers are informed about signs and symptoms of serum sickness before discharge. An urticarial rash developing within a few days to weeks is the most common sign, although malaise, myalgias, and arthralgias also may occur. More serious problems are rare. We recommend discharging the patient with prescriptions for antihistamines (hydroxyzine or diphenhydramine) and a tapering dose of corticosteroids to be started if serum sickness develops. Any persons treated with antivenin must be warned that they are allergic to serum products from the animal species used. Repeated use of antivenin for subsequent envenomations is relatively contraindicated but can be undertaken with extreme caution if necessary. Consultation with toxicologists experienced in treating C. exilicauda envenomations can be obtained by calling the Samaritan Regional Poison Center at (602) 253-3334 or the Arizona Poison and Drug Information Center at (520) 626-6016.
PREVENTION Many scorpion stings result from human practices that place persons at risk. Residences with small cracks and crevices offer many hiding places, increasing the risk of human-scorpion interactions. In several countries, playing or working outdoors with inadequate protective clothing, especially in the early evening during warm months, is associated with most scorpion stings. In scorpion-infested areas, clothing, shoes, packages, and camping gear should be shaken out and checked for scorpions. Footwear is recommended. Unnecessary ground cover and debris should be removed to reduce potential nesting places. Certain insecticides, including organophosphates, pyrethrins, and several chlorinated hydrocarbons, are known to kill scorpions. Home spraying is often ineffective because the insecticide does not come in contact with the scorpion. Spraying insecticides around the home can work indirectly by killing other insects in the area and reducing the scorpions' food supply.
860
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Chapter 36 - North American Arthropod Envenomation and Parasitism Sherman A. Minton † H. Bernard Bechtel Timothy B. Erickson
The phylum Arthropoda contains about four fifths of the known animals of the world, and insects are the largest group of arthropods. Insects are an important part of the biota of all terrestrial and freshwater environments that support life; only in marine environments are they relatively unimportant. More species of insects exist than of any other form of multicellular life, and they may well exceed all other land animals in biomass. Insects can use most animal and plant substances as food, and their feeding plays a vital role in recycling organic compounds. They compete with other organisms for the world's food supplies but are themselves a major food source for many forms of life. They are essential for the pollination of many plants. Insect life cycles are diverse and often complex, involving developmental and sexual stages that are widely different in morphology and ways of life. Although sexual reproduction is the rule, parthenogenesis (unisexual reproduction) and pedogenesis occur. Some groups, such as ants, bees, and termites, have developed a high degree of social organization. During at least part of its life cycle, an insect's body is divided into three distinct regions (head, thorax, and abdomen), with three pairs of legs attached to the thorax. Except for a few primitive or parasitic groups, most adult insects have wings. The greatest direct medical importance of insects is associated with their feeding on human blood and tissue fluids. In doing so, they often inject salivary secretions. This is a highly effective method of transmitting pathogenic microorganisms; moreover, the secretions are often allergenic and sometimes toxic. Other insects may carry human pathogens passively on their feet or mouthparts or in their digestive tracts. Venoms have evolved in several insect groups, and venomous insects may attack humans, sometimes with lethal results. Skin, hair, and secretions of insects may be irritant or allergenic, producing cutaneous and respiratory syndromes. Finally, insects can be highly annoying.
HYMENOPTERA (BEES, WASPS, AND ANTS) By far the most important venomous insects are members of the order Hymenoptera, including bees, wasps, and ants ( Figure 36-1 ). They vary in size from minute to large (up to 60 mm in body length). The abdomen and thorax are connected by a slender pedicle that may be quite long in certain wasps and ants. Bees and most wasps are winged as adults; ants are wingless, except for sexually mature adults during part of the life cycle. Mouthparts are adapted for chewing but in some species are modified for sucking. The life cycle includes egg, larva, and pupa stages before emergence of adults. Immature stages may be protected and provided with food by the adult. Both animal and plant foods are used. Many species are parasitic on other arthropods. All ants and many species of bees and wasps are social insects. Colonies range in size from a few dozen individuals to many thousands. In cold climates, most individuals die in autumn, leaving the fertilized females to winter over and found new colonies in the spring. Bees The honeybee (Apis mellifera) is one of the few domesticated insects and is maintained in hives in many countries ( Figure 36-2 ). Numerous geographic races of the honeybee exist; the Italian bee (A. m. ligustica), a common domestic strain of Europe, is also widely distributed in the United States. Feral honeybee colonies usually nest in hollow trees or crevices in rocks but may nest in the walls of occupied buildings. An event of considerable health and economic significance in the Americas was the introduction of an African race of the honeybee (A. m. scutellata, also referred to as A. m. adansoni). This race was introduced from Africa into Brazil because it was thought to be a more efficient honey producer in the tropics. It is characterized by large populations (one queen may lay tens of thousands of eggs), frequent swarming (6 to 12 swarms a year), nonstop flights of at least 20 km, and a tendency toward mass attacks on humans after minimal provocation. As a result, these Africanized honeybees, also known as "killer bees," are much more aggressive than typical Hymenoptera. They attack in swarms of hundreds and chase their victims much greater distances from the hive than does any other species.[54] [57] The first escapes from hives occurred in the state of São Paulo in 1957, and the "Brazilian killer bees," †Deceased.
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or "Africanized bees," have spread widely. These bees are actually hybrids between A. scutellata and European honeybee races. Cold climate seems to have stopped their southern spread in Argentina, but they have moved steadily northward at 200 to 300 miles
Figure 36-1 Representative venomous Hymenoptera: A, hornet (Vespula maculatal); B, wasp (Chlorion ichneumerea); C, yellowjacket (Vespula maculiforma); D, honeybee (Apis mellifera); E, fire ant (Solenopsis invicta); F, bumblebee (Bombus species).
per year and in October 1990 reached the southern border of the United States. By mid-1991, 103 swarms had been captured in southern Texas. Populations are established in Arizona, New Mexico, and California.[108] Future populations may eventually be distributed 865
as far east as North Carolina.[133] At least four human deaths have occurred from multiple stings. Unless the bees acquire greater resistance to winter conditions, their range will be confined to the southern third of the United States and may also be restricted by scarcity of suitable flowers in the arid Southwest. The greatest impact of Africanized bees in the United States will probably be economic, related to decreased honey production and less effective pollination of crops. The bees also present a threat to human health. Africanized bee colonies are extremely sensitive to disturbance, respond faster in greater numbers, and are up to 10 times more active in stinging than European bees. The quantity of venom per sting is slightly less in African bees, however, with no significant biochemical or allergenic difference between the venoms.[75] [83] [110] About 50 simultaneous stings can cause systemic envenomation, and an estimated 500 are necessary to cause death by direct toxicity.[53] About 350 fatal attacks have been documented worldwide, of which at least 70 occurred in Venezuela during 1977 and 1978. More than 300 bee
Figure 36-2 Worker honeybee.
Figure 36-3 A, Yellowjacket (Vespula maculiforma). B, Early nest of yellowjacket.
attacks occurred in Mexico between 1987 and 1992, with 49 fatalities.[82] A more recent account puts the fatalities at 190, with future estimates of 60 deaths per year.[108] Since Mexico and the southern United States have many feral and domestic honeybee populations, researchers thought that the aggressiveness of the African bees could be dampened by hybridization. Large numbers of male European bees were released to facilitate this, and African queens were replaced by European stock when possible. Recent studies indicate, however, that European bee populations are becoming rapidly Africanized with little reciprocal gene flow, as African females take over European hives.[43] [117] [134] Bumblebees (Bombus and related genera) are a largely holarctic group often found in quite cold environments. Small colonies usually nest just under the surface of the ground, often in mammal burrows. Some species are aggressive if disturbed, although most have mild dispositions. Sweat bees (family Halictidae) are small bees of cosmopolitan distribution. They are attracted to sweaty skin and ingest perspiration. They nest in burrows, often in clay banks. Females sting if squeezed or trapped under clothing. The sting is not very painful, but anaphylactic reactions have been reported. The allergens are immunologically unrelated to those in other bee and wasp venoms.[86] Wasps Social wasps occur throughout most of the world but are recognized as a medical problem chiefly in the United States and Europe. They often establish colonies close to human dwellings. Yellowjackets (Vespula species) may be more important than honeybees as a cause of human stings in the northeastern United States ( Figure 36-3 ). They make underground nests in rotted-out tree stumps, cavities under stones, and mammal burrows. They are strongly attracted to garbage. Paper
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wasps (Polistes) suspend their nests in shaded places, often in shrubbery near houses or below eaves, gutters, or window frames ( Figure 36-4 ). Old World hornets (Vespa species) and white-faced hornets (Dolchiovespula maculata) create large paper nests that may be plastered to buildings but more typically are hung from tree branches ( Figure 36-5 ). Solitary wasps are predators, feeding largely on other insects and spiders. Adults often carry the prey alive and paralyzed to the nest as food for the larvae. Some wasps excavate burrows, whereas others make mud nests that may be plastered on shaded walls of buildings or under bridges. Although many nests may be grouped together, the adult wasps have no social organization and make little effort to defend them. The cicada killers (Specius speciosus) and tarantula hawks (Pepsis species) are among the largest North American wasps. Velvet ants (family Mutillidae) are actually wingless wasp females that are nest parasites of other Hymenoptera ( Figure 36-6 ). They occur in deserts and other dry and open habitat and can inflict a painful sting. Ants Ants are social insects, worldwide in distribution over a wide range of habitats. Many ants sting, and others have repugnant secretions. The ant species of greatest medical significance in the United States is the imported fire ant Solenopsis invicta (see Figure 36-1, E ). It apparently was introduced from South America into Mobile, Alabama, in 1939 and has subsequently spread throughout the southern states from southeastern Virginia to central Texas and Oklahoma, largely eliminating another introduced fire ant (S. richteri) and two native species. Mound nests are usually found in open grass settings, often in urban areas ( Figure 36-7 ). Other states at risk of harboring fire ants include Arizona, California, New Mexico, Oregon, and Washington.[54] As many as 600 mounds per acre have been reported. Worker
Figure 36-4 Paper (Polistes) wasp.
colonies may reach a maximum size of 500,000 ants in 2 years and rapidly give rise to satellite colonies.[118] S. invicta is an extremely irritable insect. Harvester ants (Pogonomyrmex) of the southwestern United States and Mexico are of some medical importance.
Figure 36-5 A, White-faced hornet, Dolchiovespula maculata, largest of the common social wasps in the United States. B, Typical nest of white-faced hornet.
Figure 36-6 Velvet ant.
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Entrances to the underground nests are usually surrounded by clear zones and sometimes by rings of soil. Some species react aggressively to disturbance of the nest. The stings are painful and may be accompanied by systemic symptoms; anaphylaxis has been reported. Stinging Patterns Multiple stings often result from disturbance of a nest, as the first insects encountered release alarm pheromones that incite aggressive behavior in other members of the colony. With large species such as the white-faced hornet, 40 to 50 stings may create a life-threatening injury.[132] The lethal dose of honeybee venom has been estimated at 500 to 1400 stings.[114] In the United States and other Western nations the incidence of serious insect stings is higher in adults than in children and higher in males than in females. Most persons are stung while engaged in outdoor work or recreation. Beekeeping is a high-risk occupation; however, many beekeepers develop considerable immunity as a result of frequent stings. Other relatively high-risk occupations are farmer, house painter, carpenter, highway worker, and bulldozer operator. Fire ants may invade houses during periods of heavy rain and in hot, dry weather as they seek food and water.[23] Wasps and bees sometimes are swept into the interior of a moving automobile, exposing the occupants to risk of both a sting and a highway accident. Many foods, particularly meats, ripe fruit, or fruit syrups, attract yellowjackets; they often swarm around picnic areas and recycling bins. Syrups, flowers, sweat, and some perfumes attract bees. In such aggregations the insects are not particularly aggressive but may become trapped in clothing or hair. In temperate zones, the incidence of hymenopteran stings is highest in late summer and early fall, when insect populations are highest.[7]
Figure 36-7 Fire ant mound.
Venom and Venom Apparatus Venom is present in many hymenopteran species and is used for both defense and subjugation of prey. The venom apparatus is located at the posterior end of the abdomen and consists of venom glands, a reservoir, and structures for piercing the integument and injecting venom. Venoms of most medically important Hymenoptera are mixtures of protein or polypeptide toxins, enzymes, and pharmacologically active low-molecular-weight compounds such as histamine, serotonin, acetylcholine, and dopamine. Melittin, a strongly basic peptide, is the principal component of honeybee venom. It damages cell membranes through detergent-like action, with liberation of potassium and biogenic amines. Peptides with similar activity occur in bumblebee venom. Histamine release by bee venom appears to be largely mediated by mast cell degranulating (MCD) peptide. A third peptide, apamin, is a neurotoxin that acts principally on the spinal cord. Adolapin, a recently described bee venom peptide, has antiinflammatory activity, which may explain the effectiveness of bee venom in treating some forms of arthritis. The chief enzymes of bee venom are phospholipase A and hyaluronidase. The former is believed to be one of the major venom allergens and, with melittin, to account for much of the acute lethality. Histamine makes up about 3% of the dry weight of bee venom. The intravenous (IV) median lethal dose (LD50 ) of honeybee venom for mice is 6 mg/kg. An average sting injects about 50 µl of venom containing approximately 0.05 mg of solids. Intense pain after stings by hornets and other social wasps is largely caused by serotonin and acetylcholine, which constitute 1% to 5% of dry venom weight. Wasp kinins (peptides) contribute to pain production and have strong, brief hypotensive effects. Mastoparans are similar in action to MCD peptide but are weaker. Phospholipase A, phospholipase B, and hyaluronidase are present in relatively large amounts. Unidentified proteins, some of which appear to be major allergens, are also present. A lethal protein in Vespa basalis venom releases serotonin from tissue cells and has hemolytic and phospholipase A activity.[47] The IV LD50 of different
hornet venoms for mice ranges from 1.6 to 4.1 mg/kg. Less is known of venoms of solitary wasps. The venom of Sceliphoron caementarium, a mud dauber, is comparatively low in protein and contains no acetylcholine, histamine, serotonin, or kinins but contains several unidentified low-molecular-weight compounds. Its proteins are immunologically different from those of honeybee, yellowjacket, and paper wasp venoms. Philanthotoxin (molecular weight 435) from venom of the beewolf (Philanthus triangulum) acts at the insect's myoneural junction and has potential value as an insecticide.
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Figure 36-8 Fire ant lesions.
Ant venoms show great variation. Those of more primitive ants (subfamilies Ponerinae, Myrmicinae, and Dorylinae) resemble venoms of social wasps, containing kininlike peptides, enzymes, and unidentified proteins. In more highly evolved ants (subfamilies Dolichoderinae, and Formicinae) a variety of low-molecular-weight compounds (terpenes, ketones, and organic acids) make up the bulk of the secretion, which may be sprayed rather than injected. Venoms of fire ants (Solenopsis species) are composed largely of piperidine alkaloids, which cause histamine release and necrosis in human skin. Proteins make up only 0.1% of dry weight of fire ant venoms but are highly allergenic.[35] Hyaluronidase and phospholipase activities have been demonstrated. Clinical Aspects Hymenoptera stings are most often inflicted on the head and neck, followed by the foot, leg, hand, and arm. Stings in the mouth, pharynx, and esophagus may occur when bees or yellowjackets in soft drink or beer containers are accidentally ingested.[113] A single wasp, bee, or ant sting in a unsensitized individual usually causes instant pain, followed by a wheal and flare reaction, with variable edema. Fire ants typically grasp the skin with their mouthparts and inflict multiple stings. These produce vesicles that subsequently become sterile pustules ( Figure 36-8 ). Multiple Hymenoptera stings may cause vomiting, diarrhea, generalized edema, dyspnea, hypotension, tachycardia, and collapse. Widespread necrosis of skeletal muscle with hyperkalemia, acute tubular necrosis with renal failure, hepatorenal syndrome with hemolysis, acute pancreatitis, and disseminated intravascular coagulation have been reported after multiple stings.[19] [34] [59] [132] Myocardial infarction, atrial fibrillation, and cerebral infarction in previously healthy individuals may follow multiple hymenopteran stings.[63] [99] [130] Large local reactions spreading more than 15 cm beyond the sting site and persisting more than 24 hours are relatively common. They represent a cell-mediated (type IV) immunologic reaction, although more than half these patients also have immunoglobulin E (IgE) antibody against venom or show a positive skin test. Later stings in these individuals usually result in another large local reaction; systemic reactions are rare.[136] Allergy is the most serious aspect of hymenopteran stings. Anaphylaxis and related syndromes from this source are relatively common outdoor emergencies. An estimated 0.4% of the U.S. population shows some clinical degree of allergy to insect venoms, and 40 to 50 deaths are reported annually.[95] Fatal anaphylaxis due to fire ant stings has also been reported.[90] Asymptomatic sensitization, as shown by positive venom skin test, was observed in 15% of 269 randomly selected subjects with no history of allergic sting reaction. [41] Sensitization is transient but may persist for years. These individuals are at higher risk of systemic allergic reactions than those with negative skin tests.[40] Sudden death from insect sting may not always be recognized. Of 142 sera obtained after sudden, unexpected death, 23% contained elevated levels of IgE to at least one insect venom. In contrast, 6% of sera from 92 blood donors contained comparable IgE levels. In eight fatal cases of Hymenoptera sting anaphylaxis, IgE to the putative venom source was elevated in all, although levels were not higher than those of some healthy individuals in the same population.[112] Anti-fire ant IgE and elevated serum tryptase were detected in a case of fatal fire ant sting.[81] Elevated levels of venom-specific IgE were detected in two fatal cases of wasp sting.[124] Wasp and bee venoms contain 9 to 13 antigens, some of which are potent allergens. Available evidence indicates little cross-sensitization between honeybee and wasp venoms. About 50% cross-sensitization occurs between Polistes and other social wasp venoms, and nearly 100% between yellowjacket and hornet venoms. Positive radioallergosorbent test (RAST) reactions to imported fire ant venom were seen in 51% of patients allergic to bee and wasp venoms but without exposure to fire ants. The allergen appears to be identical to antigen 5 of wasp venoms.[48] Examination of sera of hypersensitive individuals for IgE and IgG antibodies against purified venom proteins indicates that phospholipase A, hyaluronidase, and acid phosphatase are important in honeybee venom, whereas phospholipase A, antigen 5, and hyaluronidase are important in wasp venoms. Antigen 5, a nontoxic protein of unknown activity, is reported to have sequence similarity to mammalian testis, human brain tumor, and certain plant leaf proteins. This may explain anaphylactic reactions to first insect stings.[58] [131] Despite the small amount of protein in fire
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ant venoms, about 12% of persons treated for fire ant stings show systemic allergic reactions, and 32 anaphylactic deaths have been confirmed. Four antigens in Solenopsis invicta venom have been reported to be allergenic.[12] Allergic sting reactions occur remote from the sting site and include flushing, pruritus, hives, and angioedema. In life-threatening reactions, marked respiratory distress with airway edema, hypotension, loss of consciousness, and cardiac arrhythmias may be seen. At least half the severe reactions occur within 10 minutes after a sting, and virtually all occur within 5 hours. Most fatalities occur within 1 hour. The interval between the first known sting and the reaction-producing sting is usually less than 3 years but may be as long as 48 years. In a group of 3236 Hymenoptera-allergic individuals, 61.5% were males and 32.3% had a history of atopy. The mean age was 30.5 years. No correlation existed between systemic reactions and number of stings in the past or number of stings per incident and severity of a systemic reaction.[67] In a series of 138 adults with a history of insect sting anaphylactic reactions, 99 had no anaphylactic reactions to later stings, 17 had more severe reactions, and 22 had mild to moderate reactions. [127] In another series of 90 adults with previous anaphylactic reactions, 60 had similar reactions when restung, and 23 had more severe reactions.[94] In children 10 years and younger, life-threatening reactions occur less often than in adults, and repeated sting episodes usually are not increasingly severe. However, 17% of children with a history of systemic bee or wasp sting reactions developed a systemic reaction after a sting challenge test, as did 5% of children who sustained a sting in the field.[44] Fatalities that occur within the first hour after a sting result from airway obstruction, hypotension, or both. In 69% of fatal cases, obstruction of the respiratory tree by edema or secretions was the principal finding at autopsy; in 12%, vascular pathology was the principal finding; and 7% of the victims had primary central nervous system involvement such as petechial hemorrhages, infarction, and cerebral edema.[4] Hemostatic defects, including reduction of all clotting factors and release of a thrombin inhibitor, may be seen with insect sting anaphylaxis. Severe fetal brain damage, presumably associated with hypoxia, has been reported. Delayed (3 to 14 days) atypical reactions after hymenopteran stings include serum sickness and Arthus reaction, which are caused by systemic and local effects of antigen-antibody complexes; nephrotic syndrome; thrombocytopenic purpura; grand mal and focal motor seizures; transient cerebral ischemic attacks; Guillain-Barré syndrome; and progressive demyelinating neurologic disease. Most appear to be immunologically mediated. In one series, elevated IgE to bee or yellowjacket venom was observed in 6 of 13 such patients.[64] [74] Identification of the individual with potentially dangerous allergy to hymenopteran sting is not always possible. Skin testing with hymenopteran venoms is the most sensitive method; RAST for IgE antibody to venoms is less sensitive. [59] A small but significant number of individuals with no history of sting reactions have IgE antibody specific for hymenopteran venoms; prevalence of this antibody is higher in summer.[139] These methods do not identify all at risk, and antibody levels do not correlate with severity of sting reactions. In a significant number of individuals, particularly children, clinical sensitivity disappears and IgE levels fall virtually to zero 3 to 18 months after a reaction-producing sting. In about 40% of cases, sensitivity may disappear within 3 years.[62] Venom antibody (both IgE and IgG) may be found in healthy individuals (40% of beekeepers, 12% of blood donors) with no history of systemic reaction to insect stings. Treatment and Prevention Treatment of anaphylaxis is conventional. Aqueous epinephrine 1:1000 should be administered subcutaneously at the first indication of serious hypersensitivity. The dose for adults is 0.3 to 0.5 ml and for children under age 12 is 0.01 ml/kg, not to exceed 0.3 ml. When symptoms are predominantly respiratory, epinephrine by
inhalation (10 to 20 puffs for an adult; 2 to 4 puffs per 10-kg body weight for a child) may provide more rapid relief.[79] In the presence of profound hypotension, 2 to 5 ml of 1:10,000 epinephrine solution may be given by slow IV push, or an infusion may be initiated by mixing 1 mg in 250 ml and infusing at a rate of 0.25 to 1 ml/min. Selective inhaled (nebulized) ß2 -adrenergic agents, such as albuterol, can also be effective in relieving bronchospasm at doses of 2.5 mg/3 ml of a 0.08% solution. Aminophylline, 5 mg/kg as a loading dose followed by 0.9 mg/kg/hr as an infusion, may relieve bronchospasm not relieved by epinephrine or albuterol. In the presence of hypotension, IV crystalloid solutions should be infused; pressor agents such as dopamine may be required. The military antishock trousers (MAST) garment may be helpful if rapid correction of decreased lower extremity peripheral resistance is desired. Oxygen, intubation, and mechanical ventilation may be needed to correct airway obstruction. Antihistamines and corticosteroids are also indicated in acute anaphylactic reactions, although the time of onset with corticosteroids is delayed. Propranolol is contraindicated because of the ß-adrenergic blockade effect on the bronchioles. Persons taking ß-adrenergic blockers may respond poorly to epinephrine. Those with insect sting anaphylaxis require close observation, preferably in the hospital, for about 24 hours.[79] For mild hymenopteran stings, ice packs often provide relief. Honeybees frequently and yellowjackets occasionally leave a stinger in the wound. Although recommendations
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were that stingers should be scraped or brushed off with a sharp edge and not removed with forceps, which might squeeze the attached venom sac and worsen the injury, recent literature has refuted this. [129] Advice to victims on the immediate treatment of bee stings now emphasizes rapid removal by whatever method.[129] Wheal size and degree of envenomation increased as the time from stinging to stinger removal increased, even for a few seconds. The response was the same whether stings were scraped or pinched off after 2 seconds. Home remedies, such as baking soda paste or meat tenderizer applied locally to stings, are of dubious value, although the latter is often regarded as effective. Topical anesthetics in commercial "sting sticks" are also of little value. Local application of antihistamine lotions or creams such as tripelennamine may be helpful. An oral antihistamine such as diphenhydramine, 25 to 50 mg for adults and 1 mg/kg for children, every 6 hours is often effective. No therapy is effective against local effects of fire ant stings, although oral antihistamines and corticosteroids may provide some relief in severe cases. Since infection is common, topical antimicrobials (e.g., mupirocin) and prophylactic oral antibiotics are recommended. Breaking fire ant blisters should be avoided.[18] [22] Corticosteroids such as methylprednisolone, 24 mg/day initial dose tapered off over 4 to 5 days, often help resolve extensive local reactions to bee and wasp stings. This may be combined with cold packs and oral antihistamines. Envenomation from multiple hymenopteran stings may require more aggressive therapy. IV calcium gluconate (5 to 10 ml of 10% solution) with a parenteral antihistamine and corticosteroid may be helpful in relieving pain, swelling, nausea, and vomiting. Development of a hyperimmune bee venom antiserum is under investigation. [109] Hypovolemic shock is managed conventionally. Plasmapheresis was used successfully to treat a person who sustained about 2000 honeybee stings.[25] Patients should be observed for 12 to 24 hours for coagulopathy and evidence of renal and neurologic damage. Urine output is monitored and urine tested for hemoglobin and myoglobin. Serum potassium, creatine kinase, and lactate dehydrogenase levels should be monitored. Oliguria with myoglobinuria, azotemia, and hyperkalemia are indications that hemodialysis may become necessary. Immunotherapy.
Desensitization with purified venoms produces an excellent blocking antibody response and prevents anaphylaxis in more than 95% of patients. A protective antiidiotypic antibody to honeybee venom has been identified.[56] Venoms for desensitization generally available in the United States are honeybee, yellowjacket, wasp (Polistes), and mixed vespid. A whole body extract of fire ant containing at least three venom antigens is also available. No firm guidelines are available for selecting patients to receive immunotherapy. Skin test results and IgE levels in RAST tests are not reliable. Any adult with a history of systemic allergic reactions should be considered for immunotherapy. Persons receiving ß-adrenergic blockers should be shifted to other appropriate medications if possible. Children under 16 with only cutaneous or mild systemic allergic reactions and persons with a history of only large local reactions do not need immunotherapy.[126] Evaluation of anaphylactic risk is recommended in children using wasp venom extract challenges.[107] Regimens for desensitization attempt to achieve tolerance to venom doses of about 100 µg. A maintenance level of immunity requires about 95 days to achieve. Rapid programs requiring 3 to 7 days for initial immunization appear to be effective.[5] [27] Some programs make use of both active and passive immunotherapy.[78] In a series of 1410 patients, 12% had systemic reactions during treatment; no fatalities were reported.[66] [68] Experience of 26 women with 43 pregnancies does not suggest significant increased risk from venom immunotherapy during pregnancy.[111] Maintenance doses are required at intervals after basic immunization. Neither skin testing nor determination of IgG and IgE antibody levels against venom will reliably indicate success of immunization, although the majority of persons will be protected by a specific IgG antibody level of 400 RAST units/ml of serum.[125] Actual sting challenge is the most reliable test for determining immunotherapy candidates and desensitization[128] but is not widely used in the United States. It must be done in the hospital with careful monitoring and consideration of economic, ethical, and safety factors.[103] If the skin test is negative after 3 years of immunotherapy, patients may be placed on immunologic surveillance. Few patients require more than 5 years of immunotherapy. [95] For unknown reasons, desensitization to wasp venoms is achieved more quickly than to honeybee venom.[8] Antivenom Therapy.
Recently a group in the United Kingdom developed an ovine Fab-based antivenin as a potential treatment for mass bee stings. Sera from sheep immunized against the venom of Apris mellifera scutellata contained high levels of specific antibodies, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and chromatography. Although effective experimentally in a mouse model, no human administration of the antivenin has been documented.[53] Preparedness and Preventive Measures.
Persons with a history of allergic reactions to insect stings (including large local reactions) should carry an emergency kit containing epinephrine and should wear medical identification tags. Kits should be available in work or recreation areas where the risk of insect sting is
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Figure 36-9 EpiPen preloaded delivery system for injection of aqueous epinephrine.
high. Two kits widely available in the United States are EpiPen ( Figure 36-9 ) and Ana-Kit. EpiPen and EpiPen Jr. are autoinjectors that deliver 0.3 mg or 0.15 mg of epinephrine, respectively. They are quick and easy to use; however, patients should be cautioned against injecting the material into fingers or buttocks or directly over veins. Ana-Kit contains two doses of 0.3 mg of epinephrine in a single conventional syringe, plus chewable antihistamine tablets and a tourniquet. It is more versatile but requires more instruction for the user. Frequent cleaning of garbage cans and disposal of decaying fruit will make premises less attractive to bees and wasps. Hymenopterans are highly susceptible to many insecticides, and their control around dwellings and other inhabited buildings is rarely difficult. Spraying the nests after dark is safer. Many hymenopterans are economically valuable as pollinators of plants or predators on other insects, so their control on a wide scale is rarely desirable. The fire ant in the southern United States has been the target of massive but marginally effective control campaigns that adversely affected local ecosystems. A new approach uses grain baits containing synthetic insect growth hormones that are carried into the nests, where they disrupt ant caste differentiation and inhibit egg production. Arrays of thousands of hormone-baited traps placed in selected areas of Mexico, however, failed to stop the northward spread of Africanized bees.
LEPIDOPTERA Venomous Species and Venoms Insects of the order Lepidoptera typically cause human envenomation, but effects generally are less serious than with hymenopterans. Injury usually follows contact with caterpillars, occurring less frequently with the cocoon or adult stage. The larval lepidopteran (caterpillar) is usually free living, is moderately active, and
Figure 36-10 Puss caterpillar, Megalopyge opercularis.
feeds on plants, although a few are parasites of insect nests or eat food of animal origin. The pupal stage may be free or encased in a silk cocoon. Wintering over in cold climates is usually in the pupal stage. Adults (butterflies and moths) have wings with microscopic chitinous scales. They primarily feed on nectar and other plant juices, but some eat semiliquid mammalian feces and urine. The adult provides no care or protection of immature stages. No social organization exists, although larvae and adults of some species assemble in large aggregations. Venomous species occur in about 16 families of Lepidoptera, with no general rules for recognition. Many venomous caterpillars are broad, flat, and sluggish. Some have the dorsal surface densely covered with long hairs. Others are spiny and may have bright, conspicuous colors and markings. Some are highly camouflaged. Venoms in Lepidoptera are purely defensive. The venom apparatus consists of spines that are simple or branched and frequently barbed. They may be scattered widely over the surface of the insect or arranged in clumps and often are intermixed with nonveniferous hairs or spines. In the most venomous caterpillars the spines are hollow and brittle with venom glands at the bases. Muscles surrounding the glands may help in expelling venom. In other Lepidoptera the spines are solid and function primarily as mechanical irritants or contain surface toxicants. Little is known of the chemistry of caterpillar venoms. Some are heat labile and contain proteins. Histamine and serotonin have been found in caterpillar venoms but are not common. Hairs of the brown-tailed moth (Euproctis chrysorrhea) contain enzymes with esterase and phospholipase activity. Probably the most important venomous caterpillar in the United States is the puss caterpillar ( Figure 36-10 ) or woolly slug (Megalopyge opercularis), which occurs in the southern states west through most of Texas
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and north to Maryland and Missouri. This hairy, flat, and ovoid caterpillar reaches a length of 30 to 35 mm and feeds on shade trees, including elm, oak, and sycamore. Some years it may be plentiful enough to be a nuisance. In southeast Texas in 1958, 2130 persons were treated for stings, with eight hospitalized. A related species, the flannel moth caterpillar (M. crispata), occurs in the eastern states north to New England. Its sting is less severe than that of M. opercularis. The large, spiny caterpillar of the io moth (Automeris io) is pale green with red and white lateral stripes ( Figure 36-11 ). It is widely distributed in the eastern United States but rarely plentiful. The saddleback caterpillar (Sibine stimula) and oak slug (Euclea delphinii) are flat and almost rectangular; both can deliver a painful injury. The gypsy moth (Lymantria dispar) feeds on a variety of plants and has caused thousands of cases of dermatitis in the northeastern United States. Other common nettling caterpillars are E. chrysorrhea, which also occurs in Europe, and the tussock or toothbrush caterpillar (Hemerocampa leucostigma), with its conspicuous red head and four tufts of bristles. Another tussock caterpillar, Oryia pseudotsuga, causes numerous cases of dermatitis and conjunctivitis among lumber-workers and foresters in the northwestern states. Stinging Patterns Caterpillar envenomation usually occurs when living insects are touched as they cling to vegetation or drop onto bare skin. Persons cutting branches, picking fruit, or climbing trees are likely to be stung. However, the largest outbreaks have been associated with spines detached from live or dead caterpillars and cocoons. These may be airborne or deposited on bedding or laundry hung outdoors. In temperate regions, caterpillar stings are most common from August to early November. Heavy caterpillar infestations seem to occur during exceptionally favorable weather and with decreases in populations of parasites and predators that serve as natural controls.
Figure 36-11 Caterpillar of the io moth, Automeris io. Widespread in the eastern United States, this species can inflict a painful sting.
Clinical Aspects Two general syndromes are associated with lepidopteran envenomations. In the case of caterpillars with hollow spines and basal venom glands (e.g., Automeris, Megalopyge, and Dirphia), direct contact with the live insect causes instant nettling pain, followed by redness and swelling ( Figure 36-12 ). Puss caterpillar stings show a characteristic gridiron pattern of hemorrhagic pinpoint papules. In typical cases, no systemic manifestations occur, and symptoms usually subside within 24 hours. However, pain may be intense with central radiation, accompanied by urticaria, nausea, headache, fever, vomiting, and lymphadenopathy. Hypotension, shock, dyspnea, abdominal tenderness, and convulsions have been reported with puss caterpillar stings. [37] [49] The second syndrome is associated with caterpillars with a less highly developed venom apparatus (e.g., Lymantria, Euproctis, Thaumetopoea). Contact with the living insect is not necessary; detached spines are often involved. Little or no immediate discomfort is experienced. An itching, erythematous, papular, or urticarial rash develops within a few hours to 2 days and persists for up to a week. Rarely the lesions may be bullous. Conjunctivitis, upper respiratory tract irritation, and rare asthmalike symptoms may be seen with or without dermatitis. Ophthalmia serious enough to require enucleation may be caused by detached spines lodged in the eye. Acute anaphylactic reactions have not been reported to follow lepidopteran stings. Patch testing has demonstrated both immediate and delayed hypersensitivity. Treatment and Prevention Treatment of lepidopteran envenomations is symptomatic. Prompt application and stripping of adhesive tape or a commercial facial peel at the site of the sting may remove many spines and serve as a diagnostic
Figure 36-12 Nettle rash from unidentified caterpillar.
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procedure, since the spines can be identified by microscopy. Patients with local symptoms usually obtain relief from group I corticosteroid creams and ointments. Over-the-counter preparations containing corticosteroids and antihistamines are not significantly better than simpler preparations such as calamine lotion with phenol. Oral antihistamines such as fexofenadine (60 mg 2 times a day) or antiinflammatory drugs such as tolmetin sodium (400 mg three times a day) are often effective in more severe cases. Occasionally, codeine (30 to 50 mg), meperidine (50 mg), or oxymorphone (1.5 mg) in combination with an antiemetic may be needed to control pain and vomiting. IV calcium gluconate has been used successfully in severe puss caterpillar envenomation. [84] [89] Trees on which caterpillars feed may be sprayed with appropriate insecticides to control species such as the puss caterpillar. Near Shanghai, where chemical insecticides would have been harmful to silkworm culture, Euproctis caterpillars were controlled by spraying with an insect virus. Screens on windows and doors protect against moths with toxic spines.
HEMIPTERA (SUCKING BUGS) The Hemiptera comprise a large order of insects characterized by sucking mouthparts, generally in the form of a beak, and a life cycle with no well-demarcated larval and pupal stages but a gradual transition from the hatchling nymph to adult. Most hemipterans are winged as adults, with the anterior wings generally divided into a chitinized and membranous section. Most feed on plant juices, but several families are predators, and two feed on the blood of humans and other vertebrates. The assassin bugs (family Reduviidae) are generally recognizable by the long and narrow head, a stout and three-jointed beak, long antennae, and typical hemipteran
Figure 36-13 Wheel bug, Arilus cristatus, a large assassin bug common in the eastern United States.
wings ( Figure 36-13 ). Most are of a dark color; a few are brightly marked or have a checkerboard pattern along the posterior edge of the abdomen. Some species attach fragments of their prey, sand grains, or other debris to their backs. Reduviidae occur on all continents. They have a variety of habitats and are often nocturnal. The triatomids (e.g., kissing bugs, flying bedbugs, Mexican bedbugs, barberos) are a subfamily of the Reduviidae adapted for feeding on blood. They feed on a wide range of mammals and often live in the nests or burrows of their hosts. Armadilloes, dogs, opossums, and pack rats are common hosts in the southern United States and Mexico. Some triatomids adapt readily to life in human dwellings, particularly those of adobe construction. Triatomids are primarily a neotropical group, with species ranging northward in the United States to Utah and southern Indiana. Triatoma protracta and T. sanguisuga are among the better-known species. The family Cimicidae, or bedbugs, are flat, ovoid, and reddish brown insects whose wings are reduced to a pair of functionless pads. Lack of large terminal claws distinguishes them from lice. Bedbugs are cosmopolitan in distribution. Two species, Cimex lectularius and C. hemipterus, feed primarily on humans and live in dwellings, where they hide in bedding, under wallpaper, behind baseboards, and in window frames. Homes of poorer persons are more likely to be heavily infested, but the insects may be carried into well-kept residences, hospitals, and hotels. Other species of Cimex, normally parasitic on bats and swallows, occasionally attack humans. Venomous aquatic Hemiptera include the giant water bugs (family Belostomatidae) ( Figure 36-14 ), back swimmers (family Notonectidae), and water scorpions (family Nepidae). Water bugs are distinguished from aquatic beetles by their beak and hemipteran wings; back swimmers have greatly elongated hind legs; and
Figure 36-14 Giant water bug, Benacus griseus, a large insect common in aquatic habitats in the eastern United States.
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water scorpions have a slender body with long, terminal breathing tubes. These insects are widely distributed in freshwater habitats. The hemipteran venom apparatus consists of two or three pairs of glands in the thorax. Secretions are ejected through half of a double tube formed by the interlocking of the elongated maxillae and mandibles, which have distal tips modified for piercing. Few hemipteran venoms have been studied. Venoms of two reduviids, Platymeris rhadamanthus of Africa and Holotrichus innesi of the Middle East, contain several enzymes and nonenzymatic proteins. [28] [138] Sialase, an enzyme unusual in invertebrates, is found in Triatoma venom; it has anticoagulant activity.[1] Venom serves primarily for subjugation and probably digestion of prey, but the insects may defend themselves by biting. Salivary secretions of blood-sucking hemipterans also contain potent allergens. Clinical Aspects Triatomids usually bite at night on exposed parts of the body. Feeding may last from 3 to 30 minutes. Bites are painless. On initial exposure there is usually no reaction. Repeated bites are followed by reddish, itching papules that may persist for up to a week. Bites are often grouped in a cluster or line ( Figure 36-15 ) and may be accompanied by giant urticarial wheals, lymphadenopathy, hemorrhagic bullae, fever, and lymphocytosis. Systemic anaphylactoid reactions with respiratory or gastrointestinal manifestations may occur.[50] [71] Entomologists and small children are most frequently bitten by assassin bugs, since handling induces the insect to bite. Bites of several U.S. species, such as the wheel bug (Arilus cristatus), black corsair (Melanolestes picipes), and masked bedbug hunter (Reduvius personatus), are described as painful as the sting of a hornet and accompanied by local swelling lasting several hours. Bedbug bites usually raise a pruritic wheal with central hemorrhagic punctum, followed by a reddish
Figure 36-15 Triatomid feeding pattern.
papule that persists for several days. Bullae, generalized urticaria, arthralgia, asthma, and anaphylactic shock are rare sequelae of bedbug bites. Bites by aquatic Hemiptera are similar to those of assassin bugs, but few cases have been described in detail. Treatment and Prevention Treatment is symptomatic and not particularly effective. Various antipruritic preparations are helpful in mild cases. Topical or intralesional steroids have generally been disappointing. Immobilization, elevation, and local heat are helpful in severe limb bites. Desensitization with triatomid salivary gland extract has been effective in a small series of patients with history of life-threatening anaphylactic reactions.[101] Triatomids and bedbugs are more difficult to eradicate with insecticides than are many household insects. Benzene hexachloride has been effective against triatomids in Latin America.
BEETLES AND OTHER INSECTS Beetles (order Coleoptera) are the largest group of insects, with at least 250,000 species. The prothorax of beetles is generally very distinct, whereas the two posterior thoracic segments are more or less fused to the abdomen. In most beetles the anterior wings are heavily chitinized, acting as covers for the posterior membranous wings used in flight. Mouthparts are of the chewing type. The life cycle involves larval and pupal stages before emergence of the adult. Many beetles feed on plants throughout their life cycle, many are predators or scavengers, and a few are parasitic. No beetles have a bite or sting venomous to humans, but several families have toxic secretions that may be deposited on the skin. The blister beetles (family Meloidae) are a cosmopolitan group with numerous representatives in deserts and semiarid regions. A species may suddenly appear by the thousands, especially after rains, persist for a few days, and be replaced by another. The majority are of medium size (about 15 mm) and have soft, leathery forewings (elytra). Some are brilliantly colored. They are plentiful on vegetation, and some species are attracted to lights. A low-molecular-weight toxin, cantharidin, is present in the hemolymph and most of the insect's tissues. It is exuded from multiple sites if the beetle is gently pressed or otherwise disturbed. In the eastern United States, blister beetle dermatitis is usually caused by Epicauta species, which occur on many garden plants. Contact with the beetle is painless and seldom remembered by the victim. Blisters appear 2 to 5 hours after contact and may be single or multiple, usually 5 to 50 mm in diameter and thin walled. Unless broken and rubbed, they are not painful. Cantharidin nephritis has been reported after unusually heavy vesication
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but more frequently is the result of using a cantharidin preparation as an aphrodisiac. Darkling ground beetles are moderately large, dark, and heavily chitinized insects that assume a characteristic posture with head down and tail up when disturbed. They are found worldwide in arid regions, where they live under stones and other cover and crawl about at night. Most species can spray irritant secretions, mostly benzoquinones, from the tip of the abdomen to a distance of 30 to 40 cm. These secretions are generally harmless to humans, but blistering of the skin has been reported, and eye injury is possible. No special treatment for beetle vesication is available. The injuries are best treated as superficial chemical burns. Local preparations containing corticosteroids or antihistamines are not particularly effective. Other types of insect envenomation are sporadic. Many insects that normally feed on plant juices occasionally inflict annoying bites. This behavior may be initiated by dehydration of the insect or by unknown factors. Small predatory insects, such as lacewing larvae, anthocorids, and Sclerodermus species, occasionally attack humans instead of their normal arthropod prey. Thrips may bite and produce itching macules.[80] A small hemipteran, Leptodemus minutus, caused numerous cases of dermatitis in Kuwait.[105] The stick insect, Anisomorpha buprestoides, a common species in Florida and adjacent states, ejects a noxious fluid from its thoracic region that deters birds and other predators. According to regional folklore, this fluid can be directed toward human eyes with painful consequences. Recently, an outbreak of a blistering disease was reported in a military unit training in the Arizona desert during an unusual heavy rainfall and flooding. Staphylinid (rove) beetles (genus Paederus, family Stapylinidae) were collected at the site. These beetles have been responsible for vesicular dermatitis in other parts of the world but were never reported in the United States before this series.[17]
DIPTERA (TWO-WINGED FLIES) Insects of the order Diptera are characterized by one pair of wings. The second pair is usually modified to form a pair of drumsticklike structures known as halteres. A typical life cycle consists of eggs, limbless larvae, pupae, and winged adults, but numerous variations exist. Mouthparts are of the sucking type. Females of many species, although free living, take blood or other tissue fluids from vertebrates, injecting salivary secretions that are not intrinsically toxic but are potent sensitizing agents for most humans. Larvae of some Diptera are human parasites. Other adult Diptera feed indiscriminately on feces and human foodstuffs. These habits make them by far the most important arthropod vectors of human disease ( Table 36-1 ). Most of these insects are cosmopolitan in distribution, except tsetse flies, which are restricted to Africa, and tropical and subtropical sand flies. Some species of mosquitoes and blackflies are adapted to cold temperate, sub-Arctic, and alpine environments, where their numbers may make areas uninhabitable during peak activity. Other mosquitoes and biting midges are equally abundant and annoying in some coastal areas and on islands. Mosquitoes are characterized by a fringe of setae along the posterior margin of the wings and delicate scales along the wing veins. Only the female feeds on blood. Her prominent beak contains a kit of piercing and sucking tools. Most mosquitoes have body lengths of 3 to 4 mm, but some large species may be about twice this size (see Table 36-1 ). The estimated 3000 species of mosquitoes are cosmopolitan in distribution. Carbon dioxide, body heat, and sweat gland secretions, especially apocrine, are attractants for mosquitoes; certain skin lipids are repellent.[55] Children under 1 year of age rarely show a skin reaction to mosquito bites, but by age 5 nearly all are reactors. Both immediate and delayed types of hypersensitivity are induced. Typically, immediate pruritic wheals are followed by red, swollen, and pruritic lesions in 12 to 24 hours. These lesions are associated with both IgE and IgG antibody complexes and a lymphocyte response.[87] [96] All the classic types of immunologic injury have been reported after mosquito bites, including injury from circulating immune complexes, asthma, and Arthus reaction.[38] [46] [120] Seasonal bullous eruptions in a coastal area of Britain were ascribed to Aedes detritus. Most of those affected were women with varicose veins or deep venous thromboses. Intense skin reactions accompanied by fever, lymphadenopathy, and hepatosplenomegaly have been described and are associated with infiltration of skin lesions by natural killer lymphocytes.[123] Nodular skin lesions lasting up to a month have been reported after mosquito bites in patients with acquired immunodeficiency syndrome (AIDS) receiving zidovudine.[26] Papulovesicular lesions with eosinophil infiltration were reported following insect (including mosquito) bites in patients with lymphocytic leukemia.[21] Among 21 Japanese patients with severe local and constitutional reactions to mosquito bites, seven died of malignant histiocytosis before age 28. Nine others retained hypersensitivity; three lost it.[46] Treatment of mosquito bites consists of local application of antipruritic lotions or creams. Antihistamines relieve the itching of early lesions but have no effect on later ones.[97] Group I corticosteroid creams and ointments may be helpful. Desensitization with insect whole body extract is difficult but occasionally successful.[72] Prolonged heavy exposure to mosquito bites
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TABLE 36-1 -- Major Groups of Biting Dipterans INSECT
RECOGNITION FEATURES OF ADULT
LARVAL AND PUPAL STAGES
Mosquitoes (Culicidae, subfamily Culicinae)
Prominent proboscis; wings with scales; palps of female much shorter than proboscis; usually rests with body parallel to substrate
Aquatic in great variety of habitats; both larval and pupal stages motile
Mosquitoes (subfamily Anophelinae) Prominent proboscis; wings with scales and often with dark mottling; palps of Same as above females about as long as proboscis; usually rests with head down and body held at an angle to substrate Blackflies, buffalo gnats (family Simuliidae)
Stout; humpbacked; short antennae; wings broad with most of veins faint; body length >2.5 mm
Sessile in flowing water; usually attached to rocks and logs, sometimes to crustaceans
Sand flies (family Psychodidae)
Small (usually >2 mm body length); hairy; wings with straight, prominent veins
In damp crevices, animal burrows, leaf litter
Biting midges, sand flies, no-see-ums (family Ceratopogonidae)
Small (>2 mm body length); wings often mottled; most of wing veins faint
In mud, wet sand, rotting vegetation, larvae very motile
Horseflies, deerflies (family Tabanidae)
Large (5–25 mm body length) with large eyes; usually brilliantly colored; body stout; In mud or shallow water wings with prominent veins
Stable flies (family Muscidae)
Similar to housefly in size and general appearance; sharp-pointed proboscis projects downward and backward
In decaying vegetable matter or urine-soaked straw
Tsetse flies (family Glossinidae)
Large (6–14 mm); proboscis projects forward; wings fold scissorlike over back
Larvae complete most of development in female; pupate in soil a few hours after birth
Snipe flies (family Rhagionidae)
Long legs; relatively slender body; large eyes; wings with prominent veins
Aquatic, in moist soil or rotten wood
causes some individuals to lose sensitivity, occasionally in less than 1 year. Delayed hypersensitivity is lost more readily than immediate hypersensitivity; with decreases in both IgE and IgG[88] (see Chapter 32 ). Biting Midges (Culicoides) Biting midges are very small flies that have a bite out of proportion to their size. Only females feed on blood. The wormlike aquatic larvae usually develop in water-saturated soil; mangrove swamps are a common habitat. Larvae of some species use axils of banana and similar plants. The genus is cosmopolitan but presents the greatest problem in subtropical and tropical coastal regions. Activity is often seasonal. The flies bite most intensely in still air and reduced light. Bites are immediately painful and result in raised, red, and pruritic lesions that persist from a few hours to a week or more. Some victims develop vesicles, pustules, and superficial ulcers, particularly if bitten by the genus Leptoconops. Hypersensitivity is involved, although some persons seem to develop intense reactions on first exposure to the insects. Treatment of bites is symptomatic and similar to that for mosquito bites. Artificial hyposensitization has not been successful; however, spontaneous decrease in skin reactivity may occur in some individuals (see Chapter 32 ). Blackflies (Simuliidae) Blackflies are small stocky flies that have a characteristic humpbacked appearance. Adults prefer open and sunny areas and are good fliers. Not all species are anthropophilic. The sessile larvae and pupae are found in flowing water, from large rivers to small brooks. Blackflies are cosmopolitan, but their abundance and medical significance vary widely. They range well into the Arctic and constitute a major problem for both humans and domestic animals in parts of Europe, Canada, and the northern United States. In the tropics they tend to be more localized, often remaining close to streams.
Blackfly bites are more common on the upper half of the body. They snip the skin and suck the pooled blood, leaving relatively large punctures that may bleed, a symptom rarely seen with bites of other small flies. The local pain, swelling, and redness that follow blackfly bites are unusually intense and persistent. Vesicles and weeping, crusted lesions may last for weeks. Systemic symptoms such as malaise, fever, and leukocytosis may occur. Enlarged indurated lymphatics, particularly in the posterior cervical region, are common in Canadian
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children living where blackflies are abundant. Hemorrhagic symptoms have been reported in Brazil. Generalized urticaria, bleeding, angioedema, cough, wheezing, toxemia, and even death may occur.[51] [60] [135] No specific treatment for blackfly bites is available. Hyposensitization has been attempted with little success. Neither repellents nor ordinary clothes provide satisfactory protection against blackflies when they are present in large numbers. Avoidance of heavily infested areas during fly season is often the most practical solution. Control measures have not proved highly effective (see Chapter 32 ). Horseflies and Deerflies (Tabanidae) Horseflies and deerflies are medium to large (10 to 25 mm body length) stocky flies whose large eyes often are brightly colored. They are strong fliers and prefer open and sunny habitats. The tabanids attack a variety of large mammals, including humans. The predacious maggotlike larvae live in water-soaked soil or shallow water. Bites from these large flies, predominantly the deerfly (Chrysops species), are painful and may cause both external and subcutaneous bleeding. An itching wheal up to 1 inch in diameter develops but usually does not last long. In some victims, severe and prolonged swelling of the face or an extremity develops. About 30 cases of systemic anaphylactoid reactions have been reported. One man with a history of systemic reactions to wasp stings had a similar reaction to a horsefly bite.[36] [45] As with other fly bites, treatment is symptomatic. Hyposensitization has been attempted in a few cases, apparently with some success (see Chapter 32 ). Other Biting Diptera Snipe flies (Rhagionidae) primarily prey on insects, but some species, such as Symphoromyia, feed on the blood of mammals. Their habits and life history are similar to those of tabanids. Reactions to snipe fly bites range from pain to anaphylaxis. A person who reacts severely may be bedridden for days. The stable fly (Stomoxys calcitrans) is related to the housefly, which it closely resembles. It is plentiful throughout most of the United States, particularly in agricultural districts. Eggs are deposited in piles of decaying vegetation, where the larvae develop. Thunderstorms seem to stimulate fly activity, which accounts for the widespread belief that houseflies bite just before a storm. Bites cause a sharp, stinging sensation, but dermal lesions are uncommon. Itching is brief. Louse flies (Hippoboscidae) are peculiar Diptera that may lack wings entirely or have them for only part of their adult life. The wingless forms are flat, leathery insects that resemble lice or ticks. They are ectoparasites of birds and mammals. Larvae are carried in the uterus until development is almost complete; the pupal stage may be spent in the soil or on the host. The sheep ked (Melophagus ovinus) is a common species in the United States and sometimes bites sheep shearers and handlers. The related deer ked (Lipoptena cervi) is a seasonal pest in wooded sections of northern Europe, causing hundreds of cases of dermatitis annually. The pigeon fly (Pseudolynchia canariensis) is an avian parasite that sometimes infests buildings and bites the occupants. Lesions from hippoboscid bites appear 1 to 24 hours after the bites as reddish itching papules that may persist for up to 3 months. Topical corticosteroids may afford symptomatic relief and hasten resolution of the lesions. Repellents are reported to be ineffective against these insects (see Chapter 32 ). Myiasis The term myiasis for parasitism by fly larvae was introduced into the medical literature in 1840, although the condition has been observed since antiquity. More than a hundred species of Diptera have been reported to cause human myiasis.[77] Some are obligate parasites for which humans are one of several hosts; some are opportunistic invaders that find parasitism an alternative to feeding on decaying tissue or its products. Nevertheless, humans are not a particularly good host for most species of fly larvae, and many infections terminate prematurely. Sensitization of host tissues to fly larvae does not occur as readily as with many other arthropod and helminth parasites. Myiasis may be classified by clinical manifestations or etiologic agents; neither method is totally satisfactory. This chapter discusses only dermal and wound myiasis. Myiasis primarily involving the gastrointestinal tract, urinary tract, eye, and nasopharynx is not covered. Furuncular Myiasis.
In furuncular myiasis the fly larva penetrates the skin but remains sedentary, producing a boil-like lesion that usually has a central opening. Here the larva completes its development but typically emerges to pupate outside the host. As a human problem, this form of myiasis is largely confined to the tropics, although imported cases are being recognized in increasing numbers in other regions of the world (see Chapter 37 ). Autochthonous furuncular myiasis may occur in the United States, usually in children. Most cases are caused by larvae of botflies of the genus Cuterebra, whose normal hosts are small rodents and rabbits. The fly eggs are attached to low vegetation and hatch on contact with skin of the host. Adult human skin seems impervious to them, but that of children may be penetrated. There is usually a history of outdoor play in weeds or grass or with a pet rabbit, but in one case, eggs apparently were deposited directly on the skin.[39] Lesions typically develop on the head, neck, or chest in
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1 or 2 weeks. Once recognized, the larvae can often be removed by simple pressure. [91] [116] The syndrome may also be caused by larvae of Wohlfahrtia vigil, a large fly native to Canada and the northern United States. Its normal hosts are newborn mammals, particularly mink, dog, and fox. The fly deposits larvae on the skin, which penetrates in about an hour. Human infections are typically in infants under 9 months, and the furuncular lesions are usually on the face. Fever, irritability, and loss of appetite are common. Larvae can usually be expressed from the lesion; surgery rarely is necessary. Netting over the crib or pram when outdoors usually affords protection. Migratory Myiasis.
One type of migratory myiasis is caused by flies of the genus Hypoderma. Adult flies are large and hairy, resembling bumblebees. Normal hosts for the parasitic larvae are cattle, deer, and horses. The flies attach their eggs to hairs. Hatchling larvae penetrate the skin and wander extensively through the subcutaneous tissues, eventually locating under the skin of the back, where they produce furuncular lesions. The condition has veterinary importance. Humans are abnormal hosts in which the parasite is unable to complete its development. Human infections usually occur in rural areas where cattle and horses are raised and are more common in winter. Larvae migrate rapidly (as much as 1 cm/hr) and erratically through subcutaneous tissues, producing intermittent, painful swellings over months. The person often senses larval movement. Larvae respond negatively to gravity, so the last lesions are usually on the head or shoulders. Eosinophilia (up to 35% eosinophils on white blood cell differential) and angioedema may be seen. Larvae may emerge spontaneously from furuncles or may die in the tissues. In rare cases, larvae invaded the pharyngeal region, orbit, and spinal canal. Another form of migratory myiasis is caused by larvae of Gastrophilus, which normally are gastrointestinal or nasal parasites of horses ( Figure 36-16 ). In human infections, which are reported more frequently from Europe than from the United States, the young larvae burrow in the skin, producing narrow, tortuous, reddish, and linear lesions with intense itching. Lesions usually advance 1.5 cm/day, but more rapid progress has been reported. Death of the larvae terminates the infection in 1 or 2 weeks without sequelae. This infection is clinically similar to creeping eruption, an invasion of the skin by larvae of the hookworms Ancylostoma braziliense and A. caninum. The helminthic parasitosis occurs more often in warm, moist regions, including the southern United States, and is associated with dogs and cats. The myiasis is seen more frequently in cooler regions and is associated with horses. Definitive diagnosis can be made only by removal of the parasite from its burrow and microscopic examination.
Figure 36-16 Larvae of the botfly Gastrophilus haemorrhoidalis from a horse's stomach.
Removal of the larvae by surgery or expression is the usual treatment for migratory myiasis, although local freezing of cutaneous burrows is sometimes successful. Ivermictin given to a patient with Hypoderma myiasis resulted in expulsion of the larva.[52] The most effective prevention is control of the infections in domestic animals. Wound Myiasis.
Opportunistic invasion of wounds by fly larvae is often seen during war and natural disasters, when injured persons are exposed to flies and medical facilities are inadequate to cope with the emergency. Wound myiasis may also be seen sporadically in nursing homes and hospitals and often is not reported for cultural and medicolegal reasons.[10] Six of 14 cases in one series were acquired in the hospital. Eleven patients were over 63 years of age, and nearly all had underlying problems, such as diabetes or peripheral vascular disease. Most of the infected lesions were on the feet or ankles.[69] In another series of 16 cases, most victims were debilitated and over age 65. Males were affected more often than females. Seven species of flies were involved.[75] Fifty Lucilia larvae were removed from the nose, mouth, paranasal sinuses, and enucleated eye socket of a hospitalized patient left in a room with an open window.[20] The most common fly species involved are Lucilia (green-bottle flies), Calliphora species (blue-bottle flies), Phorima regina (black blowfly), Sarcophaga haemorrhoidalis (flesh fly), and Musca domestica (housefly). The flies, whose larvae normally feed on decaying animal tissues, often deposit eggs or larvae in wounds or around body orifices if a malodorous discharge is present. The larvae feed on necrotic tissue, and damage to healthy tissues and secondary infection are uncommon. They actually may debride wounds, and "maggot therapy" with aseptically bred larvae was briefly used in the 1930s. Recently, laboratory-bred fly larvae have been used to debride venous stasis ulcers and other superficial necrotic areas when antibiotic therapy
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and surgical debridement were unsuccessful.[115] [119] Maggots serendipitously present have been used to debride lesions,[92] but this can be risky. [76] Diagnosis is usually obvious on inspection of the wound. Species identification often requires the larvae to reach maturity. If this is not feasible, examination of the spiracular plates on the last segment of the larva and the chitinized oral structures usually permits adequate identification. Irrigation of the wound and mechanical removal of larvae are generally sufficient for treatment.
LICE (ORDER ANOPLURA) Species, Life Cycle, and Distribution Lice are small wingless insects that are ectoparasites of mammals. They are mostly host specific, and two species are human parasites: Pthirus pubis (pubic louse) and Pediculus humanus, with two varieties, P. h. capitis (head louse) and P. h. corporis (body louse). They are obligatory parasites, subsisting on blood from the host, and have mouthparts modified for piercing and sucking. The mouthparts are drawn into the head of the louse when not in use. The adult head louse is about 2 to 4 mm long with an elongated body that is flattened dorsoventrally ( Figure 36-17 ). The head is only slightly narrower than the thorax. The three pairs of legs are about equal in length and possess delicate hooks at the distal extremities. The entire life is spent on the host's body. The eggs (nits) are deposited on hair shafts, generally one nit to a shaft. The nits hatch in about 1 week, and the freshly hatched larvae, which must feed within 24 hours of hatching or die, mature in about 15 to 16 days. The adult female lives for approximately 1 month and may deposit more than 100 eggs during her reproductive life. Body lice are slightly larger than head lice but are similar in appearance with a similar life cycle, although the nits are deposited on fibers of clothing. Head lice and body lice interbreed. Adult public lice are about 1 to 2 mm long, the head is much smaller than the thorax, and the broadly oval body is flattened dorsoventrally ( Figure 36-18 ). The anterior legs are much shorter than the second and third pairs, and the insect resembles a miniature crab. Nits are deposited on hair shafts, often several per shaft, and the egg-to-egg life cycle is approximately 1 month. Lice are found wherever people are found. Able to exist only briefly away from the human body, lice are spread by close personal contact and by sharing of clothing and bedding. The various species not only have a particular host but often prefer a particular part of the host's body, so generalizing about transmission of the three varieties that parasitize humans is impossible. During biting and feeding, secretions from the louse cause a small red macule. Severe pruritus and marked
Figure 36-17 Male of the human head louse, Pediculus humanus capitis.
Figure 36-18 Pubic or crab louse, Phthirus pubis, grasping a hair.
inflammatory responses to bites are caused by the sensitization that occurs after repeated exposure to bites. Thus a victim may have lice for weeks before pruritus becomes marked. Not all people are equally attractive to lice, possibly because of differences in odor and chemical composition of sweat. Lice are medically important as vectors of systemic illnesses, as well as for dermatitis and discomfort. Clinical Aspects The head louse localizes on the scalp and rarely on other hairy areas of the body. Children are most frequently affected, but adults, particularly women, may also be affected. Lice are particularly common in young girls, possibly because of their long hair. Infestation is uncommon in blacks, at least in the United States, probably because the shaft of African hair has an oval cross section that makes it difficult for the louse to grip while depositing eggs. However, pediculosis capitis is found in Africa, where the indigenous head louse is adapted to grip the oval hair shafts. Since nits initially attach to the hair shaft close to the skin and are carried higher as the hair grows, the presence of nits near the tips indicates a longstanding infestation.
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Itching is the principal symptom, and physical findings vary with duration and extent of the infestation, cleanliness, excoriations, and degree of secondary infection. Diagnosis is established by identifying nits and lice. It is not always easy to find lice, especially in early and mild cases, when they may be few in number. Lice are very active, but nits are always present and easy to identify. Nits are whitish ovals, about 0.5 mm long, and attached firmly to one side of the hair. Flakes of dandruff, which resemble nits superficially, are not attached to the hair shafts. Occipital and posterior cervical adenopathy is common and may be present even in less severe cases. A pruritic scalp accompanied by adenopathy should prompt a thorough search for lice and nits. In severe cases, oozing and crusting may be present, sometimes with matting of the hair, and lice may be numerous. The body louse lives chiefly in the seams of clothing and is rarely seen on the skin. These lice leave clothing to feed on the skin or remain attached to the clothing while feeding, and thus they are most abundant where clothing abuts the skin (e.g., beltline). The bite results in a small red macule with a characteristic central hemorrhagic punctum. Excoriations, crusts, eczematization, and other secondary lesions generally obscure the primary lesions by the time the victim seeks medical attention. Shoulders, trunk, and buttocks are favorite sites for bites, and parallel scratch marks on the shoulders are a common finding. The diagnosis is confirmed by identifying parasites or nits from the clothing. Bands of trousers, side seams, and underarm seams are sites of preference. Untreated cases may persist indefinitely, and massive infestations are sometimes seen in vagabonds who have no ready access to frequent laundering or change of clothing or who cannot bathe regularly. Pediculosis pubis is usually acquired during sexual activity, although it may result from unchanged bedding or nonsexual activity, either from lice that live briefly away from the human body or from egg-infested public hairs that are shed. The lice localize principally in the pubic hair, but they are found occasionally in eyebrows, eyelashes, and axillary hairs. Adult public lice are not active and hug the skin at the base of the hair shafts, with their heads buried in the follicular orifice. They are not easy to find, but one or more can usually be found if suspicion of the diagnosis is strong enough to prompt a thorough search. A loupe is helpful. Nits are more easily found. Primary bite lesions are almost never seen, but the intense pruritus and public scratching are pathognomonic. The secondary infection, crusting, oozing, excoriations, and eczematization that often accompany head and body lice are rarely seen with public lice. Peculiar steel-gray macules (maculae caeruleae) may appear in association with some cases of public lice. These lesions do not appear until the infestation has been present for several weeks and are most common on the trunk and thighs. Treatment and Prevention Treatment of all types of lice strives to eradicate lice and nits and prevent reinfestation. Head lice may be treated with one application of 1% permethrin cream rinse (Nix). Hair should be washed, rinsed, and dried, and the rinse is applied for 10 minutes before being washed off. A fine-toothed comb may be used to remove nits after rinsing. Failure to remove all the nits is a frequent cause of treatment failure. If lice or nits are found after 7 days, retreatment is indicated. Family members and contacts should be treated simultaneously. Hats and scarfs should be machine washed with hot cycle and bed clothing dry-cleaned. Other pediculicides are available if the lice are resistant. Two products, RID (Pfizer, New York, N.Y.) and Triple X (Young's Drug Product, Weatherfield, Conn.) contain 0.3% pyrethrins and 3.0% piperonyl butoxide. One application of either preparation usually eradicates both lice and nits. A few persons may require another application 7 days after the initial treatment.[6] Lindane 1% (hexachlorocyclohexane, Kwell) may be used on persons who fail to respond or who are intolerant of permethrin. Kwell is the medication used most often in the United States for treatment of louse infestations. Lindane penetrates human skin and has potential for central nervous system toxicity. It is contraindicated in neonates and must be used according to strict guidelines in children, pregnant women, and nursing mothers. Alternative treatments contain pyrethrums and piperonyl butoxide as active ingredients. Ivermectin, a macrocyclic lactone antibiotic highly effective against filarial worms and Strongyloides, has recently been demonstrated to be effective against lice both topically and orally, but it is not approved for this use at present.[11] Body lice may be treated with the same medications, but parasites and nits are not generally found on the skin. Eradication of these from the clothing is the primary
objective. Treatment includes bathing, laundering all clothing, and changing to fresh clothes free of lice and nits. Dry cleaning eradicates lice and nits, as does ordinary laundering at hot settings. Malathion preparations and ?-benzene hexachloride formulations may be used for mass delousing. Public lice may be treated with the same medications used for head lice. Treatment consists of permethrin 1% cream rinse applied for 10 minutes or lindane 1% shampoo applied for 5 minutes and rinsed. Sexual partners should also be treated.[32] Crotamiton lotion rubbed into the affected area daily for several weeks to destroy hatching ova may also be used. Eyelash infestations may be managed with physostigmine ophthalmic ointment using a cotton-tipped applicator. Machine washing
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and drying of sheets and clothing at hot settings will kill lice and nits.
FLEAS (ORDER SIPHONAPTERA) Species, Life Cycle, and Distribution Fleas are small ectoparasites of mammals and birds. The wingless body, which is covered by a hard shiny integument, is compressed laterally, enabling the fleas to scurry easily among the hairs and feathers of the hosts. They are active insects with legs adapted for jumping, capable of prodigious leaps. Adult fleas subsist on blood. Some species must obtain blood from one particular host, others are less host specific, and all have mouthparts adapted for piercing and sucking. The eggs are laid on or near the host and drop to the ground as the host moves about or shakes. They hatch into small wormlike larvae that feed on droppings from adult fleas, flakes of dried blood from the host, and other organic matter. The life cycle varies among species and may vary considerably within the same species, since each developmental stage is influenced by prevailing temperature and humidity. The customary larval stage of 9 to 15 days may be prolonged for months by adverse conditions, and the pupal stage varies from a week to nearly a year. Individual adult fleas may live for years when circumstances are favorable and can live for months without feeding. Fleas exist universally, although the distribution of various species is restricted by climate and host. They are of medical importance because of the discomfort resulting from their bites, as a cause of papular urticaria, and as vectors of disease. They are more active in warm weather and cause more problems in warmer climates with a longer breeding season, such as the southwestern United States. They are a particular nuisance in California. High standards of sanitation and personal hygiene in developed countries have discouraged the human flea, Pulex irritans, while the same popularity of household pets has been conducive to the proliferation of dog and cat fleas, Ctenocephalides canis and C. felis. The incidence of other species in mammals and birds remains high. Since dog, cat, and many other fleas are only partially host specific, the fleas associated with many mammals and birds cause disease in humans. Most current flea bite problems are caused by animal fleas. Hungry fleas are more often attracted to people from an area frequented by an animal than from the animal itself. If the family dog is absent, hordes of hungry fleas may persist for months. Consequently, anyone with pet cats or dogs or near domesticated animals is more likely to be bitten, but outbreaks in the absence of pets are common. One epidemic of flea bites among children in a day nursery was traced to dog fleas in a deserted fox nesting area beneath the building.[102] Another outbreak among poultry workers was caused by an infestation of hen fleas, Ceratophyllus gallinae.[122] Fleas from flying squirrels also have been documented as the source of bites. Clinical Aspects The appearance of flea bites is not diagnostic, and the clinical features depend on degree of sensitivity. A bite produces a small, central hemorrhagic punctum surrounded by erythema and urticaria. A small wheal at the bite site may be nonallergic because of primary urticogenic substances in the flea saliva, but increasingly severe reactions are caused by sensitization to substances in the saliva. Bullae or even ulceration may result from flea bites in highly sensitive individuals. Flea bites are intensely pruritic, and scratching often results in crusting and impetiginization. Fleas have a habit of sampling several adjacent areas while feeding, and bites characteristically appear in irregular groups. Feet, ankles, and legs, as well as the hips and shoulder areas, where clothing fits snugly, are favorite targets. Although an individual lesion produced by a flea bite is not diagnostic, the typical clinical picture of grouped multiple bites is generally sufficient to establish a diagnosis, which is usually confirmed by locating and identifying fleas. Treatment and Prevention Ordinary flea bites require symptomatic treatment directed at relief of pruritus and prevention of secondary infection. Corticosteroid creams or calamine lotion with phenol, systemic antihistamines, and antibiotics are helpful when indicated, but the management of flea bites consists largely of prevention. The animals that host the fleas must be treated, as well as such places as chicken coops, rat nests, sleeping sites for dogs and cats, and often dwellings where pets live. Many effective insecticides are available. Typically, N,N-diethyl-meta-toluamide (DEET), pyrethrins, piperonyl butoxide, and d-trans allethrin are ingredients in sprays and foggers. An insect spray containing permethrin may be effective. Spraying or dusting must eradicate not only adult fleas but also the many larvae and pupae in grass, carpet, floorboards, furniture, and beds. Lindane, carbaryl, and malathion are the active ingredients in many sprays and dusts, and the services of professional exterminators may be necessary. Veterinary prescriptions are available for control of fleas on dogs and cats. Preparations containing 9.1% imidacloprid (Advantage, Bayer) eliminate or reduce fleas on dogs when applied to the skin; 98% to 100% of fleas are killed within 12 hours of application, and reinfesting fleas are killed for 4 weeks after a single application. An oral preparation used for both dogs and cats contains lufenuron, an inhibitor of insect development. Lufenuron does not kill adult fleas but rather
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controls flea populations by interrupting the life cycle at the egg stage.
MITES (CLASS ARACHNIDA, ORDER ACARINA) Species, Life Cycle, and Distribution Mites make up the largest group in the class Arachnida. Most are small arthropods, and many are barely visible. Mites have two body regions, a small cephalothorax and a larger, unsegmented abdomen. The cephalothorax and abdomen are broadly joined, giving most mites an oblong to globular appearance. Newly hatched larvae have three pairs of legs, and larvae acquire a fourth pair after the first molt. Mites are highly diverse. Some are parasitic, with both vertebrates and invertebrates serving as hosts; some are scavengers, some feed on plants, and many are free living and predaceous. Although most species are oviparous, some are ovoviviparous, and a few are viviparous. They occur worldwide and frequently in great numbers. Mites have been associated with disease transmission, allergies, and dermatologic manifestations. Of the approximately 35,000 species, about 50 are known to cause human skin lesions, and most of the cutaneous lesions are caused by mites feeding or burrowing in the skin. Since children and adults of all races are susceptible to these ubiquitous arthropods, they are responsible for considerable morbidity. The mites of medical importance are some of the sarcoptic mites, some of the trombiculid mites, a number of other acariform mites that infest organic substances such as grains and produce, and the gamasid mites that are vectors of several rickettsial and viral diseases. Dermatologic manifestations of mite bites may be seasonal, as with the trombiculids; individual cases or outbreaks of varying magnitude may be related to contact with mites that infest animals or various foods. Epidemics may occur, as is presently the case with scabies. Scabies Life Cycle.
The human scabies mite is Sarcoptes scabiei var. hominis, an obligate human parasite that completes its entire life cycle in and on the epidermis of humans. Unless treated, scabies can persist indefinitely. The adult female is responsible for the symptoms accompanying the infestation. After impregnation, she burrows into the epidermis and remains in the burrow for a life span of about 1 month. She slowly extends the burrow, feeding during travel, during which time several eggs are deposited daily. The ovoid female mite is approximately 0.3 to 0.4 mm long. Numerous transverse corrugations and dorsal spinous processes are adaptations to prevent backward movement in the burrow. The males are much smaller than females, spend more time on the surface, and have a brief life, dying shortly after copulation. The mite is passed in the vast majority of cases by intimate contact, but adult human scabies mites can survive off the host for 24 to 36 hours at room conditions and still remain infestive.[2] Thus scabies can be acquired from infested bedding, furniture, and clothing. Outbreaks not related to sexual activity occur frequently among nursing home patients and personnel; epidemics in schools for small children are also common. Scabies became uncommon after World War II (during the war it was a common problem), but the disease has increased in frequency since 1964 to epidemic proportions worldwide.[85] Clinical Aspects.
Severe nocturnal pruritus is the hall-mark of scabies. Itching also may be provoked by any sudden warming of the body and generally does not involve the face. A warm bath or radiant heat may cause a paroxysm of itching. Since the pruritus is caused by sensitization, 4 to 6 weeks may elapse between infestation and the onset of severe pruritus. Reinfestation is common, since eradicating the disease from all contacts simultaneously is often difficult, and reinfestation after cure results in prompt recurrence of symptoms. Cutaneous manifestations are varied. The primary lesion is the epidermal burrow, a tiny linear or serpentine track, rarely longer than 5 to 10 mm. The female mite may burrow anywhere on the body, but sites of predilection include the interdigital spaces, palms, flexor surfaces of the wrists, elbows, feet and ankles, beltline, anterior axillary folds, lower buttocks, and penis and scrotum. The distribution of burrows in infants may be atypical, with burrows frequently found in the scalp and on the soles. In the present epidemic, involving many people with excellent hygiene, cutaneous changes may be almost absent and burrows difficult to find. On the other hand, after the disease has been present for some time, eczematization, lichenification, impetiginization, myriad nonspecific papules and excoriations, and even urticaria may be present. The burrows are often the least conspicuous of various skin changes. The clinical picture varies with differences in personal hygiene, topical treatments used before diagnosis, and individual scratch threshold. Diagnosis is based on the combination of nocturnal pruritus and cutaneous findings and is confirmed by microscopic examination of burrow contents. The burrow and contents may be collected for examination by scraping with a scalpel blade or by pinching the skin to elevate it and shaving off a superficial layer. Burrows are often inflamed and no longer typical after the disease has been present for some time. The most productive sites to find burrows for examination are finger webs, sides of fingers, wrists, and elbows. Ectoparasites, ova, egg castings, feces, or pieces of mites are diagnostic.
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Norwegian scabies is a term describing a particularly severe form of scabies occasionally seen in senile and mentally impaired patients, those with debilitating illnesses, and immunosuppressed patients. Extensive crusting occurs, particularly of the hands and feet. Erythema and scaling may develop, and patients are literally "crawling with mites." This form of scabies is highly contagious resulting from the incredible number of mites on the patient and in the immediate vicinity.[13] [61] Nodular scabies is another troublesome clinical variation. Persistent pruritic nodules develop, particularly on the male genitalia or in the groin, but usually on some covered body part. Nodules may be the only finding and may persist for months after adequate antiscabetic therapy. Treatment and Prevention.
A number of topical treatments are available. In most cases a single overnight application of 5% permethrin cream (Elimite) is curative. Permethrin has the advantages of low mammalian toxicity and high cure rate.[121] Even after adequate therapy, symptoms may persist more than a month until the mite and mite products are shed with the epidermis. The chemical must be applied even beneath the fingernails, since ova and live mites are frequently lodged there as a result of frenzied scratching. If the itching has not abated in several weeks, the patient should be reexamined for treatment failure or reinfestation. Permethrin may be used for retreatment, or alternative scabicides may be considered. Lindane lotion is highly effective but has the potential for central nervous system toxicity, and percutaneous absorption may occur. It is contraindicated in infants and pregnant women and persons known to be allergic to hexachlorocyclohexane. Sulfur in petrolatum (5% to 10%) or another suitable vehicle applied for three consecutive nights is a suitable alternative. Crotamiton 10% cream or lotion applied for two consecutive nights is also used. In the treatment of Norwegian scabies, salicylic acid ointment may be needed to soften scales and permit penetration of the scabicide. Nodular scabies can be a perplexing therapeutic problem and may necessitate intralesional injections of corticosteroids in addition to adequate antiscabetic therapy. Application of crude coal tar to the nodules has been recommended. Contacts must be treated simultaneously. Clothing and linens should be laundered the morning after treatment to kill mites that may have strayed from the skin. When many members of a household are infested, live mites may be on the furniture; ?-benzene hexachloride sprays are available. Control of scabies outbreaks in nursing homes and similar epidemic situations can be almost insurmountable because of the number of patients and contacts that must be treated simultaneously. An uncured case of Norwegian scabies as the focus of an epidemic may be surrounded by millions of mites. Ivermectin is an effective antiscabetic when taken orally. A single dose of 250 µg/kg cured 10 of 11 patients with Norwegian scabies and all in a group of otherwise healthy persons with scabies; however,[73] it is presently approved in humans for strongyloidiasis and onchocerciasis. Zoonotic Scabies.
Other burrowing mites similar to the human scabies mite infest animals such as swine, cattle, horses, mules, sheep, dogs, and wild animals. They are relatively host specific but under conditions of close contact may cause self-limited dermatitis in humans. Because of humans' close association with dogs, the most common animal scabies is canine, caused by Sarcoptes scabiei var. canis. Studies indicate that the dog scabies mites are able to survive for at least 96 hours on human skin, even burrowing and laying eggs, but whether a perpetual life cycle can be established is not yet determined. [29] Infested dogs have reddish papules, scaling, crusting, and evidence of scratching. Humans develop itchy papules, often with some urtication, and scratching may give rise to varying degrees of secondary infection. The initial lesions are most often on areas of skin that come in contact with dogs: forearms, chest, anterior abdomen, and anterior thighs. Outbreaks are frequently traced to a kennel or litter of puppies. In one case, 15 patients developed an itchy dermatitis from five puppies in a single litter.[16] Human infestation with dog scabies mites subsides spontaneously when contact with dogs is discontinued or when the dogs are cured. The dogs must be treated with scabicides and the human victims with
symptomatic therapy for pruritus. Cats, also closely associated with humans, have been known to harbor mites that can infest humans. Notoedres cati infestation is seen more often in Czechoslovakia and Japan than is dog sarcoptic scabies.[14] Trombiculid Mites Mites of the family Trombiculidae are distributed worldwide. In the United States the most important species is Eutrombicula alfreddugesi (red bug, chigger, harvest mite). Another species, E. batatas, is also indigenous to parts of the United States. Adults are free living and predaceous on small arthropods and their eggs, but the larvae are ectoparasites of vertebrates. Wild and domestic mammals, as well as reptiles, serve as hosts. The larval bite causes human dermatitis. Adult mites lay their eggs among vegetation, and newly hatched larvae crawl up on the vegetation, waiting to attach themselves to a passing host. They attach themselves to the skin with hooked mouthparts and feed on blood, falling off when full. However, humans are not good hosts, and larvae usually do not stay long. Severity of the response depends on the species of
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trombiculid, the irritating qualities of the mites' saliva, and the host's allergic response. The typical bite is a maddeningly pruritic, hemorrhagic punctum that usually becomes surrounded by intense erythema within 24 hours. Bites may number in the hundreds and can be associated with an allergic reaction. Hypersensitivity causes blisters and weeping of clear fluid with crusting. The surrounding area may be purplish in color, with severe swelling, particularly of the feet and ankles ( Figure 36-19 ). The lesions regress in 1 to 2 weeks, but pruritus is persistent and often paroxysmal during this time, with secondary infection in excoriated skin. Treatment is symptomatic and consists of topical antipruritic agents, corticosteroids, systemic antihistamines, and occasionally, pulse therapy with systemic corticosteroids. Superpotent topical corticosteroid creams and ointments, such as 0.05% clobetasol, applied sparingly to individual bites several times daily, are effective but must be used properly. Prolonged application can result in atrophy, and absorption can be significant if excessive body surface is treated. Phenol 1% in calamine often is effective. As in all self-limited conditions with no satisfactory cure, home remedies abound, such as meat tenderizer rubbed into the moistened skin. Application of clear nail polish to the individual lesions is a popular home remedy, even though no evidence suggests that this is effective. Preventive measures consist of avoidance and insect repellents used on skin and clothing. Clothing pretreated with permethrin has resulted in 74.2% increase in protection compared with unprotected controls.[9] Other repellents suggested for treating clothing are ethylhexandiol, DEET, and flowers of sulfur. The symptoms are allergic, and permanent residents in infested areas may develop tolerance to repeated bites. Miscellaneous Mites Parasitiformes.
This group contains gamasid mites that are parasites of birds, mammals, snakes, insects, and rarely, humans. In addition to being vectors of disease, gamasid mites are responsible for some cases of dermatitis. The chicken mite, Dermanyssus gallinae, is responsible for most of the dermatitis caused by this group. This pest of poultry is widespread and is associated with both domestic and wild birds. Poultry workers are common targets, but other persons may be infested from insidious sources, such as a pet canary or bird nest near an intake for ventilation or air conditioning. The clinical picture is nonspecific, but the diagnosis may be made by identifying the mite. Treatment consists of symptomatic therapy and eradication of the mite source. The tropical rat mite Ornithonyssus bacoti has also been reported to cause dermatitis, from such diverse sources as a rat nest in the attic or a colony of laboratory mice.[15] [33] Snake mites have been implicated as a
Figure 36-19 Chigger bites.
cause of dermatitis. Four members of one family developed a vesicobullous eruption from Ophionyssys natricis harbored by a pet python.
[106]
Acariniformes.
This huge group includes mites that infest foods, feathers, and furs. Individual infestations and larger outbreaks are common, with increased exposure by occupation, resulting in such terms as grocer's itch, miller's itch, and copra itch. Dogs, cats, and rabbits are primary hosts for mites of the genus Cheyletiella, and domestic pets are increasingly the source of mite dermatitis. Pet house cats are often involved.[100] Mites of the genus Dermatophagoides are said to be the principal inhaled allergen of house dust. D. scheremetewskyi is an unusual mite that has been found in kapok and feather pillows, in a sparrow's nest, in monkey food, and on rats and other animals. This mite has been reported as the cause of feather pillow dermatitis.[3] The most common type of dermatitis in this group is grain itch caused by Pyemotes ventricosus. This tiny mite parasitizes various insects often found in and around grain and straw. It attacks humans when a large mite population has no ready access to normal hosts. Grain itch implies an occupational bias, but outbreaks not involving farmers or rural workers have been described. During a widespread epidemic of Pyemotes infestation of farm workers in the midwestern United States in 1950 to 1951, straw used at the Indiana State Fair was infested. During a 2-year period, 642 visitors were treated for grain itch at a dispensary maintained
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on the fairgrounds, and about 1100 animal attendants and fair workers were treated over the same period at a separate facility. The reservoir of infestation by Pyemotes may be quite obscure. Several cases have been reported associated with the common furniture beetle Anobium punctatum in the floor joists of a house.[31] Therapy is symptomatic. Large-scale eradication measures may require services of professional exterminators.
DELUSIONS OF PARASITOSIS Patients with delusions of parasitosis are convinced, against all evidence to the contrary, that parasites infest their skin and often their homes and clothing. No single cause is known for this condition, although some cases may be associated with proven parasitic infestation. The idea may also be suggested by infestations of relatives or acquaintances. Patients over 50 years are most often female; patients under 50 are equally male and female. Most cases of delusions of parasitosis commence with pruritus, which may be accompanied by crawling, creeping, stinging, and burning sensations. The initial reaction is to scratch, replaced soon by digging to remove the "parasites." Self-mutilation and suicidal behavior may develop. Generally the first contact with a physician is to bring in evidence of the "infestation." Evidence typically consists of scales, lint, crusts, hairs, dust, and small pieces of skin, carefully collected and stored in a small box or folded in facial tissue. Medical attention is often sought not to relieve the symptoms but to eradicate the parasites. Patients may take the evidence to a professional entomologist for identification and may employ professional exterminators for repeated fumigation. Patients may be so convincing that household members or acquaintances come to share the delusion.[24] [30] Many patients with parasitophobia know that their fear is groundless but are still unable to overcome it. Other patients with delusions of parasitosis are convinced that they have an infestation and regard as incompetent the physician who makes the correct diagnosis of no infestation. A complete examination of the patient and the evidence is essential, and investigation of the home or workplace may be indicated. Other medical conditions that may produce cutaneous sensations include liver and renal disease, alcoholism and toxic states, diabetes mellitus, cardiovascular disease, lymphoma, anemia, sideropenia, vitamin B12 deficiency, pellagra, peripheral neuritis, dermatitis herpetiformis, drug reactions, and environmental irritants (e.g., arthropods, fiberglass).[70] [137] Psychiatric intervention is often unsatisfactory to both patient and physician. Convinced that the physician is wrong, patients often seek repeated opinions and finally become despondent. Pimozide, a neuroleptic medication used to treat other monosymptomatic hypochondriacal psychoses, has been found useful in treating this condition.[81] [93] [98] In one group of 14 patients treated with pimozide and followed for an average of 34 months, seven had complete remissions, three had relapses that responded to treatment with pimozide, and four were treatment failures. [65] IN MEMORIAM It is with great sadness that we observe the passing of Sherman Minton, MD, who was an outstanding teacher, scientist, and friend. His contributions to this book and the entire wilderness medicine community were extensive and generous, and we will always be in his debt. Paul Auerbach, MD
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Chapter 37 - Non-North American Arthropod Envenomation and Parasitism Sherman A. Minton † H. Bernard Bechtel Timothy B. Erickson
HYMENOPTERA (BEES, WASPS, AND ANTS) Hymenoptera insects are worldwide in distribution and often consistute a major part of a region's insect fauna. Honeybees are exploited for their honey throughout the world; even the aggressive Apis mellifera scutellata is used for honey production in Africa. Honeybees in southern Asia attach huge nests to limbs of forest trees. The giant bee, Apis dorsata, of southeast Asia has a reputation for savagery, and deaths from multiple stings have occurred. Yellowjackets and hornets are common in Europe and the Middle East and have similar medical importance as in the United States. Two species, Vespula orientalis and V. vulgaris, have recently been introduced into Australia, where they have become a significant problem.[30] Paper wasps of the genus Polistes are plentiful in tropical America and Australia. Another Australian paper wasp, Ropalidia revolutionalis, constructs nests that resemble belts of bullets and hangs them from shrubs and fences. Fire wasps (Polybia) are found from Mexico to northern South America. The common species are black with yellow markings. They construct globular, cylindric, or cone-shaped paper nests up to 70 cm long that are usually hung from trees and sometimes under bridges. They may defend these nests with great vigor. Ants have numerous stinging species in the tropics. Although native to South America, fire ants do not seem to be a major medical problem there, perhaps because of native competitors, predators, and parasites. Two fire ant species are important in areas outside the United States. Solenopsis geminata has been introduced into Okinawa and Guam and is widespread in Central America, Mexico, and some Caribbean islands. S. xyloni is common in Mexico and also occurs in California and Texas. S. invicta has been introduced into Puerto Rico. Amino acid sequences of all fire ant venoms are very similar.[23] Presumably, all fire ant stings are similar and can be managed medically in the same manner. The samsum ant, Pachycondyla sennaarensis, is an ecologic counterpart of the fire ant widely distributed in the African tropics and Arabian peninsula. It nests in the ground but does not make a conspicuous mound. In the United Arab Emirates it is plentiful in urban areas and the cause of many stings.[13] Australian bull ants are large insects (about 20 mm) with prominent jaws ( Figure 37-1 ). They are ground dwelling and common in suburban areas in southeastern Australia. Many neotropical stinging ants live in trees. The giant black ants (16 to 22 mm) of the genus Paraponera are found from Nicaragua to the Amazon basin. Although they nest in the ground, workers forage in trees from almost ground level to high in the forest canopy. They are most active at night. The green tree ant of northeastern Australia makes a leaf nest in trees. It has no true sting but ejects formic acid into wounds made by its jaws. Clinical Aspects No unique features distinguish Hymenoptera envenomations in other parts of the world from those in North America. Venoms of the various groups show little geographic variation. This is also true of groups at risk, with the possible exception of a few honey-gathering Asian tribes. The incidence of Hymenoptera sting allergy may be slightly higher in western Europe than in the United States, and fatal allergic reactions may be slightly more common.[8] Systemic anaphylactic reactions to stings of Australian bull ants and samsum ants are increasing, with reports of a few fatalities. Patients with history of systemic reactions to samsum ant stings have immunoglobulin E (IgE) and positive skin test reactions to fire ant venom.[13] Paraponera ant stings are intensely painful for several hours and may be accompanied by fever and lymphadenitis.
LEPIDOPTERA The Lepidoptera show high diversity in the tropics with correspondingly greater medical importance, particularly in Latin America. Caterpillars of the genus Lonomia native to northern South America can inflict life-threatening stings ( Figure 37-2 ). These caterpillars are 50 to 70 mm long and have numerous branched dorsal spines. They live in primary tropical forests in groups of up to about 50 individuals. Disturbance of their habitat has resulted in an increasing number of envenomations. Venom of Lonomia is a protein that activates prothrombin and is stimulated by factor V and calcium ions.[21] Stings cause intense pain but not much local reaction. Signs of coagulopathy, such as ecchymoses, †Deceased.
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bleeding gums, hematuria, and melana, may develop in a few hours or be delayed a week or more. Fibrinogen, factor V, factor XII, and plasminogen are decreased; fibrin degradation products are increased; and platelets usually are normal. Acute renal failure, cerebral hemorrhage, and pulmonary hemorrhage may occur. Coagulopathy lasts 2 to 5 weeks. In one series of 33 cases, four were fatal. [1] [6] [16] Treatment with prednisone, plasma, and whole blood is ineffective. An antivenom has been developed, and a preliminary report indicates possible clinical effectiveness.[11] [12] Neotropical caterpillars of the genera Dirphia, Megalopyge, and Automeris are large, stout, spiny, and sometimes covered with hair. Most are forest species but can adapt to areas of cultivation. Agricultural workers are most often stung; the incidence of stings is higher in the rainy season. Intense, centrally radiating pain with local edema and erythema is typical; lymphadenopathy is often seen. Systemic symptoms include nausea, headache, malaise, chills, and fever. Hypotension, shock, and convulsions have been reported. An Automeris caterpillar bite reported from French Guyana produced syncopal pain and edematous infiltration of the thigh lasting several days.[10] Symptoms usually subside within 24 hours. Treatment is symptomatic. Oral antihistamines are often effective if given within about
Figure 37-1 Red bull ant.
Figure 37-2 A, Caterpillar of Lonomia achelous, which can inflict injuries characterized by potentially fatal coagulopathy. B, Moth of L. achelous, which has no venomous spines.
an hour after the sting. Codeine or meperidine is occasionally needed to control pain. A chronic granuloma of the hands of Brazilian rubber tappers known as pararama results from contact with caterpillars of Premolis semirufa. Permanent disability may result. [39] Moths of the genus Hylesia occur from southern Mexico to Argentina. The caterpillars have venomous spines, but the greatest problem is created by the moths, which have a coating of spines on their abdomen. The spines or setae are hollow and pointed, contain a toxin of unknown nature, and are freely shed into the air. The moths are attracted to lights in enormous numbers, and their airborne spines can cause great discomfort. Their activity has created serious problems at airports, shipping docks, and tourist resorts. Within a few minutes to a few hours after contact with the spines, victims develop a pruritic, erythematous rash that progresses to urticaria and excoriation. Any portion of exposed skin may be involved, but palms and soles are often spared. Irritation of eyes and mucous membranes is unusual. Symptoms subside in about a week if there is no further exposure. Topical and systemic treatments have had little success.[14] In Korea, outbreaks of dermatitis, presumably caused by setae of the yellow moth Euproctis flava, are well known. In the summer of 1980, hundreds of U.S. soldiers were affected.[3] The caterpillars feed on hardwood trees; great numbers of moths appear in summer and are attracted to lights. Dermatitis usually involves direct contact with moths or their cocoons or with clothing contaminated with setae. The lesions are similar to those described for Hylesia and are equally refractory to treatment. Other outbreaks of dermatitis ascribed to Euproctis moths and caterpillars have been reported in Japan and China. One outbreak in Shanghai in 1972 affected about 500,000 individuals. Cases of Euproctis dermatitis and ophthalmia have also been reported
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in Australia and Great Britain. Sensitization with elevated IgE levels may occur. [39] [44] In the Mediterranean region and Middle East the pine processionary caterpillar, Thaumetopoea pityocampa, is plentiful and makes silk nests in trees. Its setae cause a maculopapular rash occasionally accompanied by urticaria, bronchitis, and conjunctivitis. Outbreaks typically occur when groups of tourists and military personnel camp in pine groves. The rash usually results from contact with detached setae rather than with caterpillars. The adult moth stage apparently does not have irritating spines. Moths of the genus Calyptera native to Southeast Asia have a serrate proboscis and feed on mammalian blood, including that of humans. Tropical species of several moth genera feed on human ocular secretions. Their medical importance is unknown.
BEETLES AND OTHER INSECTS Small rove beetles of the genus Paederus are troublesome in many tropical and subtropical regions. The whiplash beetle or Finch Hatton bug (Paederus australis) caused evacuation of an entire aboriginal community in northern Australia,[46] and a large suburban hospital in Sri Lanka had 108 cases of painful dermatitis among members of its staff on night duty.[27] Staphylinid (rove) beetle dermatitis epidemics have been reported in Nigeria in 1990, Egypt in 1994, and Kenya in 1998 after sudden floods.[9] These beetles are slender with elongate abdomens and very short rectangular elytra. They frequent damp habitats and may be plentiful in irrigated crop fields. They usually fly after dark in hot, humid weather and are attracted to lights. Their vesicant secretion is an alkaloid present in greatest concentration in hemolymph; it is usually deposited on human skin when the beetles are pressed or crushed but may occasionally be spontaneously secreted. There is no immediate reaction to the secretion, but after 12 to 24 hours, painful erythematous lesions develop and soon become vesicular. The vesicles last 3 to 7 days and are followed by crusting and pigmentation. Conjunctivitis results if the secretion is rubbed into the eyes. This condition is known in parts of the world as "Nairobi eye" or "Christmas eye."[9] Some persons with extensive skin involvement may show generalized symptoms. Treatment is symptomatic and not very effective. Prompt soap and water washing after insect contact is recommended. Screening of sleeping and working quarters is the best prevention. Lady beetles (ladybugs, family Coccinellidae) are widely distributed and highly beneficial as predators on aphids and scale insects. Species in the eastern United States often overwinter in houses and do no harm. However, an Australian lady beetle, Diomus notescens, is reported to bite, causing papules with small necrotic centers.[40] Two cases of human ear invasion by a predaceous beetle, Crasydactylus punctatus, or the carabid beetle, have been reported from Oman. One victim had a severe otologic injury caused by biting and chewing on the external auditory canal and tympanic membrane.[4]
DIPTERA (TWO-WINGED FLIES) Most dipterans are cosmopolitan in distribution. However, two groups of biting flies and several species involved in human myiasis are largely confined to the tropics and are discussed here (see Table 36-1 ). Sand flies (Phlebotomus and related genera) are very small biting flies quite distinct from Culicoides and its relatives. They are widely distributed in tropical and subtropical regions. They live in damp, shaded places such as mammal burrows, rock crevices, and cracks in walls of houses and other structures. Favorite habitats in Central America are gambas, deep clefts between the buttresses of large forest trees. Larval and pupal stages are found in moist detritus in holes and crevices. The adults usually emerge at night when air is still and temperatures are above 13° C (56° F). They are poor fliers. Sand flies are vectors of leishmaniasis and of Bartonella bacilliformis in Peru. Sand fly populations can be controlled with pyrethroid insecticide sprayed into the mounds and burrows. Spraying of a 100-m-wide barrier zone around a campsite can reduce sand fly numbers for an extended period.[17] Tsetse flies (Glossina species) are of great importance as vectors of human and animal trypanosomiasis in sub-Saharan Africa. Although not closely related to deerflies and other tabanids, they are similar in appearance and habits (see Chapter 36 ). Their life history is peculiar in that a single large larva develops in the uterus of the female and is expelled shortly before pupation, which takes place in the soil. Tsetse fly bites produce comparatively little local reaction other than brief pain and itching. Myiasis Furuncular Myiasis.
This type of myiasis is caused by flies whose larvae penetrate human skin and develop in that location, producing boil-like lesions with an external opening. Formerly, this condition was encountered almost exclusively in the tropics, but with the growing popularity of ecotourism and other travel to unconventional destinations, cases are being seen in many other parts of the world. A German travel clinic reported 13 cases in travelers returning from tropical countries during a 3-year period.[25] The classic agent of furuncular myiasis is the so-called human botfly, Dermatobia hominis ( Figure 37-3 ). Actually, humans are only one of many mammals that serve as suitable hosts for the obligately parasitic larvae of this fly. It is widely distributed in the American
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tropics and is an important parasite of domestic cattle in many places. Human infection seems to be most prevalent in Central America and northern South America. Adult flies resemble a bumblebee (body length about 15 mm). The do not feed and are infrequently seen. The life cycle of this fly is unique in that the female attaches her eggs to the body of another arthropod for transfer to the host. Large mosquitoes of the genus Psorphora are often used (8% were found bearing Dermatobia eggs in one study), but about 40 species of insects and ticks have been reported to be egg carriers. When the carrier alights on a mammal, the eggs hatch immediately, and the larvae enter the skin through the bite of the carrier or some other small trauma. Small larvae are fusiform and later become pyriform to ovoid as they reach full development at
Figure 37-3 Dermatobia larva.
lengths of 15 to 20 mm. They are encircled by several rings of spines. The larval stage lasts 6 to 7 weeks, after which the larva emerges from the skin and drops to the ground, where pupation occurs. Infection is fairly common among rural people of Central America. Cases in returned tourists and visitors from Latin America have been diagnosed in many parts of the United States. Six cases occurred in one group of tourists visiting archaeologic sites in Guatemala.[15] [26] [28] [37] [45] Lesions may be on any part of the body exposed to insect bites and may be single or multiple. An initial pruritic papule becomes a furuncle, with a characteristic opening from which serosanguineous fluid exudes. Pain often accompanies movements of the older larvae, but the lesion is not particularly tender to palpation. Lymphadenopathy, fever, and secondary infection are rare. This form of myiasis should be suspected in patients with furuncular lesions and history of residence or travel in endemic areas. It must be differentiated from leishmaniasis and onchocerciasis, which have a different prognosis and treatment. The sensation of movement within the lesion, accompanied by pain but little tenderness or inflammation, suggests myiasis. The tip of the larva may protrude from the central opening, or bubbles produced by its respiration may be seen. Often, simple pressure will extrude the organism, particularly if it is small.[36] Occlusion of the breathing hole may cause the larva to emerge sufficiently for it to be grasped and withdrawn. An effective folk remedy is binding a piece of fat, such as bacon, over the opening ( Figure 37-4 ).[5] This often causes the larva to leave its
Figure 37-4 A, Lateral view of three lesions cased by infestation with D. hominis larvae. The nodules were initially assumed to be furunculosis. A central breathing aperture is present in each nodule. Serosanguineous fluid is draining from two of the nodules. Larval spiracles are visible emerging from the uppermost nodule. B, The fatty portion of multiple strips of raw bacon were placed over the larval apertures to obstruct the air supply and encourage the larvae's egress from the skin. C, After approximately 2 hours of treatment with bacon therapy, the D. hominis larvae have emerged far enough from the subcutaneous tissues to be grasped with forceps. The larva is removed intact. (From Felsenstein D et al: JAMA 270:2087, 1993.)
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burrow. Another technique is injection of about 2 ml of a local anesthetic into the base of the lesion, thus extruding the larva by fluid pressure. If these methods are unsuccessful, surgical excision under local anesthesia is indicated. Whatever method is used, care should be taken not to break or rupture the larva. This may cause a strong inflammatory reaction, often followed by secondary infection. Repeated infections tend to confer some immunity that may abort larval development. Screens, protective clothing, and use of insect repellents are helpful in preventing infestation. Furuncular myiasis in tropical Africa is caused by the tumbu fly, Cordylobia anthrophophaga. The larval stage of this fly is an obligate parasite of many mammals, of which rats and dogs are most important epidemiologically. The adult is about the size of a housefly, but stockier. It prefers shade and is most active in early morning and afternoon. Females lay eggs on dry sandy soil or on clothing. They are attracted by the odor of urine. The eggs hatch in 1 to 3 days, and hatchling larvae can survive up to 2 weeks waiting for contact with skin of a suitable host. They can penetrate unbroken skin. They become fusiform to ovoid and reach a length of 13 to 15 mm. The larval stage is completed in 9 to 14 days. Human infections occur in most nations of sub-Saharan Africa. Transmission increases during the rainy season. Among indigenous peoples, infection is most frequent in children; adults evidently acquire some immunity. Infections among Americans and Europeans visiting Africa are reported regularly.[24] [25] [43] Lesions may be on any part of the body but are more common on the legs and buttocks. The furuncles are discrete, elevated, and nontender and have a central opening. The number of lesions, up to about 50, is greater than with Dermatobia. Infections in children have been mistaken for chickenpox,[35] but the course of the infection is much shorter. An exceptionally heavy infection (about 150 larvae) was caused by Cordylobia rodhaini, normally a parasite of forest mammals. It was accompanied by lymphadenopathy,
leukocytosis, and elevated IgA. Clothing left to dry on the ground was the presumed source of the parasites.[38] Principles of diagnosis and treatment are much the same as for Dermatobia. Avoidance of skin contact with potentially contaminated soil and ironing of clothing and bedding after open-air drying are preventive measures that often are difficult to achieve. Hematophagous Myiasis.
The sole cause of hematophagous myiasis is the Congo floor maggot, Auchmeromyia luteola. It is dark, distinctly segmented, ovoid, 15 to 18 mm long, and assumes the larval stage of a moderate-size yellowish fly. It is widely distributed in sub-Saharan Africa and is essentially a human parasite. It is unique among parasitic fly larvae in living apart from its host in the earthen floor of native dwellings. It seeks persons lying or sitting on the floor or on mats and feeds intermittently on blood, usually at night. The bites are trivial but may interfere with sleep. Sensitization appears to be uncommon. Wound Myiasis.
About 85% to 90% of cases are caused by larvae of flies of the family Calliphoridae, which includes both obligate parasites and opportunists. The most dangerous type of myiasis may be caused by larvae of the screw-worm flies Callitroga (Cochliomyia) americana (hominivorax) in the Americas and Chrysomyia bessiana in Asia and Africa. The adults are rather stocky flies, 8 to 12 mm in body length, and metallic blue-green to purplish black. The parasitic larvae are pinkish, fusiform, and strongly segmented, providing the common name. Length at maturity is 12 to 15 mm. They are obligate parasites whose chief hosts are cattle, sheep, and goats. They are a major cause of economic loss among livestock. Enzootic areas are mostly in the tropics and subtropics; in the past, summer infections have occurred as far north as Colorado and Nebraska. Female flies deposit eggs near any break in the skin or around the nose, mouth, or ears if a discharge is present. Larvae invade healthy tissue, often causing considerable damage. The larval stage lasts 4 to 8 days, and the entire cycle is 15 to 20 days in enzootic areas. Screw-worm has been eradicated in the southern United States and some other areas primarily through the release of large numbers of laboratory-bred male flies sterilized by gamma irradiation. Females mate only once, so mating with a sterile male nullifies the female's reproductive effort, greatly reducing the population. Flies may be dispersed by prevailing winds. Infection is often acquired while resting outside during the day or may result from trauma.[32] Lesions may appear on any exposed part of the body. Those on the scalp may be associated with pediculosis capitis. Typical dermal lesions are ulcers or sinuses that may contain up to 200 larvae. These are surrounded by a zone of induration. Pain is variable. Secondary bacterial infection is common. Tissue destruction may be extensive and mortality is associated with nasopharyngeal invasion. Topical application of 5% chloroform in olive oil followed by irrigation and manual removal of larvae is often sufficient in dermal infections. Deeper nasopharyngeal and orbital infections require surgery. Antimicrobial therapy as dictated by culture and sensitivity tests, is often necessary. The most effective prevention is elimination of the disease in domestic animals.
BURROWING FLEA Flea infestations tend to be similar clinically and associated with the distribution of animal hosts. However, one flea, Tunga penetrans, is responsible for a distinctive infestation known as tungiasis. The flea has a number of common names: burrowing flea, chigo, sand flea,
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and jigger. Infestation is common in Central and South America and in Africa, where the burrowing flea is widely distributed, but more cases are seen in the United States as increasing numbers of tourists visit exotic places. One woman resident of New York City developed lesions of tungiasis on her toes after visiting several countries in East Africa, where she frequently wore sandals in rural areas.[47] The primary lesions of tungiasis are produced by the female flea. As soon as it is impregnated, it burrows into the skin until only the posterior end protrudes. Sucking blood, the insect becomes as large as a small pea and deposits eggs that fall to the ground. Lodged in the skin, the gestating female produces a firm itchy nodule, with the posterior end of the flea visible as a dark plug or spot in the center of each nodule. Lesions occur most often on the feet, buttocks, or perineum of persons who wear no shoes or frequently squat, since the burrowing flea is not a good jumper and abounds in the dusty soil surrounding human habitations. If the infestation is extensive, numerous papules may aggregate into plaques with a honeycomb appearance. Secondary infection around each flea is inevitable, resulting in suppuration, ulceration, and rarely gangrene. The lesions become painful or even crippling, and severe infections may lead to death. If the burrowing flea is not removed, the pustule ruptures, leaving an ulcer. Wearing shoes will prevent most cases of tungiasis. Cases should be treated promptly. One method is curettage of each nodule under local anesthesia, with concomitant use of systemic antibiotics to prevent secondary infection. Ether pledgets applied to the skin will kill the fleas before curettage is begun. Where burrowing fleas are endemic, eradication is important. Floors must be swept free of dust, and insecticides may be sprayed or dusted.
CENTIPEDES AND MILLIPEDES Centipedes are elongate, flattened arthropods with one pair of legs for each of the typical body segments, which
Figure 37-5 A, Centipede, Scolopendra armidale. B, Centipede fangs.
may number from 15 to more than 100. The first segment bears a pair of curved hollow fangs with venom glands at the bases. The last segment bears a pair of filamentous to forcepslike caudal appendages not associated with the venom apparatus. The largest species reach lengths of about 30 cm (12 inches). Most centipedes live in crevices or beneath objects on the ground. Some are burrowers, and others are climers. Many are nocturnal. Scutigera coleoptrata, with body length of 25 mm and long thin legs, is a common house arthropod in much of the United States. Lithobius is a cosmopolitan ground-dwelling genus. A species common in eastern U.S. gardens is orange and 30 to 50 mm long. Centipedes prey chiefly on invertebrates, but larger species occasionally eat small vertebrates. Female centipedes of some species curl around their egg clusters and newly hatched young and may actively defend them. Centipedes use venom primarily to kill prey and only secondarily for defense. Venom may also have a digestive function. Enzymes, including acid and alkaline phosphatase and amino acid naphthylamidase, lipoproteins, histamine, and serotonin, are variably present.[33] Venom of Scolopendra subspinipes produces hypotension followed by hypertension. The major lethal toxin is an acidic protein with molecular weight of 60,000 daltons. It produces vasoconstriction, increased capillary permeability, and cardiac arrest.[19] [20] As with spiders, any centipede whose fangs can penetrate human skin can cause local envenomation. Centipede bites are typically pointed in shape, a feature that can help differentiate a bite from a large centipede from a snake. [18] Contrary to popular folklore, centipedes do not inject venom with their feet or caudal appendages. The jaws inject a neurotoxic venom through venom ducts. Centipede bites have been reported from numerous tropical and subtropical regions, but never as a serious medical problem. Most bites have been ascribed to species of Scolopendra, which has a wide distribution with several species in the southern United States ( Figure 37-5 ). Fatalities are almost unknown; however, a death in the United
894
Figure 37-6 Spirobolus millipede.
States was recently mentioned, but with no locality or details.[29] Burning pain, local swelling, erythema, lymphangitis, and lymphadenopathy are common manifestations of a centipede bite. Swelling and tenderness may persist for as long as 3 weeks or may disappear and recur. Superficial necrosis may occur at the site of fang punctures. Few bites with serious systemic reactions have been reported in detail. In one case ascribed to Scolopendra heros in the southwestern United States, a woman had massive edema of the leg, necrosis of the peroneal muscles, loss of motor function in the foot, myoglobinuria, and azotemia. [31] An Israeli patient bitten on the neck complained of inability to turn her head, probably because of muscle spasm.[34] Other cases have been characterized by dizziness, nausea, collapse, and pyrexia. [7] An infant that ingested a centipede identified as Scutigera morpha developed hypotonia, vomiting, and lethargy, presumably from being bitten in the mouth or pharynx. The child recovered spontaneously after about 48 hours.[2] Although some centipede bites may be excruciatingly painful, they are not fatal and seldom require more than supportive care. Treatment of centipede envenomation is symptomatic. Infiltration of the bitten area with lidocaine or another anesthetic promptly relieves pain. Antihistamines and steroids have been suggested for more severe reactions. Tetanus prophylaxis is advisable. Millipedes differ from centipedes in having two pairs of legs per body segment and in lacking apparatus for injecting venom. Several large species of the genus Spirobolus are common in the southern United States ( Figure 37-6 ). Some species are broad and short and roll into a ball when disturbed ( Figure 37-7 ). Millipedes are generally ground dwelling and secretive. Occasionally, they aggregate in enormous numbers. They generally feed on decaying vegetation. Millipedes are exceptionally well endowed with defensive chemical secretions that include hydrogen cyanide, organic acids, phenol, cresols, benzoquinones, and hydroquinones. These effectively deter most
Figure 37-7 Giant Madagascar millipede.
predators. Some large species can eject secretions for distances up to 80 cm (32 inches). Human injury from millipede secretions has been reported from a number of tropical regions. The most common injury is dermatitis that begins with a brown-stained area, which burns and may blister and exfoliate. Millipede secretion in the eye causes immediate pain, lacrimation, and blepharospasm. This may be followed by chemosis, periorbital edema, and corneal ulceration. Blindness has been reported. [22] [41] Individuals exposed to large millipede aggregations may complain of nausea and irritation of the nose and eyes. No specific treatment is available. Prompt irrigation with water or saline should be followed by analgesics, antimicrobials, and other measures appropriate for superficial chemical burns. Ophthalmologic evaluation is mandatory for eye injuries.
GENERAL TREATMENT OF INSECT BITES Oral antihistamines can be effective in reducing the symptoms of insect bites. Cetirizine was given prophylactically in a double-blind, placebo-controlled, 2-week crossover trial to 18 individuals who had previously experienced dramatic cutaneous reactions to mosquito bites.[42] Subjects given the active drug had a 40% decrease in both the size of the wheal response at 15 minutes and the size of bite papule at 24 hours. The mean pruritus score, measured at 15 minutes and 1, 12, and 24 hours after being bitten, was 67% less than that of the untreated controls. These studies have not been done with astemizole, loratadine, or fexofenadine. In highly sensitized individuals, prophylactic treatment with nonsedating antihistamines may safely reduce the cutaneous reactions to insect bites. A 3.6% ammonium solution (After Bite), relieves the type I hypersensitivity symptoms associated with mosquito bites. In a double-blind, placebo-controlled laboratory trial, 64% of mosquito-bitten subjects experienced complete relief of symptoms after a single application of the ammonium solution, and the remaining 36% had partial relief lasting 15 to 90 minutes.
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No subjects treated with placebo reported complete symptom relief.[48]
PROTECTION AND PREVENTION An integrated approach to personal protection is the most effective way to prevent arthropod bites, regardless of location and species. Insect repellents containing diethyltoluamide (DEET) are the most effective products currently on the market, providing broad-spectrum repellency lasting several hours. Topical insect repellents alone do not provide complete protection. Mosquitoes, for example, can find and bite any untreated skin and may even bite through thin clothing. Deerflies, biting midges, and some blackflies prefer to bite around the head and will crawl into the hair to bite unprotected areas. Wearing protective clothing, including a hat, reduces the chances of being bitten. Treating clothes and hats with permethrin maximizes protection by repelling any insect that crawls or lands on the treated clothing. To prevent chiggers or ticks from crawling up the legs, pants should be tucked into boots or stockings. Persons traveling to a part of the world where insect-borne disease is a potential threat should be certain to learn about indigenous insects and the diseases they might transmit. Protective clothing, mesh insect tents or bedding, insect repellent, and permethrin spray should be carried.
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Gomes A et al: Isolation, purification, and pharmacodynamics of a toxin from the venom of the centipede Scolopendra subspinipes dehaani, Indian J Exp Biol 21:203, 1983.
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Guererro B, Arocha-Pinango CL: Activation of human prothrombin by the venom of Lonomia achelous caterpillars, Thromb Res 66:169, 1992.
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Haneveld GT: Eye lesions caused by the exudate of tropical millipedes. I. Report of a case, Trop Geo Med 10:165, 1958.
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Hoffman DR: Reactions to less common fire ants, J Allergy Clin Immunol 100:679, 1997.
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Johnston M, Dickinson G: An unexpected surprise in a common boil, J Emerg Med 14:779, 1996.
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Komaladasa SD, Perera WDH, Weeratunga L: An outbreak of Paederus dermatitis in a suburban hospital in Sri Lanka, Int J Dermatol 36:34, 1997.
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Kpea N, Zywoanski C: "Flies in the flesh": a case report and review of cutaneous myiasis, Cutis 55: 47, 1995.
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Langley RL, Marrow WE: Deaths resulting from animal attacks in the United States, Wilderness Environ Med 8:8, 1997.
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Levick N, Winkle KD, Smith G: European wasps an emerging hazard in Australia, Med J Aust 167:650, 1997.
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Logan JL, Ogden DA: Rhabdomyolysis and acute renal failure following the bite of the giant desert centipede Scolopendra heros, West J Med 142:549, 1985.
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Mehr Z, Powers NR, Konkol KA: Myiasis in a wounded soldier returning from Panama, J Med Entomol 28:553, 1991.
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Mohamed AH et al: Proteins, lipids, lipoproteins and some enzymes characteristic of the venom extract from the centipede Scolopendra morsitans, Toxicon 21:371, 1983.
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Mumcuoglu KY, Liebovici V: Centipede (Scolopendra) bite: case report, Isr J Med Sci 25:47, 1989.
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Nunn P: Tangling with tumbu larvae, Lancet 343:646, 1994.
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Olulmide YM: Cutaneous myiasis—a simple and effective technique for extraction of Dermatobia hominis larvae, Int J Dermatol 33:148, 1994.
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Pallali L et al: Case report: myiasis—the botfly boil, Am J Med Sci 303:245, 1992.
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Pampiglione S, Schiavon S, Fioravanti ML: Extensive furuncular myiasis due to Cordylobia rodhaini larvae, Br J Dermatol 126:418, 1992.
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Poskitt L, Duffill MB: Sleeping with a ladybird: suspected bites from Diomus notescens, NZ Med J 105:132, 1992.
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Chapter 38 - North American Venomous Reptile Bites Robert L. Norris Jr. Sean P. Bush
INTRODUCTION North America is unique in that it is home not only to venomous snakes, but also to the world's only known venomous lizards. Fortunately, bites by venomous reptiles in North America are relatively uncommon, although precise statistics are not available. The only systematic attempt to evaluate the incidence of venomous snakebite in the United States was done in the late 1960s by Dr. Henry Parrish. He estimated that there were approximately 7000 bites by venomous snakes, of which approximately 15 ended in death.[106] The incidence of venomous snakebite may have changed significantly since Parrish's study, but given that snakebite is not a reportable "disease," no mechanism exists for obtaining reliable data. The incidence of snakebite in Canada is lower than that in the United States because fewer snakes species are found farther north up the continent. In Mexico, however, snakebite takes on increasing medical importance because this country has more venomous snake species than any other nation in the New World.[16] As many as 150 deaths may be caused by snakebite in Mexico each year.[46] Establishing credible estimates of the incidence of venomous lizard bites is even more difficult than for snakes. The vast majority of victims are bitten while intentionally interacting with the lizard, and since these creatures are legally protected, many bites are probably never reported. Many physicians called on to render acute care to snakebite victims have had limited experience with the potentially complex syndromes of snake venom poisoning. In addition, convincing research sponsors to fund needed studies evaluating prehospital care techniques, hospital management principles, and antivenom development is difficult when the targeted population size is only a few thousand individuals. Snake venoms are highly complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, minerals, and other unidentified substances. Venoms vary among species, within a single species depending on its geographic distribution, and even within an individual snake depending on factors such as age, diet, and health. [118] The effects of a particular venom may be different depending on the species of prey or research animal that has been poisoned. Such variables make it difficult to conduct meaningful research into snakebite management techniques. Table 38-1 lists the species of venomous reptiles found in North America.[16] [46] [52] [74] [115] The medically important North American venomous snakes all fall into the families Viperidae (subfamily Crotalinae, the crotalines or pit vipers) and Elapidae (elapids, the coral snakes). Although there are reports of human envenoming by a handful of species of Colubridae—the family of snakes traditionally regarded as harmless—the cases from North America have all been relatively minor and non-life threatening (see Chapter 39 ). Pit vipers are widely dispersed throughout most of North America below southern Canada (south of 55 degrees north latitude).[96] In the United States, for example, all 48 contiguous states except Maine have at least one pit viper species.[107] Being poikilothermic and relying on environmental heat energy to support locomotion, feeding, digestion, and reproduction, snakes tend to increase in numbers of species as one moves southward toward the equator. At least 34 species of pit vipers are found in North America, with many more subspecies. Pit vipers can be further divided into rattlesnakes (genera Crotalus and Sistrurus, approximately 30 species); copperheads, cottonmouth water moccasins, and cantils (genus Agkistrodon, three North American species and a number of subspecies); and lance-heads (genus Bothrops, with one species in eastern Mexico, B. asper).[46] Rattlesnakes are the most widespread of pit vipers, found throughout most of North America ( Figure 38-1 , Figure 38-2 , Figure 38-3 , Figure 38-4 , Figure 38-5 , Figure 38-6 , Figure 38-7 , Figure 38-8 , Figure 38-9 ). Copperheads (Agkistrodon contortrix) are found in the central and southeastern United States and westward into the Big Bend region of Texas ( Figure 38-10 ). Cottonmouth water moccasins (Agkistrodon piscivorus) are found in the southeast from Virginia to Florida and extend westward into central Texas ( Figure 38-11 ). In Mexico the copperhead and cottonmouth are replaced by the cantil, Agkistrodon bilineatus ( Figure 38-12 ). [52] The pit vipers of North America come in a wide range of sizes. Among the smaller rattlesnakes are the sidewinders (Crotalus cerastes), ridge-nosed rattlesnakes (C. willardi), and
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TABLE 38-1 -- Venomous Reptiles of North America PRESENT (?) IN GENUS
SPECIES/SUBSPECIES COMMON NAME
Crotalus
CANADA U.S. MEXICO
Rattlesnakes adamanteus
Eastern diamondback rattlesnake
—
?
—
atrox
Western diamondback rattlesnake
—
?
?
basiliscus
Mexican West Coast rattlesnake
—
—
?
catalinensis
Santa Catalina Island rattlesnake
—
—
?
cerastes
Sidewinder
—
?
?
durissus
Neotropical rattlesnake
—
—
?
enyo
Lower California rattlesnake
—
—
?
exsul
Cedros Island diamond rattlesnake
—
—
?
horridus
Timber/canebrake rattlesnake
?
?
?
intermedius
Small-headed rattlesnake
—
—
?
lannomi
Autland rattlesnake
—
—
?
lepidus
Rock rattlesnake
—
?
?
mitchelli
Speckled rattlesnake
—
?
?
mitchelli stephensi
Panamint rattlesnake
—
?
—
molossus
Black-tailed rattlesnake
—
?
?
polystictus
Lance-headed rattlesnake
—
—
?
pricei
Twin-spotted rattlesnake
—
?
?
pusillus
Tancitaran dusky rattlesnake
—
—
?
ruber
Red diamond rattlesnake
—
?
?
scutulatus
Mojave rattlesnake
—
?
?
stejnegeri
Long-tailed rattlesnake
—
—
?
tigris
Tiger rattlesnake
—
?
?
tortugensis
Tortuga Island diamond rattlesnake
—
—
?
transversus
Cross-banded mountain rattlesnake
—
—
?
triseriatus
Dusky rattlesnake
—
—
?
unicolor
Aruba Island rattlesnake
—
—
?
viridis abyssus
Grand Canyon rattlesnake
—
?
—
viridis caliginis
Coronado Island rattlesnake
—
—
?
viridis cerberus
Arizona black rattlesnake
—
?
—
viridis concolor
Midget faded rattlesnake
—
?
—
viridis helleri
Southern Pacific rattlesnake
—
?
?
viridis lutosus
Great Basin rattlesnake
—
?
—
viridis nuntius
Hopi rattlesnake
—
?
—
viridis oreganus
Northern Pacific rattlesnake
?
?
—
viridis viridis
Prairie rattlesnake
?
?
?
willardi
Ridge-nosed rattlesnake
—
?
?
Sistrurus
Rattlesnakes catenatus
Massasauga
?
?
?
miliarius
Pygmy rattlesnake
—
?
—
ravus
Mexican pygmy rattlesnake
—
—
?
Agkistrodon
Copperheads, water moccasins, cantil bilineatus
Cantil
—
—
?
contortrix
Copperhead
—
?
?
piscivorus
Cottonmouth water moccasin
—
?
—
—
—
?
—
?
?
Bothrops
Lancehead vipers asper
Terciopelo, cuatro narices
Micruroides
Coral snakes euryxanthus
Micrurus
Sonoran (Arizona) coral snake Coral snakes
bernadi
Saddled coral snake
—
—
?
bogerti
Bogert's coral snake
—
—
?
browni
Brown's coral snake
—
—
?
diastema
Variable coral snake
—
—
?
distans
Clear-banded coral snake
—
—
?
elegans
Elegant coral snake
—
—
?
ephippifer
Double black coral snake
—
—
?
fulvius
North American coral snake
—
?
?
laticollaris
Double collar coral snake
—
—
?
latifasciatus
Long-banded coral snake
—
—
?
limbatus
Tuxtlan coral snake
—
—
?
nebularius
Neblina coral snake
—
nigrocinctus
Black-banded coral snake
—
—
?
proximans
Nayarit coral snake
—
—
?
Heloderma
?
Venomous lizards suspectum
Gila monster
—
?
?
horridum
Mexican beaded lizard
—
—
?
Figure 38-1 Eastern diamondback rattlesnake (Crotalus adamanteus) is the largest pit viper of the United States and can attain lengths of 2 m. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
pygmy rattlesnakes (Sistrurus miliarius), whose adult sizes are routinely less than 65 cm.[74] At the other extreme, the eastern diamondback rattlesnake (Crotalus adamanteus) can exceed 2 m.[74] Outside of North America the family Elapidae contains a number of extremely dangerous species, such as cobras (genus Naja), mambas (genus Dendroaspis), and all the potentially lethal snakes of Australia (e.g., Oxyuranus, Notechis, Pseudonaja) (see Chapter 39 ). The
Figure 38-2 Western diamondback rattlesnake (Crotalus atrox) causes many serious bites in the U.S. Southwest. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
elapids of North America are all coral snakes and belong to one of two genera, Micrurus and Micruroides ( Figure 38-13 Figure 38-14 Figure 38-15 ). These colorful reptiles are found in Arizona (Sonoran coral snake, Micruroides euryxanthus), the southeastern United States (eastern coral snake, Micrurus fulvius fulvius), and Texas
(Texas coral snake, Micrurus fulvius tenere). Mexico has 15 species of coral snake, including M. euryxanthus and 14 Micrurus species. Because of the inoffensive habits of 899
Figure 38-3 Mojave rattlesnake (Crotalus scutulatus) has two geographic populations in terms of venom composition, one with predominantly neurotoxic effects and one with more local sequelae. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-4 Timber rattlesnake (Crotalus horridus) is a large, dangerous snake of the eastern United States. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-5 Prairie rattlesnake (Crotalus viridis viridis) is a widely distributed species of the western United States. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-6 Northern Pacific rattlesnake (Crotalus viridis oreganus) is a moderate-sized but very toxic snake of the Pacific Northwest. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-7 Southern Pacific rattlesnake (Crotalus viridis helleri) is one of nine subspecies of western rattlesnakes (C. viridis subsp.). (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-8 Tropical rattlesnake (Crotalus durissus durissus) is one of the large, dangerous subspecies of C. durissus distributed from southern Mexico through South America. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
900
Figure 38-9 Western pygmy rattlesnake (Sistrurus miliarius streckeri) is one of the smaller rattlesnake species of North America. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-10 Southern copperhead (Agkistrodon contortrix contortrix) has markings that make it almost invisible when lying in leaf litter. (Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
Figure 38-11 Cottonmouth water moccasin (Agkistrodon piscivorus) exhibiting its threat display. This snake is found most often around standing water sources in the southeastern United States. (Courtesy Sherman Minton, MD.)
Figure 38-12 Cantil (Agkistrodon bilineatus) is a close relative of the copperheads (A. contortrix) and cottonmouths (A. piscivorus) of the United States. This pit viper is found in Mexico and Central America. (Courtesy Michael Cardwell and William W. Lamar.)
Figure 38-13 Texas coral snake (Micrurus fulvius tenere) has a highly potent venom but is secretive, and bites are uncommon. (Courtesy Michael Cardwell and the Gladys
Porter Zoo.)
these fossorial (burrowing) snakes and their less efficient venom delivery device (see later discussion), bites are very uncommon. Although Parrish and Khan[109] estimated that fewer than 20 coral snake bites occurred in the United States each year, the 1998 report of the American Association of Poison Control Centers (AAPCC) Toxic Exposure Surveillance System listed 61 cases.[90] The only two known species of venomous lizards in the world are found in North America and belong to the genus Heloderma. The Gila monster (Heloderma suspectum, with two subspecies) is found in the southwestern United States (Arizona, western New Mexico, southeastern California, southern tip of Nevada, extreme southwestern Utah) and northwestern Mexico ( Figure 38-16 ). [133] The range of the Mexican beaded lizard (Heloderma horridum, with three subspecies) is below that of the Gila monster, south to Guatemala
901
Figure 38-14 Comparison of Texas coral snake (Micrurus fulvius tenere) with harmless Mexican milk snake (Lampropeltis triangulum annulata). Coral snake (bottom) has contiguous red and yellow bands, whereas the milk snake has its red and yellow bands separated by black. (Courtesy Charles Alfaro.)
( Figure 38-17 ).[124] The helodermatids are discussed in more detail later in this chapter.
VENOMOUS SNAKES Anatomy Pit Vipers.
The term pit viper comes from the presence of paired, highly sensitive, thermoreceptor organs (pits) present on the forward portion of these snakes' heads ( Figure 38-18 ). These structures, also known as foveal organs, serve the snake in locating prey, aiming strikes, and adjusting venom dose ( Figure 38-19 ). The foveal organs can detect temperature changes of as little as 0.003° C (0.0054° F).[96] A neurologic feedback loop between the foveal organs and the venom delivery apparatus may allow the snake to adjust the volume of venom it injects into a potential meal or a perceived threat.[149]
Figure 38-15 Sonoran coral snake (Micruroides euryxanthus) is also known as the Arizona coral snake. No documented fatality has followed a bite by this species. (Courtesy Michael Cardwell and Jude McNally.)
Figure 38-16 Gila monster (Heloderma suspectum) is one of only two known venomous lizards and the only species found in the United States. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 38-17 Mexican beaded lizard (Heloderma horridum) is located south of the Gila monster's range in Mexico. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
902
The anatomy of the venom delivery system of crotalines is the most sophisticated of all snakes ( Figure 38-20 ). Bilateral glands located at the sides of the head, above and behind the eyes, produce and store the venom. These glands are connected through ducts to more anterior accessory glands that probably serve to activate or potentiate the venom.[118] From here the venom is passed forward through other ducts into the
Figure 38-18 Pit viper's head. Note the elliptic pupil and the heat-sensing pit for which these reptiles are named. Viewed from above, the head has a distinctly triangular shape. Many nonvenomous snakes also possess triangular-shaped heads, however, this is not a reliable means of differentiation. (Marlin Sawyer, 1994.)
Figure 38-19 Paired heat-sensing pits of the pit vipers used to help the snake locate its prey, direct its strike, and probably determine the volume of venom to be expended. (Marlin Sawyer, 1994.)
proximal portion of the hollow fangs with which the snake pierces its victim in a stabbing motion. These fangs, found on the anterior surfaces of the maxillary bones, are large (up to 20 mm in large rattlesnakes[74] ) and highly mobile. At rest the snake folds the fangs against the roof of its mouth. For the strike, the fangs are brought into an upright position, perpendicular to the maxilla. The snake has voluntary control over its fangs and can open the mouth without raising the fangs or can raise each fang individually. The fangs are relatively brittle and fracture or become dull with time and use. Replacement fangs at varying stages of development behind the functional set move forward on the maxillary bone when needed ( Figure 38-21 ). The speed of a pit viper's strike has been clocked at 8 feet per second; the snake can reach distances of approximately one half of its body length.[149] Table 38-2 lists venom yields for various North American pit vipers. The fastest crotaline can crawl at a maximum speed of approximately 3 miles per hour, which equates to an average adult walking pace.[149] Pit vipers do not chase people. Accounts suggesting otherwise can be explained by snakes' poor eyesight; when threatened, they may retreat in the direction of people. The characteristic forked tongue of the snake is an olfactory tool and possesses none of the offensive "stinging" function ascribed to in folklore. The snake extends its tongue to detect chemical odors in its environment. The tongue is then retracted and its tips placed into the paired Jacobson's organs, lined with olfactory epithelium, in the roof of its mouth. This sensory
903
system is highly sensitive, allowing the snake to identify potential mates, locate food, and track down a prey item that has been struck and released. Pit vipers have elliptic, or catlike, pupils, whereas most North American harmless snakes have round
Figure 38-20 Venom delivery apparatus of a pit viper. Venom is produced in large venom glands just posterior to the eyes and is passed through a duct system into the hollow, anterior fangs when the snake bites. (Marlin Sawyer, 1994.)
Figure 38-21 Rattlesnake skull. Replacement fangs are behind the primary, functional fangs. The smaller teeth of the palatine, pterygoid, and mandibular bones are used for gripping food. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
pupils. A few essentially harmless, rear-fanged colubrids, such as the night snake (Hypsiglena torquata) and lyre snake (Trimorphodon biscutatus), also possess elliptic pupils but lack facial pits. Although these species possess a special venom gland (Duvernoy's gland) in the rear of the mouth, they are innocuous creatures. They are reluctant to bite humans, and their salivary toxins cause few signs or symptoms, other than slight swelling, bruising, and pain. This contrasts with the truly dangerous rear-fanged colubrids of other parts of the world (see Chapter 39 ). The two species of boas in North America, the rosy boa (Lichanura trivirgata) and rubber boa (Charina bottae), also possess elliptic pupils, but their body form (more cigar shaped and lacking the broad, triangular head of a pit viper) and skin patterns are very different from any pit viper. The caudal rattle of the rattlesnake is composed of loosely interlocked plates of keratin that emit a buzzing sound when the snake rapidly vibrates its tail. This characteristic sound serves as a warning to a perceived threat. A new segment to the rattle is added each time TABLE 38-2 -- Venom Yields of Some Medically Important Snakes of North America MAXIMUM VENOM YIELD (mg DRY WEIGHT)
SPECIES Crotalus adamanteus Crotalus atrox Crotalus cerastes
REFERENCE 848
[74]
1145
[74]
63
[74]
Crotalus durissus
514 (average)
[74]
Crotalus horridus horridus
160 (average)
[97]
Crotalus horridus atricaudatus
229
[74]
Crotalus molossus
540
[74]
Crotalus scutulatus
141
[74]
Crotalus viridis helleri
390
[74]
Crotalus viridis oreganus
289
[74]
Crotalus viridis viridis
162
[74]
33
[41]
Sistrurus catenatus Sistrurus miliarius
18 (average)
Agkistrodon contortrix
[74]
45
[107]
150
[107]
6
[115]
Micrurus fulvius
38
[115]
Micrurus nigrocinctus
20
[115]
Agkistrodon piscivorus Micruroides euryxanthus
904
the snake sheds its skin, which can be from one to several times each year, depending on its age, health, and feeding success. Newborn rattlesnakes have a single button present at birth. Not until after their first shed do they possess a true rattle that can create a sound. Rattles may be broken off during the snake's life and cannot be used reliably to determine age. Although rattlesnakes are quick to sound out a warning when threatened, it is a misconception that they will always do so before striking in defense. Another distinct anatomic feature of pit vipers is the scale pattern on the underside of the tail, the subcaudal scales. The junction of the snake's body and its tail can be easily ascertained by viewing its ventral side. At this location is a large scale (sometimes divided) known as the anal plate. Just distal to this in pit vipers is a sequence of single scales that entirely cross the ventral surface. In nonvenomous snakes and in coral snakes the subcaudal scales are paired (i.e., each covers approximately half the width of the tail) ( Figure 38-23 ). This feature becomes clinically useful when a snakebite
Figure 38-22 Coral snake's skull. Note the slightly enlarged anterior fang that is fixed in its upright position. (Marlin Sawyer, 1994.)
Figure 38-23 Subcaudal scale pattern of pit viper vs. a harmless snake. Pit viper (here, a rattlesnake) has a single scale that spans the ventral side of its tail, just distal to the anal plate, whereas harmless colubrid snake has a double row of scales. Coral snakes also possess a double row of subcaudal scales. (Marlin Sawyer, 1994.)
victim brings in the body of a decapitated snake for identification and when the skin pattern is unfamiliar to the physician. There are very few exceptions to this anatomic rule. The harmless long-nose snake (Rhinocheilus lecontei) and the rosy boas (L. trivirgata) and rubber boas (C. bottae) possess single subcaudal scales. Coral Snakes.
Coral snakes are identified primarily by color pattern. U.S. coral snakes are banded in a red-yellow-black-yellow-red pattern (see Figure 38-13 ), and the bands completely encircle the snake's body. The contiguity of the red and yellow bands distinguishes U.S. coral snakes from a number of harmless mimics (e.g., several king snakes and milk snakes, genus Lampropeltis), which generally have red and yellow bands separated by black bands. This can best be remembered by recalling the phrase "red on yellow, kill a fellow; red on black, venom lack" or by considering that the red and yellow lights on a traffic signal are the warning lights. Contiguous red
and yellow bands on a North American snake warn of its venomous potential. Exceptions to this rule are found south of Mexico city, including some routinely bicolor (red and black) specimens.[98] Although one harmless U.S. colubrid has a contiguous red and yellow banding pattern (the shovel-nosed snake, Chionactis species), this is an inoffensive reptile, and its bands do not completely encircle its body. In exceptionally rare cases, coral snakes can be all black (melanistic) or albino.[94] The coral snake venom apparatus is much less complex than that of the pit vipers. The paired venom glands connect through ducts to slightly enlarged, hollow, maxillary fangs that are fixed in an upright position in the forward portion of the jaw ( Figure 38-22 ). In
905
order for the coral snake to inflict a potentially serious bite, it must chew on the victim to inject a sufficient volume of venom through its relatively small fangs. These animals are not capable of striking out with the stabbing motion of the crotalines. In the vast majority of coral snakebite cases, the victim was handling the creature when bitten. Venoms Crotaline venoms contain proteins and peptides capable of damaging vascular endothelial cells, leading to increased permeability to plasma and erythrocytes. This results in translocation of fluids, which may progress to hypotension and shock. [148] Specific enzymes common to pit viper venom include proteolytic enzymes, hyaluronidase, thrombinlike enzymes, phospholipase A2 , L-amino acid oxidase, collagenase, RNase, DNase, and arginine ester hydrolase. Proteolytic enzymes damage muscle and subcutaneous tissue and are responsible for necrosis. Hyaluronidase decreases the viscosity of connective tissue, allowing venom to spread. Thrombinlike enzymes act by cleaving either fibrinopeptide A or fibrinopeptide B from fibrinogen without activating factor XIII. This results in formation of an abnormal, unstable fibrin clot, which is readily lysed by both endogenous plasmin and proteolytic enzymes in the venom.[118] This leads to hypofibrinogenemia and increased fibrin degradation products. Phospholipase A2 , common to all pit viper venoms, causes muscle necrosis by damaging cell membranes, which allows calcium influx and release of creatine and creatine kinase (CK). In addition, phospholipase A2 increases permeability of red blood cell (RBC) membranes, leading to ab-normal RBC morphology and potential hemolysis. Lysolecithin, a by-product of the enzymatic action of phospholipase A2 , damages mast cell membranes and results in histamine release.[21] Pit viper venom has both offensive (i.e., food gathering) and defensive functions. In predatory strikes the venom immobilizes the prey, facilitates its retrieval by altering its scent, and accelerates digestion.[19] [60] [62] Defensive strikes are meant to deter predators and tormentors. The amount of venom injected differs from bite to bite. Factors such as prey size and species, duration of fang contact, and time elapsed since last meal influence the amount of venom released. [60] [62] Rattlesnakes have been shown to inject significantly more venom into large mice than into small mice.[60] The mass of venom expended probably differs between predatory and defensive bites. In preliminary comparisons, venom expenditure by North American pit vipers appears greater in defensive bites than in predatory bites.[62] In one comparison the northern Pacific rattlesnake (Crotalus viridis oreganus) expended almost 4 times more venom when biting a hand model (defensive) than a mouse (predatory). [60] [62] The most important factor influencing potential venom delivery is the size of the snake.[62] A direct relationship has been demonstrated between snake length and mass of venom expended in both predatory and defensive bites.[58] [62] A popular belief is that juvenile rattlesnakes are more dangerous than adult snakes because their venom is more toxic and they are unable to control the volume they release. The venom of some juvenile rattlesnakes may be slightly more toxic, but larger rattlesnakes are capable of delivering much greater amounts of venom in a bite. Juvenile prairie rattlesnakes (Crotalus viridis viridis) have venom that is 2 to 3 times more toxic than that of adults.[33] Large adult snakes, however, deliver an average of 17 times more venom than do juveniles.[58] The ability to control venom expenditure has been demonstrated in juvenile rattlesnakes. In a series of first exposures to different-sized prey, "naïve" juvenile rattlesnakes injected similar quantities of venom into all size classes. However, in the second series of exposures, "experienced" snakes injected significantly more venom into larger prey.[59] The clinical relevance of this is uncertain. In many species, venom composition appears to change as the snake ages. Phospholipase A2 activity decreases with age, probably accounting for some decrease in toxicity. Proteolytic activity, however, increases with age, possibly to aid digestion of larger prey eaten by older, larger snakes.[58] Coagulopathic effects can be different between juvenile and adult western diamondback rattlesnakes (Crotalus atrox), partly due to greater amounts of thrombinlike enzymes in younger snakes.[113] Venom characteristics may vary with geographic origin of the snake. [44] Certain populations of the Mojave rattlesnake (Crotalus scutulatus scutulatus) cause human neurotoxicity with severe envenomation while causing minimal local tissue destruction and no hemorrhagic effects.[24] [69] Neurotoxic findings may include respiratory difficulty, generalized weakness, and cranial nerve palsies.[24] The venoms of these snakes possess a presynaptic neurotoxin, Mojave toxin, and are classified as venom A populations. Venom B populations lack Mojave toxin and are less toxic. Bites by venom B snakes result in consequences more typical of most rattlesnake venom poisoning: soft tissue swelling, necrosis, and coagulopathy. Venom A populations range from California, across western Arizona, Nevada, Utah, New Mexico, and Texas. Venom B populations are found in more eastern parts of Arizona. A zone of intergradation between venom A and venom B populations occurs along a line between Phoenix and Tucson. [53] [147] Toxins with structure and physiologic effects similar to those of Mojave toxin have been isolated from venoms of other species of rattlesnakes, including prairie rattlesnakes (Crotalus viridis viridis), midget faded rattlesnakes (C. v. concolor), tropical rattlesnakes (C. durissus), canebrake rattlesnakes (C. horridus), and tiger rattlesnakes (C.
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tigris).[42] [43] [61] [144] Geographic differences occur in the venoms of other snakes as well. Canebrake rattlesnakes (C. horridus) from Florida, Georgia, and South Carolina possess more neurotoxic and myotoxic "canebrake toxin" than do specimens from Alabama, Mississippi, Tennessee, and North Carolina.[43] Differences in concentration of this toxin correlate with variable clinical effects seen after bites by this species from different geographic regions.[17] Neurotoxicity has been clinically associated with severe myotoxicity in many cases.[13] [17] [27] [69] Severe rhabdomyolysis and myoglobinuric renal failure have been reported after Mojave rattlesnake envenomation and are thought to be related to Mojave toxin.[69] The association between neurotoxicity and myotoxicity has been confirmed in laboratory animals.[3] C. horridus specimens possessing significant amounts of the neurotoxin (canebrake toxin) produce a rise in serum CK levels as a biochemical signature of significant venom poisoning. The rise in CK appears to parallel the severity of poisoning by these snakes.[17] Autopsy findings have demonstrated that myonecrosis in this setting is systemic and not focused at the bite site.[17] [73] Concomitant rises in MB fractions of creatine kinase can occur in the absence of any clinical evidence of cardiac damage. In one such case, troponin-T was measured as negative despite abnormal total CK and CK-MB.[17] Lesser CK elevations (usually less than 500 U/L) may be seen with other rattlesnake bites, such as that of the eastern diamondback (Crotalus adamanteus). In these cases the elevations appear to more closely parallel local effects.[17] Mojave toxin is thought to inhibit acetylcholine release at the presynaptic terminal of the neuromuscular junction.[24] Myokymia, or muscle fasciculation, is often considered a manifestation of neurotoxicity. This phenomenon, however, occurs through a different mechanism than Mojave toxin-induced neurotoxicity. Muscle fasciculations are believed to be caused by the interaction of certain venom components with calcium or calcium binding sites on the nerve membrane.[24] Fasciculations may occur after envenomation by various species of rattlesnakes, including northern and southern Pacific rattlesnakes (C. viridis oreganus and C. v. helleri, respectively), eastern diamondback rattlesnakes (C. adamanteus), western diamondback rattlesnakes (C. atrox), Mojave rattlesnakes (C. scutulatus), and timber rattlesnakes (C. horridus). [6] [24] [141] Coral snake venoms have received less research attention; they are also less complex than pit viper venoms. Micrurus and Micruroides venoms have minimal proteolytic activity but contain the spreading enzyme hyaluronidase and some phospholipase A2 . [124] The primary lethal component is a low-molecular-weight, postsynaptic neurotoxin that blocks acetylcholine binding sites at the neuromuscular junction.[18] [139] In addition, the venom contains at least one myotoxic component that may clinically produce a rise in CK levels.[51] What coral snake venom lacks in complexity, it makes up in potency. Among U.S. snakes, Micrurus and Micruroides venom potency, as determined by median lethal dose (LD50 ) values in mice, are surpassed only by that of the Mojave rattlesnake (Crotalus scutulatus).[118] It is estimated that a full-grown coral snake carries enough venom in its delivery apparatus to kill four to five adult humans.[34] It is indeed fortunate that these toxic reptiles are shy, inoffensive, and possess a less effective venom delivery device than the pit vipers. Clinical Presentation Pit Vipers.
The clinical presentation of pit viper venom poisoning is quite variable, depending on the circumstances of the bite. Important factors include the species, size and
health of the snake, age and health of the victim, circumstances that led up to the bite, number of bites and their anatomic locations, and quality of the care rendered to the person, both in the field and in the hospital. Although statistics vary, most accidental bites occur to the lower extremities.[106] The next most common anatomic site is the upper extremity. Many of these bites occur while the victim is intentionally interacting with the snake (e.g., tormenting the animal, trying to catch it, or working with a captive specimen). Less often, bites occur to the head, neck, or trunk. Most bites occur around dawn or dusk, during warmer months, when snakes and people are more active outdoors.[106] A young, intoxicated male bitten on the hand while intentionally interacting with a snake is the most common clinical profile in the United States. About 75% to 80% of pit viper bites result in envenoming. Approximately one in every four to five bites is "dry," meaning no venom has been injected.[108] [118] The snake may voluntarily choose to save its venom for its next meal rather than waste it on a large human. Alternatively, the feedback mechanism may "short-circuit" between the pit organs and the venom apparatus, so that when faced with a huge, heat-radiating mass (a human), the system fails and no venom is expelled. Other possible causes of dry bites include glancing blows that fail to penetrate the skin and an exhausted venom supply. Approximately 35% of cases are mild envenomations, 25% moderate, and 10% to 15% severe.[108] Given their less efficient venom delivery system, coral snakes only effectively envenom approximately 40% of the time.[118] The clinical findings found in crotaline venom poisoning can be divided into local and systemic signs and symptoms ( Table 38-3 ). After most pit viper bites, severe burning pain at the site begins within minutes. Soft tissue swelling then progresses outward to a variable extent from the bite site. Over hours a bitten extremity can swell all the way to the trunk. Blood may
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TABLE 38-3 -- Signs and Symptoms of Rattlesnake Bites SIGN OR SYMPTOM
FREQUENCY*
Fang marks
100/100
Swelling and edema
74/100
Pain
65/100
Ecchymosis
51/100
Vesiculations
40/100
Change in pulse rate
60/100
Weakness
72/100
Sweating, chills
64/100
Numbness or tingling of tongue and mouth, scalp, or feet
63/100
Faintness or dizziness
57/100
Nausea, vomiting, or both
48/100
Blood pressure changes
46/100
Change in body temperature
31/100
Swelling regional lymph nodes
40/100
Fasciculations
41/100
Increased blood clotting time
39/100
Sphering of red blood cells
18/100
Tingling or numbness of affected part
42/100
Necrosis
27/100
Respiratory rate changes
40/100
Decreased hemoglobin
37/100
Abnormal electrocardiogram
26/100
Cyanosis
16/100
Hematemesis, hematuria, or melena
15/100
Glycosuria
20/100
Proteinuria
16/100
Unconsciousness
12/100
Thirst
34/100
Increased salivation
20/100
Swollen eyelids
2/100
Retinal hemorrhage
2/100
Blurring of vision
12/100
Convulsions
1/100
Muscle contractions
6/100
Increased blood platelets
16/100
Decreased blood platelets
42/100
Modified from Russell FE: Snake venom poisoning, New York, 1983, Scholium International. *Number of times the symptom or sign was observed per total number of patients.
persistently ooze from fang marks, marking the presence of anticoagulant substances in the venom. Ecchymosis is common, both locally and at more remote sites, as the vasculature becomes leaky and RBCs escape into the soft tissues ( Figure 38-24 and Figure 38-25 ). Fang marks are usually evident as small puncture wounds, but the precise bite pattern can be misleading.[100] Most nonvenomous snakebites result in multiple rows of tiny puncture wounds (from the maxillary, palatine, pterygoid, and mandibular teeth), which usually coagulate quickly. Pit vipers also possess palatine, pterygoid, and
Figure 38-24 Mottled rock rattlesnake (Crotalus lepidus lepidus) bite in a young man at 24 hours. Note the exudation of red cells into the soft tissues remote from the bite site. The man was bitten on his left thumb. (Robert Norris, MD.)
Figure 38-25 Hemorrhagic bleb at the site of a western diamondback rattlesnake (Crotalus atrox) bite at 24 hours. (Robert Norris, MD.)
mandibular teeth, which can result in more than the classic paired puncture marks. Also, a snake may make contact only with a single fang. Thus the associated signs and symptoms should be considered more than the bite pattern in determining whether a bite was inflicted by a pit viper or another snake. Some rattlesnake bites result in little or no local pain despite envenoming; the best example is the Mojave rattlesnake (Crotalus scutulatus). Specimens containing significant amounts of Mojave toxin in their venom tend to cause few local findings. This can lead the treating physician to misjudge the severity of envenoming.[149] Systemic findings after pit viper bites can be extremely variable because any organ system can be affected. Nausea with or without vomiting is common and may occur early in serious bites. The victim may complain of an overall sense of weakness. An odd sense of taste, such as a rubbery, minty or metallic taste, may be present.[118] Occasionally the victim complains of a numb sensation of the mouth or tongue. The vital signs may be abnormal. The respiratory and heart rates may be increased. The victim may experience respiratory
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distress due to neurotoxic components of the venom, especially after bites by venom A—producing Mojave rattlesnakes (C. scutulatus). [118] Another important cause of respiratory distress is pulmonary edema from pulmonary artery congestion and translocation of intravascular fluid into alveoli. This can be compounded by myocardial depressant factors in some venoms.[118] The victim's blood pressure may be elevated; however, hypotension, which may progress to frank shock, is more common in severe cases. In the first several hours, hypotension is usually caused by pooling of volume in the pulmonary and splanchnic beds. Later, as swelling progresses and fluids exude into remote soft tissues, intravascular volume can become significantly depleted. A rare cause of early shock is an anaphylactic reaction to the venom. [14] [29]
Musculoskeletal and neurologic abnormalities can be present. As mentioned, a number of rattlesnake venoms possess a component that can result in local or systemic muscle fasciculations as a sign of significant envenoming. These fasciculations can persist for many hours despite adequate treatment with antivenom. Other findings of neurologic dysfunction can include paresthesias, numbness, and frank motor weakness, especially after bites by some Mojave rattlesnakes (C. scutulatus) and eastern diamondback rattlesnakes (C. adamanteus). Although uncommon, hemorrhage can occur at multiple anatomic locations because of the complex procoagulant and anticoagulant fractions of some venoms.[118] Bleeding can occur in the gingival membranes, renal system (microscopic or frank hematuria), gastrointestinal tract (hemoccult-positive stools or frank blood per rectum), pulmonary tree (hemoptysis) or central nervous system. Laboratory evaluation of a victim of significant pit viper bite may reveal significant abnormalities. The white blood cell count may be elevated. The hematocrit may be elevated from hemoconcentration or may be depressed secondary to bleeding or hemolysis. Serum chemistries may be abnormal. Blood sugar may be elevated. Muscle damage can result in elevated serum potassium and CK levels. Renal dysfunction may result from hypotension, myoglobin and hemoglobin deposition, and direct venom effects.[22] Hepatic dysfunction with elevations of serum transaminases may be seen.[93] Coagulation studies may reveal significant abnormalities. Prothrombin time (PT) and partial thromboplastin time (PTT) can be prolonged. Fibrinogen levels may be depressed, along with an elevation of fibrin degradation products and d-dimers. [4] Major abnormalities may be seen in serum coagulation studies in the absence of any clinically significant bleeding (i.e., more serious than gingival oozing or microscopic hematuria).[9] This is particularly relevant in determining when to use blood products in treating these victims. Recurrent coagulopathic parameters may persist or recur for as long as 2 weeks after envenomation.[24] Urinalysis should be obtained to identify hematuria. Proteinuria and glycosuria may also be seen.[123] Each time the victim voids, the urine should be evaluated with bedside testing strips for the presence of blood. If venom poisoning seems severe or if the victim has significant underlying medical problems (e.g., cardiovascular or respiratory disease), an electrocardiogram (ECG), arterial blood gases (ABGs), and chest radiograph should be obtained. The ECG may reveal evidence of myocardial ischemia. ABGs give important information regarding adequacy of tissue perfusion and respiratory status. Pulmonary vascular congestion or frank pulmonary edema may be seen on the radiograph. Coral Snakes.
The findings of significant coral snake envenoming reflect the predominant neurotoxic effects of these venoms. The victim may have some early, mild, transient pain.[117] Local swelling is uncommon. Fang marks may be difficult to see and should be carefully sought.[102] Systemic signs and symptoms may be delayed as long as 12 or 13 hours after significant bites and can then progress rapidly.[73] The earliest findings may be nausea and vomiting, followed by headache, abdominal pain, diaphoresis and pallor.[32] Victims may complain of paresthesias or numbness or may have altered mental status, such as drowsiness or euphoria.[94] The victim may develop cranial nerve dysfunction (e.g., ptosis, difficulty speaking, difficulty swallowing), followed by peripheral motor nerve dysfunction.[94] In severe cases, respiratory insufficiency and aspiration are significant risks. [73] Cardiovascular insufficiency may also be seen. [123] Unlike many crotaline envenomations, coagulopathy is not a feature of coral snake venom poisoning. Laboratory studies are of little value in the evaluation of a victim of coral snake bite. Occasionally, a rise in serum CK and myoglobinuria occur, reflecting myotoxicity.[73] ABGs may be useful in evaluating the victim's respiratory status if endotracheal intubation is considered. A chest radiograph is indicated in the setting of apparent cardiac dysfunction or following intubation. Management Prehospital Care PIT VIPERS.
Recommendations for first-aid and prehospital treatment of pit viper venom poisoning are often based on speculation and anecdotal experience. Much of the literature is contradictory. In one large retrospective series, first-aid treatment had no relationship to ultimate envenomation severity.[148] Some first-aid measures recommended in the past cause more injury than the snakebite itself, and delays in care have been shown
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to increase morbidity and mortality.[29] [54] It is inappropriate to use any technique that could potentially injure the patient or impede immediate travel to the nearest facility where antivenom can be administered. General support of the airway, breathing and circulation should be provided based on the capabilities at hand. Oxygen, cardiac monitoring, and intravenous (IV) fluids should be used in the field when available. Although it may be necessary for the victim to hike out from the scene of the incident, activity should be minimized as much as possible. Alternative methods (e.g., helicopter or boat) of extracting the victim from a wilderness setting can be used when available and when conditions such as weather and terrain allow. Jewelry and tight-fitting clothing are removed from the involved extremity in anticipation of swelling. The border of advancing edema is marked with a pen every 15 minutes so that emergency personnel can estimate severity of poisoning by following the rate of progression. A negative pressure venom extraction device, The Extractor (Sawyer Products, Safety Harbor, Fla.) has been advocated by the Wilderness Medical Society as a temporizing or adjuvant measure before antivenom is available.[35] [45] This device, applied directly over fang marks, delivers approximately one atmosphere of negative pressure and requires no skin incisions. [53] To retrieve venom, the device needs to be applied as soon after the bite as possible, probably within 3 minutes.[7] Some recommend that suction continue for 30 to 60 minutes.[2] As blood, tissue fluid, and possibly venom fill the transparent suction cup, the vacuum is lost. The cup is emptied as needed and reapplied as the victim is transported to the hospital. Two small studies suggest some venom retrieval with this device. [7] [8] Two patients envenomed by C. atrox were treated within 1 minute with an Extractor.[8] The device was applied to each victim a total of 5 times and was left on each time until the
suction cup filled. An average of 27.5 µg of venom per milliliter of serosanguineous fluid was removed during the initial suction period, decreasing to 4.4 µg/ml by the end of the fifth application. This is much less than 1 mg of total venom retrieved and probably was not significant because the average venom yield for C. atrox is approximately 250 mg.[74] Tissue effects and outcome were not described. In a rabbit study, an estimated 34% of artificially injected, radiolabeled rattlesnake venom was retrieved using the Extractor.[7] The effects on local tissue were not described. Some suggest the Extractor may exacerbate tissue damage.[38] A study evaluating use of the device in pigs injected with rattlesnake venom demonstrated no difference in swelling between the Extractor group and controls.[11] A circular lesion corresponding to the size of the suction cup, however, developed in some animals and progressed to necrosis. This may have been caused by venom sequestration at the site of envenomation or suction-induced tissue ischemia. Use of the device clinically in humans has been documented in a few anecdotal case reports in nonmedical literature.[55] Its effect on outcome in these cases is difficult to determine, but in two of five cases a dark hemorrhagic bleb conforming precisely to the size of the suction cup formed over the fang puncture sites. Further research is needed to define the risks and benefits of mechanical suction in crotaline venom poisoning. Other devices producing lesser degrees of suction, such as kits with small, rubber suction cups, are of no benefit. Mouth suction is contraindicated because of the potential for contaminating the wound with oral flora. Incising the bite site across fang marks is not recommended. This creates additional injury and has never been shown to be effective. Because viperid fangs are curved, incisions may miss the track along which venom is actually injected. Incisions made by laypersons can cause serious injury to underlying blood vessels, nerves, or tendons. In the face of venom-induced coagulopathy, bleeding from such incisions can be severe.[53] Furthermore, the lack of sterile conditions in a field setting increases the risk of infection. Venom sequestration techniques, such as proper application of a lymphatic/superficial venous constriction band or pressure immobilization, inhibit the systemic spread of venom.[10] [135] In a porcine model, lymphatic constriction bands decreased systemic venom absorption without increasing local tissue swelling.[10] It is not clear, however, whether such measures improve outcome after pit viper envenomation. Some argue that restricting spread of potentially necrotizing venom to local tissues may intensify injury.[56] Since local sequelae are the predominant complications after pit viper venom poisoning in North America, and since permanent systemic injury and death are extremely rare, such attempts to limit venom to the bite site may be ill advised.[29] Also, proper placement of a constriction band can be difficult for a lay provider. The band is applied several inches proximal to the bite site and just tight enough (at a pressure of approximately 20 mm Hg) to occlude lymphatic and superficial venous flow while sparing arterial and deep venous perfusion.[10] Appropriate tightness, however, is difficult to gauge. If applied more loosely, the band would be ineffective. If placed too tightly or with ongoing swelling, the band could become an arterial tourniquet.[10] [56] Tourniquets have worsened injury when used for snakebite and are contraindicated. [53] Use of a constriction band for a pit viper bite should be based on the situation. If the victim has been bitten by a potentially lethal snake, such as a large rattlesnake (greater than three feet), and is more than 60 minutes from medical care, a constriction band may reduce the chances of a poor systemic outcome, although local
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necrosis could worsen. More research is also needed on constriction bands. Pressure immobilization has been used effectively in Australia for field management of elapid snakebites (see Chapter 39 ).[136] The technique involves wrapping the entire extremity, starting at the bite site, with an elastic or compressive bandage and immobilizing it with a splint. Although one small study suggests this technique is effective in experimental eastern diamondback rattlesnake (C. adamanteus) venom poisoning,[135] the concerns about severely restricting venom movement at the site and worsening local necrosis again apply. Patients bitten by pit vipers often complain of severe pain and do not tolerate pressure immobilization well.[56] The Venom Ex device (Arachnodata, Frauentalweg 97, CH-8045 Zurich) combines a constriction band, incision, and suction.[55] The device consists of six parallel cutting blades (5 mm wide and adjustable to 5 mm in length), a buckled tourniquet (used as a constriction band), and a spring-loaded syringe (20 ml) for suction. The concept is to apply the constriction band, inflict multiple incisions into the bite site, and apply suction to the bleeding wounds. No evidence indicates that this device is beneficial in crotaline bites, and because it uses controversial interventions with potential risks, it is not recommended. Simple immobilization of the extremity with a splint has not been studied but is unlikely to cause any direct harm. The optimal position for the splinted extremity is not known. The bitten appendage should probably be maintained at heart level, if possible, to balance systemic spread of venom against extremity swelling. All field management recommendations are based primarily on theory and speculation, with very little science available on which to make an informed decision. This area is open for future research. Until more definitive data are available, the following principles can be used as guidelines. The victim should be calmed, reassured, and transported as expeditiously as possible to the hospital. A splint can be applied en route if materials are immediately available, and the extremity should be kept at heart level unless the victim is required to walk. These measures suffice as adequate prehospital care for the vast majority of cases of pit viper bites in the United States. Decisions regarding the use of a mechanical suction device (e.g., Extractor), a constriction band, or pressure immobilization must take into consideration the risk of worsening local tissue damage. For the victim of a pit viper bite who is many hours or days from medical care, the best course of action is even less clear and highly dependent on the situation. First-aid measures (reassurance, splint, maintenance of extremity at heart level) should be applied. If present, a companion may hike out for help, if conditions allow for prompt return of a rescue team. At times, if sufficient rescuers are available, the victim can be carried out. The victim who must hike out should use a makeshift crutch (for a lower extremity bite), should rest frequently, and should maximize oral intake of fluids unless vomiting becomes pronounced. Electrotherapy was proposed in the late 1980s for first-aid treatment of snakebites and subsequently was popularized by the lay press.[55] [63] Guderian et al[49] described 34 indigenous people bitten by unidentified snakes in Ecuador who were treated with electric shocks. Four or five direct-current (DC) shocks (20 to 25 kV, less than 1 mA) were applied to each bite site. Shocks were given every 5 to 10 seconds and lasted 1 to 2 seconds each. The victims apparently developed no local or systemic effects of envenomation, and the authors concluded that treatment was effective. Early proponents recommended application of high-voltage, low-amperage, DC shocks to the bite site using a source such as an outboard motor or lawn mower engine.[48] A "stun gun," typically designed for self-defense, was even modified by one company and marketed for snakebite treatment. [55] This marketing was prohibited by the U.S. Food and Drug Administration (FDA) in 1990 because of total lack of testing or evidence of efficacy. Critics of the Ecuadorian observations suggest many reasons for Guderian's findings. Many of the bites may have been delivered by nonvenomous species, which closely resemble dangerous reptiles in this part of the world, and many indigenous peoples consider all snakes dangerous. The victims who made it to the missionary hospital from the Ecuadorian jungles may have been a self-selected population with less severe bites that would have done well without any treatment.[55] [125] In subsequent controlled animal studies, electric shock showed no efficacy in reducing morbidity or mortality after rattlesnake poisoning in mice, rats, or rabbits.[67] [70] [132] In humans, application of electric shock for snakebite has been associated with acute myocardial infarction and increased local tissue damage secondary to electrical burns.[28] [119] Because of its lack of efficacy and inherent risks, electric shock should not be used in the treatment of snakebites. Local application of ice to the bite wound as a first-aid measure has not been adequately studied as to its benefits or risks. This should not be confused with "cryotherapy," or packing the injured limb in ice for extended periods. This form of treatment was popularized in the 1950s and 1960s. The results of cryotherapy were a significant increase in tissue loss and amputation rate after pit viper bites, and it has now been completely abandoned.[116] Whether brief (e.g., less than 1 hour) application of ice is beneficial (by reducing venom activity or decreasing pain) or harmful (by worsening local ischemia and resulting necrosis) is unknown. The American Red Cross recommends that no
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cooling measures should be applied in the field management of venomous snakebite. [141] Indigenous peoples in many parts of the world have long used plants in the treatment of snakebite, either topically or systemically, but little formal research has been done in this area. No current data support the use of any plants in the management of North American snakebite.[66] Other first-aid measures lacking therapeutic value or potentially more harmful than the snakebite itself include scarification of the bite wound, ingestion of alcohol, use of stimulants, and various folk remedies such as application of ammonia, silver nitrate, oil, potassium permanganate, or saliva. Similarly ineffective is the application of poultices made from various parts of the offending reptile (or other creatures), such as the snake's crushed head, bile, or fat.[118] Antivenom use in the field can be recommended only when a qualified physician is on scene and when all equipment and drugs are available to manage a potential anaphylactic/anaphylactoid reaction to the serum (including definitive airway management equipment). Newer, potentially safer antivenoms produced using Fab
technology (see later discussion) may prove to be safe enough for field use, although monetary costs could be prohibitive.[31] Attempts to secure or kill the snake are not recommended because of the risk of additional bites to the victim or rescuer and because precious time can be wasted. Currently the same treatment principles and antivenoms apply for all pit viper bites in North America, so absolute identification of the snake is not necessary. Focus is on "treating the bite, not the snake." Serious morbidity and even death have been reported after envenomation by decapitated rattlesnake heads. [17] [73] [134] In addition, an apparently dead snake or a decapitated snake head can have a bite reflex for up to 1 hour after death. Therefore emergency personnel and hospital care providers should exercise extreme care if handling any specimens accompanying the victim. CORAL SNAKES.
After a bite by a potential coral snake, the animal's skin color pattern should be noted if possible. Because of the potential delay in onset of signs and symptoms after coral snake envenoming and because the recommendation is to administer antivenom to such victims even in the absence of clinical findings, distinguishing between a coral snake and a harmless mimic becomes important. If the snake can be safely captured and contained, this can be helpful if done quickly. Although research into field management measures for coral snake envenoming is minimal, the Australian pressure immobilization technique would probably be useful. Being elapids, coral snakes are related to the venomous snakes in Australia for which this technique has been shown to be highly effective in limiting venom absorption (see Chapter 39 ). Hospital Care ( Box 38-1 ) PIT VIPERS.
As in all emergent medical care, initial attention must be focused on the victim's airway, breathing, and circulation. Most victims should receive supplemental oxygen until it is clear that they are stable. Pulse oximetry and cardiac monitoring should be instituted and two large-bore IV lines established. The initial management of hypotension or shock should include vigorous fluid resuscitation with crystalloids (normal saline or Ringer's lactate). If organ perfusion remains inadequate after vigorous fluid infusion (e.g., 2 L of crystalloid in an adult, 20 to 40 ml/kg in a child), a trial infusion of albumin should be started. Evidence supports the utility of adding albumin early in this setting because of the rapid onset of increased vascular permeability after significant pit viper envenomation.[126] Vasopressors should be used to treat venom-induced shock only as a last resort, after adequate volume infusion and initiation of antivenom therapy. Prolonged, inadequately treated hypotension has been strongly implicated in fatal cases of venom poisoning. [29] [56] Antivenom is the definitive treatment for serious pit viper envenomation. Antivenin (Crotalidae) Polyvalent (Wyeth-Ayerst Laboratories, Philadelphia, Pa.) has been the only commercially available antivenom in the United States for crotaline envenomation since 1954. Antivenin (Crotalidae) Polyvalent is derived from the serum of horses immunized to the venom of two North American and two South American pit vipers: the eastern diamondback rattlesnake (C. adamanteus), western diamondback rattlesnake (C. atrox), South American rattlesnake (C. durissus terrificus), and fer-de-lance (Bothrops atrox). This antivenom can be used for bites by any North American pit viper, as well as all the Central and South American crotalines and some Asian pit vipers. The degree of protection, however, varies according to the species involved. Since this product is manufactured using only four different snake venoms, its ability to protect against crotalines with significantly different venoms (e.g., the Mojave rattlesnake, C. scutulatus) is lessened. As a heterologous serum product, Antivenin (Crotalidae) Polyvalent carries some significant risks in its use. Early, acute reactions to antivenom can be either anaphylactic (type I, IgE mediated) or anaphylactoid (due to direct complement activation).[148] These immediate reactions are clinically indistinguishable and may manifest with urticaria, pruritus, flushing, facial edema, vomiting, diarrhea, crampy abdominal pain, bronchospasm, laryngeal edema, and hypotension. Approximately 20% of patients who receive the Wyeth product can be expected to have an early reaction, and
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about half of these are serious.[28] [71] Deaths from allergic reactions to antivenom (airway obstruction, cardiovascular collapse) are rare.[71] [120] Risk factors for allergy to antivenom (e.g., previous exposure to equine serum, history of allergy to horses) should be considered when deciding on a course of therapy.
Box 38-1. 38-1 MANAGEMENT PRINCIPLES IN TREATING A VICTIM OF POTENTIAL PIT VIPER BITE IN NORTH AMERICA Determine: was the snake venomous? Determine: is there evidence that venom poisoning has occurred? Assess and support: airway, breathing, and circulation. Establish two large-bore intravenous lines for crystalloid infusion. Obtain appropriate laboratory studies. Measure the bitten limb's circumference at two or more sites every 15 minutes. If systemic signs or symptoms or laboratory abnormalities are present, obtain and reconstitute an appropriate antivenom. Obtain informed consent for antivenom infusion if possible. Have epinephrine (appropriate subcutaneous dose) drawn up at the victim's bedside for possible acute reaction to antivenom. Perform skin testing for possible allergy to antivenom if indicated. If the skin test is negative or if antivenom is to be given without skin testing, pretreat with H1 - and H2 -blocking antihistamines. Expand the victim's intravascular volume with crystalloid fluids unless contraindicated. Dilute the vials of antivenom to be given in crystalloid (1 L for adult, 20–40 ml/kg for child). Begin antivenom by slow intravenous infusion. Gradually increase the rate of infusion in the absence of an acute reaction. If a reaction occurs, stop the antivenom and treat as necessary. Consider the need for further antivenom: Further antivenom to be withheld: provide conservative care only. Further antivenom to be given: dilute the antiserum further; administer intravenous steroids; restart the antivenom at a slower rate. If reaction continues in the face of severe poisoning: Admit to the intensive care unit (ICU). Institute maximal monitoring as needed. Consult an expert in snake envenomation. Titrate epinephrine drip against the reaction. Provide wound care. Determine management approach: Apparent dry bite: admit to hospital or observe for a minimum of 8 hours. Any degree of envenomation: admit to hospital. Severe venom poisoning: admit to ICU.
Another, more common reaction to Antivenin (Crotalidae) Polyvalent is serum sickness (type III, IgM- and IgG-mediated hypersensitivity reaction), characterized by rash, fever, chills, arthralgias, lymphadenopathy, and malaise. In severe cases, there may be renal or peripheral nerve involvement. Serum sickness may occur in as many as 50% to 75% of patients 3 days to 3 weeks after antivenom administration. [71] [149] The likelihood of serum sickness increases with total antivenom dosage and it usually occurs when eight or more vials of Antivenin (Crotalidae) Polyvalent are given.[71] The risks of adverse reactions to antivenom must be weighed against the potential benefit of improved mortality and morbidity from its administration. Informed consent should be obtained whenever possible. Severity grading and dosage of antivenom.
Deciding when to use antivenom in a case of pit viper venom poisoning can be difficult. The risks of adverse reactions to the antivenom must be weighed against the benefits of reducing venom toxicity. Antivenom should certainly be given when evidence indicates serious envenomation (e.g., cardiovascular insufficiency, respiratory difficulty) or imminent risk of an acute complication (e.g., life-threatening bleeding, tissue necrosis, compartment syndrome, rhabdomyolysis). Snake venom poisoning is a dynamic process. Initiation of antivenom or administration of additional vials is indicated in the victim with a worsening clinical course ( Figure 38-26 ). Antivenom therapy is predicated on imparting passive immunity to the victim against circulating snake venom antigens. Once these deleterious antigens bind to their target tissues, antivenom is unable to pull them off or reverse their effects. Therefore, to be most effective, antivenom should be given as soon as possible after the bite, preferably within 4 to 6 hours.[75] Antivenom may be useful, however, in patients with significant coagulopathy or acute renal failure for days after envenomation.[121] Venom antigens have been detected as late as 13 days after venomous snakebite.[39] The clinical implications of prolonged, recurrent, isolated, and mild coagulopathy and the utility of late antivenom administration remain unresolved. No clear endpoints for antivenom's therapeutic window have been established. Decisions about initial dosing of antivenom in cases of venomous snakebite are based on the apparent or predicted severity of poisoning. The grading scale described in Table 38-4 can be very useful to physicians in determining the severity of North American pit viper bites, but it should not be applied to bites by non-crotaline
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Figure 38-26 A, Soft tissue swelling, hemorrhagic blebs, and early necrosis after red diamond rattlesnake (Crotalus ruber) bite to the long finger (day 2). Victim received 10 vials of antivenom 6 hours after the bite and 10 more vials for severe thrombocytopenia on day 2. B, Seven weeks later. Note the degree of necrosis. (Sean Bush, MD.)
TABLE 38-4 -- Clinical Severity Grading Scale for Pit Viper Bites in North America LOCAL FINDINGS SYSTEMIC SIGNS AND LABORATORY STUDIES SYMPTOMS
SEVERITY Nonenvenomation (dry bite)
Puncture wounds only
and None
and Normal
Minimal envenomation
Puncture wounds
and None
and Normal
and Mild (e.g., nausea, vomiting, general weakness, mildly abnormal vital signs)
or
Mildly abnormal (e.g., slightly decreased platelet count or fibrinogen; presence of fibrin degradation products; slightly increased PT/PTT; hemoconcentration)
or
Profoundly abnormal (e.g., coagulopathy; hemolysis/severe anemia; renal dysfunction)
Swelling limited to bite site Bloody ooze from bite site Local ecchymosis Local pain (may be severe) Moderate envenomation
As for minimal, but swelling may involve entire extremity Severe pain
Severe envenomation
May be severe (e.g., severe soft tissue swelling and pain)
and Very abnormal vital signs Shock
May be less severe than expected (especially if deep or intravenous deposition of venom)
Respiratory distress
Significant clinical bleeding species. A more detailed snakebite severity score was developed as a research tool, but is not intended for clinical use.[30] The grade of envenomation at any given time is determined by whichever parameter (local effects, systemic effects, or laboratory abnormalities) is most severely affected. In nonenvenomations, or "dry bites," fang marks are present but there are no other clinical signs or symptoms and no laboratory abnormalities. The victim has only superficial punctures that require
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standard wound care, including tetanus prophylaxis as necessary. Minimal envenomation results in effects confined to the immediate area around the bite site (pain, swelling, erythema, ecchymosis). Systemic effects are absent and laboratory values normal. In a moderate envenomation, local effects progress beyond the immediate bite area but involve less than the entire body part (arm or leg). Local effects are generally quantified in relation to the extent of involvement of the bitten extremity. Systemic effects begin to appear when venom poisoning reaches moderate severity and may include paresthesias, strange taste sensations, numbness of the mouth and tongue, muscle fasciculations (myokymia), generalized weakness, and mild hypotension. Along with systemic signs and symptoms, laboratory abnormalities occur. Coagulation times (e.g., PT, PTT, international normalized ratio) may be elevated, platelets may drop to less than 90,000/mm3 , fibrinogen may fall below 90 mg/dl, and CK levels may exceed 500 to 1000 U/L. Although evidence is limited that antivenom corrects venom-induced thrombocytopenia, rhabdomyolysis, or myokymia, [4] [24] these abnormalities serve as markers of systemic injury and the need for antivenom therapy. With severe venom poisoning, local effects may rapidly involve the entire body part and may become limb threatening. Systemic manifestations may include shock, clinically significant hemorrhaging (e.g., hematemesis), respiratory difficulty, and multifactorial renal failure. Severe muscle fasciculations may contribute to respiratory difficulty. Profound laboratory abnormalities, such as thrombocytopenia less than 20,000/mm3 , coagulopathic parameters associated with potentially life-threatening bleeding, or rhabdomyolysis/myoglobinuric renal failure, also indicated severe envenomation. Antivenom dosing is directed by clinical severity of venom poisoning. No antiserum is necessary in dry bites, and it is questionable whether the risks associated with the use of Antivenin (Crotalidae) Polyvalent ever justify its use in mild venom poisoning. Some authors recommend a starting dose of 5 vials in mild cases.[118] For moderate poisoning the initial dose should be 10 vials, and for a severe case, 15 to 20 vials. If symptoms, signs, or laboratory parameters continue to deteriorate after the initial dose of antivenom, further dosing in 5- to 10-vial increments every 30 minutes to 2 hours is indicated. A typical total dose of Antivenin (Crotalidae) Polyvalent for a serious rattlesnake envenomation is approximately 20 to 40 vials. Although few studies have compared children with adults in terms of the effects of crotaline venom poisoning, higher doses of antivenom should be used in pediatric victims.* Children may receive a higher dose of venom per kilogram of body weight, which may predispose them to greater toxicity. With adequate antivenom administration, however, children do not appear any more susceptible to systemic venom effects than adults. [29] Special bite situations.
Systemic findings may be delayed after bites by venom A-producing Mojave rattlesnakes (C. scutulatus), with deceptively minimal local tissue effects. This can lead to underestimation of severity based on the grading scale in Table 38-4 . Therefore, in geographic areas where this variant is found, some recommend that antivenom be started empirically for known Mojave bites, regardless of the initial apparent severity of the bite.[12] [148] Antivenin (Crotalidae) Polyvalent provides relatively poor coverage for C. scutulatus venom, which supports this recommendation.[122] To compensate for reduced overall efficacy in these cases, Wyeth's Antivenin (Crotalidae) Polyvalent is usually given early and in larger doses than for most other rattlesnake bites. Copperheads (Agkistrodon contortrix) and cottonmouths (A. piscivorus) generally cause less severe clinical effects that do most rattlesnakes. Many Agkistrodon envenomations can be treated without Antivenin (Crotalidae) Polyvalent.[30] [146] Severe envenomation, however, regardless of the crotaline species involved, requires antivenom therapy. Antivenom administration.
Reconstituting lyophilized Antivenin (Crotalidae) Polyvalent can be an onerous task. Each vial must be dissolved in 10 ml of diluent. Although the antivenom comes with a vial of 10 ml of sterile water for this purpose, any typical diluent (e.g., sterile water, normal saline) can be used. Using warm diluent helps facilitate reconstitution. Gentle agitation of each vial for several minutes is required to redissolve the proteins. Care must be taken to not denature the antiserum with overzealous shaking. It may take as long as 30 minutes to fully reconstitute the antivenom, so this process should be started as soon as the need for antiserum has been identified. Wyeth recommends a skin test for possible allergy to equine-derived products before administration of Antivenin (Crotalidae) Polyvalent. This involves intradermal injection of 0.02 to 0.03 ml of a 1:10 dilution of normal horse serum into an unbitten extremity (e.g., volar forearm). A small vial of normal horse serum is packaged along with the lyophilized antivenom and diluent. A positive test is manifested by a wheal and flare reaction within 5 to 30 minutes. Skin testing, however, is very unreliable. As many as 10% to 28% of persons with a negative skin test still manifest an acute reaction to antivenom, and up to 30% with a positive skin test have no reaction if antivenom is still given.[71] [130] Furthermore, people can develop an acute reaction or delayed serum sickness to the skin test alone.[130] Since the test takes up to 30 minutes to be called negative, it is reasonable to forego *References [ 1]
[ 14] [ 26] [ 29] [ 142] [ 148]
.
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testing in a patient with clear indications for antivenom treatment. If antivenom might be withheld with a positive skin test (e.g., non-life-threatening, moderate envenomation), testing can be considered. In these cases, using actual reconstituted antivenom (further diluted to 1:10 or 1:100) rather than normal horse serum may increase the predictive value of the test. Along with the serum skin test, a similar volume of normal saline should be injected intradermally in the opposite arm as a negative control. Skin testing may be useful in predicting immediate hypersensitivity but has no value in predicting eventual serum sickness. Furthermore, skin testing can sensitize individuals to antivenom, making use of this product even more risky in the event of a future venomous snakebite. Skin testing is not recommended when antivenom is either not indicated (dry bite) or clearly indicated (severe bite). Antivenom is still indicated for severe venom poisoning, even with a positive skin test. In this case, management should proceed as for the victim with severe poisoning who reacted adversely to the antivenom during its infusion (see later discussion). Any time antivenom is given, an acute adverse reaction should be anticipated and preparations made to manage a life-threatening situation. Airway equipment must be immediately available and two functional IV lines secured. Before beginning antivenom infusion (but after interpreting any administered skin test), the patient may be premedicated with appropriate doses of antihistamines. Both an H1 blocker (e.g., diphenhydramine, 1 mg/kg) and an H 2 blocker (e.g., cimetidine, 5 mg/kg up to 300 mg) can be given intravenously to prevent or mitigate any acute reaction. Expanding the victim's intravascular volume with an appropriate bolus of crystalloid (e.g., 1 to 2 L in an adult, 20 to 40 ml/kg in a child) may also prevent or blunt such a reaction.[1] If the risk of allergy is high (e.g., past history of known allergy to horses or horse serum products), a prophylactic dose of epinephrine can be considered as well. Epinephrine has been shown to reduce the incidence of acute reactions to antivenom. Subcutaneous administration of 0.25 ml of epinephrine (1:1000 aqueous) reduced acute adverse reactions from 43% to 11% in one randomized, controlled, prospective series of 105 patients.[111] No patients pretreated with epinephrine had severe reactions to antivenom, whereas 8% of patients who did not receive epinephrine had reactions. Epinephrine must be used with caution in persons at risk for ischemic heart disease or stroke. If coagulopathy is present, prophylactic epinephrine should be avoided because of the risk of elevating blood pressure and causing intracranial bleeding.[145] The very short half-life of epinephrine would certainly limit any potential benefits from its prophylactic use. Routine premedication with corticosteroids is not common practice in the United States; it is more common in Australia. Since the beneficial effects of steroids in limiting allergic phenomena would not be present for 4 to 6 hours, and since steroids may worsen local effects of venom poisoning by North American pit vipers,[128] steroids are generally not given unless an acute reaction has occurred. Once the vials of antivenom are dissolved, each should be further diluted before administration. Many early reactions to antivenom are related to the concentration of the product that is given intravenously[1] ; therefore Antivenin (Crotalidae) Polyvalent should be given in a relatively dilute form. For adults without preexisting cardiac insufficiency the initial total dose can be placed into a liter of normal saline or Ringer's lactate. For children, the total starting dose should be placed into a volume equivalent to 20 to 40 ml of crystalloid fluid/kg up to 1 L. The infusion should be started at a slow rate (e.g., 1 ml/min) for the first 10 to 20 minutes, with the attending physician monitoring for signs of acute reaction. If no adverse reaction occurs, the rate is increased to complete the infusion over 1 to 2 hours; children should receive approximately 10 to 20 ml/kg/hr. If an acute reaction develops, the antivenom infusion should be stopped immediately and the response treated. This may require administration of epinephrine, further antihistamines (both H1 and H2 blockers), and steroids. Appropriate ventilatory and circulatory support should be instituted as needed. Once these interventions have stopped the reaction, the physician must determine if antivenom therapy is still indicated. In most cases, antivenom infusion can be restarted, but after further dilution of the antiserum (twofold if the patient's cardiovascular reserve will tolerate the increased volume) and at a slower rate. If the reaction was serious or persists after restarting the antivenom, and if the venom poisoning is life threatening, the patient should be placed in an intensive care setting with maximal cardiovascular monitoring. Invasive monitoring (e.g., arterial line access) is helpful as long as no coagulopathy would make such line placement risky. An epinephrine IV infusion should be established (starting at 0.1 µg/kg/min) and titrated to hold the anaphylactic reaction at bay as further antivenom is infused. Generally, enough antivenom can be administered using this technique to benefit the patient's outcome.[13] [91] Careful reevaluation of the need for antivenom should be made before embarking on this hazardous approach. It is advisable to consult with a specialist who manages difficult envenomations. New antivenoms.
Much work has been done worldwide to develop new, more effective, and safer antivenoms for snakebite therapy. For North American pit vipers, a new product may be more potent and less allergenic than Antivenin (Crotalidae) Polyvalent. [25] [31]
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This antivenom (CroFab, Protherics, London) is derived from four groups of sheep, each immunized to the venom of one of four species of crotaline: eastern diamondback rattlesnake (Crotalus adamanteus), western diamondback rattlesnake (C. atrox), venom A-producing Mojave rattlesnake (C. scutulatus scutulatus), and eastern cottonmouth water moccasin (Agkistrodon piscivorus piscivorus). These four genetically dissimilar snakes were chosen to optimize the degree of cross-protection against venoms of all clinically important North American pit vipers.[25] The ovine IgG molecules from each resulting monospecific antiserum are papain digested into Fc and Fab fragments. The immunogenic Fc portion is precipitated and discarded. The protective Fab portions are isolated by affinity chromatography to the venom against which they are active. These Fab fragments are subsequently desorbed and combined in equal parts to yield a polyspecific, crotaline, Fab antivenom. [25] [31] This antivenom should cause fewer allergic reactions than Antivenin (Crotalidae) Polyvalent. Ovine IgG is not glycosylated, unlike equine IgG(T), and therefore is less immunogenic. In addition, Fab fragments, with their single binding site, are incapable of cross-linking immune complexes and stimulating the cascade of mediator release that results in anaphylaxis.[72] Immunologic response is less likely because the immunogenic Fc portion is eliminated and the molecule is smaller.[129] Also, this ovine Fab for injection, with its smaller molecular size, is more rapidly cleared by the kidneys; thus it may prevent serum sickness by reducing immune complex deposition in tissues. A smaller molecule may also allow improved tissue penetration and better access to available venom.[65] In animal models CroFab has been shown to be 3 to 10 times more potent than Antivenin (Crotalidae) Polyvalent in protecting mice against lethal effects of venom from various North American pit vipers.[25] [95] In clinical trials the initial dosage of CroFab ranged from 4 to 12 vials, with repeated doses of 2 to 6 vials given for recurrence or progression of swelling or systemic effects.[24] [31] [127] Venom effects may recur after initial treatment because Fab fragments are cleared before all venom antigens are neutralized.[127] In the first 42 patients treated with CroFab, there were 7 early serum reactions (5 with "urticaria," 1 "cough," and 1 "allergic reaction" manifested by urticaria, dyspnea, and wheezing).[104A] There were also 5 late serum reactions (2 with "rash," 1 with "pruritus," 1 with "urticaria," and 1 "serum sickness" manifested by severe rash and pruritus.)[104A] CroFab received FDA approval in October 2000. Per the manufacturer, it is indicated for mild and moderate North American pit viper venom poisoning.[104A] Almost certainly, the product will be effective in severe cases, as well. The precise degrees of cross protection, however, for crotaline species other than those used in its manufacture remains to be determined. It is intended for IV administration. No skin test is recommended. No premedication is mentioned in the package insert, but appropriate medications (epinephrine and antihistamines) should be immediately available if a reaction occurs.[104A] The starting dose for CroFab is 4 to 6 reconstituted vials, further diluted to 250 ml of normal saline.[104A] Similar to Antivenin (Crotalidae) Polyvalent administration, CroFab should be started slowly for the first several minutes while observing the patient closely for any signs of adverse reaction. If all goes well, the rate is increased to get the initial dose administered in 1 hour. The victim should then be observed over the course of an additional hour for evidence that control of abnormalities has been achieved. If there is evidence of progression of local findings or if coagulation studies and systemic signs and symptoms fail to return to normal, 4 to 6 additional vials should be given until such stabilization occurs. Then 2 vials should be given every 6 hours for up to 18 hours (3 doses). Further dosage requirements after that time period have not been determined. There is evidence that patients with significant coagulopathies during the initial phase of their poisoning may have recurrence of these findings during the first 2 weeks after the bite.[104A] The clinical significance of these findings and the need for additional antivenom remains to be determined. Certainly, patients should be warned of this potential recurrence of coagulopathy and the need to return if there is any evidence of bleeding and to avoid elective surgical procedures during this time period. Monitoring therapy.
Antivenom administration should continue until the patient is stabilized. This may include reduced swelling, subjective systemic improvement, and stabilization or
normalization of vital signs and laboratory values. Muscle fasciculations should not be used as a guide for continued administration of Wyeth's Antivenin (Crotalidae) Polyvalent, since they may be refractory to this therapy. Preliminary reports, however, suggest that myokymia improves with administration of the new Fab antivenom.[24] Neurotoxicity has been documented to improve with antivenom administration, even with delayed administration. [13] [24] The efficacy of antivenom in treating venom-induced coagulopathy and thrombocytopenia is not established. Although Antivenin (Crotalidae) Polyvalent binds to venom antigens responsible for these effects, abnormalities in hemostatic parameters may persist or recur.[4] [127] In several reports, venom-induced thrombocytopenia improved after antivenom infusion. [9] [57] [114] Other reports contradict these findings.[112] [138] In a series of patients envenomed by timber rattlesnakes (Crotalus horridus), PT and PTT, but not thrombocytopenia, normalized after antivenom therapy.[4] In another series, rattlesnake venom-induced thrombocytopenia usually
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improved after antivenom infusion, although the degree of improvement was small, frequently incomplete, and did not appear to be related to the total dose of antivenom given.[15] Seifert et al[127] reported investigational use of Fab antivenom (CroFab) in a thrombocytopenic victim of western diamondback rattlesnake (Crotalus atrox) venom poisoning. Although the platelet counts rebounded from 12,000/mm3 to 227,000/mm3 within 1 hour, recurrent thrombocytopenia was documented from day 5 through day 10, possibly because of more rapid clearance of Fab fragments than venom antigens. Blood products.
In the rare situation of significant clinical hemorrhage after pit viper venom poisoning (e.g., gastrointestinal bleeding, central nervous system hemorrhage), transfusion of blood products, including platelets, plasma or packed RBCs, may be necessary. Antivenom should always be started before factor replacement to avoid adding further fuel to an ongoing consumptive coagulopathy. Packed RBCs should be considered for acute, severe anemia (e.g., hemoglobin less than 7 g/dl). Solvent/detergent-treated plasma or fresh-frozen plasma may be needed to replace depleted coagulation factors if bleeding is significant, and cryoprecipitate may be added as needed for fibrinogen levels less than 100 mg/dl.[9] Regardless of the presence or absence of bleeding, platelet transfusion should be considered for a count of less than 20,000/mm3 . Any improvement in platelet count after transfusion, however, may be temporary.[4] [138] Patients with dangerously low platelet counts should be placed on bed rest to lower the risk of bleeding until counts rebound. Analgesia and wound care.
Pain control can be a significant issue after pit viper venom poisoning. Analgesia is best obtained using appropriate, titrated doses of opiates (e.g., IV morphine sulfate, 2 to 10 mg in adults and 0.1 mg/kg in children; repeated as needed if vital signs allow). Aspirin and nonsteroidal antiinflammatory drugs should be avoided because they may exacerbate coagulopathies. Wound care for pit viper venom poisoning follows standard principles. Tetanus immunization (diphtheria-tetanus toxoid, 0.5 ml intramuscularly) is recommended if the patient's immunization is not up-to-date. Any wounds should be cleaned and the extremity placed in a well-padded splint with additional padding between the digits. The extremity is then elevated above the heart to reduce swelling. Antivenom, if indicated, should be started before elevating the limb. Although snakes' mouths are colonized with several potentially pathogenic organisms, such as Pseudomonas aeruginosa, Staphylococcus epidermidis, Enterobacteriaceae species, and Clostridium species, wound infections from bites are uncommon, and prophylactic antibiotics are unnecessary in most cases.[23] [143] Pit viper
Figure 38-27 Rarely indicated fasciotomy in a victim of severe rattlesnake bite (Crotalus viridis helleri). Compartment pressures were greater than 60 mm Hg despite aggressive antivenom therapy. (Robert Norris, MD.)
venom has antibacterial activity, which may account in part for the low incidence of wound infections.[137] If misdirected first-aid efforts included incisions into the bite wound or mouth suction, an appropriate broad-spectrum antibiotic (e.g., amoxicillin/clavulanate) should be considered. If secondary infection occurs, appropriate aerobic and anaerobic wound cultures (and possibly blood cultures, depending on the clinical situation) should be obtained. Empiric therapy should then be started (e.g., ciprofloxacin, 500 mg orally twice a day in adults). If anaerobes are suspected, metronidazole or clindamycin in appropriate doses can be added. Children and pregnant women can be treated with an initial dose of ceftriaxone (50 mg/kg up to 1 g IV or IM) followed by oral amoxicillin/clavulanate (40 mg/kg divided 3 times a day). Daily wound monitoring will guide decisions regarding repeat doses of ceftriaxone until culture and sensitivity results are available. Abscesses should be drained as usual. An infected snakebite should prompt further examination of the wounds for potential retained teeth or fangs. Radio-graphs may be helpful but are not particularly sensitive. Compartment syndrome is a rare occurrence after venomous snakebite. [36] [101] The diagnosis can be difficult because an envenomed arm or leg is often very swollen, discolored, tender, and painful on attempted range of motion of the digits. These findings may closely mimic a compartment syndrome. To differentiate the subcutaneous swelling from intramuscular swelling, it is relatively simple to measure intracompartmental pressures using a wick catheter or digital readout device. If compartmental pressures exceed 30 to 40 mm Hg, antivenom should be started or continued while the extremity is elevated above heart level. The hemodynamically stable patient should receive IV mannitol (1 to 2 g/kg) over 30 minutes. These measures may reduce the pressures to safe levels.[20] If the pressures fail to decrease within 60 minutes, a fasciotomy
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is needed ( Figure 38-27 ). A surgical consultant (hand, orthopedic, or general) should be involved if compartment syndrome is a possibility. Prophylactic fasciotomy, however, is not recommended. In animal studies, prophylactic fasciotomy did not reduce the amount of muscle necrosis when rattlesnake venom was injected intramuscularly.[37] Muscle necrosis after pit viper envenomation is primarily caused by direct myotoxic venom effects rather than any increase in intracompartmental pressure. Although the fangs of many pit vipers are long enough to penetrate muscle compartments, most crotaline bites result in subcutaneous deposition of venom.[118] Management approach.
Disposition decisions for patients bitten by pit vipers are generally straightforward. Admission to an intensive care unit (ICU) is prudent for victims with severe envenomations or with progressive clinical findings and need for further antivenom administration. Persons bitten in the head, neck, or trunk should be monitored in an ICU because of the greater risks associated with these bites. Patients who develop a serious adverse reaction to antivenom, such as anaphylaxis, should also be admitted to the ICU. Victims who require a higher level of care than available at the treating institution should be transferred to an appropriate facility. After antivenom infusion and clinical stabilization, victims of moderately severe poisoning can be admitted to a basic floor. Admission to the hospital should be strongly considered for all persons with apparent envenomation. In one series, more than half of persons with minimal or no signs of envenomation at presentation subsequently developed significant envenomation with moderate to severe swelling, elevated PT, or thrombocytopenia. [68] About 25% of these persons deteriorated more than 8 hours after envenomation. Even with apparent resolution of swelling, victims may later develop severe toxicity.[50] Because onset and progression of signs and symptoms after a pit viper bite vary greatly, all potential victims should be closely watched in the emergency department for a minimum of 8 hours if not admitted. Because of the delayed onset of findings with some Mojave rattlesnake bites, all persons with suspected Crotalus scutulatus bites should be admitted to the hospital for 24 hours of observation. Admission is also highly recommended for children with potentially venomous snakebites. Discharge is considered after 8 hours of observation for victims who apparently sustained a dry bite. These victims have no symptoms or signs other than puncture wounds. All laboratory studies and vital signs must be normal. On discharge, patients should be instructed to return for onset of swelling, increased pain, bleeding, blood in the urine, severe headache, difficulty breathing, rash, joint pain, swollen lymph nodes, fever, or signs of wound infection. The victim should be scheduled for a follow-up reexamination in 24 to 48 hours and should be accompanied and assisted by another if needed. At time of hospital discharge, patients who received antivenom should be reminded about the possibility of developing serum sickness and that they need prompt
medical attention if they develop fever, arthralgias, myalgias, urticaria or other findings consistent with a type III reaction within the first few weeks after treatment. Serum sickness is usually benign and self-limited. Most patients can be adequately treated as outpatients with steroids (e.g., oral prednisone, 1 to 2 mg/kg/day) and antihistamines (e.g., oral diphenhydramine, 25 to 50 mg 4 times a day in adults and 5 mg/kg/day in divided doses for children). Steroids should be continued until signs and symptoms of serum sickness resolve, then tapered over 1 to 2 weeks. In patients more severely affected, treatment can begin in the hospital with IV steroids in equivalent doses. Discharge instructions to patients should also include information on ways to prevent venomous snakebite. More than half of bites occur during intentional interaction with the reptiles.[99] These usually involve attempts to handle, harass, capture, or kill the snake. The bite may be inflicted by a specimen in captivity. Avoiding intentional interaction with venomous snakes can prevent most injuries. Wearing shoes and long pants can prevent some strikes. In areas where snakes are common, young children should be closely supervised and older children educated to avoid snakes. Animal control services should be called to remove snakes found close to human habitation. If a snake is encountered in the wilderness, people should carefully move a safe distance away from the snake. Assistance with managing a victim of snakebite can be obtained from regional poison control centers, including the University of Arizona Poison and Drug Information Center (520-626-6016), Rocky Mountain Poison Control (303-739-1123), and San Diego Regional Poison Control (accessed via a central number for California poison control centers, 800-411-8080). The Antivenom Index, published by the American Zoo and Aquarium Association (8403 Colesville Rd., Suite 710, Silver Springs, MD 20910; 301-562-0777) and the AAPCC list U.S. antivenom sources. CORAL SNAKES.
Hospital management of coral snake bite victims can be challenging. The first priority in the stable victim is to determine that a coral snake was actually the culprit; photographs of coral snakes and nonvenomous mimics indigenous to the area can be useful. If a coral snake is identified and appears to have inflicted an effective bite, management should proceed in anticipation of a significant envenoming, even if systemic abnormalities are currently absent. Evidence supports
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this approach because the progression of neurotoxicity can be extremely difficult to halt once it begins, even with antivenom administration.[117] The patient should receive cardiac and pulse oximetry monitoring, and an IV line should be established. A history and careful physical examination should be performed; local findings are minimal, and fang marks can be difficult to see. The victim typically has little or no swelling and variable local pain. The victim should be carefully assessed for any neurologic abnormalities. Evidence of respiratory dysfunction or difficulty with secretions demands aggressive airway management. Early endotracheal intubation should be considered in such cases to prevent aspiration and its complications. Laboratory studies have little benefit except for ABGs if respiratory insufficiency is suspected. Bedside pulmonary function testing may be of some benefit in monitoring the patient's status. If a coral snake inflicted an effective bite, preparation for antivenom administration should begin, even in the absence of systemic signs or symptoms. [73] Several antivenoms are produced for coral snakes of the Western Hemisphere. The antivenom currently available in the United States is manufactured by Wyeth-Ayerst (Antivenin [Micrurus fulvius]) using eastern coral snake (M. fulvius) venom. It is effective against bites by the eastern (M. f. fulvius) and Texas (M. f. tenere) coral snakes. It has no proven benefit against Sonoran coral snake (Micruroides euryxanthus) venom. No antivenom is currently produced for this species, but it is a small, inoffensive creature, and no deaths have been reported after its bite. Treatment of patients bitten by the Sonoran coral snake is entirely supportive. There is little information regarding efficacy of Antivenin (Micrurus fulvius) for other Micrurus species of North America. If a significant bite has occurred by a Mexican Micrurus, its use is probably warranted. Preparation for antivenom administration is similar to that for pit vipers. Informed consent is obtained if possible. Skin testing for potential allergy to horse serums is inaccurate and of little benefit in making therapeutic decisions. The victim's intravascular volume should be expanded with prudent crystalloid infusion and the patient premedicated with intravenous antihistamines (both H1 and H2 blockers). The starting dose for the antivenom is three to six vials, diluted in 500 to 1000 ml of crystalloid (in 20 ml/kg for pediatric patients). [149] IV infusion is begun at a slow rate, with the physician and epinephrine at the bedside, to ensure no adverse response occurs (anaphylactic or anaphylactoid reaction). The rate is then increased to administer the entire dose over approximately 2 hours. If a reaction occurs, the antivenom infusion should be temporarily halted and the patient treated as necessary (e.g., epinephrine, further antihistamines, steroids). Once the reaction is treated, the antivenom can usually be restarted at a slower rate after further dilution of the dose. If a severe reaction occurs, a difficult decision must be made: whether to continue antivenom administration efforts, as outlined for pit viper antivenom reactions, or to treat the patient conservatively (endotracheal intubation as needed and respiratory support). Respiratory paralysis after severe bites can be prolonged and may require days to weeks of mechanical ventilation. [73] All victims of potential coral snake bite should be admitted to an ICU for close monitoring even if a dry bite is suspected. If signs of neurotoxicity progress after initial antivenom infusion, three to five more vials should be administered; rarely are more than 10 vials required.[104] Snakebites in Pregnancy As with all disease states that can occur in pregnant women, the management approach that optimizes fetal outcome is the one that best supports the mother. Fortunately, snake bites are rare in pregnant women in North America. The potential effects of snake venom on the fetus have not been well studied, although fetal malformation has been described.[92] Preterm labor and abruptio placentae have also been reported after pit viper envenomation. [103] [150] The anticoagulant and proteolytic actions in most crotaline venoms probably are responsible for disrupting integrity of the placental attachment to the uterus. To inhibit these systemic venom effects, antivenom administration is important, even though antivenom carries an FDA "Category C" designation for safety in pregnancy (i.e., "uncertain safety—animal studies show an adverse effect, no human studies"). Informed consent may be even more important to obtain, if possible, in this situation. Standard doses of antivenom should be used, although the severity rating should be liberally upgraded in pregnant patients. If an acute allergic reaction develops during antivenom administration, antivenom should be temporarily stopped. Epinephrine should be avoided because of its adverse effects on uterine blood flow. Instead, ephedrine should be given at a dose of 25 to 50 mg by slow IV push.[105] This dose can be repeated every 30 minutes as needed. Other drugs (e.g., antihistamines, steroids) should be given as for the nonpregnant patient. Antivenom administration can usually be restarted in a more dilute concentration and at a slower rate. Additional consultation is advisable. Other management principles for snake-bitten pregnant women include early obstetric consultation, fetal monitoring, and early ultrasonography for fetal/placental assessment. Morbidity and Mortality Pit Vipers.
Reliable estimates of morbidity and mortality from snakebite in the United States are not available,
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TABLE 38-5 -- Snake-Related Deaths Reported to American Association of Poison Control Centers, 1983–1998 YEAR DEATHS TOTAL BITES SPECIFICS REPORTED* 1983
1
717 Rattlesnake
1984
1
1347 Rattlesnake
1985
0
1676
1986
0
2416
1987
1
2701 Rattlesnake
1988
0
3076
1989
1
3851 Prairie rattlesnake: 27 year-old male was bitten on two fingertips by 2-foot-long prairie rattlesnake (Crotalus viridis viridis). He arrived in ED 15 minutes later. Swelling rapidly progressed to upper arm over next 2 ½ hours. He skin-tested positive to antivenom but was pretreated with diphenhydramine, epinephrine, and methylprednisolone; 5 vials of antivenom in 250 ml D5W started. After 20 minutes, with 60% of antivenom given, he developed anaphylaxis. He was given IV epinephrine, and cricothyroidotomy was performed because he could not be intubated secondary to laryngospasm. He arrested. Autopsy revealed bronchospasm but no swelling of the upper airway.
1990
0
4461
1991
1
5255 Unidentified rattlesnake: 52-year-old male was bitten on thumb by an unidentified rattlesnake in central Oregon at high altitude. In ED 20 minutes later, he complained of circumoral numbness, tingling, and flushing. Vitals were BP 140/94, pulse 92, and respiration 16. Thumb had "two entrance wounds and minimal swelling." No skin test was performed. He was given 6 ml of a solution of 5 vials of antivenom in 500 ml D5W when he became diaphoretic and dyspneic with increased pulmonary secretions. He became near syncopal. Antivenom was discontinued, and he was intubated and given epinephrine and steroids. He became hypotensive and developed asystole within 15 minutes. Studies showed acidosis, hemoconcentration, and mild coagulopathy. Autopsy revealed extensive coronary artery disease.
1992
2
1055 Northern Pacific rattlesnake: 20-year-old male was handling snake when it bit him on the lips. He collapsed, began vomiting, and then was driven 3 miles to hospital. Forty minutes later he was intubated, but arrested during procedure. He was resuscitated with epinephrine, atropine, and 5 vials of antivenom for 30 minutes before recovering a sinus rhythm and BP of 100/60. He developed profound coagulopathy and was given 30 vials of antivenom. He was later determined to be brain dead. Autopsy showed brain edema and herniation. Blood alcohol level was 207 mg/dl. Black Indian cobra: 25-year-old male snake expert was bitten on the toe by gravid pet black Indian cobra. He died within minutes. Autopsy revealed bloody pulmonary exudate, cerebral edema, and fine petechial rash.
1993
0
5653
1994
2
6317 "Presumptive ... Mohave [sic] Green rattlesnake": 40-year-old male was bitten while working in bushes. He collapsed 20 minutes later. In ED 4 ½ hours later, he was comatose and in atrial fibrillation with labile blood pressure. He was intubated for poor respiratory effort. Fasciculations and metabolic acidosis were noted. Two small puncture wounds 1 cm apart were then noted on the forearm and lower leg. The presumptive diagnosis of Crotalus scutulatus scutulatus bite was made and antivenom administered. He was cardioverted to normal sinus rhythm and dopamine was started, but he remained hypotensive. He developed disseminated intravascular coagulation and died on hospital day 8. Rattlesnake: 34-year-old male "snake handler" was bitten on the hand when he picked up a rattlesnake on the road. He collapsed 10 minutes after being bitten, and his family began CPR. Medics arrived 30 minutes later, and he was in full arrest. He was intubated, given IV fluids, dopamine, antivenom, and hydrocortisone. He died within 3 hours. Autopsy revealed hemorrhage in the myocardium, alveoli, pancreas, and kidney. Although the airway was patent, he had laryngeal edema, pulmonary edema, and evidence of aspiration. His right coronary artery was 75% stenotic. Blood alcohol level was 118 mg/dl.
1995
2
7100 Canebrake rattlesnake: 35-year-old male was bitten near radial artery while playing with Crotalus horridus. He was asystolic when medics arrived 30 minutes later. At autopsy, no necrosis was noted. Blood alcohol level was 250 mg/dl. Reptile other/unknown
1996
0
7494
1997
2
7045 Rattlesnake: 4-year-old male bitten on the thigh was treated with 5 vials of antivenom and transferred. He was intubated en route, subsequently developing massive swelling. He arrested, was resuscitated, and given additional antivenom, then arrested again in PICU 7 hours after envenomation. Poisonous exotic snake
1998
0
TOTAL
13
7194 67,358 2 deaths appeared to be caused by anaphylaxis to antivenom. All were male. Ages: 4, 20, 25, 27, 35, 40, 52. 10 rattlesnakes, 2 exotics, 1 unknown. 2 autopsies revealed coronary artery disease. 3 victims were intoxicated with alcohol. Bites: 1 facial, 4 upper extremity, 2 lower extremity, 1 both. Time to death varied from minutes to 8 days.
ED, Emergency department; D5W, 5% dextrose in water; BP, blood pressure; CPR, cardiopulmonary resuscitation; PICU, pediatric intensive care unit. *Includes all bites by reptiles (including exotics, nonpoisonous, and unknowns).
but mortality is extremely rare. Extensive work by Parrish in the late 1950s revealed an estimated 7000 venomous snakebites per year with approximately 15 deaths.[106] No one to date has repeated Parrish's systematic evaluation of the problem. The best current information comes from the AAPCC. In 1997, about 7000 reptile bites were reported to regional centers in the AAPCC.[89] Only 10 deaths from endemic venomous snakes were reported to the AAPCC between 1983 and 1998 ( Table 38-5 ).[76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [140] When the offending reptile was identified, almost all were rattlesnakes. These numbers are underestimates and can be used only as a rough gauge of incidence and mortality. Not all venomous snakebites, even fatal ones, are reported to the AAPCC. The 1998 statistics, for example, reveal that no fatal snakebite cases were reported to the AAPCC Toxic Exposure Surveillance System.[90] Snakebite is not classified as a reportable disease, and no reliable government statistics exist. Mortality from snakebite depends on treatment. Before the introduction of Wyeth's Antivenin (Crotalidae) Polyvalent in 1954, mortality rates were estimated as high as 5% to 25%.[108] After this time, mortality rates in patients treated without antivenom declined to approximately 2.6%, largely because of improvements in other aspects of care (e.g., ICU, fluid resuscitation). Antivenom, however, further reduces the mortality rate to 0.28%, a statistically and clinically significant tenfold reduction.[108] This difference should be even more significant when newer, safer, and more effective antivenoms become available. Other than death, permanent systemic morbidity after pit viper envenomation is rare.[29] Local sequelae are more common. The reported incidence of permanent local morbidity is less than 10%, although this does not include complications that may follow surgical interventions.[46] Most patients recover fully after rattlesnake envenomation in the United States, but the incidence of local complications is probably underestimated. Unless careful follow-up is done, including range of motion and sensory testing, permanent disabilities that impact lifestyle and occupation can be missed.[128] Although not clearly substantiated, children are probably more susceptible to systemic morbidity and mortality from snakebites.[1] [26] [142] Better pediatric supportive care and improved understanding of how antivenom should be administered have blurred any distinction between pediatric and adult prognosis.[29] Elderly patients appear to have a higher case-fatality rate, probably related to comorbid conditions.[29] Morbidity and mortality from snakebites also result from efforts to treat the victim. Significant wound complications can follow ill-advised incisions in and around the bite site and application of mouth suction.[40] [149] Serious burns and systemic complications, such as myocardial infarction, can follow application of electric shocks to the wound. [28] [119] Tourniquets or ice may increase the risk of tissue damage. Equine antivenoms
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can precipitate early anaphylactic or anaphylactoid reactions and delayed serum sickness (see earlier discussion). Coral Snakes.
Although no deaths have been reported from coral snake bites in the United States since Antivenin (Micrurus fulvius) was introduced,[118] the mortality rate if bites were untreated is estimated at approximately 10%.[109] Prolonged muscle weakness is common after severe envenoming, and victims with respiratory compromise may require mechanical ventilation for many days. There are no reports of permanent sequelae in patients who survive coral snake envenomation.
VENOMOUS LIZARDS Anatomy The two venomous lizards of the world are impressive creatures about which much misinformation has been spread for centuries. They have been thought to possess supernatural features such as poisonous breath, a stinging tail and the ability to spit their venom.[118] The Gila monster (Heloderma suspectum) reaches a maximum length of approximately 50 cm, whereas the beaded lizard (Heloderma horridum) is larger, reaching almost a meter. They are both heavily built and possess massive muscles of mastication with powerful biting capacity. The venom delivery apparatus consists of a pair of anterior, multilobed, interior labial glands that open through a series of ducts into the labial mucosa. Their teeth are lancet shaped, grooved, and loosely attached to the jaws. When the reptile becomes agitated, it salivates heavily, producing a flow of venom into the labial mucosa. It bites with a powerful, chewing motion, instilling venom into the wounds by capillary action along the grooves of the teeth. Teeth may be left in the wounds, especially if the lizard must be forcefully removed from the victim ( Figure 38-28 ). The tenacious creature may still be attached when help arrives. Effective envenomation occurs in only about 70% of bites.[5] Venom Gila monster and beaded lizard venoms are similar in composition and are as potent as some rattlesnake venoms.[131] They possess enzymatic components, including hyaluronidase (spreading factor), protease, phospholipase A2 , and kallikrein-like substances, and nonenzymatic substances such as serotonin. Venom kallikreins stimulate the release of vasoactive kinins, such as bradykinin, which are largely responsible for occasional hypotension seen after helodermatid bites.[133] Clinical Presentation The vast majority of victims bitten by a lizard are attempting to catch or handle the reptile; accidental bites
Figure 38-28 Teeth of the helodermatid lizards are grooved to aid instillation of venom during a bite. These teeth are loosely adherent and may become dislodged in the bite wound. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
are rare. Most bites involve captive animals, and many are not reported. Significant bleeding often occurs from punctured and torn tissues. Throbbing or burning pain may radiate proximally along the bitten extremity. Local edema may be progressive. Victims may complain of generalized weakness, nausea and vomiting, difficulty breathing, profuse sweating, dizziness, and paresthesias.[64] [118] [133] On examination the victim may be tachycardic, hypotensive (related to kinin release), and diaphoretic.[64] The wounds generally reveal significant local tissue trauma with variable bleeding. The site may be cyanotic or ecchymotic with local vasospasm.[118] Regional lymphadenopathy may be present on arrival to medical care or appear later. [5] Management Prehospital Care.
Data are minimal regarding prehospital care of venomous lizard bites. In some cases the first priority is to detach the lizard from the victim. The lizard can be placed under running hot water, or the jaws can be pried apart using a stick or metal instrument.[133] Care must be taken not to injure the victim further and to avoid a second bite, perhaps to the rescuer. Once freed from the lizard, the victim should be placed at rest and the bite site rinsed and cleaned as much as possible. Any bleeding should be stopped with direct pressure. No evidence supports the use of suction devices, ligatures, or pressure immobilization. Some advocate local ice to reduce pain,[131] but signs of vasoconstriction must be monitored to prevent later tissue loss.[118] A dressing to stop bleeding and a splint to limit movement may be beneficial. Transport to a medical facility should be carried out as expeditiously as possible. Incisions and electrotherapy should be strictly avoided.
923
Hospital Care.
Assuming the lizard has been detached before arrival at the hospital, the victim's airway, breathing and circulation are assessed. Vital signs should be obtained while the patient is being placed on oxygen and cardiac/pulse oximetry monitoring. At least one large-bore IV line should be established with either normal saline or Ringer's lactate. If the victim is hypotensive or tachycardic, a second line should be placed. The victim with hypotension should receive an infusion of physiologic saline (1 to 2 L for an adult, 20 to 40 ml/kg for a child). Hypotension rarely persists after volume resuscitation. If necessary, vasopressors can be added after the victim's intravascular volume has been repleted.[133] Laboratory studies include complete blood count, serum electrolytes, renal function studies, and coagulation studies. Total WBC may be elevated, and in severe cases, platelets may be decreased.[118] Although lizard venoms do not appear to possess anticoagulant fractions, coagulopathy of unclear mechanism has been reported after severe bites.[5] Hemostatic abnormalities in these victims may not result from the venom but rather from endothelial damage.[133] Urinalysis is useful to assess for microscopic hematuria or renal casts. These bites can cause transient electrocardiogram (ECG) abnormalities, such as T-wave anomalies and conduction delays.[5] [64] Myocardial infarction has been reported after Gila monster bites. [5] An ECG is recommended if the victim shows any sign or symptom of venom poisoning. Once the victim's overall status is stabilized, attention focuses on wound care. A soft tissue radiograph of the bite site may identify retained lizard teeth but does not replace careful exploration of the wounds.[64] After an assessment of functional status, the wound can be anesthetized using a local or regional block. The bite site should then be carefully explored for damage to underlying vital structures and for retained teeth. Thorough cleansing and irrigation should follow exploration. The wounds are dressed and splinted with generous padding. The extremity is then elevated to reduce swelling and discomfort. Opiates may be necessary in the management of pain during the victim's initial evaluation and for any pain not controlled by local or regional anesthesia. The victim's tetanus immunization status should be updated. Prophylactic antibiotics are not required.[133] Daily wound care should include cleansing with soap and water, followed by hydrogen peroxide, application of a topical antiseptic, and redressing. After the first 24 hours a course of physical therapy can be helpful in more rapidly returning the patient to full function. If the bite appears to be dry (i.e., victim relatively asymptomatic, vital signs/studies/ECG normal), the victim can be discharged home after approximately 6 hours of observation in the emergency department. This assumes the victim has proper resources for care at home and can return if status deteriorates. Proper wound care instructions should be given and the patient scheduled for reevaluation in approximately 24 to 48 hours. An oral opiate analgesic may be prescribed. Evidence of envenoming (i.e., signs or symptoms besides simple wounds; test or ECG abnormalities) or pain that is difficult to control requires admission. Systemic findings (e.g., chest pain, ECG changes, hypotension, coagulopathy) require monitoring for at least 24 hours.[133]
Morbidity and Mortality No fatalities from helodermatid bites have been documented in the last 50 years,[95] but a bite might be fatal if a large helodermatid hangs on to the victim for minutes. Such a bite to a child or ill adult is especially dangerous. Although pain may be prolonged for several hours or even days after these bites, necrosis is rare.[95] [118] Wound infections are uncommon. If infection occurs, cultures should be obtained and the victim started on broad-spectrum antibiotic coverage for both gram-positive cocci and gram-negative rods. Culture and sensitivity results should guide further treatment.
ALLERGY TO REPTILE VENOMS Snake and lizard venoms are highly immunogenic substances, and occasionally, a bitten victim presents with an acute, anaphylactic reaction.[47] [110] The risk of such reactions increases in victims previously bitten by venomous reptiles or who work with snake or lizard venoms (e.g., in a venom production or research facility). The presentation can be typical for anaphylaxis, with bronchospasm, hypotension, and urticaria, but differentiating an acute allergic reaction to venom from direct venom toxicity can be difficult. If the precise etiology for hypotension or respiratory distress is unclear, treatment can be rendered for anaphylaxis while antivenom preparation (in the case of snakebite) and supportive care proceed.
BITES BY EXOTIC SNAKES IN THE UNITED STATES With the growing popularity of herpetoculture in the United States, bites by captive venomous reptiles have increased. Many involve species indigenous to North America, but an increasing number are caused by exotic species. Russell [120] estimated that exotic venomous snakes were responsible for 30 bites in 1984. In 1998, however, 100 such cases were reported to the AAPCC Toxic Exposure Surveillance System.[90] An emergency physician anywhere in North America may see a victim who has been bitten by a king cobra, black mamba, or other exotic species. Management principles in these cases are similar to those outlined earlier (see also Chapter 39 ).
924
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Weed HG: Nonvenomous snakebite in Massachusetts: prophylactic antibiotics are unnecessary, Ann Emerg Med 22:220, 1993.
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Weinstein SA, Minton SA, Wilde CE: The distribution among ophidian venoms of a toxin isolated from the venom of the Mojave rattlesnake (Crotalus scutalatus scutulatus), Toxicon 23:825, 1985.
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Whitley RE: Conservative treatment of copperhead snakebites without antivenin, J Trauma 41:219, 1996.
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Wilkinson JA et al: Distribution and genetic variations in venom A and B populations of the Mojave rattlesnake (Crotalus scutulatus scutulatus) in Arizona, Herpetologica 47:54, 1991.
148.
Wingert WA, Chan L: Rattlesnake bites in southern California and rationale for recommended treatment, West J Med 148:37, 1988.
149.
Wingert WA, Wainschel J: Diagnosis and management of envenomation by poisonous snakes, South Med J 68:1015, 1975.
150.
Zugaib M et al: Abruptio placentae following snakebite, Am J Obstet Gynecol 151:754, 1985.
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Chapter 39 - Non-North American Venomous Reptile Bites Robert L. Norris Jr. Sherman A. Minton †
Snake envenomation is a significant cause of morbidity and mortality in some parts of the world. The only attempt to survey snakebite as a global problem was undertaken in 1954 under the auspices of the World Health Organization.[72] The estimate was an annual incidence of 300,000 bites with 30,000 to 40,000 deaths. Due to methodologic problems, the estimate of incidence was probably much too low. In more recent estimates, as many as 2.5 million envenomations and 125,000 deaths may occur each year.[10] Although reporting from many parts of the world is inadequate, the highest incidence of snakebite occurs in regions where dense human populations coexist with a dense population of venomous snakes, people are engaged in agriculture by nonmechanized methods, and most people reside in small villages. Geographically, these regions include Southeast Asia, sub-Saharan Africa, and tropical America. The epidemiologic patterns of snakebite in the United States and Europe have changed since 1950. Before that time the bites largely involved persons engaged in agriculture or living in rural environments, although the number was far fewer than those reported from tropical regions. Over the past 40 to 50 years the number of bites from handling captive snakes in a hazardous fashion has increased. In Minton's series of consultations in the United States from 1977 to 1995, 54 of 160 venomous snakebite cases involved nonnative snakes, and 53 of these were by animals in captivity.[48] In addition, 25 of the 106 bites inflicted by native snakes involved captive animals. The popularity of snake keeping as a hobby is increasing. Although most snakes kept in captivity are not dangerous, some people acquire venomous species. In rare cases, venomous snakes may be incorrectly identified and sold as innocuous species. Many snakes in the "pet" trade are not native to the nations where they are sold. Boa constrictors and ball pythons are harmless exotic snakes popular in the United States, whereas the nonvenomous North American king snakes (Lampropeltis spp.) and rat snakes (Elaphe spp.) are popular in Europe. Venomous species also appear in the international trade. Cobras, large African vipers of the genus Bitis, and green arboreal vipers (Trimeresurus spp.) from Southeast Asia are among the species commonly sold in the United States, whereas rattlesnakes are prized by collectors in Europe. An informal survey in southern California indicated that nearly 2000 venomous snakes were kept by herpetologists and snake collectors in that area in the early 1960s.[60] Before 1960, bites by nonnative venomous snakes in the United States made up approximately 4% of total bites, largely confined to workers in research laboratories, zoos, and other public displays. In 1972, however, 15% of 410 hospital-treated snakebites were inflicted by nonnative species.[30] An emergency department physician in an urban hospital in the eastern or midwestern United States is almost as likely to be confronted with a bite of an exotic venomous snake as with that of a species native to North America. Snakebite is a minor hazard for tourists engaged in sightseeing or recreation unless they deliberately capture or handle local reptiles. The risk for those involved in engineering projects, exploration, military operations, scientific fieldwork, and humanitarian activities in regions where venomous snakes are common is somewhat higher but still small. Hardy[26] reported three bites by the large pit viper Bothrops asper during 1.5 million person-hours in the field at four operations in Belize, Costa Rica, and Guatemala.
SNAKES OF MEDICAL IMPORTANCE Snakes are a distinctive and specialized group of reptiles represented by about 2700 species. However, their classification at the family level and beyond has always presented problems to taxonomists. Recent taxonomic changes involving medically important species include redivision of the pit viper genera Agkistrodon (North America and Asia), Bothrops (tropical America), and Trimeresurus (southern Asia) and recognition that some wide-ranging species, such as the Asian cobra (Naja naja) and saw-scaled viper (Echis carinatus), are actually groups of several similar species.[18] [95] Table 39-1 summarizes the major snake families. All species in the families Viperidae, Elapidae, Hydrophiidae, and Atractaspididae, plus an unknown but significant number in the family Colubridae, are venomous. Box 39-1 lists the most medically important venomous species for certain areas of the world. †Deceased.
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TABLE 39-1 -- Major Snake Families REMARKS
GROUP
DISTRIBUTION
Blind snakes
Tropical and warm temperate zones
Very small, wormlike snakes; none venomous
Mostly tropical and warm temperate zones; pythons in Old World only
Includes both large and small species; none venomous
Almost worldwide except for Arctic, Antarctic, southern Australia, and certain islands
Large and extremely varied family; many species with venom glands and posterior maxillary fangs, but few capable of causing clinically significant envenomation
Africa, limited areas of Middle East
About 15 species, all venomous; rather small burrowers; large maxillary fangs used singly with backward stabbing motion
Families: Typhlopidae and Leptotyphlopidae Boas and pythons Family: Boidae "Typical" snakes Family: Colubridae Burrowing asps Family: Atractaspididae Cobras, mambas, coral snakes, Tropical and warm temperate zones kraits, and others
About 180 species, all venomous; fangs at anterior end of maxillae
Family: Elapidae Sea snakes
Mostly Southeast Asian and Australian coastal waters
About 50 species, all venomous; fangs similar to those of Elapidae
The Americas and much of Asia
About 120 species, all venomous; highly movable fangs on much reduced maxillae; heat- sensing pits between eyes and nostrils
Africa, Europe, and Asia
About 40 species, all venomous; fangs like those of pit vipers; no heat-sensing pits
Family: Hydrophiidae Pit vipers Family: Viperidae Subfamily: Crotalinae Old World vipers Family: Viperidae Subfamily: Viperinae
Box 39-1. MOST IMPORTANT SPECIES OF VENOMOUS SNAKES IN VARIOUS REGIONS OF THE WORLD
UNITED STATES AND CANADA Diamondback rattlesnakes (Crotalus adamanteus, C. atrox) Timber rattlesnake (C. horridus) Prairie rattlesnake (C. viridis viridis) Pacific rattlesnake (C. viridis oreganus and C. v. helleri) Pigmy rattlesnake (Sistrurus miliarius) Copperhead (Agkistrodon contortrix) Cottonmouth (Agkistrodon piscivorus)
MEXICO, CENTRAL AMERICA, WEST INDIES Western diamondback rattlesnake (Crotalus atrox) Mexican west coast rattlesnake (C. basiliscus) Tropical rattlesnake (C. durissus), several subspecies Cantil (Agkistrodon bilineatus) Terciopelo, barba amarilla (Bothrops asper) Fer-de-lance (Bothrops lanceolatus, B. caribbaeus) Lora, green palm viper (Bothriechis lateralis) Eyelash viper (Bothriechis schlegelii) Hognose viper (Porthidium nasutum) Central American coral snake (Micrurus nigrocinctus)
NORTHERN SOUTH AMERICA (TO ABOUT 15° S) Tropical rattlesnake (Crotalus durissus), several subspecies Terciopelo, mapana, vibora equis (Bothrops asper, B. atrox) Neuwied's lancehead (Bothrops neuwiedi) Amazonian tree viper (Bothriopsis bilineata) Hog-nose vipers (Porthidium nasutum, P. lansbergii) Bushmaster (Lachesis muta) Amazonian coral snake (Micrurus spixii) Red-tail coral snake (M. mipartitus)
SOUTHERN SOUTH AMERICA Brazilian rattlesnake (Crotalus durissus terrificus) Jararaca (Bothrops jararaca) Jararacussu (B. jararacussu) Neuwied's lancehead (B. neuwiedi) Urutu (B. alternatus) Southern coral snake (Micrurus frontalis)
EUROPE European viper (Vipera berus) Asp viper (V. aspis) Nose-horned viper (V. ammodytes)
NEAR AND MIDDLE EAST Levantine viper (Macrovipera [Vipera] lebetina) Palestine viper (V. palaestinae) Saw-scaled vipers (Echis carinatus, E. coloratus)
Levantine viper (Macrovipera [Vipera] lebetina) Palestine viper (V. palaestinae) Saw-scaled vipers (Echis carinatus, E. coloratus) Desert horned viper (Cerastes cerastes)
INDIAN SUBCONTINENT AND SRI LANKA Russell's viper (Daboia russellii) Saw-scaled viper (Echis carinatus) Hump-nose viper (Hypnale hypnale)
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Indian krait (Bungarus caeruleus) Asian cobras (Naja naja, N. kaouthia) Sea snakes, especially beaked sea snake (Enhydrina schistosa), important in some coastal areas
SOUTHEAST ASIA INCLUDING PHILIPPINES AND MOST OF INDONESIA Russell's viper (Daboia russellii) Malayan pit viper (Calloselasma rhodostoma) White-lipped tree viper (Trimeresurus albolabris) Wagler's pit viper, temple viper (T. wagleri) Mangrove viper (T. purpureomaculatus) Malayan krait (Bungarus candidus) Asian cobras (chiefly Naja atra, N. kaouthia, N. philippiensis, N. sputatrix, N. sumatrana) King cobra (Ophiophagus hannah) Beaked sea snake (Enhydrina schistosa) Annulated sea snake (Hydrophis cyanocinctus) Hardwicke's sea snake (Lapemis curtus hardwickii)
FAR EAST (EASTERN CHINA, TAIWAN, KOREA, JAPAN) Mamushi (Agkistrodon blomhoffii, A. halys, A. intermedius) Hundred-pace snake (Deinagkistrodon acutus) Okinawa habu (Trimeresurus flavoviridis) Chinese habu (T. mucrosquamatus) Chinese green tree viper (T. stejnegeri) Many-banded krait (Bungarus multicinctus) Chinese cobra (Naja atra) Annulated sea snake (Hydrophis cyanocinctus)
NORTHERN AUSTRALIA, NEW GUINEA AND ASSOCIATED ISLANDS Death adders (Acanthophis antarcticus, A. praelongus) Taipan (Oxyuranus scutellatus) Mulga snake, king brown snake (Pseudechis australis) Papuan black snake (Pseudechis papuanus) Brown snakes (Pseudonaja textilis, P. nuchalis) Ikaheka snake (Micropechis ikaheka) Sea snakes, particularly Astrotia stokesi, Aipysurus laevis, Lapemis curtus
SOUTHERN AUSTRALIA AND TASMANIA Tiger snakes (Notechis scutatus, N. ater) Copperhead (Austrelaps superbus) Death adder (Acanthophis antarcticus) Mulga snake, king brown snake (Pseudechis australis)
Copperhead (Austrelaps superbus) Death adder (Acanthophis antarcticus) Mulga snake, king brown snake (Pseudechis australis) Red-bellied black snake (Pseudechis porphyriacus) Brown snakes (Pseudonaja), several species
NORTH AFRICA TO SOUTHERN EDGE OF SAHARA Desert horned viper (Cerastes cerastes) Saw-scaled vipers (Echis pyramidum, E. ocellatus) North African rock viper (Vipera mauritanica) Puff adder (Bitis arietans) Egyptian cobra (Naja haje) Red spitting cobra (Naja pallida) Burrowing asp (Atractaspis microlepidota)
CENTRAL AND SOUTHERN AFRICA Saw-scaled vipers (Echis pyramidum, E. ocellatus) Puff adder (Bitis arietans) Rhinoceros viper (B. nasicornis) Gaboon viper (B. gabonica) Green tree viper (Atheris squamiger) Night adders (Causus rhombeatus, C. maculatus) Spitting cobras (Naja mossambica, N. nigricollis) Egyptian cobra (N. haje) Cape cobra (N. nivea) Ringhals (Hemachatus haemachatus) Black mamba (Dendroaspis polylepis) Green mambas (D. angusticeps, D. viridis) Burrowing asps (Atractaspis), several species Boomslang (Dispholidus typus)
Cobras Strictly speaking, cobras are snakes of the genus Naja ( Figure 39-1 , Figure 39-2 , Figure 39-3 ), but the term is often applied to other snakes of cobralike habitus, particularly the king cobra (Ophiophagus hannah) ( Figure 39-4 ), ringhals (Haemachatus) ( Figure 39-5 ), water cobras (Boulengerina), and tree cobras (Pseudohaje). Spreading the neck to form a hood is common to all, although this behavior is seen in numerous other snakes of several families, including some nonvenomous species. Nearly all cobras are large snakes, 1.2 to 2.5 m in total length, with the king cobra occasionally reaching 5 m. Cobras of the genus Naja occur throughout Africa and tropical and subtropical Asia, except in deserts. They live in a wide variety of habitats and adapt well to agricultural and
Figure 39-1 Chinese cobra (Naja atra). Cobras are among the world's most venomous snakes, dangerous by virtue of potent venom and distribution in densely populated regions. (Sherman Minton, MD.)
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Figure 39-2 The monocellate cobra (Naja kaouthia) is one of many cobra species whose venom is known to cause significant local necrosis. (Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
Figure 39-3 The African red spitting cobra (Naja pallida) is capable of spraying its venom with great accuracy for distances up to 3 m. (Courtesy Michael Cardwell and Carl
Barden Venom Laboratory.)
Figure 39-4 The king cobra (Ophiophagus hannah) is the largest of the venomous snakes, can reach lengths of up to 5 m, and is widely distributed in Asia. (Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
Figure 39-5 Cobralike ringhals (Hemachatus haemachatus) of Africa spreads a hood when threatened and can also spit venom. Some specimens feign death, as shown here, causing bites in unsuspecting keepers. (Michael Cardwell and Cape Town Snake Park.)
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Figure 39-6 Green mamba (Dendroaspis angusticeps). These large, slender arboreal African snakes are quick, alert, and often dangerous. (Sherman Minton, MD.)
suburban situations. The king cobra is restricted to forest areas in southeastern Asia; the ringhals, water cobras, and tree cobras inhabit sub-Saharan Africa. The African spitting cobras, Naja nigricollis, N. mossambica, N. katiensis, N. pallida, and Hemachatus, have fangs modified for ejecting jets of venom anteriorly and upward for distances up to 3 m with remarkable accuracy. This habit is rarely seen in Southeast Asian cobras. Mambas Mambas are slender elapid snakes constituting the genus Dendroaspis ( Figure 39-6 and Figure 39-7 ). They are usually 1.5 to 2.2 m long, although the black mamba (D. polylepis) may reach 4 m. The four species inhabit most of tropical Africa. Mambas are at least partially arboreal, alert and active, and aggressive under some circumstances. Kraits There are about a dozen species of south Asian elapids of the genus Bungarus ( Figure 39-8 ). Their average lengths are 1 to 1.2 m, with two species reaching 2 m. Kraits have short fangs and highly toxic venom, are nocturnal, and are often found close to human dwellings. Bites are uncommon, but the case fatality rate is high. Coral Snakes All medically important species of coral snakes are in the genus Micrurus, which includes about 50 species distributed
Figure 39-7 Relatively large anterior fangs of green mamba (Dendroaspis angusticeps). Elapids tend to have smaller fangs than do most viperids, but some, as shown here, can be quite large. (Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
Figure 39-8 Many-banded krait (Bungarus multicinctus). Kraits are widely distributed in southern Asia and have highly lethal neurotoxic venoms. They are nocturnal and rarely aggressive. (Sherman Minton, MD.)
from the southern United States to central Argentina ( Figure 39-9 ). Nearly all are in the 0.6 to 1.2 m size range. Most have tricolor patterns of red, yellow, and black. A few species are bicolor. The rules and mnemonics for distinguishing coral snakes from their 932
Figure 39-9 Amazonian coral snake (Micrurus spixii). This South American species demonstrates how color patterns can be misleading in identification of coral snakes outside the United States. its red and yellow bands are separated by black rather than being contiguous. (Courtesy Michael Cardwell and Extreme Wildlife Photography.)
Figure 39-10 Coastal taipan (Oxyuranus scutellatus) Australia's largest venomous snake can reach a length of 3 m and can be aggressive. Its range is largely in semitropical Queensland. (Sherman Minton, MD.)
mimics become progressively less reliable from central Mexico southward (see Chapter 38 ). Coral snakes are secretive and not often encountered. The dozen or more species of oriental coral snakes (Calliophis, Maticora) are widely distributed but uncommon and not well studied.
Australian Elapids Elapids are the dominant snakes of Australia, New Guinea, and proximity islands north to the Solomons. The 85 or more species are closely related and part of one evolutionary radiation, which also includes the sea snakes. The diverse elapids range from small (40 to 60 cm), inoffensive burrowers to the potentially aggressive coastal taipan (Oxyuranus scutellatus), which may reach a length of 3.3 m ( Figure 39-10 ). Death adders (Acanthophis) are viperlike in appearance, with wide heads
Figure 39-11 Death adder (Acanthophis antarcticus). This viperlike Australian snake is actually an elapid with highly neurotoxic venom. (Courtesy Michael Cardwell and William W. Lamar.)
Figure 39-12 Tiger snake (Notechis scutatus). This highly venomous elapid snake is found in the densely populated eastern part of Australia. (Sherman Minton, MD.)
and thick bodies ( Figure 39-11 ). Other dangerous species are tiger snakes (Notechis), which may be plentiful in well-populated eastern coastal districts of Australia ( Figure 39-12 ); brown snakes (Pseudonaja), which are quick and may be dangerous if cornered; and large snakes of the genus Pseudechis, including the red-bellied black snake (P. porphyriacus) and the king brown snake (P. australis). Venoms of most of these snakes are highly toxic. Sea Snakes The 50 or more species of sea snakes inhabit tropical and subtropical sections of the western Pacific and Indian Oceans over the continental shelves, but the pelagic sea snake (Pelamis platurus) also occurs on the western coasts of America from Baja California to Ecuador and is occasionally found in Hawaiian waters
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Figure 39-13 Pelagic sea snake (Pelamis platurus) is the most widely distributed sea snake and the only species found in American waters. (Sherman Minton, MD.)
Figure 39-14 Nose-horned viper (Vipera ammodytes) is an important cause of snakebites in Europe, but cases are rarely fatal. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
( Figure 39-13 ). Similarity in plasma and venom proteins indicates that sea snakes are closely related to Australian terrestrial elapids (see Chapter 61 ). Eurasian Vipers The genus Vipera includes approximately a dozen species. Dangerous, large species include the Levantine viper (V. lebetina), found from North Africa to Pakistan, and the Palestine viper (V. palaestinae), which is native to the Middle East. The European viper (V. berus) has one of the most extensive ranges of any land snake and is found from the British Isles to Korea and the eastern limits of Russia. V. berus is relatively small (60 to 75 cm). Other species important in Europe are the asp viper (V. aspis), Iberian viper (V. latasti), and nose-horned viper (V. ammodytes) ( Figure 39-14 ). These cause numerous bites, but the case fatality rate is low. The Russell's viper (Daboia [formerly Vipera] russellii) is found from
Figure 39-15 Russell's viper (Daboia russellii). Plentiful in agricultural regions of southern Asia, these large vipers are a leading cause of fatal snakebites. (Sherman Minton, MD.)
Figure 39-16 Desert horned viper (Cerastes cerastes). These relatively small Egyptian vipers are highly adapted to their desert environment. Bites are rarely fatal. (Courtesy Michael Cardwell and The Living Desert.)
Pakistan to Taiwan and is one of the world's most dangerous snakes, having a highly lethal venom ( Figure 39-15 ). It adapts well to agricultural environments. Desert Vipers The saw-scaled vipers (Echis) may cause more fatalities than any other snakes in the world.[83] These snakes live in arid and semiarid regions from India through the Middle East to west Africa; however, they often thrive on cultivated land. Their name comes from the sawtoothed ridges on the lateral scales that are rubbed together to produce a warning sound. These small snakes are rarely more than 60 cm in length but are highly irritable and quick to strike. The venoms cause severe coagulopathy. Cerastes has two species in North Africa and the Middle East, including the horned viper of Egypt ( Figure 39-16 ). These snakes are highly adapted to desert conditions. They are relatively small, and their
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Figure 39-17 Puff adder (Bitis arietans). This large African viper is widely distributed and extremely dangerous. As shown here, its color pattern allows it to blend into background leaf clutter. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 39-18 Gaboon viper (Bitis gabonica). This impressive African viper possesses the longest fangs of any venomous snake, up to 5 cm. It can deliver massive quantities of hightly toxic venom. (Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
bites are rarely fatal. Two other species in this group are the Persian horned viper (Pseudocerastes persicus) and the leaf-nosed viper (Eristicophis macmahoni), both occurring in the Middle East and Pakistan. They are uncommon and of little medical importance. African Vipers The genus Bitis has 12 species and occurs throughout Africa, exclusive of the northern deserts. The wide-ranging puff adder (B. arietans) also occurs in western Saudi Arabia ( Figure 39-17 ). All are stout-bodied, wide-headed snakes. They vary in size from B. peringueyi (rarely exceeds 30 cm) to the Gabon viper (B. gabonica) ( Figure 39-18 ), which may reach a length of 2 m and a weight of about 10 kg. Habitat ranges from desert to rainforest. The puff adder is a major cause of snakebites in most parts of Africa where it is found. It prefers grassland and often lives near villages. Atheris is an arboreal African viper genus with eight species. They are usually 50 to 65 cm long, and some have a bizarre appearance that makes them popular with zoos and hobbyists; bites are infrequent. Night adders of the genus Causus are widespread in Africa south of the Sahara. They are usually 50 to 70 cm long and may be plentiful around fields and villages. Bites are numerous, but fatalities are almost unknown. Agkistrodon Complex Pit Vipers The 15 species in the Agkistrodon pit viper group are found from the eastern United States to Central America and throughout most of Asia. They are characterized by large shields on the crown of the head, a presumably primitive condition in viperid snakes. American copperheads (A. contortrix) and cottonmouths (A. piscivorus) are discussed in Chapter 38 . The closely related cantil (A. bilineatus) is native to Mexico and Central America. The mamushi (A. blomhoffii) of Japan, Korea, and eastern China, Siberian pit viper (A. halys) of Asian Russia and Mongolia; and central Asian pit viper (A. intermedius), found from Iran to Korea, are all common snakes, usually 60 to 80 cm long and of moderate build. They are the only venomous snakes in much of central and northeastern Asia and account for many snakebites. The case fatality rate is low. The Malayan pit viper (Calloselasma rhodostoma) is a distinctive species of Southeast Asia that inhabits forests at low elevation and is particularly common on rubber plantations. It is a major cause of snakebites. The hundred-pace snake (Deinagkistrodon acutus) is a large (1.2 to 1.5 m) snake with a strongly upturned snout. It is native to forests in south China and Taiwan and is dangerous but uncommon. Asian Lance-Head Pit Vipers The genus Trimeresurus is now subdivided by many herpetologists. It includes approximately 40 species. They are distributed from southern India to Indonesia, the Philippines, and the southern islands of Japan ( Figure 39-19 ). The most dangerous species are large (up to 2.3 m), slender snakes with very wide heads. They are often called "habu," a Japanese name. They are mostly terrestrial and may have large populations in sugar cane fields and other areas of cultivation. The Okinawa habu (T. flavoviridis) accounts for a high incidence of snakebites on the southern Ryukyu Islands.[63] The Chinese habu (T. mucrosquamatus) has a wide range in Southeast Asia and is another plentiful and dangerous species. Arboreal species are often predominantly green, 60 to 100 cm long, and are found throughout the range of the group. T. albolabris, the white-lipped bamboo viper, is the most widely distributed member of this group. These vipers cause many snakebites, but fatalities are rare. A third group (Ovophis to some) includes five species of stout, short vipers found in mountainous terrain. They seem to be of little medical importance. Wagler's pit viper is a widely
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Figure 39-19 Chinese green tree viper (Trimeresurus stejnegeri) is found in southern and eastern Asia. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 39-20 Wagler's pit viper, temple viper (Tropidolaemus wagleri). This Asian pit viper is popular with amateur snake keepers. (Courtesy Michael Cardwell and William W. Lamar.)
distributed arboreal species usually assigned to the genus Tropidolaemus ( Figure 39-20 ). Its venom contains a peculiar heat-stable toxin, but its bites do not seem to differ from those of arboreal Trimeresurus. Neotropical Pit Vipers Most of these snakes were formerly assigned to the genus Bothrops, which ranges from eastern Mexico to southern Argentina and a few islands of the West Indies ( Figure 39-21 ). The genus contains approximately 30 species, most of which are of medical importance. These are medium to long snakes (0.7 to 2.5 m) of moderate to heavy build with distinctly triangular heads. Habitat ranges from semiarid grasslands to rainforests; several species adapt well to banana and sugar cane plantations. Among the more dangerous species are B. atrox, B. asper, B. jararaca, and B. lanceolatus. They have many Spanish and Portuguese names, but the name
Figure 39-21 Urutu (Bothrops alternatus). This large, dangerous South American pit viper is responsible for many severe bites in its distribution. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
Figure 39-22 Eyelash viper (Bothriechis schlegelii) is found in southern Mexico, Central America, and northern South America and is popular with amateur snake keepers.
(Courtesy Michael Cardwell and Carl Barden Venom Laboratory.)
"fer-de-lance" is often used for these snakes in English language publications. Species of Bothrops account for most of the serious snakebites in Latin America. Fifteen arboreal species formerly in Bothrops are now in the genera Bothriopsis and Bothriechis. They are slender snakes with large heads and are 50 to 100 cm in length. Most have green in their pattern. The eyelash viper (Bothriechis schlegelii) is a well-known example that accounts for about 20% of venomous snakebites in Costa Rica ( Figure 39-22 ). Fatalities are rare. Fourteen other 936
Figure 39-23 Bushmaster (Lachesis muta) is the largest pit viper, up to 3.6 m and is found in southern Central America and northern South America. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)
former Bothrops species constitute the genus Porthidium, which has been further subdivided by some authorities. These are small to moderate-sized snakes (45 to 100 cm) with heavy bodies and wide heads. They are found from eastern Mexico to northern South America, usually in forests and often in highlands. They are terrestrial. Bites are common but fatalities rare. The bushmaster (Lachesis muta) is the largest pit viper, usually 1.5 to 2.5 m long but occasionally reaching 3.6 m ( Figure 39-23 ). It has extraordinarily rough scales in the middorsal region and a distinct tail spine. It is found in lowland forests from southern Nicaragua to eastern Brazil and is uncommon. Bushmaster bites are rare, but the case fatality rate is high. Rattlesnakes The 31 species of rattlesnakes occur from southern Canada to Uruguay and eastern Argentina, although only two species occur south of the isthmus of Tehuantepec in Mexico. All except one insular species in Baja California can be identified by the presence of a rattle (see Chapter 38 ). Burrowing Asps The 15 species of the genus Atractaspis were formerly considered vipers because they have viperlike fangs; however, they have several unique features that justify their recognition as a separate family (Atractaspididae). They are small (50 to 80 cm), moderately slender with small heads, and uniformly black or brown. They are found throughout most of sub-Saharan Africa and in some areas of the Middle East. They frequent habitats ranging from forest to semidesert and are burrowers that may emerge at night and after rains. Bites are fairly common in some parts of Africa, but fatalities are infrequent.
Figure 39-24 Boomslang (Dispholidus typus) is the most dangerous of the rearfanged colubrid snakes. This arboreal snake is widely distributed in Africa. (Sherman Minton, MD.)
Colubrid Snakes The colubrids are a large, taxonomically varied family of snakes that lack anterior fangs and the primitive features (e.g., labial heat-sensing pits, pelvic spurs, and so on) associated with boas and some other snakes. Some herpetologists partition this family, but little agreement exists on recognized divisions. In most parts of the world, colubrids make up the majority of snake species, absent only from the Arctic and Antarctic, southern Australia, and some islands. Many species have grooved fangs in the rear of the upper jaw, and others have enlarged but ungrooved rear teeth. Although the vast majority of these species are harmless, more than 50 species of colubrid snakes in 30 genera have caused human envenoming. Most cases are mild because the venom-injecting apparatus is inefficient and the quantity of venom small; however, serious and fatal envenomations have occurred.[47] Most colubrid bites involve the handling of snakes believed to be harmless. The more important species include the boomslang (Dispholidus typus) ( Figure 39-24 ), twig snakes (Thelotornis spp.), Japanese garter snake (Rhabdophis tigrinus), and brown tree snake (Boiga irregularis).
VENOM APPARATUS The venom apparatus of snakes functions mainly to immobilize and kill prey, although it may also be an important means of defense. Dentition is modified in all venomous snakes, although some colubrids have only an enlarged pair of posterior maxillary teeth. The most highly modified dentition is that of vipers, in which a single, large, tubular or deeply grooved fang is attached to a greatly reduced maxillary bone. These fangs have a wide range of rocking movement. Burrowing asps (Atractaspis spp.) have large, viperlike fangs used one at
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a time with a backward stabbing motion as the lower jaw is shifted to the opposite side. They can bite with the mouth virtually closed. Fangs of elapid snakes are short, tubular or grooved, and attached to the anterior end of a longer maxillary bone that may bear additional teeth and has a limited degree of rocking movement. Fangs of sea snakes are even shorter; the maxillary bone is long and usually bears additional teeth. The enlarged teeth or grooved fangs of colubrids are at the rear of the maxillary bone and are typically preceded by additional teeth. Snake venoms are produced in a pair of glands usually located between the eye and the angle of the mouth. In one genus of oriental elapids (Maticora), two species of burrowing asps (Atractaspis), and two species of night adders (Causus), however, the glands are tubular and extend well back into the body. Histologic and histochemical studies show secretory cells of various types in all snake venom glands.[3] [36] Space for venom storage in the lumen of the gland is greatest in viperids and some elapids (e.g., cobras), less in other elapids and sea snakes, and minimal in colubrids. Musculature for emptying the glands is best developed in viperids, moderately effective in elapids and sea snakes, and relatively ineffective in colubrids. This is reflected in quantities of venon injected in natural bites and amounts that can be obtained by extraction.
SNAKE VENOMS The biochemistry and pharmacology of snake venoms are well studied. The venoms are colorless to amber liquids with solid content that is mostly protein. Pharmacologically active substances include enzymes, polypeptide toxins, glycoproteins, nucleotides, small peptides, and biogenic amines. Many of the enzymes and toxins are very stable. Dried snake venoms can retain lethality and some enzyme activity after three decades of storage. The postsynaptic neurotoxins, found in most elapid and sea snake venoms, are probably the best understood snake venom toxins. They bind to the nicotinic acetylcholine receptors competitively with acetylcholine and produce a nondepolarizing neuromuscular blockade. The short toxins have 60 to 62 amino acids and four disulfide bridges; the long toxins have 71 to 74 amino acids and five disulfide bridges. Presynaptic neurotoxins inhibit release of acetylcholine at the neuromuscular junction. Toxins in this group have phospholipase A2 activity, occur in a variety of elapid and viper venoms, and are similar to myotoxins in some sea snake venoms. The phospholipases of this group have 110 to 125 amino acids and six or seven disulfide bonds. Their neurotoxicity and myotoxicity are not related to hydrolytic activity. With the exception of sea snake venom, nearly all snake venoms affect blood coagulation, although not always to a clinically significant degree. Thrombinlike activity that converts fibrinogen to fibrin is characteristic of pit viper venoms; the fibrin is abnormal and easily lysed. Enzymes responsible for this activity have been isolated from a number of venoms, including the Malayan pit viper (Calloselasma rhodostoma), eastern diamondback rattlesnake (Crotalus adamanteus), hundred-pace snake (Deinagkistrodon acutus), Gaboon viper (Bitis gabonica), and jararaca (Bothrops jararaca). In sublethal doses these enzymes produce nonclotting blood and do not cause platelet aggregation. Prothrombin activation with formation of thrombin is seen particularly with venoms of the Russell's viper (Daboia russellii) and saw-scaled vipers (Echis spp.), from which the enzymes responsible have been isolated. Prothrombin activation is also seen with venoms of several Australian elapids, some pit vipers, and dangerous colubrids. Some venoms have more than one type of anticoagulant activity. Hemorrhage and necrosis are often seen with snakebites, particularly those inflicted by vipers. Although attributed to proteolytic enzymes, several hemorrhagic factors have little or no proteolytic activity.[55] Their main mode of action is disruption of the vascular basement membrane. Extensive myonecrosis is often seen with bites by sea snakes, some Australian elapids, and some pit vipers. Myotoxins have been isolated from several venoms. Most myotoxins show phospholipase A2 activity, which is more pronounced in those derived from elapids. The so-called cardiotoxin first described from cobra venom and subsequently found in venoms of some other related snakes is a strongly basic polypeptide whose main action is to produce irreversible depolarization of cell membranes. A specific cardiotoxin with quite different structure and action is found in venoms of some burrowing asps (Atractaspis spp.). Its action is directly on the heart, producing coronary vasoconstriction and atrioventricular block.[43] [90] Hyaluronidase is found in most reptilian venoms and facilitates absorption and spread of other venom components. Other enzymes, such as phosphodiesterase, L-amino acid oxidase, 5' nucleotidase, and acetylcholinesterase, are present in many snake venoms, but their roles in envenomation are poorly understood. Most of the clinical effects of envenomation result from several venom components acting in concert, and venom effects may be compounded by endogenous release of autopharmacologic compounds such as histamine and bradykinin.
SIGNS AND SYMPTOMS OF SNAKE VENOM POISONING The complexity and diversity of snake venoms are reflected in the wide array of signs and symptoms that can occur after envenomation. The precise clinical picture
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and degree of severity of any specific venomous snakebite depend on many factors, including the species of snake and its age, size, health, and geographic origin; anatomic location of the bite; size and health of the victim; and therapeutic interventions. The treating physician must anticipate multisystem dysfunction in any victim of snake venom poisoning and must remain vigilant for any constellation of signs, symptoms, and laboratory findings, regardless of the species of snake implicated ( Box 39-2 ). Box 39-2. SIGNS AND SYMPTOMS AFTER SNAKE VENOM POISONING
ELAPIDS (COBRAS, MAMBAS, KRAITS, AUSTRALIAN VENOMOUS SNAKES, CORAL SNAKES) Local Findings may be absent or minimal Significant pain occurs with some species Regional lymphadenopathy Necrosis occurs with some species Systemic Neurotoxicity (cranial nerve dysfunction, altered mental status, peripheral weakness and paralysis, respiratory failure) Cardiovascular failure Coagulopathy Myonecrosis Renal failure
SEA SNAKES Local Trivial Fang marks may be difficult to identify Systemic Neurotoxicity (cranial nerve dysfunction, peripheral weakness and paralysis, respiratory failure) Myotoxicity with resulting muscle pain and tenderness, myoglobinemia, myoglobinuria, and hyperkalemia (may precipitate cardiac dysrhythmias and renal failure)
VIPERS AND PIT VIPERS Local Pain Soft tissue swelling Regional lymphadenopathy Ecchymosis, bloody exudate from fang marks Early absence of local findings does not rule out significant envenomation Local necrosis may be significant
SYSTEMIC Any organ system may be involved Cardiovascular toxicity (hypotension, pulmonary edema) Neurotoxicity (cranial nerve dysfunction, peripheral weakness) with some species Hemorrhagic diathesis Renal failure
Hemorrhagic diathesis Renal failure
BURROWING ASPS Local Single fang puncture Pain Some swelling Occasional local necrosis Systemic Nausea, vomiting Diaphoresis Fever Occasional respiratory distress, cardiac dysrhythmias (atrioventricular block) Rare fatalities
COLUBRIDS (REAR-FANGED) Local Mild to moderate local swelling, pain, and ecchymosis Bloody exudate from fang marks Systemic Nausea, vomiting Coagulopathy and associated complications Renal dysfunction
Elapids Local findings after most elapid envenomations are unimpressive compared with those seen after typical viperid venom poisoning ( Figure 39-25 ). In many cases it may be difficult to find distinct fang marks. [69] [93] The degree of pain varies depending on the species involved. Often, local pain is a minor complaint, but it may be significant after bites by certain cobra species, such as the king cobra (Ophiophagus hannah) (see Figure 39-4 ).[22] Regional lymphadenopathy may be present. Although significant, local soft tissue swelling is uncommon after most elapid envenomations.[11] Some species, such as the African spitting cobras (Naja mossambica, N. nigricollis) [76] and some Asiatic cobras (Naja spp.),[58] [67] [75] may produce early edema as an indication of envenomation. Swelling can progress with time to involve the entire bitten extremity. With some of these species, local tissue necrosis may be profound ( Figure 39-26 ).[59] [75] [85] Some Australian elapids, such as the taipan (Oxyuranus spp.) and tiger snake (Notechis spp.), also can induce myonecrosis and coagulopathy.[16] [59] [93] Renal failure has been reported as a complication of envenomation by some elapids.[12] [28] [59]
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Figure 39-25 Bite of a small Australian elapid snake (Hemiaspis signata) resulting in localized swelling with some discoloration but no systemic symptoms. (Sherman Minton, MD.)
Neurotoxicity is seen after most elapid envenomations. The time of onset of neuropathic signs and symptoms after envenomation is quite variable. It is usually most rapid after serious cobra and mamba bites and most delayed after some coral snake envenomations. In certain situations the onset may be delayed for 10 hours or more.[59] The earliest systemic manifestations of envenomation by most elapids are signs of cranial nerve dysfunction, especially ptosis, but also difficulty swallowing, dysphonia, and blurred vision.[75] Paresthesias, muscle fasciculations, peripheral weakness, and paralysis, including that of respiratory muscles, may soon follow. Mental status (drowsiness, hallucinations) may be altered.[75] Associated systemic symptoms include hypersalivation and diaphoresis.[11] [56] In cases of severe envenomation, cardiovascular depression may result in hypotension and pulmonary edema.[59] [91] Eye exposure to venom from any of the spitting cobras or ringhals results in immediate burning pain and tearing. Significant systemic absorption does not occur, but corneal ulceration, uveitis, and permanent blindness can follow untreated cases.[59] [84] Bites by spitting cobras often manifest violent local reactions with hemorrhage and necrosis, but rarely neurotoxicity. Sea Snakes Local findings at the bite site after sea snake envenomation are usually trivial. In serious cases, systemic symptoms usually appear within 2 hours. [78] The bite site may show several tiny puncture wounds from the fangs and other teeth, but local pain and soft tissue swelling are negligible ( Figure 39-27 ). Fang marks may be difficult to see.[79] Sea snake venoms demonstrate significant neurotoxicity in animal studies and in human envenomations.[12] [59] [79] Neurologic dysfunction is manifested by hypersalivation, dysphagia, dysarthria, muscle spasm, and paralysis. Victims remain conscious if hypoxia is
Figure 39-26 Sharply demarcated necrosis, sometimes extensive, often follows bites by both African and Asian cobras. (Sherman Minton, MD.)
Figure 39-27 Bite of a Southeast Asian water snake (Enhydrina plumbea), generally considered to be nonvenomous. Swelling and ecchymosis were still present after 24 hours. (Sherman Minton, MD.)
prevented.[79] Envenomation is also characterized by trismus and diffuse myopathic findings.[56] [59] The myotoxic components of sea snake venoms may cause significant outpouring of potassium and myoglobin from injured muscle. Hyperkalemia may precipitate cardiac dysrhythmias, and myoglobinuria can lead to acute renal failure.[5] Untreated sea snake envenomation may result in muscle pain and weakness that persists for months.[59] Death after sea snake envenomation may result from respiratory failure caused by paralysis of the diaphragm, hyperkalemic cardiac arrest, or acute renal failure[79] (see Chapter 61 ). Vipers and Pit Vipers (Viperids) The effects of envenomation by Eurasian and African vipers and Asian and neotropical pit vipers are similar to those seen after bites by the pit vipers of North America ( Chapter 38 ). Severe pain, local soft tissue swelling, subcutaneous ecchymosis, and bloody exudation from the fang marks usually begin within minutes. Regional lymphadenopathy may be present within 30 to 60 minutes,
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and soft tissue swelling may progress extensively over several hours. The trunk and contralateral extremity may become edematous. Lack of soft tissue swelling, however, does not rule out significant poisoning by some species or after deep intramuscular or intravascular envenoming. After 12 to 24 hours, serum-filled vesicles and hemorrhagic bullae may appear, and ecchymoses may spread throughout the involved extremity.[12] Systemic envenomation may result in blurred vision, altered taste, weakness, dizziness, diaphoresis, nausea, vomiting, diarrhea, fever, headache, abdominal pain, and bleeding at various anatomic sites.[46] [56] [59] Hypotension and shock may occur over a variable time course. Early hypotension is caused primarily by pooling of blood in the pulmonary and splanchnic vasculatures. After several hours, transudation of fluid into the bitten extremity and peritoneal cavity, hemolysis, and systemic bleeding may play a role. Coagulopathy is a characteristic finding after systemic venom poisoning by saw-scaled vipers (Echis spp.).[46] [57] [59] It is also seen after bites by some populations of Daboia russellii and many neotropical and Asian pit vipers.[53] Victims can bleed at multiple sites, including the bite wound, soft tissues, gastrointestinal tract, respiratory tract, brain, eyes, and kidneys. The venoms of some populations of D. russellii can also cause massive intravascular coagulation and hemolysis.[31] [53] Neurologic findings after pit viper venom poisoning in North America are uncommon (with the notable exception of the Mojave rattlesnake [Crotalus scutulatus]; see Chapter 38 ). Neurotoxicity is a major concern, however, after bites by the South American rattlesnake (Crotalus durissus terrificus) [61] and vipers in the Eastern Hemisphere, including the Berg adder (Bitis atropos),[84] Palestine viper (Vipera palaestinae),[81] and some populations of Russell's viper (D. russellii). [82] Signs and symptoms include cranial nerve dysfunction, muscle paralysis, and respiratory failure.[29] [52] Victims may have an altered sensorium (from lethargy to coma) as a result of hypotension, hypoxia, intracranial bleeding, and possibly direct venom effects. Seizures may occur but are uncommon and probably secondary to cerebral hypoxia. Renal failure may complicate viperid envenoming, as with North American pit vipers or Australian elapids. Etiologic factors include myoglobinuria, hemoglobinuria, hypotension, and direct venom nephrotoxicity. This is especially common after bites from the Russell's viper and saw-scaled viper (Echis carinatus).[12] [57] [59] Onset may be delayed for several days, and any complaints of costovertebral angle pain should arouse suspicion of impending renal failure.[53] Local bite site necrosis and myonecrosis may be severe after viperid envenomation and may necessitate surgical intervention (amputations, grafting procedures). [46] Although most viperid bites result in venom deposition into subcutaneous tissues, subfascial injection is possible. In these rare cases, direct myotoxicity can produce muscle necrosis. If muscle swelling is significant, a compartment syndrome may develop. The signs and symptoms of compartment syndrome are closely mimicked by the findings after a typical subcutaneous envenomation (swelling, discoloration or cyanosis, pain on palpation, paresthesias). The diagnosis of a compartment syndrome can be confirmed by documenting elevated intracompartmental pressures. This has significant treatment implications, as discussed later. Burrowing Asps Envenomation by any of the burrowing asps (Atractaspis spp.) may result in severe symptoms, although fatalities have thus far been reported from only A. microlepidota and A. irregularis.[14] [15] Persons bitten by these snakes may have severe local pain followed by numbness, soft tissue swelling, lymphadenopathy, vomiting, diaphoresis, and fever.[15] [84] Systemic coagulopathies may occur.[15] [24] Local vesicles can be seen at the bite site, and local tissue necrosis occurs rarely.[8] [15] [84] The cause of death after experimental Atractaspis envenomation has been attributed to venom-induced coronary vasospasm.[39] Colubrids (Dispholidus, Thelotornis, Rhabdophis) Envenomation by some rear-fanged colubrids may have severe consequences. Fatalities have been reported after bites by the boomslang (Dispholidus typus), the bird or twig snake (Thelotornis kirtlandii), and the Japanese garter snake or yamakagashi (Rhabdophis tigrinus). [38] [49] [51] Life-threatening envenomation has also occurred after bites by the red-necked keelback (R. subminiatus).[6] [20] [41] Signs and symptoms of envenomation by these snakes include mild soft tissue swelling and, in severe cases, coagulopathy, similar to that seen with viperid venom poisoning. [47] [89] Associated findings may include variable local pain, headache, nausea, vomiting, ecchymoses, jaundice, and abdominal pain.[47] Renal dysfunction has been reported after D. typus, T. kirtlandii, and R. tigrinus envenomations.[38] [42] [51] [66] Onset of signs of serious envenomation may be delayed by many hours and possibly even days.[11] [21]
MANAGEMENT Prehospital Care Prehospital management of a bite by any potentially venomous snake involves placing the victim at rest, offering reassurance, and providing expeditious transport to the nearest facility equipped to handle such an emergency ( Figure 39-28 ). First-aid measures should not cause further harm and should not delay medical care.
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Figure 39-28 First-aid measures for venomous snakebites.
A proven technique of limiting systemic distribution of venom after most elapid and sea snake bites is the Australian pressure immobilization technique ( Figure 39-29 ). This involves immediately wrapping the entire bitten extremity with a crepe bandage, elastic bandage, or article of clothing as tightly as for an acute sprain. This is followed by splinting with any available object.[19] [26] [71] [78] The splinted extremity should be maintained at approximately heart level if possible. The use of pressure immobilization in cases of bites by snakes capable of causing significant local necrosis (e.g., most viperids, certain cobra species) is controversial.[19] A laboratory study found that pressure immobilization limits pit viper (eastern diamondback rattlesnake, Crotalus adamanteus) venom dispersal from the bite site without worsening necrosis.[70] However, localizing a necrotizing venom in the region of the bite site may exacerbate tissue loss.[69] [80] Clinical experience with pressure immobilization in human victims of viperid envenomation is limited; the rescuer must weigh the risks against potential benefits. If the offending reptile is a small, innocuous species and transport time to medical care will be short, it may be best to avoid pressure immobilization. If a large or particularly virulent snake is involved and the bite may be life threatening, immobilization may be indicated, especially if in evacuation to medical care will be delayed. More definitive recommendations on the use of pressure immobilization in viperid envenoming must await further research and clinical reports. Respiratory and cardiovascular status should be supported to the extent possible under field conditions. If the time to reach medical care is prolonged and nausea and vomiting are not present, the victim should be encouraged to drink frequent, small volumes of clear, nonalcoholic liquids to support intravascular volume. Other first-aid measures occasionally recommended for snakebites lack sufficient laboratory or clinical evidence to prove their effectiveness. Using any sharp instrument to incise fang marks in the field does more harm than good by exacerbating local bleeding (especially in the face of coagulopathy), introducing bacteria into the wound under nonsterile conditions, and further devascularizing the wound when perfusion may already be impaired. Applying mechanical suction to the wound using a device such as the Extractor (Sawyer Products, Safety Harbor, Fla; Figure 39-30 ) without incising the bite may remove a small percentage of venom from the site.[4] [5] Further description of the Extractor, including controversies regarding its use, is found in Chapter 38 . Measures such as local cooling, electric shock, and the application of topical agents should be avoided because they lack efficacy
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Figure 39-29 Australian compression and immobilization technique has proved effective in the management of elapid and sea snake envenomations. Its efficacy in viper bites has yet to be evaluated clinically.
Figure 39-30 The Extractor device. The efficacy of this device for applying mechanical suction to snakebites in the field continues to be studied.
and may actually worsen local tissue damage or the overall clinical outcome. Cold application may drive deleterious venom components deeper into tissues[60] (see Chapter 38 ). Evacuating a snakebite victim from a remote field situation can be problematic.[44] The key principles are applying potentially effective first-aid measures (reassurance, splinting, with or without mechanical suction or pressure immobilization), transporting the victim to medical care as soon as possible, and limiting the victim's physical activity to minimize cardiac output and systemic circulation of venom. If the victim is alone and unlikely to be found for several hours, he or she should attempt to hike out, pausing for frequent rest stops and maintaining oral intake of fluids. If a lower extremity is involved, a crutch can be improvised to assist ambulation. If a single companion is present and prompt transportation to medical care is unavailable, first-aid measures should be applied and the victim placed at rest. If unconscious, the victim should be placed in a recovery position (left lateral decubitus position with the head downhill and the left
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Figure 39-31 Guidelines for the hospital management of venomous snakebite.
knee bent) to keep the airway open and decrease the risk of aspiration. The companion can then hike out in search of help. Any plan to carry the victim out must taken into account the local terrain, weather conditions, and overall distance (see Chapter 25 , Chapter 26 , Chapter 27 ).
Hospital Care Initial hospital management of a victim of snake venom poisoning should involve assessment of respiratory and cardiovascular status ( Figure 39-31 ). A patient with significant respiratory distress or in extremis should be
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Figure 39-31
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Figure 39-31
promptly intubated to support ventilation and prevent aspiration. Oxygen should be administered to all victims while rapid assessment takes place. Cardiac and pulse oximetry monitoring should be started. If intubation is required, the treating physician should choose the most familiar method. Nasotracheal intubation may be considered, but epistaxis is a risk in victims with coagulopathy. Rapid sequence intubation (RSI) uses sedative-hypnotics and paralytic agents to facilitate oral intubation and is safe and effective. The depolarizing neuromuscular agent succinylcholine should be avoided in RSI of a victim with potential hyperkalemia (e.g., sea snake bite). A nondepolarizing agent, such as vecuronium or rocuronium, can be substituted. Hypotension is treated initially with intravenous (IV) fluids. Crystalloid, such as Ringer's lactate or normal saline, should be started through at least two large-bore IV lines. Having two lines also allows simultaneous administration of fluids, drugs, and antivenom when indicated. If hypotension persists after the rapid infusion of approximately 2 L of crystalloid in an adult or 20 to 40 ml/kg in a child, then 5% albumin should be added. Animal research has demonstrated an improvement in physiologic parameters and survival with the use of albumin compared with crystalloids and dextran.[64] Vasopressors should be used only after intravascular volume has been restored. The inappropriate use of vasopressors when volume is required leads to prolonged hypotension, multiple organ failure, and preventable deaths.[25] If a victim reports being bitten by a snake but appears well, providers must first determine whether the snake is venomous. Identifying the venomous species indigenous to an area is important. Hospital emergency wards should maintain color photographs of the local snake species to aid in identification. The keeper of an exotic snake involved in a bite probably knows its identity, although an amateur hobbiest may know the snake only by its common name. Common names are extremely variable and often applied to a number of unrelated species of snakes. Assistance in definitive identification may be obtained from a local zoo, university, or museum with a herpetologist on staff.
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If the snake has been identified as venomous and the victim remains asymptomatic, a careful search for puncture wounds should be made. With bites by sea snakes and smaller venomous snakes, such as coral snakes, identifying fang marks can be difficult.[54] [79] Many bites by venomous snakes occur without injection of venom. These dry bites occur in 20% to 30% of viper bites and 50% to 70% of elapid bites. [37] [68] The incidence of dry bites reaches approximately 75% with sea snakes[37] and is even higher with rear-fanged colubrids.[47] A careful history regarding current symptoms and a rapid physical examination looking for abnormalities should be performed. Careful evaluation and monitoring of the victim's vital signs are important. If a pressure immobilization device has been applied in the field and the patient is asymptomatic, it should be removed (after IV access has been secured and appropriate antivenom has been located) to assess the bitten extremity. If obvious signs of envenomation develop, the device should be immediately reapplied and left in place until antivenom administration has begun. If a totally occlusive vascular tourniquet has been applied in the field, a looser constriction band (only tight enough to impede superficial venous and lymphatic return) should be applied more proximally and IV access secured. The arterial tourniquet can then be removed while closely observing the victim for possible deterioration as stagnant, acidotic blood (with or without venom) is released to the central circulation. If signs of significant envenomation are present on arrival, appropriate antivenom administration should begin before removal of any pressure immobilization device or constriction band. Tourniquets are best replaced by constriction bands as soon as possible, however, to avoid adding ischemic insult to venom-induced tissue damage.
Box 39-3. DIAGNOSTIC STUDIES IN EVALUATION OF VENOMOUS SNAKEBITE VICTIMS
BLOOD AND SERUM Type and cross-match Complete blood cell count Peripheral smear Coagulation studies (fibrinogen, fibrin degradation products, D-dimer, partial thromboplastin time, prothrombin time) Electrolytes, glucose, creatinine, blood urea nitrogen, liver enzymes, bilirubin Arterial blood gases Myoglobin, creatine kinase
URINE Bedside tests (glucose, blood, myoglobin [on each voided specimen]) Urinalysis
STOOL Test for blood
RADIOGRAPHS Chest (if over 40 years old, history of underlying cardiopulmonary disease, or severe envenomation) Bite site soft tissue films (if retained fangs possible; poor sensitivity) Computed tomography of the brain (if presentation suggests intracranial hemorrhage)
ELECTROCARDIOGRAM If patient is over 40 years old, has a history of underlying cardiopulmonary disease, or has a severe envenomation
Snake venom detection kits are available in Australia and in other regions to help detect the presence of venom in a bitten individual and identify the offending indigenous species.[59] [73] This technique, which is both sensitive and specific, uses an enzyme-linked immunosorbent assay (ELISA) to identify venom in tissue fluid taken from the bite site or in the victim's urine. The test is less reliable using blood samples.[93] The severity of envenomation is assessed. If the victim shows signs of cardiovascular collapse or respiratory distress, prompt action is needed, including antivenom administration. If the patient appears stable, however, the approach is more complicated. Snake venom poisoning is a dynamic process, so a patient who looks well may suddenly develop respiratory distress and hypotension. The physician must anticipate multisystem involvement after snake venom poisoning and be prepared for deterioration in the victim's clinical status. Furthermore, with some snake species, many hours may pass before significant signs or symptoms appear. The history and physical examination help determine severity. The bitten extremity should be marked at two proximal locations and the circumferences at these sites monitored every 15 minutes for progressive swelling. Rapidly progressive edema indicates a worsening clinical situation. Lack of swelling, however, does not rule out significant venom poisoning. Laboratory evaluations are also important in judging severity ( Box 39-3 ). A complete blood cell count may reveal a drop in hematocrit with significant bleeding or hemolysis or evidence of hemoconcentration as intravascular fluids leak into soft tissues. Leukocytosis is common, and platelet count may reflect consumptive coagulopathy. The peripheral blood smear may reveal microangiopathic hemolysis. A sample for blood typing
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and screening should be obtained as soon as possible, since both venom toxins and antivenom may later interfere with this procedure. Blood coagulation studies (prothrombin time, partial thromboplastin time, fibrinogen level, fibrin degradation products) can aid in gauging severity in species known to induce coagulopathy. Urine samples should be checked at the bedside with reagent strips for the presence of blood. If positive, formal urinalysis and measurement of urine myoglobin should be performed as well. Stool should be tested for gross or occult blood. Baseline electrolyte and renal function studies are important when hyperkalemia and renal failure are potential complications. Liver function parameters help assess hepatic toxicity. Creatine kinase level, as a marker for myotoxicity, may help determine the presence of envenomation. If elevated, cardiac markers should also be checked to rule out myocardial involvement. If systemic poisoning is evident, an electrocardiogram and chest radiograph should also be obtained. Arterial blood gases should be measured and followed if there is evidence of respiratory involvement or circulatory embarrassment. Signs or symptoms of intracranial bleeding should prompt computed tomographic scanning. The key principles of treating significant snake venom poisoning are sound supportive care of the victim's physiologic status and the use of appropriate antivenom when available. Antivenoms are available for the vast majority of the world's medically important venomous snakes. Although most antivenoms are still of equine origin, an increasing number of countries are putting ovine Fab or Fab2 antivenoms into clinical use. These antivenoms appear to have an increased safety profile in regard to allergic phenomena and may be more effective than their equine predecessors (see Chapter 38 and Chapter 40 ). [18] [33] Currently, no specific antivenom exists for Atractaspis species, and the majority of these bites follow a benign clinical course.[76] Likewise, no antivenoms for colubrid envenomations are widely available, although antivenoms against Dispholidus typus and Rhabdophis tigrinus venoms are produced in South Africa and Japan, respectively. Management of envenomation by burrowing asps and colubrids relies almost entirely on sound supportive care. The bitten extremity should be splinted and elevated. Mild analgesics may be required in some cases, and antibiotics are indicated if secondary infection occurs. If a coagulopathy develops, careful assessment of the coagulation status of the patient is vital. Fresh-frozen plasma may replace depleted coagulation factors,[51] [62] and blood products may be needed to counter a declining hematocrit. However, adding fuel to an ongoing consumptive coagulopathy may exacerbate intravascular clotting. [42] IV steroids (hydrocortisone, 15 mg/kg/day) and aminocaproic acid (70 mg/kg initially, then 15 mg/kg/day) have been beneficial in some cases.[40] The use of heparin for intravascular coagulation has
also been recommended but is controversial.[38] [66] These modalities have no effect on any direct venom toxicity to the vasculature or internal organs.[51] For an antivenom to be effective in snake venom poisoning, it must contain antibodies to the specific deleterious antigens present in the offending snake's venom. In regions where more than one antivenom is available to treat bites by various indigenous snakes, identifying the specific snake takes on added importance. In Australia, where multiple monospecific antivenoms are available, this task is aided by ELISA kits. In regions where the only antivenom available is a polyvalent product, identifying the specific snake is less critical as long as all medically important indigenous species are covered by the antivenom. In some situations, antivenom produced for a snake in a particular region may be largely ineffective in treating bites by the same species found in a different region because of significant differences in venom composition. Important examples include the carpet viper (Echis carinatus) and Russell's viper (Daboia russellii). Bites by these species should be treated with antivenoms produced using snakes from the same geographic region as the responsible animal.[34] Using an antivenom developed for unrelated species is generally of no benefit unless cross-protection has been previously demonstrated. Significant risk surrounds use of a heterologous antivenom, however, since all commercially available products carry some variable risks of allergic phenomena (see Chapter 40 ). In some instances, however, heterologous antivenoms have demonstrated significant cross-protection.[45] An excellent example of this is the efficacy of Commonwealth Serum Laboratory's tiger snake (Notechis) antivenom against sea snake venoms.[2] [65] [78] This should be considered the second-line agent to be used if specific sea snake antivenom is not available.[79] Further research and clinical experience will clarify the antigenic relationships between venoms of seemingly unrelated snake taxa, increasing the list of cross-protective antivenoms. If there is a choice between a polyvalent antivenom developed to counter the effects of venom poisoning by several snake species found in a geographic area and a monovalent serum specific for one species of snake, the monovalent product should be used if the snake has been definitively identified. It will provide more specific protection with a smaller burden of extraneous, allergenic proteins ineffective against the offending snake's venom. Recommendations regarding antivenom choices can be obtained from experts in snake envenomation or from the Antivenom Index.[1] [2] This resource contains a list of medically important snakes of the world (scientific and common names), recommended
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antivenoms for these species, a list of antivenom inventories maintained by participating institutions in the United States, and a list of manufacturers of antivenoms around the world. Assistance in locating stocks of antivenom within the United States can be obtained by using the Antivenom Index or consulting the University of Arizona Poison and Drug Information Center (602-626-6016). Assistance in obtaining an appropriate, exotic antivenom may be obtained from law enforcement agencies or the military. Once the decision has been made to administer antivenom and an appropriate agent has been obtained, preparations for administration should begin promptly. The patient's intravascular volume should be expanded using crystalloid infusion unless there is a contraindication (e.g., a history of congestive heart failure). Volume expansion may blunt a hypotensive response as a result of direct complement activation by antivenom proteins. An appropriate dose of 1:1000 aqueous epinephrine (0.01 ml/kg, up to 0.5 ml total) should be drawn up in a syringe and placed at the patient's bedside so that it is immediately available for subcutaneous or intramuscular injection if an allergic reaction occurs to the antivenom. Although most antivenom manufacturers suggest an intradermal test for possible allergy to their product before infusion begins, these tests are extremely nonspecific and unreliable; a significant number of false positives and false negatives occur.[32] [88] Furthermore, a positive skin test does not contraindicate the use of antivenom if a significant threat to life or limb exists. If indicated, antivenom should be administered without first performing any test for sensitivity. The treating physician should be at the patient's bedside during the initiation of the infusion in order to intervene immediately if a reaction occurs (see Chapter 40 ). The antivenom package insert should be consulted in determining an appropriate starting dose. Antivenom can generally be withheld in an apparently dry bite or minor envenomation while the victim is closely observed for any development or progression of signs or symptoms. For a few species of snakes, antivenom should be administered after any bite by an identified specimen regardless of whether symptoms or signs are present. Examples include bites by kraits (Bungarus spp.) or large (greater than 50 cm in length) coral snakes (Micrurus spp.). Once symptoms begin in these scenarios, they may be difficult to stop even with antivenom. The potency of different antivenoms is variable, and it is difficult to make general recommendations regarding dosages. For many antivenoms, 20 to 50 ml (further diluted as above) is a reasonable starting dose in treating moderately severe poisoning. In a severe envenomation, especially with evidence of neurotoxicity, 100 to 150 ml is more appropriate.[59] If signs and symptoms or laboratory abnormalities continue to progress after the initial dose is given, more antivenom should be administered. Children should receive the same starting doses as adults or even higher, since children receive larger doses of venom in proportion to their body surface area and intravascular volume.[50] [59] In the future, antivenom dosing may be guided by ELISA techniques that quantitate circulating venom.[9] Before antivenom infusion the patient should be premedicated with IV antihistamines. Fifty to 100 mg of diphenhydramine (1 to 2 mg/kg in children) and 300 mg of cimetidine (5 to 10 mg/kg in children) or equivalent agents can be given. Where antivenom is clearly needed and risk of anaphylaxis is increased (e.g., history of allergy to horses, prior reaction to antivenom), premedicating the patient with a small dose of subcutaneous 1:1000 epinephrine (0.3 ml in adults, 0.01 ml/kg in children) can be considered if there are no contraindications (e.g., coronary artery disease, severe hypertension). The total antivenom dose to be administered should be added to a bag of diluent (5% dextrose in water or crystalloid) at a dilution of 1:50 to 1:100. The infusion should be begun intravenously at a very slow rate (a few milliliters per minute) with the physician in attendance. If no reaction occurs after a few minutes, the rate can be progressively increased so that the total dose is administered in approximately 1 to 2 hours. If the patient is in extremis, however, the infusion should be more rapid. Antivenom should not be administered by local or intramuscular injection, because it is less effective by these routes, and if a reaction occurs, the drug cannot be discontinued.[11] If an early reaction occurs, the antivenom should be temporarily halted and the reaction treated (see Chapter 38 ). The infusion can then usually be restarted at a slower rate. Further diluting the antivenom may also be helpful. Patients who receive equine antivenom are at risk for immune complex-mediated delayed serum sickness, usually 1 to 2 weeks after administration. This risk increases in direct proportion to the total dose of antivenom administered. Victims definitely envenomed, particularly those requiring antivenom, should be admitted for close cardiopulmonary monitoring for a minumum of 24 hours and until overall stability is achieved. Any abnormal laboratory values should be remeasured frequently for at least 24 to 48 hours or until normalized. Delayed coagulopathy after antivenom treatment may result from delayed release of venom from depot sites such as skin blisters.[59] Persons who remain asymptomatic after being bitten by venomous snakes create challenging disposition decisions. If a viperid snake is implicated in such a bite,
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it is usually safe to discharge the victim after 6 hours of close observation, provided the clinical picture remains normal. For sea snakes, 8 hours is reasonable; for elapids, 24 hours is safer.[11] [79] Suspected boomslang (Dispholidus typus), bird snake, or twig snake (Thelotornis spp.) bites should be observed in the hospital for 24 hours. If coagulation studies remain normal at that time, the patient can be discharged. If discharged, the person should be instructed about bed rest for 24 hours, increased fluid intake, and monitoring for symptoms, such as increased pain, swelling, dizziness, shortness of breath, numbness, and weakness. Follow-up within 24 hours should be arranged for reevaluation. With evidence of clinically significant bleeding in the patient with a coagulopathy, administration of appropriate blood products should be considered. Antivenom should be started if possible before blood products are given to stop the continued activation and depletion of coagulation factors. Many viperid bites have laboratory evidence of coagulopathy without significant clinical hemorrhage.[46] [57] Such cases can be treated with antivenom, bed rest, and close observation while withholding blood products. Other treatment modalities for snake venom poisoning have demonstrated variable anecdotal benefit, but they do not replace proper conservative care and appropriate antivenom use. Edrophonium and neostigmine, for example, can temporarily reverse neuromuscular blockade after cobra envenomation.[59] [75] [87] These agents must be used cautiously because either may stimulate cholingeric crisis. Edrophonium combined with atropine might be effective in reversing respiratory muscle weakness in
a victim of cobra or krait bite when antivenom is not immediately available. Attempts to temporize in a patient with impending respiratory failure can result in aspiration.[35] It is best to proceed with prompt endotracheal intubation before frank respiratory failure occurs. Ethylenediaminetetraacetic acid (EDTA) has been touted as an inhibitor of snake venom proteases,[46] [60] but its clinical efficacy has not been demonstrated. In fact, increased mortality occurred in animal models when EDTA was given intravenously to treat pit viper venom poisoning.[60] Other modalities recommended in the past without evidence to support routine use include topical agents (e.g., potassium permanganate) to "deactivate" venom; routine fasciotomy of the bitten extremity (see following discussion); immediate exploration, debridement, or excision of the bite site; administration of heparin to counter disseminated intravascular coagulation; and high-dose steroids. Renal failure can best be prevented by aggressively treating hypotension, maintaining adequate urine output, and using antivenom appropriately. Myoglobinuria should be treated in standard fashion with sodium bicarbonate, mannitol, or loop diuretics. If renal failure develops, care should be directed at maintaining proper electrolyte balance. Peritoneal dialysis or hemodialysis is often required in such cases. Hemodialysis has been anecdotally reported to improve peripheral muscle weakness in victims of severe sea snake envenomation with acute renal failure, probably by reversing hyperkalemic and uremic effects on venom-damaged muscle fibers.[65] Dialysis does not remove circulating venom components, however, and the indications for dialysis are the same as for any other cause of acute renal failure. Wound care of the bitten extremity should be provided (see Chapter 38 ). Although controversial, broad-spectrum antibiotics may be used prophylactically for a few days in victims with significant potential for necrosis in an attempt to limit secondary infection. Although the incidence of such infection is low,[13] the risks increase after misdirected attempts to incise or open the bite site under field conditions.[94] Early physical therapy aimed at returning the bitten extremity to its maximal level of function is important, especially in patients with significant soft tissue swelling or necrosis. If concerned about compartment syndrome, the physician should measure intracompartmental pressures using an appropriate device. Sustained pressures greater than 30 to 40 mm Hg in a normotensive patient may exceed capillary perfusion pressure in the muscles. Ischemia may result if the situation is not addressed, usually by means of a fasciotomy. The pressure at which ischemia ensues is even lower in hypotensive snakebite victims, and the threshold for performing a fasciotomy may need to be lowered in this setting. The overall incidence of compartment syndromes after venomous snakebite, however, is low.[17] [23] [86] Prophylactic fasciotomies in patients without objectively documented elevated intracompartmental pressures are inappropriate. The management of a victim with ocular exposure to spitting cobra venom begins with immediate and copious irrigation of the eyes with any readily available, nonirritating fluid.[59] [84] Prompt treatment may help prevent local complications. Close ophthalmologic follow-up is important to rule out corneal ulceration or uveitis.
ACTIVE IMMUNIZATION Rituals and techniques for immunization against snake venom have been practiced for centuries in various parts of the world.[49] More recently, modern immunologic methods have been used. Beginning in 1965, 43,446 individuals in the Ryukyu Islands of Japan, an area of high snakebite incidence, were immunized with habu (Trimeresurus flavoviridis) venom toxoid. Follow-up after about 5 years indicated equivocal results, and no further large-scale trials were undertaken, but experimental
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work continues. Individuals have also been immunized against other snake venoms. [63] [77]
MORTALITY Although mortality rates vary greatly throughout the world, more than 95% of deaths from snakebites occur in underdeveloped countries with inadequate or remote medical resources.[9] The causes of death in fatal cases of elapid envenomation are respiratory paralysis, coagulopathy, renal failure, and cardiac failure.[11] [60] [92] In viperid-related fatalities the cause is usually protracted hypovolemic shock.[11] This is often related to inadequate fluid resuscitation, inappropriate use of vasopressors, or inadequate or delayed use of antivenom. Sea snake fatalities are related to respiratory failure, cardiac arrhythmias, or renal failure.[7] [59] [79] The average time to death after envenomation is 5 hours in elapid bites, 2 to 3 days in viperid bites, and 12 to 24 hours in sea snake bites.[58]
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Chapter 40 - Antivenins and Immunobiologicals: Immunotherapeutics of Envenomation Rivka S. Horowitz Richard C. Dart
The ideal therapeutic agent effectively treats or prevents a specific medical condition and is free of adverse effects. Commercially available antivenins (antivenoms) are not ideal. The vast majority of antivenins are equine derived and thus possess the potential adverse immunologic effects inherent in the administration of foreign proteins. Although antivenin lowers the morbidity and mortality associated with envenomation, it may have life-threatening side effects. As a result, many physicians are reluctant to administer antivenin even to patients who have a clear indication for its use. Worldwide, more than 60 commercial laboratories produce almost 200 different antivenin preparations for the treatment of snake, arachnid, fish, and coelenterate envenomations. Theakston and Warrell[48] compiled a list of hyperimmune sera available for the treatment of venom poisoning. The available crotalid antivenin in the United States is effective against all indigenous North American pit vipers. However, zoos and amateur snake enthusiasts are likely to house non-indigenous, exotic snakes for which the anticrotalid antivenin would be useless. Physicians must expeditiously exploit all available resources to identify and acquire the appropriate antivenins for unusual envenomations. One such resource, the Antivenin Index, is compiled by the American Association of Zoological Parks and Aquariums and the American Association of Poison Control Centers (AAPCC). The Index lists the location of foreign antivenins stocked by zoos in the United States. Guidance for use of these antivenins and general snakebite management may be obtained through an AAPCC-certified poison center.
PRINCIPLES OF ANTIVENIN THERAPY Historical Perspective Immunotherapy against snake venom dates to 1887 with the first report of successful immunization in birds. Sewall[39] reported that pigeons injected with increasing but sublethal doses of Sistrurus catenatus catenatus (Eastern massasauga) venom became resistant to venom inoculations seven times the lethal dose. Seven years later, contemporaneous experiments by Calmette[8] and Phisalix and Bertrand[33] demonstrated that immunization with cobra (Naja naja) and European viper (Vipera berus) venoms, respectfully, protected animals against inoculation with these venoms. Within a decade of Sewall's landmark experiment, Calmette[9] produced the first therapeutic antivenin derived from immunizing horses with cobra venom. Although Calmette overestimated the effectiveness of his antivenin, erroneously believing that it would protect against all neurotoxic venoms,[8] he recognized an important principle of immunotherapy still operative today: interspecies cross-reactivity. Another pioneer in the study and production of antivenin, Vital Brazil, further demonstrated both specificity and cross-reactivity through the production of numerous monospecific and polyspecific antivenins. A monospecific antivenin is derived from immunizing animals with the venom of a single species, whereas polyspecific antivenin is produced either by inoculating animals with the venom of more than one species or by pooling different monospecific antivenins into a final product. Brazil recognized the need for polyspecific antivenins, since snakebite victims were often unable to differentiate among the variety of poisonous snakes indigenous to an area.[14] To ensure an adequate supply of venom for his research, Brazil organized a unique exchange network throughout the countryside of São Paulo, Brazil. He convinced government and railroad officials to allow free passage for snakes shipped to his institute and sent devices for snake capture and crates for transport to anyone requesting them. For every snake shipped to him, Brazil would send a vial of serum (antivenin); for every six snakes sent, he would provide a needle and syringe for administering the serum.[14] After more than a decade of operating his exchange, Brazil claimed a significant decrease in mortality from snakebites.[5] [14] Neutralizing Antibody The foundation of antivenin therapy is the antigen-antibody interaction. The component of antivenin responsible for its therapeutic activity is the immunoglobulin G (IgG) antibody molecule. This neutralizing antibody inactivates the antigen by specific, noncovalent, antigen-antibody binding. Thus a neutralizing antibody to phospholipase A2 , a common constituent of snake venoms, prevents or attenuates the
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neurotoxic or myotoxic activity associated with this venom component. Understanding the structure of IgG helps to explain both the mechanism of action and the adverse reactions of antivenins. An IgG molecule weighs approximately 150,000 daltons and is composed of two functional parts: the antigen-binding site, consisting of two Fab portions, and the effector site, or Fc region ( Figure 40-1 ). Specific binding of the antigen to the Fab sites neutralizes further activity of the antigen. The Fc region of IgG is responsible for binding and activating immune system cells (e.g., phagocytes, macrophages, mast cells) and triggering a host of immunologic responses. These reactions, which include degranulation of mast cells and activation of the complement cascade, are partly responsible for the immediate, life-threatening allergic reactions to antivenin. The large size of the IgG antibody has important implications for the immunogenicity, distribution, and elimination of these neutralizing antibodies. Large-molecular-weight entities in general (IgG and other large antivenin components) are more likely to trigger immunologic reactions than smaller ones.[49] The ideal neutralizing antibody would be expected to have a large volume of distribution, implying more extensive tissue penetration and access to venom components. The large size of IgG, however, confines it primarily to the intravascular space and may limit more extensive distribution into tissue compartments. Theoretically, this may limit the effectiveness of IgG in binding antigen within tissue compartments.
Figure 40-1 Schematic diagram of an IgG molecule. The antigen-binding region (Fab portion) is present at the amino-terminal end. The effector region (Fc portion) interacts with the immune system cells and resides at the carboxyl end of IgG. Note the disulfide bridge.
The large molecules that make up most antivenin proteins have long elimination half-lives, and may predispose recipients to further immunologic complications. Large antivenin proteins exceed the threshold for filtration and excretion by the kidneys and therefore are eliminated primarily by the reticuloendothelial system (RES), a much slower process than renal elimination. Theoretically, the longer it takes to clear foreign proteins from the body, the more time they will be available to form immune complexes with the patient's endogenous antibodies. These complexes, composed of infused antivenin proteins and the patient's own IgG molecules, may precipitate in susceptible tissue, resulting in clinical disease such as serum sickness. Enzymatic cleavage of IgG with pepsin and papain produces smaller substituent Fab2 and Fab fragments that are capable of neutralizing venom components. Snake antivenin composed of Fab or Fab2 fragments avoids many of the serious adverse effects of IgG antivenin and thus represents a significant advance in treatment of envenomation ( Figure 40-2 and Figure 40-3 ) (see later discussion). Modern Production of Antivenin Antivenin (Crotalidae) Polyvalent, the IgG crotalid antivenin manufactured by Wyeth, has been the mainstay of therapy for crotalid envenomation despite its numerous potential deleterious effects. Efforts to maximize the neutralizing potential of antivenin while minimizing its immunogenicity have become the principal goal of modern antivenin production. Despite major advances in our understanding of the biology of antivenin production, the commercial manufacture of antivenin relies on the same principles of host animal immunization with snake venom described more than a century ago. All antivenins follow a two-step production process. First, a neutralizing antibody is produced by immunization of a host animal with sublethal doses of venom. This antibody is one of many proteins present in the resulting immune serum preparation. Step two involves purification of antivenin with reduction in the fraction of nonneutralizing proteins. The preparation is then concentrated and packaged in its final lyophilized or liquid form. Antivenin (Crotalidae) Polyvalent Wyeth.
In 2000 the ovine-derived antigen-binding fragment (Fab) anticrotalid antivenin became available for clinical use. Before this, the only available antivenin in the United States against pit viper envenomation was Antivenin (Crotalidae) Polyvalent Wyeth. Manufacture of that antivenin has changed little since its introduction in 1954. In this process, horses are immunized with increasing doses of venom from four crotalid species: Crotalus adamanteus (eastern diamondback), C. atrox (western diamondback),
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Figure 40-2 Proteolytic cleavage of IgG results in predictable substituent fractions. Pepsin digestion produces Fc and Fab 2 fractions. Fab2 consists of two Fab portions connected by a disulfide bridge. Molecular weight of Fab2 is 100,000 daltons.
Figure 40-3 Proteolytic cleavage of IgG results in predictable substituent fractions. Papain digestion of IgG yields the Fc and two Fab segments for each IgG molecule. Molecular weight of Fab is 50,000 daltons.
C. durissus terrificus (South American or tropical rattlesnake), and Bothrops atrox (fer-de-lance), plus adjuvant for immune system stimulation. The resultant hyperimmune serum is subjected to an ammonium sulfate precipitation, which removes a variety of plasma proteins. Unfortunately, a fraction of neutralizing antibody is also lost in this process, resulting in diminished potency. The product is then precipitated, filtered, resuspended, and lyophilized. The final concentrated antivenin contains 1.5 to 2 g of horse protein, only 15% to 25% of which is IgG.[43]
ADVERSE EFFECTS Incomplete purification of Antivenin (Crotalidae) Polyvalent Wyeth results in the presence of significant amounts of nonneutralizing proteins, such as albumin, a- and ß-globulins, and IgM. Sullivan[43] has quantified the relative contributions of nonneutralizing proteins to the final antivenin product ( Box 40-1 ). The heterologous nature of this antivenin enhances immunogenicity and is responsible for life-threatening anaphylactic and anaphylactoid reactions and the
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more common, but self-limiting, serum sickness (see later discussion). In addition, since the purification process results in denaturation of a portion of the protective IgG fraction,[43] multiple vials of antivenin must be administered for adequate reversal of venom poisoning. Box 40-1. QUANTITATION OF PROTEINS IN SAMPLES OF WYETH ANTIVENIN
IgG
2900 mg/ml
IgM
75 mg/ml
Total protein
9.4 g/dl
Albumin
0.28 g/dl
a1 -Globulin
0.74 g/dl
a2 -Globulin
3.50 g/dl
ß-Globulin
2.76 g/dl
?-Globulin
2.12 g/dl
Despite these impurities and being prepared from only four species, the Wyeth antivenin preparation is effective against all crotalids native to North, Central, and South America. This cross-reactivity enables a single preparation of antivenin to be effective against any clinically significant pit viper envenomation. Anaphylactic and Anaphylactoid Reactions The spectrum of human immunologic responses to antivenin is well documented. Introduction of heterologous protein may induce type I hypersensitivity (anaphylactic) reactions. This syndrome results from IgE-mediated degranulation of mast cells and release of vasoactive mediators, including histamine, leukotriene, platelet activating factor, adenosine, and neutrophilic and eosinophilic chemotactic factors.[26] These substances induce vasodilation and increased capillary permeability resulting in hemodynamic instability and hypotension. Bronchospasm, laryngospasm, and death can result without airway management and pharmacologic intervention. Anaphylactoid reactions are clinically indistinguishable from anaphylaxis but are not IgE mediated. In this syndrome, mast cell degranulation is postulated to result from direct interaction of nonneutralizing antivenin protein or the Fc segment of the IgG molecule itself with mast cell membranes. This is often associated with activation of the complement cascade.[45] In addition, large nonneutralizing proteins present in antivenin, as well as aggregates of IgG itself,[3] [13] [19] may directly activate the complement system, resulting in release of vasoactive mediators. The subsequent hypotension, bronchospasm, and airway compromise require rapid, appropriate interventions. These life-threatening sequelae may occur whether antivenin is administered as the skin test or in the full antivenin dose. Management of allergic reactions should include epinephrine (intravenous bolus or infusion), antihistamines (both H1 and H2 blockers), and aggressive airway support if necessary ( Table 40-1 ). Allergic Reactions Patients with significant envenomation and a history of allergy to equine-derived antivenin or to horse serum present a difficult challenge. The decision to treat with Antivenin (Crotalidae) Polyvalent Wyeth must be based on strong clinical and laboratory indications and requires careful but rapid risk-benefit analysis. A patient with a history of allergy to antivenin who requires antivenin because of life- or limb-threatening symptoms may be successfully supported with epinephrine, antihistamines, and airway management. Patients who have experienced life-threatening allergic reactions to antivenin may not necessarily have recurrent reactions when rechallenged. Nevertheless, it is prudent to pretreat such patients with epinephrine and antihistamines (diphenhydramine and cimetidine) before antivenin administration (see Table 40-1 ). Serum Sickness In addition to the acute effects associated with antivenin administration, a delayed type III hypersensitivity reaction is well described. This entity, known as serum sickness, is common,[12] [46] particularly in persons receiving more than seven or eight vials of antivenin.[17] [50] The syndrome of serum sickness was originally described in 1905 by two pediatricians, von Pirquet and Schick, who noted that children receiving equine-derived streptococcal antitoxin sometimes developed fever, lymphadenopathy, and rash.[29] They first used the term serum sickness to describe this constellation of symptoms resulting from the administration of heterologous serum. Modern definitions of this syndrome have varied little from the original description. Serum sickness is a spectrum of disease, typically characterized by fever, malaise, urticaria, lymphadenopathy, arthralgias, and less commonly, glomerulonephritis and neuritis. The onset of symptoms usually occurs within 1 to 2 weeks after exposure to foreign antigens, in this case, heterologous protein in antivenin. The pathophysiology of serum sickness results from nonspecific deposition of immune complexes (antigen-IgG) in susceptible tissue. Under nonpathologic conditions, these complexes are cleared by the RES without sequelae. With abnormal vascular permeability and slight antigen excess, however, precipitation of immune complexes occurs. In addition, immune complex deposition tends to occur in tissues where the vasculature has a filtering function.[6] These complexes diffuse between endothelial cells and deposit along the basement membrane.[27] The interaction of immune complexes
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TABLE 40-1 -- Treatment Recommendations for Antivenin-Induced Anaphylaxis or Anaphylactoid Reaction EPINEPHRINE ANTIHISTAMINES INFUSION Adult 1–4 µg/min IV
BOLUS
DIPHENHYDRAMINE
CIMETIDINE
0.5–1 ml of 1:10,000 solution IV
50 mg IV stat, 50 mg IV q6h, prn
300 mg IV stat, then 300 mg IV q6h, prn
Child 0.01–1 µg/kg/min IV
0.01 mg/kg of 1:10,000 solution IV
1 mg/kg IV stat, then 1 mg/kg IV q6h, prn
5–10 mg/kg IV stat, then 5–10 mg/kg IV q6h, prn
IV, Intravenously; stat, immediately; q6h, every 6 hours; prn, as needed. trapped in the vascular wall with vasoactive mediators results in complement activation, further release of vasoactive mediators, and exacerbation of the inflammatory process. This process characteristically occurs in skin, synovial joints, and the glomerular apparatus, resulting in the clinical manifestations of serum sickness.[10] [26] [52] Treatment of Serum Sickness
A large percentage of patients receiving more than seven or eight vials of the standard, equine-derived anticrotalid antivenin develop serum sickness. [17] [50] The spectrum of illness in this syndrome is highly variable and may range from mild urticaria, malaise, and low-grade fever to debilitating arthralgias and myalgias. Fortunately, although well described, glomerulonephritis and neuritis are rare complications. The variability of the syndrome requires that treatment be tailored to individual clinical needs. Patients with serum sickness should receive antihistamines such as diphenhydramine or hydroxyzine and, except in the mildest cases, a 7- to 10-day course of high-dose steroids. Clinical illness typically resolves within 1 to 2 weeks.
SPECIFIC ANTIVENINS This section covers general aspects of antivenin therapy following envenomation by the black widow spider, coral snake, and pit vipers. Specific indications for each antivenin are covered in their respective chapters (see Chapter 34 , Chapter 38 , and Chapter 39 ), as are specialized or experimental antivenins directed against the venoms of such creatures as scorpions (see Chapter 35 ) and stonefish, box-jellyfish, and sea snakes (see Chapter 61 and Chapter 62 ). Arachnid Antivenin: Black Widow Spider The only nonsnake antivenin approved by the FDA for use in the United States is indicated for envenomation by the black widow spider Latrodectus mactans (see Chapter 34 ). Antivenin (Latrodectus mactans) MSD is derived from hyperimmunizing horses with Latrodectus venom and is effective in counteracting the pain associated with severe envenomations. A similar antivenin frequently used in Australia is associated with a low but measurable incidence of anaphylaxis and serum sickness.[47] Fortunately, the venom from the black widow spider rarely results in life-threatening manifestations. Patients can usually be managed effectively with adequate doses of narcotic analgesics and benzodiazepines. In certain conditions, however, Latrodectus antivenin may be indicated. In general, patients with underlying medical problems, such as coronary artery disease or chronic obstructive pulmonary disease, whose pain may trigger secondary ischemic events, and those who may not be able to tolerate large doses of narcotics or benzodiazepines may be appropriate candidates for antivenin. Pregnancy and extremes of age have often been cited as indications for antivenin.[28] [38] Patients with severe pain who do not respond to narcotics and benzodiazepines, however, will obtain prompt relief with intravenous (IV) administration of one vial of Latrodectus antivenin. [28] Snake Envenomation In contrast to black widow spider bites, venomous snakebites do not allow withholding antivenin when signs of envenomation are present (see Chapter 38 and Chapter 39 ). No effective alternative therapy exists for clinically significant snake envenomations other than antivenin.[37] The FDA-approved new, safer anticrotalid antivenin (CroTAb) is available for clinical use. Before this, only equine-derived Antivenin (Crotalidae) Polyvalent Wyeth was available for the treatment of crotalid envenomation from indigenous snakebites in the United States. Coral Snakes (Elapidae).
The AAPCC reported 61 coral snake bites (family Elapidae) in 1998. [22] An effective antivenin is available only for the Eastern (Micrurus fulvius fulvius) and Texas (M. fulvius tenere) coral snakes. Envenomation by these two species is associated with more serious systemic findings than typically occurs with their Arizona (Sonoran, Micruroides euryxanthus) counterpart.[20] [36] Signs of local envenomation are minimal, with neurotoxicity in the form of bulbar and respiratory paralysis developing up to 12 hours after the bite.
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Immunotherapy for M. fulvius envenomation requires IV administration of four to six vials of Antivenin (Micrurus fulvius) Equine Origin.[35] Additional vials may be necessary as clinically warranted.[20] Antivenin should be given to patients who have been bitten by an Eastern coral snake that has "chewed" on the affected part and who have evidence of fang penetration through the skin.[20] Early antivenin treatment is recommended, since cranial nerve dysfunction and respiratory paralysis from Eastern coral snake envenomation may be easier to prevent than to reverse.[20] Once venom components are bound to neuronal target tissue, they may not be readily removed by antivenin, or the end-organ toxicity may not be readily reversible. Thus early administration of antivenin, preferably within 8 hours of the bite, has been advocated.[20] As with any equine-derived product, skin testing is mandatory, and preparations for treatment of anaphylaxis must be in place. Skin testing may be omitted if the patient is hemodynamically unstable as a result of envenomation. Pit Vipers (Crotalidae).
A sheep-derived Fab antivenin, Affinity Purified, Mixed Monospecific Crotalid Antivenom, Ovine Fab for Injection (CroTAb), approved in 2000, represents a major advance in the immunotherapeutics of snake envenomation. Indications for the use of anticrotalid antivenin include signs and symptoms of progressive envenomation, as manifested by increasing local or systemic effects, or laboratory abnormalities consistent with envenomation (see Chapter 38 ). Antivenin (Crotalidae) Polyvalent Wyeth.
A careful history must be elicited from all envenomed patients. This should include allergy to horse dander, history of atopic reactions, and previous allergy or exposure to horse serum. Patients with positive histories may be at greater risk for allergic reactions to antivenin. Once the decision to administer antivenin has been made, a skin test determines horse serum sensitivity. Skin testing may be omitted for patients in extremis from snake envenomation, since immediate treatment may be lifesaving. Skin testing should never be done unless a decision to administer antivenin has been made, since life-threatening allergic reactions may occur from skin testing alone. The patient must be in an emergency department or other intensive care setting, with adequate IV access and resuscitation equipment at hand. The attendant staff must be prepared to treat acute anaphylaxis whenever skin testing is performed or antivenin is infused. PROTOCOL FOR SKIN TEST.
The manufacturer recommends the following protocol for skin testing [34] : 1. From 0.02 to 0.03 ml of a 1:10 dilution of antivenin or 0.02 to 0.03 ml of horse serum (provided in the kit as prediluted 1:10 solution) is injected intradermally. 2. A similar control dose of normal saline is injected at a distant site for comparison. 3. Patients with a history of sensitivity to horse serum who require antivenin therapy should be skin tested using a dilution of 1:100 of antivenin or normal horse serum. 4. A positive skin test is usually manifest within 5 to 30 minutes and is characterized by a wheal or without erythema. A significant percentage of both false-positive and false-negative skin tests occurs. Therefore a negative skin test does not rule out the potential for anaphylaxis associated with the administration of antivenin. Equally important, a positive skin test does not contraindicate the use of antivenin if the patient's life or limb is threatened.[25] [34] [37] The purpose of a skin test is to identify a patient with obvious severe hypersensitivity so that the health care team can be prepared to manage an allergic reaction. ADMINISTRATION.
In general, the initial dose of this antivenin is 10 vials, although the clinical severity of the bite may necessitate higher initial doses. Eastern diamondback rattlesnake (C. adamanteus) envenomations, for example, are typically more severe and may require an initial dose of 10 to 20 vials of antivenin. Although seemingly a minor detail, dissolving the lyophilized antivenin is yet another challenge in managing the envenomed victim. Provided with each antivenin kit, 10 ml of diluent (bacteriostatic water for injection, USP) is added to the lyophilized antivenin. Gentle swirling and rotating of the vials are mandatory to avoid inactivating the neutralizing component, IgG. Vigorous handling or shaking while solubilizing the antivenin may result in partial denaturation of IgG. Dissolving lyophylized antivenin
takes 20 to 30 minutes per vial, so enlisting the help of staff will result in more rapid completion of the process. Once in solution, the vials of antivenin are diluted in 250 to 500 ml of 5% dextrose in water or normal saline. The initial rate of infusion should be slow, with frequent clinical assessment for evidence of an allergic reaction. If well tolerated, the remainder of the infusion should be administered over 1 hour. The initial rate of antivenin infusion in patients with positive skin tests should be even slower than for patients with negative skin tests. We support pretreatment of these patients with epinephrine and antihistamines,[31] but this is not universally recommended. If no allergic reaction occurs, the residual infusion may proceed over the next 1 to 2 hours. If anaphylaxis develops during administration of antivenin, the infusion is stopped, and aggressive airway management and pharmacologic intervention are initiated.
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Patients should receive epinephrine and antihistamines (both H1 and H2 blockers) (see Table 40-1 ). Persistent life-threatening, systemic signs of venom poisoning may necessitate restarting the antivenin infusion. Under these conditions the antivenin should be further diluted and given at a slower rate than the initial infusion. The patient should be pretreated with antihistamines and epinephrine, and when required, epinephrine should be simultaneously infused at a second IV site (see Chapter 38 ). Antigen-Binding Fragment.
A major advance in immunotherapy for envenomation involves the use of specific Fab to neutralize venom (see Figure 40-3 ). Theoretically, use of these smaller antibody fragments has advantages. The ideal immunotherapeutic agent should have: (1) high specificity and affinity for the antigen, (2) rapid and extensive tissue distribution so that it will reach and bind the antigen in a timely fashion, (3) low antigenicity, and (4) rapid clearance from the body.[43] Based on clinical and experimental data, Fab appears to satisfy these criteria. ADVANTAGES OF FAB VS. IMMUNOGLOBULIN G.
Both animal and human experiments, especially with digoxin intoxication, support the efficacy of purified Fab and its superiority to whole IgG. Extensive experience with the digoxin antidote Digibind demonstrates that ovine-derived digoxin-specific Fab fulfills the criteria for an effective immunotherapeutic agent and is superior to whole IgG antibodies.[7] [23] [41] In baboon and rabbit models, distribution and elimination half-lives for digoxin-specific Fab were significantly shorter (0.28 to 0.32 and 9 to 13 hours, respectively) than those of the digoxin-specific IgG molecules (4 and 61 hours). [41] In addition, the volume of distribution for digoxin-specific Fab is significantly greater than that of the whole IgG antibody, reflecting its more extensive tissue distribution. In this model, therefore, Fab was more rapidly and extensively distributed to tissue sites than IgG.[41] Similar kinetic analysis in the dog model of digoxin poisoning revealed significantly shorter distribution half-lives with Fab than with the whole IgG antibody (0.54 hour vs. 2.28 hours). This correlated with shorter mean time to reversal of digoxin-induced cardiotoxicity in the Fab-treated group (36 minutes vs. 85 minutes in the IgG group).[23] Besides its proven efficacy,[1] [40] [53] ovine-derived Fab has not caused anaphylaxis or serum sickness despite its extensive use in clinical practice. Digoxin-specific Fab (Digibind) is safe, effective therapy for the rapid reversal of digoxin-induced cardiotoxicity. ADVANTAGES AND DISADVANTAGES OF FAB ANTIVENIN.
Clinical manifestations of crotalid envenomation using polyspecific anticrotalid Fab can be successfully reversed based on (1) the effectiveness of digoxin-specific Fab immunotherapy, (2) the successful clinical trials using Fab antivenin directed against V. berus,[18] and (3) the protection against venom-induced lethality in mice after the administration of specific Fab.[44] Although successful treatment of digoxin toxicity with Digibind is similar to the use of purified Fab fragment antivenin for snake envenomation, important differences include the following: 1. Unlike digoxin, snake venom is a heterogenous mixture of antigens varying greatly in size and structure. The antigenicity of each venom component may vary greatly depending on its physical characteristics. 2. Unlike snake venom, digoxin does not cause permanent cellular damage to target cells. Thus, once digoxin is released from target tissue and bound to Digibind, the cellular toxicity is reversed. The same may not be true of toxic effects of venom. 3. The relatively small size of the digoxin (781 daltons)-Fab (50,000 daltons) complex permits it to be renally excreted. In addition, evidence supports endogenous renal catabolism of such small complexes.[2] [21] [42] [51] Venom is a complex mixture of proteins, glycoproteins, and peptides, with molecular weights ranging from several thousand to greater than 100,000 daltons. [37] Although Fab complexed to small-molecular-weight venom components may be cleared renally, most of venom proteins have molecular weights greater than 20,000 daltons and are too large to be filtered and excreted by the kidney when complexed to Fab. This may result in significantly longer elimination half-lives of venom-Fab complexes. Theoretically, this may allow sufficient time for dissociation of the venom-Fab complex, resulting in the release of active venom components. ADMINISTRATION.
The new CroTAb antivenom is an affinity-purified, lyophilized preparation of ovine Fab obtained from healthy sheep, each immunized with one of the following North American crotalid snake venoms: C. atrox (Western diamondback rattlesnake), C. adamanteus (Eastern diamondback rattlesnake), C. scutulatus scutulatus (Mojave rattlesnake), and Agkistrodon piscivorus piscivorus (cottonmouth or water moccasin). The final product is prepared by isolating the immunoglobulin from the ovine serum, digesting it with papain, and isolating the venom-specific Fab fragments on affinity columns. This procedure produces four different monospecific antivenoms, which are then mixed in equal proportions to prepare the final antivenom. In mouse lethality studies, CroTAb averaged 5.3 times more potent than Antivenin (Crotalidae) Polyvalent
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Wyeth in neutralizing the venoms of 10 clinically important North American crotalid snakes.[11] In two prospective, open-labeled, multicenter trials, 42 patients ages 10 and or older had minimal or moderate North American crotalid envenomation (excluding copperhead bites) within 6 hours before admission and showed evidence of worsening in the emergency department. Rapid onset of action was noted in both trials, with reversal of progressive swelling, neurologic, and gastrointestinal symptoms, and prolonged prothrombin time (PT) during the initial CroTAb infusion. The short half-life of Fab compared with IgG resulted in recurrent signs of envenomation. Therefore a novel dosing schedule for CroTAb is recommended. Four to twelve vials of CroTAb are infused to achieve initial control of the envenomation syndrome, followed by two vials every 6 hours for three additional doses (18 hours), particularly in patients with severe coagulopathy. COMPLICATIONS.
As with all products containing animal proteins, CroTAb causes adverse reactions in about 20% of all reactions during infusion. Nearly all effects were mild. The most severe reaction was bronchospasm, which responded promptly to therapy. No cases of anaphylaxis have been reported. The serum sickness rate is approximately 6%, much lower than with nonpurified serum products, which typically produce serum sickness in 70% to 80% of patients.
Monoclonal Antibodies Advances in molecular biology have made the use of monoclonal antibodies commonplace in research.[15] A monoclonal antibody is a single, unique molecule produced in large quantity by a clone of cultured B cells. Reports describe the production of monoclonal antibodies directed against specific venom components and activities. For example, monoclonal antibodies with antithrombin-like,[30] antihemorrhagic,[16] [32] antimyotoxic,[24] and other activities have been purified. Preincubation of several classes of antiphospholipase A2 monoclonal antibodies in mice neutralized the myotoxic activity typically seen with Bothrops asper (ferde-lance) envenomation. [24] Monoclonal antibody-based enzyme-linked immunosorbent assays can be used to measure the concentration of venom components and may be more accurate and sensitive than other bioassays.[4] This technique also has diagnostic potential because it can be used to detect unique venom components after envenomation.[30] Despite these advances, use of monoclonal antibodies for venom poisoning has significant theoretic problems. Traditionally, an effective antivenin has a broad spectrum of activity and can counteract a wide array of clinical sequelae. Because of the complex and heterogenous nature of venoms with their innumerable antigenic sites, such antivenin would require pooling of many different monoclonal antibodies. A major advantage of a polyclonal antivenin is its ability to neutralize the effects of venoms of related species within the same genus or family. The very specificity that enables monoclonal antibodies to target unique antigenic determinants might render this approach impractical as an isolated therapeutic modality against envenomation.[25] Nevertheless, with continued isolation of monoclonal antibodies capable of neutralizing specific clinical effects of envenomation, such as myotoxic effects[24] and thrombinlike activity,[30] "libraries" of monoclonal antibodies may target and counteract predominant signs and symptoms of envenomation. Adjunctive immunotherapy with monoclonal antibodies and a broad-spectrum antivenin may provide the exquisite sensitivity against specific adverse reactions typically absent in standard antivenin. After a slow start, advances in molecular biology are finally being applied to envenomation therapeutics. We can anticipate a multitude of novel immunotherapeutic modalities in the future.
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Cochrane CG, Koffler D: Immune complex disease in experimental animals and man, Adv Immunol 16:185, 1973.
Consroe P et al: Comparison of a new ovine antigen binding fragment (Fab) antivenin for United States Crotalidae with the commercial antivenin for protection against venom-induced lethality in mice, Am J Trop Med Hyg 53:507, 1995. 11.
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Kitchens C, Van Mierop L: Envenomation by the eastern coral snake (Micrurus fulvius fulvius): a study of 39 victims, JAMA 258:1615, 1987.
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Chapter 41 - Bites and Injuries Inflicted by Domestic Animals Sean Keogh Michael L. Callaham
Domestic animal bites are common, and their incidence is rising. [15] [120] [148] Wild animal attacks are often more spectacular, but in the developed world, injuries from domestic animals have a much greater health and economic impact. Humans are not a natural prey of any animal, and most attacks are caused by fear of humans (real or perceived), territoriality, protective instinct, or accident. Occasionally a bite may result from disease (e.g., rabies) or rogue behavior. Injuries range from minimal to fatal, are regularly contaminated with a wide array of pathogens, and may spread systemic disease.
EPIDEMIOLOGY OF BITES AND INJURIES The 1998 National Pet Owner Survey estimated that more than 39 million households own at least one dog and that 32 million households own at least one cat.[4] The great majority of bites (about 80% to 90%) are inflicted by dogs.[92] Domestic cats account for about 5% to 15%, although some studies report a figure as high as 25%.[92] [133] [214] An estimated 1.8% of Americans are bitten by a dog every year, resulting in 4.5 million bite wounds. More than 750,000 of these bite victims seek medical attention.[118] [173] From 15 to 30 bites per 10,000 population occur per year, based on patient visits to the emergency department (ED).[120] [199] In a survey of 274 million ED visits in the United States between 1992 and 1994, more than 333,000 new dog bite injuries were seen, a rate of 12.9 per 10,000 persons. These injuries produced 0.4% of all ED visits in the United States. Bites to children were common, with boys aged 5 to 9 years having the highest incidence rate at 60.7 per 10,000 persons, which is 3.6% of all injury-related ED visits in this group. [210] These figures represent only bite victims who sought medical attention; one analysis of dog bite incidence in Pittsburgh showed that 790 bites were reported but that an estimated 1388 were unreported, an annual incidence of 58.9 per 10,000 population.[33] Urban areas have a higher reported rate of biting, and some studies suggest that dog bite incidence correlates inversely with socioeconomic status.[184] [199] The victim of a bite is often a pet owner or a member of the owner's family, and injury is frequently sustained while playing with the animal.[38] Surveys of schoolchildren have shown that 55% of boys and almost 40% of girls have been bitten, with 17% requiring medical attention.[12] Childhood bites can produce significant psychologic morbidity.[179] In Thailand, where Buddhist cultural beliefs encourage feeding and protection of stray animals, most dog bites are inflicted by strays and are unprovoked.[14] The annual incidence of cat bites is about 400,000 in the United States,[5] [76] [92] which is probably an underestimate. Biting cats are typically stray females, and most human victims are also female. Human bites on other humans are more common in urban areas, with a reported incidence of 3.6% to 23% of all bites.[27] [29] [129] One district in Brooklyn, New York, has reported a rate as high as 60.9 bites per 100,000 population. [129] In contrast, human bites in rural communities are less common, with one study reporting that 0.03% of all bites are caused by humans. [177] Children are frequently both the inflicters and the recipients of bite wounds. In a study of day-care centers, 46% of children were bitten by another child over a 1-year period.[73] About 30 million Americans ride horses, 50,000 of whom are treated for horse-related injury in an ED annually, principally because the rider is unrestrained and can fall off while travelling at speeds up to 40 mph. Horses can kick with a force of up to 1 ton[115] and frequently bite. A 2-year review of animal bites in Oslo revealed that 2% of 1051 recorded bites were caused by horses; 53% of these horse bite victims were children.[43] The American Ferret Association estimates 6 to 8 million domesticated ferrets reside in the United States. The risk of attack by a ferret is greatest in infants and small children. Bite statistics are scarce, but in Arizona, 11 ferret bites were reported over 11 months, with the ferret population estimated at 4000, about a 0.3% reported bite to ferret population ratio. During the same period, 2265 dog bites occurred, with the dog population estimated at 100,000, for a bite ratio of 2.2%.[180] Certain occupations carry a greater risk for animal bite; U.S. letter carriers reported 2851 dog bites in 1995,[35] and 64% of veterinarians have sustained a major animal-related injury in their careers. [119] Incidence of biting species varies with exposure. Among veterinarians, most injuries are inflicted by cattle, followed by dogs and then horses.
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Box 41-1. ADVICE TO AVOID BEING ATTACKED AND BITTEN BY COMMON PETS*
DOGS Do not leave a young child alone with a dog. Never approach or try to pet an unfamiliar dog, especially if it is tied up or confined. Always ask owners if you can pet their dog. Do not lean over a dog or pet it directly on the head; do not kiss a dog. Avoid quick, sudden movements that may startle a dog. Never pet or step over a sleeping dog. Never try to take a bone or toy from a dog (other than your own). Know the appearance of an angry dog: barking, growling, snarling with teeth showing, ears laid flat, legs stiff, tail up, and hair on back standing up. Never step between two fighting dogs; if you need to separate them, use a bucket of water or a hose. Do not approach a female dog that is nursing her pups. Teach injury prevention advice to children from an early age.
CATS Be aware that some cats do not like prolonged petting. Know warning signs of an impending bite: twitching of the tail, restlessness, and "intention" bites (i.e., cat moves to bite but does not bite).
FERRETS Do not sell or adopt a ferret that is known to bite. Do not push your fingers through the wires of a ferret cage. Reach for a ferret from the side, palm upward, rather than from above. Do not handle food and then handle young ferrets without washing your hands first. Do not poke a ferret or pull on its tail or ears. Never leave a ferret alone with a child or infant. If a ferret bites and locks on very tightly, pour cold and fast-running water over its face.
* Prevention of bites and injuries from other animals is addressed in the appropriate sections.
BITE AND INJURY AVOIDANCE Domestic animals of any kind rarely attack unless provoked, although unrestrained dogs are exceptions.[156] Physical attack is often a last resort, but an animal will often fight if it perceives that it is trapped. Reducing the risk of injury is often based on common sense and knowledge of animal behavior. For example, horses kick backward and with both rear feet, whereas cattle kick forward with only one foot. How humans react during a confrontation with an animal is also important. Nonpredator species such as cattle and deer are very susceptible to human intimidation, whereas a direct stare to a dog is seen as a challenge. Specific recommendations can reduce the chance of being attacked and bitten by a domestic animal ( Box 41-1 ). Dogs are guided by memory and instinct; fear and self-preservation are very strong instincts, so any perceived threat can lead to an attack. Territoriality is still ingrained in domestic dogs, even if humans provide for them. Protection of food can cause aggression, even in a docile dog. Any threat to a dog's mate, off-spring, or owner may result in an attack. Personality changes may lead to aggression; causes include illness (e.g., distemper) or physiological factors (e.g., female in heat).[211] Specific actions can be taken when threatened or under attack by a dog ( Box 41-2 ).
FIELD CARE Local wound treatment should be initiated at the scene of the bite. This is often more important in determining the course of healing than any later therapy. When skin is unbroken, but tissue contusion is present, treatment should include prompt and liberal application of ice or other cold packs during the first 24 hours. In wounds producing a penetrating injury, pressure usually controls bleeding; the use of pressure point occlusion or proximal tourniquets should be avoided unless blood loss is extreme and cannot otherwise be controlled. If
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the victim is more than an hour from treatment, the wounds should be cleansed promptly after resuscitation. Early cleansing reduces the chance of bacterial infection and is extremely effective in killing rabies and other viruses. Tap or drinking water is safe to use. Ordinary hand soap adds some bactericidal, virucidal, and cleansing properties; at least a pint of soapy water should be used. The wound should be thoroughly irrigated and then gently debrided of dirt and foreign objects by swabbing with a soft, clean cloth or sterile gauze. This is particularly important if the biting animal might be rabid, since simple irrigation without actual swabbing of the wound edges may not remove rabies virus. If possible, irrigation should be with a syringe under pressure. Box 41-2. SUGGESTED ACTION IF YOU ARE UNDER THREAT OR ATTACKED BY A DOG Stand totally still, and let the dog come to you. Stand passively, rather than in an aggressive or submissive pose. Do not pat the dog. Keep your eye on the dog, but do not stare at it. To reprimand the dog, say "no" in a harsh voice; do not attempt to hit the dog. Do not make any threatening or provocative movement. Do not fight back, especially against a "fighting" dog. Do not let the dog get behind you; keep turning to face it. If you are knocked down, feign death and curl up into a ball until the dog loses interest. If the dog punches you with its nose, ignore it. If a dog puts one of your legs in its mouth without tearing the flesh, waiting for a reaction, stay still if you can. If attacked by more than one dog, try and stand with your back to a wall or car.
Modified from Wilson S: Bite busters: how to deal with dog attacks, New York, 1997, Simon & Schuster.
Box 41-3. HUMAN AND DOMESTIC ANIMAL BITE RISK FACTORS
HIGH RISK Location Hand, wrist, or foot Scalp or face in infants (risk of cranial perforation) Over a major joint (risk of perforation) Through-and-through bite of cheek Type of wound Puncture (impossible to irrigate) Tissue crushing that cannot be debrided (typical of herbivore) Carnivore bite over vital structure (artery, nerve, joint) Biting species Human (hand wound) Cat (hand and lower extremity wounds) Pig Patient factors Older than 50 years of age Asplenia Chronic alcoholic Altered immune status (chemotherapy, AIDS, immune defect) Diabetes Peripheral vascular insufficiency Chronic corticosteroid therapy Prosthetic or diseased cardiac valve (consider systemic prophylaxis) Prosthetic or seriously diseased joint (consider systemic prophylaxis)
LOW RISK Face, scalp, ears, or mouth Self-bite of buccal mucosa (not through-and-through) Large clean lacerations that can be thoroughly cleansed Partial-thickness lacerations and abrasions
After thorough cleansing, the wound should be covered with sterile dressings or a clean, dry cloth. Wounds of the hands or feet require immobilization. If the wound is high risk ( Box 41-3 ), antibiotics should be started if available, preferably within an hour of wounding. In severe cases, antibiotics are worthwhile even if administered many hours later.
EVALUATION OF INJURIES Many domestic animals are large, heavy and strong. All victims of animal attacks should be evaluated using advanced trauma life support (ATLS) guidelines, except for the most minor and isolated bite injuries. Severe blunt trauma and life threatening injuries may initially be less obvious than a bite wound. Even apparently minor wounds ultimately require meticulous exploration, because injuries that appear superficial may overlie fractures or lacerated tendons, vessels, and nerves, or may penetrate into joint spaces.[69] With large herbivores, most of the bite injury may consist of severe contusion without skin disruption.[130] [205] Broken skin may result in local wound infection and the transmission of systemic disease. Infection can be caused by organisms carried in the animal's saliva or nasal secretions, by skin microbial flora carried into the wound, or by environmental organisms that enter the wound during or after the attack. Fortunately, most wounds do not become infected, particularly after adequate wound care. The need for tetanus prophylaxis should be assessed and rabies immunoglobulin and vaccine given if required. Few tests are routinely indicated in the evaluation of most animal bite injuries. Radiographs are useful to exclude fractures, foreign bodies (e.g., teeth), air in the joint after a deep bite wound to the hand, and osteomyelitis in older bite wounds. Films should be taken after any fight-bite injury (e.g., clenched fist) and also after any cranial or facial bite in an infant or small child to exclude bony penetration of the skull or facial fracture.[208] In the first few hours after a bite, white blood cell count or wound culture is not helpful.
DEFINITIVE WOUND CARE The same principles of irrigation and cleansing used in the prehospital environment apply in the hospital.
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Although tap water[9] and normal saline are acceptable wound irrigants,[6] 1% povidone iodine solution should also be used if rabies transmission is a possibility, as it is virucidal. [181] [187] Although 1% benzalkonium has been shown experimentally to kill the rabies virus, no data support its use in humans.[48] Besides gauze, a finely porous sponge may be used to cleanse the wound.[36] [51] [121] Irrigation is best performed with a 19-gauge needle or plastic intravenous (IV) catheter on a 35-ml syringe.[30] Puncture wounds tend to have a higher infection rate because irrigation is difficult, but it can be attempted if the wound is large enough to be held open. Irrigation does not remove dead or devitalized tissue common in bites, so thorough debridement may be required. Fleisher[69] advises that wounds should be treated and left open initially if they (1) are punctures rather than lacerations, (2) are not potentially disfiguring, and (3) involve the limbs, particularly the hand or foot. Delayed repair is advised if wounds are older than 6 to 12 hours (bites to the arms and legs) or 12 to 24 hours (facial bites). In contrast, many surgeons now advocate primary closure for dog bite wounds of the face, even when several days old.[105] One study from Ghana, where a delay of several days before hospital presentation after injury is common, indicated that immediate closure of human bite injuries to the face is safe. In 90% of cases, wound healing was complete at suture removal, even though some of the wounds sutured were up to 4 days old.[53] Bites of the hand are common and at high risk for infections and impaired healing. Although dog bites to other areas of the body have wound infection rates of 5% to 10%,[209] dog bite wounds of the hand have infection rates of up to 30%.[26] [30] [171] Treatment of hand bites should be aggressive, with irrigation, debridement, and antibiotic prophylaxis. The wounds are usually left open, although some authors recommend closing nonpuncture hand wounds.[209] If a dog bite wound to the hand or foot is closed primarily, the part should be immobilized in a bulky dressing and elevated. If infection is present, admission and antibiotics are indicated, with surgical drainage if required. If admission is not possible or practical, the wound should be rechecked daily until signs of infection are no longer present. If there is no evidence of infection, 5 days of splinting and oral antibiotics should be adequate.
WOUND INFECTIONS Tetanus Prophylaxis Clostridium tetani is an anaerobic gram-positive rod; its spores are found in the saliva and on teeth of animals and can survive in soil for years. Bite wounds often contain devitalized and crushed tissue, as well as puncture sites. These injuries are particularly suited to the release of the exotoxin tetanospasmin, which causes clinical tetanus. The number of cases of human tetanus after bite wounds is small but is double that of bite-related human rabies.[194] Therefore a thorough immunization history is vital for appropriate immunoprophylaxis [161] (see Chapter 66 ). Risk Factors for Wound Infection Risk factors for wound infection after a bite are summarized in Box 41-3 .[30] [49] Indications for Cultures Cultures of fresh bite wound surfaces have no value in the prediction of subsequent infection. Many of the pathogens causing infection take several days to grow and may be very fastidious or difficult to identify, particularly by routine diagnostic laboratory methods. The choice of empiric therapy for infected wounds can occasionally be guided by organisms identified on Gram's stain, but therapeutic decisions are usually made before culture results are known. Once infection is established, wound culture is indicated if prophylaxis or empiric therapy has failed; if the patient has systemic illness with signs such as pyrexia, rigors, or hypotension (in this case, blood cultures are mandatory); or if the wound or patient is at high risk. Cultures should be both aerobic and anaerobic. Gram's stain of pus may be helpful in determining predominant pathogens. The laboratory must be informed that prolonged cultures of up to 14 days may be necessary, depending on the organism sought. Using specific media for fastidious organisms, such as Brucella-supplemented agar to culture Porphyromonas, may also increase the isolation rate.[76] This is also important if Pasteurella or Capnocytophaga canimorsus infection is suspected. Isolates of coliforms should not be dismissed as contaminants and must be identified with antibiotic sensitivities. Reference laboratories, such as those of state health departments or at the Centers for Disease Control and Prevention (CDC) in Atlanta, are more likely to isolate unusual pathogens from bite wound cultures than are local laboratories.[198] Prophylactic Antibiotics Surgical wound care rather than antibiotic treatment is the most important factor in decreasing wound infection,[136] but whether to administer "prophylactic" antibiotics after bite wounds remains controversial. Some authors still recommend antibiotic prophylaxis for all dog bites.[134] [164] [172] Prospective, blinded clinical trials of dog bite wounds suggest that although persons treated with antibiotics may have lower infection rates, this is not statistically significant. [28] Such results have been extrapolated to the bite wounds of other animals. Unfortunately, many trials lacked standardization of wound care, antibiotic choice and dose, and evidence of compliance.
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In 1994, Cummings[42] performed a meta-analysis of eight randomized trials to determine whether prophylactic oral antibiotics prevent infection in persons with dog bite wounds. The relative risk for infection in persons given antibiotics was 0.56. This means that 14 persons need to be treated to prevent one infection. This conclusion is skewed, however, because one study had an atypically high infection rate of 60%. If this study is excluded, the benefit of prophylaxis in low-risk wounds is even less convincing. Antibiotic therapy is not cost-effective in low-risk dog bites and should be reserved for wounds at high risk for infection.[28] [50] (see Box 41-3 ). A small controlled trial of antibiotic prophylaxis in cat bites showed a decrease in wound infection in persons given prophylaxis.[60] Deep cat bites are prone to infection and mandate prophylaxis, whereas superficial injuries in low-risk areas do not require it. The bite victim needing prophylactic antibiotic treatment should be identified early in a wilderness setting or during triage on entry to the ED. After a few hours, bacteria bind to proteins and become encapsulated in a blood and fibrin coagulum that protects them to some extent from antibiotics.[59] [207] If infection risk is very high, parenteral antibiotics may be warranted,[207] but in most cases a 3- to 5-day oral regimen is sufficient. Previous recommendations for choice of antibiotic often assumed that Pasteurella, although common in cat bites, was a rare isolate in wounds resulting from dog bites. Recent work by Talan et al[198] suggests that this may not be true. Although 42% of dog bite wounds harbored Pasteurella stomatis, P. canis, and P. dagmatis,[71] 12% of wounds grew the more virulent P. multocida. [198] When infection presents less than 8 hours after injury, Pasteurella is probably the infecting organism. Empiric therapy for dog and cat bites should cover at least Pasteurella, Streptococcus, Staphylococcus, and anaerobes (see Box 41-5 ). Pasteurella isolates appear susceptible to amoxicillin-clavulanate, ampicillin, penicillin, second- and third-generation cephalosporins, doxycycline, trimethoprim/sulfamethoxazole, fluoroquinolones, azithromycin, and clarithromycin, although the latter two are somewhat less effective.[75] [76] [77] [78] [80] [82] [83] [84] [85] Common antibiotics often used for soft tissue wound infections, such as antistaphylococcal penicillins and first-generation cephalosporins, are less active in vitro against Pasteurella. Erythromycin, often chosen for the penicillin-allergic patient, is a poor choice for Pasteurella; serious clinical failures are well documented.[81] [123] Pasteurella is resistant to clindamycin.[75] Amoxicillin-clavulanate is recommended as a first-line agent for cat, dog, human, and most other bite wounds. It is ß-lactamase stable and therefore covers all Bacteroides, Staphylococcus, and Streptococcus species as well as most gram-negative bacteria. It shows activity against all 173 aerobic and anaerobic isolates tested from one series of animal bites.[78] Other options are a second-generation cephalosporin with anaerobic activity (e.g., cefoxitin) or combination therapy with either a penicillin and a first-generation cephalosporin, or clindamycin and a fluoroquinolone (e.g., ciprofloxacin).[198] Azithromycin, which is superior to clarithromycin for treating Pasteurella, and the new ketolide antibiotics, such as HMR 3004,[76] [85] show in vitro promise, although this may not translate into in vivo success. For the penicillin-allergic nonpregnant woman, clindamycin and ciprofloxacin are effective in high-risk wounds. For a pregnant woman whose only history of penicillin allergy is a rash, cefoxitin can be given because the chance of cross-sensitivity is low. In the penicillin-allergic pregnant woman the choice is a more difficult. Because neither azithromycin nor clarithromycin is approved for use in pregnancy, erythromycin may need to be prescribed. Because of its limited effectiveness against Pasteurella, careful observation of the patient is warranted. Tetracyclines should not be prescribed in pregnancy; ciprofloxacin and tetracycline should not be prescribed for young children ( Table 41-1 and Table 41-2 ). Follow-Up and Indications for Admission Follow-up of animal bites depends on risk factors (see Box 41-3 ) and the victim's response to treatment. With a superficial abrasion, infection is unlikely, so a return visit is usually not needed. With a typical, low-risk bite wound, one follow-up visit (in 2 days, to assess any infection) is sufficient. If the patient is well and no sutures have been placed, this visit may not be necessary. Infected wounds need close follow-up. In a wound that is at high risk for infection, the initial follow-up should be the next day. If an infected wound fails to respond to 5 days of initial antibiotic treatment, a wound culture is usually advised, although switching to a broader spectrum antibiotic may be considered. Rarely, the victim requires hospitalization ( Box 41-4 ). Response to initial or secondary therapy (particularly in a high-risk patient), age, general health, previous medical history, and social circumstance can influence this decision.
Box 41-4. INDICATIONS FOR CONSIDERATION OF HOSPITAL ADMISSION Hand bite Involvement of bone, joint, or tendon Deep space infection or tenosynovitis Septicemia from animal bite Severe wound infection causing systemic toxicity in immunocompetent patient Cellulitis or local infection in severely immunocompromised patient (diabetes, AIDS, chronic alcoholism, asplenia)* Cranial injury in an infant Major trauma inflicted by a large animal
*Possible indication, depending on patient circumstances.
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TABLE 41-1 -- Antibiotic Sensitivities of Common Wound Isolates BACTEROIDES SP. ANTIBIOTIC
Pasteurella spp.
ANIMAL ORIGIN
HUMAN ORIGIN
Fusobacterium Eikenella Capnocytophaga Streptococcus pyogenes
Staphylococcus aureus
Penicillin or ampicillin
+++
+++
+
+++
++
+++
+++
±
Amoxycillin plus clavulanate
+++
+++
+++
+++
++
+++
+++
+++
Erythromycin
-
+
+
-
+
++
++
++
Cephalexin
-
-
-
-
-
+
++
++
Tetracycline*
+++
++
++
+
+
+
++
+
Cefoxitin
++
++
+†
+
++
++
++
++
Clindamycin
-
+
+
++
-
++
+++
+++
Trimethoprim/sulfamethoxazole +
-
-
-
-
++
++
++
Imipenem
+++
+++
+++
+++
+++
+++
+++
+++
Piperacillin plus tazobactam
+++
+++
+++
+++
+++
+++
+++
+++
Ciprofloxacin*
+++
-
-
-
±
+++
±
+
Oxacillin
-
-
-
-
-
±
-
+++
+++, Very sensitive; ++, moderately sensitive; +, some sensitivity; ±, predominantly insensitive; -, insensitive. *Tetracycline should not be prescribed for pregnant women. Ciprofloxacin and tetracycline should not be prescribed for young children. †Bacteroides fragilis may be resistant to cefoxitin.
PROPHYLAXIS
TABLE 41-2 -- Suggested Initial Antibiotic Prophylaxis for Domestic Animal and Human Bites ADULT CHILD
Standard
Amoxicillin-clavulanate
Amoxicillin-clavulanate
If penicillin allergic
Clindamycin plus ciprofloxacin
Azithromycin Tetracycline if child is older
Azithromycin Tetracycline If pregnant
Amoxicillin-clavulanate
—
If pregnant and rash only with penicillin
Cefoxitin*
—
If pregnant and penicillin allergic
Erythromycin†
—
In the case of pig bite, ciprofloxacin, when not contraindicated, should be added to amoxicillin-clavulanate. *Chance of cross-sensitivity with penicillin is low. †Erythromycin has poor activity against Pasteurella species, so close clinical observation is necessary.
Treatment If inoculated in sufficiently large numbers, aerobic and anaerobic bacteria can cause localized cellulitis and abscess formation, which are the most common forms of infection. Wound infection may progress to sepsis. Treatment of wound infection from animal bites is the same as that for other traumatic wounds: elevation and immobilization of the affected part, removal of sutures or staples, and antibiotic therapy. Empiric initial antibiotic therapy is the same as that for prophylaxis (see Table 41-2 ), except with severe cellulitis or sepsis (see later discussion). Transmission of Systemic Infection Approximately 150 systemic diseases of mammals can be transmitted in some manner to humans, but relatively few are transmitted through a bite or scratch. These include rabies, cat scratch, cowpox, tularemia, leptospirosis, infection with Sporothrix schenckii, and brucellosis. House cats are an increasing source of human
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plague in the U.S. Southwest. Since the onset of the human immunodeficiency virus (HIV) epidemic, Rochalimaea infection (bacillary angiomatosis) has also become more prominent and is closely associated with exposure to cats. Sepsis Secondary to Bite Wounds Although theoretic risks with any animal bite pathogen, bacteremia and sepsis have been reported with only a limited number of organisms. Capnocytophaga canimorsus, formerly CDC alphanumeric strain DF-2, is a fastidious, slender, tapering, and gram-negative rod. This facultative aerobe grows poorly in most standard media, making identification difficult. Growth of C. canimorsus from blood often takes a week, making Gram's stain of the blood buffy coat taken on admission a useful diagnostic test.[117] Most infections occur after dog bites. Some cases have occurred after nonbite exposure to dogs or no animal exposure.[6] About 80% of persons who become seriously ill with this infection are immunocompromised, particularly because of splenectomy, hematologic malignancy, or cirrhosis. A minor bite in a previously healthy person can also result in catastrophic infection.* Clinical manifestations include cellulitis, endocarditis, meningitis, pneumonitis, Waterhouse-Friderichsen syndrome, renal failure, shock, and death. Purpuric lesions are seen in one third of cases and may progress to symmetric peripheral gangrene and amputation. Malar purpura is characteristic. In some cases, cutaneous gangrene develops at the bite site, a finding classic to this species of bacteria. When the diagnosis is known, optimal treatment is with penicillin or a cephalosporin. C. canimorsus is susceptible to cefuroxime, ampicillin, erythromycin, and vancomycin. Ciprofloxacin has been used with success.[140] Unlike most gram-negative bacilli, C. canimorsus is resistant to aminoglycosides, often used in empiric treatment of sepsis. If C. canimorsus infection is suspected, the laboratory should be alerted, and additional blood cultures should be sent to reference laboratories (e.g., the CDC) for identification. Pasteurella multocida can also produce bacteremia.[143] Usually the source is a cat bite, but dog bites also contribute. Most persons who develop bacteremia, as with those dying of Capnocytophaga infection, have cirrhosis, HIV infection, malignancy, or other immunosuppression. The mortality rate can be as high as 36%. Some victims may have been healthy, and even a seemingly trivial bite may produce life-threatening sepsis.[109] Several options exist for empiric IV antibiotic therapy in severe cellulitis and sepsis ( Box 41-5 ). Clindamycin plus ciprofloxacin is an appropriate combination; clindamycin inhibits toxin production in streptococcal infection and covers Staphylococcus aureus and anaerobes, and ciprofloxacin has good gram-negative coverage, including Pasteurella and C. canimorsus. Both drugs can also be given orally, either in the field or as continuation therapy on discharge from hospital.
Box 41-5. SUGGESTED EMPIRIC ANTIBIOTIC THERAPY FOR SEVERE CELLULITIS AND SEPSIS FROM BITES Ciprofloxacin plus clindamycin* Cefoxitin Ceftriaxone Imipenem-cilastatin
*May be given orally in the field or on discharge from hospital.
DOG BITES Dogs are the only species whose bites have been well studied in large numbers. Most factors contributing to dog bites are related to the owner's level of responsibility.[174] Although domesticated for at least 12,000 years, dogs retain many of their wild instincts, such as territoriality in a guard dog. Although many people keep dogs to repel burglars, a burglar is a fatal dog attack victim in only 1 of 177 attacks. A fatal dog attack victim is a child in 7 of 10 cases.[35] Besides the physical and emotional trauma of a dog attack, the financial impact is huge. Recent estimates put the total annual U.S. national cost of ED services for new dog bite-related injuries at more than $102 million.[210] When combined with charges for physician services and subsequent postdischarge care, direct medical care charges for dog bites rise to an estimated $165 million.[165] Dogs under 1 year of age are responsible for the highest incidence of bites.[215] The incidence of biting increases substantially during the warm summer months. Most bites occur between 1 and 9 PM, probably because more people are on the street.[95] Many bites are inflicted on children coming home from school or playing outdoors. The increased susceptibility of children results from their smaller size, relative inability to defend themselves, interest in animals, and unintentional abuse of animals. Biting dogs (not necessarily those causing fatal wounds) are more likely to be certain breeds, particularly German shepherd, pit bull, and chow chow in the United States. [9] [74] [90] In a United Kingdom survey of patients receiving plastic surgery for bite wounds, the most common *References:
[ 49] [ 96] [ 100] [ 134] [ 147] [ 170] [ 172]
.
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biting dogs were Staffordshire bull terriers, followed by Jack Russell terriers, medium-sized mongrels, and German shepherds.[182] Pit bulls have become popular in recent years and are often bred for aggressive behavior. Fatal attacks from pit bulls have increased dramatically. [175] Many towns and counties are passing legislation limiting or outlawing ownership of pit bulls, and owners may be charged with manslaughter after fatalities.[39] Wound Pathophysiology Although most wounds are minor, the jaws of adult dogs can bite with a force of up to 450 pounds per square inch, enough to puncture light sheet metal.[72] Wounds may comprise a mixture of biting, clawing, and crushing forces. These give a characteristic pattern of lacerations and punctures and may result in avulsion of soft tissues. A dog's bite can break human long bones.[46] [48] Treatment may naturally focus on the crushing component of the wound, but the penetrating component may cause the most morbidity.[200] The dog may move and shake its head during the attack, further tearing tissue.[114] Some owners replace their dogs' natural teeth with metal ones to increase their wounding capabilities. Snorting, grunting, or wound manipulation by the biting animal may force air into the tissues.[72] Besides infective organisms, foreign debris and even teeth may be deposited. In a severe attack the dog may eat tissue and blood or scavenge on an unconscious or intoxicated victim. [91] [160]
Wound Location Hand, arm, and lower extremity bites are reported most often in the adult population, with children primarily receiving head and neck wounds.[49] Injuries are typically centered around the nose, lips, and cheeks, and a bite can fracture the victim's maxilla.[70] In one large study the leading sites for wounds in victims of all ages were the face, neck, and head (29%), followed by the upper and then lower limbs.[210] In children up to age 9 years, 73% of injuries were to the face, neck, and head. [210] In Germany, 8500 dog bite injuries to the face are reported each year, and more than 50% of victims are infants or children. [178] Microbiology of Dog and Cat Wounds A comprehensive study that evaluated 50 patients with dog bites and 57 patients with cat bites identified a median of five bacterial isolates per culture ( Box 41-6 ). [198] Pasteurella species were the most common pathogens in bites of both dogs (50%) and cats (75%), in contrast to many previous studies, where Pasteurella was rarely isolated from dog bite wounds.[28] The association of Pasteurella with infections of rapid onset was confirmed. In other studies, Pasteurella multocida subspecies multocida and septica were the most common isolates in cat bite wounds and P. canis in dog bites.[16] [62] [98] Streptococcus, Staphylococcus, Moraxella, Corynebacterium, and Neisseria were the next most frequent aerobic isolates. Eikenella corrodens, usually associated with human bite infections, was found in only one cat and one dog bite wound.[198] Capnocytophaga species and Weeksella zoohelcum, both of which can cause invasive sepsis, were uncommon in this study and may be opportunistic pathogens. Fusobacterium, Bacteroides, Porphyromonas, and Prevotella were common anaerobic isolates. Wound Infection in Dog Bites Typical nonbite lacerations in an adult ED population have an infection rate of 5% to 15%.[51] [89] The rate is lower in the pediatric population.[10] This rate is similar to that of typical outpatient-treated dog bite wounds, when managed properly with irrigation and debridement. Dog bites of the head and neck, all sutured and none treated with antibiotics, have an infection rate as low as 1.4%. [93] Bites of the face and ears, although often requiring extensive plastic surgery, also heal well when treated aggressively and with antibiotics, as do dog bites of the genitalia.[54] [195] [213] Therefore, dog bite wounds that are not high risk are probably no more infection prone than nonbite, accidental cutaneous lacerations. Antibiotic therapy for infected dog bite wounds is initially the same as for prophylaxis, unless prophylaxis failed (see Table 41-2 ). Law Enforcement Dog Bite Wounds Law enforcement dogs are usually trained to bite and hold onto a victim until commanded to release. This is not the normal pattern for an attacking dog. The bite-and-hold technique results in deep puncture wounds, severe crush injuries, and large tissue avulsions. Attention should focus on the greater risk for deep nerve, vessel, and musculoskeletal injury.[158] Over 3 years in 486 patients evaluated on a jail ward for police dog bites, 7.2% required angiography of an extremity, and 21% of these had arterial injury.[188] A change in policy, from a bite-and-hold to a find-and-bark technique has been evaluated in Los Angeles. This resulted in a decrease in bites, injuries, and complications and a reduction in hospital admissions from 52% to 33.8% after police dog bite injuries. [102] Fatal Attacks by Dogs A dog bite-related fatality can be defined as death caused by acute trauma from a dog attack, often from an exsanguinating neck wound.[72] Fatal attacks by dogs in the United States cause many more deaths than rabies. A vicious attack cannot be predicted from a dog's prior behavior, since most offending dogs revert to normal, friendly behavior after the episode. A review between
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1979 and 1988 identified 157 fatalities, a rate of 6.7 deaths per 100 million population per year. Seventy percent of these were in children younger than 10 years.[175] For infants less than 1 year the annual death rate was 68 per 100 million, with half occurring while the infant was sleeping in a crib. Only a minority of fatal attacks were caused by stray dogs. Most victims died at the scene of the attack. Fatal attacks from pit bulls increased from 20% to 62%. German shepherds, huskies, malamutes, and wolf hybrids were the next most common fatal attackers. A review of fatal dog attacks in the US from 1989 to 1994 revealed 109 episodes.[174] Fifty-seven percent of the victims were children under 10 years. The rate of death for neonates was twice that for adults. Most attacks involved an unrestrained dog on the owner's property. Pit bulls were involved in 24 deaths, rottweilers in 16, and German shepherds in 10.
Box 41-6. BACTERIA ISOLATED FROM DOG AND CAT BITES
AEROBES Pasteurella multocida Other Pasteurella spp. Streptococcus mitis Streptococcus mutans Streptococcus pyogenes Streptococcus sanguis II Streptococcus intermedius ß-Hemolytic streptococci, group G ß-Hemolytic streptococci, group F Other Streptococcus spp. Staphylococcus aureus Staphylococcus epidermidis Staphylococcus warneri Staphylococcus intermedius Other Staphylococcus spp. Neisseria weaverii Neisseria subflav Other Neisseria spp. Corynebacterium minutissimum Other Corynebacterium spp. Moraxella (Branhamella) EF-4b Enterococcus faecalis Enterococcus avium Other Enterococcus spp. Bacillus Pseudomonas aeruginosa Other Pseudomonas spp. Actinomyces Brevibacterium EF-4a Weeksella zoohelcum Other Weeksella spp. Klebsiella Lactobacillus Citrobacter Flavobacterium Micrococcus Proteus mirabilis Stenotrophomonas maltophilia Capnocytophaga Eikenella corrodens Flavimonas oryzihabitans Acinetobacter Actinobacillus Alcaligenes Enterobacter cloacae Erysipelothrix rhusiopathiae
Actinobacillus Alcaligenes Enterobacter cloacae Erysipelothrix rhusiopathiae Reimerella anatipestifer Rothia dentocariosa Aeromonas hydrophilia Pantoea agglomerans Rhodococcus Streptomyces
ANAEROBES Fusobacterium Bacteroides fragilis Other Bacteroides spp. Porphyromonas Prevotella Propionibacterium Peptostreptococcus Eubacterium Clostridium sordellii Veillonella
Data from Talan DA et al: N Engl J Med 340:85, 1999.
In the most recent American review on dog bite fatalities, covering 1995 to 1996, dogs killed at least 25 people, although this is probably a marked underestimate because of death certificate unavailability.[32] Eighty percent of these deaths involved children, continuing a worrisome trend. Three were neonates less than 30 days old. The rottweiler was the most common breed involved. Sixty-four percent involved more than one dog. Pack behavior increases the likelihood that social facilitation and pack instinct will prolong the attack. [18] A report from southern Ireland notes that many dogs are very timid when alone, but when exposed to a pack environment, their behavior deteriorates dramatically. Of the seven pack attacks in the Irish report, five
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were by greyhounds.[114] Packs of aggressive dogs should be avoided and aggressive pack behavior toward humans punished by the owner. [18] Dogs represent a significant potential cause of death for infants and small children. A dog may accept an immobile baby but may have an unpredictable predatory response when the child starts crawling. Severe dog attacks on children occur most frequently in those under 5 years old.[21] Children and severely disabled persons should never be left alone with a dog, regardless of its reputation and prior behavior. Certain breeds (e.g., pit bulls) account for a disproportionate number of cases and should be considered for more effective supervision and controls. Prevention of Dog Bites Risk factors for increased biting propensity include male gender and unneutered status. Many dogs that seriously wound or kill humans have long histories of aggressive behavior. Strategies that reduce biting risk include education of owners and the public, selection of dogs, training, care, and socialization.[74] Other strategies, such as the compulsory trimming of canine teeth of sled dogs in Greenland, are also useful.[88] Laws regarding dangerous dogs should be enforced, although these are not a panacea. In 1991 the Dangerous Dogs Act was quickly enacted in the United Kingdom in response to violent attacks by American pit bull terriers and specified tight restrictions. Any offense meant the dog was euthanized and the owner prosecuted. Unfortunately, difficulties in clearly identifying pit bull terriers in the absence of clear breed standards led to confusion, and the act has received much criticism. [52] It has not yet been shown to decrease injuries by so-called dangerous breeds.[113] Animal control programs should be introduced and supported. Animal control associations, veterinary societies, and the Humane Society offer such courses. [215] Training in bite avoidance and canine behavior is recommended; for example a dog wagging its tail still may attack. This training should be offered to persons at greatest risk, such as animal control officers and postal workers; children might also benefit.[184] Dog bites should be reported as required by local or state ordinances.
DOMESTIC CAT BITES Domestic cats are becoming an increasing problem in the United States as the population of strays has exploded, with some estimates at 90 million. [192] This is important because of the opportunity for exposure to wild vectors of rabies. Cats now account for 50% of animal control calls, which has led to proposals for leash and licensing laws for cats. Little information for cat bites by breed is available. Women, particularly those aged 30 to 40 years, are more likely than men to be bitten by a cat, and 63% of bites are on a hand or finger, usually the right (dominant) hand.[133] [198] [214] Twenty-three percent of wounds are to the shoulder, arm, or forearm.[198] Seventy percent of wounds are scratches, and 27% are punctures of the skin.[214] Cats have a weaker biting force than dogs, but possess sharp, slender teeth, often producing deep puncture wounds.[48] Cat bites are notorious for their high infection rate, with 15% to 80% becoming infected.[47] [198] Cat bites result in a higher incidence of osteomyelitis and septic arthritis than dog bites.[75] Cat bites frequently possess two risk factors for infection: location on the hand and increased depth of puncture. Other risk factors associated with wound infections include an older victim, longer delay until ED treatment, wound inflicted by a pet rather than a stray, wound care at home, and a more severe wound.[47] Wound infections are more likely to develop in patients with lower extremity wounds who did not receive prophylactic oral antibiotics and in those with puncture wounds without benefit of prophylactic oral antibiotics. Scratches very seldom become infected.[47] Because the hand and lower extremities are common sites of injury and wounds are deep and penetrating, most cat bites are considered high risk. Such wounds should prompt administration of prophylactic antibiotics (see Table 41-2 ). Superficial cat bites and scratches elsewhere on the body are not high risk and should receive standard wound care without antibiotic coverage. Bacteria from cat bites and scratches can seed in distant arthritic and prosthetic joints and cause Pasteurella septic arthritis, endocarditis, and even mycotic thoracic aortic aneurysm[7] [86] [99] (see Table 41-2 and Box 41-6 ).
HUMAN BITES Human bites are common, particularly in urban areas. They were previously thought to be associated with a higher incidence of infection than other animal bites, but this may not be true. A study of 434 human bites found an infection rate of only 17.7% compared with 13.4% in 803 lacerations in the same patient group. [125] Others have cited a 10% infection rate for human bite wounds.[24] The important high-risk exception is human bites to the hand, especially if treatment is delayed. Unfortunately, bites of the hand often present several days after injury. Most human bites occur during fights. A wound sustained when human teeth actually bite a part of the human anatomy is termed an occlusional bite; in forensic cases this is most common on the hands and arms of men and the breasts and genitalia of women.[75] [92] Bites may occasionally be self-inflicted as a result of psychiatric or organic illness. [166] [201]
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Human bite wounds in developing countries pose special problems. Presentation may be significantly delayed,[127] [135] [145] and victims may have advanced infections. Many bites are inflicted by women on other women, and many are bites of the face, particularly the lip.[34] [53] [145] These wounds are intended to be disfiguring and can carry significant social stigma, further delaying treatment. Initial treatment in developing countries may be inappropriate, such as treating fresh bites with very hot water.[127] In the Micronesian Islands the tip of the nose may be bitten off adulterous wives to provoke shame.[20] [124] This form of punishment was known under ancient Roman law and Indian custom, and the art of nasal reconstruction originated in India as early as 1000 BC. [151] Traumatic love bites to the neck are well documented, as are bites to the face, breasts and penis during sexual activity.[65] [212] Microbiology At least 42 different species of bacteria have been identified in human saliva,[128] and 190 species have been found when gingivitis or periodontitis is present ( Box 41-7 ).[137] [138] Anaerobes include Bacteroides fragilis, Prevotella, Porphyromonas, Peptostreptococcus, Fusobacterium, Veillonella, and Clostridium species. Anaerobes are found in more than 50% of human bite wounds[75] and frequently produce ß-lactamase, unlike those from animal bites. Studies show that 41% to 45% of B. fragilis infections from human bite wounds are resistant to penicillin.[22] [81] Common pathogenic aerobes include ß-hemolytic streptococci, Staphylococcus aureus, and Haemophilus species.[75] [92] Eikenella corrodens, a fastidious, slow-growing, and gram-negative anaerobic rod, is found on 8.2% of human tooth scrapings and in 0.6% of salivary samples.[167] E. corrodens is frequently implicated in fight-bite injury infections and has been found in 10% to 29% of human bite wounds[92] (see Table 41-2 ).
Box 41-7. BACTERIA ISOLATED FROM HUMAN BITES
AEROBES Acinetobacter Branhamella (Moraxella) catarrhalis Corynebacterium Eikenella corrodens Enterobacter cloacae Other Enterobacter spp. Escherichia coli Haemophilus aphrophilus Haemophilus influenzae Haemophilus parainfluenzae Klebsiella pneumoniae Micrococcus Moraxella Neisseria gonorrhoeae Other Neisseria spp. Nocardia Proteus mirabilis Pseudomonas aeruginosa Other Pseudomonas spp. Serratia marcescens Staphylococcus aureus Staphylococcus epidermidis Staphylococcus intermedius Staphylococcus saprophyticus a-Hemolytic streptococci ß-Hemolytic streptococci ?-Hemolytic streptococci
a-Hemolytic streptococci ß-Hemolytic streptococci ?-Hemolytic streptococci
ANAEROBES Acidaminococcus Actinomyces Arachnia propionica Bacteroides fragilis Clostridium Eubacterium Fusobacterium nucleatum Peptostreptococcus anaerobius Peptostreptococcus prevotti Other Peptostreptococcus spp. Prevotella Propionibacterium acnes Other Propionibacterium spp. Veillonella
Modified from Griego RD, Rosen T, Orengo IF, Wolf JE: J Am Acad Dermatol 33:1019, 1995.
Human Bites and Systemic Disease Transmission of actinomycosis has been reported after a human bite,[139] as has syphilis, herpes, hepatitis C, hepatitis B, and tuberculosis.[45] [66] [67] [68] [110] [193] Tetanus from a human bite has been documented. [1] [144] Herpetic whitlow (infection of the distal phalanx) from herpes simplex virus is a well-known occupational hazard of nurses, physicians, dentists, and oral hygienists.[107] Toxic shock has been reported after a clenched-fist injury.[126] Human bites had not been thought to pose a significant risk of HIV.[169] HIV is usually not present in the saliva of infected patients, and when present, the titer of virus is very low. Recent data suggest that a slight risk does exist, however, and a human bite is thought to have been the mode of HIV transmission in at least two cases.
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In one report from Slovenia, a man was bitten while trying to control the airway of a person with acquired immunodeficiency syndrome (AIDS) who had bitten his own tongue during a seizure.[206] The second occurred after a lip bite in a male from a female prostitute.[112] When bitten by a person who is infected with or at high risk for HIV, the victim should receive unusually vigorous and thorough wound irrigation with a virucidal agent such as 1% povidone-iodine. A baseline HIV blood test and follow-up test in 6 months should be considered. Human Bites of the Hand The two forms of bite injury to the hand are the simple, direct occlusional bite to a finger and the fight-bite, or clenched-fist, injury. Osteomyelitis may occur after either injury.[87] [204] The fight-bite injury is more common and at higher risk for infection. Presentation is frequently delayed.[204] From 60% to 80% of fight-bite injuries occur in males, most in the dominant fist after striking an opponent's tooth.[135] In this position the extensor tendon and its underlying bursa are pulled distally over the metacarpophalangeal (MCP) joint. The result is a deep laceration that can disrupt superficial and deep fasciae, the extensor tendon and its bursa, and the joint capsule. When the fingers are extended, the skin and tendon retract proximally, sealing off the contaminated wound. Any penetrating injury in the vicinity of the MCP joint should be considered a human fight-bite wound until proved otherwise. Radiographs should be requested, and up to 70% of patients may have positive findings[56] ( Figure 41-1 ). Films should be obtained in a
Figure 41-1 Intraarticular fracture of the third metacarpal resulting from a human fight-bite injury.
lateral or steep oblique attitude, since this is the best view for initial soft tissue swelling.[168] The ideal view is the skyline view of the metacarpal head, taken with the x-ray beam in the same plane as the proximal phalanx, with the MCP joint fully flexed.[64] Treatment of clenched-fist injuries should be rapid and aggressive. Significant injuries should be explored and debrided, preferably in the operating room.[11] [204] In the wilderness setting the wounds should be thoroughly irrigated and not sutured. These wounds are at high risk for infection, and antibiotics should be prescribed as soon as possible. Oral antibiotic therapy should result in a very low infection rate.[216] Although evidence is contradictory, few indications exist for primary repair of any type of hand bite. The affected extremity should be immobilized and elevated. A person with established infection is usually hospitalized and treated with IV antibiotics, although closely supervised outpatient oral therapy is an alternative in the compliant patient after wound cleansing and debridement. [56] [191] An appropriate initial antibiotic choice for both prophylaxis and treatment of a clenched-fist injury is amoxicillin-clavulanate. Human Bites to the Face and Cheek Facial wounds are at low risk for infection, and a large series of sutured facial human bites treated in a plastic surgery clinic had an infection rate of only 2.5%.[57] Treatment includes aggressive debridement, irrigation, and suturing. Cosmetic considerations are important. Antibiotics are indicated for the same risk factors as in
animal bites (see Box 41-3 ). Self-inflicted bite wounds of the oral or buccal mucosa have not been well studied. Accidental bites of the mouth and lips have low infection rates, possibly because of protective effects from saliva and resistance of mucosal tissues to the victim's own flora. However, a case of Haemophilus aphrophilus vertebral osteomyelitis secondary to an accidental lip laceration was reported in a healthy 36-year-old male despite prophylactic antibiotics.[97] The literature suggests that oral-cutaneous (through-and-through) wounds are high risk and may benefit from penicillin prophylaxis.[3] [155] [190] Lacerations that involve only the buccal mucosa, particularly those that do not need suturing, do not require prophylaxis. Human Bite Forensics Bite mark evidence has become accepted as a powerful tool in the investigation of crime.[202] Human bite marks are found most often in cases of murder, rape, child abuse, or altercation.[106] The examining physician should document the appearance of the bite carefully, including its shape, color, and size. Determining the age of the bite can be difficult but is often a critical legal issue. The healing dynamics of these bite wounds is
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poorly understood,[44] and accurate description is better than unsupported speculation. The physician must determine if a criminal act may have occurred; if so, the wound should be photographed. Salivary deoxyribonucleic acid (DNA) can be recovered from bite marks on human skin.[197] Physical comparison of a suspect's teeth to a bite mark injury using hollow-volume comparison overlays is a common forensic odontology technique.[196] Since most physicians are not familiar with these procedures, consultation with a forensic pathologist or dentist is recommended and may be arranged through the local law enforcement agency.
FERRET BITES Egyptians kept ferrets long before the cat.[154] The two species of ferret in the United States are the common ferret Mustela putorius furo, sold as a domestic pet, and the wild black-footed ferret Mustela nigripes, which is an endangered species. The pet ferret was domesticated from the wild European polecat and was first introduced into the United States in about 1875.[131] Ferrets are kept in increasing numbers as domestic pets, especially by urban apartment dwellers. Because of its speed, an attacking ferret can easily run over the shoulders and head of an adult human and inflict multiple bites without stopping. [40] Ferrets were bred to hunt and kill small game and rodents in their burrows and are particularly attracted to suckling animals, possibly because of the scent of milk. Along with a mouth containing 34 teeth, sharp claws are found on all four feet.[8] Severe injuries caused by ferrets are not common. When they occur, an infant is often the victim and typically is sleeping or in a crib. The face, ears, and nose may be mutilated. [154] Scratches, lacerations, and puncture wounds are seen, and the ferret may chew on a victim (e.g., a baby's ear). The neck is also a common target. In a comprehensive review of 452 ferret attacks over 10 years, virtually all the unprovoked attacks were on the faces of unattended infants.[40] Most victims were less than 3 years of age and were attacked while sleeping or lying down. Several injuries were severe, and one child died. Bites were usually multiple, and sometimes the ferret's jaws had to be pried open or the ferret had to be killed to secure release.[154] Ferrets are unusually adept at escaping from cages and enclosures, guaranteeing that they will occasionally be loose unsupervised in the house and also that they can escape to the wild, where they will be exposed to endemic rabies. In one study, 4% of biting ferrets were positive for rabies virus.[40] At the University of Georgia, 50 ferrets were inoculated with rabies virus; no animal with virus in the central nervous system showed any evidence of viral shedding in saliva, and only one had rabies in their salivary glands.[55] Ferrets are now classified in the same category as cats and dogs regarding rabies pathogenesis and viral shedding patterns, rather than as wild terrestrial carnivores. They may be confined and observed for 10 days rather than being routinely euthanized after biting.[103] An effective rabies vaccine for ferrets (IMRAB-3) has been available since 1990. Little is known of infection rates or bacteriology in ferret-inflicted wounds although unusual species such as Mycobacterium bovis have been observed.[108] Initial treatment should be as for dog bites.
BITES AND INJURIES FROM DOMESTIC HERBIVORES Horses and Donkeys The horse is inclined to both bite and kick, but most horse-related injuries follow a fall during riding activities. More accidents occur per hour horse riding than motorcycling.[37] Young females are most often injured by falls,[23] and head injuries cause the majority of deaths.[94] When a half-ton horse lands on top of a rider after a fall, pelvic ring injuries and knee ligament injuries are a particular risk.[58] Appropriate helmets and footwear help to reduce the severity of injury.[37] Horse bites are common but not severe injuries. The occlusal surfaces of both lower and upper incisors are flattened. Most male horses possess canines, however, that may be used to grab onto a mare's neck during mounting. A penetrating wound to the chest after a horse bite in a child has been described. [104] The soft tissue contusions inflicted by a horse can be severe, but in a series of 24 horse bites, 21 healed uneventfully.[58] Bites can produce significant injury, including muscle rupture and fat necrosis, with no external wound. Ultrasound may be useful in the diagnosis of such injuries. [205] Horses also have a propensity for biting human nipples, which are at the same height as a horse's mouth. Horse kicks from the rear legs can be extremely powerful, causing severe blunt trauma, including cardiac rupture.[19] Kicks have also resulted in massive pulmonary embolism.[159] Donkeys also bite. One rural worker was bitten twice the same year by the same donkey. The bites were on different forearms, and both resulted in multiple fractures.[189] Death has been reported from fat embolism caused by fractures after a donkey bite.[17] Cattle and Sheep Cattle and sheep are usually docile but can inflict a variety of injuries. Serious bites are infrequent, since these animals possess neither upper incisors nor canines. A cow typically weighs 1400 pounds, and a bull can exceed 3000 pounds. Accidental treading on the human victim or butting can cause major crush injuries and fractures. Rams have killed farmers by repeated blunt
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trauma.[146] Farm animals in Wisconsin kill about six people a year.[25] One hospital in rural Wisconsin treated an average of 22 persons a year for horse and cattle injuries, most of them inflicted by a kick or other assault. Domestic cattle and horses are fairly frequently infected with rabies, but because veterinary workers are immunized against the virus, these animals seldom account for human infection. Cattle horn injuries (or gorings) present typical and unique damage patterns. The horns are used in an inward hooking motion to butt and fling the victim, or the horn tip can be used for goring. Goring injuries seen in bullfighting typically involve the perineum and thigh; they tend to be deep and sometimes fatal. Scrotal skin avulsion is common in bullfight gorings.[183] By contrast, bull horn injuries from domestic cattle involve a sweeping arc at the level of the bull's head, which is at the level of the human abdomen. The semicircular motion of the horn often produces a relatively superficial laceration, leaving deeper structures of the abdomen intact. In one series of 29 cases in which the peritoneum was breached, usually producing prolapse of bowel or omentum, 27 laparotomies demonstrated no additional injuries. In only a few cases was the bowel itself damaged.[183] The wound infection rate in this series was high (54%), probably because of delayed treatment. Gorings to the eye have also been described; in one case a metal horn cover complete with decorative ribbons was impacted in the orbit.[186] Farmers or veterinarians examining a sick animal should always have a second person present to assist and warn them.[31] Bulls should be approached only with a protective device (e.g., a heavy stick) and a preplanned exit. A ring in the bull's nose gives a victim something to hang onto besides the horns and a way to yank the bull's nose up, which may stop the attack. Dehorning the bull will not eliminate the potential for crushing. If struck by a bull or cow, the victim should not attempt to stand, since this will provoke being thrown to the ground again, and should try to crawl to safety. Children must be educated about the risks of large animals and kept away from them whenever possible. Camels In regions where camels are used for domestic or agricultural purposes, bite injuries are quite common.[176] Although herbivores and usually docile, camels are much more likely to bite in the winter rutting season, and bite fatalities have been reported. Camels have 34 teeth, including large backward-inclined upper canines, or tushes. The lower tushes are placed relatively forward, and the resultant mouth grip is very effective. Jerking movements of the head result in severe tissue damage and sometimes limb avulsion. This whipping motion can also break the victim's neck. The forearm is often injured, and bites to the face are well documented.[150] [185] Virtually all bites are single.[176] Injury or death can also occur if the camel presses the victim to the ground and crushes, after gripping the person in its jaws. Domestic Deer The most common domesticated deer are the reindeer and the more recently domesticated red and fallow deer. Female deer bite other deer when fighting. Males bite when testosterone levels are low, because at these times antlers are soft, pain sensitive, and cannot be used as weapons. Foreleg kicks are more common, since the deer stands on its back legs. Domestic deer only bite humans when threatened. Since they have a dental pad instead of upper incisors, bites are rarely serious and are usually directed at an arm and the back, which are normally well covered by clothing. These bites are usually single nips. Microbiology of Herbivore Bites Little is known about wound infection from herbivore-inflicted injuries. Infection after camel bites is common, up to 86%,[176] although this series did not specify time from injury to treatment. Species of Actinobacillus lignieresii and A. suis, as well as Pasteurella multocida, have been isolated from infected horse and sheep bites.[13] [157] All are common organisms in the mouths of herbivores. Actinobacillus and Pasteurella are closely related genera, distinguished chiefly by biochemical tests. Most domestic herbivores carry Pasteurella, and most are given frequent and regular doses of different antibiotics, especially in their feed, leading to antibiotic resistance of bite wound organisms.[162] Pasteurella caballi has been isolated from a horse bite wound.[63] Staphylococcus hyicus subspecies hyicus, a well-known cause of disease in many animals, has been reported as a human wound pathogen after a donkey bite.[153] One child developed Acinetobacter anitratus osteomyelitis after a pet hamster bite to his finger.[132] Bites from horses, donkeys, cattle, sheep, camels, deer, and most other herbivores are treated with the same antibiotics as bites from dogs, cats, and humans (see Table 41-2 and Box 41-5 ).
INJURY FROM DOMESTIC SWINE Bites from domestic swine are fairly rare, although pigs have bitten 12% of veterinarians.[119] When they do attack, domestic swine can be aggressive and inflict deep goring or bite injuries, often on the posterior thigh as the pig approaches from behind.[11] [149] Goring wounds may be deep, even while deceptively small on the surface.[203] Among veterinarians, pigs have a reputation of inflicting bites at high risk for infection. Thorough wound exploration and debridement are essential. The usual
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wide range of bacterial pathogens is reported, including Pasteurella aerogenes, Bacteroides, Proteus, and hemolytic streptococci, including Streptococcus milleri.[11] [122] Actinobacillus suis has also been reported.[61] Like many domestic animals, pigs often carry Pasteurella multocida. Unusual gram-negative bacteria, such as Flavobacterium group IIb, have been isolated, as has Mycoplasma. [79] [141] Both these organisms are resistant to amoxicillin-clavulanate, so the addition of ciprofloxacin is recommended as prophylaxis for a serious pig bite wound.[141] [142]
INJURY FROM BIRDS Birds may be kept as domestic pets or on farms. They can inflict serious injuries. Attacks on joggers by non-domesticated birds may also occur. European buzzards, red-tailed hawks, and starlings are known to be aggressive on occasion. On farms, rooster attacks, often by male fowl defending their territory, are well documented. Children, especially infants, are particularly vulnerable to attack. Rooster injuries have included serious clawing to the face and a fractured skull.[163] A 2-year-old child sustained a ruptured globe from a rooster attack in a petting zoo.[116] In one report a rooster spur was retained in a wound, resulting in chronic infection. [41] Septic arthritis was reported in a child after a bite from a domestic fowl.[101] The ostrich is responsible for one to two deaths a year, mostly in Africa, where it is raised commercially. Most of the fatal attacks are kicks to the head and abdomen. The ostrich can kick only forward; a sharp toe-nail flicks out like a switchblade and can penetrate the abdomen. Since an ostrich can easily outrun a human, the only protection is to lie prone to protect against disembowelment and to cover the neck to protect against pecks. Eventually, the ostrich loses interest and allows the victim to escape.
MEDICOLEGAL IMPLICATIONS In certain locations and circumstances, animal bites must be reported to public health authorities. Reporting suspected exposure to rabies is mandatory in most regions. If the offending animal is a pet, the victim may seek compensation from the owner, and that the health care provider may be summoned and the medical record reviewed in court. Injuries and their circumstances should be documented as fully as possible, with line drawings or photographs added to the medical record whenever possible. Hand wounds are particularly prone to infection and can lead to permanent, litigation-prone complications. A legible, precise, and complete medical record is the best protection for the health care provider. Human bites are often inflicted in assaults or fights and may be a marker for child, spousal, or elder abuse. All these conditions must be reported to law enforcement agents in most jurisdictions. Subsequent criminal investigation may depend heavily on the initial medical record, which must be extensive and complete. Human bites of the hand have a propensity for infection and complications. In addition to providing and documenting thorough and appropriate care of the wounds, the physician should warn the victim of possible complications despite current care.
ACKNOWLEDGMENT
I thank Dr. Marina Morgan for her microbiologic advice and review of this chapter.
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Chapter 42 - Bites and Injuries Inflicted by Wild Animals Luanne Freer
Wild animal bites are distinct from the other assorted injuries suffered by humans. Tearing, cutting, and crushing injuries are sometimes combined with blunt trauma caused by falls. Animal bites may cause local infection, but this complication is hardly unique. Many offending bacteria reside in numerous environmental sources. However, few traumatic lacerations are as regularly contaminated with as broad a variety of pathogens as are animal bites. Other special features are as follows: 1. Many victims have been terrorized by an attacking animal. 2. Animals can transmit various systemic diseases, many of which induce substantial morbidity and mortality; detailed discussion of zoonoses is found in Chapter 44 . 3. In contrast to the extensive scientific literature on traumatic injuries that do not involve bites, the literature on animal bites, especially wild animal bites, is largely unscientific and often simply anecdotal. As a result, rational treatment decisions are often made without a completely satisfactory scientific basis. 4. Many decisions involved in the treatment of wild animal attack victims are based on experience with domestic animal attacks, namely dog and cat bites. 5. Perhaps most importantly, animal attack injuries are usually preventable. When experience allows humans to understand typical behavior for a species, they can take proper precautions in the vicinity of a potentially dangerous animal. This chapter interprets the present state of knowledge to make logical, specific recommendations for all of these features.
INCIDENCE OF BITES Neither the annual number of bites nor the base population at risk can be reliably estimated, especially when the human population is only those exposed to a wild animal or in a wilderness setting. The world supports approximately 4600 species of mammals, 10,000 species of birds, and 6000 species of reptiles,[90] but the actual number of wild animals in the world is estimated to be in the billions. Many people who suffer relatively minor injuries from wild animals do not seek medical attention unless infection or some other complication occurs, or they fear exposure to rabies. If the injury is minor, patients will continue to be treated, released, and unrecorded. Few studies have examined the incidence of wild animal bites ( Table 42-1 ). In Sweden, three of 1000 inhabitants were injured by animals each year.[19] Domestic animals accounted for over 90% of the total, moose accounted for 6% (almost all involved in auto accidents), and all other animals totaled 4%. However, bites were not examined separately, and many injuries occurred during accidents caused by animals. Some officials estimate there are two bites for every one reported, but a survey of children 4 to 18 years old estimated an incidence of more than 36 times the reported bite rate. Such figures are most likely based on domestic bites, although this was not specifically stated. [14] [15] No reported statistics exist on the typical wild animal attack victim. If all animal bites (including domestic) are considered, two U.S. state health departments report animal bites most often occurring in male children age 5 to 9 years,[120] [122] but over 90% of animal attacks in these states are caused by domestic animals so this group is probably not representative of a wild animal attack. In undeveloped countries, many persons are exposed every day to bites from species considered "exotic" in the developed world. Persons in certain occupations in developed countries, such as veterinary and animal control workers and laboratory workers, are at greatest risk of wild animal bite. A British survey reported a 70% incidence of animal-handling injuries during a typical veterinarian career; the rate was 42% in veterinary technical staff.[32] The U.S. Bureau of Labor Statistics reported that in 1 year, less than 0.3% of all occupational injury fatalities were caused by mammals.[130] In one study of 102 animal control officers, the overall bite rate was 2/57 per working day, 175 to 500 times the estimated rate in the general population (this study did not differentiate between wild and domestic animal bites).[14] It is difficult to make conclusions about the financial sequelae of wild animal bites because the incidence is substantially lower than with domestic animal bites. In every statistical series of bites, small numbers of exotic animals, such as ocelots, jaguars, lions, leopards,
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TABLE 42-1 -- Incidence (Percent) of Bites by Species in the United States REFERENCE SPECIES
A
B
C
Dog
89
91.6
78
75
Cat
4.6
4.5
16
20
Rodent
2.2
3
50 secs) indicates immediate transfer to a tertiary center with transplant capability. Persons with significant hepatic failure may require monitoring of blood glucose every 2 to 4 hours and supplemental glucose administration for symptomatic hypoglycemia. No specific antidote or treatment is available for fulminant hepatic failure. The appropriate timing or necessity of liver transplantation is uncertain. In persons with fulminant hepatic failure from infectious causes, prolonged PT (unresponsive to fresh-frozen plasma) and development of hepatorenal syndrome, grade II hepatic encephalopathy, hypoglycemia, and uncorrectable metabolic acidosis are used as signs that transplantation is needed on an emergent basis. Persons with fulminant hepatic failure from toxic ingestion, elevated bilirubin level, and young age are important indicators of a poor prognosis.[32] [75] Mortality from gyromitrin poisoning is reported to be 15% to 35%.[33] [76]
Renal Toxicity Although originally thought to be an edible mushroom, Cortinarius orellanus was associated with 81 cases of renal toxicity in the 1950s. [40] This led to isolation of the toxin orellanine, which is found in the mushrooms C. orellanus, C. speciosissimus, and C. gentilis. Most cases occur in Europe and Japan. Causative Mushroom.
C. orellanus has a small, brown to brownish red, smooth cap 30 to 80 cm in diameter. The stalk is somewhat yellow, often darker toward the soil. Gills are orange to rust with rust-colored spores. It grows in deciduous woods, most often in sandy soil underneath oaks and birches. It is ubiquitous throughout Europe. Other Cortinarius species are found in the United States and may be toxic ( Box 49-6 ). Toxin.
The two toxins isolated from C. orellanus, orellanine and orelline, are structurally related to paraquat and diquat. Their mechanism of action remains a mystery. These are heat-stable compounds, unaffected by cooking. The toxin appears to cause intense interstitial nephritis with early fibrosis.[47] Amanita smithiana, which contains the nephrotoxins norleucine (aminohexadrenoic acid) and chlorocrotylglycine,
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grows in the Pacific Northwest and may be mistaken for pine mushrooms.[104] Amanita proxima is found in France and also causes renal failure.[17] Box 49-6. MUSHROOMS REPORTED OR SUSPECTED OF CONTAINING ORELLINE OR ORELLANINE Cortinarius gentilis Cortinarius orellanus Cortinarius speciosissimus Cortinarius splendena Cortinarius venenosus
Clinical Presentation.
Persons who ingest C. orellanus are generally asymptomatic for 2 to 20 days. After this latent period, acute renal failure develops. Some persons develop neurologic changes, including paresthesias, taste impairment, and cognitive disorders. Symptoms vary greatly. One case report described 26 soldiers who ate soup made of C. orellanus in nearly identical quantities.[11] Acute renal failure developed in 12 on or about day 11. Eight soldiers later recovered normal renal function, whereas four required long-term dialysis or kidney transplantation. The other 14 soldiers showed no rise in BUN or creatinine levels but developed leukocyturia and hematuria that persisted for more than 1 month. Renal failure reportedly occurs in 30% to 46% of persons who ingest these mushrooms and become ill. Renal function returns in 46% to 66% of victims. Renal biopsy in patients with orellanine-induced renal failure shows tubule lesions with epithelial necrosis and disruption of the tubular basement membrane. These biopsy changes may persist for up to 3 months. [11] Treatment.
In most persons who ingest renally toxic mushrooms, unexplained acute renal failure develops many days later. If a person presents early after eating orellanine-containing mushrooms, gastric emptying and activated charcoal administration (1 g/kg orally or via gastric tube) might prevent some absorption, decreasing the resultant toxicity. Early presentation, however, is rare. Once acute renal failure develops, baseline and repeated monitoring of BUN, creatinine, electrolytes, CBC, differential, and urinalysis should be performed to monitor renal function. Urine output should be monitored, and if it decreases, fluid administration should be used to achieve optimal hydration. Serum potassium, calcium, and magnesium should be monitored closely. If renal failure progresses, the victim should be transferred to a facility for hemodialysis and possible renal transplantation. Renal function may return to normal after months of dialysis dependency. Steroids seem to have no effect on the course of the disease, but they may have been given too late. Amatoxin The mushrooms that contain amatoxins are responsible for 90% to 95% of fatalities caused by mushrooms ( Table 49-6 and Box 49-7 ). A. phalloides is most common in central and eastern Europe; immigrants to the U.S. may have carried mushroom spores in wood products TABLE 49-6 -- Look-Alikes of Mushrooms Containing Amatoxin TOXIC SPECIES
EDIBLE SPECIES
Amanita phalloides
Amanita fulva
Amanita virosa
Amanita bisporus
Amanita verna
Lepiota flavovirens
from eastern Europe. A. verna and A. virosa are more common in the United States.
Box 49-7. MUSHROOMS REPORTED OR SUSPECTED OF CONTAINING AMATOXINS Amanita ocreata Amanita phalloides Amanita verna Amanita virosa Galerina autumnalis Galerina marginata Galerina venenata Lepiota castanea Lepiota jasserandii Lepiota helveola
Causative Mushrooms.
The common names of A. phalloides (see Figure 49-3 ) and its relatives A. verna and A. virosa are death cap, death angel, and destroying angel, reflecting their association with fatal outcome. A. phalloides has a white to greenish cap 4 to 16 cm in diameter, often with remnants of the veil (warts). The stalk is generally thick, 5 to 18 cm long, with a large bulb at the base, often with a vulva or cup. A thin ring is usually present on the stalk. Gills are generally free and white to green in color; spores are white. The mushrooms grow under deciduous trees in the autumn. A. virosa is more common in the United States (Figure 49-18 (Figure Not Available) ). It resembles A. phalloides, but the cap is more yellow or white. A. verna is characteristically white. All grow in deciduous woods. Even mushroom experts have been tempted by the large white mushroom, which is tasty. The fatality rate, however, is 35% in adults and 50% in children. Some Lepiota mushrooms, including L. castanea and L. jasserandii, contain high concentrations of amatoxin. Human toxicity has been reported. Mushrooms that contain amatoxin may have a positive Meixner test. This test was first described by Wieland in 1949[107] and popularized by Meixner.[70] A drop of liquid is expressed from a fresh mushroom onto print-free (ligand-free) newspaper and allowed to dry. A drop of concentrated (10 to 12 N) hydrochloric acid is added. A blue color develops within 1 to 2 minutes in the presence of amatoxins. Control tests on newspaper without mushroom juice and paper containing
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Figure 49-18 (Figure Not Available) Amanita virosa, which causes delayed hepatotoxicity. (From Phillips R: Mushrooms of North America, Boston, 1991, Little, Brown.)
ligand should be conducted. False-positive results are common and can be elicited from excessive drying temperatures (greater than 63° C [145° F]) or exposure to sunlight. False-positive tests also occur from mushrooms containing psilocybin, terpenes, and bufotenin. Nearly 20% of gilled mushrooms that did not contain amatoxins tested positive in one study,[90] placing the usefulness of this technique in doubt. Thinlayer chromatography (TLC) more accurately identifies the presence of amatoxin and can be done on mushroom liquid, human serum, or urine. [81] Radioimmunoassay (RIA) of serum or urine can detect amatoxins in the body. Toxin.
The mushroom A. phalloides contains two groups of toxins: amatoxins and phallotoxins. Each group contains several toxins. There are now eight identified amatoxins: a-amanitin, ß-amanitin, ?-amanitin, e-amanitin, amanin, amaninamide, amanullinic acid, and amanullin.[103] [105] Of these, a-amanitin is thought to be primarily responsible for human disease. a-Amanitin injected into animals produces hepatic toxicity characteristic of human ingestion of A. phalloides. Phallotoxins include phalloidin, phalloin, phallisin, phallacidin, phallacin, phallisacin, and prophalloin.[103] Phalloidin is the primary phallotoxin. Phallotoxins bind to F-actin, disrupting plasma membranes and causing massive efflux of calcium and potassium. Phallotoxins cause death in animals within 2 hours but are not believed to play a role in human toxicity.[34] Humans may not even absorb these toxins, which may be responsible for local gastric irritation. A. virosa contains amatoxins and virotoxins. Virotoxins resemble phallotoxins biochemically, and also bind F-actin and cause death within a few hours. Six different virotoxins have been isolated, but none is thought to play a role in human Amanita hepatotoxicity. [105] After ingestion, amatoxins are absorbed from the gut and actively transported into the liver through transport systems shared by bile acids and xenobiotics. [106] a-Amanitin is rapidly cleared from plasma. [52] Amatoxins are not protein bound. They bind to ribonucleic acid (RNA) polymerase II and inhibit the formation of messenger RNA (mRNA).[60] This in turn inhibits transcription as the reservoir of RNA is depleted.[25] Amatoxins are excreted into the bile, where they are reabsorbed and once again transported into the liver.[12] Interruption of this enterohepatic circulation may be an important therapeutic tool. Within the liver, a-amanitin may undergo some metabolism through the cytochrome P450 system. Animal studies suggest that a more toxic metabolite is produced through this metabolism.[87] [89] Nuclear fragmentation and condensation of chromosomal material have been observed within 15 hours of injection.[24] Glycogen is rapidly depleted, and fatty degeneration occurs within the liver parenchymal cells.[20] Mitochondria become swollen, and microvesicules appear throughout the cytoplasm.[76] Direct renal toxicity may occur, but renal failure (10% of cases) is more likely to be caused by hepatorenal syndrome. Clinical Presentation.
Persons who ingest A. phalloides feel well for 4 to 16 hours. Severe nausea, vomiting, abdominal cramps, and diarrhea follow this characteristic latent period. Early complications include fluid and electrolyte imbalance (hypoglycemia, hypokalemia, elevated BUN). Persons in whom symptoms develop earlier (4 to 10 hours) are more likely to experience severe hepatotoxicity. Over the next 12 to 24 hours the victim's GI symptoms abate. The second latent period is followed by hepatic failure, which develops 48 to 72 hours after ingestion in most victims. Hepatic failure may be of varying severity; it is frequently worse in children and depends minimally on the amount of mushroom ingested. Children have greater toxicity and higher mortality, perhaps because of the relative quantity of mushrooms ingested or the varying metabolism in young children (differing levels of P450 -metabolizing enzymes). Previous experiments showed that concurrent ethanol with A. phalloides ingestion (whole mushroom lyophilized) decreased hepatotoxicity.[30] Therefore decreased toxicity in adults could result from ingestion of ethanol with an Amanita mushroom dinner. More recently, however, ethanol failed to alter hepatoxicity in an animal model poisoned with a-amanitin, which raises doubts about this explanation for increased toxicity in children.[86] In addition to hepatic failure, endocrinopathies may develop, with hypocalcemia, decreased thyroid function, and elevated insulin levels in the presence of hypoglycemia.[53] Hypocalcemia may be caused in part by loss of calcium through diarrhea or may be a direct effect
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on osteoclasts. Renal failure may contribute to hypocalcemia. The thyroid abnormalities probably result from decreased hormone synthesis caused by overwhelming
illness and blocked peripheral conversion of thyroxine (T4 ) to triiodothyronine (T3 ). Thyroid-stimulating hormone (TSH) depression may result from decreased synthesis caused by the inhibition of RNA polymerase II by amatoxin. Hypothyroidism has not been clinically significant. Hypoglycemia is probably the result of several processes, including impaired hepatic gluconeogenesis, increased insulin release from the initial hyperglycemia, or tissue destruction of the pancreas.[53] Bone marrow toxicity with decreased neutrophils, lymphocytes, and platelets has been noted.[84] Disseminated intravascular coagulation and coagulopathies secondary to hepatic dysfunction are common.[84] Pancreatitis occurs in up to 50% of patients.[28] Hypophosphatemia is particularly common in children, for unknown reasons. Myopathy has been associated with Amanita toxicity.[39] Hepatic biopsy shows diffuse and severe steatosis with periportal inflammation and necrosis. Extremely high levels of hepatic enzymes are seen. ALT/AST level is not helpful in predicting the victim's prognosis. A precipitous drop may occur just before death. Treatment.
Attempts to treat A. phalloides poisoning have ranged from scientific to purely empiric. Noting that rabbits were able to eat the A. phalloides mushroom with impunity, clinicians fed ground raw rabbit to victims of Amanita poisoning, without success.[100] Hemodialysis was long recommended but has been shown to be ineffective, since the toxin is rapidly cleared. Amatoxin is taken up in liver cells within 5 hours after IV administration. [22] In a retrospective study of 205 cases of amatoxin ingestion,[32] hemodialysis worsened the prognosis, and charcoal hemoperfusion did not improve outcome. Plasmapheresis appears to be ineffective for similar reasons.[80] Amatoxins are enterohepatically circulated. Attempts have been made to divert the enterohepatic circulation. Although animal studies showed some benefit with this treatment,[23] it is not recommended. Multidose activated charcoal (1 g/kg orally or via gastric tube, 15 to 20 g every 4 to 8 hours with a cathartic given every second or third dose if no diarrhea) may adsorb the amatoxins and interrupt the enterohepatically circulated drug. Antigen-binding fragment (Fab) monoclonal antibodies against amatoxin were developed by immunizing rats and fusing their spleen cells to mouse myeloma cells. The amatoxin-specific clones were selected and their immunoglobulin separated into Fab fragments. When this Fab antibody was used in a-amanitinpoisoned mice, renal toxicity was 50 times greater. All animals died of renal failure but had no hepatic damage.[21] The Fab-amatoxin compound may have dissociated in the kidney, leading to severe local damage. Thioctic acid is used throughout Europe as a treatment for A. phalloides poisoning. Although its exact mechanism is unknown, it may act as a free-radical scavenger or interfere with the hepatic transport of toxin. In animal studies, thioctic acid has been ineffective against a-amanitin or extracts of the mushroom.[2] In a large retrospective study, thioctic was more frequently associated with a fatal outcome in humans.[32] Its use is not recommended. Silymarin is the active component of the milk thistle Silybum marianum. A water-soluble preparation (silibinin) is effective against amatoxin in both animals and humans. Silibinin also may interrupt the enterohepatic circulation or act as a free-radical scavenger. Patients treated with silibinin were more likely to survive in one study.[50] In a retrospective study, silibinin was associated with increased survival.[32] IV silibinin is not available in the United States, but an oral form may be found in health food stores. High-dose penicillin decreased toxicity in an animal study evaluating hemodialysis with penicillin used prophylactically.[31] The control group (penicillin alone) showed a decrease in toxicity. Other animal studies have indicated penicillin's effectiveness in reducing hepatotoxicity.[27] [88] In humans, penicillin has been very effective. [32] Other antibiotics, including rifampin and cephalosporins, have been shown to protect against amatoxin poisoning.[26] [73] Penicillin's exact mechanism of action is unclear. Sterilization of the intestines may lead to decreased GABA production, which may diminish ensuing cerebral encephalopathy. Penicillin may share a common transport system with amatoxin, which interferes with uptake.[29] Regardless of the mechanism, large doses of IV benzylpenicillin (300,000 to 1 million units/kg/day) are recommended. This dose may be associated with seizures. French physicians have used hyperbaric oxygen as a treatment for Amanita toxicity.[57] Hyperbaric oxygen may facilitate hepatic regeneration and lessen toxicity. It is most often used with high-dose penicillin. Animal data suggest other therapies. High-dose cimetidine (4 to 10 g/day IV in adults) appears to inhibit formation of more toxic metabolites by blocking the cytochrome P450 system.[87] Cimetidine has not been given in children for Amanita ingestion. Other drugs under investigation in animals include vitamin C,[102] zinc, and thiol compounds.[29] Gastric aspirate or emesis can be sent for spore analysis if mushroom specimens are not available for identification. Persons with documented or suspected amatoxin ingestion should receive activated charcoal (1 g/kg orally or via gastric tube followed by 15 to 20 g every 4 to 8 hours). Repeated administration may bind
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drug that is enterohepatically circulated. Cathartics are generally not necessary, since diarrhea is prominent. IV normal saline or Ringer's lactate is needed to replace GI fluid losses. Electrolyte losses (particularly potassium) may be great. BUN, creatinine, CBC with differential, platelet count, electrolytes, glucose, calcium, phosphorus, magnesium, urinalysis, PT, PTT, fibrinogen, amylase, protein, and albumin should be initially measured and repeated at least daily to monitor liver and renal function. Hyperglycemia is common on the first day, but insulin is generally not required. Hypoglycemia occurs after 24 hours and may be significant, requiring concentrated IV glucose. Bedside determinations of glucose should be performed at least every 6 hours. Tests of liver function, including ALT, AST, alkaline phosphatase, PT, and PTT, should be repeated at least daily and more often if findings become abnormal. Levels rapidly rising or greater than 2000 IU for ALT/AST and 50 seconds for PTT should signal severe toxicity and the need for referral to a transplant center. To confirm the diagnosis of amatoxin ingestion, a serum RIA is ordered for amatoxins. Urine can also be studied. The nearest laboratory performing this RIA is usually known to the regional poison information center. Specific treatment should begin as soon as diagnosis is suspected, either by symptoms or confirmed by the fresh specimen or spores. Benzylpenicillin (penicillin G), 300,000 to 1 million U/kg/day, should be given IV in divided doses. Silibinin, if available, can be given intravenously, 20 to 40 mg/kg/day in divided doses. Hyperbaric oxygen treatments (dives to 2 atm for 30 minutes once or twice a day) can be tried. Cimetidine (4 to 10 g IV for adults for 2 days) is experimental but has few side effects. Once liver failure begins, hypoglycemia becomes more likely. Supplemental glucose should be readily available. Dietary protein should be limited and thiamine and multivitamin supplementation given. Oral lactulose, 30 to 45 ml every 6 to 8 hours, may reduce hepatic encephalopathy. Clotting studies should be performed several times a day and vitamin K or fresh-frozen plasma (or both) used to correct abnormalities. If hepatic failure progresses, liver transplantation may be required. The timing is highly controversial, and criteria for transplant in other forms of fulminant hepatic failure are often applied to this setting. Factors associated with poor prognosis in acetaminophen-induced hepatic damage include metabolic acidosis, elevated PT and elevated serum creatinine.[75] In viral hepatitis and other drug reactions, however, factors such as bilirubin, victim's age, and duration of jaundice before clinical encephalopathy are important. [65] In the few pertinent studies of A. phalloides ingestion, poor outcome was related to age less than 10 years, a short latent period, and the severity of coagulopathy.[32] The largest study suggests that a person with ALT or AST level greater than 2000 IU, grade II hepatic encephalopathy, or PT greater than 50 seconds is at serious risk for death and should be considered for emergency liver transplantation.[19] Persons who met these criteria have survived.[64] [82] A recent report suggests that increased reparative enzymes correlate with hepatic recovery.[49] Because hepatic failure develops rapidly, victims with significant hepatic dysfunction must be transferred early to a transplantation site. Patients undergoing liver transplantation for fulminant hepatic failure (not caused by A. phalloides) have a 62% survival rate. Recently a temporary liver transplant sustained a child while her liver recovered.[83] Persons who survive acute hepatic failure without needing hepatic transplant may have persistent elevation in liver transaminases. In one study of 14 persons with severe hepatotoxicity, eight had elevated AST/ALT without normalization over a 1-year follow-up.[19] All had biopsy evidence of chronic active hepatitis, with positive anti-smooth muscle antibody and cryoglobulins. It is not known whether these persons will have an increased risk of hepatoma or develop more serious complications of chronic active hepatitis.[79] Amatoxin ingestion during pregnancy does not appear to have serious consequences to the fetus provided the mother remains healthy.
APPROACH TO THE VICTIM OF MUSHROOM POISONING Four types of individuals develop mushroom toxicity: foragers, children, those seeking hallucinogenic "highs," and rarely, victims of attempted homicide. Most victims seek medical care after symptoms develop. Caregivers who observe small children chewing on lawn mushrooms should call the nearest poison center. Children who have ingested an entire lawn mushroom or more should receive ipecac and be observed for symptoms at home. Follow-up calls should be made to ensure that emesis has occurred and at 1, 4, and 24 hours to assess symptoms. Persons with agitation, altered perceptions, or frank hallucinations temporally related to mushroom ingestion are probably intoxicated with isoxazole or hallucinogenic mushrooms. Whether the mushrooms are picked accidentally or ingested intentionally, the treatment and clinical course are identical. Persons who develop muscarinic symptoms (salivation, urination, diaphoresis, GI upset, emesis) present a classic picture that is rarely confused with any other presentation. Some drugs (e.g., bethanechol) may cause similar symptoms when taken in overdose. Victims of mushroom poisoning generally remain
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mentally clear and should be able to relate an appropriate history. Victims with GI symptoms can be divided into those with early and those with delayed presentations. Those with early (within 2 hours) GI symptoms generally have a benign course, except for persons with a mixed ingestion. Most guidebooks for mushroom hunters recommend eating only one variety of mushroom at a time, but more daring or foolish individuals mix multiple mushrooms and eat them frequently over a day. This makes diagnosis based on time of symptom onset difficult. Early onset of GI symptoms may mask more significant delayed symptoms. In these cases, identification of ingested mushrooms becomes essential to planning therapy. Accurate botanical identification of the mushroom can be difficult. Only 800 of the 3000 species found in Europe can be identified without a microscope. [100] When multiple mushrooms are eaten together, the residual specimens may not be those causing toxicity. Cooking and refrigeration alter identifying features. Fresh mushroom specimens should be transported in a paper bag rather than a plastic container to limit the effects of humidity. Finally, precise identification of even a good specimen can be difficult and should be done by an expert. Mycologists can be contacted through a poison center, university, museum, or commercial mushroom grower. In difficult cases, spores can be obtained from emesis or gastric emptying procedures. Specimens should be refrigerated while awaiting analysis. More specific diagnosis can be made through TLC or RIA techniques. Botanical identification may not match the victim's symptoms. The victim should be treated according to time of symptom onset and current condition when examined. Victims with early-onset GI symptoms require supportive care with fluid and electrolyte replacement. For those with delayed GI symptoms or mixed ingestions of amatoxin or gyromitrin mushrooms, treatment should begin as soon as possible. These mushrooms generally can be differentiated by the description or by the season (spring for Gyromitra, autumn for Amanita). Persons who have disulfiram-like reactions to alcohol should be questioned about prior mushroom ingestion. This situation is rarely diagnosed correctly, because symptoms are thought to result from panic attacks, alcohol intoxication, or even an allergic reaction. Persons rarely relate their symptoms to the dinner of mushrooms eaten days earlier. Any person with unexplained acute renal failure should be questioned about prior wild mushroom ingestion. Although Cortinarius orellanus is more common in Europe and Japan, it is found with increasing frequency in the United States. Because of the long delay before the onset of renal failure (1 to 2 weeks), the history of mushroom ingestion may be missed.
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Chapter 50 - Ethnobotany: Plant-Derived Medical Therapy Kevin Jon Davison
The history of ethnobotany begins before the advent of written records. In all ancient civilizations, plants served as important elements of food, shelter, dyes, ornamentation, religious rituals, and medicines. The term ethnobotany refers to an individual culture's use of specific plants. The medicinal use of the plant kingdom has been termed herbalism, plant medicine, natural-based medicine, and phytomedicine in its current application. The word "herb" is broadly defined as a nonwoody plant that dies down to the ground after flowering. The most commonly used interpretation, however, is any plant used for medicinal therapy, nutritional value, food seasoning, or dyeing another substance. The precise medicinal discovery of the uses of plants by humans remains conjectural. Many scenarios probably occurred. Perhaps, in a prehistoric jungle of South America, a pool of water containing fallen plant material leached out some of the precious medicinal constituents of leaves, flowers, stems, and bark. Tannins, glycosides, sugars, and alkaloids from the bark were infused into the waters. Because of burning fever and severe dehydration, an extremely ill native drank from the pool, and his fever miraculously disappeared. The pond became known for its magical healing powers. If the water held bark from the cinchona tree, the native may have serendipitously discovered quinine. Archeologic evidence shows that prehistoric humans used plants extensively to treat physical ailments. Instinct and trial and error led to the realization that, for example, cinchona bark controlled intermittent fevers, animals fed on ergotized grain aborted their fetuses, and latex from the opium poppy could be eaten to alleviate pain. Innumerable medicinal plant traditions that remain intact to the present originated as far back as 2700 BC. Ethnobotanically, the use of plant-based medicines represented much more than a culture's individual efforts to survive. Analyzing the methods and degrees of use of indigenous medicines reveals much about cultural philosophy, ingenuity, and sophistication. The Chinese developed an extensive and elaborate system for prescribing, classifying, and processing herbs, which dates back to the third millennium BC. The formulas identified the specific effect of each herb and interactions with other herbs. Less tolerable herbs were blended with those that would counteract undesirable effects. Formulas were custom blended, taking into account a victim's constitution and the stage of the disease. Some of the ancient knowledge from these writings is being used in many contemporary herbal preparations commercially sold as "patent" (readily available in pill form) medicines. Many native tribes of New Guinea, Indonesia, and the Amazon use single-herb formulations as they did thousands of years ago to treat nearly all their medical conditions. In the West, written records dating to the Sumerians accurately describe the medicinal uses of specific plants.[101] In the same period of about 3000 years ago, the first Asian written record, the Ben Tsao Gan Mu, was compiled by the Chinese. It listed more than 360 medicinal plants and their classification, uses, contraindications, and methods of action as perceived at that time. Roman and Greek herbal remedies were described in the writings of Hippocrates and later in those of Galen, providing a pattern for the development of the Western medical tradition. Hippocrates was an advocate for using a few simple plant preparations along with fresh air, rest, and proper diet to help the body's own "life force" eliminate problems. Conversely, Galen promoted the use of direct intervention to correct the imbalances that cause disease, employing large doses of complicated "drug" mixtures that included animal, plant, and mineral ingredients.[114] The earliest European compendium that listed the uses and properties of medicinal plants, De Materia Medica, was written by the Greek physician Dioscorides in the first century AD. He described about 600 plants, and his work remained the authoritative herbal medicinal resource into the seventeenth century.[41] Herbalism was practiced in many different ways during and after the Middle Ages. There were learned traditional herbalists and lay practitioners, as well as wandering herbalists who professed pagan animism or Christian superstitions that often were more influential in healing than the herbs' properties. Little was added to the knowledge of herbalism during this period. After the Middle Ages and invention of the printing press in the 1400s, hundreds of herbal publications were compiled. Most early works were available only in Latin or Greek; it was not until the fifteenth through seventeenth centuries that the great age of herbalism was appreciated in English.[101] Tides changed in European herbalism when a Swiss pharmacist-physician named Theophrastus Bombastis von Hohenheim, better known as Paracelsus (1490–1541), introduced a new dimension. He advocated chemistry and chemical processing and used mineral salts, acids, and other preparations in medicinal therapies. This was a
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departure from the plant-based medicinal methods of the past. During the latter seventeenth century, the predominance of plant medicines slowly eroded. In 1806, Freidrich Serturner, a small-town German pharmacist, became known for his efforts to isolate organic acids from plants in an attempt to find the active ingredient in opium. He discovered organic alkaloids, which became known as the first set of active plant constituents.[149] Because of their physiologic activity, the search for plant alkaloids continued into the twentieth century. Discoveries quickly followed. The bronchodilator and antitussive ephedrine, from the herb Ephedra sinica, was often used in Chinese medicinal formulas for bronchial asthma. The discovery of morphine led to creation of all the narcotic analgesics. The bark of cinchona was found to contain quinine in 1819, which led to development of antimalarial drugs. The traditional herbal extract from rhubarb (Rheum species) has several active compounds. These compounds mediate many of the pharmacologic effects, such as its purgative action (from sennosides); antibacterial, antifungal, and antitumor activities (from anthraquinones); antiinflammatory and analgesic activities; and improvements of lipid metabolism (from stilbenes). Treatment of leukemias from an extract of Madagascar periwinkle (Catharanthus roseus), known as vincristine, has been highly effective.[42] Discoveries in the nineteenth and twentieth centuries included atropine (from belladona leaves, Atropa belladona) in 1831, cocaine (from coca leaves, Erythoxylum coca) in 1860, ergotamine (from Claviceps purpurea) in 1918, and tubocurarine in 1935.[114] European settlers brought herbal knowledge and their medicinal methods to the Americas. Because of the abundance and wide use of plants on the new continents, they also learned much from the indigenous peoples. The colonists found that conditions afflicting them, such as malaria and scurvy, were treated effectively with herbs by the Native Americans.[115] In the 1700s, herbal medicine continued to have popular applications in lay circles but also was investigated by the new medical establishment. Although the creation of a small elite group of learned professionals was thought to violate the political and constitutional concepts of the early American democratic movement, the practice of medicine was carried over from England and Scotland during prerevolutionary days. Before a professional medical class was established, most illness in America was treated within the family or extended family network. Many concepts were modified in the colonies between 1765, when the first medical school opened, and 1850, when more than 42 schools of medicine had been recognized. The inquiry into Digitalis purpurea (foxglove) by William Withering exemplified the change in perspective from anecdotal folk medicine to a critical examination for specific uses of botanicals from a biochemical point of view. During the early 1800s the trend was to look at the efficacy of botanicals and their intrinsic value from a more scientific perspective. Several developments delayed the appreciation of herbalism by physicians in the colonies. For instance, Samuel Thomson promoted a system of herbal medicine by proselytizing about his patented method of herbal prescribing, which used many Native American herbs. A central theme in his approach was the advocacy of self-prescribing based on the philosophies and herbal prescriptions found in his book New Guide to Health. The right to sell "family franchises" for use of the Thomsonian method of healing was the basis of a widespread lay movement between 1822 and Thomson's death in 1843. Thomson adamantly believed that no professional medical class should exist and that democratic medicine was best practiced by lay persons within a Thomsonian "family unit."[39] Although his methods
were considered crude and unscientific, he had over 3 million faithful followers in 1839. Founded on ignorance, prejudice, and dogma, the Thomsonian school did little to help physicians accept European and American herbal medicines. European physicians in the Thomsonian movement wished to separate themselves from the lay practitioners by creating requirements and standards for the practice of Thomsonian medicine. Thomson was adamantly against this, but a decade after his death the Thomsonian physicians formed the Eclectic School of Medicine, which attempted to unite "professional physicians," Thomsonianism, and traditional herbal medicine. The establishment of several Eclectic medical schools was a step toward validating herbal medicine, but it failed to bring herbalism into the mainstream medical establishment. The founding of the American Medical Association and the Flexner Report on medical education in 1910 thoroughly established the modern pharmaceutical industry in the medical education system.[39] Because of the availability of pure, active constituents from plant drugs and the synthetic drugs that began to appear on the market toward the end of the nineteenth century, the prescribing habits of physicians began to change. The sensibility and predictability of administering exact doses were appealing. For example, the pure alkaloid of quinine could be prescribed for malaria rather than a foul-tasting extract of cinchona bark containing variable percentages of quinine and other alkaloids with different physiologic properties. Many "crude drugs" were standardized for therapeutic activity. Digitalis, which still retains its status in the United States Pharmacopeia (USP), is one example. Of the 200 plant drugs officially listed in the USP in 1936, about 19% are still official today.[149] An estimated 25% of all prescriptions dispensed in community pharmacies between 1959 and 1980 contained ingredients extracted from higher plants. For a significant number of synthetic drugs, natural drug products continue to serve as either models or starting points for synthesis.
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EVOLUTION OF PHYTOPHARMACEUTICALS The drive toward patenting and ownership in the pharmaceutical industry has been a strong incentive to research and develop plant-based products. Because a plant cannot be patented, however, little U.S. effort has gone into developing herbal medicines during the last century. Active principles of botanicals are investigated for their biologic activity, although in many cases the active constituent is less effective than the whole crude extract of a herb.[114] One problem in the development of the botanical pharmaceutical industry in the United States has been quality control. In addition, lack of standardization plagues plant-based products. Quality control and standardization of crude plant extracts for herbal medicines were virtually nonexistent until recently,[114] or we might be using more botanical medicines for common ailments. In Europe and Asia, where pharmaceutical firms have been producing standardized phytopharmaceuticals (plant-based standardized extracts) for decades, research and development have demonstrated economic and medical sense. Europeans use phytopharmaceuticals as part of their "mainstream" medical practice. In hospitals they are used primarily as adjuvant therapies. More that 70% of general practitioners in Germany prescribe phytopharmaceuticals, and the public health insurance system pays for most of these prescriptions. The total annual market for phytopharmaceuticals in Germany alone is $1.7 billion. Beginning in 1993 the licensing procedure for German physicians required a knowledge of phytotherapy. [130] Production and evaluation of botanical medicines have improved significantly in the past six decades. In crude plant evaluation, modern laboratory analysis can determine the percentage of active principles, as well as solubility, specific gravity, melting point, optical rotation, and water content. Scientists detect resins, alkaloids, flavonoids, enzymes, essential oils, fats, carbohydrates, and protein content. They can precisely assay using liquid, high-pressure liquid, paper, and thin-layer chromatographies; spectrophotometry; atomic absorption;
Figure 50-1 A, Calendula officinalis. B, Calendula drying and dried in a jar. (Courtesy Cascade Anderson Geller.)
and magnetic resonance imaging. These methods improve the predictability and therapeutic effectiveness of standardized crude botanical medicines, which are then evaluated for their efficacy in animal studies to determine pharmacologic potency, activity, and toxicity. U.S. and European companies have set strict quality control guidelines to ensure optimum yields of pharmacoactive principles and acceptable levels of impurities, bacterial counts, pesticides, residual solvents, and heavy metals. Specific cultivation and harvesting techniques affect the therapeutic value of a given herb, which is related to the amount of active constituents in a specific medicinal plant. Methods of packaging, storage, and transport can dramatically affect the stability of active compounds. Both extracts and concentrates are obtained by adding appropriate solvents to raw herbs, which removes the active constituents. The most common method is infusion. As a tea bag is steeped in hot water to make a cup of tea, the water acts as a solvent. If the water were slowly evaporated, the concentrate would contain the active constituents. Pure ethanol is an effective solvent often used to concentrate active herbal constituents. Immersing a high-quality bulk or raw herb in pure ethanol for hours or days, depending on the herb and the part used, then pressing it out, yields an herbal tincture. The alcoholic tincture is remixed with water to yield a 20% alcohol tincture. In another method, a 20% alcohol mixture is the solvent. Fluid extracts are made by distilling off some of the alcohol with vacuum distillation to avoid elevating the temperature, which may affect some of the active constituents. Another concentration process, solid extraction, yields a solid or semisolid product that can then be powdered or granulated for administration. Once an extract is produced, qualitative and quantitative analyses can be performed to assist in standardization. The percentage of known active constituents is assayed, to obtain predictable clinical results. An herbal infusion is generally a better source of active compounds than an air-dried or sun-dried powdered herb ( Figure 50-1 ), but it may not be as strong in
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action as concentrates such as tinctures, solid extracts, and fluid extracts. Potency of an extract can be defined by (1) percentage of active constituents or (2) concentration. Herbalists express concentration as an equivalency; a four-to-one extract is equivalent to or derived from four parts of the crude herb to yield one part extract. This is usually written as "4:1 solid extract." Longer shelf life, greater effectiveness, and higher concentration of active constituents make a more standardized (better) product than does the raw powdered herb; however, efficacy is difficult to compare. An example of a product that is standardized to the percentage concentration of pharmacoactive glycosides is the extract of Gingko biloba, marketed in Europe under the trade names Tanakan, Rokan, and Tebonin. It is typically standardized as 24% flavonoid glycoside. G. biloba extract has been shown to prevent metabolic and neuronal disturbances of cerebral ischemia and hypoxia in experimental models.[86] [96] Quality control is addressed for many herbal products when the known clinical effectiveness can be attributed to a specific active constituent. Improved analytic methods and use of high-quality herbs (high in active principles) helps ensure standardization. In Europe the dosage is expressed in milligrams of active constituents, which favors consistency. The main difference between this method and chemical isolation or synthesis is that the extracts still contain all the synergistic cofactors that enhance the function of the active ingredient. This important aspect of herbal medicine is lost once the active constituent is removed from the whole plant.
HERBAL PREPARATIONS FOR CLINICAL AND WILDERNESS USE Botanical preparations are readily applicable in acute prescribing for travelers and wilderness enthusiasts. Throughout the ages, botanicals have been useful adjunctive therapeutic agents. Knowing how and what preparations from the natural pharmacopeia can be used provides a sense of integration with the natural environment. Indigenous peoples who have depended on the botanical world throughout their existence hold a vast amount of untapped knowledge. Wilderness enthusiasts should help engender and preserve this understanding of the natural world and help save natural habitats. Further investigation into the plant kingdom for useful medicinal agents will aid in these efforts. Herbal medicines can be prepared by decoction or infusion of bulk or raw herbs or by the use of extracts, concentrates, and tinctures. Infusions are prepared like a standard tea. The soft parts of plants, flowers, stems, and leaves—are placed in a warmed pot. Boiling water is poured over the herb, and the pot is covered to prevent beneficial essential oils from evaporating. The mixture infuses for about 10 minutes, then is strained. The supernatant can be used immediately or refrigerated in an airtight container for as long as 2 days. A standard adult dose of an herbal preparation would be 1 ounce (28 g) of dried herb to 1 pint (or 500 ml) of water, or a teaspoon per cup. The amount is doubled if the herb is fresh. Generally, it is best to take infusions hot by the cupful three times daily for a chronic problem and up to every hour or two during an acute illness. To make infusions palatable, many herbalists have added licorice, aniseed, or honey. The hard or woody parts of plants, such as bark, seeds, roots, rhizomes, and nuts, have tough cell walls that must be broken down by great heat before they can impart their constituents to water. The herbs can be broken into small pieces by chopping, crushing, or hammering. Traditionally, a decoction was prepared in an earthen crock reserved especially for making herbal preparations. In the past, herbalists believed that some of the quality of the medicine was affected by the type of vessel or container in which the brew was prepared. Contemporary practitioners generally recommend the use of stainless steel, ceramic, or enamel and specifically discourage the use of aluminum or other alloyed metal pots. The herb is placed in an appropriate container and covered with cold water. The mixture is brought to a boil, covered, and simmered for 10 to 45 minutes, depending on the type and part of the herb being used. A decoction can be strained, flavored, or sweetened like an infusion, and it is consumed while hot. Modern practitioners use the most efficient and predictable forms of specific herbal medicines. Concentrates in capsule form are most effective and easiest to administer. The standard herbal concentrate found in the marketplace is in the ratio of 4:1. Ease of administration and dosage and the predictable clinical effects have made this the industry standard. Herbal tinctures are extracted into a specific percentage of alcohol and can be mixed easily to make formulas tailored to personal conditions. A combination may be many times more effective than a single herb. Formula prescribing is an art. Classic formulas for common ailments have been cataloged since the first herbal compendiums were recorded centuries ago. For the purposes of this chapter, however, single herbs and their specific uses, identification, and preparation are detailed.
HOMEOPATHIC USE OF BOTANICALS Medical pioneer Samuel Hahnemann developed a radically different system of medicine nearly 200 years ago. Homeopathy is derived from the Greek words homoios, which means "similar," and pathos, which means "disease" or "suffering." The "law of similars" states that a substance that causes a set of symptoms in pharmacologic dosages can create a cure for similar symptoms (even if the etiologic agent is different) if that substance
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is given in a homeopathic dilution. Most homeopathic remedies are prepared from plant, mineral, and animal products. In homeopathic medicine, there is a perfectly matched similimum (the most effective medicine) if the predominant symptoms of a disease or illness match the symptoms produced when the substance is taken in large doses in a healthy individual. For example, the herb Atropa belladona, which contains atropine, is poisonous. In excessive doses the herb causes death; in moderate doses it creates hot, feverish states; and in tiny (homeopathic) doses it can effectively treat certain types of fevers, viral syndromes, and inflammatory states. A homeopathic dilution is created by taking a prepared tincture (mother tincture) of a botanical or an extract from nonplant sources and diluting it in a sequential or serial method. The difference in a homeopathic dilution is in its methodology. A homeopathic medicine must be succussed (shaken or agitated) mechanically or manually a prescribed number of times between each serial dilution to be effective. The succussion method originally discovered by Hahnemann is said to "dynamize" the medicine. The succussion method may affect the water molecules, creating a "memory" that the water molecules store in a lattice formation. This is similar to the storage of information on a magnetic disk or tape, except the signature resonance pattern is created from the interaction of the original tincture within the water's lattice structure. The dilution can range from a 1x potency, which is a decimal dilution of a given ingredient (one part mother tincture per nine parts solute), to a 1c (one part mother tincture to 99 parts solute), to an extremely dilute 200c (one part mother tincture per 99 solute, serially diluted 200 times). A high-potency dilution (serially diluted more than 30 times in the x potencies and more than 12 times in c potencies) would be taken much less frequently than a low-potency dilution. To make a 30x homeopathic preparation of Arnica montana, one drop of the plant tincture is added to nine drops of pure water, and the mixture is succussed 50 to 100 times. Next, one drop from that solution would be added to nine drops of pure water and again succussed 50 to 100 times. This is repeated 30 times to yield the desired 30x homeopathic remedy. The number refers to the number of succusions and the letter to the ratio of the mother tincture to pure water. The mechanisms by which homeopathy works have yet to be elucidated, even though it has been practiced effectively for several hundred years. In 1900 an estimated 15% of U.S. physicians were prescribing homeopathic remedies.[105] Recent studies have shown effective results in clinical trials using homeopathic medicines.[28] [80] [91] Mechanisms of action for many common pharmaceuticals also remain unknown. Many theories in medicine are still based largely on empiric observations rather than theoretic understanding. One herbal folk remedy for bruises, sprains, strains, and rheumatism in European and native American medicine was topical application of the plant Arnica montana (leopard's bane). Consistent with the homeopathic principle, the toxic effects of the whole-plant extract of Arnica produce the same set of symptoms it is intended to cure when administered internally in a homeopathic dosage or if the tincture or oil is applied topically to the affected area. Arnica is contained in herbal and homeopathic dosages in numerous ointments, salves, and poultices for the treatment of trauma resulting from localized sprains, strains, or contusions. Controlled studies in Germany have shown that effective products for sprains from athletic activity use an ointment that contains homeopathic Arnica. [158]
TOPICAL APPLICATION The earliest method of plant administration was topical application. Although many plants contain generalized moisture-enhancing properties, some were found to be particularly effective in ameliorating specific acute conditions when applied topically. Two methods are used to apply remedies to the skin. The endermatic method applies medicine on the skin without friction, as when applying a compress to the dermis and epidermis after an abrasion or laceration. The epidermatic method uses friction and is most effective with botanical oils, liniments, ointments, and medicated warm and cold friction rubs, primarily for subdermal contusions and trauma to effect circulatory changes.[51] Topical application of medicinal plants is useful for many conditions, including abrasions, lacerations, burns, insect bites, infections, rashes, and dermatoses. Other applications include contusions, varicosities, joint pain, inflammation, and musculotendinous aches, strains, and sprains. Topical herbal remedies are applied with a poultice, compress, fomentation, or ointment. Probably the most common, the poultice is used to apply a remedy to a skin area with moist heat. A poultice is prepared by bruising or crushing the medicinal parts of the plant to a pulpy mass, then applying this to the affected area and covering it all with a moist heat source. If dried plants are used (or fresh plants if necessary), the materials are moistened by mixing with a hot, soft, adhesive substance such as moist flour or corn meal. A good way to apply a poultice is to spread the paste or pulp on a wet and hot cloth, which is wrapped around the affected area to help retain moisture and heat. The cloth is moistened with hot water as necessary. With irritant plants, as in a mustard "plaster," the paste is kept between two pieces of cloth to prevent direct contact with the skin. After the poultice is removed, the area is washed well with water to remove any residue. A poultice can be used to soothe, to irritate, or to draw impurities
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from the affected area, depending on which plants are applied. A fomentation is a hot cloth soaked with an herbal infusion or decoction. Fomentations are generally less active than poultices. A cold compress is used for conditions that require an antiinflammatory cure. A cold, infusion- or decoction-soaked cloth is applied to an area and then removed when the body's circulation has warmed the cloth to body temperature. The botanicals' active principles determine what actions the external applications will impart. For example, a poultice with an astringent herb such as Hammamelis (witch hazel) has an entirely different effect than one made with a strong vasodilator and rubefacient, such as Capsicum (cayenne pepper). Ointments are another method of topical administration. Most ointments are made in a base of petroleum jelly, stable vegetable oils, beeswax, or a combination of these. The extract from the desired botanical is suspended within the base to create a stable solid product. Topical botanical products have the same function as topical pharmaceutical ointments and are used to treat lacerations, abrasions, infections, and insect bites. Other uses for botanical topicals include hemostatic, antiinflammatory, antihistamine, rubefacient, analgesic, emollient, and circulatory stimulant actions. As with pharmaceutical topical agents, herbal poultices, compresses, and ointments deliver their active compounds transdermally. The first uses of most medicinal plants were probably topical. In contemporary herbology, many of these plants are also used internally. Whole plants containing more than one ingredient with biologic activity generally invoke synergistic action of several components to produce the therapeutic action. Thus most botanicals have multiple applications for therapeutic purposes. Herbalists and homeopaths treat trauma of the skin, muscles, tendons, ligaments, and joint tissue with a topical agent in ointment or poultice form and give the same medicine internally in minute (homeopathic) doses to enhance the activity, as with concurrent use of Arnica ointment and homeopathic Arnica. The major precaution in medical botany is to identify toxicity. Some of the most effective topical agents can be toxic if ingested. Most of these plants found in the wild could not be taken in sufficient doses to be fatal before causing gastrointestinal (GI) upset. A tincture, herbal concentrate, or powdered version of the plant, however, could have deadly potential.
USE OF HERBAL MEDICINE IN THE WILDERNESS Travelers in the wilderness can choose preprocessed herbal preparations or naturally available plants in the immediate vicinity. A surprisingly large number of minor medical conditions encountered in an outdoor setting can be treated with plants in that location. North American recreational areas are home to medicinal plants that have been used by Native Americans for centuries. Recreationists in desert, alpine, and river environments can find medicinal plants in abundance. Nearly all the vegetation encountered during an alpine trek in North America has some medicinal property. Many plants in tropical and subtropical regions have medicinal properties. Considerations for using herbal products in the wilderness are availability, ease of application, incidence of side effects, toxicity, spectrum of applicability, affordability, and effectiveness. Availability and Application If a condition can be improved by application of a local botanical growing in the immediate vicinity, the pharmacy is immediately available. Plants may be in season, plentiful, and easily harvested. Finding the appropriate plants can be challenging, however, depending on the location, season, the traveler's familiarity with botanicals, and the type of medical condition. During the popular mild seasons and at elevations conducive to plant growth in the continental United States, the chances of finding common plants are good. If not, standardized commercial preparations of these herbs can be carried. These are packaged for long storage life, sanitary and convenient application, and standardization of active ingredients. Hundreds of plants can be applied topically for a variety of conditions. Most of the readily available plants, even if properly identified, require some form of processing for the active constituents to be used fully. Furthermore, expertise in the field requires years of training by a knowledgeable botanist and herbalist. It also requires knowledge of plant seasonal variation, ecologic niches, and precise plant identification. However, a non-botanist-herbalist can gain a basic understanding of a few plant medicines that have a wide spectrum of applicability and a broad range of geographic distribution. Side Effects and Toxicity The American Association of Poison Control Centers annually reports plant ingestion as a significant category of accidental poisoning. In 1997, 5.6% of U.S. poisonings came from plants and mushrooms. Of the substances that were involved in pediatric poisonings, plants were responsible for 7.4% of exposures. Side effects or toxic reactions from botanicals are rarely experienced. In those covered in this chapter, toxicity is not a major consideration. Anything can be toxic when used excessively or indiscriminately. Many toxic plants produce GI distress, vomiting, or diarrhea before any severe neurologic or cardiorespiratory derangement. Often, toxic side effects are caused by one substance in a plant. When isolated, minute amounts of an
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alkaloid may be potentially dangerous, but when ingested in a form modified by other constituents the altered drug effect allows tolerance of larger amounts of the toxic substance or substances. As with any medication, medicinal plants should be applied appropriately, and dosages for internal use should not exceed recommendations. Pregnancy and nursing may pose contraindications. Dosages for almost any herb can be found in numerous references.[114] Felter[51] stated that "as a rule, doses usually administered are far in excess of necessity and it is better to err on the side of insufficient dosage and trust to nature, than to overdose to the present or future harm or danger of the patient." In general, for the self-harvested herbs presented in this chapter, the dry, crushed, herbal adult dosage should be 1 teaspoon per pint of water; when the fresh herb is used, the amount should be twice that. Although no absolute law exists in administering medicines to children, Cowling's rule takes the child's age at the next birthday and divides by 24 to determine what fraction of the adult dose should be given.[51] Spectrum of Applicability Most herbal medicines that have been catalogued and used historically are specifically indicated for one condition, although additional therapeutic effects have been noted over time. All the botanicals covered here have multiple uses. Comfrey (Symphytum officinale) may be used as a topical antiinflammatory agent; it also has principles that are effective for GI conditions when taken internally.[101] Aloe vera gel is an excellent topical agent for abrasions and burns; taken internally, the latex portion serves as an effective laxative.[101] Calendula officianalis has antimicrobial properties that make it an effective topical dressing for mild infectious conditions, whereas internally it has antipyretic effects.[101] Affordability If the herbalist collects plants and processes them personally, the cost is minimal. The purchase price of botanicals depends on the rarity and origin. Some exotic and rare botanicals from Asia and the Amazon rainforest demand a high price on the world market. Panax ginseng has long been regarded by Asian peoples as a prized herbal tonic and can cost hundreds of dollars per root, depending on the size, origin, and age. Panax quinquefolius, or American ginseng, can cost as much as $52 per pound, and was valued at $62 million as a cash crop in 1992.[15] Many exotic herbal and animal-derived medicines from China have prices as high as those of precious metals. Most of the herbs produced in the continental United States used for common ailments average 20 to 30 cents per dose (equivalent to 1 teaspoon of herbal tincture). Prices are not yet standardized. Quality control for production and supply and demand seem to dictate the cost of the mass-marketed herbal products. The best way to obtain a standardized product with a good quality/price ratio is to acquire the product from a botanical company that has been in business for at least 10 years and sells only to licensed health care practitioners.
NORTH AMERICAN PLANT MEDICINES Ephedra (Ephedra viridis) Description and Habitat.
Common names for Ephedra include Brigham Young weed, desert herb, Mormon tea, squaw tea, and teamsters' tea. Ephedra species are shrubs with erect strawlike branches found in desert or arid regions throughout the world and in the southwestern deserts of the United States ( Figure 50-2 ). The Chinese Ephedra called Ma Huang, Ephedra sinica, is found throughout Asia; E. distacha is found throughout Europe; E. trifurca or E. viridis (desert tea), E. nevadensis (Mormon tea), and E. americana (American Ephedra) are found in North America; and E. gerardiana (Pakistani Ephedra) is found in Pakistan and India. The 2- to 7-foot shrubs grow on dry, rocky, or sandy soils. The broomlike shrub has many jointed green stems with two or three small scalelike leaves that grow at the joint of stems and branches. Pharmacology.
Ephedra is generally utilized for its alkaloid content, which tends to be ephedrine, pseudoephedrine, and norpseudoephedrine. The various species vary significantly in both alkaloid type and content. In E. sinica the total alkaloid content can be from 3.3% to 20%, with 40% to 90% being ephedrine and the remainder pseudoephedrine.[46] The North American varieties, such as Mormon tea (E. nevadensis), are reported to contain no ephedrine. Ephedra's pharmacology centers on the actions of ephedrine. Ephedrine and pseudoephedrine are used widely in prescription and over-the-counter drugs to treat asthma, hay fever, and rhinitis.[58]
Figure 50-2 Ephedra viridis. (Courtesy Cascade Anderson Geller.)
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The central nervous system (CNS) effects of ephedrine are similar to those of epinephrine but are much milder and longer in duration of action. The cardiovascular effects are increased blood pressure, cardiac output, and heart rate. In addition, ephedrine increases brain, heart, and muscle blood flow while decreasing renal and intestinal circulation.[58] Relaxation of bronchial, airway, and uterine smooth muscles also occurs.[58] Pseudoephedrine has weaker CNS and cardiovascular system actions but has bronchial smooth muscle relaxation effects. Because of fewer side effects, it is used more often than ephedrine for asthma.[58] Pseudoephedrine also demonstrates significant antiinflammatory activity.[70] [87] Per 100 g, the dry leaf of Ephedra is reported to contain 5 g protein, 5810 mg calcium, and 500 mg potassium.[46] Native and European Medicinal Uses.
Ephedra has been used extensively in the West and in Asia for upper respiratory conditions such as asthma, bronchitis, and hay fever. It has also been used to treat edema, arthritis, fever, hypotension, and urticaria.[34] It is said to be valuable as a diuretic, febrifuge, and tonic.[101] The Navajo Indians used the dried, crushed, long leaf of Ephedra to apply to syphilitic sores, and the Hopi Indians drank a tea from the branches and twigs of a related species for the same condition.[152] Other tribes used the ground and roasted root for making bread.[46] Mormon tea is a folk remedy for colds, gonorrhea, headache, nephritis, and syphilis.[46] Mexicans mix the leaves with tobacco and smoke them for headaches.[46] Modern Clinical and Wilderness Applications.
Ephedra has proved to be an effective bronchodilator for treating mild to moderate asthma and hay fever. The common preparations include other herbs that have antitussive and expectorant effects, such as licorice (Glycyrrhiza glabra) and grindelia (Grindelia camporium). Ephedrine promotes weight loss.[114] Appetite suppression plays a role, but an increase in metabolic rate of adipose tissue is the main mechanism.[7] The weight reduction effects can be enhanced by up to 60% with the addition of methylxanthine.[47] Clinically, standardized Ephedra preparations are used because of the predictable alkaloid content. E. sinica extracts are available with a standardized 10% ephedrine alkaloid content. The dosage of a 10% alkaloid content extract is 125 to 250 mg three times a day. In the wilderness, specifically the desert, the raw herb Mormon tea from E. nevadensis or E. viridis can be useful for hay fever, mild asthma, bronchitis, or an upper respiratory infection (URI). These species contain minimal amounts of ephedrine and principally contain pseudoephedrine; thus they can be used without some of the unpleasant side effects of the Asian species. They can also be used for mild fevers associated with influenza or URI. The shrubs are typically found growing on dry, rocky, or sandy slopes. The leaves can be picked fresh or sun-dried for 6 to 8 hours and can be prepared as a steeped tea or an infusion. Generally, the dose should be the equivalent volume of 1 tablespoon of dried, crushed stems per 4 ounces of water, steeped for 10 minutes. The patient should not exceed a dosage given six times per day. Once harvested, the leaves can be kept for an indefinite period for later use if stored in an airtight container. Toxicity.
According to Duke,[46] an infusion of Ephedra produced a "prompt and extensive contraction of uterine muscle when applied to smooth muscle strips of virgin guinea pig uteri." Ephedra may also elevate blood pressure. Frequent use may result in nervousness and restlessness. It should be used with caution if the patient has hypertension, heart disease, thyrotoxism, diabetes, or benign prostatic hypertrophy. Ephedrine should not be used with antihypertensive or antidepressant medications. Goldenseal (Hydrastis canadensis) Description and Habitat.
Hydrastis has a perennial root or rhizome, which is tortuous, knotty, and creeping. The internal color is bright yellow, with numerous long fibers. The stem is erect, simple, herbaceous, and rounded, from 15 to 30 cm (6 to 12 inches) in height, becoming purplish and bearing two unequal terminal leaves. The leaves are alternately palmate with three to five lobes, hairy, dark green, and cordate at the base. The flowers, which are evident in early spring, are solitary, terminal, small, and white or
rose colored. The plant is a native of eastern North America and cultivated in Oregon and Washington. The parts used are the dried rhizome and roots. Pharmacology.
The alkaloids derived from Hydrastis are hydrastine (1.5% to 4%), berberine (0.5% to 6%), berberastine (2% to 3%), canadine, hydrastinine, and related compounds. Other constituents include meconin, chlorogenic acid, phytosterins, and resins.[114] Native and European Medicinal Uses and Folklore.
Native Americans used Hydrastis extensively as an herbal medicine and clothing dye. The Cherokee Indians used the roots as a wash for local inflammations and as a decoction for general debility, for dyspepsia, and to improve appetite. The Iroquois Indians used a decoction of the root for whooping cough, diarrhea, liver trouble, fever, sour stomach, flatulence, pneumonia, and heart trouble.[109] Early European uses date back to 1793; in the Collections for an Essay Towards a Materia Medica of the United States, Benjamin Smith Barton noted that Hydrastis was useful as an eyewash for conjunctival inflammation and as a bitter tonic. In the pharmacy of the nineteenth
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century (1830), goldenseal was listed among the official remedies in the first revision of the New York edition of the USP. It was listed in the USP until 1926 and recognized in the National Formulary until 1955.[71] Modern Clinical and Wilderness Applications.
Goldenseal is among the top sellers in the American herbal medicine market. It is used as an antiseptic, hemostatic, diuretic, laxative, tonic, and antiinflammatory for inflammation of the mucous membranes. It has also been recommended for hemorrhoids, nasal congestion, sore mouth and gums, conjunctivitis, external wounds, sores, acne, and ringworm.[98] Modern research into the active ingredients berberine and hydrastine has shown why some of the folk applications are effective. The most widely studied component is berberine. This isoquinoline alkaloid has demonstrated antibiotic, immunostimulatory, anticonvulsant, sedative, febrifugal, hypotensive, uterotonic, choleretic, and carminative activities (promoting the elimination of intestinal gas). [114] Berberine has broad-spectrum antibiotic activity. The antimicrobial activity has been demonstrated on protozoa, fungi, and bacteria, both in vitro and in vivo. Antimicrobial action has been noted against Staphylococcus, Streptococcus, Chlamydia, Corynebacterium diphtheriae, Escherichia coli, Salmonella typhi, Vibrio cholerae, Pseudomonas, Shigella dysenteriae, Entamoeba histolytica, Trichomonas vaginalis, Neisseria gonorrhoeae and N. meningitidis, Treponema pallidum, Giardia lamblia, Leishmania donovani, and Candida albicans.[114] Berberine inhibits the adherence of bacteria to host cells.[140] Active ingredients in the crude botanical may be responsible for the wide-spectrum effectiveness of Hydrastis. The antifungal properties, for example, prevent the overgrowth of Candida that frequently occurs with the use of other antibiotic therapies. Other studies have shown the immunostimulatory activity of berberine-containing plants. Berberine increases blood flow through the spleen; improved circulation may augment the immune function of this lymphoid organ.[125] Berberine also activates macrophages.[91] Historically, berberine-containing plants have been used as febrifuges, and in rat studies they have an antipyretic effect three times as potent as that of aspirin.[114] Plants such as goldenseal are very effective in treating acute GI infections. In several clinical studies, berberine has successfully treated acute diarrhea caused by E. coli, Shigella dysenteriae, Salmonella, Klebsiella, Giardia, and Vibrio cholerae.* Berberine-containing plants, in addition to their antimicrobial properties, influence the enterotoxins produced by offending pathogens.[24] [141] [142] GI illness is a major concern of the traveler to areas where sanitation is questionable. Both waterborne and food-borne bacterial and protozoal infections are concerns for persons in wilderness and Third World environments. Some experts recommend using a berberine-containing botanical source prophylactically at least 1 week before a visit to questionable areas and for 1 week after return.[114] Various eye complaints involving the conjunctivae and surrounding mucous membranes have been effectively treated with forms of berberine extract. Recent studies point to the effectiveness of berberine in treating the infection caused by Chlamydia trachomatis. Clinical trials found that a 2% berberine solution compared favorably to sulfacetamide. Although the symptoms resolved more slowly with the berberine extract, the rate of relapse was much lower in the berberine-treated group.[9] [110] A standardized form of Hydrastis canadensis is beneficial for generalized digestive disorders (acute dysentery, gastritis) and infective, congestive, and inflammatory states of the mucous membranes (sinusitis, pharyngitis, stomatitis). A typical dose depends on the source and method of the extract. For the previous conditions, the following three-times-a-day dosage is recommended: dried root or as infusion, 2 to 4 g; tincture (1:5), 6 to 12 ml (1.5 to 3 teaspoons); or solid extract (4:1 or 10% alkaloid content), 250 to 500 mg. Hydrastis can also be used as a wash or rinse for conjunctivitis, sinusitis, and pharyngitis. Eye drops, nasal lavage, and gargle are applied in a 5% preparation of a 1:5 tincture, or 1 to 2 teaspoons of powdered herb to 8 ounces water to create an infusion for application to inflamed mucous membranes. This can be repeated three times a day. Toxicity.
Berberine and berberine-containing plants are generally nontoxic. In recommended doses, berberine-containing plants have not been shown to be toxic in clinical trials. The median lethal dose (LD50 ) of berberine sulfate in mice is approximately 25 mg/kg, and in dogs, intravenous (IV) doses up to 45 mg/kg do not produce lethal or gross toxic effects.[125] Hydrastis should not be used during pregnancy, and long-term ingestion may interfere with the metabolism of B vitamins. Arnica (Arnica montana) Description and Habitat.
Arnica is a perennial plant generally found in mountainous areas of Canada, the northern United States, and Europe. The plant reaches a height of 30 to 60 cm (1 to 2 feet) and generally contains from one to nine large daisylike flowerheads, which bloom during summer months ( Figure 50-3 ). Pharmacology.
The flower is used both internally and externally for medicinal effects. The rootstock is used to make commercial preparations for tinctures and oils that are applied topically. The active principles of the plant drug are flavonoids, volatile oils, and plant pigments (carotinoids).[153] Specific constituents include arnicine, *References [ 11]
[ 37] [ 45] [ 66] [ 85] [ 126] [ 131]
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Figure 50-3 Arnica latifolia.
formic acid, thymohydroquinone, lobelamine, and lobeline (piperidine alkaloid).[28] Native and European Medicinal Use and Folklore.
The Catawa Indians administered the tea of Arnica roots to treat back pain. In Europe the flowerheads have been used since the sixteenth century as an application for bruises and strains.[151] European Arnica was included in the USP from the early 1800s until 1960 and was recognized for its effects on the healing of bruises and sprains. Specific instructions given in the American Dispensory in 1922 listed Arnica as effective for "muscular soreness and pain from strain or overexertion; advanced stage of disease, with marked enfeeblement, weak circulation, and impaired spinal innervation; ... tensive backache, as if bruised or strained; [and] ... headache with tensive, bruised feeling and pain on movement."[51] Arnica in tincture (concentrated) form has been a popular but not necessarily safe medicine to treat inflammatory swellings and to relieve the soreness of myalgia and the effects of bruises and contusions. Doses above the therapeutic range cause vagal inhibition when ingested and may cause toxicity if the concentrated tincture is applied topically. Therefore the most common use has been fomentation of the flowers for topical applications in treatment of strains and sprains. Modern Clinical and Wilderness Applications.
Contemporary use of Arnica montana is generally limited to topical commercially prepared ointments and salves, in conjunction with internal homeopathic (low-dose) use for the same indications. Although its alkaloid (arnicine) and volatile oil (thymohydroquinone) are both relatively toxic, the actions of these constituents are extremely useful in resolving contusions and soft tissue injury. Most ointments are found to contain a 1x homeopathic dilution of Arnica tincture, which is about 4% by volume. Oral dosage is given in homeopathic potencies of 6x to 200c, depending on the severity of the condition.
Figure 50-4 Garlic blossom (Allium species). (Courtesy Cascade Anderson Geller.)
For application in the wilderness, most naturopathic first-aid kits include both the ointment and the oral homeopathic forms of Arnica. For direct use of the plant in treating minor sprains and strains, 2 teaspoons of the dried flower tops can be steeped in 1 cup of water for 10 minutes, and the infusion can be applied in a cold compress to the affected area. This should be repeated each 2 hours in addition to standard first-aid procedures. The infusion lasts a day if refrigerated and a few hours if not; therefore it is best to use a fresh infusion whenever possible. In addition, if available, the oral homeopathic preparation (30x to 200c) should be taken three times daily until the swelling is reduced significantly. A topical ointment can be applied every 2 to 3 hours for this condition in place of the compress. According to Weiss,[152] Arnica is safe and effective for topical contusions and for stimulating granulation and epithelialization. A tablespoon of tincture is added to 500 ml of water, and the gauze compress is then placed on the wound. This stimulates local circulation and acts on the peripheral vasculature. After granulation has occurred, ointments may be applied. Toxicity.
Arnica tincture or infusion can be toxic if the concentration is too high. Undiluted tincture should not be used internally or in compress form over an open wound. Vagus nerve inhibition is the primary toxic effect; GI irritation is also noted. Toxic reactions include gastric burning; nausea; vomiting; headache; decreased temperature; dyspnea; cardiovascular collapse; convulsions; motor, sensory, and vagal paralysis; and death.[28] Garlic (Allium sativum) Description and Habitat.
Garlic is a member of the lily family. It is a perennial plant cultivated worldwide ( Figure 50-4 ). The garlic bulb is composed of individual cloves enclosed in a white skin. The medicinal herb is found in the bulb and is used either fresh or dehydrated. Garlic oil, which also has medicinal value, is obtained
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by steamed distillation of the crushed fresh bulbs.[98] Pharmacology.
The medicinal compounds in garlic generally contain sulfur and have been the subject of most research on garlic. Two primary compounds are an odorless chemical called alliin and the enzyme allinase, which begins a cascade of chemical reactions when the garlic clove is cut, crushed, or bruised. Alliin is converted to allicin, which is responsible for the characteristic odor of garlic. Allicin is strongly antibacterial and considered to be the major source of the antimicrobial effects of garlic. Diallyl sulfide, disulfide, and trisulfide are yielded from the breakdown of allicin. Heat speeds up the reaction, so cooked garlic and steamed distilled garlic oil contain little or no allicin. Within garlic, about 0.1% to 0.36% of the volatile oil is composed of sulfur-containing compounds (e.g., allicin, diallyl sulfide, diallyl trisulfide). These volatile oils are considered to be responsible for most of the pharmacologic properties of garlic. Other constituents of garlic include s-methyl-L-cysteine sulfoxide, protein (16.8% dry weight basis), a high concentration of trace minerals (particularly selenium and germanium), vitamins, glucosinolates, and enzymes, which are composed of allinase, peroxidase, and myrosinase.[114] [122] Native and European Medicinal Use and Folklore.
Throughout history, garlic has played an important part in medicinal herbology. Clay garlic bulbs dating back to 3750 BC were found in Egypt. Preserved garlic bulbs were discovered in the tomb of Tutankhamen. An entire basket of these bulbs from the tomb of Kha at Thebes is in the Turin Museum. The Greek historian Herodotus recorded that an enormous amount of money was spent on garlic for the builders of the great pyramids. One of the earliest Sanskrit manuscripts, The Bower Manuscript, devotes its entire first section to garlic, describing its legendary origins. It says that garlic keeps in order the three fluids and can cure thinness, weakness of digestion, lassitude, coughs, inflammation of the skin, piles, glandular swellings in the abdomen and enlargement of the spleen, indigestion, constipation, excessive urination, worms, wind in the body (rheumatism), leprosy, epilepsy, and paralysis. Within the traditional medical circles of Greece and Rome, medieval Europe, and the Far East, similar claims may be found. Galen, Dioscorides, and Aristotle extolled garlic as an excellent medicine. Hippocrates recommended garlic as a diuretic; to regulate digestion; to treat bowel pains, inflammations, and infections; and to regulate menstruation. Early Chinese and European herbalists used garlic for heating and drying and therefore to prevent and cure diseases arising from cold, poisons, excesses of diet and drink, and sluggish metabolism. Pasteur noted garlic's antibiotic properties in 1858. Albert Schweitzer used garlic in Africa to treat amebic dysentery. Garlic was also used as an antiseptic to prevent
gangrene during both world wars. Modern Clinical and Wilderness Applications.
The pharmacologic effects of garlic are based on its activity as a hypoglycemic and hypolipemic regulating agent,* anticoagulant,† antihypertensive,[103] [124] antimicrobial,‡ detoxifier of heavy metals,[2] and immune system modulator.[82] Animal and human studies have substantiated that garlic lowers serum cholesterol and triglyceride levels and increases the amount of high-density lipoproteins. Dietary atherosclerosis was significantly reduced in rabbits fed garlic consistently for weeks; also, extract of garlic and onions was more effective than clofibrate against hyperlipidemia and subsequent lipid deposition within the aorta. [23] After 4 months of feeding the rabbits a high-cholesterol diet, the average lipid content in the aorta of the control animals rose from 5.95 to 13.75 mg/100 g dry weight. Animals taking clofibrate for 4 months had 7.95 mg and garlic-fed animals 6.23 mg/100 g dry weight of lipid content in the aorta.[23] Other studies of experimental atherosclerosis in rabbits support these findings. [76] [88] Decreased atheromatous lesions seem to be a consistent finding in rabbits fed high-cholesterol diets supplemented with garlic. Of various sulfur-containing amino acids isolated from garlic, s-methylcysteine and s-allylcysteine exert the greatest antilipidemic effects.[74] Components of garlic can combine with the sulfhydryl group, the functional part of coenzyme A that is necessary for the biosynthesis of fatty acids, cholesterol, triglycerides, and phospholipids. The lipid-lowering effect may best be attributed to inactivation of the sulfhydryl group.[8] Both in vitro and in vivo tests show reduced conversion of acetate into cholesterol by liver tissues.[35] Since the sulfhydryl groups are involved at all levels of metabolic activity, the impact of garlic could be more extensive. Studies suggest that garlic may lower blood pressure by acting similar to prostaglandin E1 , which decreases peripheral vascular resistance.[118] As a nutritional supplement, garlic is composed of magnesium, iron, copper, zinc, selenium, calcium, potassium chloride, germanium, sulfur compounds, amino acids, and vitamins A, B1 , and C. Garlic increases the body's capacity to assimilate thiamine by enhancing its absorption. Thiamine is a key part of the co-carboxylase enzyme system, which has beneficial effects on liver cells; this may explain why garlic offers prophylaxis against liver and gallbladder damage. In one study, garlic was shown to protect hepatocytes in tissue *References [ 6] [ 8] [ 12] [ 17] [ 18] [ 20] [ 21] [ 26] [ 35] [ 36] [ 65] [ 74] [ 75] †References [ 5] [ 16] [ 19] [ 24] [ 25] [ 57] [ 77] [ 102] [ 119] [ 127] [ 137] . ‡References [ 3] [ 4] [ 32] [ 53] [ 93] [ 102] [ 115] [ 144] [ 146]
[ 78] [ 79] [ 80] [ 83] [ 84] [ 88] [ 89] [ 116]
.
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culture from the damage of carbon tetrachloride.[118] Antioxidant activity has been attributed to garlic and garlic derivatives. The free radical scavenger action of garlic may be explained by its germanium, glutathione, selenium, and zinc content. The last three are key components of the antioxidant enzyme superoxide dismutase and glutathione peroxidase. Animal studies show that feeding garlic oil enhanced physical endurance in normal rats and also reduced the decrease in physical endurance induced by isoproterenol, a synthetic catecholamine that induces necrosis of the myocardium.[129] Garlic inhibits platelet aggregation in animals; similar effects can be demonstrated in vitro and in vivo in humans.[43] [137] An antiplatelet extract of garlic, ajoene, was found to potentiate the antithrombotic effect of antiinflammatory drugs. Under fasting conditions inhibition of platelet aggregation by garlic or its extracts is dose related.[138] The garlic effect may be linked to inhibition of thromboxane synthesis or to altered properties of the plasma membrane. Methyl (2-propenyl) trisulfide, another component of garlic, is 10 times more potent as an inhibitor of platelet aggregation than is diallyl disulfide or trisulfide.[5] Thrombocyte aggregation inhibition is enhanced by two other compounds, 2-vinyl-1,3-dithiene and allyl-1,5-hexidienyl-trisulfide.[14] Garlic and its juice or oil also enhance fibrinolysis.[22] In a double-blind placebo-controlled trial, cycloalliin, a component of garlic, was given to volunteers and patients after myocardial infarction and significantly increased fibrinolysis 1 ½ hours later.[49] Chutani and Bordia[38] observed that the increase took place 6 ½ to 12 hours after garlic intake. Daily garlic ingestion for 1 month generated a 72% to 85% increase in fibrinolysis in patients with ischemic heart disease.[124] The pharmacologic versatility of garlic is best reflected by its antiviral, antifungal, antiprotozoan, antiparasitic, and antibacterial activities.* Laymen are credited with being the first to describe the scientific basis for the medicinal use of garlic extract.[155] Huddleson et al[72] and Cavallito et al[33] demonstrated in 1944 that garlic juice and allicin inhibited the growth of Staphylococcus, Streptococcus, Bacillus, Brucella, and Vibrio species at low concentrations. Recent studies using serial dilutions and filter paper disk techniques have shown that fresh garlic, powdered garlic, and vacuum-dried preparations were effective antibiotic agents against many bacteria, including Staphyloccus aureus, a- and ß-hemolytic Streptococcus, E. coli, Proteus vulgaris, Salmonella enteritidis, Citrobacter, and Klebsiella pneumoniae.[114] These studies compared the antimicrobial effects of antibiotics, including penicillin, streptomycin, chloramphenicol, erythromycin, and tetracycline, with those of garlic. Besides confirming garlic's well-known antibacterial effects, studies demonstrated its effectiveness in inhibiting the growth of some antibiotic-resistant bacteria.[1] [48] [132] Garlic has also demonstrated significant antifungal activity against a wide range of fungi.* From a wilderness perspective, inhibition of fungi that can affect the skin (Microsporum, Trichophyton, Epidermophyton, and Candida albicans) can be significant. Garlic juice applied topically is an effective alternative in treating fungal skin diseases.[3] Garlic compares well with nystatin, gentian violet, and six other reputed antifungal agents to treat C. albicans.[1] [111] [121] [128] Garlic has long been associated with prophylaxis against influenza virus. In vivo studies with mice revealed that garlic administration protected mice against intranasal inoculation with influenza viruses and enhanced reproduction of neutralizing antibodies after vaccine administration.[115] In vitro studies have shown that garlic has antiviral activity against influenza B virus and herpes hominis virus type I.[145] Preliminary studies have revealed significant enhancement of natural killer (NK) cell activity in humans administered raw or cold, aged whole-clove garlic preparations daily for 3 weeks.[82] The antiviral activity of garlic in humans may be secondary to the direct toxic effect on viruses and enhanced NK cell activity that destroys virus-infected cells. Wilderness Medical Applications.
The use of garlic in the outdoor setting can be extensive. Its use as a food should be encouraged despite its odor, particularly in people with elevated cholesterol levels, heart disease, hypertension, diabetes, asthma, fungal infections, respiratory infections, and GI disorders (intestinal parasites, dysentery). A macerated garlic poultice and garlic slices serve as topical agents for fungal infections, ulcerated wounds, pyoderma, and other skin infections. The poultice can be used directly on the dermatologic problem and as a suppository can be used to treat vaginitis, particularly infections caused by C. albicans. For this application, one to two fresh chopped cloves can be made into a poultice. This should be kept on the affected site for several hours and changed at least once every 6 hours with a fresh preparation. If the garlic causes epidermal irritation, its use is discontinued. Prophylactic use during the flu season can reduce the incidence of infection. Within the first 48 hours of onset of a flu or URI, one or two cloves can be consumed with a carbohydrate source to prevent stomach irritation. Alternatively, two or three oil of garlic capsules can be taken. For persons concerned about the social segregating aspect, extracts that preserve the allicin content but remain odorless can be used. *References [ 3]
[ 4] [ 32] [ 53] [ 115] [ 143] [ 157]
.
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Toxicity.
For the vast majority of individuals, garlic is nontoxic at usual dosages. However, some people develop allergic contact dermatitis or irritation of the digestive tract. Apparently, they are unable to detoxify allicin and other sulfur-containing components. Prolonged consumption of large amounts of raw garlic by rats results in anemia, weight loss, and failure to grow.[117] Ginger (Zingiber officinale)
Description and Habitat.
Ginger is an upright perennial herb with tuberous rhizomes, from which grows an aerial stem to 1.5 m (5 feet) in height. It is native to southern Asia, although it is cultivated in the tropics. Extracts and dried ginger are produced from dried unpeeled ginger; peeled ginger loses much of its essential oil content. [148] Pharmacology.
Ginger is composed of a rich variety of nutrients and enzymes. The general composition is starch (50%); protein (9%); lipid (6% to 8%) composed of phosphatidic acid; lecithin; free fatty acids; triglycerides; protease (up to 2.26%); volatile oils (1% to 4%), the principal components of which are three sesquiterpenes (bisabolene, zingiberene, zingiberol); vitamins, especially niacin and vitamin A; and resins.[148] Native and European Medicinal Use.
Zingiber officinale is native to southern Asia and tropical Africa. Therefore it did not have a role in the early herbal preparations of European and Native American herbal medicine. Modern Clinical and Wilderness Applications.
Clinical use of ginger for antiinflammatory action, cholesterol-lowering effects, and relief of dizziness and motion sickness is noted in herbal texts.* A choleretic effect (the promotion of bile flow to the gallbladder and small intestine) and the conversion of cholesterol into bile acids are enhanced by ginger ingestion and may be responsible for its overall cholesterol-lowering effect. An early eclectic medical text listed ginger as local stimulant, sialogogue, diaphoretic, and carminative.[51] Powdered ginger in a large quantity of cold water taken before sleep frequently "breaks up" a severe cold, and a hot infusion of ginger tea is a popular remedy for similar use to mitigate the pains of dysmenorrhea.[51] Ginger may relieve painful spasmodic contractions of the stomach and intestine. The antiinflammatory action of ginger is thought to be caused by potent inhibition of inflammatory compounds, such as prostaglandins and thromboxanes.[90] Ginger is also known to contain strong plant proteases such as bromelain, ficaine, and papain, which may explain some of its antiinflammatory action.[148] Ginger has been used historically for major GI complaints. It is generally regarded as an excellent carminative (promotes the elimination of intestinal gas) and intestinal spasmolytic.[114] One of the most noted uses of ginger in contemporary herbal medicine that applies to wilderness medicine is its action on the symptoms of motion sickness and seasickness.[62] [63] [113] Ginger is also a significant antiemetic. It has long been used in the treatment of nausea and vomiting associated with pregnancy. The efficacy of ginger has been confirmed in hyperemesis gravidarum, a severe form of nausea and vomiting during pregnancy. Ginger root powder at a dose of 250 mg four times a day brought a significant reduction in both the severity of nausea and the number of attacks of vomiting during pregnancy. [52] To treat motion sickness and vertigo, two 500-mg capsules of powdered ginger root are eaten 20 to 30 minutes before the precipitating event. The same dose is used for the nausea of pregnancy during the acute attack. The raw ginger root can be grated using 1 teaspoon in 4 ounces of water, steeped for 10 minutes, and taken every 30 minutes until the symptoms of motion sickness abate. Toxicity.
There appears to be no toxicity associated with ginger root ingestion. Comfrey (Symphytum officinale) Description and Habitat.
Comfrey is a perennial herb with a stout spreading root that is essentially divisible for propagation. Comfrey grows about 1 m (3 feet) high and has coarse, bristly, oblong, lanceolate leaves. The tubular flower can be purplish, blue, white, red, or yellow ( Figure 50-5 ). About 25 Symphytum species are described; they are indigenous to countries around the Mediterranean Sea and in northern Asia. Comfrey is typically found in moist meadows and other wet places in the United States and Europe. Pharmacology.
The chemical constituents of Symphytum officinale roots include carbohydrate, predominantly sucrose; the amino acids serine and asparagine; the phenolic acids chlorogenic acid, caffeic acid, and
Figure 50-5 Comfrey (Symphytum officinale). (Courtesy Cascade Anderson Geller.) *References [ 51]
[ 52] [ 62] [ 63] [ 64] [ 90] [ 113] [ 134] [ 138] [ 139] [ 148]
.
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p-coumaric acid; the alkaloids choline and allantoin; and the pyrrolizidine alkaloids viridiflorine, echinatine, heliosupine, symphytine, echimidine, and lasiocarpine.[150] The most concentrated (0.88% to 1.71%) alkaloid, allantoin, is generally credited with comfrey's beneficial effects. Native and European Medicinal Uses and Folklore.
In Europe, comfrey is a common perennial grown in the garden for animal fodder. Russian comfrey is often promoted as a medicinal herb for use as a tonic. Comfrey is also cultivated in Japan as a green vegetable and tonic and has been used in American herbal medicine for hundreds of years.[95] Comfrey has long been known as an external agent for the rehabilitation of musculoskeletal and orthopedic injuries. Its former name, "bone knit," derives from the external use of poultices of leaves and roots, which were believed to help heal burns, sprains, swellings, and bruises. Comfrey has been claimed to heal gastric ulcers and hemorrhoids, suppress bleeding, and relieve bronchial congestion and inflammation. [13] The healing action of a poultice derived from the roots and leaves is probably related to the presence of allantoin, an agent that promotes cell proliferation. The underground parts contain 0.6% to 1.3% allantoin and 4% to 6.5% tannin.[30] [107] Comfrey extracts applied topically have been reported to heal wounds and bones in about half of the normal time. In herbology a general rule is that if anything is broken, use comfrey.[156] Herbalists have also found that the allantoin concentration from a fluid extract of comfrey can increase the rate of wound healing of lacerations sufficiently to avoid the use of sutures. [154] In European folklore, comfrey was regarded as an herb having unsurpassed ability to heal any injured or broken tissue. The mucilage (gelatinous mucopolysaccharide) of the comfrey root was named "the great cell proliferator," helping new flesh and bones to grow. Comfrey was one of the main herbs found in any poultice or fomentation. European herbalists considered comfrey exceptional for coughs and soothing inflamed tissues. Comfrey is effective for treating upper respiratory inflammation and has been used successfully to treat hemorrhagic conditions of the lungs. Modern Clinical and Wilderness Applications.
Comfrey lotions and salves containing 0.5% to 2.5% allantoin have been used for sprains, strains, and contusions. In the 1980s, comfrey became controversial because of potential hepatotoxicity. Members of the family Boraginaceae (Heliotropium, Symphytum) contain a variety of related pyrrolizidine alkaloids reported to cause hepatotoxicity in animals. Although no hepatotoxic episodes from the ingestion of comfrey have been reported in humans, the potential exists, so caution is advised when using comfrey for internal consumption.[95] Topical use of comfrey products as yet poses no concern for toxicity.
As a topical agent after acute trauma for musculoskeletal injuries, strains and sprains, or contusions, comfrey is an exceptional medicine.[31] A prepared gel of comfrey with a standardized allantoin concentration should be carried during travel or camping expeditions in the wilderness. The raw herb can be used if the person is in the plant's environment. The herb is readily identifiable, although it should not be confused with foxglove (Digitalis purpurea) and should be used with caution when taken internally in its raw state. For use in a poultice or compress, the leaves may be picked damp, macerated, and applied topically for up to 24 hours. Toxicity.
Comfrey is not recommended for routine internal ingestion. Animal studies indicate that hepatic damage is an eventual outcome if the herb is consumed over a long period. Aloe (Aloe vera) Description and Habitat.
The aloe is a perennial plant native to South and East Africa and is also cultivated in the West Indies and other tropical and temperate areas. The leaves, which emerge from a central rosette produced by a central fibrous root, are 30 to 60 cm (1 to 2 feet) long, narrow, fleshy, and light green with spiny teeth on the margins ( Figure 50-6 ). Aloe is easily cultivated as a houseplant and can be grown in a sunny warm spot with good drainage. The genus Aloe comprises more than 300 species, which are members of the Liliaceae (lily) family. Aloe species are perennial succulents native to Africa. They are not cacti and should not be confused with American aloe, the century plant. Pharmacology.
Two important products are derived from aloe: a gel and a latex. Aloe gel is a clear gelatinous material extracted from the mucilaginous cells found in the inner tissue of the leaf. The gel is obtained by crushing the leaves and repeated straining to remove
Figure 50-6 Aloe claviflora. (Courtesy Cascade Anderson Geller.)
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cellular debris. The result is a clear gel, which is the product most frequently used in the health food and cosmetic industries. It is generally devoid of anthraquinone glycosides. A variety of compounds have been identified in the aloe species, including polysaccharides, tannins, organic acids, enzymes, vitamins, minerals, saponins, and steroids.[95] The bitter yellow latex of aloe contains cathartic anthraquinone glycosides, mostly barbaloin, as the active principles. The concentrations of the glycosides vary with the type of aloe, ranging from 4% to 25% of aloe in concentration. The water-soluble fraction of aloe is called aloin and is a mixture of active glycosides. Cathartics have been derived from extracts of the latex and can create strong purgative effects by stimulating the large intestine. Native and European Medicinal Uses and Folklore.
Fresh Aloe vera gel is well known for its domestic medicinal values.[59] [97] [112] [120] Aloe has been dubbed the burn plant, first-aid plant, and medicine plant. When fresh, the gel relieves thermal burns and sunburns and promotes wound healing. It also has moisturizing and emollient properties. Because of these effects, aloe is widely used as a home remedy. Aloin and other anthraquinone derivatives of aloe are extensively used as active ingredients in laxative preparations. Aloin is also used as an antiobesity preparation.[98] Aloe or aloin extracts are also used in sunscreens and other cosmetic preparations and in drugs for moisturizing, emollient, or wound-healing purposes. In folk medicine, aloe is used for condylomas, warts, abnormal skin growths, and cancers of the lip, anus, breast, larynx, liver, nose, stomach, and uterus.[46] Other folklore suggests that parts of the plants be chewed to purify the blood. The pulp is said to possess wound-healing hormonal activities and "biogenic stimulators" and is used for intestinal ailments, sore throat, and ulcers. In India it is used to treat piles and rectal fissures. Slukari hunters in Africa's Congo basin rubbed their bodies with the gel to eliminate the human scent, making them less likely to disturb prey. During epidemics of influenza, Lesotho natives take a public bath in an infusion of Aloe latifolia. [46] Modern Clinical and Wilderness Application.
Although numerous claims have been made for aloe gel, its most common lay use is in the treatment of minor burns and skin irritations. In 1935 a report described the use of aloe in the treatment of radiation-induced dermatitis. [40] This study followed a 5-week course of topical applications of either the whole leaf or leaf macerated into gel, resulting in complete wound healing after 4 months. In 1937, studies used a calamine and lanolin-based aloe preparation to treat skin irritations resulting from burns, pruritus vulvae, and poison ivy. The results suggested that aloe stimulated tissue granulation and accelerated wound healing.[95] Barnes[10] evaluated the effect of 5% aloe ointment on sandpaper-abraded fingertips and found that the wound-healing rate was two to three times that of control subjects, as measured by decreased electrical potential of the wound. Other studies measured tensile strength of the healed surgical wounds of mice. Healing occurred within 9 days, an improvement over the control mice.[60] Studies of antibacterial activity of aloe extracts have been attempted several times, yielding mixed results. In 1963, studies of the antibacterial effect of macerated Aloe vera gel found no activity against S. aureus and E. coli. [54] Other studies have determined that Aloe chinensis is effective against S. aureus, E. coli, and Mycobacterium tuberculosis, although Aloe vera showed no inhibitory effect.[61] The latex possesses in vitro activity against several pathogenic strains of bacteria, although the whole leaf minus the latex from the leaf epidermis and mesophyll of aloe showed no activity.[99] Two commercial preparations of aloe gel were found to exert antimicrobial activity against gram-negative and gram-positive bacteria and C. albicans when used in concentrations greater than 90%.[67] The moisturizing effect of aloe may be beneficial in the treatment of burns. The healing process may be related to mucopolysaccharides along with sulfur derivatives and nitrogen compounds in the gel, but this has not been well substantiated. [94] In attempts to document the antiinflammatory effects of aloe, a 1976 study found that Aloe vera had bradykinase activity in vitro, but this was not confirmed in vivo.[56] Evidence for the internal use of aloe has been limited to studies involving mucous membrane tissue repair. Corneal ulcers treated with aloe extracts had more healing, less cellular reaction, and fewer signs of irritation than did control groups.[95] Topical application of Aloe vera gel after periodontal flap surgery reduced postoperative pain more than the saline control, and swelling of the treated tissue was less marked than with the control.[69] Because of easy recognition and administration, use of the aloe plant in the wilderness environment is practical. The wild plant can yield an excellent preparation for dermal abrasions, cuts, and superficial wounds. A leaf cut from the base of a healthy plant can be conveniently carried. This allows the gel to remain intact, protected by the outer skin of the leaf. It can be squeezed from the inside through the cut portion directly onto superficial wounds with or without a gauze dressing. A standardized preparation of Aloe vera may be used as an antibacterial agent and an emollient for superficial wounds or dermatitis.
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In the event of constipation, the mixture of aloe gel and latex can be scraped or squeezed from the leaf cortex and ingested, 1 tablespoon three times daily, or until a mild laxative effect is noted. A gel and latex mixture produces less cathartic effect than only latex. Because of the bitterness of the gel and the latex, it should be taken with food or a flavored beverage. Toxicity.
Because of its cathartic effects, oral aloe is not advised if gripping pain is associated with constipation. Aloe taken orally is contraindicated in pregnancy. Otherwise it has no reported toxicity. Plantain (Plantago major) Description and Habitat.
The common broadleaf plantain is a familiar perennial "weed" that may be found along roadsides and in meadowlands. Plantain belongs to the order Plantaginaceae, which contains more than 200 species, 25 or 30 of which have a domestic use. The plant is a small weed with a rosette of ribbed leaves and small projecting seed stalks. Its seeds, known as psyllium seeds in North America, resemble those of another species, Plantago psyllium. The leaves contain 84% water, 2.5% protein, 0.2% fat, and 14% carbohydrate, trace amounts of calcium, phosphorus, iron, sodium, and potassium, as well as ß-carotene, riboflavin, niacin, and ascorbic acid. Biochemically identified compounds include allantoin, adenine, baicalein, baicalin, benzoic acid, chlorogenic acid, choline, cinnamic acid, ferulic acid, L-fructose, fumaric acid, gentisic acid, D-glucose, P-hydroxybenzoic acid, indicain, lignoceric acid, neochlorogenic acid, oleanolic acid, plantagonine, planteose, saccharose, salicylic acid, scutellarein, sitosterol, sorbitol, stachyose, syringic acid, tyrosol, ursolic acid, vanillic acid, and D-xylose. [46] Native and European Medicinal Uses and Folklore.
Historically, plantain has been used for stings, bites, and irritations from venomous insects and reptiles. The folk medicine of the eastern United States suggests using crushed plantain leaves to stop the itching of poison ivy. It has also been reported to help relieve toothache. Ancient herbalists maintained that plantain had refrigerant (imparts a cooling sensation to the mucosa and allays thirst), diuretic, and astringent properties. When the leaves are applied to a bleeding surface wound, hemorrhage lessens. In the highlands of Scotland, plantain is still called slan-lus, or plant of healing. In the United States, plantain has been known as snake weed, from the belief that it is effective for bites from venomous creatures. Felter[51] noted that "the crushed leaves were very effective for the distressing symptoms caused by puncture by the horny appendages of larvae of Lepidoptera and the irritation produced by certain caterpillars, as well as the stings of insects and bites of spiders." In native American folklore, the plant was known as "white man's foot," in reference to its trait of growing in the settlements of white men. The Shoshoni Indians heated the leaves and applied them in a wet dressing for wounds.[153] Modern Clinical and Wilderness Applications.
Plantain is readily available in the recreational areas of North America. This plant is extremely useful for various superficial wounds, abrasions, stings, and bites of mildly venomous insects. The constituents in the crushed leaves have an antihistaminic effect, and anesthetic quality. In the event of a tooth fracture, a compress or poultice of ½ teaspoon of fresh leaves may be used on the exposed nerve root of a tooth. The seeds of the plantago plant are useful for spastic colon, an effect that appears to be related to their mucilaginous properties. Psyllium seeds, known on the Asian continent as flea seed husk, are often used as a bulk laxative. The seeds are collected from the stalk, and 1 teaspoon of fresh seeds in 4 ounces of water is taken twice a day for mild constipation. Water should be ingested throughout the day to alleviate the condition and assist the laxative effect. Because of its astringent effects, an infusion of the leaves is recommended to treat diarrhea. The preparer pours 1 pint of boiling water on 1 ounce of the herb and leaves it in a warm place for 20 minutes. After, straining and cooling, ½ cup is ingested three or four times a day. Toxicity.
No known toxicities are attributed to Plantago. Chamomile (Matricaria chamomilla) Description and Habitat.
Chamomile is a low-growing perennial with a hairy prostrate branching stem. It blooms late in July through September and is found growing throughout North America and Europe. Chamomile is derived from the Greek chamos (ground) and melos (apple), which refer to the plant's low growth and the applelike scent of its fresh blooms.[135] The flower head is about 2.5 cm (1 inch) in diameter, has a conical receptacle, and is covered by yellow disk flowers surrounded by 10 or 20 white down-curving ray flowers. Pharmacology.
The most important chemicals associated with chamomile are the volatile oils containing tiglic acid esters, chamazulene, farnesene, and a-bisabolol oxide. These volatile oils are destroyed if the herb is boiled.[136] Native and European Medicinal Uses and Folklore.
A distinction should be made between German and Roman chamomile, which have been used interchangeably for centuries. The German chamomile is preferred on the European continent, whereas the Roman chamomile has been used widely in Great Britain. In
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the United States, German chamomile is by far the more widely consumed of the two species.[104] German chamomile has a long tradition as a folk or domestic remedy. Its uses include external compresses or fomentations for gout, sciatica, inflammations, lumbago, rheumatism, and skin ailments. Infusions, decoctions, and tinctures have long been used internally to treat colic, convulsions, croup, diarrhea, fever, indigestion, insomnia, teething, toothaches, and bleeding or swollen gums. Historically, Roman chamomile was used similarly.[46] [98] Chamomile is also a folk cancer remedy. Modern Clinical and Wilderness Applications.
The biochemical constituent of chamomile is chamazulene. It is found in both species of chamomile and is reported to have antihistaminic properties. [50] Both histamine release and inhibition of histamine discharge have been considered mechanisms for the potential antiallergic action of chamazulene. In Germany, chamomile products include tinctures, extracts, teas, and salves, widely used as antiinflammatory, antibacterial, antispasmodic, and sedative agents.[104] Studies have shown that both chamazulene and a-bisabolol have antiinflammatory activity. Chamazulene may constitute as much as 5% of the essential oil. Other studies have shown that a-bisabolol has a protective effect against peptic ulcer, as well as antibacterial and antifungal effects. a-Bisabolol has also reduced fever and shortened the healing time of skin burns in laboratory animals.[44] Most commercial European chamomile preparations have been standardized with regard to the chamazulene and a-bisabolol content.[149] According to Rudolph Weiss,[152] one action of chamomile is to reduce gastric motility and secretions, which would alleviate colic and painful spasm. About 20 flavones and flavonols, such as apingenin, are found in the aqueous portion of the distillation process. These are three times as effective at spasmolytic activity as the opium
alkaloid papaverine. Chamomile also has a significant calming effect and has been traditionally applied as a mild sedative. Chamomile is a good botanical to have on hand when traveling or camping. For infants experiencing restlessness and discomfort from teething, one third of the adult dosage may provide relief. For the treatment of conditions that may arise from excessive nervous tension (intestinal gas, colic, peptic ulcers), 2 teaspoons (or one standard teabag) of the flower tops can be added to a cup of boiling water and infused for 5 to 10 minutes; 2 to 3 cups may be taken in 30 minutes for acute intestinal colic. Echinacea (Echinacea angustifolia) Description and habitat.
Echinacea is a perennial herb native to the midwestern region of North America, from Saskatchewan to Texas. The plant produces a characteristic large pale-purple flower and thick hairy leaves and grows 60 to 90 cm (24 to 36 inches) high. The dried root is typically used for medicinal purposes. Pharmacology.
The compounds currently identified from Echinacea species are inulin, glucose, fructose, betaine, echinacin, echinacoside, trihydroxyphenyl proprionic acid, and nonspecific resins. Native and European Medicinal Uses.
This medicinal herb came to the attention of American herbalists in the late 1800s. Echinacea was originally used by the Indian tribes of Nebraska and the Sioux for the treatment of snakebite and as an antiseptic and analgesic. Eclectic practitioners used it externally for the same purposes but used it internally to treat "bad blood," or any condition that manifested signs of local or systemic infection, whether bacterial or viral. Modern Clinical and Wilderness Applications.
Echinacea is probably the most common botanical used and known by the public, especially in relation to its immunomodulating effects. Many have found that echinacea can reduce symptoms and derail the onset of URIs and minor influenza episodes. Echinacea is also a good systemic adjunct to the treatment of any contusion or laceration. The polysaccharide component echinacin can maintain the structure and integrity of the collagen matrix in connective tissue and ground substance and can accelerate wound healing experimentally.[114] Echinacin also has a cortisone-like effect, with intermediate stabilization of inflammation reactions. Inulin, a major component of Echinacea, is a powerful activator of the immune system's alternative complement pathway. It may increase host defense mechanisms for the neutralization of viruses, destruction of bacteria, and increased action of white blood cells (lymphocytes, neutrophils, monocytes, eosinophils) within areas of infection. Extracts of the root have been shown to possess interferon-like properties. As an immune stimulant early in infection, and for posttrauma rehabilitation, dosages are taken orally three times a day: tincture (1:5), 30 to 60 drops, or solid extract (dry powdered extract 6:1), 250 to 500 mg. Calendula (Calendula officinalis) Description and Habitat.
Calendula is found throughout Asia, North America, and Europe and is in the daisy and dandelion family. It is most often known as the marigold. The flower is generally used for the production of the tincture. Pharmacology.
Calendula's chemical constituents include flavonoids, carotenes, saponin, resin, and volatile oil. The volatile oil content is responsible for a localized increase in blood circulation and diaphoresis. The resin
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content is responsible for the antimicrobial and antiinflammatory action of the topical application. Native and European Medicinal Uses.
Native Americans apparently did not use calendula extensively, and the early European literature only mentions its medicinal role. Calendula, however, is one of the best topical applications for the treatment and prevention of infection and skin irritation. Early American surgeons highly regarded its ability to treat and prevent postsurgical infections. Modern Clinical and Wilderness Applications.
A fluid/water extraction or oil infusion (prepared as a tincture but using vegetable oil instead of alcohol) of Calendula should be used in the initial treatment of lacerations, abrasions, and scalds; immediately after any required debridement and cleaning of a wound; and for generalized inflammation of the mucous membranes. It has shown its usefulness in dermatitis and vaginal, sinus, ophthalmic, and middle and external ear infections over the decades. The application of calendula ointments, tinctures, or fluid extracts depends on the wound. The succus (fluid extract) of the flower should be applied for irrigation of wounds and in ophthalmic uses.
NATURAL PRODUCTS FIRST-AID KIT A natural products first-aid kit should contain a variety of products that are easy to obtain and replace and that have a wide spectrum of use, including herbs ( Box 50-1 ), homeopathic preparations, and vitamin and enzyme supplements ( Table 50-1 ). Homeopathic Medicines Homeopathy can be an excellent source of relief and treatment for emergencies and general first-aid situations. Homeopathic preparations include powders, tablets, tinctures, lotions, ointments, creams, and sprays. The advantages of homeopathy are the ease of administration, lack of toxicity, rapid action, and small volume of material. The disadvantages are the degree of understanding and competence required to become an effective prescriber and the lack of readily available sources of each medicine at most North American pharmacies.
Box 50-1. HERBAL MEDICINES RECOMMENDED FOR FIRST-AID KIT Aloe gel and powder capsules Arnica ointment Calendula gel, ointment and tincture Chamomile tincture Comfrey gel or ointment Echinacea tincture or freeze-dried powder capsules Ephedra freeze-dried powder capsules Goldenseal tincture or ointment Hypericum ointment or tincture Plantain tincture Witch hazel fluid extract or tincture
A kit made exclusively of homeopathic medicines can cover most first-aid emergency situations. For the acute, straightforward injury or malady without a complex presentation, the correct similimum and rapid amelioration of symptoms are not difficult to achieve. This section discusses a few indications for the use of homeopathic medicines and the preparation most often used. Unless otherwise noted, a 6x to 12x potency in lactose pellet form should be given every 15 to 30 minutes immediately after the injury until noticeable improvement occurs. If no effect is noted after the first two doses, one must reconsider the medicine selection. A personal experience exemplifies the relief that can be obtained from an acute injury with the appropriate homeopathic medicine. I was bitten on the lip by a small centipede while sleeping. I instantly experienced swelling and intense burning pain. Local application of ice provided no relief. I chose the homeopathic medicine Apis mellifica in a 6c potency because the wound was shiny and felt hot and swelling was increasing. After sublingual ingestion of two pellets I waited 1 to 2 minutes, still in excruciating pain with no change in symptoms. My next selection was Cantharis in a 6c potency, since a key symptom for this remedy is extreme red and hot burning pain of the face. Less than 30 seconds after administration the pain was almost undetectable. Total relief was obtained within a few minutes after being bitten. For comparison, I have had no homeopathic kit available after other centipede bites, and the pain generally lasted for hours and the residual swelling for days. Reactions from different centipedes can cause different sensations and symptoms, however, so Cantharis may not work for all bites. Proper selection of the similimum or indicated homeopathic medicine requires the ability to note the subtle differences in the way the victim responds to an apparently similar traumatic or toxologic influence. An appropriate homeopathic field guide that lists the specific indications and differentiation for each of the homeopathic remedies should accompany any first-aid kit. Unlike with Western pharmaceutical medications, it is essential to understand the specific homeopathic indications (similimum) for each of the remedies on hand. Without this, the chance of obtaining a successful outcome using homeopathics is small. Practitioners and the homeopathic industry have realized the difficulty of single remedy prescribing, which involves understanding and memorizing the indications
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TABLE 50-1 -- Physiologic Responses from Phytopharmaceuticals PLANT MEDICINES
ANALGESICS ANTIBIOTICS ANTIFUNGALS ANTIINFLAMMATORIES ASTRINGENTS ANTISEPTICS DECONGESTANTS SEDATIVES
Aconitum nopellus
Homeopathic internal
Apis mellifica Arnica montana
Homeopathic topical, internal Homeopathic internal
Homeopathic topical, internal
Botanical topical Arsenicum alfum
Homeopathic internal
Bromalain Calendula
Internal Botanical internal, topical
Botanical topical
Botanical topical Botanical topical
Chamomile
Botanical Botanical internal, topical internal, topical
Comfrey Echinacea
Botanical internal, topical
Botanical topical
Botanical internal
Botanical homeopathic internal
Botanical topical Botanical Botanical Botanical internal, topical internal, topical internal, topical
Botanical internal
Botanical homeopathic topical
Ephedra Goldenseal
Botanical internal Botanical Botanical internal, topical internal, topical
Botanical topical
Botanical internal, topical
Hypericum
Botanical topical Homeopathic internal, topical
Peppermint
Botanical internal, topical
Plantain Rhus toxicodendron
Homeopathic internal
Botanical topical Botanical topical Homeopathic topical, internal
Witch hazel
Botanical topical Botanical topical
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for every homeopathic medicine. Therefore medicines have been developed that combine individual preparations to cover a large number of symptoms and symptom characteristics that typically accompany most ailments. These medicines, known as complex or combination homeopathic preparations, can be very helpful for the new user. Single Preparations and Indications ACONITE.
Tincture of the whole plant with root is derived when monkshood or wolfsbane (Aconitum napellus) begins to flower. Aconite is indicated for acute states of emotional disturbance, including anxiety and intense fear or pain. This is one of the key remedies that should be administered after an acute injury that has dazed, shocked, or frightened the victim. Persons who are fearful or restless, cannot tolerate being touched, and have pain followed by numbness and tingling sensations are most responsive to aconite. Those with sudden onset of fever, nausea, and vomiting and who exhibit symptoms of fear, restlessness, and anxiety may also benefit. APIS.
The original tincture is manufactured from the whole honeybee and from dilutions of the venom (Apis mellifica). Apis is used for insect stings, particularly from bees and related insects, when the wound is swollen, shiny, and hot to the touch. Treatable symptoms from other conditions are histamine reactions (resulting in facial flushing, puffiness or swelling around the mouth, face, and eyes) sunburn, hives, burns, and early stages of abscesses and frostbite. If symptoms include a stinging, burning, or swelling quality and subside by applying cold rather than heat, Apis is the indicated remedy. ARNICA.
The tincture comes from the whole fresh plant, flowers, and dried roots of leopard's bane or Fallkraut (Arnica montana). Arnica is indicated for blunt traumatic wounds (resulting in both deep and superficial hematomas), contusions, swelling, and localized tenderness. This is also effective for sore muscles, as well as sprains, fractures, dislocations, and internal bleeding. I recommend taking a 6x to 30x potency every 15 minutes to 3 hours for the first few days for a severe injury. The more severe the injury, the more frequently the dosage is taken for the first day. As the symptom severity decreases, the medicine is taken less often. Arnica can be helpful in decreasing severity and recovery time. ARSENICUM.
Derived from arsenic trioxide, arsenicum is used for skin rashes (which feel warm but are relieved by hot applications), hay fever, asthma (especially when accompanied by notable anxiety), diarrhea, vomiting, and gastroenteritis (especially from food-borne microbes). HYPERICUM.
The tincture comes from the whole fresh plant and flowers of St John's wort (Hypericum perforatum). Indications include any pain that affects the peripheral or central nervous system and exhibits shooting pains that travel in a dermatomal pattern (e.g., sciatica). Wounds that affect the nerve endings, such as injuries to the fingers, toes, or teeth, are improved by Hypericum. Pain from dental surgery, toothaches, injuries to the coccyx, and first- and second-degree dermal burns are other indications. LEDUM.
Ledum is made from the leaves and stems of the whole fresh plant of wild rosemary (Ledum palustre). Homeopathic indications include puncture wounds from small, sharp objects (e.g., nails, needles) and some mosquito bites when the injured area feels cold, swollen, and numb and pain is relieved by cold application. RHUS.
This homeopathic preparation comes from the leaves and stems of the whole fresh plant of poison ivy (Rhus toxicodendron). This is the remedy of choice for the urticaria caused by poison ivy exposure and is also helpful for some cases of poison oak. Other skin rashes that are red, weeping, blistered, and swollen with itching can be treated with Rhus. It is also effective for the treatment of connective tissue irritations with swelling, stiffness, and tightness. Rhus is often used for overuse injuries (e.g., fasciitis, tendinitis) and some forms of arthritis, especially when the injured area feels better with warm applications and movement. Combination Preparations for Acute Sprains and Strains.
Homeopathic companies have created combination remedies for the general public that can be used without the need for in-depth understanding of homeopathic prescribing. These remedies are designed to cover a broad range of symptoms associated with acute ailments and trauma-induced medical conditions. Traumeel (Heel Biotherapeutics, Albuquerque, NM) is a combination homeopathic formula that is effective in the treatment of trauma and inflammatory changes affecting skin, connective tissue, and muscle. The preparation comes in liquid, tablet, and ointment form. Traumeel includes remedies indicated for traumatic injuries (sprains, strains, contusions) and the resulting pain, swelling, and ecchymoses. Many German studies have demonstrated its effectiveness.[27] Traumeel may be the primary homeopathic medicine chosen for the first-aid kit because of its wide range of application and multiple delivery system. Herbal Combination Formulas
Acute Gastroenteritis.
In the tradition of Chinese herbal medicine, many formulas have been developed over the centuries to treat acute ailments. Many of these
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formulas were kept secret from the general populace and reserved for the nobility and ruling class. As the field of Chinese herbology developed and became more accessible to the general populace, some of the secret formulas have been mass produced into convenient pill form known as patent medicines. Many of these are extremely useful for acute conditions. Pill Curing (Kang Ning Wan, "Healthy Quiet Pill"), botanically called Coix Formula, consists of 16 herbal medicines that are collectively effective for relieving the disturbances caused by motion sickness, food poisoning, overeating, excessive alcohol consumption (nausea, headache, vomiting) difficulty passing stool or loose stools, and GI cramping and pain. Coix Formula is currently produced in a convenient globule form (Metagenics, San Clemente, Calif). One or two capfuls of globules are swallowed with warm water every hour until symptoms improve. Relief should occur within 4 hours of administration. Acute Hemorrhagic Conditions.
The product Yunnan Bai Yao ("Yunnan White Medicine"), produced in the western Chinese province of Yunnan, has been used for centuries as a first-line approach to trauma that results in internal or external bleeding. It is prescribed in China for excessive menstrual cramps and bleeding, bleeding ulcers, trauma-induced swelling, bleeding wounds, and allergic reactions to insect bites. It comes in powder (4-g bottles) and capsule (packets of 20) form and contains one red pellet that is to be ingested only for serious bleeding conditions. Dosage is 1 to 2 capsules four times per day. The powder can be applied externally after the wound has been properly cleaned. This product is exclusively produced in China from a proprietary formula and can be obtained from most Chinese herbal pharmacies. Nutritional Supplements For immune system support, antiinflammatory action, and pain relief, many natural products in the nutritional supplement category have proved to be effective agents. Bromelain.
Bromelain is a naturally occurring proteolytic enzyme found in pineapple that is used to reduce pain and swelling after sprains and strains of soft tissues. Ingested on an empty stomach, the complex proteases in bromelain are absorbed intact and have significant antiedema, antiinflammatory, and coagulation-inhibiting effects. Bromelain shows fibrinolytic activity and acts to inhibit fibrinogen synthesis, decreasing kininogen and bradykinins.[100] For treatment of injuries and postsurgical recovery, 125 to 400 mg is ingested three times daily at 30 minutes before or 90 minutes after a meal. Bromelain is nontoxic even at high doses and is generally prepared as 100-mg tablets. Papain.
As with bromelain, papain is a naturally occurring plant enzyme (papaya fruit) that exhibits proteolytic activity. Papain is generally used externally to neutralize bee, ant, or wasp venom. Papain is available as commercial meat tenderizer (e.g., Adolph's) or in tablet form. After removal of the stinger, a thick paste is prepared from water and tenderizer or from five or six crushed tablets and applied to the area as soon as possible. Vitamin C.
Ascorbic acid has both wound-healing and antiinflammatory effects. Vitamin C is required for hydroxylation of proline and subsequently for the synthesis of strong collagen. Studies have shown that the stress associated with injury and wound healing results in an increased need for vitamin C.[106] For acute trauma and acute upper respiratory allergy, vitamin C in larger dosages (2 to 5 g/day in divided doses) can greatly reduce anaphylactic reactions and recovery time.[68] Therefore, for any traumatic event, high-dose vitamin C should be administered as part of the treatment.
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APPENDIX
Companies Nature's Apothecary 997 Dixon Rd Boulder, CO 80302 800-999-7422 Small herbal kits include Dental Poultice Pac for toothaches and abscesses, Clear Eyes Eyewash Kit (including Eyebright Euphrasia extract), and reformulated Home Herbal Medicine Kit. Boiron 1208 Amosland Rd PO Box 54 Norwood, PA 19074 800-258-8823 Natural Home Health Care LeKit contains 36 single-remedy medicines in distinctive blue tubes, including the commercial flu remedy Oscillococcinum. The home kit also contains four external remedies: tinctures of Calendula and Hypericum and ointments of Arnica and Calendula. Travel LeKit is a more compact collection of single remedies (22 multidose and 16 unit-dose tubes) plus the flu remedy. Dolisos America 3014 Rigel Ave Las Vegas, NV 89102 702-871-7153, 800-365-4767 Single Remedy Family Kit contains 48 single remedies, a Flu-Solution remedy, Calendula ointment and tincture, and Arnica cream. The 48 combination Energy Medicine Kit includes remedies for bruises, insect bites, and poison ivy.
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Biological Homeopathic Industries (BHI) 11600 Cochiti S.E. Albuquerque, NM 87123 800-621-7644 BHI is the U.S. distributor of the German line of complex homeopathic remedies manufactured by Heel.
Books Natural Health and Medicine Encyclopedia of Natural Medicine by Michael Murray, and Joseph Pizzorno, Rocklin, Calif, 1991, Prima Publishing. Health and Healing: Understanding Conventional and Alternative Medicine by Andrew Weil, Boston, 1983, Houghton Mifflin. The Natural Remedy Bible by John Lust, and Michael Tierra, New York 1990, Pocket Books. Herbs and Herbalism The Healing Power of Herbs by Michael Murray, Rocklin, Calif, 1991, Prima Publishing. Herbal Medicine by Rudolph Fritz Weiss, Beaconsfield, England, 1988, Beaconsfield Publisher. Homeopathy Books Boericke's Materia Medica with Repertory by William Boericke, and Oscar Boericke, New Dehli, India, 1991, B. Jain Publishing. The Homeopathic Emergency Guide by Thomas Kruzel, Berkeley, Calif, 1992, North Atlantic Books/Homeopathic Education Services. Homotoxicology by Hans Rekeweg, Albuquerque, NM, BHI. Sports & Exercise Injuries: Conventional, Homeopathic & Alternative Treatments by Steven Subotnick, Berkeley, Calif, 1991, North Atlantic Books.
Further Information Practitioners American Association of Naturopathic Physicians 601 Valley St, Suite 105 Seattle, WA 98109 206-323-7610 www.naturopathic.org Herbal Medicines Herb Research Foundation 1007 Pearl St, #200F Boulder, CO 80302 303-449-2265 Homeopathy
International Foundation for Homeopathy 2366 Eastlake Ave E, #329 Seattle, WA 98102 206-324-8230 Nutritional Products Thorne Research 25820 Highway 2 West PO Box 25 Dover, ID 83825 800-228-1966 Metagenics 100 Avenida La Pata San Clemente, CA 92673 800-692-9400 PhytoPharmica 825 Challenger Dr PO Box 1745 Green Bay, WI 54305 800-553-2370
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Part 8 - Food and Water
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Chapter 51 - Field Water Disinfection Howard D. Backer
Waterborne disease is a risk for international travelers who visit countries that have poor hygiene and inadequate sanitation and for wilderness users relying on surface water in any country, including the United States. Natural water may be contaminated with organic or inorganic material from land erosion, dissolution of minerals, decay of organic vegetation, biologic organisms that reside in soil and water, industrial chemical pollutants, and microorganisms from animal or human biologic wastes.[38] [67] Fecal pollution with enteric pathogens is the primary reason for disinfecting drinking water. However, chemical contamination of groundwater is increasing at an alarming rate in the United States and worldwide from industrial, agricultural, and individual sources. Of the 1700 million square miles of water on earth, less than 0.5% is potable. [221] According to the National Water Quality Inventory Report by the U.S. Environmental Protection Agency (EPA), as of 1994, about 40% of the nation's surveyed rivers, lakes, and estuaries are too polluted for basic uses such as fishing and swimming. Natural organic and inorganic material may not cause illness but can impart unpleasant turbidity, color, and taste to the water. Appearance, odor, and taste are not reliable to estimate water safety.
ETIOLOGY Infectious agents in contaminated drinking water with the potential for waterborne transmission include bacteria, viruses, protozoa, and parasites ( Box 51-1 ). The number of pathogenic microorganisms capable of waterborne transmission is more than 100 and similar to that of potential etiologic agents of travelers' diarrhea. Separating the contribution of waterborne transmission of these pathogens from food-borne and person-to-person transmission is impossible. The latter two are probably more common. The source of fecal contamination in water may be either human or animal. Some bacterial pathogens (Shigella, Salmonella typhosa) occur exclusively in human feces, whereas others (Yersinia, Campylobacter, nontyphoidal Salmonella) may be present in wild or domestic animals. The enteric viruses seem to occur exclusively in human feces. No enteric viruses excreted by animals have been shown to be pathogenic to humans.[162] The major source of these enteric pathogens is fecal contamination from infected human residents. Legionella pneumophila and Vibrio cholerae exist as natural organisms in water. However, the mode of transmission of Legionella is inhalation of aerosolized water.[194] No evidence exists of human immunodeficiency virus (HIV) transmitted via a waterborne route, and no epidemiologic evidence exists of casual transmission by fomites or by any environmentally mediated mode.[168] Viruses Hepatitis A virus (HAV), Norwalk virus, and rotavirus are the main viruses of concern for potable water supplies; the last two are responsible for about 77% of acute waterborne gastroenteritis.[221] In addition to HAV, waterborne transmission of hepatitis E is suspected in outbreaks among travelers from Asia.[26] [100] During 1993 and 1994 an explosive waterborne epidemic of hepatitis E virus occurred in Islamabad, Pakistan, with about 4000 cases of acute icteric hepatitis.[185] Many other viruses are capable and suspected of waterborne transmission, and more than 100 different virus types are known to be excreted in human feces.[72] [175] The most frequent waterborne illness (acute infectious nonbacterial gastroenteritis of unknown etiology) in the United States may be caused by undetected viruses.[43] [119] [189] Protozoa Six protozoa cause enteric disease and may be passed via waterborne transmission: Giardia lamblia, Cryptosporidium parvum, Entamoeba histolytica, Cyclospora cayetanesis, Isospora belli, and the microsporidia. [118] The first two are the most important for wilderness travelers. Cryptosporidium is a recently recognized enteric pathogen.[27] Many aspects of the epidemiology and transmission appear similar to Giardia; large waterborne outbreaks of Cryptosporidium have been documented.[25] [49] [78] Waterborne transmission of E. histolytica is common in developing countries. Cyclospora has been epidemiologically linked to waterborne transmission in the United States and in Nepal, but the reservoir and host range are not known. Unlike Giardia and Cryptosporidium, Cyclospora is not infectious when passed in feces and requires up to two weeks in the laboratory to sporulate.[187] Surface water is a common environmental source for microsporidia, however, the route of infection is unknown. Naegleria fowleri is a waterborne protozoan that enters the body through the nasal epithelium during swimming in contaminated surface water and causes meningoencephalitis.
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Box 51-1. WATERBORNE ENTERIC PATHOGENS
BACTERIAL Escherichia coli Shigella Campylobacter Vibrio cholerae Salmonella Yersinia enterocolitica Aeromonas
VIRAL Hepatitis A Hepatitis E Norwalk virus Poliovirus Miscellaneous enteric viruses (more than 100 types: adenovirus, enterovirus, calcivirus, ECHO, astrovirus, coronavirus, etc.)
PROTOZOAL Giardia lamblia Entamoeba histolytica Cryptosporidium Blastocystis hominis Isospora belli Balantidium coli Acanthamoeba Cyclospora
Balantidium coli Acanthamoeba Cyclospora
PARASITIC Ascaris lumbricoides (roundworm) Ancylostoma duodenale (hookworm) Taenia spp. (tapeworm) Fasciola hepatica (sheep liver fluke) Dracunculus medinensis (Guinea tapeworm) Strongyloides stercoralis Trichuris trichiura (whipworm) Clonorchis sinensis (Oriental liver fluke) Paragonimus westermani (lung fluke) Diphyllobothrium latum (fish tapeworm) Echinococcus granulosus (hydatid disease)
Data from Drinking Water Health Effects Task Force, US Environmental Protection Agency: Health effects of drinking water treatment technologies, Chelsea, Mich, 1989, Lewis; and Gelreich EE: Microbiological quality of source waters for water supply. In McFeters GA, editor: Drinking water microbiology, New York, 1990, Springer-Verlag.
Parasitic Organisms Parasitic organisms other than Giardia and E. histolytica are seldom considered in discussions of disinfection. Infectious eggs or larvae of many helminths are found in sewage, even in the United States.[164] [184] The frequency of infection by waterborne transmission is unknown, since food and environmental contamination or skin penetration is more prevalent.[228] The most obvious risk is from nematodes with no intermediate hosts that are infectious immediately or soon after eggs are passed in stool. Ascaris lumbricoides (roundworm) is transmitted by ingestion of the eggs in contaminated food or drink. In endemic areas, 85% of the population is infected; this leads to daily global environmental contamination by 9 × 1014 eggs. [228] Ancylostoma duodenale (hookworm) usually infects as larvae penetrate the skin of the foot, but it also may be acquired by mouth. Oral entry of the larvae causes pulmonary (Wakana) disease. Necator americanus does not appear to be infectious via the oral route. Taenia solium (pork tapeworm) is infectious to humans in cyst or egg form. Eggs passed in stool are ingested in food or water and develop into tissue cysts, often in the brain, resulting in cysticercosis. Echinococcus granulosus (dog tapeworm) can use humans as intermediate hosts. Eggs from the feces of an infected dog or other carnivore are ingested in food and water. Hydatid disease generates cysts in the liver, peritoneum, and other sites. Fasciola hepatica (liver fluke of herbivores and humans) is normally acquired by ingestion of encysted metacercariae on water plants or free organisms in water. Cercariae of schistosomiasis, which live in fresh water and normally enter through skin, can enter through the oral mucosa. The cercariae are killed by stomach acid. Dracunculus medinensis (Guinea tapeworm) is a tissue nematode of humans and causes the only such disease transmitted exclusively through drinking water.[218] Dracunculus larvae are released in water from subcutaneous worms on the legs of infected bathers or water-gatherers. Larvae are ingested by a tiny crustacean (Cyclops species), which acts as the intermediate host and releases infectious larvae when ingested by humans. Bacterial Spores Bacterial spores can cause serious wound and gut infections but are not likely to be waterborne enteric pathogens. Clostridium is ubiquitous in soil, lake sediment, tropical water sources, and the stool of animals and humans.[79] [183] C. botulinum and C. perfringens type A food poisoning are not waterborne because they require germination of spores in food by inadequate cooking, then production of an enterotoxin, which is ingested. C. perfringens type C causes enteritis necroticans,
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probably through in vivo production of an enterotoxin, and thus has the potential for waterborne transmission in the tropics. However, the epidemiology of these infections, as in infant botulism, is related to food-borne sources in the United States. Chemical Hazards Chemical hazards are also becoming an alarming source of pollution in surface water. In the United States, chemical contamination is routinely responsible for about 30% of waterborne gastroenteritis where an etiology can be identified. [30] [31] Most common sources include lead that leaches into water lines, as well as copper, nitrate, fluoride, and a variety of other chemicals. Industrialization proceeds worldwide without adequate environmental protection. A vast array of toxins are sold with little concept of safe use and no means of safe disposal. Inorganic chemicals in drinking water include common salts, heavy metals, asbestos, fluorides, nitrates, radionuclides, and some heavy metals (arsenic, copper, iron, lead, selenium). Natural organic chemicals predominate from soil runoff, forest canopy aquatic biota, and human and animal wastes. Synthetic organic matter includes pesticides, herbicides, and chemicals from industrial or human activities.[53] Major underground aquifers are becoming contaminated. Streams and rivers in rural areas are contaminated by individual carelessness, leaching landfills, and agricultural runoff. Atmospheric spread has resulted in pesticides being found in remote wilderness lakes and in the well-publicized acid rain. Numerous pesticides have been found in runoff and rivers in agricultural areas of the Midwest.[125] Wilderness users may soon need to ensure removal of chemical, as well as microbiologic, contaminants.
RISK EVALUATION Risk of waterborne illness depends on the number of organisms consumed, which is determined by the volume of water, concentration of organisms, and treatment system efficiency.[42] [89] Additional factors include virulence of the organism and defenses of the host. Infection and illness are not synonymous; the overall likelihood of illness from multiple studies for all three categories of microorganisms (bacterial, viral, protozoan) is 50% to 60%. Death is unlikely except with specific organisms (e.g., Escherichia coli O157:H7, Vibrio cholerae), hepatitis E in pregnant women, and Cryptosporidium with underlying malnutrition. Total immunity does not develop for most enteric pathogens and reinfection may occur.[89] Waterborne outbreaks do not give a complete picture of the potential for waterborne illness. Most outbreaks of waterborne disease are not identified because not enough people become ill, providing an insensitive mechanism for detecting water contamination. When an outbreak is identified, it is very difficult to prove TABLE 51-1 -- Estimated Infectious Dose of Enteric Organisms INFECTIOUS DOSE
ORGANISM Salmonella
105
Shigella
102
Vibrio
103
Enteric viruses
1–10
Giardia
10–100
Cryptosporidium 10–100 (?) conclusively that the source was waterborne. The supply may have been only transiently contaminated; water samples from the time of exposure are seldom available; some organisms are difficult to detect; and almost everyone has some exposure to water. [204] The data on concentration of microorganisms in surface water show widely varying values, but the testing is insufficient for risk assessment and dose-response models. Instead, infectious dose data and statistical techniques have been used to devise models for determining risk ( Table 51-1 ).[89] These cannot be applied unless the microbial content of water is known. Few water sites are monitored. The excretion and loading of microbial contaminants are dynamic and change over time. Pathogenic microorganisms clearly exist in most raw source waters, especially in surface waters. [53] Most microbiologic testing is done on community water intake sources and sewage treatment effluent. Less information is available for more remote water sources.[42] [175] [227] Protozoan cysts can be found even in pristine water, but their levels are a small fraction of the number in polluted water.[177] Recreational Contact Inadvertent ingestion during recreational water contact is a risk for swimmers and white-water boaters. The microorganisms that cause infection require only a small dose. Recreational water activities have resulted in giardiasis, cryptosporidiosis, typhoid fever, salmonellosis, shigellosis, viral gastroenteritis, and hepatitis A, as well as in wound infections, septicemia, and aspiration pneumonia due to Legionella. [43] From 1993 to 1994, 36 outbreaks of gastroenteritis (excluding hot tub dermatitis) from recreational water were reported. Sixteen outbreaks were caused by Cryptosporidium, four by Giardia, six by E. coli O157:H7, three by Shigella sonnei, and one by Norwalk virus.[31] Six isolated cases of primary amebic meningoencephalitis (Naegleria fowleri) were reported, with 100% fatality. Underdeveloped Countries In tropical areas and developing countries, water has a complex relationship with spread of disease. Table 51-2
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TABLE 51-2 -- Water and Spread of Disease EXAMPLES
TYPE
MECHANISM
PREVENTION
Waterborne
Fecal contamination of drinking water by infectious organisms
Typhoid fever, cholera, campylobacteriosis, giardiasis, hepatitis A
Sanitation and disinfection of water
Water washed
Person-to-person fecal-oral spread via direct contact, food, or water (all these are also waterborne)
Shigellosis, amebiasis, ascariasis, eye and skin infections
Handwashing and personal hygiene
Water based Organism or agent that lives in water
Schistosomiasis, dracunculosis, parasitic worms
Prevention of exposure from bathing
Water related Spread by insects that breed in water or collecting water
Malaria, sleeping sickness, yellow fever, dengue
Insect protection and piped water
Modified from Bradley DJ: Health aspects of water supplies in tropical countries. In Feachem R et al, editors: Water, wastes and health in hot climates, New York, 1977, Wiley. presents a useful classification, and Steiner et al[195] proposed adding the category "water carried" for infections resulting from accidental ingestion in recreational water. Worldwide, 1.5 billion rural people and 200 million urban people in the world lack safe drinking water and adequate sanitation. An estimated 80% of the world's diseases are linked to inadequate water supply and sanitation. Between 10 and 25 million people die each year (28,000 to 68,000 persons each day) from diseases caused by contaminated water and unsanitary conditions. In undeveloped countries, these illnesses account for 1 billion cases of diarrhea every year and 95% of deaths in children under 5 years of age.[79] [218] Of the four diseases that may cause the most morbidity and death in underdeveloped parts of the world—cholera, hepatitis, malaria, and typhoid—malaria is the only one that is not waterborne.[89] The sanitary situation in many undeveloped countries is illustrated by current statistics from Peru evaluated during a recent cholera epidemic. Only 73% of the urban population have access to a water distribution system and only 50% to sanitation services. In rural areas, only 23% have access to a water supply and 6% to a sanitation system. In urban areas over the past 5 years the quality of water has deteriorated because of the lack of water treatment chemicals, laboratories for monitoring, and operators to control the processes. Institutional barriers impede improvements for adequate water and sanitation systems.[44] The statistics for Egypt are only slightly better. In certain tropical countries the influence of high-density population, rampant pollution, and absence of sanitation systems means that available raw water is virtually wastewater.[35] Contamination of tap water must be assumed because of antiquated and inadequately monitored disposal, disinfection, and distribution systems. Water from springs and wells and even commercial bottled water may be contaminated with pathogenic microorganisms.
Box 51-2. ENTERIC PATHOGENS IN U.S. WILDERNESS OR RECREATIONAL WATER
OFTEN REPORTED Giardia Cryptosporidium
OCCASIONALLY REPORTED, WITH FIRM EVIDENCE FOR WATERBORNE Campylobacter Hepatitis A Hepatitis E Enterotoxigenic Escherichia coli E. coli O157:H7 Shigella Enteric viruses
UNUSUAL OCCURRENCES, WATERBORNE SUSPECTED Yersinia enterocolitica Aeromonas hydrophila Cyclospora
United States Waterborne pathogens account for most outbreaks of infectious diarrhea acquired in U.S. wilderness and recreation areas ( Box 51-2 ). From 1920 to 1980, 178 waterborne outbreaks caused by use of contaminated, untreated surface water or groundwater were reported in systems serving parks, campgrounds, and recreation areas.[43] Between 1970 and 1990, gastroenteritis of undefined etiology accounted for most cases overall, while Giardia caused the most cases of defined etiology.[43] [81] A distinct seasonal variation is seen, with the majority of cases from recreational areas occurring during summer months.[43] This is probably a result of both
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increased contamination and number of persons at risk. Between 1993 to 1996, Giardia continued to be one of the most common waterborne infections, but Cryptosporidium epidemics were being identified with increasing frequency in both public and surface water supplies.[78] [174] An outbreak of Cryptosporidium in a public water supply in Milwaukee affected more than 400,000 people.[115] A surface water outbreak occurred at Lake Mead. During this period, bacteria linked to water ingestion included Salmonella, Campylobacter, Shigella sonnei, Plesiomonas shigelloides, and another emerging pathogen, E. coli O157:H7.[30] [31] Enteric bacteria are still associated with 12% of waterborne outbreaks in the United States.[177] Viruses Testing in the United States, Europe, and developing countries shows consistent, sometimes astounding, degrees of viral contamination of drinking and surface water.* Even remote surface lakes and streams tested in California showed disturbing levels of viral contamination.[72] Widespread enteric viral contamination was found at multiple sites in a popular recreation canyon in Arizona. Viruses included poliovirus, echovirus, coxsackievirus, rotavirus, and other unidentifiable viruses, and exceeded the recommended state level for recreational water use in several areas. Virus levels correlated with human activity but not with excess levels of standard coliform indicators.[175] All surface water supplies in the United States and Canada contain naturally occurring human enteroviruses.[221] The infectious dose of enteric viruses is only a few infectious units in the most susceptible people.[119] [217] [227] Protozoa New methods to detect Giardia cysts in surface water have found widespread contamination[91] [169] [193] ( Table 51-3 ). Cysts have been found as frequently in pristine water and protected sources as in unprotected waters.[82] [176] Repeated sampling of "negative" sources invariably produced positive results. A zoonosis with Giardia is known, but with at least three different species, the extent of cross-species infection is not clear.[12] [225] Many of the species apparently capable of passing Giardia cysts to humans, including dogs, cattle, ungulates (deer), and beaver, are present in wilderness areas. Forty percent of beaver in Colorado were infected and shedding 1 × 108 cysts per animal per day. All 386 muskrats found were infected. Up to 20% of cattle examined were infected.[82] Beaver have been implicated in multiple municipal outbreaks of giardiasis. Samples from Rocky Mountain National Park[106] [128] and the California Sierra Nevada[193] [197] show a direct correlation between numbers of cysts and levels of human use or beaver habitation. In Yukon, Canada, 13 of 61 scat samples from various wild animals yielded Giardia cysts.[170] Ten G. lamblia cysts may result in infection, although the infections in this widely quoted study were asymptomatic. [165] Even with a low infectious dose, the environmental cyst recovery data indicate that the risk of ingesting an infectious dose of Giardia cysts is small.[230] [231] However, the likely model that poses a risk to campers is pulse contamination-a brief period of high cyst concentration from fecal contamination. Beaver stool and human stool may contain 1 × 106 cysts/g. Stream contamination from a beaver has been calculated to reach 245 cysts/gallon.[91] In this instance, small amounts of water may cause infection, similar to an outbreak among lap swimmers from inadvertent water ingestion in a fecally contaminated pool. [152] Cryptosporidium oocysts are found widespread in surface water, and the cyst is durable in the environment. A large zoonosis is evident. Environmental occurrence appears ubiquitous.[173] [174] Cryptosporidium is now found more frequently than Giardia in surface water, but in smaller numbers. Persistence of Enteric Pathogens Once environmental contamination has occurred, a natural inactivation or die-off begins. However, enteric pathogens can retain viability for long periods ( Table 51-4 ).[53] [177] Factors promoting survival of microorganisms are pH near neutral (between 6 and 8) and cold temperatures, which explain the risk of transmission in mountain regions. In temperate and warm water, survival is measured in days, with densities of infectious agents decreasing by 90% every 60 minutes. However, tropical water differs from temperate in nutrients, creating a microbiologically rich environment. Coliform bacteria can survive several months in natural tropical river water and may even proliferate. Survival of other bacteria is also much longer (about 200 hours in tropical compared with 30 hours in temperate water). E. coli and Vibrio cholerae may
occur naturally in tropical waters and are capable of surviving indefinitely.[44] [79] [148] Most enteric organisms, including Shigella, resist freezing.[52] Salmonella typhosa (typhi) can survive for up to 5 months in frozen debris and ice. [221] HAV survives 6 months at below-freezing temperatures. [203] Cryptosporidium may be able to survive a week or more in home freezers.[195] Natural Purification Mechanisms It is widely believed that streams purify themselves and that certain water sources are reliably safe for drinking. These concepts have some truth but do not preclude the need for disinfection to ensure water quality. *References [ 40]
[ 67] [ 72] [ 119] [ 189] [ 227]
.
1191
SOURCE
TABLE 51-3 -- Giardia Cysts and Cryptosporidium Oocysts in North American Surface Water POSITIVE SAMPLES NUMBER OF CYSTS
REFERENCE
GIARDIA Surface water from 301 municipalities in the U.S. Pristine surface waters Unprotected watersheds
798 of 4423
[176]
0.4–5 cysts/100 L 0.33–104 cysts/100 L Rocky Mountain National Park, California Sierra Nevada
44% in high-use areas
Average 3–10 cysts/1000 L, up to 100–600 cysts/1000 L (not adjusted for 10%–30% recovery rate)
[106] [128] [193] [197]
3 pristine rivers and 12 tributaries in Pacific Northwest
94/224 (42%) samples over 9 months
0.1–5.2 cysts/L (adjusted for 22% recovery rate)
[143]
3 high-quality surface creeks in California and Washington
1.3–6 cysts/gallon
[143A]
Yukon Canada pristine surface water
7/22
[170]
Raw surface water entering U.S. treatment plants
87%
[195]
Surface water samples from 17 states
55% of 257 samples positive (39% from pristine sources positive)
0.43 oocysts/L
[176]
Western U.S.
77% rivers, 75% lakes, 28% treated drinking water samples
Average 0.02–1.3 oocysts/L; pristine areas: 0.02–0.08/L; streams and rivers: 0.58–0.91/L
[143A]
Yukon water
None found in pristine water but some found in water that received sewage effluent
CRYPTOSPORIDIUM
[170]
ORGANISM
TABLE 51-4 -- Viability of Enteric Pathogens in Water CONDITIONS SURVIVAL
Vibrio cholerae
Cold
4–5 weeks
Tropical
> 1 year
Cold
3–5 weeks
[18]
Temperate stream
3–10 days
[186]
Temperate stream
13 hours
[186]
Tropical
> 1 year
[148]
Salmonella
Temperate stream
Half-life 16 hours
[148]
Yersinia
Temperate stream
540 days
[186]
Shigella
Temperate stream
Half-life 22 hours
[186]
Freeze/thaw
Yes
[54]
Enteric pathogens
Freeze/thaw
Yes
[52]
Salmonella typhosa
Ice/frozen debris
5 months
Viruses
Cold
17–130 days
Enteric viruses
15°–25° C water
6–10 days
[177]
4° C water
30 days
[177]
Cold
1 year
Fresh, sea, wastewater
12 weeks
[16]
< 0° C
6 months
[203]
Cold
2–3 months
[15] [51]
15° C lake, river
10–28 days
[51]
Entamoeba histolytica
Cold
3 months
[34]
Microsporidia
4° C
> 1 year
Cryptosporidium
Cold
12 months
[48]
Ascaris eggs
Wet or dry
6–9 years
[228]
Hookworm larvae
Wet sand
122 days
[228]
Campylobacter Escherichia coli
Hepatitis A virus
Giardia
REFERENCES [60] [148]
[221] [182] [227]
[16] [203]
[118]
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Surface water is subject to frequent, dramatic changes in microbial quality as a result of activities on a watershed. Storm water causes deterioration of source water quality by increasing suspended solids, organic materials, and microorganisms. Some of these contaminants are carried by rain from the atmosphere, but most come from ground runoff. In water sources downstream from towns or villages, storms may overload sewage facilities and cause them to discharge directly into the receiving
water. However, rainwater can also flush streams clean by dilution and by washing microbe-laden bottom sediments downstream.[67] [79] Every stream, lake, or groundwater aquifer has limited capacity to assimilate waste effluents and storm water runoff entering the drainage basin. Self-purification is a complex process that involves settling of microorganisms after clumping or adherence to particles, sunlight providing ultraviolet destruction, natural die-off, predators eating bacteria, and dilution. Environmental factors include water volume and temperature, hydrologic effects, acid soil contact, and solar radiation. The process is time dependent and less active during wet periods and winter conditions. Hours needed in flow time downstream to achieve a 90% bacterial kill by natural self-purification vary with pollution inflow and rate of water flow. They have been measured at approximately 50 hours in the Tennessee River in summer, 47 hours in the Ohio River in summer, and 32 hours in the Sacramento River. [67] Storage in reservoirs or lakes also improves microbiologic quality, with sedimentation as the primary process. A 100- to 1000-fold increase in fecal coliform bacteria can be found in bottom sediments compared with overlying water. This removal must be considered temporary, influenced by recirculation of organisms trapped in bottom sediments.[51] [66] In optimal conditions, 10 days of reservoir storage can result in 75% to 99% removal of coliform bacteria and 30 days can produce safe drinking water. Generally, 80% to 90% of bacteria and viruses are removed by storage, depending on inflow and outflow, temperature, and no further contamination. Cysts, with a larger size and greater weight, should settle even faster than bacteria and viruses.[3] Groundwater is generally cleaner than surface water because of the filtration action of overlying sediments, but wells and aquifers can be polluted from surface runoff. Spring water is generally of higher quality than surface water, provided that the true source is not surface water channeling underground from a short distance above the spring. Drawing conclusions from the preceding factors is difficult. The major factor governing the amount of microbe pollution in surface water is human and animal activity in the watershed. The settling effect of lakes may make them safer than streams, but care should be taken not to disturb bottom sediments when obtaining water. Benefits of Water Treatment Methods for treating water are found in Sanskrit medical lore, and pictures of apparatus to purify water appear on Egyptian walls from the fifteenth century BC. Boiling and filtration through porous vessels, sand, and gravel have been known for thousands of years. The Greeks and Romans also understood the importance of pure water.[127] Safe and efficient treatment of drinking water was one of the major public health advances of the twentieth century.[195] As the percentage of the U.S. urban population served by water treatment utilities increased after 1900, the annual death rate from typhoid decreased. Drinking water treatment processes provide enormous benefits with minimal risk. Without disinfection and filtration, waterborne disease would spread rapidly in most public water systems served by surface water.[43] [53] Disinfection alters the incidence of certain enteric diseases but does not eliminate diseases. In underdeveloped countries, improving water quality decreases incidence of diarrhea and improves health status.[7] [90] Standards Because coliforms originate primarily in the intestinal tracts of warm-blooded animals, including humans, they are used as indicators of possible fecal contamination.[79] Although compelling reasons exist for testing other organisms before determining the safety of drinking water, cost and relative difficulty in testing for viruses and protozoa are major obstacles to expanding routine water testing. Coliforms remain the worldwide standard indicator organism. Only recently have U.S. regulations stated that testing must be done for specific organisms, mainly Cryptosporidium. In the future, molecular probes should make this process much easier.[127] The basic federal law pertaining to drinking water is the 1974 Safe Drinking Water Act, which was expanded and strengthened by amendments in 1977, 1986, and 1996.[127] The U.S. Public Health Service recommendations for potable water specify a mean of one coliform organism/100 ml of water, or 10 organisms/L. Absolute limits are three coliform bacteria/50 ml, four/100 ml, and 13/500 ml.[214] In 1989 the standards for detection of fecal coliform bacteria in drinking water were relaxed slightly in recognition that coliform bacteria occur in large numbers in many water distribution systems that have no problem with waterborne disease.[212] Generally the goal is to achieve a 3- to 5-log reduction in the level of microorganisms. Treatment must reduce Giardia by 99.9% (3 log) and enteric viruses by at least 99.99% (4 log).[161] All standards acknowledge the impracticality of trying to eliminate all microorganisms from drinking water; they allow a small risk of enteric infection.[189] Risk models are used to predict levels of illness and desired levels of reduction. For example, EPA guidelines suggest Giardia cyst removal
1193
with the goal of ensuring high probability that consumer risk is no more than one infection per 10,000 people per year.[162] The concept of risk is important for wilderness travelers as well, since it is impossible to know the risk of drinking the water in advance and not practical to eliminate all risk with treatment. Definitions Disinfection, the desired result of field water treatment, means the removal or destruction of harmful microorganisms. Technically, it refers only to chemical means such as halogens, but the term can be applied to heat and filtration. Pasteurization is similar to disinfection but specifically refers to the use of heat, usually at temperatures below 100° C (212° F) to kill most pathogenic organisms. Disinfection and pasteurization should not be confused with sterilization, which is the destruction or removal of all life forms.[107] The goal of disinfection is to achieve potable water, indicating only that a water source, on average over a period of time, contains a "minimal microbial hazard," so that the statistical likelihood of illness is acceptable. Water sterilization is not necessary, since not all organisms are enteric human pathogens.[84] Purification is the removal of organic or inorganic chemicals and particulate matter to remove offensive color, taste, and odor. It is frequently used interchangeably with disinfection, but purification may not remove or kill enough microorganisms to ensure microbiologic safety.[218]
HEAT Heat is the oldest means of water disinfection. It is used worldwide by residents, travelers, and campers to provide safe drinking water. In countries with normally safe drinking water, it is often recommended as backup in emergencies or when water systems have become contaminated by floods or a lapse in water treatment plant efficacy. Fuel availability is the most important limitation to using heat. One kilogram of wood is required to boil 1 L of water.[35] For wilderness travelers without access to wood, liquid fuel is heavy. Heat inactivation of microorganisms is exponential and follows first-order kinetics. Time plotted against temperature yields a straight line when plotted on a logarithmic scale.[96] Thus the thermal death point is reached in shorter time at higher temperatures, whereas lower temperatures are effective with a longer contact time. Pasteurization uses this principle to kill enteric food pathogens and spoiling organisms at temperatures between 60° and 70° C (140° and 158° F), well below boiling.[64] Therefore the minimum critical temperature is well below the boiling point at any terrestrial elevation. Microorganisms have varying sensitivity to heat; however, all common enteric pathogens are readily inactivated by heat ( Table 51-5 ). Bacterial spores (e.g., Clostridium species) are the most resistant; some can survive 100° C (212° F) for long periods but, as discussed, are not likely to be waterborne enteric pathogens. Protozoal cysts, including Giardia and Entamoeba histolytica, are the most susceptible to heat. Cryptosporidium is also inactivated at these lower pasteurization levels. Parasitic eggs, larvae, and cercariae are all susceptible to heat. For most helminth eggs and larvae, which are more resistant than cercariae and Cyclops, the critical lethal temperature is 50° to 55° C (122° to 131° F). [184] Common bacterial enteric pathogens (E. coli, Salmonella, Shigella) are killed by standard pasteurization temperatures of 55° C (131° F) for 30 minutes or 65° C (149° F) for less than 1 minute.[64] [137] Recent studies confirmed safety of water contaminated with V. cholerae and E. coli after 10 minutes at 60° to 62° C (140° to 143.6° F) or after boiling water for 30 seconds.[76] [166] Viruses are more closely related to vegetative bacteria than to spore-bearing organisms[96] and are generally inactivated at 56° to 60° C (132.8° to 140° F) in less than 20 to 40 minutes. [2] [149] [199] Inactivation at higher temperatures is similar to that of vegetative bacteria. Death occurs in less than 1 minute above 70° C (158° F). This has been confirmed in milk products, despite some degree of thermal protection from particles.[198] Given its environmental stability and clinical virulence, hepatitis A virus is a special concern. It should respond to heat as do other enteric viruses, but data indicate that it has greater thermal resistance. Widely varying data probably result from different models for virus infectivity and destruction and from the use of various test media. Boiling Time The old recommendation for treating water is to boil for 10 minutes and add 1 minute for every 1000 feet (305 m) in elevation. However, available data indicate this is not necessary for disinfection. Evidence indicates that enteric pathogens are killed within seconds by boiling water and rapidly at temperatures above 60° C (140° F). In the wilderness the time required to heat water from 55° C (131° F) to boiling temperature works toward disinfection. Therefore any water brought to a boil should be adequately disinfected. An extra margin of safety can be added by boiling for 1 minute or by keeping the water covered and allowing it to cool slowly after boiling. Although the boiling point decreases with increasing altitude, this is not significant compared with the time required for thermal death at these temperatures ( Table 51-6 ). The boiling time required is important when fuel is limited. In recognition of the difference between pasteurizing water for drinking purposes and sterilizing for surgical purposes, many other sources now agree with this recommendation to bring water to a boil. Because of scant data for hepatitis A the Centers for Disease Control and Prevention (CDC) and EPA still recommend boiling for 1 minute to add a margin of safety.[28] Some sources still
1194
ORGANISM Giardia
TABLE 51-5 -- Heat Inactivation of Microorganisms LETHAL TEMPERATURE (° C)/TIME
REFERENCES
55 for 5 min
[94]
100 immediately
[15]
50 for 10 min (95% inactivation)
[143]
60 for 10 min (98% inactivation) 70 for 10 min (100% inactivation) 55 Entamoeba histolytica
Similar to Giardia
Nematode cysts, helminth eggs, larvae, cercariae
50–55
Cryptosporidium
45–55 for 20 min
[6]
[184] [5]
55 warmed over 20 min 64.2 within 2 min
[59]
72 heated up over 1 min Escherichia coli
55 for 30 min
[64]
60–62 for 10 min
[76]
50 for 10 min ineffective
[137]
60 for 5 min 70 for 1 min Salmonella, Shigella
65 for < 1 min
Vibrio cholerae
60–62 for 10 min
[166]
100 for 30 sec E. coli, Salmonella, Shigella, Campylobacter 60 for 3 min (3-log reduction)
[8]
65 for 3 min (all but a few Campylobacter) 75 for 3 min (100% kill) Viruses
55–60 within 20–40 min 70 for < 1 min
[2]
Hepatitis A
98 for 1 min
[105]
85 for 1 min
[203]
61 for 10 min (50% disintegrated) 60 for 19 min (in shellfish)
[150]
Hepatitis E
60 for 30 min
[203]
Bacterial spores
>100
[2]
TABLE 51-6 -- Boiling Temperatures at Various Altitudes BOILING POINT (° C)
ALTITUDE [ft (m)]
5000 (1524)
95
10,000 (3048)
90
14,000 (4267)
86
19,000 (5791)
81
suggest 3 minutes of boiling time at high altitude to give a wide margin of safety. [32] [66] [87] [174] Hot Tap Water Although attaining boiling temperature is not necessary, it is the only easily recognizable end point without using a thermometer. Other markers, such as early bubble formation, do not occur at a consistent temperature. When no other means are available, the use of hot tap water may prevent travelers' diarrhea in developing countries. Newman[137] [138] cultured samples from the hot water tap of 17 hotels in west Africa and in 15 found no coliforms, one yielded a single colony and another two colonies. Water temperature ranged from 57° to 69° C (131° to 140° F). As a rule of thumb, water too hot to touch fell within the pasteurization range. Bandres et al[8] also measured hot tap water temperature in 14 hotels in four different countries outside the United States. Most temperatures were 55° to 60° C (131° to 140° F), but one was 44° C (111.2° F), only one was 65° C (149° F), and several were 52° C (125.6° F). The authors concluded that hot water from taps would not be safe to drink. Groh et al[76] showed that tolerance to touch is too variable to be reliable, since some people found 55° C too hot to touch. If water has been sitting in a tank near 60° C for a prolonged period, enteric pathogens will be significantly reduced, likely to potable levels. Neumann's suggestion is reasonable if no other method of water treatment is available. Solar Heat Pasteurization has been successfully achieved using solar heating. A solar cooker constructed from a foil-lined
1195
Figure 51-1 Filtration. (Courtesy Dan Vorhis, Marathon Ceramics.)
ORGANISM
TABLE 51-7 -- Microorganism Susceptibility to Filtration AVERAGE SIZE (µm) MAXIMUM FILTER SIZE (µm)
Viruses
0.03
Escherichia coli
0.5 × 3–8
0.2–0.4
Campylobacter
0.2–0.4 × 1.5–3.5
0.2–0.4
Microsporidia
1–2
N/S
Cryptosporidium oocyst
2–6
1
Giardia cyst
6–10 × 8–15
3–5
Entamoeba histolytica cyst
5–30 (average 10)
3–5
Cyclospora
8–10
3–5
Nematode eggs
30–40 × 50–80
20
Schistosome cercariae
50 × 100
Coffee filter or fine cloth adequate
Dracunculus larvae
20 × 500
Coffee filter or fine cloth adequate
N/S
N/S, Not specified. cardboard box with a glass window in the lid can be used for disinfecting large amounts of water by pasteurization. Bottom temperatures of 65° C have been obtained for at least 1 hour in up to three 3.7-L jugs. Exposure to full sunshine in Kenya destroyed E. coli in 2-L clear plastic bottles within 7 hours if the maximum temperature reached 55° C. Inactivation in this situation was a combination of thermal and ultraviolet irradiation.[97] [120] This could be a low-cost method for improving water quality, especially in refugee camps and disaster areas.
PHYSICAL REMOVAL Filtration Filters have the advantages of being simple and requiring no holding time. They do not add any unpleasant taste and may improve taste and appearance of water. However, they add space and weight to baggage. All filters eventually clog from suspended particulate matter (present even in clear streams), requiring cleaning or replacement of the filter. A crack or eroded channel allows passage of unfiltered water. Filtration is both a physical and a chemical process, so many variables influence filter efficiency. The characteristics of the filter media and the water, as well as flow rate, determine the interactions. Filtration can reduce turbidity, bacteria, algae, viruses, color, oxidized iron, manganese, and radioactive particles.[47] The size of a microorganism is the primary determinant of its susceptibility to filtration ( Table 51-7 and Figure 51-1 ). Filters are rated by their ability to retain particles of a certain size, which is described by two terms. Absolute rating means that 100% of a certain size of particle is retained. Nominal rating indicates that more than 90% of a given particle size will be retained. Filter efficiency is generally determined with hard particles (beads of known diameter), but microorganisms are soft and compressible under pressure. A membrane with pore size of 0.2 µm can remove enteric bacteria. Giardia and E. histolytica cysts are easily
1196
filtered, requiring a maximum filter size of 5 µm. Cryptosporidium cysts are somewhat smaller than Giardia and more flexible; 57% are able to pass through a 3 µm membrane filter, so a filter with 1- to 2-µm pores is recommended. [174] Helminth eggs and larvae, which are much larger, can be removed by a 20-µm filter. Cyclops that transmits dracunculosis can be removed by passage through a fine cloth.[184] Filters are constructed with various designs and materials, and many filters are designed for field use. Surface, membrane, and mesh filters are very thin with a single layer of fairly precise pores, whose size should be equal to or less than the smallest dimension of the organism. These filters provide little volume for holding contaminants and thus clog rapidly, but can be cleaned easily by washing and brushing without destroying the filter. Maze or depth filters depend on a long, irregular labyrinth to trap the organism, so they may have a larger pore or passage size. Contaminants adhere to the walls of the passageway or are trapped in the numerous dead-end tunnels. Granular media, such as sand or charcoal, diatomaceous earth, or ceramic filters function as maze filters. A depth filter has a large holding capacity for particles and lasts longer before clogging but may be difficult to clean effectively, since many particles are trapped deep in the filter. Flow can be partially restored to a clogged filter by back flushing or surface cleaning, which removes the larger particles trapped near the surface. For ceramic filters, surface cleaning is highly effective but destroys some of the filter medium. As a filter clogs, it requires increasing pressure to drive the water through, which can force microorganisms through the filter. Portable filters can readily remove protozoan cysts and bacteria but may not remove viruses, which are another order of magnitude smaller than bacteria. Only the semipermeable membranes in reverse-osmosis filters are inherently capable of removing viruses. However, adsorption and aggregation reduce viruses using other mechanical filters. Virus particles may adhere to the walls of diatomite (ceramic) or charcoal filters by electrostatic chemical attraction.[58] [71] [163] Viruses in heavily polluted water often aggregate in large clumps and become adsorbed to particles or enmeshed in colloidal materials, making them amenable to filtration. [53] [159] Thus turbidity (cloudiness from contaminants) may help remove pathogens with filtration while it inhibits halogens. In one study, however, only 10% of total virus particles detected were recovered on 3- to 5-µm pore prefilters, suggesting that most were not associated with the suspended sediment. [141] Furthermore, adsorbed viral particles can be subsequently dislodged and eluted from a filter.[158] [206] Some filters now can remove 99% to 99.9% of viruses, but the fourth log required by water treatment units remains a challenge. Recently, the First Need filter (General Ecology, Exton, Pa.) was able to meet the EPA standards for water purifiers, including 4-log removal of viruses. It is not clear how this filter succeeded when others have failed[71] (see Appendix ). In general, however, mechanical filters should not be considered adequate for complete removal of viruses, except with special equipment.[219] Additional treatment with heat or halogens before or after filtration guarantees effective virus removal.[163] New designs and materials may overcome this limitation of microfiltration. For domestic use and in pristine protected watersheds where pollution and viral contamination are minimal and the main concerns are bacteria and cysts, filtration can be used as the only means of disinfection. For foreign travel and for surface water with heavy levels of fecal or sewage contamination, however, most filters should not be used as the sole means of disinfection.[58] One rational use of filtration is to clear the water of sediment and organic debris, allowing lower doses of halogens with more predictable residual levels.[134] Filters are also useful as a first step to remove parasitic and Cryptosporidium organisms that have high resistance to halogens. Filtration using simple, available products is of interest for use in developing countries and in emergency situations. Sand filtration is still used widely in municipal plants. A column of fine sand 60 to 75 cm deep that permits no more than 200 L/m2 /hr is capable of removing turbidity and greater than 99% of organisms.[161] Rice hull ash filters are moderately effective. The United Nations International Children's Emergency Fund has devised a filter containing crushed charcoal sandwiched between two layers of fine sand that can filter 40 L/day and requires cleaning only once a year, but it has not been well tested.[35] Reverse Osmosis.
A reverse-osmosis filter uses high pressure (100 to 800 psi) to force water through a semipermeable membrane that filters out dissolved ions, molecules, and solids.[53] This process can desalinate water, as well as remove microbiologic contamination. If pressure or degradation causes breakdown of the membrane, treatment effectiveness is lost. Even Giardia cyst passage has been shown to occur in a compromised reverse-osmosis unit.[45] Small hand-pump reverse-osmosis units have been developed. Their high price and slow output currently prohibit large-scale use by wilderness travelers, but they are important survival items for ocean travelers. Battery-operated units are often used on boats. The U.S. Department of Defense uses large-scale mobile reverse-osmosis units for water purification units because these are capable of producing potable water from fresh, brackish, or salt water, as well as from water contaminated by nuclear, biologic, or chemical agents. Moreover, these are considered the most fuel-efficient mobile
1197
units, producing the highest quality water from the greatest variety of raw water qualities. The units use pretreatment, filtration, and desalination, then disinfection for storage.[219] Granular Activated Carbon (GAC).
Granular charcoal has been used as an adsorbent for water purification since biblical times.[108] It is still in use for water treatment and for medical detoxification. When activated, charcoal's regular array of carbon bonds is disrupted, yielding free valences that are highly reactive and adsorb dissolved chemicals.[68] [178] GAC is the best means to remove organic and inorganic chemicals from water (including disinfection byproducts) and to improve odor and taste.[53] [134] Thus it is widely used in municipal disinfection plants and in home undersink devices. GAC is also a common component of field units as a filter and water purifier. GAC can be compressed into block form that acts both as a depth filter and adsorbent charcoal. The block carbon is more effective than granular because the passages are smaller, forcing closer contact with the carbon. Many, but not all, viral particles and bacteria adhere to GAC, [134] and some cysts are trapped in the matrix. [113] However, using a bed of GAC to filter particles and microorganisms results in more rapid saturation of binding sites and clogs the bed. An alternative means of disinfection should always be used. GAC does not kill microorganisms, so it does not disinfect. In fact, bacteria colonize beds of GAC and slough off into the effluent water. Bacteria attached to charcoal are resistant to chlorination because the chlorine is adsorbed by the GAC.[53] [108] [134] This bacterial contamination has not been found to be harmful because the usual heterophilic bacteria are not enteric pathogens. Enteric pathogens have been shown to survive on GAC, but if an active biofilm exists, the pathogens are rapidly displaced by
heterophilic bacteria and fail to become established. Therefore nonpathogenic bacterial colonization is encouraged in municipal plants. [163] Eventually the binding sites on the carbon particles become saturated and no longer adsorb; some molecules are released as others preferentially bind. [134] Unfortunately, no reliable means are available to determine precisely when saturation is reached. Filters using charcoal in compressed block form as the filter element may clog before the charcoal is fully adsorbed. Presence of unpleasant taste or color in the water can be the first sign that the charcoal is spent. To test the charcoal, filter iodinated water or water tinted with food coloring. With regular use the lifetime of GAC is probably measured in months; it is substantially longer with infrequent use. GAC can be "recharged," but this is not practical for small-quantity use. Ingested particles of charcoal are harmless. GAC can be used before or after disinfection. Before disinfection, GAC removes many organic impurities that result in bad odor and taste and that are precursors to trihalomethane formation. GAC is best used after chemical disinfection to make water more palatable by completely removing the halogen[134] [221] and other chemical impurities. With increasing industrial and agricultural contamination of distant groundwater, final treatment of drinking water with GAC may become a necessity for wilderness users. GAC also removes radioactive contamination. Silver Impregnation.
Silver impregnation of filters neither prevents microbial contamination of the filter nor sustains its action as a bactericide in the effluent water.[11] Although silver has slow antibacterial effect on coliform organisms, filter cartridges impregnated with silver typically become colonized with heterotrophic bacteria, which increase the total bacterial count in the effluent water but have not been linked to increased illness.[11] [58] [68] [163] In GAC filters designed to operate in line with chlorinated tap water, silver merely exerts selective pressure on the kinds of bacteria that will colonize the filter. Colonization of filters with pathogenic coliforms has not been demonstrated, but protective effect cannot be attributed to silver impregnation.[58] [163] Commercial Devices Using Mechanical Filtration.
Portable water treatment products are the third highest intended purchase of outdoor equipment after backpacks and tents.[95] Some are designed as purely mechanical filters, whereas others combine filtration with GAC. Filters that contain iodine resins are considered in the discussion on halogens (see Appendix ). Environmental Protection Agency Registration.
Until recently, no testing criteria were mandated for EPA registration. The EPA does not endorse, test, or approve mechanical filters; it merely assigns registration numbers.[39] However, registration requirements distinguish between two types of filters: those that use mechanical means only and those that use a chemical, designated as a pesticide. Standards were developed to act as a framework for testing and evaluation of water purifiers for EPA registration, as a testing guide to manufacturers, to assist in research and development of new units, and as a guide to consumers.[212] To be called a "microbiologic water purifier," the unit must remove, kill, or inactivate all types of disease-causing microorganisms from the water, including bacteria, viruses, and protozoan cysts, so as to render the processed water safe for drinking. An exception for limited claims may be allowed for units removing specific organisms to serve a definable environmental need, for example, removal of Giardia only. The EPA standards include performance-based microbiologic reduction requirements, chemical health
1198
limits for substances that may be discharged, and stability requirements for chemical(s) sufficient for the shelf life of the device. The unit should signal the end of effective lifetime (e.g., by terminating discharge of treated water) or give simple instructions for servicing or replacing within measurable volume, throughput, or time frame. There are currently no national guidelines for the removal of chemicals by portable filters. Challenge water seeded with specific amounts of microorganisms is pumped through the filters at given intervals during the claimed volume capacity of the filter. Between the bacteriologic challenges, different test waters without organisms are passed through the unit. Water conditions are specified to include average and worst-case conditions, which are 5° C with high levels of pollution, turbidity, and alkaline pH. Testing must be done with bacteria (Klebsiella), viruses (poliovirus and rotavirus), and protozoa (Cryptosporidium has replaced Giardia). A 3-log reduction is required for cysts, 4-log reduction for viruses, and 5- to 6-log reduction for bacteria. Testing is done or contracted by the manufacturer; the EPA neither tests nor specifies laboratories. Filter Testing.
Current registration of mechanical filters requires only that the product make reasonable claims and that the location of the manufacturer be listed; no disinfection studies are required.[24] However, many companies now use the standards as their testing guidelines. For mechanical filters the standards should be applied only for those microorganisms against which claims are made, such as protozoa and bacteria, excluding viruses. Despite criticisms of the methodology and inconsistencies and loopholes in the reporting process, the EPA standards are currently the best means to compare filters. The ceramic filters (especially Katadyn) have been tested most extensively and generally perform well.[58] [143] [206] Results may not apply to all ceramic filters because efficacy depends on the characteristics of the ceramic, water quality, product engineering, and prior extent of filter use. Comparative testing of different filters is in progress. Available data are from testing organized by one filter manufacturer, so the results are not generally accepted, despite nearly all filters performing well ( Table 51-8 ). Turbidity and Clarification River, lake, or pond water is often cloudy and unappealing. Turbidity (cloudiness) is an optical measurement of light scattering as it passes through water. Visibility in water with turbidity of 10 nephelometric turbidity units (NTU) is about 30 inches and with 25 NTU is 10 inches. Turbidity is caused by suspended organic and inorganic matter, such as clay, silt, plankton, and other microscopic organisms. High turbidity is often associated with unpleasant odors and tastes, most often caused by organic compounds and metallic hydroxides with a much smaller particle size.[38] [109] Clayorganic complexes may also carry pesticides or heavy metals. Bacteria, as well as viruses, may be adsorbed to particulate matter or be embedded in it, and in highly contaminated water, microorganisms tend to aggregate and clump. In one study, 17% of turbidity particles contained attached microbes, averaging 10 to 100 bacteria per particle.[109] Organisms in the center of these conglomerates are afforded some protection from disinfectants. Even the flocculate produced by a chlorination-flocculation tablet may harbor viable organisms.[155] Thus, removing particulate matter also decreases the number of microorganisms and halogen demand.[98] [134] Removal of turbidity and particulates may be important in preventing chemical or infectious illness. Even if turbidity is caused by benign inorganic particles, such as clay, removal is desirable for improving esthetic quality of the water. Filtration can remove larger particles, but cloudy water can rapidly clog a filter. Sedimentation and coagulation-flocculation are other clarification techniques routinely used in municipal disinfection plants that can be easily applied in the wilderness for pretreatment of cloudy water, which is then disinfected by filtration or halogenation. Coagulation-flocculation and filtration are also used to remove Giardia and Cryptosporidium cysts that are more resistant to chlorine. Early experiments with water heavily contaminated with feces containing hepatitis A virus demonstrated that filtration and sedimentation alone did not prevent infection but reduced the severity of the illness. Water pretreated with coagulation, settling, and filtration was subsequently disinfected with 0.4 ppm of residual chlorine, whereas water chlorinated to 1 mg/L without pretreatment remained infectious.[135] [136] Sedimentation.
Sedimentation is the separation of suspended particles large enough to settle rapidly by gravity, such as sand and silt. The time required depends on the size of the particle. Generally, 1 hour is adequate if the water is allowed to sit without agitation. After sediment has formed on the bottom of the container, the clear water is decanted or filtered from the top. Microorganisms, especially protozoal cysts, eventually settle, but this takes longer and the organisms are easily disturbed during pouring or filtering. In one test in Tanzania, 4 days were required for sedimentation to improve microbiologic quality of the water.[35] Sedimentation should not be considered a means of disinfection. Coagulation-Flocculation.
Smaller suspended particles and chemical complexes too small to settle by gravity are called colloids. Most of these can be removed by coagulation-flocculation, a technique that has been used to remove unpleasant color, smell, and taste in water since 2000 BC.
Coagulation is achieved with addition of an appropriate chemical that alters the physical state of dissolved
1199
REFERENCE CHALLENGE
TABLE 51-8 -- Performance Evaluations of Portable Filters FILTERS RESULTS CONCLUSIONS/COMMENTS TESTED BACTERIA PROTOZOA VIRUS
[157]
Challenged Katadyn filter with 108 B. subtilis spores, 106 Naegleria cysts, 105 Giardia cysts using EPA test waters 1 and 3 (clear and cloudy) at 20° and 4° C.
Katadyn
N/A
Clear
Pass
Pass
Cloudy
Pass 2/3
Fail 3/3
Survivor (reverse osmosis) tested with above plus Survivor 35 107 poliovirus and rotavirus, using EPA test water Clear Pass 1 and 3% seawater. Sea-water Fail
Pass Pass
Katadyn filter failed unless cleaned regularly; failure was related to mechanical pump forcing organisms through a clogged filter. Recommend prefilter.
Survivor failure was due to growth of the test organism on and throughout the filter membrane. Recommend biocide Pass treatment of membrane. Pass BACTERIA PROTOZOA VIRUS
[133]
Condensed EPA standard testing protocol using bacteria, viruses, and Cryptosporidium oocysts with three test waters from average to "worst" case conditions at beginning, middle and end of claimed filter lifetime; "Pass" indicates removal of 99.9999% bacteria, 99.9% protozoa, 99.99% viruses; "N/A" indicates not applicable because no claims for virus removal.
PUR hiker
N/A
New
99.96% 99.8% pass
200 gal
99.6%
Katadyn
Pass
Pass
This testing was sponsored by several outdoor retailers and by Sweet Water but is the best comparative testing available to date.
N/A
Minifilter Timberline
N/A
New
99%
Pass
200 gal
91.5%
Pass
General Ecology First Need
Timberline made no claims for bacteria.
N/A Pass
Pass
Microlite New
99.96% Pass
MSR waterworks
Pass
Pass
SweetWater
Pass
Pass
N/A
N/A
Guardian PUR Scout Pass
99.8%
200 gal
99.9%
99.8% pass
88.7%
Explorer failed to perform after only 100 gal, although claimed capacity Pass greater. Passed tests with average 95.2% case water, but failed worst case water. 85.8%
Pass
Pass
99.7%
SweetWater Pass with iodine (See note)
Pass
99.7% SweetWater failed viral removal at end of filter life.
TEST 1 [90A]
N/A
New
Explorer (See note)
97%–99% virus removal by this mechanical filter.
TEST 2
4 × 108 /L B. diminuta bacteria; filters tested at limit of design life after MSR passing 92–345 L high-quality river water, then tested after 4, 5, 6, and Miniworks 99.998% 99.9% 7 L seeded water; test 2 done after passing high-turbidity water until clogged, then cleaning filters. Miniworks 99.99999% II
Although independent laboratory, the testing was sponsored by MSR. Note very high levels of bacteria. PUR Scout and Explorer and SweetWater plus contain iodine resin.
Katadyn Pocket
99.8%
Combi Sweet Water
99.99999% 96.3%
Guardian + iodine PUR Scout
96.7% 99.9999%
99.999% 99.9%
Explorer Hiker
99.6%
99.999% 57.7%
97.7%
1200
and suspended solids, causing particles to stick together on contact because of electrostatic and ionic forces.[38] [53] Lime (alkaline chemicals principally containing calcium or magnesium and oxygen) and alum (an aluminum salt) are commonly used, readily available coagulants. Rapid mixing is important to obtain dispersion of the coagulant. The second stage, flocculation, is a purely physical process obtained by prolonged gentle mixing to increase interparticle collisions and promote formation of larger particles. The flocculate particles can be removed by sedimentation and filtration. Coagulation-flocculation removes most coliform bacteria (60% to 98%), viruses (65% to 99%),[47] [159] [189] Giardia (60% to 99%), helminth ova (95%), [184] heavy metals, dissolved phosphates, and minerals.[38] [53] [113] [227] Organic and inorganic compounds may be removed by forming a precipitate or by adsorbing onto aluminum hydroxide or ferric hydroxide floc particles.[53] Despite removal of most microorganisms, a subsequent disinfection step is advised. The sequential use of coagulation and activated carbon is often beneficial. Coagulation is generally found to remove large molecules that absorb poorly on GAC. On
the other hand, carbon has limited effectiveness for removing organic matter from water.[4] To clarify water by this means in the field, add 10 to 30 mg of alum per liter of water. The exact amount is not important, so it can be done with a pinch of alum, lime, or both for each gallon of water, using more if the water is very cloudy. Next, stir or shake briskly for 1 minute to mix the coagulant, then agitate gently and frequently for at least 5 minutes to assist flocculation. Settling requires at least 30 minutes, after which the water is carefully decanted or poured through a cloth or paper filter. Finally, filtration or halogenation should be used to ensure disinfection. TOXICITY.
Questions have been raised concerning the association of aluminum with central nervous system (CNS) toxicity in mammals, but these effects have been observed only after exposures other than ingestion. Most of the aluminum in alum is removed with the floc. A report from the National Academy of Sciences concluded that aluminum in drinking water does not present a significant risk.[53] Alum is a common chemical used by the food industry in baking powder and for pickling. It can be found in some food stores or at chemical supply stores. ALTERNATIVE AGENTS.
Many substances can be used as a coagulant, including lime or potash. In an emergency, baking powder or even the fine white ash from a campfire can be used.[209] Other coagulation-flocculation agents used traditionally by native peoples include seeds from the nirmali plant in southern India and rauwaq (a form of bentonite clay) or seeds from moringa plants in Sudan.[35]
HALOGENS Worldwide, chemical disinfection is the most widely used method for improving and maintaining microbiologic quality of drinking water. Halogens, chiefly chlorine and iodine, are the most effective chemical disinfectants. Understanding the principal factors of halogen disinfection allows intelligent and flexible use. Germicidal activity results from oxidation of essential cellular structures and enzymes.[33] [107] [134] [139] Halogenated amines may be synthesized by white blood cells as part of the body's natural defenses to destroy microorganisms.[220] The disinfection process is determined by characteristics of the disinfectant, the microorganism, and environmental factors.[34] [86] [131] Dilute solutions do not sterilize water. Variables with Halogenation Concentration and Contact Time.
The major variables in the disinfection reaction with chlorine or iodine are the amount of halogen (concentration) and the exposure time of the microorganism to the halogen disinfectant (contact time). Concentration of halogen in water is measured in parts per million (ppm) or milligrams per liter (mg/L), which are equivalent. Contact time is usually measured in minutes but ranges from seconds to hours. In field disinfection, concentrations of 1 to 10 mg/L for 10 to 60 minutes are generally effective. Theoretically the disinfection reaction follows first-order kinetics. The rate of the reaction is determined by the initial concentration of reactants, and a given proportion of the reaction occurs in any specified interval.[86] [221] This means concentration and time are inversely related, and their product results in a constant for specified disinfectant, organism, percent reduction of viable microorganisms, and given conditions of water temperature and pH: concentration × time = constant (Ct = K) ( Figure 51-2 ).[221] When concentration and contact time are graphed on logarithmic coordinates, a straight line results. This means that concentration and time can be varied oppositely and still achieve the same result.[9] In field disinfection this can be used to minimize halogen dose and improve taste or to minimize the required contact time. In reality the disinfection reaction deviates from first-order kinetics, and Ct values do not follow the exponential rates described by the empiric equation because microorganisms do not act as chemical reagents (Cn t = K). An initial lag period may be seen before inactivation begins (e.g., because of penetration of the cyst wall), and inactivation declines for more resistant organisms or those protected by aggregation or association with other particulate matter ( Figure 51-3 ). [77] [82] [86] Contaminants.
Organic and inorganic nitrogen compounds from decomposition of organisms and their
1201
Figure 51-2 Relationship of halogen concentration and contact time for a given temperature and pH. The first-order chemical reaction results in a straight line over most values for each microorganism and halogen compound. (Data from Change SL: J Am Pharm Assoc 47:417, 1958; and Water and Sanitation for Health [WASH] Project: Report on mobile emergency water treatment and disinfection units, WASH Field Report No 217, Arlington, Va, 1980.)
wastes, fecal matter, and urea complicate disinfection with halogens and must be considered in field water treatment. Vegetable matter, ferrous ions, nitrites, sulfides, and humic substances also affect oxidizing disinfectants.[55] [134] [221] These contaminants react with halogens, especially chlorine, to form compounds with little or no disinfecting ability, effectively decreasing the concentration of available halogen. Halogen Demand and Residual Concentration.
Halogen demand is the amount of halogen reacting with impurities. Residual halogen concentration is the amount of active halogen remaining after halogen demand of the water is met. To achieve microbial inactivation in aqueous solution with a chemical agent, a residual concentration must be present for a specified contact time. Failure of chlorination in municipal systems to kill cysts or other microorganisms is usually caused by difficulty maintaining adequate residual halogen concentration and contact times, rather than by extreme resistance of the organism.[196] Halogen demand and residual concentration of surface water are the greatest uncertainties in field disinfection. Nitrogen appears in most natural waters in varying amounts, which relate directly to the sanitary quality of water. Cysticidal dose of halogens is strongly affected by the level of contamination (cyst or viral density) in otherwise clean water.[34] [75] [196] Scant data are available on halogen demand for surface water ( Table 51-9 ). Clear water is assumed to have minimal demand and cloudy water high demand. Surface water in the wilderness contains 10 times the organic carbon content
Figure 51-3 Effect of concentration and temperature on Giardia cyst inactivation by iodine. Low concentrations are effective at cold temperatures with prolonged contact time. (From Fraker LD et al: J Wilderness Med 3:351, 1992.)
of aquifer groundwater. The green or brown color in stagnant ponds or lakes or in tropical and lowland rivers is usually caused by organic matter with considerable halogen demand. In some cases, such as runoff after storms and snowmelt, cloudy water may be caused by inorganic sand and clay that exert little halogen demand. In general, chlorine demand rises with increased turbidity.[109] In addition, particulate turbidity can shield microorganisms and interfere with disinfection.[47] [98] [109] The initial dose of halogen must consider halogen demand. For clear alpine waters, 1 mg/L demand can
1202
TABLE 51-9 -- Halogen Demand of Surface Water SOURCE Cloudy river water, Portland, Oregon Cloudy water from clay particles
HALOGEN DEMAND (mg/L)
REFERENCE
3–4
[93]
None
[34]
Clear water with 10% sewage added
2
[34]
Lily pond and turbid river water
5–6
[34]
Colorado River, cloudy from inorganic sand, clay
0.3
[207]
Unspecified surface waters
2–3
[46]
Municipal wastewater
20–30
[46]
High-elevation spring
0.3
[142]
Western river
0.7
[142]
0.4–1.6
[109]
1.3
[202]
Six watersheds in western Oregon Small stream, Australia
be assumed; for cloudy waters the assumption is 3 to 5 mg/L. If a method is used that adds 4 mg/L to clear water, extra time can compensate for the lower expected residual concentration. In cloudy water, however, where the demand may be nearly 4 mg/L, an increased dose of halogen, rather than prolonging the contact time, is needed to ensure free residual. The usual field recommendation to compensate for the unknown demand of cloudy water is a double dose of halogen (to achieve 8 to 16 mg/L). This crude means of compensation often results in a strong halogen taste on top of the taste of the contaminants. If the cause of turbidity is uncertain, the water should be allowed to sit; inorganic clay and sand will sediment, clarifying the water considerably. Other means of clarification, such as coagulation-flocculation or filtration, significantly reduce halogen demand. Several simple color tests (most often used to test swimming pools and spas) measure the amount of free (residual) halogen in water. Testing in the wilderness for halogen residual may be reasonable for large groups but is not practical for most. Smell of chlorine usually indicates some free residual. Color and taste of iodine can be used as indicators. Above 0.6 ppm, a yellow to brown tint is noted. [221] pH.
Two other variables in the disinfection reaction are pH and temperature. [55] [107] [134] Halogen oxidizes water to form several compounds, each with different disinfection capabilities. The percentage of each halogen compound is determined by pH. The optimal pH for halogen disinfection is 6.5 to 7.5.[34] [130] As water becomes more alkaline, approaching pH 8.0, much higher doses of halogens are required. Although pH can be measured in the field, the relationship is too complex to allow meaningful use of the information. Most surface water pH is neutral to mildly acidic, which is within the effective range of the halogens used. Granite keeps many alpine waters mildly acidic. Unfortunately, acid rain is affecting some high mountain lakes.[122] The EPA found the average pH in western alpine lakes to be no less than 5.5; other US lakes are beginning to show lower pH levels. On the alkaline side, some surface water with pH 7.0 to 8.0 begins to affect the chemical species of chlorine, favoring less active forms. [86] Certain desert water is so alkaline that halogens would have little activity; however, these waters are usually not palatable. At this time, compensating for pH is not necessary. Tablet formulations of halogen have the advantage of some buffering capacity. Temperature.
Temperature influences the rate of the disinfection reaction. Cold water affects germicidal power and must be offset by longer contact time or higher concentration to achieve comparable disinfection.[74] The common rule is a twofold to threefold increase in inactivation rate per 10° C increase in temperature. Unusual retardation of rates as temperatures approach 0° C has not been seen.[86] Temperature can be estimated in the field. Some treatment protocols recommend doubling the dose of halogen in cold water, but if time allows, time can be increased instead of dose. Data for killing Giardia in very cold water (5° C) with both chlorine and iodine indicate that contact time must be prolonged three to four times, not merely doubled, to achieve high levels of inactivation.[63] [83] If feasible, raising the temperature by 10° to 20° C allows a lower dose of halogen and more reliable disinfection at a given dose. Susceptibility of Microorganisms.
The final variable is the target microorganism. Sensitivity to halogen is determined by the diffusion barrier of the cell wall or capsule and the relative susceptibility of proteins and cellular respiration to denaturation and oxidation.[33] [134] Organisms, in order of increasing resistance to halogen disinfection, are enteric (vegetative) bacteria, viruses, protozoan cysts, bacterial spores, and parasitic ova ( Table 51-10 and Table 51-11 ); for example, E. histolytica cysts are 160 times as resistant as E. coli and 9 times as resistant as hardier enteroviruses to chlorine (HOCl). Virucidal residuals of I2 and HOCl are 5 to 70 times higher than bactericidal residuals.[33] [134] Relative resistance between organisms is similar for iodine and chlorine.
1203
HALOGEN ORGANISM
TABLE 51-10 -- Disinfection Data for Chlorine CONCENTRATION (mg/L) TIME (min) pH TEMPERATURE (° C) DISINFECTION CONSTANT (Ct) REFERENCE
HOCl
Escherichia coli
0.1
0.16
6.0
5
0.016
FAC
Campylobacter
0.3
0.5
6.0–8.0
25
0.15
[19]
FRC
20 enteric viruses
0.5
60
7.8
2
30
[22]
Free Cl
6 enteric viruses
0.5
4.5
6.0–8.0
5
2.5
[56]
FRC
Hepatitis A virus
0.5
1
6.0
25
0.5
[75]
Free Cl
Hepatitis A virus
0.5
5
6.0
5
2.5†
[189]
HOCl
Amebic cysts
3.5
10
25
35
[33]
FRC
Amebic cysts
3.0
10
7.0
30
30
[196]
Free Cl
Giardia cysts
2.5
60
6.0–8.0
5
150
[167]
Free Cl
G. lamblia cysts
0.85
90
8.0
2–3
77
[216]
Free Cl
G. muris cysts
3.05
50
7.0
5
153
[180]
5.87
25
7.0
5
139
[180]
6.0
0.5
170
[83]
6.0
5
120
[83]
7200
[221]
30
[228]
*
Free Cl
Giardia
[221]
Free Cl
Cryptosporidium
80
90
FRC
Schistosome cercariae 1.0
30
7.0
Free Cl
Nematodes
2–3
120
(Not lethal)
[134]
95–100
30
(95% lethal)
[134]
200
20
5.0
FRC
Ascaris eggs
28
37
HOCl, Hypochlorous acid; FAC, free active chlorine; Free Cl, free chlorine; FRC, free residual chlorine. *These represent nearly equivalent measurements of the residual concentration of active chlorine disinfectant compounds. †Four-log reduction. Most experiments use 2- to 3-log (99% to 99.9%) reduction as the end point.
2000
[104]
HALOGEN*
ORGANISM
TABLE 51-11 -- Disinfection Data for Iodine CONCENTRATION (mg/L) TIME (min) pH TEMPERATURE (° C)
Escherichia coli
1.3
I2
Amebic cysts
3.5
10
25
35
[33]
6.0
5
25
30
[33]
12.5
2
25
25
[33]
1.25
39
6.0
25
49
[13]
12.7
5
6.0
25
63
[13]
6
7.0
18
6
[13]
7.0
5
15
[13]
23
80
[34]
0–5
160
[34]
Poliovirus 1
2–5
REFERENCE
FRI
FRI
1 6.0–7.0
DISINFECTION CONSTANT (Ct) 1.3
[134]
I2
Poliovirus 1
1
I2
Coxsackievirus
0.5
30
Added I2
Amebic cysts
8
10 4.0–8.0
Bacteria, viruses
8
20
Giardia cysts
4
15
5.0
30
60†
[63]
4
45
5.0
15
170†
[63]
4
120
5.0
5
480†
[63]
FRI
*FRI (free residual iodine) and I2 (elemental iodine) are nearly equivalent measurements of the residual concentration of active iodine disinfectant compounds. Added I 2 indicates initial dose. †100% kill; viability tested only at 15, 30, 45, 60, and 120 minutes.
1204
BACTERIA.
All vegetative bacteria are extremely sensitive to halogens. Inactivation involves oxidation of enzymes on the cell membrane and does not require penetration.[221] Little modern work has focused on bacterial agents because they are more sensitive than viruses and cysts, and little difference is evident between the bacterial pathogens.[86] Although halogens were first used to disinfect water during cholera epidemics in 1850, recent cholera epidemics prompted review of data to ensure the susceptibility of V. cholerae to low levels of chlorine and iodine. [44] Campylobacter has susceptibility similar to that of other enteric pathogens.[19] Bacterial spores, such as Bacillus anthracis, are relatively resistant to halogens, but with chlorine, spores are not much more resistant than Giardia cysts.[9] [221] Quantitative data are not available for iodine solutions, but iodine does kill spores. Fortunately, sporulating bacteria do not normally cause waterborne enteric disease.[84] VIRUSES.
Enteroviruses are more resistant than enteric bacteria,[134] but they constitute such a large and diverse group of organisms that generalization is especially difficult.[33] [53] [107] Most studies have used poliovirus, a phage virus, or coxsackievirus. The mechanism of action for halogen inactivation of viruses has not been resolved. It is not clear whether the oxidant injures protein on the shell, a process similar to bacterial inactivation,[23] or penetrates the protein capsid by chemical transformation and then attacks the nucleic acid core, as in cyst inactivation.[221] Most viruses tested against chlorine have shown resistance 10 times greater than that of enteric bacteria, but inactivation is still achieved rapidly (0.3 to 4.5 minutes) with low levels (0.5 mg/L) of chlorine.[56] [210] Current data suggest that HAV is not significantly more resistant than other enteric viruses.[75] [151] [190] [203] In one test using iodine tablets, HAV was inactivated under difficult conditions more readily than poliovirus or echovirus.[191] Norwalk virus may be more resistant to chlorine than several other viruses, which may account for its importance in waterborne outbreaks.[101] Powers et al[155] [156] found that poliovirus was more slowly inactivated than rotavirus and Giardia muris by both chlorine and iodine, but this is inconsistent with other data. Clumping and association of viruses with cells and particulate matter are thought to be significant factors affecting viral disinfection, causing departure from first-order kinetics.[56] [191] [210] Cell-associated hepatitis A virus was 10 times more resistant than dispersed hepatitis A virus. CYSTS AND PARASITES.
Protozoal cysts are considerably more resistant than enteric bacteria and significantly more resistant than enteric viruses, probably because of cysts' physiologically inactive outer shell, which the disinfectant must penetrate to be effective.[33] [221] Early data exist for E. histolytica, but recent work on G. lamblia indicates similar sensitivity to both iodine and chlorine.[94] Higher pH and lower temperature decrease the effectiveness of halogens on Giardia. [82] [91] [191] Review literature frequently attributes exaggerated resistance of Giardia to halogens; Hoff[85] traced this to misquoted data. Jarrol et al[92] [93] tested two chlorine methods and four iodine methods for effectiveness against Giardia cysts. They found all methods effective in warm water, but only two methods destroyed all cysts in cold water in recommended doses. Higher doses or longer contact times would make all these methods effective. Halogens can be used in the field to inactivate Giardia cysts* (see Figure 51-3 ). However, longer contact time is required in cold and dirty water.[73] Cryptosporidium oocysts differ greatly from other protozoan cysts and are highly resistant to halogens. The Ct constant for Cryptosporidium in warm water with chlorine was estimated at 9600.[29] From 65% to 80% of Cryptosporidium oocysts were inactivated after 4 hours by two iodine tablets in "general case" water. [73] This implies that 3-log inactivation could have been achieved after 3 to 4 more hours. Although halogens can achieve disinfection of Cryptosporidium in the field, this is not practical. [48] [174] [221] The resistance of Cyclospora and microsporidia is not well studied, but the oocysts are similar to Cryptosporidium and thus may resemble this protozoa more than Giardia. Schistosome cercariae are susceptible to low concentrations of chlorine.[223] Limited data on parasitic helminth larvae and ova indicate such high levels of resistance that chemical disinfection is not useful.[104] [134] [184] However, these are not common waterborne pathogens and can be readily removed or destroyed by heat, filtration, or coagulation-flocculation. DISINFECTION CONSTANT.
The best comparison of disinfection power is the disinfection constant (Ct). Disparate results may be caused by lack of standardized experimental conditions of pH, temperature, chemical species of halogen, and species of microorganism or by different techniques for concentrating, counting, and determining viability of organisms.[86] [134] The latter is especially a problem for cysts and viruses, which cannot be cultured easily.[182] The end point for disinfection effectiveness is now becoming standardized by the EPA guidelines, but most older studies used 99.9% for all organisms, with some using 99% or 99.99%. Differences between laboratory and field conditions also make extrapolation from data to practice inaccurate and suggest the need for a safety factor in the field. Despite variation, Ct remains a useful and widely used concept; values provide a basis for comparing the effectiveness * References
[ 63] [ 83] [ 86] [ 91] [ 154] [ 155] [ 156] [ 180]
.
1205
of different disinfectants for inactivation of specific microorganisms.[86] To use halogens for disinfection, a consensus organism (the most resistant target) determines
the Ct.[86] [107] [221] For wilderness water this has been protozoan cysts. The resistance of Cryptosporidium will not raise the threshold for halogen use; rather, it will force an alternative or a combination of methods to ensure removal and inactivation of all pathogens. Chlorine Chlorine has been used as a disinfectant for 200 years. Hypochlorite was first used for water disinfection in 1854 during cholera epidemics in London and was first used continuously for water treatment in Belgium in 1902. It is currently the preferred means of municipal water disinfection worldwide, so extensive data support its use[221] (see Table 51-10 ). Chemistry.
Chlorine reacts in water to form the following compounds[55] [221] : HOCl + H+ + Cl-
Cl2 + H2 O HOCl
OCl- + H+
At neutral pH, negligible amounts of diatomic chlorine are present. The major disinfectant is hypochlorous acid (HOCl), which penetrates cell and cyst walls easily. Dissociation of HOCl to the much weaker disinfectant hypochlorite (OCl- ) depends on temperature and pH. In pure water at pH 6.0, 97% of chlorine is HOCl; at pH 7.5, HOCl/OCl- ratio is 1:1; and above pH 7.5, OCl- predominates.[221] The combination of these two compounds is defined as free available chlorine. Both calcium hypochlorite (Ca[OCl]2 ) and sodium hypochlorite (NaOCl) readily dissociate in water, allowing the same equilibrium to form as when elemental chlorine is used.[107] [221] Chloride ion (Cl- , NaCl, or CaCl2 ) is germicidally inactive. In addition, chlorine readily reacts with ammonia to form monochloramines (NH2 Cl), dichloramines, or trichloramines, referred to as combined chlorine. In field disinfection these compounds are not considered, and only free residual chlorine should be measured. However, chloramines have weak disinfecting power and are calculated as a disinfectant in municipal sewage plants.[86] [130] [134] [221] Toxicity.
Acute toxicity to chlorine is limited; the main danger is irritation and corrosion of mucous membranes if concentrated solutions (for example, household bleach) are ingested. Numerous cases have been reported of short-term ingestion of very high residuals (50 to 90 ppm) in drinking water; one military study used 32 ppm for several months without adverse effects.[221] Animal studies using long-term chlorination of drinking water at 100 to 200 ppm have not shown toxic effects.[134] Sodium hypochlorite is not carcinogenic; however, reactions of chlorine with certain organic contaminants yield chlorinated hydrocarbons, chloroform, and other trihalomethanes, which are considered carcinogenic.[53] [134] Public health departments limit residual chlorine in public systems to decrease ingestion of trihalomethane. The concern is now fueled more by public fears than by scientific conclusion.[221] The risk of death from infectious diseases if disinfection is not used is far greater than any risk from chlorine disinfection by-products.[53] These compounds are not likely to form in clean wilderness surface water, since the organic precursors are not present. Formulations.
Chlorine is available in liquid and tablet forms for field use ( Table 51-12 and Table 51-13 ). BLEACH.
Liquid household bleach is a hypochlorite solution that comes in various concentrations, usually 5.25%. This has the convenience of easy availability, low cost, high stability, and administration with a dropper. If bleach containers break or leak in a pack, the liquid is corrosive and stains clothing. Sodium hypochlorite solutions are vulnerable to significant loss of available chlorine over time. Stability is greatly affected by heat and light. Five percent solution loses about 10% available chlorine over 6 months at 21° C (70° F) and freezes at -4.4° C (24° F). TABLETS
Halazone.
Tablets contain a mixture of monochloraminobenzoic and dichloraminobenzoic acids.[55] Each tablet releases 2.3 to 2.5 ppm of titratable chlorine.[140] These tablets have been criticized because the alkaline buffer necessary to improve halazone dissolution decreases disinfectant efficiency, requiring unacceptably high concentrations and contact times (6 tablets = 15 mg/L for 60 minutes) for reliable disinfection under all conditions.[172] Tablets have the advantage of easy administration and can be salvaged if the container breaks. However, they lose effectiveness with exposure to heat, air, or moisture. Although no significant loss of potency results from opening a glass bottle intermittently over weeks, 75% of activity is lost after 2 days of continuous exposure to air with high heat and humidity. The shelf life is 6 months; potency decreases 50% when stored at 40° to 50° C (104° to 122° F). A new bottle should be taken on each major trip or changed every 3 to 6 months. Halazone is being replaced by newer formulations of chlorine tablets. Aquaclear and Puritabs.
Each tablet contains 17 mg of sodium dichloroisocyanurate (NaDCC) in a paper/foil laminate. The effervescent tablet releases 10 mg of free chlorine (HOCl) when dissolved in 1 L of water. Fifty percent of the available chlorine remains in compound
1206
TABLE 51-12 -- Water Disinfection Techniques and Halogen Doses ADDED TO 1 LOR QT OF WATER IODINATION TECHNIQUES
AMOUNT FOR 4 ppm
AMOUNT FOR 8 ppm
Iodine tabs: tetraglycine hydroperiodide
½ tab
1 tab
0.2 ml
0.4 ml
5 gtts
10 gtts
0.35 ml
0.70 ml
8 gtts
16 gtts
Saturated solution: iodine crystals in water
13 ml
26 ml
Saturated solution: iodine crystals in alcohol
0.1 ml
0.2 ml
CHLORINATION TECHNIQUES
AMOUNT FOR 5 ppm
AMOUNT FOR 10 ppm
EDWGT (emergency drinking water germicidal tablet) Potable Aqua Globaline 2% iodine solution (tincture) 10% povidone-iodine solution*
Household bleach: 5% sodium hypochlorite
0.1 ml
0.2 ml
2 gtts
4 gtts
AquaClear: sodium dichloroisocyanurate
1 tab
AquaCure, AquaPure, Chlor-floc: chlorine plus flocculating agent
8 ppm/tab
Measure with dropper (1 drop = 0.05 ml) or tuberculin syringe. *Povidone-iodine solutions release free iodine in levels adequate for disinfection, but scant data are available.
TABLE 51-13 -- Recommendations for Contact Time with Halogens in the Field CONTACT T IME IN MINUTES AT VARIOUS WATER TEMPERATURES CONCENTRATION OF HALOGEN
5° C
15° C
30° C
2 ppm
240
180
60
4 ppm
180
60
45
8 ppm
60
30
15
Recent data indicate that very cold water requires prolonged contact time with iodine or chlorine to kill Giardia cysts. These contact times have been extended from the usual recommendations in cold water to account for this and for the uncertainty of residual concentration. and is released as free chlorine is consumed by halogen demand. NaDCC is a stable, nontoxic chlorine compound that forms a mildly acidic solution, which is optimal for hypochlorous acid, the most active disinfectant of the free chlorine compounds. To disinfect large quantities of water, tablets are also available in 340 and 500 mg of NaDCC and in screw-cap tubs. Chlorination-flocculation.
Chlor-floc, AquaPure, and AquaCure tablets were devised for the military in South Africa and are now becoming widely available in the United States. They contain alum and 1.4% available chlorine in the form of dichloroisocyanurate (sodium dichloro-s-triazinetrione) with proprietary flocculating agents. Bicarbonate in the tablets promotes rapid dissolution and acts as a buffer. One 600-mg tablet yields 8 mg/L of free chlorine. In clear water without enough impurities to flocculate, the alum causes some cloudiness and leaves a strong chlorine residual. However, this is an excellent one-step technique for cloudy and highly polluted water. After treatment, water should be poured through a special cloth to remove floc and decrease turbidity. Testing by the U.S. military demonstrated biocidal effectiveness similar to iodine tablets under most conditions.[153] [155] [156] Extended contact time was necessary for complete viral removal in some of the tests. Because of the ability to flocculate turbid water, the action was superior to iodine in some poor-quality water. The tablets are stable for 3 years if stored in their packaging out of the heat. (See Table 51-15 .) SUPERCHLORINATION-DECHLORINATION.
The Sanitizer is a method of field chlorination that uses first superchlorination and then dechlorination. High doses of chlorine are added to the water in the form of calcium hypochlorite crystals. Concentrations of 30 to 200 ppm of free chlorine are reached at the recommended doses. These extremely high levels are above the margin of safety for field conditions and rapidly kill all bacteria, viruses,
1207
and protozoa but probably not Cryptosporidium. After at least 10 to 15 minutes, several drops of 30% hydrogen peroxide solution are added. This reduces hypochlorite to chloride, forming calcium chloride (a common food additive), which remains in solution, as follows: Ca(OCl)2 + 2 H2 O ? 2 HOCl + Ca++ (OH- )2 Ca(OCl)2 + 2 H2 O2
CaCl2 + 2 H2 O + 2 O2
Excess hydrogen peroxide reacts with water to form oxygen and water. Chloride has no taste or smell. Hydrogen peroxide is also a weak disinfectant, [229] although not in common use. The process of superchlorination-dechlorination with different reagents is used in some large-scale disinfection plants to avoid long contact times and to remove tastes and smells. High doses of chlorine remove or oxidize hydrogen sulfide and some other chemical contaminants that contribute to poor taste and odor. Chlorine bleaches organic matter, making water sparkling blue, as in swimming pools. [221] The minor disadvantage of a two-step process is offset by excellent taste. Measurements to titrate peroxide to the estimated amount of chlorine do not need to be exact, but some experience is needed to balance the two and achieve optimal results. This is a good technique for highly polluted or cloudy water and for disinfecting large quantities. It is the best technique for storing water on boats or for emergency use. A high level of chlorine prevents growth of algae or bacteria during storage; water is then dechlorinated in needed quantities when ready to use. The two reagents must be kept tightly sealed to maintain potency of the reagents. Properly stored, calcium hypochlorite loses only 3% to 5% of available chlorine per year. Thirty-percent peroxide is corrosive and burns skin, so it should be used cautiously. Iodine Iodine has been used as a topical and water disinfectant since the beginning of the twentieth century.[107] Iodine is effective in low concentrations for killing bacteria, viruses, and cysts, and in higher concentration against fungi and even bacterial spores, but it is a poor algicide[34] [74] [134] (see Table 51-11 and Figure 51-3 ). Iodine has been used successfully in low concentrations for continuous water disinfection of small communities.[103] Despite several advantages over chlorine disinfection, it has not gained general acceptance because of concern for its physiologic activity. Chemistry.
Iodine is the only halogen that is a solid at room temperature. Of the halogens, it has the highest atomic weight, lowest oxidation potential, and lowest water solubility. Its disinfectant activity in water is quite complex because of formation of various chemical intermediates with variable germicidal efficiencies. Seven different ions or molecules are present in pure aqueous iodine solutions, but only elemental (diatomic) iodine (I2 ) and hypoiodous acid (HOI) play major roles as germicides. Diatomic iodine reacts in water to form the following compounds[34] [74] : I2 + H2 O
HOI + I- + H-
I2 is two to three times as cysticidal and six times as sporicidal as HOI, because it more easily diffuses through the cyst wall. Conversely, HOI is 40 times as virucidal and three to four times as bactericidal as I2 , since inactivation of organisms depends directly on oxidation potential, without involving cell wall diffusion.[33] Their relative concentrations are determined by pH and concentration of iodine in solution.[34] At pH 7.0 and 0.5 ppm of iodine, the concentrations of I2 and HOI are approximately equal, resulting in a broad spectrum of germicidal action. At pH 5.0 to 6.0, most of the iodine is present as I2 , whereas at pH 8.0, 12% is present as I2 and 88% as HOI.
At higher concentrations of iodine, more HOI is present. Under field conditions, I2 is the major disinfectant for which doses are calculated.[34] Other chemical species, including triiodide (I3 - ), iodate (HIO3 ), and iodide (I- ), form under certain conditions but play no role in water disinfection.[34] [47] Iodide is important because it readily forms when reducing substances are added to iodine solution. Iodide ion is without any effect for water disinfection and also has no taste or color, but is still physiologically active. Toxicity.
The main issue with iodine is its physiologic activity, potential toxicity, and allergenicity.[147] Acute toxic responses generally result from intentional overdoses of iodine, with corrosive effects in the gastrointestinal tract leading to hemorrhagic gastritis. Mean lethal dose is probably about 2 to 4 g of free iodine or 1 to 2 ounces of strong tincture.[62] Toxicity is limited by rapid conversion of iodine to iodide by food (especially starch) in the stomach and early reflex vomiting. Iodide is absorbed into the bloodstream but has minimal toxicity (it is used widely for radiographic imaging). Sensitivity reactions, including rashes and acne, may occur with usual supplementation levels of iodine. Given the necessity of iodine, it is not clear why some people react to certain forms of the substance, such as iodized salt. As with other sensitivity reactions, these may occur with very low doses. Acute allergy to iodide is rare and manifests as individual hypersensitivity, such as angioneurotic and laryngeal edema.[147] Chronic iodide poisoning, or iodism, occurs after prolonged ingestion of sufficiently high doses, but marked individual variation is seen. Symptoms simulate
1208
upper respiratory illness, with irritation of mucous membranes, mucus production, and cough. A major disadvantage of iodine is its physiologic activity with effects on thyroid function. Iodine is an essential element for normal thyroid function and health in small amounts of 100 to 300 µg/day, but excess amounts can result in thyroid dysfunction. Maximum safe level and duration of iodine ingestion are not clearly defined, making it difficult to provide recommendations for prolonged use in water treatment. THYROID EFFECTS OF EXCESS IODINE INGESTION.
Most persons can tolerate high doses of iodine without development of thyroid abnormalities, because the thyroid gland has an autoregulatory mechanism that effectively manages excessive iodine intake. Initially, excess iodine suppresses production of thyroid hormone, but production usually returns to normal in a few days. Iodine-induced hyperthyroidism can result from iodine ingestion by persons with underlying thyroid disease or when iodine is given to persons with prior iodine deficiency.[21] [179] During the worldwide campaign to eliminate endemic goiter and cretinism, 1% to 2% of residents developed hyperthyroidism from small amounts of dietary iodine supplementation. Groups at higher risk were elderly persons, Graves' disease patients (especially after antithyroid therapy), and patients taking pharmacologic sources of iodine. Hyperthyroidism has been reported from iodine use as a water disinfectant in two travelers. Both were from iodine-sufficient areas and had antithyroid antibodies, suggesting underlying thyroiditis; one had a mother and sister with Hashimoto's thyroiditis.[111] Iodine-induced hypothyroidism or goiter is much more common from excessive iodine intake. Hypothyroidism is attributed to prolonged suppression of thyroid hormone production induced by excess iodine levels, but the mechanism through which iodide goiter is produced is not well understood. The incidence of goiter varies and does not correlate well with quantity of iodine or with the level of hypothyroidism. Recently, goiters were discovered among a group of Peace Corps volunteers in Africa and were linked epidemiologically to the use of iodine resin water filters.[102] Forty-four (46%) of the volunteers had enlarged thyroids, but 30 of these had normal thyroid function tests. Iodine-induced hypothyroidism or goiter may occur with or without underlying thyroid disease but is more common in several groups[21] [179] [224] : (1) those with underlying thyroid problems, including prior treatment for Graves' disease or subtotal thyroidectomy; (2) fetuses and infants, from placental transfer of iodide from mothers treated with iodides; (3) persons with subclinical hypothyroidism, especially elderly persons, in whom the incidence is 5% to 10%; and (4) patients with excessive iodide from medications (formerly potassium iodide; currently amiodarone). Neonatal goiter is especially worrisome because it can lead to asphyxia during birth or hypothyroidism with mental impairment. Daily intakes as small as 12 mg have been reported to produce congenital iodide goiters, but generally much higher doses are required. DOSE-RESPONSE OR THRESHOLD LEVEL.
It is unclear what percent of the population will respond adversely to excess iodine or what should be defined as excess intake. The majority of people can tolerate high doses of iodine with no ill effects.[21] The reported incidences of goiter, hypothyroid effects, and hyperthyroid response vary so widely that they provide no clear dose limits.[147] The use of iodine for decades in the military and civilian population without reports of associated clinical thyroid problems suggests that the risks are minimal and would be outweighed by the risk of enteric disease. However, biochemical assays show that changes in thyroid function tests are common with excess iodine intake. In controlled trials, iodine was administered to healthy volunteers, 30 to 70 mg/day for 14 to 90 days.[132] [171] Two studies simulated field use of four iodine tablets (32 mg) per day.[69] [110] All found the same changes in thyroid function: an increase in thyroid-stimulating hormone (TSH) and decrease in triiodothyronine (T3 ) and thyroxine (T4 ) within 1 to 2 weeks and persisting throughout iodine ingestion. Paul et al,[145] studied the minimum dose that would cause alterations in thyroid function and found that 1.5 mg/day decreased TSH, but not 500 and 750 µg/day. These changes were statistically significant from baseline but usually remained within the range of normal values. Even when outside the normal range, the changes in thyroid function remained sub-clinical. Thyroid enlargement was sometimes noted when evaluated by ultrasound. All changes reverted to normal within weeks to months without persistent thyroid disease. Studying longer duration of ingestion, Freund[65] found minimal changes and no clinical problems when water with 1 mg/L of iodine was given to prisoners for up to 3 years. Referring to the same project, Thomas et al [201] reported that after 15 years of ongoing iodine use at 1 mg/L, iodinated water caused no decrease in serum concentrations of T4 below normal values and no allergic reactions. Patients with prior thyroid disease had no recurrence with iodinated water; four patients with active hyperthyroidism were treated in standard fashion, and their condition remained well controlled despite the extra iodine intake. Also, 177 inmates gave birth to 181 full-term infants, and no neonatal goiters were detected.[200] The military studied long-term toxic effects of iodine, adding sodium iodide to drinking water at a naval base for 6 months.[129] The estimated daily dose of iodine per person was 12 mg for the first 16 weeks and 19.2 mg for the next 10 weeks. No evidence of functional changes or damage in the thyroid gland, cardiovascular
1209
system, bone marrow, eyes, or kidneys was noted. No increase in skin diseases, no sensitization to iodine, and no impaired wound healing or resolution of infections was evident. Treatment of subclinical thyroid disease is controversial, even the chronic cases found on a serologic diagnostic battery.[41] [80] With a history of excess iodine ingestion, most experts would first stop the iodine intake and follow thyroid function before treating hypothyroidism. Recommendations.
The tenth edition of the recommended dietary allowances (RDAs, 1989) set the allowable dose to 1.0 mg/day for children and up to 2.0 mg/day for adults (increased from 0.5 to 1.0 mg in the ninth edition, 1980), primarily based on the data from Freund and Thomas.[147] Possible toxicity with intermediate- to long-term use of iodine and the question of iodide toxicity remain controversial. The EPA and the World Health Organization
(WHO), supported by the American Water Works Association (AWWA), have recommended iodine use for water disinfection only as an emergency measure for short periods of about 3 weeks.[218] [233] However, this period of short use appears arbitrary. The following groups should not use iodine for water treatment because of their increased susceptibility to thyroid problems: Pregnant women Persons with known hypersensitivity to iodine Persons with a history of thyroid disease, even if controlled by medication Persons with a strong family history of thyroid disease (thyroiditis) Persons from areas with chronic dietary iodine deficiency
Available data suggests the following: 1. High levels of iodine, such as those produced by recommended doses of iodine tablets, should be limited to periods of 1 month or less. 2. Iodine treatment that produces a low residual (1 mg/L or less) appears safe, even for long periods in people with normal thyroid function. Iodine resin devices with a charcoal stage to remove residual iodine, or iodination followed by microfiltration that includes a charcoal stage, should allow prolonged use. Concern for International Space Station crew members who would be using iodinated water for 6 months prompted the National Aeronautics and Space Administration (NASA) to use an exchange resin to reduce residual iodine concentration from 3 or 4 to 0.25 mg/L. [121] 3. Persons planning to use iodine for a prolonged period should have the thyroid gland examined and thyroid function measured to ensure that a state of euthyroidism exists.
TABLE 51-14 -- Iodine Solutions IODINE (%) IODIDE (%)
PREPARATION
TYPE OF SOLUTION
Iodine topical solution
2.0
2.4 (sodium)
Aqueous
Lugol's solution
5.0
10.0 (potassium)
Aqueous
Iodine tincture
2.0
2.4 (sodium)
Aqueous-ethanol
Strong iodine solution
7.0
9.0 (potassium)
Ethanol (85%)
Formulations.
Several forms of iodine are available for field use ( Table 51-12 , Table 51-13 , Table 51-14 ). IODINE SOLUTIONS.
Iodine solutions commercially sold as topical disinfectants are inexpensive and can be measured accurately with a dropper but are staining and corrosive if spilled. These contain iodine, potassium, or sodium iodide in water, and ethyl alcohol or glycerol ( Table 51-14 ). Iodide improves stability and solubility but has no germicidal activity and adds to the total amount of iodine ingested and absorbed into the body. Iodophors are solutions in which diatomic iodine is bound to a neutral polymer of high molecular weight, giving the iodine greater solubility and stability with less toxicity and corrosive effect.[34] [74] Povidone-iodine is a 1-vinyl-2-pyrrolidinone polymer with 9% to 12% available iodine. The iodophors are routinely used for topical disinfection, since they have less tissue toxicity than iodine solutions. Although they are not approved for water disinfection in the United States, they are used in other countries for this purpose.[10] According to the manufacturer, approval for this use in the United States was not pursued because the anticipated use did not justify the expense. Povidone is nontoxic and was used as a blood expander during World War II. In aqueous solution, povidone-iodine provides a sustained-release reservoir of halogen; free iodine is released in water solution depending on the concentration (normally, 2 to 10 ppm is present in solution). In dilutions below 0.01%, povidone-iodine solution can be regarded as a simple aqueous solution of iodine. [74] One report found these compounds similar in germicidal efficiency to other iodine-iodide solutions.[34] Data indicate persistence of about 2 ppm of free iodine at a 1:10,000 dilution, [74] which corresponds to a 0.001% solution made by adding 0.1 ml (2 drops) to 1 L of water. However, another study found conflicting values for
1210
available iodine and free iodine (measured by different techniques). Bactericidal effect on Pseudomonas and Staphylococcus bacteria increased at dilutions of 1:100, compared with 10% stock solutions, but dilutions of 1:10,000 were not bactericidal.[14] The complex chemistry of povidone-iodine solutions accounts for these conflicting data. Since free residual iodine can be measured at the concentration used for water disinfection, it should be effective. Personal and anecdotal experience of others attest to its effectiveness in field use. [10] TABLETS.
The two types of iodine tablets are those that depend on a chemical reaction to convert iodide into iodine and those in which the iodine exists as hydroperiodide. [172] The tablets used by the U.S. military and sold in the United States for water disinfection contain tetraglycine hydroperiodide, which is 40% I2 and 20% iodide.[34] [131] Tetraglycine hydroperiodide tablets are sold as Globaline, Potable Aqua, and EDWGT (emergency drinking water germicidal tablet). Each tablet releases 8 mg/L of elemental iodine into water.[34] [131] [140] [172] An acidic buffer provides a pH of 6.5, which supports better cysticidal than virucidal capacity but should be adequate for both. Tablets have the advantages of easy handling and no danger of staining or corroding if spilled. They are stable for 4 to 5 years under sealed storage conditions and for 2 weeks with frequent opening under field conditions, but they lose 30% of the active
HALOGEN DOSE ChlorFloc
1 or 2 tabs
TABLE 51-15 -- Data on Microcidal Efficacy of Iodine and Chlorine Tablets FRH (mg/L) TIME (min) TEMPERATURE (° C) ORGANISM 4–7
Globaline
REFERENCE
10–20
Bacteria
6
20
10–20
Giardia muris
3
5
10–20
Rotavirus
4
20
10–20
Poliovirus
Inadequate
1 tab
12
25
Poliovirus
Inadequate
2 tabs
20
Various
Bacteria
6
45
5
G. muris
3
20
5
Rotavirus
4
60
5
Poliovirus
60
4–14
5
LOG REDUCTION
[156]
AquaPure
2 tabs
7–11
1 tab
Globaline
Iodine
40
[155]
15–25
Bacteria
6
15–25
Rotavirus
4
15–25
Polio virus
2
20
15–25
G. muris
2
60
15
Giardia
3
1 tab
180
5
Giardia
3
2 tabs
120
5
Giardia
3
8–16
60
5–25
Hepatitis A
4
8
60
5
Poliovirus, echovirus
Inadequate
16
60
5
Poliovirus, echovirus
4
2 tabs
1 or 2 tabs
30–40
5
10
[157]
[192]
FRH, Free residual halogen. iodine if bottles are left open for 4 days in high heat or humidity. Tetraglycine hydroperiodide was originally developed and chosen as a preferred technique by the military for individual field use because of its broad-spectrum disinfection effect, ease of handling, rapid dissolution, stability, and acceptable taste.[34] [99] [131] [140] [154] The military requirements dictated a short contact time (10 minutes in clear, warm water)-thus the relatively high concentration of iodine (8 ppm) compared with other iodination techniques. The recommended dose has been increased to two tablets in cold water to ensure disinfection with short contact times. With adequate contact time, one tablet can be added to 2 quarts of water to yield 4 ppm of free iodine ( Table 51-15 ). Potable Aqua is now sold with "neutralizing" tablets made of ascorbic acid. Ascorbic acid converts iodine to iodide, removing the taste and color and stopping the disinfection action of iodine, but does not change the physiologic load of ingested iodine. The Australian military developed the other type of iodine tablet (e.g., Afses). The tablet contains a combination of potassium iodide and potassium iodate together with an acidic material (potassium permanganate) that catalyzes a reaction to form iodine.[172] The advantage is this tablet's resistance to thermal deterioration, but it is highly sensitive to traces of moisture. It is formulated to release 8 mg/L of free iodine, but the
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actual amount measured in water is more variable than that released by Potable Aqua, so its biocidal performance is not as good. The tablet also contains more iodide than Potable Aqua, which contributes to potential adverse effects.[202] CRYSTALS (SATURATED SOLUTION).
Because of limited solubility in water, iodine crystals may be used for disinfection. In one technique for field use, 4 to 8 g of crystalline iodine is put in a 1- to 2-ounce bottle, which is then filled with water.[99] A small amount of elemental iodine goes into solution (no significant iodide is present); the saturated solution is used to disinfect drinking water. Water can be added to the crystals hundreds of times before they are completely dissolved. Since the amount of iodine dissolved depends on the temperature of the solution (200 ppm at 10° C, 300 ppm at 20° C, 400 ppm at 30° C), [34] [74] [221] the bottle should be kept warm or the amount added to drinking water adjusted for temperature of the iodine crystal solution. In the field, it may be easier to warm the bottle in an inner pocket than to estimate temperature and adjust the dose. The supernatant should be carefully decanted or filtered to avoid ingestion of the crystals[232] ; this is aided by the weight of the crystals, which causes them to sink. Many people prefer crystalline iodine because of its large disinfectant capacity, small size, and light weight. A commercial product (Polar Pure) has made iodine crystals readily available in camping supply stores. An alternative technique is to add 8 g of iodine crystals to 100 ml of 95% ethanol.[222] Increased solubility of iodine in alcohol makes the solution less temperature dependent and allows much smaller volumes to be used (8 mg/0.1 ml), which can be measured with a 1-ml syringe or dropper (2 drops). The stability and simplicity of iodine crystals have led to their testing for in-line systems that provide continuous water disinfection for remote households and small communities. In these designs, residual iodine is removed with GAC.[57] [205] RESINS.
Iodine resins have great potential for water disinfection in individual or small systems and have been incorporated into many different filter designs available for field use. They provide many advantages over chlorination systems by eliminating the need for chemical feed systems, residual monitoring, and contact time.[218] Iodine resins are considered demand disinfectants because they are minimally insoluble in water and little iodine is released into aqueous solution. However, when a microorganism comes into contact with the resin, iodine apparently transfers to the microorganism aided by electrostatic forces, binds to the wall or capsule, penetrates and kills the organism.[116] Iodine resins are engineered to produce low residuals in effluent water. The initial iodine residual with pentaiodide resin produces a constant 1 to 2 ppm after initial use, whereas triiodide resin produces a residual iodine concentration of less than 0.20 ppm at equilibrium.[116] The concentration in the eluent of triiodide resin is temperature dependent. Concentrations less than 1.0 ppm were obtained with water at 42.2° C (108° F), but this increased to a total iodine content of 6 to 10 ppm at 71° C (160° F). After returning to room temperature, the iodine residual returned to nominal values.[116] Measurable iodine is attached to bacteria and cysts after resin treatment, effectively exposing the organisms to high iodine concentrations. This allows reduced contact time compared with dilute iodine solutions.[61] [116] Some contact time still appears necessary. [117] Fifty percent of Giardia cysts were viable 10 minutes after passage through a triiodine resin. Viable Giardia cysts could be recovered in 4°-C (39.2°-F) water 40 minutes after passage through an iodine resin.[117] PUR Traveler cup filters failed to pass the EPA protocol for "worst-case" water unless water was passed through the filter twice. The data implied that a holding (contact) time could have achieved the same results.[70] The Canadian Health Department, challenging an in-line triiodine resin with highly polluted water, also found that a 15-minute contact time was necessary for warm water and 30-minute contact time for cold water.[57] The EPA conducted tests of triiodide resin against E. coli but not against other organisms, for which it relied on independent testing. It concluded that the product depends on a 0.2-ppm residual and that additional testing would be necessary below this level. Resins are chemically and physically stable during conditions of dry storage at room temperature. Aqueous suspensions or resins retain biocidal potential for 15 years. No alteration in activity was observed after dry storage for 1 month at 50° C (122° F).[116] Resins have proved effective against bacteria, viruses, and cysts but not against Cryptosporidium parvum oocysts or bacterial spores.[116] When Cryptosporidium oocysts were passed through a triiodide resin column, most were retained in the resin column, probably by electrostatic attraction to the resin. Of those that passed through, only a small percentage were inactivated within 30 minutes by the iodine. [208] Despite the controversy regarding contact time, most of the testing done with iodine resins has shown high levels of effectiveness, and products have demonstrated their ability to meet the EPA guidelines for reduction of microorganisms (see Table 51-8 ). Recently, however, iodine resin products from two different companies (SweetWater with Viralguard and PUR filters) were withdrawn from the market when company testing showed that they failed to meet viral inactivation standards of 4-log reduction. The units had previously
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obtained EPA registration on the basis of successful testing contracted through a laboratory that does the majority of testing for the filter industry. This variation of test results is disconcerting for several reasons, including the source of test variability, credibility of the original laboratory, and the effectiveness of the iodine resin, which is used in the products of other manufacturers. Iodine resin filters.
Iodine resins have been incorporated into a broad line of filters for field use (see Appendix ). Optimal designs incorporate two stages in addition to the iodine resin. A microfilter, generally 1 micron (micrometer), effectively removes Cryptosporidium, Giardia, and other halogen-resistant parasitic eggs or larva. Since iodine resins kill bacteria and viruses rapidly, no significant contact time is required for most water.[70] The addition of a third stage of activated charcoal removes dissolved residual; however, the importance of iodine residual for disinfection has not been determined.[117] [205] Testing by one filter company demonstrated that a carbon block could reduce 16 mg/L of iodine to less than 0.01 mg/L for 150 gallons, which was close to the expected lifetime of its ceramic filter.[181] The effective removal of residual iodine makes the iodine resin filters safe for long-term use. For effective performance of activated charcoal, it must be replaced periodically. In conclusion, iodine resins are effective disinfectants that can be engineered into attractive field products, including use in the space shuttle and large-scale units for international disasters. They may prove useful for small communities in undeveloped and rural areas where chlorine disinfection is technically and economically unfeasible. However, more testing is needed on specific products to ensure adequate resin contact, to define the need for contact time, and to confirm whether a residual iodine concentration is needed. Chlorine vs. Iodine A few investigators have reported data suggesting ineffectiveness of common halogen preparations. Jarroll et al[93] [94] tested six methods of field disinfection and found that none achieved high levels of Giardia inactivation at the recommended dose and times. However, this failure simply reflected the need for longer contact times in cold water.[112] Ongerth et al[143] tested seven chemical treatments for Giardia inactivation in clear and turbid water at 10° C (50° F). None achieved 99.9% reduction in 30 minutes. All iodine-based chemical methods were effective at 8 hours, but none of the chlorine preparations was effective, even after this extended time. Although these results after 30 minutes in cold water are to be expected, the 8-hour results do not conform with other experimental data on chlorine. Unfortunately, the authors did not test for residual halogen, although initial levels achieved should have been effective, and they did not test at regular time intervals to determine when the iodine methods had achieved the target reduction of organisms. A large body of data proves that both iodine and chlorine are effective disinfectants with adequate concentrations and contact times (cold temperatures equate with slow disinfection time for both). Comparing effectiveness between chlorine and iodine is difficult because of the different ionic species and compounds that may exist under varying conditions.[84] Chlorine and iodine tablets have been directly compared under identical water test conditions and found to be similar in their biocidal activity in most conditions using recommended dose and contact time[153] (see Table 51-12 , Table 51-13 , and Table 51-15 .) Contact times in Table 51-13 are extended from the previous recommendations for treatment in cold water to provide a margin of safety and to ensure high levels of cyst destruction. Iodine has several advantages over chlorine. Of the halogens, iodine has the lowest oxidation potential, reacts least readily with organic compounds, is least soluble, is least hydrolyzed by water, and is less affected by pH, all of which indicate that low iodine residuals should be more stable and persistent than corresponding concentrations of chlorine.[47] [74] [103] [134] Taste Objectionable taste and smell are the major problems with acceptance of halogens. These depend on specific chemical compounds. Most people are familiar with the taste of chlorine (hypochlorite); tap water usually contains 0.2 to 0.5 ppm of chlorine, swimming pools 1.5 to 3.0 ppm, and hot tubs 3.0 to 5.0 ppm. Most persons note a distinct taste at 5 ppm and a strong, unpleasant taste at 10 to 15 ppm.[172] Hypochlorous acid and chloride have no taste or odor.[221] Most objectionable tastes in treated water are derived from dissolved minerals, such as sulfur, and from chlorine compounds, chloramines, and organic nitrogen compounds, even at extremely low levels. Elemental iodine at 1 mg/L is undetectable. Most persons can detect iodine solutions at 1.5 to 2 mg/L but do not find it objectionable.[17] [47] [66] Eight ppm of iodine produces a distinct taste and odor; however, tablets yielding these concentrations were preferred by military personnel over tincture of iodine in equivalent doses.[34] [131] Iodide ion has no color or taste. Taste tolerance or preference for iodine over chlorine is individual. Opposite preferences have been documented when direct comparisons are done.[140] [155] I believe that most persons prefer the taste of iodine to chlorine at concentrations typically used in the field. In addition, iodine forms fewer organic compounds that produce highly objectionable taste and smell. Minimal Dosage.
Taste can be improved by several means ( Box 51-3 ). One method is to use the relationship
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between halogen concentration and time and to give the minimum necessary dose, allowing a longer contact time (see Table 51-13 ). Giardia cysts and viruses can be killed with doses of chlorine or iodine of 2 ppm or less (see Figure 51-3 ).[63] [83] [107] Wilderness travelers usually can allow a longer contact time for water disinfection. Box 51-3. IMPROVING THE TASTE OF HALOGENS Decrease dose and increase contact time. Clarify cloudy water, allowing decreased halogen. Use iodine resin. Remove halogen: Granular activated carbon Chemical reduction Ascorbic acid Sodium thiosulfate Chlorination-dechlorination (Sanitizer) KDF (zinc-copper) brush or media Use alternative techniques: Heat Filtration
Theoretically, doubling the contact time allows a 50% reduction of halogen dose at any level. Although this relationship holds true at the higher field doses of halogens,
as the levels drop, the reaction departs from mathematical models, and the straight-line graph has a "tail" (see Figure 51-2 ). This departure from strict first-order kinetics and the uncertainty of halogen demand in field disinfection mean that a margin of safety must be incorporated into contact times at lower doses. Of all standard iodine doses, iodine tablets yield the highest dose (8 mg/L with an intended contact time of 10 minutes in warm water). The tablets cannot be broken in half but can be added to 2 quarts instead of 1 quart to yield concentrations consistent with the other preparations. In recommended doses the liquid preparations of iodine yield 4 mg/L. Since even clear surface water has some halogen demand, this dose of 4 mg/L should generally not be reduced. The exception would be for backing up tap water in developing countries, when the dose may routinely be cut in half for an added dose of 2 ppm with a few hours of contact time. For chlorination methods that add 5 mg/L, adding half the amount to clean surface water should be adequate if the contact time is tripled. Even less could be used for tap water. None of these concentrations will destroy Cryptosporidium oocysts. Effective disinfection with low iodine residual can also be achieved by use of iodine resin filters. Temperature and organic matter in the water may be manipulated. Increasing the temperature of the water, especially when initially near 5° C, decreases the Ct constant (see Table 51-13 and Figure 51-2 ). Filtering water before adding halogen improves the reliability of a given halogen dose by decreasing halogen demand, allowing a lower dose of halogen.[134] Sedimentation or coagulation-flocculation cleans cloudy water and lowers the required halogen dosage considerably, in addition to removing many of the contaminants that contribute to objectionable taste. Dehalogenation.
Halogen can be removed from water after the required contact time. Activated charcoal removes iodine or chlorine, allowing standard or even high doses to be used without residual taste. The relative instability of chlorine in dilute solutions can be used to decrease taste over time. Chlorine residual in an open container decreases 1 mg/L in the first hour, then 0.2 mg/L in the next 5 to 8 hours, for a total of 2.0 to 2.5 mg/L in 24 hours. Ultraviolet light also depletes free chlorine.[221] Alteration of Chemical Species (Reduction).
Several chemical means are available to reduce free iodine or chlorine to iodide or chloride that have no color, smell, or taste. These "ides" have no disinfection action, so the techniques should be used only after the required contact time. The Sanitizer uses hydrogen peroxide to "dechlorinate" the water by forming calcium chloride. This reaction with hydrogen peroxide works best if calcium hypochlorite is used as a disinfectant. If bleach (sodium hypochlorite) is used, hydrogen peroxide reacts with chlorine in water to form hydrochloric acid in harmless amounts. Two other chemicals that may be safely used with any form of chlorine or iodine are ascorbic acid (vitamin C) and sodium thiosulfate. Ascorbic acid is widely available in the crystalline or powder form. Grinding up tablets that have binders may cloud the water. Ascorbic acid is a common ingredient of flavored drink mixes, which accounts for their effectiveness in covering up the taste of halogens. [140] [172] Sodium thiosulfate similarly "neutralizes" iodine and chlorine. A few granules in 1 quart of iodinated water decolorizes and removes the taste of iodine by converting it to iodide. In reaction with chlorine, it forms hydrochloric acid, which is not harmful or detectable in such dilute concentration. Thiosulfate salts are inert in vivo and poorly absorbed from the gastrointestinal tract. Sodium thiosulfate is available at chemical supply stores. Zinc-copper alloys act as catalysts to reduce free iodine and chlorine through an electrochemical reaction. They also remove or reduce dissolved metals, including heavy metals such as lead, selenium, and mercury. One product incorporated such an alloy into the bristles of a small brush to be stirred in the water after halogen disinfection. It is effective but slow, which limits its
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use to small volumes of water. Stirring for 1 minute removes 10 mg/L of chlorine from 250 ml of water. Environmental Protection Agency Registration Products that are used for treating municipal or private water supplies for drinking are considered pesticides and must be registered by the EPA Pesticide Branch. Registration signifies the following: 1. 2. 3. 4.
The composition is such as to warrant the proposed claims. The labeling and other material required to be submitted comply with the requirements of the act. The method will perform its intended function without unreasonable adverse effects on the environment. When used in accordance with widespread and commonly recognized practice, the method will not generally cause unreasonable adverse effects on the environment.
Thus EPA registration implies only that the "pesticide" agent is not released into the water at unsafe levels.[24] [39] This is less stringent than for filters that contain halogens.
MISCELLANEOUS DISINFECTANTS Silver Silver ion has bactericidal effects in low doses. The literature on antimicrobial effects of silver is confusing and contradictory.[88] [134] [221] [226] Concentrations in water less than 100 parts per billion (ppb) are effective against enteric bacteria. The reaction follows first-order kinetics and is temperature dependent. Calcium, phosphates, and sulfides interfere significantly with silver disinfection. Organic chemicals, amines, and particulate or colloidal matter may also interfere, but no more than with chlorine. Silver is physiologically active. Acute toxicity does not occur from small doses used in disinfection, but argyria, which is permanent discoloration of the skin and mucous membranes, may result from prolonged use. For this reason a maximum limit of 50 ppb of silver ion in potable water is recommended. At this concentration, disinfection requires several hours. Experimental results indicate 18% survival of E. coli at 3 hours at 40 µg/L. Salmonella typhi was reduced more than 5 log at 50 µg/L with a 1-hour exposure; poliovirus was not reduced at 50 µg/L with a 1-hour exposure.[11] Water disinfection systems using silver have been devised for spacecraft, swimming pools, and other settings.[221] The advantage is absence of taste, odor, and color. Persistence of residual silver concentration allows reliable storage of disinfected water. Silver can be supplied through a silver nitrate solution, desorption from silver-coated materials, or electrolysis. When coated on surfaces, silver acts as a constant-release disinfectant that produces aqueous silver ion concentrations of 0.006 to 0.5 ppm, which are sufficient to disinfect drinking water.[116] Because of this attractive feature, silver-based devices are being designed and tested in developing countries. In Pakistan a nylon bag with silver-coated sand was designed to be placed in earthenware pitchers that store water. Silver incorporated into alum is also being tested in India.[35] Filters and granular charcoal media are sometimes coated with silver to prevent bacterial growth on the surface, but this does not maintain sterility. A slow, selective action against total coliform count is noted, but none against total bacterial count. Long-term use might overcome any bacteriostatic action initially shown.[68] In an EPA study, effluent populations from the silver-containing units were about as large as those from the units without silver.[11] Bacteria can develop resistance to silver ions through generation of silver reductase. Large-scale use of silver for water disinfection has been limited by cost, difficulty controlling and measuring silver content, and physiologic effects. Short-term field use is limited by its marked tendency to adsorb onto the surface of any container (resulting in unreliable concentrations) and interference by several common substances. Data on silver for disinfection of viruses and cysts indicate limited effect, even at high doses.[33] [134] The use of silver as a drinking water disinfectant has been much more popular in Europe where silver tablets (MicroPur) are sold widely for field water disinfection. They have not been approved by the EPA for this purpose in the United States, but they were approved as a water preservative to prevent bacterial growth in previously treated and stored water. Potassium Permanganate Potassium permanganate is a strong oxidizing agent with some disinfectant properties. It was used extensively before hypochlorites as a drinking water disinfectant. [131] It is still used for this purpose and also for washing fruits and vegetables in parts of the world. It is used in municipal disinfection to control taste and odor and is usually employed in a 1% to 5% solution for disinfection. Bacterial inactivation can be achieved with moderate concentrations and contact times (45 minutes at 2 mg/L, 15 minutes at 8 mg/L). A 1:5000 (0.5%) solution controlled V. cholerae and S. typhi contamination of fruits and vegetables. The virucidal action has been tested, but without titrations of virus that remained after various periods of contact time, so the rate of action is not known. In most instances, however, a 1:10,000 solution destroyed the infectivity of virus suspensions in ½ hour at room temperature; 30 mg/L was effective in inactivating HAV within 15 minutes. [203] Although potassium
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permanganate clearly has disinfectant action, it cannot be recommended for field use, since quantitative data are not available for viruses and no data are available for protozoan cysts, despite the chemical's frequent use in some parts of the world. Packets of 1 g to be added to 1 L of water are sold in some countries. A French military guide from 1940 instructed users: "To sterilize water, use a solution of 1 gram of KMnO4 for 100 grams of water. Add this solution drop by drop to the water to sterilize until the water becomes pink. The operation is considered sufficient if the water remains pink for half an hour."[36] The solutions are deep pink to purple and stain surfaces. The chemical leaves a pink to brown color in water at concentrations above 0.05 mg/L. Small deposits of brown oxides settle to the bottom of the water container. A few drops of alcohol will cause this residual color to disappear. Hydrogen Peroxide Hydrogen peroxide is a strong oxidizing agent but a weak disinfectant. [20] [134] [229] Small doses (1 ml of 3% H2 O2 in 1 L water) are effective for inactivating bacteria within minutes to hours, depending on the level of contamination. One million colony-forming units/ml of seven bacterial strains were killed overnight, with 80% kill in 1 hour. Viruses require extremely high doses and longer contact times. Although information is lacking on the effect of hydrogen peroxide on protozoa, it is a promising sporicidal agent in high (10% to 25%) concentrations. Hydrogen peroxide was popular as an antiseptic and disinfectant in the late nineteenth century and remains popular today as a wound cleanser; for odor control in sewage, sludges, and landfill leachates; and for many other applications. It is considered safe enough for use in foods. It is naturally present in milk and honey, helping to prevent spoilage. It yields the innocuous end products oxygen and water. Solutions lose potency in time, but stabilizers can be added to prevent decomposition.[20] Although hydrogen peroxide can sterilize water, lack of data for protozoal cysts and quantitative data for dilute solutions prevents it from being useful as a field water disinfectant. Its application in superchlorination-dechlorination is effective. Ultraviolet Light The germicidal effect of ultraviolet (UV) light is the result of action on the nucleic acids of bacteria and depends on light intensity and exposure time. It is well established that UV light can inactivate bacteria, viruses, and protozoans when administered in sufficient dose. However, cysts should probably be removed by filtration. UV treatment does not require chemicals and does not affect the taste of the water. It works rapidly, and an overdose to the water presents no danger; in fact, it is a safety factor. UV light has no residual disinfection power; water may become recontaminated, or regrowth of bacteria may occur.[58] Particulate matter can shield microorganisms from UV rays. UV disinfection units are cumbersome and require power, so they are not well adapted to use by small groups in the wilderness. However, an intriguing question is whether direct sunlight can disinfect small quantities of water. One investigation tested the ability of sunlight to disinfect oral rehydration salt solution in clear polyethylene bags or plastic containers contaminated by sewage.[1] After 1 hour in sun the coliform bacteria count was zero. UV and thermal inactivation were strongly synergistic for the solar disinfection of drinking water in transparent plastic bottles that was heavily contaminated with E. coli for temperatures above 45° C (113° F). Above 55° C (131° F) thermal inactivation is of primary importance.[120] Whereas thermal inactivation is effective in turbid water, UV effects are inhibited.[97] Where strong sunshine is available, solar disinfection of drinking water is an effective, low-cost method for improving water quality and may be of particular use in refugee camps and disaster areas. However, thermal effects of sunshine are probably more important than UV rays, with insufficient data to quantify UV results.
Copper and Zinc A copper and zinc alloy (KDF) has electrochemical properties that can aid in water treatment. Its main actions are through its strong oxidation-reduction (redox) potential of 500 millivolts due to its propensity to exchange electrons with other substances. It is bacteriostatic with some bactericidal activity. Microorganisms are killed by the electrolytic field, and by formation of hydroxyl radicals and peroxide water molecules. Although KDF has been ruled a "pesticidal device" by the EPA and is used in industry to decrease bacteria levels and control bacterial growth, it should not be used as the sole means of water treatment. KDF is most often used to reduce or remove chlorine, hydrogen sulfide, and heavy metals from water. The redox reactions change contaminants into harmless components: chlorine into chloride, soluble ferrous cations into insoluble ferric hydroxide, and hydrogen sulfide into insoluble copper sulfide. Up to 98% of lead, mercury, nickel, chromium, and other dissolved metals are removed by KDF simply by bonding to the media. KDF controls the buildup of bacteria, algae, and fungi in GAC beds and carbon block filters, extending the life of carbon and improving its effectiveness. KDF media can be manufactured as brushes with wire bristles, fine steel woollike media, or granules. A KDF brush removes the taste of chlorine or iodine from treated water. KDF has been incorporated into a few portable field filters but has not yet gained widespread use. In series with charcoal, KDF extends the life of charcoal and increase its effectiveness. Products that
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claim to be purifiers, with KDF destroying all microorganisms, should be rigorously tested to prove the claims. Ozone and Chlorine Dioxide Ozone and chlorine dioxide are highly effective disinfectants widely used in municipal water treatment plants, but until recently, not available in stable form for field use.[221] These are the only disinfectants that have been demonstrated effective against Cryptosporidium in typical concentrations.[146] Two products currently being tested may revolutionize the use of chemicals for field water disinfection. A stabilized solution of chlorine dioxide (Aquamira, McNett Corp., Bellingham, Wash.) is mixed with phosphoric acid, which activates the chemical and is then mixed with water for disinfection. EPA registration for use as a water purifier is pending. Testing data will be available from the company when EPA approval is obtained. Developed for military use, an electrochemical process converts simple salt into a mixed-oxidant disinfectant containing free chlorine, chlorine dioxide and ozone (MIOX Corp., Albuquerque, NM).[215] The device is currently used in large- and medium-volume water treatment operations but has been reduced to a cigarsized unit that operates on camera batteries. This will be developed for the civilian market after testing is completed. Other Disinfection Products Other products marketed for water disinfection for travelers cannot be recommended until more data become available. These were initially introduced into the health food market but are now being offered to the general travel market. Citrus juice has biocidal properties. Lemon juice has been shown to destroy V. cholerae at a concentration of 2% (equivalent of 2 tablespoons per liter of water) with a contact time of 30 minutes. A pH less than 3.9 is essential, which depends on the concentration of lemon juice and the initial pH of the water. Its activity is greatly reduced in alkaline water.[50] Traveler's Friend is a product marketed for water disinfection that contains citrus extract. Company-sponsored data are convincing for antibacterial and antiviral activity. However, the product was not tested against Giardia cysts. The active chemical disinfectant has not been identified, and a time/dose response has not been generated. Without better data, this product cannot be recommended. Aerobic Oxygen is advertised not only as a water disinfectant, but also as a cure for headaches and tropical fish diseases. Company literature implies that the active disinfectant could be chlorine dioxide or ozone, but this is not chemically feasible. Company-sponsored testing demonstrates activity against bacteria and viruses, but not against cysts. No dose/time response has been developed to compare the product against other disinfectants.
PREFERRED TECHNIQUE Field disinfection techniques and their effects on microorganisms are summarized in Table 51-16 . The optimal technique for an individual or group depends on the number of persons to be served, space and weight available, quality of source water, personal taste preferences, and availability of fuel ( Table 51-17 ). The most effective technique may not always be available, but all methods will greatly reduce the load of microorganisms and reduce the risk of illness. For alpine camping with a high-quality source water, any of the primary techniques is adequate. The only limitation for halogens is Cryptosporidium cysts, but in high-quality pristine surface water the cysts are generally found in insufficient numbers to pose significant risk. Surface water, even if clear, in undeveloped countries where there is human and animal activity should be considered highly contaminated with enteric pathogens. Optimal protection requires either heat or a two-stage process of filtration and halogens. Iodine resin filters that combine microfiltration, halogen, and activated charcoal are a simple alternative to a two-stage process, but questions have recently surfaced concerning effectiveness against viruses under all water conditions. New techniques utilizing chlorine dioxide may prove to be highly effective. Water from cloudy low-elevation rivers, ponds, and lakes in developed or undeveloped countries that does not clear with sedimentation should be pretreated with coagulation-flocculation, then disinfected with heat or halogens. Filters can be used but will clog rapidly with silted or cloudy water. Even in the United States, water with agricultural runoff or sewage plant discharge from upstream towns or cities must be treated to remove Cryptosporidium and viruses. In addition, water receiving agricultural, industrial, or mining runoff may contain chemical contamination from pesticides, other chemicals, and heavy metals. A filter containing a charcoal element is the best method to remove most chemicals. Coagulation-flocculation or KDF resin will also remove some chemical contamination. Halogens need to be used when water will be stored, such as on a boat, in a large camp, or for disaster relief. When only heat or filtration is used before storage, recontamination and bacterial growth can occur. Hypochlorite still has many advantages, including cost, ease of handling, and minimal volatilization in tightly covered containers.[126] A minimum residual of 3 to 5 mg/L should be maintained in the water. Superchlorination-dechlorination
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BACTERIA VIRUSES
TABLE 51-16 -- Summary of Field Water Disinfection Techniques GIARDIA, AMEBAE CRYPTOSPORIDIUM
NEMATODES, CERCARIAE
Heat
+
+
+
+
+
Filtration
+
±*
+
+
+
Halogens
+
+
+
-†
±‡
*Reverse osmosis is effective. Most filters make no claims for viruses; however, General Ecology claims 4-log virus removal. †Chlorine dioxide may be effective. ‡Eggs are not susceptible to halogens but have a low risk of waterborne transmission.
HEAT
TABLE 51-17 -- Advantages and Disadvantages of Disinfection Techniques FILTRATION HALOGENS FILTRATION PLUS HALOGEN
Availability
Wood can be scarce
Many commercial choices
Many common and specific products
Includes iodine resin filters
Readily available
Cost
Fuel and stove costs
Moderate expense
Inexpensive
Mainly filter costs
Depends on second stage
Effectiveness
Can sterilize or pasteurize
Most filters not reliable against viruses
Cryptosporidium and some parasitic eggs Covers all organisms are resistant
Optimal application
Clear water, but effective for cloudy water
Clear or slightly cloudy; turbid water clogs filters rapidly
Clear; need increased dose if cloudy
Clear; need increased dose if Cloudy / turbid water cloudy
Taste
Does not change Can improve taste, taste especially if charcoal stage
Tastes worse unless remove or "neutralize" halogen
Depends on sequence; can improve if allows reduced halogen dose or if filter has charcoal
Improves
Time
Boiling time (minutes)
Filtration time (minutes)
Contact time (minutes to hours)
Combination of two processes
Combination of two processes
Other considerations
Fuel is heavy and bulky
Adds weight and space; Works well for large quantities and for requires maintenance to water storage; some understanding of keep adequate flow principles is optimal; damaging if spills or if container breaks
CLARIFICATION (C–F) PLUS SECOND STEP
Highly effective because most microbes removed by C–F
Use halogens first if filter has Best means of cleaning charcoal stage turbid water, followed by halogen, filtration, or heat
C–F, Coagulation-flocculation. is especially useful in this situation because high levels of chlorination can be maintained for long periods, and when ready for use, the water can be poured into a smaller container and dechlorinated. Iodine works for short-term but not prolonged storage, since it is a poor algicide. Silver has been approved by the EPA for preservation of stored water. Storage techniques can decrease risk of contamination. For prolonged storage, a tightly sealed container is best. For water access, narrow-mouth jars or containers with water spigots prevent contamination from repeated contact with hands or utensils.[188] On oceangoing vessels where water must be desalinated during the voyage, only reverse-osmosis membrane filters are adequate. Halogens should then be added to the water in the storage tanks.
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PREVENTION AND SANITATION In remote settings in developing countries, potable water alone does not necessarily make a substantial difference in the incidence of many gastrointestinal diseases. A study in a Brazilian village showed no reduction in incidence of diarrhea with use of disinfected water. This emphasizes the importance of general hygiene, which requires education and sanitation.[35] A combination of drinking water treatment and sanitation can decrease episodes of diarrhea. [90] [124] Hygiene is also essential for wilderness travelers. A Shigella outbreak among river rafters on the Colorado River was investigated and assumed to be waterborne from adjacent Native American communities, but no source was found in the tributaries. It was finally traced to infected guides who were shedding organisms in the stool and contaminating food through poor hygiene.[123] Personal hygiene, mainly handwashing, prevents spread of infection from food contamination during preparation of meals.[123] Simple handwashing with soap and water purified with hypochlorite (bleach) significantly reduced fecal contamination of market-vended beverages in Guatemala.[188] No one with a diarrheal illness should prepare food. Dishes and utensils should be disinfected by rinsing in chlorinated water, prepared by adding enough household bleach to achieve a distinct chlorine odor. Prevention of food-borne contamination is also important in preventing enteric illness (see Chapter 52 ). Washing fruits and vegetables in purified water is a common practice, but little data support its effectiveness. Washing has a mechanical action of removing dirt and microorganisms while the disinfectant kills microorganisms on the surface. However, neither reaches the organisms that are embedded in surface crevices or protected by other particulate matter. When lettuce was seeded with oocysts, then washed and the supernatant examined for cysts, only 25% to 36% of Cryptosporidium parvum and 13% to 15% of C. cayetanensis oocysts were recovered in the washes. Scanning electron microscopy detected oocysts on the surface of the vegetables after washing.[144] Chlorine, iodine, or potassium permanganate are often used for this purpose. Higher concentrations can be used than would normally be palatable for drinking water. With superchlorination-dechlorination, high-chlorine concentrations are used to rinse vegetables because the chlorine can be removed with the second step. Aquaclear (NaDCC) chlorine tablet instructions suggest 20 mg/L for washing vegetables. Although effective against most microorganisms, these levels would not be effective against Cryptosporidium or Cyclospora. The ultimate responsibility is proper sanitation to prevent contamination of water supplies from human waste. UV rays in sunlight eventually inactivate most microorganisms, but rain may first wash pathogens into a water source. In the soil, microorganisms can survive for months.[211] A Sierra Club study found more prolonged survival in alpine environments.[160] The investigator marked group latrines in alpine terrain and returned 1 to 2 years later to dig test trenches. He found a thin crust of decomposition covering unaltered raw waste with high coliform bacteria counts. Microorganisms may percolate through the soil. Most bacteria are retained within 20 inches of the surface, but in sandy soil this increases to 75 to 100 feet[209] ; viruses can move laterally 75 to 302 feet.[182] When organisms reach groundwater, their survival is prolonged, and they often appear in surface water or wells.[211] Some suggest that campers smear feces on rocks. Although desiccation occurs, UV disinfection is not reliable, and feces may wash into the watershed with rain runoff.[37] Moreover, it will be repulsive to other campers. In the Sierras, feces left on the ground generally disappeared within 1 month, but it was not known whether disinfection occurred before decomposition or whether the feces washed away, dried, or were blown in the wind.[160] Despite more rapid decomposition in sunlight rather than underground, burying feces is still preferable in areas that receive regular use. The U.S. military and U.S. Forest Service recommend burial of human waste 8 to 12 inches deep and a minimum of 100 feet from any water.[209] [213] Decomposition is hastened by mixing in some dirt before burial. Shallow burying is also not recommended because animals are more likely to find and overturn the feces. Judgment should be used to determine a location that is not likely to allow water runoff to wash organisms into nearby water sources. Groups larger than three persons should dig a common latrine to avoid numerous individual potholes and inadequate disposal. To minimize latrine odor and improve its function, it should not be used for disposal of wastewater. In some areas the number of individual and group latrines is so great that the entire area becomes contaminated. Therefore sanitary facilities (outhouses) are becoming common in high-use wilderness areas. Popular river canyons require camp toilets, and all waste must be carried out in sealed containers.
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Saaski B, Bicking M: Evaluation of the Mountain Safety Research carbon and ceramic filter cartridges: iodine reduction, New Brighton, Minn, 1992, Spectrum Labs.
182.
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183.
Schaffner W: Gas gangrene (other Clostridium-associated disease). In Mandell G et al, editors: Principles and practice of infectious disease, New York, 1990, Churchill Livingstone.
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Shephart M: Helminthological aspects of sewage treatment. In Feachem R et al, editors: Water, wastes and health in hot climates, New York, 1977, Wiley.
Siddiqi S et al: Water-borne hepatitis E virus epidemic in Islamabad, Pakistan: a common source outbreak traced to the malfunction of a modern water treatment plant, Am J Trop Med Hyg 57:151, 1997. 185.
186.
Singh A, McFeters G: Injury of enteropathogenic bacteria in drinking water. In McFeters G, editor: Drinking water microbiology, New York, 1990, Springer-Verlag.
187.
Soave R et al: Cyclospora, Infect Dis Clin North Am 12:1, 1998.
Sobel J et al: Reduction of fecal contamination of street-vended beverages in Guatemala by a simple system for water purification and storage, hand-washing, and beverage storage, Am J Trop Med Hyg 59:380, 1998. 188.
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Sobsey M: Enteric viruses and drinking water supplies, J Am Water Works Assoc 67:414, 1975.
Sobsey M et al: Inactivation of hepatitis A virus and model viruses in water by free chlorine. In Proceedings of Conference on Current Research in Drinking Water Treatment , Cincinnati, 1988, US Environmental Protection Agency. 190.
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Sobsey M et al: Inactivation of cell-associated and dispersed hepatitis A virus in water, J Am Water Works Assoc 83:64, 1991.
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Sobsey M et al: Comparative inactivation of hepatitis A virus and other enteroviruses in water by iodine, Water Sci Technol 24:331, 1991.
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Sorenson S et al: Isolation and detection of Giardia cysts from water using direct immunoflourescence, Water Resources Bulletin 22:843, 1986.
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States S et al: Legionella in drinking water. In McFeters G, editor: Drinking water microbiology, New York, 1990, Springer-Verlag.
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Steiner T et al: Protozoal agents: what are the dangers for the public water supply? Annu Rev Med 48:329, 1997.
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Stringer R, Kruse C: Amoebic cysticidal properties of halogens in water. In Proceedings of National Specialty Conference on Disinfection, 1970, American Society of Civil Engineers.
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APPENDIX: Water Disinfection Devices and Products* PRODUCT
PRICE STRUCTURE/FUNCTION
KATADYN (Suunto USA, 2151 Las Palmas Dr #F, Carlsbad, CA 92009; 800-543-9124) Pocket Filter ( Figure 51-4 )
All filters contain a 0.2 micron ceramic candle filter, silver impregnated to decrease bacterial growth. Large units also contain silver quartz in center of filter. $250 Hand pump; 40-inch intake hose and strainer, zipper case; size: 10 × 2 inches; weight: 23 oz; flow: 0.75–1.0 L/min; capacity: 13,000–50,000 L. $165
Replacement filter element Minifilter ( Figure 51-5 )
$90 Smaller, lighter hand pump; 31-inch intake hose and strainer; hard plastic enclosure and pump; size: 7 × 2.75 × 1.75 inches; weight: 9 oz; flow: 0.5 L/min; capacity: about 7000 L.
Combi ( Figure 51-6 )
$160 Small hand pump with ceramic filter and activated charcoal stage; can brush ceramic to clean or separately replace elements; size: 2.4 × 10.4 inches; weight: 19 oz; flow: 0.5 L/min; capacity: up to 50,000 L, 200 L for charcoal.
KFT Expedition ( Figure 51-7 )
$1150 Large hand pump with steel stand; size (packed in case): 23 × 6 × 8 inches; weight: 12 lb; flow: 4 L/min; capacity (per filter element): 100,000 L. $90
Replacement filter element
Figure 51-4 Katadyn Pocket Filter.
Figure 51-5 Katadyn Minifilter. *Prices vary considerably and product lines change regularly.
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PRODUCT
PRICE STRUCTURE/FUNCTION
Drip filter TRK ( Figure 51-8 ) Replacement filter (same filter element as hand pump) Syphon ( Figure 51-9 )
$275 Gravity drip from one plastic bucket to another with 3 ceramic candle filter elements; size: 18 × 11-inch diameter (26 inches high when assembled); weight: 9 lb 4 oz; flow: 1 pt/hr (10 gal/day); capacity: 100,000 L. $80 $100 Gravity siphon filter element: 12 × 2 inches; weight: 2 lb; flow: 2 gal/hr; capacity: 5000–20,000 L.
Claims Filter removes bacterial pathogens, protozoan cysts, parasites, and nuclear debris and clarifies cloudy water. If filter clogs, brushing the filter element (which can be done hundreds of times before replacing filter element) can restore flow. Claims for removal of viruses not made in United States, although testimonials imply effectiveness in all polluted waters. Pocket Filter has a lifetime warranty.
Figure 51-6 Katadyn Combi.
Figure 51-7 Katadyn KFT Expedition filter.
1221
Comments Well-designed, durable products are effective for claims. However, high filter volume capacity is optimistic and not likely to be achieved filtering average surface water. Field tests found the flow comparatively slow, requiring more energy to pump and frequent cleaning. Abrading the outer surface can effectively clean ceramic filters, but the gauge must be used to indicate when filter thickness is excessively diminished.
Pocket Filter is the original, individual or small-group filter design. Metal parts make it durable but the heaviest for its size. Minifilter was designed to be lighter and more cost competitive. Expedition filter is popular for larger groups, especially river trips, where weight is not a factor. Complete virus removal cannot be expected, although most viruses clump or adhere to larger particles and bacteria that can be filtered. Silver impregnation does not prevent bacterial growth in filters.
Figure 51-8 Katadyn drip filter TRK.
Figure 51-9 Katadyn Syphon.
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PRODUCT
PRICE STRUCTURE/FUNCTION
GENERAL ECOLOGY, INC. (151 Sheree Blvd, Exton, PA 19341; 610-363-7900; www.general-ecology.com)
All filters (except Microlite) contain 0.1-micron (0.4-micron absolute) Structured Matrix filter in removable canister.
First-Need Deluxe direct-connect water filter ( Figure 51-10 )
$70 Hand pump with intake strainer; outflow end connects directly to common water bottle; self-cleaning prefilter float; size: 6 × 6 inches, weight: 15 oz; flow: 1.6 L/min; capacity: 100–400 L.
Extra canister
$32
Prefilter replacement
$7
New pump assembly
$23
Filtermate
$8 Connects older-design filter to wide-mouth Nalgene bottle.
Matrix pumping system
$9 2-L carry bag, polyethylene liners; 18-inch hose and hose adapter for creating gravity filter unit from filter elements.
Microlite ( Figure 51-11 ) Replacement cartridges (set of two) Trav-L-Pure ( Figure 51-12 ) (carrying case included) Replacement canister Base Camp ( Figure 51-13 ) (carrying case included) Replacement cartridge
$30 Structured Matrix filter 0.5 µm (nominal) with activated carbon; hand pump, 24-inch intake hose and strainer; attaches directly to wide-mouth or bike bottle, soda bottle, or outlet spout; size: 5.5 × 2.5 inches; weight: 8 oz; $10 flow: 0.5 L/min; capacity: 50 L/cartridge. $120 Filter and hand pump in rectangular housing (1.5-pt capacity); pour water into housing, then pump through prefilter and microfilter; size: 4.5 × 3.5 × 6.75 inches; weight: 22 oz; flow: 1–2 pt/min; capacity: 100–400 L. $30 $500 Stainless steel casing and hand pump connected with tubing; capacity 1000 gal; canister size: 4.8 × 5.4 inches; pump: 1.5 × 10.5 inches; weight: 3 lbs; flow: 2 L/min $60
Figure 51-10 General Ecology First-Need Deluxe unit.
Figure 51-11 General Ecology Microlite unit.
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Claims First-Need filter is a proprietary blend of materials including activated charcoal. "Microfiltration removes bacteria and larger pathogens" (cysts, parasites). "Adsorption and molecular sieving": carbon absorbers remove chemicals and organic pollutants that cause color and taste; cavities in surface of adsorption material draw particles in deeper. Filter does not remove all dissolved minerals or desalinate. Proprietary process also creates ionic surface charge that removes colloids and ultrasmall particles, including viruses, through "electrokinetic attraction." Microlite removes sediment, protozoan cysts, algae, and chemicals (including iodine) and improves color and taste of water. Iodine tablets are included to kill bacteria and viruses when these organisms are a concern. Comments Reasonable design, cost, and effectiveness. All units (except Microlite) use the same basic filter design. Most testing with E. coli and Giardia cysts show excellent removal. Charcoal matrix will remove chemical pollutants. This is the only company that claims to meet EPA standards for 4-log reduction of viruses through mechanical filtration, not inactivation. However, they do not claim to remove all viruses, since they have not been able to test with the hepatitis virus. Despite viral claims, recommend caution in highly polluted water; prior disinfection with halogen would guarantee disinfection, and carbon would remove halogen. The filter cannot be cleaned, although it can potentially be back-flushed, so it must be replaced when clogged.
Microlite is designed primarily for day use or light backpacking. Used alone, it makes microbiologic claims for protozoan cysts (Giardia and Cryptosporidium) only. Iodine tablets or solution should be used as pretreatment with this filter for all water except pristine alpine water in North America. This filter is compact, lightweight, and designed for low-volume use with inexpensive, easily changed filter cartridges. Base Camp is for large groups. It also comes with an electric pump and can be hooked up in parallel to provide large quantities of water for disaster relief.
Figure 51-12 General Ecology Trav-L-Pure.
Figure 51-13 General Ecology Base Camp.
1224
PRODUCT
PRICE STRUCTURE/FUNCTION
STERN'S OUTDOORS (FORMERLY BASIC DESIGNS) (Box 1498, St Cloud, MN 56302; 800-697-5801; www.stearnsinc.com) High-flow ceramic water filter (B240) ( Figure 51-14 ) Replacement filter
$45 Ceramic filter with 0.5-micron absolute retention size and carbon center; gravity filtration with element placed near the end of a 6-foot outflow tube connected to a 7.5-L heavy plastic collection bag, providing 2–3 lb of hydrostatic pressure through the in-line filter; packing size: 4 × 4 × 8 inches; weight: 13 oz; flow rate: 15 L/hr; capacity: 1000 L. $29
Water carrier bag, 2.5 gal with fitting for filter output
$9
Ceramic Filter Pump ( Figure 51-15 )
$22 Hand pump with ceramic cartridge at end of intake tubing and polyurethane prefilter; size: pump 8 × 1 inches, filter 4 × 3 inches, 18-inch tubing; weight: 7 oz; flow: 0.4 L/min; capacity: 500 gal.
Replacement filter
$12
Claims Ceramic filter removes Giardia, bacteria, Cryptosporidium, cysts, tapeworm, flukes, and other harmful pathogens larger than 1 micron. Carbon removes color, tastes, and odors. Filter can be cleaned with an abrasive pad. Pump is easily serviced in the field; ceramic cartridge is replaceable. Comments Ceramic candle filters are effective filtering elements, and charcoal is an effective adsorbent. No claims for virus removal. Although the pore size is larger than most filters, the low pressure depth filter increases retention of bacteria. The simple gravity design decreases cost and moving parts. Filtration rate will be slow, and this filter could clog rapidly, since there is no prefilter for larger particles. Gravity drip can be convenient after making camp, if no time restraints. The filter pump is the most practical and is reasonably priced, but the ceramic filter can break. The intake is close to the pump, which can be awkward, and the foam sleeve makes it float, requiring an extra hand to hold underwater. This filter rated poorly on field user tests. Fifteen liters per hour is not realistic for a gravity filter.
Figure 51-14 Stern's Outdoors high-flow ceramic water filter (B240).
Figure 51-15 Stern's Outdoors Ceramic Filter Pump (B250).
1225
PRODUCT
PRICE STRUCTURE/FUNCTION
MSR AND MARATHON (3800 First Ave S, Seattle, WA 98124; 800-877-9677; www.msrcorp.com; www.marathonceramics.com) MSR Waterworks II ( Figure 51-16 ) total filtration system Dromedary beverage bag (All filter elements and parts replaceable.) Miniworks ( Figure 51-17 ) Replacement filter
$140 Four filter elements of decreasing pore size: porous foam intake filter, 10-micron stainless steel wire mesh screen, cylindric ceramic filter with block carbon core, then 0.2-micron pharmacologic-grade membrane filter; pressure relief valve releases at 90–95 psi; hand pump with intake tubing; storage bag (2 or 4 L) $20 attaches directly to outlet of pump; size: 9 × 4 inches diameter; weight: 17 oz; flow: 1 L/90 sec; capacity: 100–400 L. $65 Similar external design to Waterworks II but slightly different ceramic filter and lacks final membrane filter; weight: 16 oz; flow rate 1 L/70 sec; capacity: 100–400 L. $30
Newton-Water
$249 High-retention ceramic filters with compressed block carbon core; gravity microfilter system with four ceramic filter elements; two stacked stainless steel 3-gal buckets; size: 12 × 22 inches; weight: 11 lbs; capacity: 25 gal/day.
e-water siphon filter E-water Group Siphon Filter
$35 Same filter element as above with siphon tubing; use any two containers to siphon water through filter; size: 2 × 7 ½ inches; weight 1 lb; capacity: 6–10 gal/day. Not yet Multiple ceramic filters with integral carbon block, in parallel to provide 1–2 L/min with no power or line available pressure (other than gravity) required; size: 7 × 21 × 30 inches with case; weight 45 lbs.
Claims Filter removes protozoa (including Giardia and Cryptosporidium), bacteria, pesticides, herbicides, chlorine, and discoloration. Both filters meet EPA standards for removal of cysts and bacteria. Ceramic filters reduced turbidity from 68.8 to 0.01 NTU. Carbon has been shown to reduce levels of iodine from 16 to less than 0.01 mg/L for at least 150 L. Ideal for emergency needs or for remote locations. Comments Excellent filter design and function. Prefilters protect more expensive inner, fine-pore filters. Effective for claims, high quality control, and extensive testing. No claims are made for viruses, although clumping and adherence remove the majority (currently 2 to 3-log removal, but not 4-log required for purifiers). The company is working on a microfilter that will effectively remove viruses. Until they succeed, the filter should not be considered reliable for complete viral removal from highly polluted waters in developing countries. Reservoir bag that attaches to outflow for filtered water storage is convenient. Design and ease of use are distinct advantages. Filter can be easily maintained in the field; maintenance kit and all replacement parts available. Ceramic filters can be effectively cleaned by abrading outer surface many times before compromising the filter. A simple caliper gauge indicates when filter has become too thin for reliable function. Miniworks was rated very highly in field tests. Marathon ceramic products will soon be available. The gravity drip buckets are excellent products for field camps and expatriates. Iodine or chlorine can be used to ensure viral destruction, and the carbon will remove excess halogen, allowing long-term safe use of iodine. Siphon filter is inexpensive and compact.
Figure 51-16 MSR Waterworks II.
Figure 51-17 MSR Miniworks.
1226
PRODUCT
PRICE STRUCTURE/FUNCTION
PENTAPURE (FORMERLY WTC—WATER TECHNOLOGY CORP) (150 Marie Ave East, West St Paul, MN 551187; 651-450-4913; www.pentapure.com) PentaPure Sport ( Figure 51-18 )
All products use PentaPure iodine resin.
PentaCell complete
$35 Drink-through sport bottle with internal (Pentacell) three-stage cartridge: 1-micron filter, iodine resin, and charcoal filter; filter and charcoal stages can be replaced independently; size: 11.5 × 3 inches; weight: 8 oz; capacity: 375 L. $26
Cysts Filter
$14
Replacement cartridges
EcoCell Filter Spring
$9 $25 Drink-through sport bottle with filter and charcoal, but no iodine resin; otherwise similar to Sport.
The following are considered "international" products. They are not marketed in the United States, but are available for export, which includes purchase for use outside the United States. They can be ordered from several companies, including TealBrook (800-222-6614). Availability is variable. Penta-Pour bucket ( Figure 51-19 ) Ecomaster Outdoor Ecopour Travel Tap ( Figure 51-20 ), Traveler Outdoor 500 ( Figure 51-21 ) Outdoor M1, Survivor
$170 Gravity drip bucket with 22-L storage capacity; sediment filter (30 micron), 1-micron filter; pentacide and carbon cartridge; size: 12 × 30 inches; weight: 3 kg; flow: 30 L/hr; capacity: 6500 L. Pentacide and carbon cartridge; rubber cup and hose fitting on cartridge unit fits any faucet; flow: ½ gal/min; capacity: 1000 gal. $1475 Expedition-size hand-lever filter with steel frame; sediment filter, iodine resin, carbon block; each can be independently replaced; size: 14 × 9.5 × 18.5 inches; weight: 7 kg; flow: 300 L/hr; capacity: 30,000 L. Drink-through straws; cartridge with prefilter, granular activated carbon filter sandwiched between two stages of PentPure resin; size: 5.5 inches long; weight: 1 oz; capacity: 100 gal (M1), 25 gal (Survivor).
Claims Resin releases iodine "on demand" on contact with microorganisms; minimal iodine dissolves in water: effluent 1.0 to 2.0 ppm iodine. Charcoal removes residual dissolved iodine. Tested effective for bacteria, Giardia, schistosomiasis, and viruses, including hepatitis. PentaCell tested against the new EPA protocol that requires removal of 105 bacteria, 104 viruses, and 103 Giardia cysts. Charcoal stage absorbs bad tastes and odors. Comments Resin is essentially inexhaustible because the filter will become irreversibly clogged long before the resin is exhausted. However, the carbon filter may become fully absorbed with iodine and other impurities allowing iodine in the effluent. Although the amount of iodine in the outflow water is supposed to be low (1 to 2 ppm), higher concentrations have been measured. For long-term use, carbon filters should be changed regularly. The company has narrowed their product line for field use and has dropped the small group hand-pump filters because of similar products on the market. They have also dropped the Travel Cup, a small pour-through plastic cup. The Sport Bottle is handy for individual use among hikers, bikers, and travelers. Pressure is generated by a combination of sucking and squeezing. Users must adapt to the effort and the slower flow compared with a regular sport bottle. Drink-through straws have limited applications, mainly survival and emergency situations. The "international" products are some of the most useful ones. Penta-Pour bucket is an excellent product for expatriates and field camps. The Outdoor series would work well for stationary or vehicle-based groups. Large units are available for large groups and disaster relief. The Traveler (formerly Travel Tap) is a small, portable unit that hooks to the end of a faucet and could be very useful for expatriates and frequent travelers.
1227
Figure 51-18 PentaPure Sport.
Figure 51-19 PentaPure Penta-Pour bucket.
Figure 51-20 PentaPure Travel Tap.
Figure 51-21 PentaPure Outdoor 500.
1228
PRODUCT
PRICE STRUCTURE/FUNCTION
TIMBERLINE FILTER (PO Box 20356, Boulder, CO, 80308; 800-482-9297) Timberline Eagle ( Figure 51-22 )
$24 1-micron fiberglass and polyethylene matrix; hand pump; size: 9 × 1–3 inches; weight: 6 oz; flow: 1 qt in 1.5 min. $12
Replacement element Claims
Removes Giardia cysts. No claims for bacteria or viruses. Comments Effective for claims; intended only for high-quality North American backcountry use where Giardia is a possible contaminant, but should also remove Cryptosporidium. Lightest pump filter available. Cartridges cannot be cleaned but are replaceable. The intake is close to the pump, which can be awkward.
Figure 51-22 Timberline Eagle filter.
1229
PRODUCT
PRICE STRUCTURE/FUNCTION
PUR/RECOVERY ENGINEERING, INC. (9300 N 75th Ave, Minneapolis, MN 55428; 800-845-7873) Explorer ( Figure 51-23 )
$140
Replacement parts Tritek cartridge
$45
Pump
$45
Intake filter/hose
$16
Carbon cartridge and bottle adapter Carbon refill pack
$15 $6
Hand pump with 130-micron prefilter; replaceable cartridge with 0.3-micron pleated glass-fiber filter and triiodine resin (Tritek); internal brush cleans filter with twist of handle; combination carbon cartridge and bottle adapter attaches to end of outflow tubing and removes residual dissolved iodine and other chemicals; size: 10.75 × 2.25 inches; intake and output hoses: 3 ft; weight: 21 oz; max flow: 1.5 L/min; capacity: 100 gal/cartridge.
Scout ( Figure 51-24 ) Replacement cartridge
$90 Hand pump with 150-micron intake filter; 0.3-micron pleated filter and triiodine resin and carbon cartridge; size: 9.5 × 2.25 inches; weight: 14 oz; max flow: 1.0 L/min (36 stokes/L); capacity: 100 gal/cartridge. $35
Optional carbon cartridge
$20
Pioneer ( Figure 51-25 )
$30 Hand pump filter (0.3-micron fiberglass disk) attaches to top of water bottle; size: 2.5 × 4.5 inches; weight: 8 oz; flow: 1 L/min; capacity: 20 gal. $8
Extra filters (2 pack) Hiker ( Figure 51-26 ) Replacement filter Voyageur
$50 Hand pump with 0.3-micron pleated glass fiber with 160-inch2 surface; microfilter and activated carbon core; size 7.5 × 2.5 × 3.5 $25 inches; weight: 11 oz; flow: 1 L/min (40 stokes/L); capacity: 200 gal. $70 Voyager uses same body and filter as Hiker but includes iodine resin; intake filter for particles; capacity: 100 gal until cartridge replacement.
Figure 51-23 PUR Explorer.
Figure 51-24 PUR Scout.
1230
Claims Explorer, Scout, and Voyageur are purifiers that meet EPA test standards to remove or destroy all types of microorganisms. Microfilter removes cysts, and iodine resin kills bacteria and viruses on contact. Explorer has self-contained brush to clean filter without disassembling. Filter will clog before resin is exhausted. The iodine resin filters will purify (render microbiologically safe) water of any quality. However, two passages through the filter are recommended for "worst case" water (below 5° C, cloudy and highly polluted). Easily replaced carbon cartridge attaches to the outflow tubing and scavenges residual iodine. This reduces the iodine concentration from an average of 2 ppm to less than 1 ppm, leaving no iodine taste. The Hiker and Pioneer are microfilters, without iodine resin, designed for higher quality surface water, not international travel. It will "eliminate Giardia and most bacteria;" activated carbon core "reduces chemicals and pesticides, plus improves taste of water." Filter surface area of 160 square inches is "guaranteed not to clog for 1 year." The Pioneer is effective against Giardia, Cryptosporidium, and most bacteria. Comments The Explorer is a well-designed, lightweight unit for individual or small-group use in any wilderness environment. The pumping action is very easy, and the internal brush seems to effectively restore flow. The Scout and Voyageur are smaller, less expensive, and contain the same elements except for the internal brush. The Hiker and Pioneer were designed for the domestic backpacking market with access to higher water quality, where cysts and bacteria are a threat, but viruses are less of a problem. The Hiker received top ratings for field tests evaluating user-friendliness. Instructions for the water purifier advise passing cold, highly polluted water through this filter twice, but an alternative would be to allow 30 to 40 minutes of contact time. The company is hesitant to recommend a contact time, believing that the public expects a filter to render water safe immediately after passage, so they offer the more cumbersome recommendation of filtering twice. In fact, the conditions of worst-case water will rarely, if ever, be encountered; most would not attempt to drink such water unless desperate. NOTE: Repeat testing of the iodine resin filters demonstrated failure to inactivate 4-log of viruses under certain conditions, leading to a product recall in 2000. The company is investigating the role of activated carbon and the need for contact time. They hope to have products back on the market early in 2001.
Figure 51-25 PUR Pioneer.
Figure 51-26 PUR Hiker.
1231
PRODUCT
PRICE STRUCTURE/FUNCTION
RECOVERY ENGINEERING Reverse-osmosis filters Survivor 06 ( Figure 51-27 ) Survivor 35 ( Figure 51-28 )
$550 Hand pump, reverse-osmosis membrane filter with prefilter on intake line; size: 2.5 × 5 × 8 inches; weight: 2.5 lb; flow: 40 strokes/min yields 1 L/hr. $1425 Hand pump, reverse-osmosis membrane filter with prefilter on intake line; size: 3.5 × 5.5 × 22 inches; weight: 7 lbs; flow: 1.2 gal/hr.
Claims Reverse-osmosis units desalinate, removing 98% salt from seawater by forcing water through a semi permeable membrane at 800 psi. In the process, bacteria are filtered out. The manual operation of these units makes them useful for survival at sea or for use in small craft without power source. Larger, power-operated units are also available.
Comments Reverse-osmosis units are included here because sea kayaking and small boat journeys in open water are becom˜ing more popular. Most large oceangoing boats use reverse-osmosis filters. These units can obviate the need for relying solely on stored water or can be carried for emergency survival. The military uses truck-mounted reverse-osmosis filters on land for their ability to handle brackish water and remove all levels of microorganisms. Reverse-osmosis filters could be used for land-based travel but are prohibitively expensive for most people, and the flow rates are inadequate (1 L/hr, not per minute). Desalination units will remove microorganisms, including viruses, that are larger than sodium molecules. The company does not make claims for viral removal because they assume that the membrane is imperfect and some pores will be imprecise, perhaps allowing viral passage.
Figure 51-27 PUR/Recovery Engineering Survivor 06 filter.
Figure 51-28 PUR/Recovery Engineering Survivor 35 filter.
1232
PRODUCT
PRICE STRUCTURE/FUNCTION
CASCADE DESIGNS (4000 1st Ave S, Seattle, WA 98134; 206-505-9500) SweetWater Guardian ( Figure 51-29 ) Micro-filtration system
$50 Lexan body and pump handle; 100-micron metal prefilter; in-line 4-micron secondary filter; labyrinth filter cylinder of borosilicate fibers removes pathogens to 0.2 micron; granular activated carbon (GAC); safety pressure-relief valve; end-of-life indicator; outflow tubing has universal adapter that fits all water bottles; optional biocide cartridge containing iodinated resin attaches to filter—water passes through resin first, then filter cartridge, then GAC; optional input adapter that attaches to sink faucet while traveling; size: 7.75 × 3.5 inches; weight: 11 oz; flow: 1.25 L/min (new filter); capacity: 200 gal (90 gal with Viral Guard).
Replacement filter
$30
Viral Guard iodine resin cartridge
$25
Tap-Adapt
$10
Silt-stopper
$10
Prefilter
$9
Filter brush
$3
Carrying bag
$6
Global Water Express
$90 Zipper carrying case with Guardian filter, Viral Guard cartridge, and 1-L storage bag.
Walkabout ( Figure 51-30 )
$35 Lightweight version with similar filter element; size: 6.5 inches high; weight: 9 oz; flow: 0.75 L/min; capacity: 125 gal.
Claims SweetWater filter eliminates Giardia, Cryptosporidium, and other critical bacterial and protozoan pathogens, as well as pollutants, heavy metals, pesticides, and flavors. Kills viruses when used with the Viral Guard cartridge accessory. Lighter, more compact, and durable than comparable models, and easiest to clean or replace. Filter cartridges are recycled by the company. Comments Well-designed filter at a reasonable price. The three major water treatment components—filtration, GAC, and iodine resin attachment—offer broad protection and maximum flexibility. Practical design features include universal bottle adapter. Pressure-release valve indicates when filter needs cleaning, but this can be a problem as the filter clogs. A brush is provided for cleaning, and cartridges are replaceable. NOTE: Viral Guard iodine resin was recently taken off the market due to company testing that demonstrated failure to inactivate viruses, despite prior testing in outside laboratories that passed EPA standards.
Figure 51-29 Cascade Designs SweetWater Guardian filter.
Figure 51-30 Cascade Designs Walkabout.
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Chapter 52 - Infectious Diarrhea from Wilderness and Foreign Travel Javier A. Adachi Howard D. Backer Hebert L. DuPont
Acute diarrhea is one of the most common medical problems in all populations, second only to acute upper respiratory diseases. Worldwide, diarrheal diseases were reported to cause nearly 1 billion episodes of illness in 1996.[45] [60] [61] [181] The rates of illness among children in developing areas of the world range from 5 to 15 bouts per child per year, with diarrhea being the most important cause of morbidity and mortality in many regions. Readily available oral rehydration solutions prevent great numbers of dehydration-associated deaths related to acute diarrhea, especially in developing areas, but invasive bacterial enterocolitis (caused by Shigella species and Campylobacter jejuni) and persistent diarrhea (defined as illness lasting 14 days or longer) still cause significant morbidity and mortality.[45] [89] [181] Specific groups of U.S. populations with diarrhea rates similar to those in the developing world include travelers, gay males, non-toilet-trained toddlers in day-care centers, and mentally impaired residents of custodial institutions. [60] [89] This chapter provides information to help to decrease exposure to enteropathogens and risk factors, reducing the chance of acquiring illness. The clinical features of acute diarrheal illnesses often do not permit differentiation of the specific etiologic agent, but fortunately, the majority of these infections do not require etiology-specific treatment.[45] [60] [61] We formulate a clinical approach to self-therapy that is likely to minimize the complications and suffering caused by these illnesses. For the purpose of this discussion, "traveler" includes business or pleasure travelers as well as wilderness venturers.
GENERAL PRINCIPLES OF ENTERIC INFECTIONS Epidemiology Transmission.
Fecal-oral contamination, through ingestion of contaminated water and food, is the usual route of transmission for enteric pathogens causing infectious diarrhea. Other, less common routes of fecal-oral transmission are through aerosols (viruses), contaminated hands or surfaces, and sexual activity. The relative importance of food and water depends mainly on location and precautions taken. Waterborne pathogens from drinking untreated surface water or from an inadvertent ingestion during water recreational activity account for most infectious diarrhea acquired in the U.S. wilderness. [89] [125] [131] Waterborne diarrheal diseases include typhoid fever, cholera, Campylobacter enteritis, cryptosporidiasis, giardiasis, and hepatitis A infection. They are usually preventable by proper sanitation and water disinfection. Enterotoxigenic Escherichia coli, enteroinvasive E. coli, Aeromonas species, Plesiomonas shigelloides, Shigella species, Vibrio cholerae, Campylobacter jejuni, and Yersinia enterocolitica can be foodborne as well as waterborne. Person-to-person transmission is seen in selected populations whose habits expose them to high levels of pathogens (e.g., infants in day-care centers, homosexuals, persons with minimal access to water); prevention of these illnesses includes adequate handwashing and personal hygiene. [45] [60] [61] Location.
In several areas of Africa, Asia, and Latin America, where satisfactory sanitation is lacking, diarrhea is still the leading cause of infant morbidity and mortality. Good sanitation is related to a much lower incidence of infectious diarrhea in industrialized areas of the world. Travelers to foreign countries and wilderness areas often leave behind sanitation in the form of flush toilets and safe tap water, as well as proximity to advanced medical care. Similar hygienic conditions are created in other settings. Outbreaks of infectious diarrhea in day-care centers among non-toilet-trained toddlers are associated with Giardia lamblia, Shigella, Campylobacter jejuni, and Cryptosporidium, which have a small infectious dose. Hospitals, especially intensive care units and pediatric wards, institutions for mentally handicapped patients, and nursing homes are also locations with high incidence of diarrheal diseases. Clostridium difficile-associated diarrhea, Salmonella species, rotavirus, and enteropathogenic E. coli are the most common etiologic agents reported[60] [89] [158] ( Table 52-1 ). Antimicrobial Therapy.
C. difficile-associated diarrhea is frequently related to recent use of an antimicrobial agent (or cytotoxic agent), usually during the last 2 to 4 weeks before the beginning of diarrheal illness.[30] [70] [104] Age.
In developing areas of the world, children below 5 years of age have higher morbidity and mortality
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AGENTS
TABLE 52-1 -- Epidemiologic Associations with Enteropathogens WATERBORNE CHILDREN* HOSPITAL/INSTITUTIONALIZED HOMOSEXUALITY IMMUNOCOMPROMISED ZOONOTIC
BACTERIA Enteropathogenic Escherichia coli
-
+
+
-
-
-
Enterotoxigenic E. coli
-
-
-
-
-
-
Enteroinvasive E. coli
-
-
-
-
-
-
Enterohemorrhagic E. coli
-
-
-
-
-
-
Enteroaggregative E. coli
-
+
-
-
+
-
Non-typhi Salmonella
-
-
+
-
-
+
Salmonella typhi
+
-
-
-
-
-
Shigella spp.
-
+
-
+
-
-
Campylobacter spp.
+
+
-
+
-
+
Vibrio cholerae
+
-
-
-
-
-
Yersinia enterocolitica
-
-
-
-
-
+
Aeromonas spp.
+
-
-
-
-
-
Plesiomonas shigelloides
-
-
-
-
-
-
Clostridium difficile
-
-
+
-
-
-
Norwalk, small round
+
-
-
-
-
-
Rotavirus
+
+
+
-
-
-
Hepatitis A
+
-
-
-
-
-
Giardia lamblia
+
+
-
-
+
+
Entamoeba histolytica
+
-
-
-
-
+
Cryptosporidium parvum
+
-
-
+
+
+
Isospora belli
-
-
-
-
+
-
Cyclospora cayetanensis
+
-
-
-
+
-
Microsporidia
-
-
-
-
+
-
Balantidium coli
-
-
-
-
-
+
Sarcocystis
-
-
-
-
-
+
Blastocystis hominis
-
-
-
-
-
-
VIRUSES
PROTOZOA
+, Association; -, no association or unknown association. *In industrialized areas or day care centers.
rates related to dehydration, from an estimated five to 15 episodes of diarrhea per year, superimposed on malnutrition. The enteropathogens more common in infectious diarrhea during childhood are rotavirus, enterotoxigenic E. coli, enteropathogenic E. coli, C. jejuni, and G. lamblia (see Table 52-1 ). Residents in industrialized countries, such as the United States, have only one to two bouts of diarrhea per person per year, with no difference between age groups. Complications, including death, are more common in elderly persons. [45] [60] [76] Reservoirs of Infection.
Organisms are shed in the stools during asymptomatic and symptomatic infection and for a period after illness. Long-term shedding or chronic carrier states are reported only with typhoid fever, amebiasis, giardiasis, cryptosporidiasis, and enteroaggregative E. coli infection. These cases may act as reservoirs for spreading infection, even in areas with low risk for infection by contaminated water. A few enteric pathogens that are zoonotic (animal reservoirs) can increase the risk for certain persons (e.g., veterinarians, field biologists) and account for wilderness-acquired infections. These zoonotic organisms include Salmonella, Yersinia, Campylobacter, Giardia, Balantidium coli, Entamoeba, Sarcocystis, and Cryptosporidium [45] [60] (see Table 52-1 ). Incubation Period.
Food intoxication caused by ingestion of preformed toxins from Staphylococcus aureus or Bacillus cereus usually has a short incubation period (7 hours or less) and may have a common source reported by multiple victims. An outbreak by any enteropathogen
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TABLE 52-2 -- Enteropathogens Found in Tropical and Wilderness Travel TRAVEL TO DEVELOPING TROPICAL REGIONS WILDERNESS TRAVEL IN INDUSTRIALIZED REGIONS
AGENTS BACTERIA Enteropathogenic Escherichia coli
Rarely
Rarely
Enterotoxigenic E. coli
Yes
Rarely
Enteroinvasive E. coli
Rarely
Rarely
Enterohemorrhagic E. coli
Rarely
Rarely
Enteroaggregative E. coli
Yes
Unknown
Salmonella spp.
Yes
Yes
Shigella spp.
Yes
Yes
Campylobacter spp.
Yes
Yes
Vibrio cholerae
Limited
No
Yersinia enterocolitica
Rarely
Limited
Aeromonas spp.
Yes
Yes
Plesiomonas shigelloides
Yes
Rarely
Norwalk, other small round
Yes
Yes
Rotavirus
Yes
Rarely
Hepatitis A
Yes
Yes
Giardia lamblia
Yes
Yes
Entamoeba histolytica
Yes
Rarely
Cryptosporidium parvum
Yes
Yes
Isospora belli
Limited
Rarely
Cyclospora cayetanensis
Limited
Rarely
Microsporidia
Limited
Rarely
Balantidium coli
Limited
Rarely
Sarcocystis
Limited
Rarely
Blastocystis hominis
Limited
Rarely
VIRUSES
PROTOZOA
that must first infect the intestine usually has an incubation period of 8 or more hours. Immunocompromised Status.
Immunocompromised patients, including those infected with human immunodeficiency virus (HIV), are prone to acquire infection by a wide variety of enteropathogens, to develop infectious diarrhea, and to experience relapses or reinfections. HIV patients with advanced acquired immunodeficiency syndrome (AIDS) often experience malabsorption and chronic diarrhea because of changes in the intestinal function secondary to HIV or because of reduced immunity that allows coinfection with other enteropathogens. The agents responsible for diarrheal diseases in HIV patients are common enteric agents, Mycobacterium avium-intracellulare complex, Cryptosporidium, Giardia, Isospora, Cyclospora, Microsporidium, cytomegalovirus, herpes simplex virus and HIV. Treatment of HIV with highly active antiretroviral therapy and treatment of the enteric infection are associated with improved symptomatology and decreased rates of infection. Etiology Enteropathogens are the most common etiologic agents of infectious diarrhea and include bacteria, viruses, and protozoa. Fungal agents have been reported rarely. Table 52-2 lists the etiologic agents often associated with travel to developing tropical areas or with wilderness travel in an industrialized region. Foodborne illness may consist of food "poisoning" or food "infection." In food poisoning an intoxication results when toxins produced by bacteria are found in food in sufficient concentrations to produce symptoms. The major forms of intoxication result from S. aureus or B. cereus. A rare cause of food poisoning is botulism, caused when the neurotoxin of Clostridium botulinum is ingested. Other food borne pathogens are viruses, including rotavirus and small round viruses (Norwalk virus, astrovirus), and intestinal protozoal
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PATHOGEN
TABLE 52-3 -- Bacterial Enteropathogens: Virulence Properties and Distribution VIRULENCE PROPERTIES DISTRIBUTION
Vibrio cholerae
Heat-labile enterotoxin
Endemic areas in Asia, Africa, and Latin America
Vibrio parahaemolyticus
Invasiveness (?), enterotoxin or hemolytic toxin
Endemic areas in Asia and Latin America
Enteropathogenic E. coli
Enteroadherence
Infants, worldwide
Enterotoxigenic E. coli
Heat-stable and heat-labile enterotoxins, colonization factor antigens
Developing countries, tropical areas, infants, travelers
Enteroinvasive E. coli
Shigella-like invasiveness
Worldwide, endemic in South America and Eastern Europe
Enterohemorrhagic E. coli Shigalike toxin (?)
Beef, other vehicles in industrialized areas
Enteroaggregative E. coli
Enteroadherence
Infants, travelers, worldwide
Salmonella spp.
Cholera-like toxin, invasiveness
Worldwide
Shigella spp.
Shigalike toxin, invasiveness
Worldwide
Campylobacter jejuni
Cholera-like toxin, invasiveness
Worldwide
Aeromonas spp.
Hemolysin, cytotoxin, enterotoxin
Worldwide, especially Thailand, Australia, and Canada
Yersinia enterocolitica
Heat-stable enterotoxin, invasiveness
Worldwide, especially Canada, Scandinavia, and South Africa
Clostridium difficile
Cytotoxin A and B
Worldwide
Clostridium perfringens
Preformed toxin
Worldwide
Bacillus cereus
Preformed toxin
Worldwide
Staphylococcus aureus
Preformed toxins
Worldwide
agents, including G. lamblia, Entamoeba histolytica, and Cryptosporidium. Pathophysiology Three intestinal mechanisms lead to diarrhea. The most common pathophysiologic mechanism in acute infectious diarrhea is alteration of fluid and electrolyte movement from the serosal to the mucosal surface of the gut (secretory diarrhea). This alteration may occur as a result of cyclic nucleotide stimulation (as a second messenger) or by an inflammatory process that releases cytokines. The second mechanism, malabsorption or presence of nonabsorbed substances in the lumen of the bowel, and third, acceleration of intestinal motility, are more important in chronic forms of infectious and non-infectious diarrhea, such as tropical and nontropical sprue, Whipple's disease, scleroderma, malabsorption, irritable bowel syndrome, and inflammatory bowel disease. Table 52-3 shows the virulence factors of the most important enteric pathogens related to infectious diarrhea.[42] [60] In general, enteropathogens cause diarrhea by the first mechanism and can be subdivided into noninvasive and invasive groups. Noninvasive microorganisms primarily colonize the proximal small bowel and cause secretory diarrhea without disruption of the mucosal surface. The unformed stools are usually voluminous and rarely bloody, and high fever is unusual. The common pathogens in this group include V. cholerae, enterotoxigenic E. coli, preformed enterotoxins, Norwalk virus, rotavirus, Giardia, and Cryptosporidium. Dehydration is the major complication, especially in the extremes of age, and without adequate therapy it can be followed by renal insufficiency. Invasive pathogens involve the distal ileum and colon, damaging the mucosa and eliciting an inflammatory response. Stools are typically liquid, small volume, and may contain blood and many leukocytes. The common microorganisms in this group are Shigella species, Salmonella species, enteroinvasive E. coli, enterohemorrhagic E. coli, Y. enterocolitica, C. jejuni, Aeromonas species, V. parahaemolyticus, and E. histolytica. Complications include dehydration and systemic involvement, especially in children with malnutrition.[42] [43]
TRAVELER'S DIARRHEA Traveler's diarrhea (TD) is the most important travel-related illness in terms of frequency and economic impact. Point of origin, destination, and host factors are the main risk determinants.[60] [158] International travel is more often associated with enteric infection and diarrhea, particularly when the destination is a developing tropical region, although the same infections can be contracted domestically. The 2% to 4% rate of diarrhea for people who take short-term trips to low-endemic areas (e.g., United States, Canada, Northwestern Europe, Australia, Japan) may be related to more frequent consumption of food in public restaurants, increased intake of alcohol, or stress. This rate of diarrhea increases to about 10% for travelers from these low-endemic areas to northern Mediterranean areas, China,
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Russia, or some Caribbean islands. This incidence increases as high as 40% to 50% for short-term travelers from low-risk countries to high-risk countries (developing tropical and sub-tropical regions of Latin America, southern Asia, or Africa). More than 25 million persons travel each year from these industrialized countries to high-risk areas, resulting in over 7 million travelers with diarrhea.[45] [60] [61] Multiple episodes of diarrhea may occur on the same trip.[158] Attack rates remain high for up to 1 year,[45] [60] then decrease, but not to the levels of local inhabitants. Immunity to enterotoxigenic E. coli (ETEC) infection, either asymptomatic or symptomatic, occurs after repeated or chronic exposure,[141] which supports the feasibility of developing a vaccine. TD is a syndrome, not a specific disease.[45] [60] [158] Although any waterborne or foodborne enteropathogen may cause TD, bacteria are the most common etiologic agents among persons traveling to high-risk areas. The bacterial flora of the bowel changes rapidly after arrival in a country with high rates of TD. At least 15% of travelers remain asymptomatic despite the occurrence of infection by pathogenic organisms, including ETEC and Shigella. However, most infected patients become ill. Definition TD refers to an illness contracted while traveling, although in 15% of sufferers symptoms begin after the return home.[44] Most studies define TD as the passage of three or more unformed stools in a 24-hour period in association with one or more enteric symptoms, such as abdominal cramps, fever, fecal urgency, tenesmus, passage of bloody, mucoid stools, nausea, and vomiting. [45] [60] [158] Etiology Since the incidence of TD reflects in part the extent of environmental contamination with feces, the etiologic agents are pathogens causing illness in local children. The list of etiologic agents changes as laboratory techniques identify new enteropathogens ( Table 52-4 ). Twenty years ago, specific pathogens were found in only 20% of cases.[112] [113] Currently, etiologic agents can be identified in up to 80% of TD episodes.[60] [158] In most studies, however, causative pathogens are not identified in 20% to 40% of cases. In most of these cases, antimicrobial therapy shortens illness, suggesting that this subset of diarrhea is caused by undetected bacterial pathogens.[23] [57] [63] [80] Overall, the major etiologic agents and their frequency of isolation are remarkably similar when one region of the world is compared with another. Enterotoxigenic E. coli has proved to be the most common cause of TD worldwide,[60] [141] [158] [178] accounting for about one third to one half of cases. Shigella and Aeromonas/Plesiomonas species are second to ETEC and TABLE 52-4 -- Major Pathogens in Traveler's Diarrhea (Travel to Developing Tropical Regions) AGENT
FREQUENCY (%)
BACTERIA
40–80
Enterotoxigenic Escherichia coli
5–40
Enteroaggregative E. coli
0–40
Salmonella
0–15
Shigella
0–15
Campylobacter jejuni
0–30
Aeromonas
0–10
Plesiomonas
0–5
Other
0–5
VIRUSES
0–20
Rotavirus
0–20
Small round viruses
0–10
PROTOZOA
0–5
Giardia lamblia
0–5
Entamoeba histolytica
0–5
Cryptosporidium parvum
0–5
UNKNOWN
10–40
cause 20% of illness. Other causes of TD include Salmonella (4% to 5% of cases), Campylobacter (3%), Vibrio, viruses (10%), and parasites (2% to 4%). Specific pathogens may predominate at a particular time or location. ETEC is more common in semitropical countries, including Mexico and Morocco, during rainy summer seasons and occurs less often in drier winters. [133] A recent study showed that enteroaggregative E. coli is the second most common etiologic organism in TD in Guadalajara (Mexico), Ocho Rios (Jamaica), and Goa (India).[3A] Clinical Syndromes Table 52-5 outlines the major syndromes in patients with enteric infection. The typical clinical syndrome experienced by travelers with diarrhea secondary to the major infectious causes (e.g., ETEC) begins abruptly with watery diarrhea and abdominal cramping. Most cases are mild, consisting of passage of one to two unformed stools per day associated with symptoms that are tolerable and do not interfere with normal activities. Approximately 30% of victims experience moderately severe illness, with three to five unformed stools per day and distressing symptoms that force a change in activities or itinerary. Only 10% to 20% of persons with TD experience severe illness with more than five unformed stools passed per day, incapacitating symptoms that force confinement to bed, or any number of unformed stools with concomitant fever and dysentery. [60] [158] Only 4% of persons with TD consult a local
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TABLE 52-5 -- Pathophysiologic Syndromes in Diarrheal Disease SYNDROME
AGENT
Acute watery diarrhea
Any agent, especially toxin-mediated diseases (e.g., enterotoxigenic Escherichia coli, Vibrio cholerae)
Febrile dysentery
Shigella, Campylobacter jejuni, Salmonella, enteroinvasive E. coli, Aeromonas spp., noncholera Vibrio spp., Yersinia enterocolitica, Entamoeba histolytica, inflammatory bowel disease
Vomiting (as predominant symptom)
Viral agents, preformed toxins of Staphylococcus aureus or Bacillus cereus
Persistent diarrhea (> 14 days)
Protozoa, small bowel bacterial overgrowth, invasive or inflammatory enteropathogens (e.g., Shigella, enteroaggregative E. coli)
Chronic diarrhea (> 30 days)
Small bowel injury, inflammatory bowel disease, irritable bowel syndrome, Brainerd diarrhea
physician, and less than 1% are admitted to a local hospital while traveling. Approximately one third of travelers are confined to bed or need to alter their travel plans when a diarrheal illness develops. Although the average duration of diarrhea is 3 to 4 days, 50% of cases resolve within 48 hours, 8% to 15% last longer than 1 week, and 1% to 3% last 1 month or longer. TD is rarely life threatening. Clinical Examination The etiologic organism of TD cannot be diagnosed reliably based only on clinical manifestations, because illnesses caused by different microorganisms share similar clinical features.[37] [60] [143] [158] [184] Although noninvasive organisms rarely cause dysentery, invasive organisms often cause watery diarrhea without dysentery or a sequential illness beginning with watery diarrhea and progressing to bloody dysentery. If multiple people acquire the illness shortly after eating a shared meal, food poisoning caused by ingestion of preformed toxins in food should be suspected, especially if the illness has a short incubation period (8 hours or less), predominant vomiting, and resolution within 24 hours. Investigators have studied the reliability of clinical factors to predict which persons will have a positive stool culture.[37] [143] [184] Bacterial pathogens are suspected when the sufferer has a large number (more than six) of stools per day, has a fever, and has had the ailment for more than 24 hours but less than 1 week. Regardless of the clinical similarities of enteropathogens causing TD, certain differences exist, with distinct clinical findings. Dehydration.
An important part of the initial assessment is to measure the level of hydration, which includes a determination of vital signs, orthostatic pulse and blood pressure, mental status, skin turgor, hydration of mucous membranes, and urine output. Dehydration is most common in pediatric and elder populations. Fever.
Fever is a reaction to an intestinal inflammatory process. High fever suggests a pathogen invasive to the intestinal mucosa, which classically includes bacterial enteropathogens such as Shigella, Salmonella, and Campylobacter jejuni. Fever can also be produced by enteroinvasive E. coli, Vibrio parahaemolyticus, Aeromonas, Clostridium difficile, and viral pathogens. Vomiting.
Vomiting as the predominant symptom suggests food intoxication secondary to enterotoxin produced by Staphylococcus aureus or Bacillus cereus or gastroenteritis secondary to viruses, such as rotavirus in infants or Norwalk virus in any age group. Dysentery.
Dysentery is defined as the passage of small-volume stools with gross blood and mucus. Common causes include Shigella, C. jejuni, Salmonella, Aeromonas, V. parahaemolyticus, Yersinia enterocolitica, enteroinvasive E. coli, enterohemorrhagic E. coli, Entamoeba histolytica, and inflammatory bowel disease. Invasive organisms most often cause dysentery. Up to 30% to 50% of cases of shigellosis or campylobacteriosis are reported to cause dysenteric diarrhea in the United States. Other enteric symptoms are tenesmus (straining without passing stools) and fecal urgency (voluntary inability to delay stool evacuation by 15 minutes), which are more common with dysentery. Abdominal Findings.
The abdominal examination in persons with TD often shows mild tenderness but should not demonstrate signs of peritoneal irritation. A rectal examination may reveal tenderness in enterocolitis, and the victim may have painful external hemorrhoids, a result of the excess stooling. Systemic Involvement.
Some of the enteric pathogens produce both diarrheal and systemic disease, such as hemolytic-uremic syndrome related to infection with shigellosis or enterohemorrhagic E. coli, Reiter's syndrome or glomerulonephritis related to Y. enterocolitica, and typhoid fever secondary to Salmonella typhi and S. paratyphi.
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LABORATORY TEST
TABLE 52-6 -- Indications for Laboratory Test in Diarrheal Diseases and Possible Diagnosis INDICATION DIAGNOSIS/AGENT
Fecal leukocytes or lactoferrin
Moderate to severe cases
Diffuse colonic inflammation, invasive enteropathogen
Stool culture
Moderate to severe diarrhea, fever, persistent diarrhea, fecal leukocytes, male homosexuals, food or water outbreaks
Any bacterial enteropathogen
Blood culture
Enteric fever, sepsis
Salmonella, less likely Campylobacter, Shigella, Yersinia
Parasite examination
Persistent diarrhea, travel to specific areas, day-care centers, male homosexuals, immunocompromised persons
Any protozoan parasite
Amebic serology
Persistent diarrhea, liver abscess
Entamoeba histolytica
Rotavirus antigen
Hospitalized infants
Clostridium difficile toxin
Antibiotic-associated diarrhea
C. difficile
Laboratory Findings Several laboratory tests are useful in evaluating patients with diarrheal disease ( Table 52-6 ). For most cases of TD, laboratory testing is reserved for illness continuing after the patient returns home. Persons with mild acute diarrhea usually need only clinical evaluation. An etiologic assessment is unnecessary, and treatment can be given empirically. Laboratory tests are reserved for persons with moderate to severe diarrhea and those with persistent diarrhea. Fecal Leukocyte Test.
The presence of fecal leukocytes is a reliable indicator of invasive and inflammatory distal gastrointestinal (GI) infection. For all moderate to severe illness, this is the most rapid, useful test and the ideal screening procedure. The fecal leukocyte test should be performed on a fresh sample. A mucus strand, if available, or liquid stool
is stained with a drop of dilute methylene blue and observed under a microscope. The stool can be heat-fixed and examined under oil immersion or viewed as a wet-mount preparation under a coverslip with the "high dry" objective of the microscope. Leukocytes are easily seen, although they can be confused with protozoal cysts. A large number of polymorphonuclear leukocytes (PMNs) per high-power field (hpf) indicates diffuse colonic inflammation ( Figure 52-1 ) rather than a specific etiology but correlates most significantly with invasive bacterial infection caused by Shigella, Salmonella, or C. jejuni. Other organisms and conditions that may lead to presence of fecal leukocytes in the stools are C. difficile-associated diarrhea, Aeromonas, Y. enterocolitica, V. parahaemolyticus, EIEC, idiopathic ulcerative colitis, and allergic colitis. Fecal leukocytes are less likely to be seen in noninvasive infections, such as diarrhea caused by
Figure 52-1 Methylene blue stain of a fecal smear from a patient with bacillary dysentery (400×). Numerous polymorphonuclear leukocytes are present, which indicates the presence of diffuse colonic inflammation.
enterotoxigenic E. coli, G. lamblia, and viral pathogens, but they are often observed in culture-negative stools.[92] Not all patients with invasive infectious diarrhea will have leukocyte-positive stools. Stool Culture.
Bacterial infection is specifically diagnosed by stool culture, although routine stool testing identifies few pathogens. A routine laboratory should be able to recover Shigella, Salmonella, and Campylobacter from a stool culture and, if specifically requested, Vibrio cholerae and V. parahaemolyticus, Aeromonas, Y. enterocolitica, and C. difficile. In the United States, only about 10% of stool cultures are positive. The percentage is higher (12% for adults, about 50% for children or travelers) among patients in developing countries when research laboratories look for all the important agents, including ETEC.[158] [184] The major indications for performing a stool culture are
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moderate to severe diarrhea, febrile and dysenteric disease, persistent diarrhea, and presence of fecal leukocytes in fecal smears. Blood Culture.
Blood culture(s) should be performed in all patients who are hospitalized with GI symptoms or those who have enteric symptoms and high fever. Systemic infections by S. typhi and non-typhi Salmonella, Shigella, Campylobacter fetus, and Y. enterocolitica may be diagnosed by blood culture. Parasite Examination.
In cases of TD, direct examination of stool samples looking for a parasite infection is less useful as a routine test than is stool culture. When using microscopy to search for parasites, multiple samples may have to be examined to identify the causative agent. Immunologic techniques to detect antigens of protozoan parasites are more efficient and in common use for parasites that inhabit the duodenum (e.g., Giardia, Cryptosporidium, E. histolytica, microsporidia).[89] [131] At times, intestinal parasites are better detected using a sample from duodenal aspiration or intestinal biopsy.[89] [131] Indications to perform parasitic examination are persistent diarrhea, diarrhea during or shortly after travel within mountainous areas of the United States or Russia, diarrhea in someone who has regular contact with an infant day care center, or diarrhea in a male homosexual or immunocompromised person. Special Tests.
The Enterotest is a gelatin capsule affixed to a nylon string that is swallowed after the end of the string is taped to the cheek. After the patient consumes a meal or after the string has been attached to the cheek overnight, it is removed so that mucus and other intestinal secretions can be scraped off and studied for enteropathogens. It may be useful to sample small bowel mucus to diagnose cases of typhoid fever, giardiasis, and strongyloidiasis. A serologic diagnostic test for typhoid fever (Widal's reaction) is only useful in endemic areas, because exposure to cross-reacting gram-negative rods other than S. typhi can lead to false-positive serologic results in areas where typhoid fever is not common.[136] In a patient with a typhoidlike systemic illness who has taken one or more doses of an antimicrobial, culture of bone marrow aspiration may help to identify the bacteria. Antibody-specific serologic tests are now widely used for the diagnosis of invasive amebiasis.[75] Rotavirus antigen testing of stool is sensitive and easy to perform. It is indicated to screen infants less than 3 years of age to help guide therapy (fluids without antimicrobials are given when the test is positive).[153] C. difficile toxin assay by tissue culture or serology is indicated for diagnosing antibiotic-associated colitis. Many
CLINICAL MANIFESTATIONS
TABLE 52-7 -- Empiric Treatment of Diarrhea in Adults RECOMMENDATIONS
Watery diarrhea with mild symptoms (no change in itinerary)
Provide oral fluids and saltine crackers plus symptomatic treatment as needed with loperamide or bismuth subsalicylate.
Watery diarrhea with moderate symptoms (change in itinerary but able to function)
Administer symptomatic treatment with loperamide or bismuth subsalicylate.
Watery diarrhea with severe symptoms (incapacitating)
Perform stool culture and fecal leukocytes; consider antimicrobial drugs* plus loperamide.
Dysentery or fever
Perform stool culture and fecal leukocytes; consider antimicrobial drugs,* no loperamide.
Persistent diarrhea (> 14 days)
Perform stool culture and parasite examination; consider empiric trial with metronidazole.
Vomiting, minimal diarrhea
Administer bismuth subsalicylate.
Diarrhea in pregnant women
As above; administer fluids and electrolytes; consider attapulgite, no fluoroquinolones.
*Fluoroquinolones (norfloxacin, ciprofloxacin, or levofloxacin) are recommended.
of the commercial serologic kit tests are easier to perform, but they detect only toxin A and are less sensitive than the tissue culture procedure. Infants and children may normally carry C. difficile toxin in the stools, negating the value of this test.[104] Sigmoidoscopy and Colonoscopy.
In selected cases, particularly clinical colitis and diarrhea persisting for 14 days or longer, sigmoidoscopy or colonoscopy is used to study colonic lesions and collect samples for culture and microscopy. Mucosal changes may not be specific, except when pseudomembranes are sought. In homosexual male patients with acute diarrhea, examination of the distal colon may show evidence of proctitis (mucosal inflammation in the distal 15 cm of the colon), proctocolitis (inflammation beyond 15 cm), or enteritis. Acute Diarrhea Where routine laboratory evaluation is available, logical approaches to patients with acute diarrhea depend on the clinical syndrome. The illness, not the infection,
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TABLE 52-8 -- Nonspecific Drugs for Prophylaxis and Therapy in Adults AGENT
THERAPEUTIC DOSE
Attapulgite
3 g initially, then 3 g after each loose stool or every 2 hours (not to exceed 9 g/day); should be safe during pregnancy and childhood.
Loperamide
4 mg initially, then 2 mg after each loose stool (not to exceed 8 to 16 mg/day); do not use in dysenteric diarrhea.
Bismuth subsalicylate 30 ml or two 262-mg tablets every 30 minutes for 8 doses; may repeat on day 2. should be treated, so most persons can be managed on the basis of symptoms and stool appearance. In certain situations, empiric therapy may be given without establishing an etiologic agent; in other cases, specific therapy follows laboratory confirmation of an etiologic agent ( Table 52-7 and Table 52-8 ). In patients with watery diarrhea and mild symptoms, only clinical evaluation is needed. An etiologic assessment is unnecessary, and symptomatic treatment can be given empirically. Persons with moderate to severe diarrhea, dysentery, fever, or presence of fecal leukocytes should have their stool cultured, if laboratory assessment is feasible, and should start empiric antimicrobial therapy. Persistent and Chronic Diarrhea Diarrhea may persist after the traveler returns home. Up to 3% of persons with TD in high-risk areas will develop persistent diarrhea. Persistent diarrhea is defined as illness lasting 14 days or longer, whereas diarrhea is considered chronic when the illness has lasted 30 days or longer.[44] [60] [158] The etiology of persistent or chronic diarrhea often differs from that of acute diarrhea. Important causes of persistent diarrhea include (1) protozoal parasitic agents (G. lamblia, Cryptosporidium, Cyclospora, E. histolytica), (2) bacterial infection (Salmonella, Shigella, Campylobacter, Y. enterocolitica), (3) lactase deficiency induced by a small bowel pathogen (G. lamblia, viral enteropathogen such as rotavirus or Norwalk virus), and (4) a small bowel bacterial overgrowth syndrome secondary to small bowel motility inhibition (as a result of enteric infection) or secondary to antimicrobial use. Occasionally, other parasitic enteric infections can cause more persistent illness. These include Strongyloides stercoralis, Trichuris trichiura, and severe infection by Necator americanus or Ancylostoma duodenale. In rare cases, more protracted diarrhea may be a prominent symptom in persons with schistosomiasis, Plasmodium falciparum malaria, leishmaniasis, or African trypanosomiasis.[44] [60] [158] When chronic diarrhea occurs, the following possibilities should also be considered: 1. After eradication of microbial pathogens, bowel habits may not return to normal for several weeks. Postdysenteric colitis resembling ulcerative colitis occasionally follows infection with invasive pathogens, especially infection caused by E. histolytica. This could represent slow repair of the damage to the intestinal mucosa. 2. Postinfective malabsorption can persist for weeks to months after acute diarrhea; it is especially common after giardiasis.[44] [61] [158] 3. A poorly defined condition, tropical sprue, may explain prolonged diarrhea in a traveler. Onset usually follows an episode of acute enteritis and is associated with substandard hygiene and longer stays. The cause may involve small bowel bacterial overgrowth, since small bowel incubation may yield a heavy growth of bacteria, and patients often respond to antimicrobial therapy. 4. An underlying condition such as inflammatory bowel disease, irritable bowel syndrome, or celiac sprue may worsen after an episode of acute enteritis. 5. Brainerd diarrhea, named after a community outbreak in Brainerd, Minnesota, may be the explanation for chronic diarrhea. This condition follows the consumption of raw (unpasteurized) milk[150] or untreated water. [155] There is no diagnostic test or therapy and the diagnosis is suspected based on the epidemiologic history (exposure to unpasteurized milk or untreated water just before onset of illness).[23] The approach to evaluate persistent or chronic diarrhea in travelers should begin with diagnostic tests for conventional bacterial pathogens in stools and at least three parasitologic evaluations in stools. Dietary modification in all cases should include avoidance of lactose. Treatment should be specific, following the results of the microbiologic tests. Because most of these chronic forms of diarrhea are self-limiting, it is unwise to keep treating these patients with multiple antibiotics, which only alters the gut ecology and encourages diarrhea. An empiric trial with metronidazole is an option if all tests are negative (see Table 52-7 ). If stools contain leukocytes, sigmoidoscopy or colonoscopy should be performed, along with empiric treatment for Shigella or Campylobacter infection. If there are no leukocytes, duodenal mucus should be examined for G. lamblia, followed by empirical treatment for Giardia, if metronidazole has not already been given. The next steps are tests for malabsorption and biopsy of the small bowel mucosa. Treatment In all cases of diarrhea, fluid and electrolyte replacement should be the primary therapy. Outpatient treatment
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with instructions for oral rehydration can be used in the vast majority of adults and children. Significant dehydration from diarrhea in travelers is unusual. Treatment with intravenous (IV) fluids is indicated for patients with hypotension, inability to retain oral fluids, or systemic compromise (high fever and toxicity), moderate toxicity or dehydration and a severe underlying disease, or at extremes of age. Selected patients may benefit from symptomatic therapy, and others may receive empiric antimicrobial therapy (see Table 52-7 ). The main goal for using therapy, such as an antimotility drug or an antimicrobial agent, is to attenuate the severity and duration of diarrhea and concomitant symptoms. Diet and Lifestyle.
Supplemental nutrition is beneficial (essential in undernourished populations) and can be given as soon as fluid deficit losses are replaced, usually after the first 4 hours. During acute diarrheal disease the intestinal tract cannot process complex dietary products, so patients are often told to avoid solid foods. As stooling decreases and appetite improves, staple foods, such as cereals, bananas, crackers, toasts, lentils, potatoes, and other cooked vegetables, are well tolerated and can be gradually added to the diet to facilitate enterocyte renewal, with progression to white meats, fruits, and vegetables. Dairy products and red meats are recommended only after diarrhea has resolved, usually after 2 to 3 days. Only foods and drinks that prolong diarrhea or increase intestinal motility should be avoided, such as those that contain lactose, caffeine, alcohol, high fiber, and fats. Breast-feeding of infants should not be suspended or should be resumed as soon as possible.[41] [45] [60] [61] [185] Patients with TD should avoid excessive physical therapy to reduce the risk of dehydration. Fluid Treatment.
The major cause of morbidity and mortality from acute diarrheal disease is depletion of body water and electrolytes. Rehydration is an essential part of therapy, especially in the extremes of age and during pregnancy. Most patients with TD do not become dehydrated, and hydration can be maintained by ingesting fluids such as sodas, juices, soup, and potable water in conjunction with a source of electrolytes (e.g., salted crackers).[23] [45] [60] [61] The most significant advance in the therapy of diarrhea in the past 25 years has been development of the oral rehydration concept. Oral rehydration solution (ORS) was first developed for treatment of cholera and has saved countless lives, primarily children. ORS precludes extensive use of scarce and expensive IV fluids in developing countries, and its use is the cornerstone of the World Health Organization (WHO) program to combat diarrheal diseases.[23] [45] [60] [61] The discovery that glucose-enhanced intestinal absorption of sodium remains intact despite active diarrhea or vomiting was the key to development of ORS.[133] [170] Other electrolytes are also absorbed nonselectively when ORS is administered. Watery diarrhea, often caused by release of an enterotoxin, has an electrolyte composition similar to plasma, varying somewhat with type of infection and age of the patient. The formula packaged and promoted by the WHO and United Nations Internations Children's Emergency Fund (UNICEF) contains powder to be mixed with 1 L of disinfected water, with the following concentrations: sodium 90 mEq, potassium 20 mEq, chloride 80 mEq, bicarbonate 30 mEq, and glucose 111 mmol. Newer formulations use trisodium citrate instead of sodium bicarbonate and complex carbohydrates instead of glucose. Cereal-based products are also available. Although this concentration of electrolytes is ideal for treating purging diarrhea associated with cholera and other dehydrating forms of diarrhea, most TD can be adequately managed with readily available soft and sport drinks, fruit juice or salt solutions, taken with salted crackers and the foods listed earlier.[23] [45] [60] [61] Fluid status in the field must be guided by physical signs related to hydration, including pulse, mucous membranes, skin turgor, and urine output. Urine color and volume are excellent measures. For travelers in the wilderness or tropics, fluid replacement must equal basic needs plus volume of diarrhea plus estimated sweat loss.
Nonspecific Therapy.
Symptomatic medications are useful for treatment of mild to moderate diarrhea, since they decrease symptoms and allow patients to return more quickly to normal activities (see Table 52-7 and Table 52-8 ). Nonantibiotic therapies that may be used in addition to fluids are best classified by their effects on pathophysiologic mechanisms. ALTERATION OF INTESTINAL FLORA.
Lactobacillus preparations and yogurt are safe, but evidence is insufficient to establish their value in the therapy of acute diarrhea.[23] [45] [60] [61] [94] ADSORBENTS.
Adsorbent agents bind nonspecifically to water and other intraluminal material, including bacteria and toxins, and potentially to other medications such as antibiotics. The most common medication in this group is attapulgite (see Table 52-8 for dosing), a nonabsorbable magnesium aluminum silicate that is more active than the combination of kaolin and pectin.[23] By adsorbing water, these agents give stools more form or consistency but do not decrease stool frequency, cramps, or duration of illness. They are reliable and should be safe in all persons, although adsorbents are not approved for use in young infants and pregnant women.[169] ANTIMOTILITY DRUGS.
Narcotic analogs related to opiates are the major antimotility drugs. In addition to slowing
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intestinal motility, these drugs alter water and electrolyte transport, probably affecting both secretion and absorption.[23] [45] [60] [61] Compared with placebo, antimotility drugs reduce the number of stools passed and the duration of illness by about 80% during their administration.[55] [56] The most frequently used product is loperamide (Imodium), 4 mg initially, followed by 2 mg after each unformed stool, not to exceed 8 to 16 mg/day. Loperamide also has a weak antisecretory effect through inhibition of intestinal calmodulin. Diphenoxylate with atropine (Lomotil) is less expensive than loperamide but has greater central opiate effects, in case of accidental overdose by a child, and more side effects without antidiarrheal benefits because of the atropine, which is added only to prevent overdoses. Tincture of opium or paregoric opium preparations are rapidly and equally effective and offer a modest relief of symptoms. Antimotility drugs should never be used alone in patients who have dysenteric or febrile diarrhea, since inhibition of gut motility may facilitate intestinal infection by invasive bacterial enteropathogens.[23] [46] However, this theoretic deleterious effect does not appear to be an issue when loperamide is used concurrently with an effective antimicrobial agent.[63] [64] [187] Antimotility drugs should not be given to children under age 3 years because of the danger of central nervous system (CNS) depression.[23] They are not recommended for more than 48 hours in acute diarrhea.
DIAGNOSIS
TABLE 52-9 -- Antibacterial Therapy for Diarrhea in Adults RECOMMENDATION
EMPIRIC THERAPY IN BACTERIOLOGICALLY UNCONFIRMED DISEASE Traveler's diarrhea or febrile dysenteric disease
Norfloxacin 400 mg bid, ciprofloxacin 500 mg bid, or levofloxacin 500 mg qd for 1 to 3 days
Persistent diarrhea
Trial with metronidazole 250 mg qid for 7 days
ORGANISM-SPECIFIC THERAPY IN LABORATORY CONFIRMED DIARRHEA Enterotoxigenic and enteroaggregative Escherichia coli Ciprofloxacin 1000 mg single dose or 500 mg bid for 3 days; norfloxacin 400 mg bid or levofloxacin 500 mg diarrhea qd for 1 to 3 days. Cholera
Ciprofloxacin 1000 mg single dose or 500 mg bid for 3 days; norfloxacin 400 mg bid or levofloxacin 500 mg qd for 3 days; doxycycline 300 mg single dose
Salmonellosis (typhoid fever or systemic infection)
Norfloxacin 400 mg bid, ciprofloxacin 500 mg bid, or levofloxacin 500 mg qd for 7–10 days; in patients with underlying disease or immunocompromised persons.
Salmonellosis (intestinal nontyphoid salmonellosis without systemic infection)
Antimicrobial therapy controversial (see text)
Shigellosis
Norfloxacin 400 mg bid, ciprofloxacin 500 mg bid, or levofloxacin 500 mg qd for 3 days
Campylobacteriosis
Erythromycin 500 mg qid for 5 days; azithromycin 500 mg qd, norfloxacin 400 mg bid, ciprofloxacin 500 mg bid, or levofloxacin 500 mg qd for 3 days
Enteropathogenic E. coli diarrhea
Unclear if antimicrobial therapy is necessary
Clostridium difficile colitis
Metronidazole 250 mg tid for 7 to 14 days
Bid, Twice daily; qd, daily.
ANTISECRETORY DRUGS.
Since increased secretion of water and electrolytes is the major physiologic derangement in acute watery diarrhea, therapy aimed at this effect is appealing. Although aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) inhibit secretion, their usefulness is limited, primarily because of mucosal toxicity. [23] [61] The salicylate moiety of bismuth subsalicylate reduces the number of stools passed and duration of diarrhea by about 50%, primarily by blocking the effect of the enterotoxin on the intestinal mucosa.[23] [56] Bismuth subsalicylate also has antimicrobial and antiinflammatory properties. New compounds are being developed that have antisecretory properties without motility effects.[58] Antimicrobial Therapy.
Although most enteric infections do not require antibiotics, empiric antimicrobial therapy is indicated in acute TD and febrile, dysenteric illness because of the high frequency of bacteria as etiologic agents ( Table 52-9 ).[23] [61] Therapy for specific infections is discussed in the corresponding sections. At times, treatment is indicated regardless of symptoms to prevent person-to-person spread (e.g., for food handlers, river guides, day-care workers) or to eradicate pathogenic strains and prevent conversion from asymptomatic to symptomatic illness (e.g., E. histolytica).[22] [163] Only fluoroquinolones and to a lesser extent trimethoprim/sulfamethoxazole (TMP/SMX) retain
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enough activity against enteric pathogens to be considered useful for empiric therapy. The drug of choice for empiric therapy of TD in adults is an oral fluoroquinolone for 1 to 3 days.[23] [60] [61] Fluoroquinolones, including those evaluated in TD (norfloxacin, ciprofloxacin, ofloxacin, levofloxacin), represent the treatments of choice for TD when individuals are traveling to areas where TMP/SMX resistance among bacterial enteropathogens is common or has not been determined. Potential advantages of the quinolones include a high degree of in vitro activity against virtually all bacterial etiologic agents (including Campylobacter) and the potential for less bacterial resistance.[23] [57] [63] Ciprofloxacin (500 mg twice a day) was equally effective in treating TD compared with TMP/SMX in an area where trimethoprim resistance was unusual.[63] TMP/SMX
(160/800 mg) and trimethoprim (200 mg) twice a day for 5 days were equally effective in reducing the number of unformed stools, duration of illness, and abdominal symptoms compared with placebo. [51] Reduced duration of illness was reported in infections caused by ETEC or Shigella and also in the group without identifiable pathogens. The main problem with TMP/SMX is the increasing in vitro resistance to this antibiotic in several areas of the world.[23] [60] [61] Because fluoroquinolones are not yet approved for use in children, TMP/SMX plus a macrolide, nalidixic acid, or azithromycin may be given, although a two-drug regimen is a major disadvantage. Azithromycin alone or a short course of a fluoroquinolone may soon be proven safe and efficacious.[118] [168] Travelers to high-risk regions should carry an antibacterial drug and a symptomatic drug, such as loperamide. Persons should be instructed to take an antimicrobial after passing the third unformed stool in all cases and to take loperamide only if they have no fever.[60] [64] [65] [187] In persons who pass a third stool in less than 24 hours, illness is likely to progress without therapy. Loperamide induces more rapid relief of symptoms, and the antimicrobial exerts curative effects. The duration of antimicrobials needed in TD appears to be short. Many cases respond to single-dose treatment, and no person needs more than 3 days of treatment.[23] [57] [60] [64] In cases of dysenteric diarrhea the same antimicrobial regimen is given promptly. Empiric therapy should be with fluoroquinolones in adults and with TMP/SMX plus a macrolide or nalidixic acid in children. Azithromycin is an alternative antimicrobial agent under current study. The antibiotic regimens are not effective against diarrhea caused by Campylobacter (in the case of TMP/SMX or trimethoprim therapy), viruses, parasites, or other noninfectious causes. Therefore antibiotics should not be continued in the face of persistent or worsening diarrhea. Prevention and Prophylaxis Dietary Precautions.
Food and water transmit the pathogens that cause infectious diarrhea and TD.[23] [45] [60] [61] [62] When diarrhea occurs, however, the exact source cannot be determined. It is clear that education can play an important role in prevention of TD, but dietary habits usually cannot be rigidly controlled. Food in developing countries is often contaminated with fecal coliforms and enteropathogens.[3] Vibrio cholerae remains viable for 1 to 3 weeks in food,[71] and Salmonella can survive 2 to 14 days in water or in the environment in a desiccated state.[62] Risk of illness appears to be lowest when most of the meals are self-prepared and eaten in a private home, intermediate when food is consumed at public restaurants, and highest when food is obtained from street vendors.[15] [62] The following standard dietary recommendations for prevention are based more on known potential vehicles for transmission of illness than on strong evidence, because most of the studies evaluating risk have found little correlation between routine precaution and presence of diarrhea[45] [61] [62] : 1. Avoid tap water, ice made from untreated water, and suspect bottled water. Bottled and carbonated drinks, beer, and wine are probably safe. Boiled or otherwise disinfected water is safe. Waterborne epidemics of almost all the enteric pathogens have occurred worldwide.[62] Tap water in high-risk countries is difficult to implicate in TD, but has been shown to contain enteric bacteria and pathogenic viruses and parasites.[62] [131] Tap water and occasionally even bottled water may be unsafe, but bottled carbonated beverages are considered safe because of the antibacterial effects of the low acidity. Alcohol in mixed drinks does not disinfect, so these may not be safe, but bottled beer and wine have not been found to be contaminated. Most enteric organisms can survive freezing and melting in common drinks, so ice is not considered safe unless made from treated or previously boiled water. Ice in block form is often handled with unsanitary methods.[43] [62]
2. Avoid unpasteurized dairy products. These may be the source of infection with Salmonella, Campylobacter, Brucella, Listeria monocytogenes, Mycobacterium tuberculosis, and others. [161] 3. Avoid raw food. Raw vegetables in salads may be contaminated by fertilization with human waste or by washing in contaminated water.[62] Anything that can be peeled or have the surface removed is safe. Fruits and leafy vegetables can also be disinfected by immersion and washing in iodinated water or by exposure to boiling water for 30 seconds. Raw seafood, including that in such traditional dishes as ceviche and sashimi, has been associated with increased risk of TD. Shellfish concentrate enteric organisms from contaminated 1249
water and can carry hepatitis A, Norwalk virus, Aeromonas hydrophila, Y. enterocolitica, V. cholerae, and V. parahaemolyticus. Raw fish can carry parasites such as Anisakis simplex, Clonorchis sinensis, and Metagonimus yokogawai. Raw meat is a source of Salmonella and Campylobacter and the vehicle for Trichinella, Taenia saginata and T. solium (beef or pork tapeworm), and Sarcocystis. Although adequate cooking kills all microorganisms and parasites, if food is left at room temperature and recontaminated before serving, it can incubate Salmonella, E. coli, or Shigella. Food served on an airplane, train, boat, or bus probably has been catered in the country of origin. The problems of food hygiene pertain to these forms of public transportation, even if the employees handling the food are from the United States. Safe foods are those served steaming hot, dry foods such as bread, freshly cooked food, foods that have high sugar content (e.g., syrups, jellies), and fruits that have been peeled.[23] [62] Prophylactic Medication.
Chemoprophylaxis may be useful for certain people making critical trips or for travelers with underlying medical conditions. It should only be used for 3 weeks or less and should be always approved by a physician and after a complete understanding of all risks and benefits. Despite the restrictive recommendations, 10% to 25% of European travelers to high-risk areas and up to one third of U.S. travelers to Mexico take prophylactic medication to prevent TD.[62] [113] Compared with empiric therapy with a single dose of an antimicrobial agent and loperamide, chemoprophylaxis is cost-effective only when its use does not exceed a few days[62] ( Table 52-10 ). Several nonantimicrobial agents have been studied for prevention of TD, with some found to be minimally effective. Lactobacilli have been tested on the assumption that they are safe and favorably modify intestinal flora, but they did not invariably reduce the incidence of TD and provided protective efficacy only up to 47%.[94] Antimotility drugs, such as loperamide, have adverse effects when used for prophylaxis.[23] [56] [62] Of the nonantibiotic drugs, only bismuth subsalicylate (BSS), the active ingredient of Pepto-Bismol, has been shown by controlled studies to offer reasonable TABLE 52-10 -- Prophylactic Medications for Prevention of Traveler's Diarrhea* AGENT
PROTECTIVE EFFICACY
PROPHYLACTIC DOSE
COMMENT Safe, temporary darkening of stools and tongue
Bismuth subsalicylate
65%
Two 262-mg tablets before meals and at bedtime
Fluoroquinolones
90%
Norfloxacin 400 mg, ciprofloxacin 500 mg, or levofloxacin 500 mg once Side effects, increased bacterial resistance a day
*Not generally recommended for travelers, only in special situations (see text) and for no longer than 3 weeks.
protection and safety. Several studies with volunteers and in the field have demonstrated that the use of BSS gives a protection rate from 40% to 77%,[53] [62] with fewer abdominal symptoms. Since the volume required is quite large with the liquid preparation, BSS in tablet form was also evaluated. The currently recommended dose of BSS is two tablets four times a day (2.1 g/day). [23] [45] [53] [60] [61] Mild side effects include constipation, nausea, tinnitus, and temporarily blackened tongue or stools. In areas where doxycycline is used for malaria prevention, concurrent BSS should be avoided because it may bind to the antimicrobial and prevent absorption. [53] [62] Ninety percent of salicylate from liquid BSS is absorbed and excreted in the urine of children. [53] Whether this salicylate cross-reacts with aspirin is unknown. However, BSS should not be used by someone with a history of aspirin allergy. Caution is recommended in small children, children with chickenpox or influenza (because of the potential risk of Reye's syndrome), patients with gout or renal insufficiency, and persons taking anticoagulants, probenecid, methotrexate, or other aspirin-containing products. BSS is not approved for children under 2 years old and is not recommended as prophylaxis for more than 3 weeks. The precise mechanism by which BSS prevents diarrhea is still unknown. Salicylate released during dissociation in the stomach exhibits antisecretory activity after exposure to bacterial enterotoxin on intestinal mucosa, and bismuth salts have antimicrobial activity.[53] Adherence of bacteria to intestinal mucosa may be affected. Since the first studies in the 1950s, a protective effect of antimicrobials in TD has been demonstrated. Several antimicrobial agents are highly effective in preventing TD
when given over short periods when at risk. Protection levels of 80% to 90% have been found with antimicrobial prophylaxis, provided that enteropathogens in the area were susceptible to the agent under investigation.[45] [61] [62] The most experience has been obtained with doxycycline, TMP/SMX, and the fluoroquinolones. Other antimicrobials (streptomycin and sulfonamides, erythromycin, mecillinam) have shown significant protection but have not been well studied.[61] [141] Studies of U.S. students in Mexico taking trimethoprim (160 mg) and sulfamethoxazole (800 mg) twice daily for 3 weeks or once daily for 2 weeks demonstrated 71% and 95% protection, respectively.[50] [52]
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The fluoroquinolones (e.g., ciprofloxacin, ofloxacin, norfloxacin, pefloxacin, fleroxacin, levofloxacin) have been shown to be highly protective when employed as prophylactic agents. Because of the emergence of resistance among enteropathogens to tetracyclines, doxycycline can no longer be recommended for prophylaxis unless the susceptibility of prevalent organisms is known. Similarly, TMP/SMX resistance has been reported in many regions of the developing world,[60] [62] including areas where resistance to this agent has not been previously reported. [24] With the antibiotics evaluated, the effect lasted only as long as the drug was continued. Subjects who remained in a high-risk area experienced an increased incidence of diarrhea during the week after cessation of prophylaxis.[44] [62] Despite dramatic protection against diarrhea, investigators do not recommend widespread use of these medications for prophylaxis by travelers because of the following reasons[23] [60] [62] : 1. Side effects. These include GI symptoms, photosensitivity, and other cutaneous eruptions and reactions. Pregnant women and children should not use fluoroquinolones for this reason. With larger numbers of people using these drugs, more serious side effects (e.g., Stevens-Johnson syndrome, hemolytic or aplastic anemia, antibiotic-associated colitis, anaphylaxis) will undoubtedly result. 2. Alteration of normal bacterial flora. Broad-spectrum antimicrobials may increase risk of infection with other antibiotic-resistant bacteria. Severe pseudomembranous colitis caused by colonic overgrowth with Clostridium difficile has occurred after therapy with most antibiotics. Vaginal candidiasis and GI side effects, including diarrhea, are common with antibiotic therapy. Changes in anaerobic flora can cause long-term alterations in the metabolism of bile acids and pancreatic enzymes, although clinical effects are unknown. 3. Development of antimicrobial resistance. Overuse of antimicrobial agents increases the prevalence of resistant strains.[49] [60] [84] [176] 4. False sense of security. Travelers taking antibiotics may relax their vigilance of dietary precautions and increase their risk of acquiring enteric infections. 5. High cost of fluoroquinolones and rapid effectiveness of presumptive therapy, often limiting the illness to 12 to 24 hours. Although the consensus is that not all travelers should use antibiotic prophylaxis, this approach may be appropriate for some.[23] [45] [60] [61] [62] Potential candidates would be residents of a low-risk country going to a high-risk area for short stays who have one or more of the following conditions or requirements: 1. An underlying illness that increases the risk of enteric infection or morbidity, such as gastric achlorhydria (from surgery or taking proton pump inhibitors), AIDS, inflammatory bowel disease, diabetes on insulin treatment, or a cardiac, renal, or CNS disorder. 2. An itinerary that is so rigid and critical to the overall mission that travelers would not tolerate even minor schedule changes caused by illness 3. Travelers who prefer prophylaxis after hearing the pros and cons of the approach No studies have evaluated prophylaxis of TD in young children, although they may be at higher risk for infectious diarrhea. Because of potential side effects, prophylaxis with BSS or antibiotics cannot be recommended in children under 5 years of age. Immunoprophylaxis.
Spurred by the emergence of in vitro resistance to antimicrobial agents among enteropathogens, including the fluoroquinolones, prophylaxis with vaccines is being developed to control bacterial diarrhea. Recent studies support the concept of immunoprophylaxis against rotavirus, Shigella, V. cholerae, and ETEC.[45] [60] [61]
BACTERIAL ENTEROPATHOGENS Escherichia Coli E. coli is the most prevalent facultative gram-negative rod in feces. Diarrheagenic E. coli is a heterogenous group of organisms that belong to one taxonomic species, but with different virulence properties, epidemiologic characteristics, and clinical features. At least six groups have been characterized, based on either genotypic or phenotypic markers.[141] Enteropathogenic E. coli.
EPEC strains were the first of the diarrheagenic E. coli described between the 1920s and 1940s, as causes of hospital nursery outbreaks.[141] Usually identified by serotypes, they are also characterized by a localized adherence pattern to a specialized cell line (HEp-2 cells).[194] EPEC strains have worldwide distribution, and their most accepted virulence property is enterocyte attachment with selective damage of the surface without cell invasion. They induce production of a receptor interacting with host cells' intima, and this interaction leads to intracellular changes in the enterocyte.[83] [115] [141] Enterotoxigenic E. coli.
ETEC strains, first identified in the 1970s, produce one or two enterotoxins that act on the small intestine through different mechanisms and time responses.[141] One of these toxins is a heat-labile cholera-like toxin (LT), a high-molecular-weight protein immunologically and physiologically similar to cholera toxin. Human ETEC strains also have a low-molecular-weight, poorly antigenic toxin that is heat stable (ST).[165] Both enterotoxins inhibit sodium reabsorption and increase secretion of anions and fluid into the intestinal lumen, resulting in secretory diarrhea without inflammatory exudate.[43] [60] [141] One
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common method for the diagnosis of ETEC is identification of specific deoxyribonucleic acid (DNA) plasmid sequences, using a hybridization technique.[141] Recently, polymerase chain reaction (PCR) has been used to improve the level of detection.[189] [203] ETEC has worldwide distribution and is the major cause of TD, accounting for 20% to 50% of cases in series from all parts of the world.[60] [141] [158] It also accounts for a large percentage and frequently the majority of enteritis in local pediatric populations of developing countries, where contaminated food and water are the primary sources of infection.[141] Most outbreaks of ETEC in the United States have been waterborne.[141] [165] Person-to-person spread is infrequent because of the large infectious dose (106 to 1010 organisms).[43] [141] Contamination of different types of food with these strains has been reported.[141] Enteroinvasive E. coli.
As with Shigella, EIEC strains possess the property of bowel mucosa invasion, resulting in microabscesses and ulcer formation. Because of the presence of the same invasive plasmid and other antigens of Shigella,[166] EIEC must be considered in the differential diagnosis of febrile dysenteric diarrhea, with Shigella, Salmonella, Y. enterocolitica, E. histolytica, V. parahaemolyticus, and inflammatory bowel disease. EIEC strains are found worldwide and have been associated with food-borne outbreaks, especially in areas of South America and Eastern Europe.[43] [141] [196] Enterohemorrhagic E. coli.
EHEC strains are also known as verotoxin-producing E. coli or Shiga toxin-producing E. coli. They have caused outbreaks of diarrhea associated with consumption of contaminated beef, often obtained at a fast-food hamburger chain, or unpasteurized apple juice. Contact with contaminated swimming pools and exposure to farm animals have also been associated with this infection.[31] [135] [141] [154] [179] EHEC produces copious bloody diarrhea with fecal mucus (hemorrhagic colitis), but fever is either low grade or absent. The most important EHEC strain thus far identified is O157:H7. The production of Shiga or a similar toxin by these strains may be related to the hemolytic-uremic syndrome (HUS), a common complication in children infected with EHEC O157:H7 and Shiga toxin-producing Shigella. HUS may be life-threatening, and no evidence indicates that HUS is prevented by antimicrobial therapy of EHEC disease.[72] [135] [156] Enteroaggregative E. coli.
EAEC strains are the most recent addition to the group of diarrheagenic E. coli. They are non-EPEC and do not produce ETEC LT or ST. EAEC adhere to HEp-2 cells in a typical aggregative pattern. The pathophysiology of these strains is uncertain; some studies suggest that they should be considered a phenotypically and genotypically heterogeneous group.[36] [120] [141] [142] These strains have been associated with persistent illness and malnutrition in children with diarrhea, especially in the developing world, but recent studies have demonstrated their association with diarrhea in adults. EAEC is also identified as an important cause of TD,[77] [80] second only to ETEC in some areas of the world. Diffusely Adherent E. coli.
Known also as enteroadherent E. coli, these non-EPEC strains show a diffuse adherence pattern to HEp-2 cells. Although associated with cases of diarrhea, the pathogenicity of these isolates has not been established in outbreaks or volunteer studies. The pathophysiology and importance of these strains are still not completely understood, and some propose that they be categorized as a subtype of EAEC.[36] [141] [142] Diagnosis.
Laboratory culture cannot differentiate the various diarrheagenic strains of E. coli from normal bowel flora or from one another. Specialized assays such as DNA probing and HEp-2 adherence technique are specifically used for research purposes.[141] New serologic techniques or PCR systems may become available in the future to help differentiate these organisms. Treatment.
Most cases of E. coli diarrhea are brief and self-limited, and their therapy should be primarily supportive with oral fluid replacement and maintenance, empirically based on the clinical manifestations. Dysenteric illness is the exception and should always be treated with antibacterial drugs, whether in a developing country or an industrialized region. In developing tropical countries, TD associated with the passage of numerous watery stools is often caused by both ETEC or EAEC, and antibiotics may shorten the duration of illness, especially when started within 48 to 72 hours of symptom onset.* Because of the increasing resistance of ETEC strains to antimicrobial agents, including fluoroquinolones, new therapeutic agents are actively being sought, such as rifaximin and azithromycin.[59] [84] [136] [141] [176] Since resistance patterns vary with geographic area and season, it is necessary to monitor susceptibility of bacterial isolates in various regions of the world. Susceptibility testing is required when treating diarrhea caused by EPEC, since strains are invariably resistant to a broad range of drugs. Immunoprophylaxis.
Oral immunization with inactivated ETEC with or without cholera toxin B subunit was shown to be safe and immunogenic in phase III trials in Egypt. [172] [173] A new vaccine, using a Salmonella typhimurium vaccine vector expressing recombinant ETEC fimbria, elicited immunogenic response in mice.[6] *References [ 23]
[ 54] [ 65] [ 80] [ 141] [ 187] [ 197]
.
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A live vaccine could offer advantages over a killed preparation in terms of duration and protection. Salmonella Salmonella infections may result in four different clinical syndromes: gastroenterocolitis, enteric (typhoid) fever, bacteremia with focal extraintestinal infection, and asymptomatic carriage,[17] [171] depending on the type of organism and the host characteristics. Gastroenterocolitis is usually a mild to moderately severe, self-limited illness, with preferential involvement of the lower intestine. Enteric fever is characterized by septicemia with a prolonged toxic course if not treated. In patients infected with Salmonella choleraesuis strains, or with sickle cell disease or immunosuppression (e.g., splenectomy, HIV infection, malignancy, immunosuppressive therapy, newborns, elderly persons), nontyphoid salmonellae may disseminate and produce localized infection, including osteomyelitis or meningitis. A person with an abdominal aortic aneurysm is prone to develop Salmonella infection, leading to aneurysm perforation. As many as 1% to 3% of patients who have recovered from typhoid fever may become chronic carriers who continue to shed the organism in the intestinal tract for 1 year or longer. Characteristically, the chronic typhoid carrier is an adult woman with cholelithiasis.[17] Microbiology.
The following discussion pertains to nontyphoid Salmonella, unless otherwise stated. Salmonellae are nonsporulating, facultative, gram-negative rods. The genus Salmonella is composed of more than 2000 serotypes that infect humans and animals. Enteric fever results from infection by Salmonella typhi or by S. paratyphi A, B, and C, which usually cause milder disease. S. typhi and S. paratyphi are further distinguished by their adaptation to humans as the only host. Although numerous other serotypes are capable of causing enteric fever, illness is usually limited to gastroenteritis. [60] [136] [158] [171] New serotypes occasionally become prominent, but most human infections are caused by only 10 serotypes, with S. typhimurium the most common. Epidemiology.
Nontyphoid Salmonella organisms infect nearly all animal species and cause zoonotic infections. They can persist in fresh water for 2 to 14 days, but they also may remain dormant in a desiccated non-sporulating state.[17] Human salmonellosis is a worldwide problem, remaining endemic in large areas of the developing world, where it is passed primarily through contaminated food and water. The Centers for Disease Control and Prevention (CDC) estimates that the 25,000 human cases of nontyphoid salmonellosis reported annually in the United States represent less than 1% of the actual number of clinical cases.[134] [136] A recent report of typhoid fever in the United States from 1985 to 1994 showed that travel to underdeveloped countries is still a risk factor for this disease.[136] Salmonella is the most common identifiable cause of foodborne illness. Contamination may occur from the animal feed, at slaughter, or most often, during food preparation. Because the infectious dose is relatively high, averaging 103 to 106 organisms (lower in water),[17] [136] the bacteria must multiply on or in food. This accounts for the high summer case incidence, when refrigeration may not be adequate.[136] The foods most commonly implicated are meat, dairy products (especially unpasteurized), poultry, and eggs. Recent outbreaks of salmonellosis have been related to different foods from toasted oat cereal to alfalfa sprouts and infant formula.[28] [136] [191] Person-to-person spread accounts for 10% of cases, but 20% to 35% of household contacts may become infected.[136] Salmonella is an occasional cause of TD, accounting for up to 15% of cases. [60] [158] Normal gastric acid, gut motility, bacterial flora, and poorly understood immune factors are elements in host resistance. Bacterial virulence factors, the vehicle of transmission, and infectious dose are the major determinants of infection. [17] [136] [171] Salmonellosis primarily affects children and elderly persons. Fifty-five percent of reported isolates in the United States are from persons under 5 years of age. The organism has an unexplained propensity to infect infants under 1 year of age, who may experience serious systemic infection, including sepsis and meningitis. Greater susceptibility has also been observed in patients with gastrectomy-induced hypochlorhydria, hemolytic disorders (e.g., sickle cell anemia), parasitic infections (e.g., malaria, schistosomiasis), and chronic illness (e.g., malignancies, liver disease).[134] [136] Pathophysiology.
Salmonellosis involves mucosal invasion and possibly enterotoxin production.[105] [171] After surviving the gastric acid barrier, the organisms reproduce in the gut, where they attach to the wall of the ileum and colon, inducing local degeneration of the microvilli. Invasion occurs through vacuolization, discharging the bacteria into the lamina propria, from where they gain entry into the bloodstream. At this point, only the strains that cause enteric fever enter and multiply within lymphatic tissue and phagocytic cells. The mechanism of diarrhea in enterocolitis is not clear. A heat-stable enterotoxin has been identified. In most cases, local inflammation of the bowel wall is not severe enough to cause mucosal sloughing and dysentery. Recent studies of pathogenesis demonstrated that interleukin-18 and ?-interferon contribute to host resistance and that deficiency of interleukin-12 or nitric oxide is related to severity of infection.[126] [132] Protection against typhoid fever is associated with the cystic fibrosis
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gene, called cystic fibrosis transmembrane conductance regulator (CFTR), similar to the protection of sickle cell against plasmodium infestation. Apparently, S. typhi uses this gene to invade the intestinal epithelial cells.[106] [160] Clinical Syndromes.
Although the incubation period for typhoid fever is usually 1 to 2 weeks, it is only 8 to 48 hours for intestinal infections with non-typhoid Salmonella. [171] Nausea, vomiting, malaise, headache, and low-grade fever may precede abdominal cramps and diarrhea. Stools are usually foul, and green-brown to watery, with variable amounts of mucus, blood, and leukocytes. Cholera-like fluid loss or dysentery with grossly bloody and mucoid stools occurs less often. The acute phase lasts only a few days. Asymptomatic excretion of organisms in the stool continues for 4 to 8 weeks, and chronic carriers are rare. Infants less than 3 months of age experience longer illnesses (average 8 days) with more complications. Among all ages, transient bacteremia is common, accounting for significant isolation of Salmonella types from blood. Fever and malaise occurring more than 1 week after resolution of diarrhea suggest a complication or another diagnosis.[136] [171] In healthy adults, Salmonella bacteremia occurs in 5% to 10% of infections and is not distinguishable from other causes of sepsis. Focal infections may be seen in any organ, but sites adjacent to the bowel are most common. Mortality is highest at the extremes of age, but deaths occur in all age groups.[136] Diagnosis.
Diagnosis of enterocolitis can be made by clinical manifestations and isolation of Salmonella organisms from stool or rectal swabs cultured onto selective media (MacConkey or Salmonella-Shigella agar). Blood cultures are useful to identify a systemic non-typhoidal salmonellosis. Blood cultures (or culture of bone marrow aspirates) for S. typhi or S. paratyphi are also used to diagnose enteric fever. Stool cultures are often negative early in the disease. Widal's serum test is useful for diagnosing typhoid fever in areas with high prevalence, but not in industrialized areas, because of the more frequent occurrence of cross-reaction with other gram-negative organisms. Treatment.
Supportive treatment with fluids is sufficient therapy for most cases of uncomplicated Salmonella enterocolitis. Antibiotics are not indicated because they do not shorten the illness, and they slightly prolong the carrier state and increase the risk of developing resistant strains.[7] [136] Antimicrobial therapy is indicated for persons who have symptomatic Salmonella infection with fever, systemic toxicity, or bloody stools. Patients with underlying debility that may predispose to septicemia or localized infection (e.g., immunosuppression), young infants (less than 3 months), elderly persons (more than 65 years), and sickle cell patients should be treated with antimicrobial agents. Fluoroquinolones are the treatment of choice because they shorten the duration of fever and diarrhea in salmonellosis.[7] [136] Doses are the same as those recommended to treat shigellosis, although treatment is continued for 7 days (14 days if the patient is immunosuppressed). In cases of enteric (typhoid) fever, septicemic salmonellosis, or local tissue suppuration, antibiotic therapy is indicated. The drugs of choice for enteric fever in the United States are the fluoroquinolones. These drugs can be given for a shorter duration (10 vs. 14 days), resistance to them is still low, and posttreatment carriage of S. typhi is reduced. [7] [66] In many developing countries the drug of choice is still chloramphenicol (25 to 50 mg/kg/day in divided doses every 6 hours) because of its low price and predictable activity. Alternative empiric therapy in the United States is a third-generation cephalosporin. Other traditional options, such as ampicillin or TMP/SMX,[24] have low in vitro activity in many areas. Local suppuration may require 2 to 6 weeks of antibiotics, depending on the adequacy of surgical drainage.
As with Shigella, Salmonella species are showing increasing resistance to multiple antimicrobial agents worldwide.[81] [87] [136] [177] Immunoprophylaxis.
Immunity to Salmonella is serotype specific. Vaccines have not been successful for nontyphoid Salmonella because of the number of serotypes. For typhoid fever, immunoprophylaxis is possible, and currently, three protective vaccines are commercially available. The traditional killed vaccine is associated with high reaction rate and has limited use in young children traveling in highly endemic areas. The two live attenuated typhoid vaccines are preferred for antityphoid immunizations. The first is a live attenuated strain Ty21a that is given as one oral dose every other day for four doses.[78] The second is a Vi polysaccharide preparation given as a single parenteral immunization. [1] Both preparations are of approximately equal cost and effectiveness. New vaccines are under evaluation. One new live attenuated S. typhimurium mutant is highly immunogenic and protective in animal models and induces cross-reactive antibodies to other enteric pathogens. [190] Shigella Microbiology.
Dysentery has been described since the beginning of recorded history. At the end of the nineteenth century, Shiga first identified Shigella dysenteriae as the cause of an outbreak of dysenteric diarrhea in Japan, and since then, shigellosis has become synonymous with bacterial dysentery. Other bacteria and protozoa are also capable of producing the bloody and mucoid stools that define this syndrome.
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Shigellae are thin, nonmotile, nonsporulating, gramnegative rods in the Enterobacteriaceae family. There are four species or groups: A (S. dysenteriae), B (S. flexneri), C (S. boydii), and D (S. sonnei); the first three contain numerous serotypes. Epidemiology.
Shigellosis occurs worldwide. S. dysenteriae 1 (Shiga bacillus), which causes severe disease, is most common in developing countries. In the US and in many other areas, particularly in more industrialized regions, Shigella remains endemic, with S. sonnei replacing S. flexneri as the most common isolate. Humans and certain primates are the only hosts for Shigella. Fecal-oral contamination is the mode of spread. Common source infections occur through water or food prepared by contaminated hands. Shigella can survive freezing and thawing in ice cubes. With an infectious dose as low as 10 to 200 organisms, person-to-person spread is common.[54] Even in countries with good sanitation, Shigella accounts for persistent endemic foci and high rates of transmission, especially among groups in close physical contact (e.g., male homosexuals, children in day-care centers), groups with poor hygiene (e.g., mentally impaired patients), and those who lack sanitary facilities and water (e.g., populations in developing countries, Native Americans on reservations). Long-term carriage of Shigella is less common than for Salmonella. Shigella is a potential pathogen in the American wilderness. Environmental persistence averages 3 to 4 weeks, with best survival in cool fresh water. Pathophysiology.
The essential virulence factor of Shigella is invasiveness associated with a large (120- to 140-megadalton) plasmid. Shigella organisms invade and proliferate within the epithelium of the large bowel, producing well-demarcated ulcers with cellular infiltrates (chiefly PMNs) and overlying suppurative exudates. These organisms interact with the epithelial cells through an initial type III secretory system, with invasion of these cells and reorganization of their cytoskeleton.[40] [83] [144] Organisms have also been demonstrated in the small bowel, but these have reduced potential for invasion or changes in the mucosa, causing a profuse watery diarrhea, possibly mediated by an enterotoxin.[40] [43] Despite similarities in pathogenesis between EIEC and Shigella strains, random amplified polymorphic DNA and typing techniques were not able to characterize and differentiate them.[11] [166] Clinical Syndromes.
As with most enteric pathogens, infection with Shigella may be asymptomatic, mild, or severe. Rarely a chronic carrier state may develop, depending on a combination of host and organism factors. Two distinct diarrheal syndromes may occur separately or sequentially in shigellosis. After a short incubation period of 1 to 3 days, illness begins with malaise, headache, nausea, fever, abdominal cramps, and watery diarrhea, representing small bowel infection. Children may present with fever, with diarrhea developing later. In the second and classic form of shigellosis, after 1 to 3 days of small bowel disease, colonic involvement causes progression to clinical dysentery. In this dysenteric form the volume of stools decreases and the frequency increases, with passage of up to 20 to 30 movements a day, containing gross blood and associated with fecal urgency and often tenesmus. Fever is common in dysenteric cases, found in up to one half of cases of shigellosis overall. Mild abdominal tenderness is also common, but without peritoneal signs. The natural history of shigellosis is varied, with most cases resolving spontaneously within 7 days, but with others persisting for weeks.[43] [47] The mortality rate is as high as 25% in developing countries when S. dysenteriae 1 (Shiga bacillus) diarrhea is untreated, but it decreases to less than 1% with adequate antimicrobial therapy. Complications.
Several potential complications of shigellosis may occur. Severe anemia and hypoalbuminemia may result from blood and protein losses. Febrile convulsions are seen in young children with shigellosis. Pneumonitis may complicate Shigella infection. A severe leukemoid reaction with white cell count up to 50,000 may result after apparent clinical improvement in patients. In some patients infected by strains that produce Shiga toxin, HUS syndrome develops, probably induced by formation of immune complexes. Reiter's syndrome has also been reported in patients with S. flexneri infection who are HLA B27 positive. Septicemia was found in less than 5% of Shigella infections, with fewer cases of metastatic abscesses.[47] [54] Diagnosis.
Laboratory tests often show a mild leukocytosis with a shift to the left (increase in number of immature granulocytes). If colitis is present, microscopic examination of the stool shows countless white (PMNs) and red blood cells, but this is not specific to shigellosis. Diagnosis is made by stool culture on selective media (MacConkey or Salmonella-Shigella agar), which is positive in most infected patients.[47] Fresh stool or sigmoidoscopic biopsy is the best source of culture material, while rectal cotton swabs, although not as reliable, can be used if plated rapidly or placed in a holding medium. In hospitalized patients, blood cultures should be obtained. Treatment.
Therapy first involves fluid replacement. Although large-volume diarrhea is unusual, significant
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dehydration may occur, especially in children. Antimotility drugs are controversial in patients with signs of toxicity[46] ; however, these medications are unlikely to be detrimental if antibiotics are used concurrently. [23] [64] [65] Patients with fever and dysentery should be treated with antimicrobial agents, since these drugs decrease duration of fever, diarrhea, and excretion of Shigella in stool. Antibiotic-resistant strains are emerging worldwide, with recent reports in Asia, Oceania, and Latin America,[24] [81A] [99] [183] showing that most of the strains are resistant to ampicillin and TMP/SMX, whereas the fluoroquinolones remain active. The current recommendation for treatment is with a fluoroquinolone: norfloxacin 400 mg, ciprofloxacin 500 mg, or levofloxacin 500 mg daily, for a total of 3 to 5 days. Single-dose therapy is probably effective in milder forms of illness. [23] [57] [63] [65] [187] Fluoroquinolones currently are contraindicated in infants and children because of the possible effects on articular cartilage. However, short-course fluoroquinolone therapy appears to be safe. Alternative treatments for children in areas where TMP resistance occurs are nalidixic acid and furazolidone.[168] Other options that need further testing are azithromycin and rifaximin.[59]
Immunoprophylaxis.
Temporary immunity to homologous Shigella strains follows natural infection.[48] [145] A vaccine composed of specific polysaccharide conjugates of S. flexneri and S. sonnei has been shown to be safe and immunogenic in children.[8] Other attenuated or killed strains or specific synthetic polysaccharides have shown promise in animal studies.[32] [162] Campylobacter Microbiology.
The organism is a small, curved, gramnegative rod, initially classified as Vibrio. Campylobacter jejuni strains are widespread in the environment. The major reservoir is animals, including dogs, cattle, birds, horses, goats, pigs, cats, and sheep.[16] [60] [158] A reemergent species, C. upsaliensis, has been recently associated with diarrheal disease, persistent diarrhea in HIV patients, and a few cases of HUS.[21] Epidemiology.
Most epidemics of gastroenteritis have been caused by contaminated food. The most important source for human illness is poultry, but epidemics have also been associated with ingestion of raw milk.[16] [18] C. jejuni has been isolated from surface water and can survive up to 5 weeks in cold water, ensuring its potential for wilderness waterborne spread. Person-to-person spread occurs but is uncommon. The prevalence of C. jejuni as a cause of TD varies with time of year. TD is caused by C. jejuni in about 3% of cases in rainy summertime and in up to 15% of cases during drier wintertime. [16] [133] Studies in the United States and abroad have demonstrated that C. jejuni accounts for up to 25% of patients with infectious diarrhea and is often more common than Salmonella or Shigella species.[16] [19] C. jejuni is now the most common cause of bacterial gastroenteritis in developed countries. Rates are highest among children and young adults.[16] [18] Pathophysiology.
The complete pathogenic mechanisms are unclear. All segments of the small and large intestine may be affected, accounting for the variety of diarrheal symptoms. Evidence of invasiveness includes recovery of bacteria from blood and presence of colitis, with cellular infiltration on intestinal biopsy. A heat-labile enterotoxin may play a role in disease pathogenesis. Clinical Syndromes.
The incubation period of C. jejuni enteritis is 2 to 7 days. Clinical symptoms are extremely variable and nonspecific. Victims often have a 1-day prodrome of general malaise and fever, followed by abdominal cramps and pain that herald the onset of diarrhea, with up to eight bowel movements a day. The diarrhea is initially watery, followed by passage of stools that are bile stained or bloody. The frequencies of reported symptoms are diarrhea (75% to 95%), cramps and abdominal pain (80% to 90%), nausea (20% to 50%), headache (50%), fever (50% to 80%), vomiting (20%), and bloody diarrhea (10% to 50%).[16] Tenesmus is unusual. Physical examination is nonspecific, with variable degrees of fever (averaging 40° C [104° F]), abdominal tenderness, and dehydration. Microscopic evaluation of stool shows blood and PMNs in 60% to 75% of samples. The enteric symptoms subside in 2 to 4 days, and the entire illness resolves spontaneously within 1 week. Organisms are shed in the stool for 3 to 5 weeks after resolution of symptoms, but chronic carrier states have not been described. Up to 20% of victims may show clinical relapse, which is usually less severe than the original symptoms. [16] Chronic diarrhea caused by C. jejuni has been reported in children and adults but is usually associated with significant underlying disease. Complications.
C. jejuni infection has been associated with Guillain-Barré syndrome.[16] [139] [164] C. jejuni infection often precedes development of the syndrome and in more severe cases is associated with axonal degeneration, slow recovery, and severe residual damage.[164] Diagnosis.
Definitive diagnosis is made by stool culture on a selective medium (e.g., Skirrow, Butzler, Campy-BAP), with isolation rates directly related to the severity of the disease. Extraintestinal sources account for 0.4% of positive Campylobacter cultures in the United States and usually are preceded by GI infection. Blood is the most common site, followed by the gallbladder and cerebrospinal fluid (in children), but since blood
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cultures are rarely drawn in the evaluation of gastroenteritis, the real frequency of bacteremia is unknown. The serologic tests available are still not well standardized and need further evaluation. Treatment.
Treatment is primarily supportive with oral fluids; dehydration is usually mild. Most patients have improved by the time the culture results return and do well without antibiotics. Antibiotic treatment does not conclusively improve C. jejuni gastroenteritis, but earlier therapy appears to be effective[19] and eradicates the organism from the stool within 48 hours. The antimicrobial antibiotic of choice is erythromycin or a fluoroquinolone. Fluoroquinolones are given in the same doses as for shigellosis because they are active against all the major causes of dysentery (C. jejuni, Shigella, Salmonella). In children, because fluoroquinolones are contraindicated, erythromycin (20 to 50 mg/kg every 6 hours for 5 days) is an option. Another alternative, in view of increased resistance to fluoroquinolones by Campylobacter strains,[79] [176] is azithromycin, a newer macrolide that can be used in children and is active against all major bacterial enteric pathogens. [84] [118] Vibrio Microbiology.
Cholera is a severe form of watery diarrhea often associated with dehydration. The disease is caused by Vibrio cholerae 0 group 1 (01), a motile, curved, gram-negative rod. These microorganisms have two major biotypes, classic and El Tor, which produce similar clinical illness, and each one contains two main serotypes, Ogawa and Inaba. Non-01 V. cholerae strains also produce diarrheal illness, but they show less potential for epidemic disease.[107] Nine other species have been associated with human disease. V. parahaemolyticus, V. fluvialis, V. mimicus, V. hollisae, and V. furnissii are associated with GI disease. Others, mainly V. vulnificus, are associated with wound infections and septicemia. All are halophilic, gram-negative rods that reside in seawater and on marine organisms, and infection is acquired by ingesting infected and undercooked seafood or by contamination of a wound with infected water.[107] Epidemiology.
V. cholerae is endemic in areas of Asia, Africa, and the Middle East. It has accounted for seven deadly worldwide pandemics since the early 1800s. The last began in 1961 in Indonesia and spread throughout Southeast Asia, the Middle East, Africa, parts of the Pacific and Europe, and in the 1990s to Latin America. In 1973, cholera resurfaced in the United States after an absence since 1911. Since then, a small number of cases have occurred along the Gulf Coast of Louisiana and Texas. Only 10 cases of cholera were reported in travelers returning from endemic areas between 1961 and 1981. In January 1991 a new outbreak of cholera started in Latin America along the coast of Peru. Since then, this disease has become endemic in most regions of Latin America, moving as close to the United States as northern Mexico.[107] The infection is associated with consumption of uncooked or poorly handled seafood and spreads rapidly because of a highly susceptible population that has not been exposed to cholera for almost a century and because of inadequate water supply and sewage service. Cholera continues to be a disease of poor and lower socioeconomic groups, and the Indian subcontinent and southwestern Asia are still the areas with the highest prevalence.[68] [107] The risk to travelers has been estimated at 1:500,000 during a journey to an endemic area,[60] [158] which should be further reduced with dietary discretion. Nonhuman reservoirs for V. cholerae 01 include marine or brackish waters.[68] [107] [158] As with other strains (V. parahaemolyticus, non-01 V. cholerae), shellfish ingest and carry these organisms. Fecal-oral spread is the major mechanism of transmission, and water is the most common vehicle, followed by food.[68] The organism
remains viable for days to weeks in various foods. Because of the large infective dose of 106 to 1010 organisms,[98] [158] person-to-person spread is uncommon. Most cases of gastroenteritis caused by noncholera vibrios have been associated with ingestion of raw seafood. Cases have been reported from travelers, particularly after visits to coastal areas of Southeast Asia and Latin America. V. parahaemolyticus causes 70% of cases of foodborne gastroenteritis in Japan (where large amounts of raw seafood are eaten), leads to sporadic outbreaks in the United States, and is a common cause of TD in Thailand. [20] Pathophysiology.
After passing through the stomach, the organism multiplies and colonizes the small bowel. The local effects of enterotoxin account for the pathophysiology of cholera. No pathologic changes are noted in the bowel wall. The binding subunits of toxin attach to the membrane of the mucosa, after which the adenylate cyclase-activating B subunit enters the cell. The enzyme acts inside the serosal cell, enhancing production of cyclic adenosine monophosphate. This molecule produces a 70% reduction in influx of water, saline, and a wide range of other substances into the gut mucosal cells, resulting in watery diarrhea. Glucose, potassium, bicarbonate, and most significantly, absorption of sodium and water linked to glucose remain intact. Thus, although plain water worsens cholera diarrhea, the addition of glucose renders the water and essential electrolytes absorbable, forming the basis for oral rehydration therapy.[107] [137] [159] [170] V. cholerae has the bacteriophage VPIphi, which encodes a receptor used by enterocytes for the phage CTXphi, which encodes the cholera toxin.[110]
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Details of the pathogenesis of infection by the noncholera vibrios remain unclear. Some strains produce an enterotoxin, but generally it is not cholera-like toxin. In the case of V. parahaemolyticus, a hemolytic toxin was thought to explain its effects, but the dysenteric illness that typically develops implies invasion. Another enterotoxin has been found in some strains.[20] Clinical Syndromes.
Some cholera infections are asymptomatic, and 60% to 80% of clinical cases are presented as mild diarrhea that never raise suspicion for cholera.[98] [158] After an incubation period of 2 days (range 1 to 5 days), fluid accumulates in the gut, causing intestinal distention and diarrhea. Diarrhea may begin as passage of brown stools but soon assumes the translucent gray watery appearance known as "rice water" stools. In serious cases, stool volume may reach 1 L/hr, leading to severe dehydration, acidosis, shock, and death. Vomiting may occur as a result of gut distention or acidosis.[107] The clinical syndrome caused by noncholera vibrios is not characteristic. Intestinal illness is associated with diarrhea, abdominal cramps, and fever, with nausea and vomiting in about 20% of cases. Diarrhea may be severe, with up to 20 to 30 watery stools per day. In outbreaks of V. parahaemolyticus infection, explosive diarrhea associated with abdominal cramps and nausea is often described, with vomiting in about 50% and fever in about 30% of cases. In Asia, a dysentery-like syndrome with mucoid bloody diarrhea is often seen.[20] Infections are usually brief, lasting an average of 3 days, with spontaneous resolution. Diagnosis.
Diagnosis for any of the vibrio diarrheas can be made by stool culture on suitable media (e.g., thiosulfate-citrate-bile salts-sucrose or TCBS agar). Vibrios can survive for 1 week on a stool-saturated piece of filter paper sealed in a plastic bag, before placing it in the culture media.[107] In the case of V. cholerae, another way to diagnose infection is using a darkfield microscopic examination of fresh stools, which may reveal the characteristic helical vibrio motion. Treatment.
Aggressive replacement of fluid and electrolytes is the cornerstone of therapy for cholera, especially in severe cases. Severe untreated cholera has a 50% mortality, which may be reduced to 1% with appropriate treatment. Children are at higher risk for complications and death. With fluid replacement, most cases of cholera last 3 to 5 days, with the peak fluid losses 24 hours after the onset of illness. When hypotension or persistent vomiting is present, IV fluids are necessary, but as soon as initial rehydration is complete, ORS is used for maintenance. Less than 5% of patients require IV maintenance after initial rehydration, and ORS alone is successful in 90% of cholera cases without shock. With voluminous losses, ORS can be given by nasogastric tube to continue fluids during the night. A normal or light diet should be resumed early in the course of treatment, after initial rehydration. Success of fluid replacement therapy was clearly demonstrated by the low mortality rate seen during the cholera outbreak in Peru, where principles of rehydration were applied.[68] [107] Antibiotics shorten the duration of diarrhea and excretion of organisms in severe cholera and reduce fluid losses but they are not as important as fluid therapy. Oral antibiotics can be started within a few hours of initial rehydration. The drug of choice is doxycycline, 300 mg single dose in adults or 50 mg/kg/day in four divided doses for children. This is perhaps the only indication for the use of tetracycline in children because a short course (2 to 4 days) is unlikely to stain teeth. Furazolidone (100 mg every 6 hours for adults and 5 mg/kg/day in four divided doses for children) for 2 days is an alternative. Vibrio strains are also susceptible to fluoroquinolones, but these medications are more expensive.[23] [45] [60] [107] Treatment of patients infected with noncholera vibrios should also focus on fluid replacement. Little information exists on the benefit of antibiotic therapy for GI disease, but antimicrobials may be reasonable in dysentery-like cases or prolonged illness. The same antimicrobial agents used in cholera could be used against this infection. Immunoprophylaxis.
Temporary immunity to homologous, but not to heterologous, strains of cholera develop after infection.[107] The current parenteral vaccine has no antitoxin activity and is only about 50% effective in reducing attack rates over a 3- to 6-month period for those living in endemic areas. It is recommended for persons who live and work under poor sanitary conditions in highly endemic areas and for those with known achlorhydia. It is not recommended for travelers to endemic areas.[107] A recent advance was the development of transgenic potatoes that synthesized cholera toxin subunit B without requiring a cold chain. This is a promising option for an inexpensive, effective vaccine for the developing world. New vaccines are in different stages of evaluation. Two studies in adult volunteers, one using a polysaccharide-cholera toxin conjugate and the other using a new El Tor strain that was CTXphi negative and hemagglutinin/protease defective, have shown promising results. A study of CVD103-HgR strain in Austrian travelers confirmed the tolerance of this oral vaccine. Finally, a bivalent (CVD103-HgR plus CVD 111) oral vaccine has been shown to be more effective than the monovalent one.[13] [90] [188] Yersinia Enterocolitica Microbiology.
Y. enterocolitica is a facultative anaerobic, gram-negative rod in the Enterobacteriaceae family, with different serogroups found to cause human infection.
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Epidemiology.
The major natural reservoir of the organism is wild, farm, and domestic animals. In the United States and Europe the organism resides in surface and unchlorinated well waters. Evidence indicates that persistence in warm water ranges from days to weeks, with longer survival at colder temperatures. Human isolates of Y. enterocolitica are found worldwide, but with preference for colder regions such as Canada and Northern European countries, with an incidence equal to or greater than those of Salmonella and Shigella.[130] [158] Transmission occurs from fecal-oral contamination, through food and water, and probably through person-to-person or animal-to-person contact.[130] [158] [192] Raw milk and oysters have also been implicated as vehicles of transmission. The infectious dose and attack rate are not well studied, but yersiniosis is suspected to be caused by ingestion of a large infectious dose based on a common source of transmission. The incubation period averages from 3 to 7 days. Patients with ß-thalassemia show a greater risk for acquisition of yersiniosis.[4] Pathophysiology.
Illness caused by Y. enterocolitica may involve three pathogenic mechanisms: bowel mucosal invasion, release of a heat-stable enterotoxin similar to that produced by ETEC, and elaboration of a cytotoxin.[43] [130] The organism multiplies in the small bowel and characteristically invades the mucosa in the region of the terminal ileum and colon. The mucosa may be diffusely inflamed with small and shallow ulcerations. Also, some bacteria migrate through lymphatics to mesenteric lymph nodes, producing adenitis with focal areas of necrosis. Clinical Syndromes.
The most common clinical presentation in yersiniosis is gastroenteritis, characterized by diarrhea, fever, and abdominal pain, with nausea and vomiting in 20% to 40% of cases and dysentery (passage of bloody stools) in 10% to 25%.[130] [192] Fever or abdominal pain without important diarrhea may be the most prominent sign, mimicking appendicitis in 20% of patients with positive stool cultures.[10] Although acute appendicitis has been associated with serologic evidence of Y. enterocolitica infection, the usual surgical findings are mesenteric adenitis or terminal ileitis. Severe colitis rarely results in septicemia, extensive necrosis, or perforation. Numerous extraintestinal manifestations of Y. enterocolitica infection include skin rash (erythema nodosum or maculopapular) and arthritis, probably related to an immune reaction. Extraintestinal infection involving lung, joints, lymph nodes, wounds, or septicemia may occur with or without enteritis. In the majority of intestinal infections, illness is mild and self-limited, with duration averaging 1 week, but some patients experience prolonged symptoms. [130] [192] Excretion of the organism in stool continues for a few weeks to months. Complications may be related to particularly severe disease and a misdiagnosis of Crohn's disease or appendicitis and development of Reiter's disease or collagenous colitis.[128] Diagnosis.
The diagnosis of yersiniosis is usually made by stool culture, but it can grow also from blood or surgical samples. The organism grows better at lower (22° to 25° C [71.6° to 77° F]) temperatures, which inhibit most other enteric bacteria. Abnormalities related to ileitis or colitis seen on contrast radiography and colonoscopy may be mistaken for other causes of colitis. [10] [130] Serologic tests are also diagnostic and especially helpful to diagnose Yersinia arthritis. Treatment.
Tetracyclines have been suggested as the drug of first choice for chronic or fulminant infections,[10] [23] but Yersinia is also susceptible in vitro to streptomycin, chloramphenicol, aminoglycosides, fluoroquinolones, and trimethoprim/sulfamethoxazole. Most are resistant to penicillins and cephalosporins and variably resistant to erythromycin and sulfonamides.[23] [130] Aeromonas Species and Plesiomonas Shigelloides Aeromonas species and P. shigelloides are gram-negative, facultatively anaerobic, nonsporulating rods. Their normal habitats are water and soil, and these bacteria have been implicated in a variety of human illnesses, most often gastroenteritis.[60] [96] [97] [101] [158] [195] Aeromonas was previously part of the Vibrionaceae family, until the family Aeromonadaceae was established to include the 14 species so far identified. Only five species (A. hydrophila, A. caviae, A. veronii, A. jandaei, and A. schubertti) have been associated with a variety of human diseases, including gastroenteritis, soft tissue infections, HUS, burn-associated sepsis, and respiratory infections. [101] [195] A. hydrophila is the most commonly isolated species, but its real prevalence is still uncertain. A. hydrophila has been associated with diarrheal illness in the United States, Australia, India, and southwestern Asia. [96] [101] [195] Association of illness with drinking untreated spring or well water was demonstrated in the United States. Pathogenicity includes production of cytotoxin, enterotoxin, and proteases, as well as the capacity of adhesion and invasion, but the exact mechanisms of disease pathogenicity remain controversial.[101] [174] Clinical illness associated with enteric infection by A. hydrophila varies from acute to chronic diarrhea and from passage of watery stools to dysentery with colitis.[101] [195] Median duration of diarrhea is 2 weeks, with occasional cases that persist a month or longer. Asymptomatic carriers have been identified. Non-GI infections, such as those of soft tissue and septicemia, have been associated with exposure of wounds to water.
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Aeromonas strains are susceptible to chloramphenicol, tetracycline, TMP/SMX, fluoroquinolones, and aminoglycosides but are resistant to ampicillin and erythromycin.[101] P. shigelloides has been isolated from patients with gastroenteritis, both in sporadic cases and outbreaks.[60] [97] [158] Infection has been associated with recent travel and ingestion of raw or inadequately cooked shellfish. Plesiomonas may cause dysenteric illness suggestive of an invasive organism, but its pathogenic mechanisms remain poorly defined. [97] Miscellaneous Bacterial Agents Klebsiella pneumoniae and K. oxytoca have been reported to occasionally cause diarrhea, but they are usually commensals of the GI flora.[88] Another cause of severe diarrhea in hospitalized (usually postoperative) patients receiving antibiotics is Staphylococcus aureus. The causative organism may be methicillin-resistant S. aureus. [175]
VIRAL ENTERIC PATHOGENS Recent studies have identified viruses as major causes of acute nonbacterial GI infections.[15] [29] [93] The most important defined agents are Norwalk virus and other caliciviruses, enteric adenoviruses, astrovirus, and rotavirus. Usually they cause vomiting with or without mild and self-limiting watery diarrhea. Transmission occurs through fecal-oral contamination or person-to-person transmission. Respiratory symptoms are common in patients with viral gastroenteritis. Caliciviruses and astroviruses are similar to Norwalk virus in structure and clinical presentation. They generally infect in early childhood and provide apparently lifetime immunity.[151] [152] Norwalk and Norwalk-like Viruses Norwalk virus was the first well-described etiologic agent in nonbacterial gastroenteritis outbreaks; an elementary school outbreak occurred in Norwalk, Ohio.[108] Soon after, several other small round viruses were identified as causes of nonbacterial gastroenteritis.[151] [152] Norwalk virus and the related viruses are nonsymmetric, single-stranded ribonucleic acid (RNA) viruses, recently classified within the family Caliciviridiae. [103] [119] They are the main cause of outbreaks of epidemic nonbacterial GI illness worldwide. They also cause "winter vomiting disease" because of their wintertime predisposition and common association with vomiting. These viruses are highly infective (10 to 100 organisms per inoculum), and the infection is spread by common-source vehicles with a propensity for secondary person-to-person spread (high secondary attack rate).[93] [119] Humans are the only known carriers of these viruses. Outbreaks have been recognized in family settings, health care facilities, nursing homes, schools, and travel settings, characteristically affecting both children and adults in the United States. They are found less often in neonates and toddlers. Contaminated water supplies, drinking water in cruise ships, recreational swimming pools, and commercial ice cubes have been implicated in outbreaks.[93] [119] Also, vehicles identified for food-borne outbreaks may be contaminated shellfish, salads, bakery products, cold foods, cooked meat, and fresh fruits.[152] Between 20% to 67% of outbreaks of Norwalk virus have been associated with food.[26] [147] After invasion of the enterocytes, the viral particles replicate inside, resulting in damage of the villi and crypt cell hyperplasia.[151] Malabsorption of fat, lactose, and xylose occurs with these histologic changes. The exact mechanisms of diarrhea production in viral gastroenteritis are not completely understood. Small numbers of viral particles are shed in stool during the acute illness, but prolonged carrier states are not seen. In the United States, antibodies in stools typically appear during late adolescence, but in tropical, developing countries, children acquire antibodies at a young age. Although antibodies persist in most people, they do not provide protection from clinical illness.[151] Transmission is followed by an incubation period of 24 to 48 hours, and illness begins abruptly with vomiting, abdominal cramps, and diarrhea. Stools are watery and usually do not contain blood or leukocytes. Other common symptoms include low-grade fever, malaise, myalgias, respiratory symptoms, and headache. Illness is almost always mild and self-limited, lasting 1 to 2 days. Complications and mortality are extremely rare and usually involve elderly and debilitated patients. Some malabsorption of fats and disaccharides persists after the acute illness. Supportive treatment with oral fluids and electrolytes is sufficient in the vast majority of cases.[151] Historically, and because of the difficulty or impossibility of growing these viruses in cell culture, electron microscopy was the initial means of detecting these viruses. Currently, there are immunoassays and molecular techniques (reverse-transcription PCR) available for detection of these small round RNA viruses in stool.[85] [102] [140] [151]
Vaccine development is not currently feasible because of difficulties culturing the virus and lack of animal models. Rotavirus Rotaviruses are 70-nm double-stranded RNA viruses that are classified by the capsid antigens, with group A and serotype G1 being the most common in human infections worldwide. Most severe infections in children are caused by serotypes G1 to G4.[14] [153] Rotavirus is the most common enteric pathogen in children causing diarrhea worldwide, resulting in up to 800,000 deaths per
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year.[29] [93] [153] Infection tends to be endemic, with peak incidence during winter months in temperate climates. Transmission is by person-to-person contact or as a result of common-source outbreaks. Viral shedding occurs in stools, and particles can retain infectivity for months. Rotaviruses have been found in almost every animal species, and in general, animal strains have reduced virulence for humans.[14] [29] Rotavirus infects humans repeatedly, at any age. It is the most frequently isolated pathogen in infantile diarrhea and is responsible for a disproportionate amount of hospitalization for dehydration.[14] [153] The majority of symptomatic infections occurs in children under 3 years old, with peak incidence in children 6 months to 2 years of age. Rotavirus can also cause illness in adults, usually associated with secondary spread within a family.[14] Nonspecific pathologic changes are seen in small bowel epithelial cells, with particles identified intracellularly. The exact mechanism of diarrhea is unknown, but a net secretion of water, sodium, and chloride occurs during the illness. Diarrheal losses contain 30 to 40 mEq/L each of sodium and potassium. Lactose malabsorption may persist for 1 to 2 weeks, associated with continued viral excretion in stool. Large numbers of viral particles are shed in the stool of ill patients, but prolonged excretion is unusual.[153] After an incubation period of 24 to 72 hours, illness begins with vomiting, followed by diarrhea associated with abdominal cramps, low-grade fever, and malaise. Vomiting usually resolves within 2 days (range 1 to 5), but the diarrhea may last 3 to 8 days or longer. Natural infection reduces the incidence and severity of subsequent episodes. Serum antibody levels are demonstrated within the first few years of life and in almost all adults but appear to be nonprotective. Severity of illness usually decreases with age. Adults are more likely to have asymptomatic or mild illness with less vomiting. Dehydration frequently occurs in children, accounting for appreciable mortality in developing countries. Fortunately, oral fluid and electrolytes can be successfully used in most cases.[153] The first rotavirus vaccine approved by the U.S. Food and Drug Administration (FDA) in 1998 is a tetravalent rhesus-human strain that provides coverage against the four common G serotypes of human rotavirus.[146] [153] [193] In clinical trials in industrialized countries, this vaccine provided 50% to 70% protection (up to 60% to 100% in severe cases). The recommendation was to give this vaccine to all children by mouth at 2, 4, and 6 months of age,[146] but concerns of vaccine-associated intussusception will delay routine use. The vaccine's efficacy and cost-effectiveness in developing countries and travelers should be further evaluated.
INTESTINAL PROTOZOA Protozoal infections may be pathogenic or commensal (little or no effect) to the human host. Most protozoal infections are suspected on the basis of subacute or chronic GI symptoms, which may fluctuate over time. Although acute self-limited diarrheal illness may occur, the symptoms are nonspecific, and the diagnosis is often made on stool examination. Several factors have increased the prevalence of intestinal parasites in the Unites States and worldwide: increase in immunocompetent persons who frequently become infected by these organisms, improvement in diagnostic techniques, changes in social behaviors (increased use of day care and nursing homes, more frequent international travel), and in the United States, increased immigration of people from Asia, Africa, and Latin America.[60] [89] [109] [158] As with enteric bacteria, symptoms from infection by intestinal protozoa depend on the level of bowel colonized. Those colonizing the small intestine, such as Giardia and coccidia, cause a wide spectrum of GI complaints, including malabsorption (foul stools and flatulence) and weight loss in persistent infections. Although many protozoa are capable of superficial mucosal invasion, only Entamoeba histolytica and Balantidium coli, which colonize the colon, can ulcerate the bowel wall, cause dysentery, and spread to other tissues.[89] All intestinal protozoa are transmitted by the fecal-oral route, so infection rates are highest in areas and groups with poor sanitation, close contact, or particular customs favoring transmission. These reemerging infections have been related to large outbreaks of communicable diseases in the United States, often secondary to water contamination. Protozoal parasites were the most frequent etiologic agent detected in waterborne outbreaks from 1991 to 1994.[116] [131] [138] In addition to spread by food, water, and person-to-person contact, mechanical vectors such as flies may spread these organisms. Transmission of intestinal protozoa is favored by a hardy cyst, which is passed in the feces of an infected host. In addition to an infective cyst, the life cycle for most intestinal protozoa includes a trophozoite, which is responsible for reproduction and pathogenicity. Only a single host is required, except for Sarcocystis, which requires ingestion of raw meat from an intermediate host. Zoonotic spread to humans has been documented for Giardia, Cryptosporidium, Entamoeba polecki, and B. coli. Treatment of intestinal protozoan infections is summarized in Table 52-11 . Giardia Lamblia G. lamblia is a flagellate protozoan that was first observed in 1681 by Leeuwenhoeck. In the last 30 years it
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DIAGNOSIS
TABLE 52-11 -- Antiparasitic Therapy for Infectious Diarrhea in Adults RECOMMENDATION
Giardiasis
Metronidazole 250 mg tid (15 mg/kg/day for children), Albendazole 400 mg qd, or quinacrine* 100 mg tid for 7 days, or tinidazole* 2000 mg single dose
Entamoeba histolytica excretion (asymptomatic)
Iodoquinol 650 mg tid for 20 days or paromomycin 500 mg tid for 7 days
E. histolytica diarrhea
Metronidazole 750 mg tid for 5 to 10 days or tinidazole* 1000 mg bid for 3 days, followed by iodoquinol 650 mg tid for 20 days or paromomycin 500 mg tid for 7 days
Cryptosporidiosis
None; in severe cases or AIDS patients, consider paromomycin 500–750 mg tid or qid for about 2 weeks or azithromycin 1200 mg qd for 4 weeks
Cyclosporidiosis
TMP/SMX 160 mg/800 mg bid for 7 days, followed by 160 mg/800 mg 3 times/week in AIDS patients
Isosporiasis
TMP/SMX 160 mg/800 mg qid for 10 days, followed by 160 mg/800 mg bid for 3 weeks, or pyrimethamine 75 mg qd with folinic acid 10 mg qd for 2 weeks
Microsporidiosis
Albendazole 400 mg bid for 2 to 4 weeks, followed by chronic suppression for AIDS patients
TMP/SMX, Trimethoprim and sulfamethoxazole; tid, 3 times a day; qd, daily; qid, 4 times a day; bid, twice daily. *Not available in the United States.
has gained recognition as an important human pathogen.[67] [123] The classification of Giardia species remains controversial. The life cycle of Giardia involves two stages. Active trophozoites are responsible for symptomatic illness. The organisms attach to the mucosa of the duodenum and proximal jejunum, where they multiply rapidly through binary division. Trophozoites are rarely infective because they rapidly die outside the body and are less resistant to gastric acidity. Responding to unknown stimuli, some trophozoites encyst during passage through the colon and are eliminated in the stools of infected hosts. Cysts are infectious as passed in the host stool; no period of maturation or intermediate development stage is required. Furthermore, they are very hardy in the external environment. When ingested by a potential host, excystation is stimulated by passage through the stomach, and the motile trophozoite migrates to the small bowel to complete the cycle.[67] [123] [148] Giardia is the most common protozoal intestinal parasite isolated worldwide. All age groups are affected.[67] [109] [148] Giardiasis usually represents a zoonosis, with cross-infectivity from animals to humans, and vice versa. Giardia has been found in stools of beavers, cattle, dogs, cats, rodents, and sheep.[148] The infective dose of Giardia for humans is low: 10 to 25 cysts caused infection in eight of 25 subjects; more than 25 cysts caused infection in 100%.[148] Person-to-person spread may be the most common means of transmission for humans. Twenty-five percent of family members with infected children become infected.[67] Areas and populations with poor hygiene and close physical contact have higher rates of infection. Venereal transmission occurs among homosexuals through direct fecal-oral contamination.[67] Epidemics and carrier rates of 30% to 60% have been found among children in day-care centers and in Native American reservations. Water is a major vehicle of infection in community outbreaks.[131] Cysts retain viability in cold water for as long as 2 to 3 months. In the United States from 1964 to 1984, 90 outbreaks (24,000 cases) of giardiasis were linked epidemiologically to water, and it is still the most frequently identified cause of waterborne diarrhea outbreaks. Most of these occurred in small water systems that used untreated or inadequately treated surface water.[121] [122] [131] Clear and cool mountain water has been so often associated with giardiasis that the illness has been called "backpacker's diarrhea" or "beaver fever" (although fever is not usually seen). An outbreak in Aspen, Colorado, in 1964 was the first well-documented waterborne outbreak in the United States, and recent outbreaks around the same area indicate that this area remains endemically infected with Giardia. In the northeastern states, large outbreaks have occurred in the mountain communities of Rome, New York, and Berlin, New Hampshire. Every U.S. region has experienced waterborne outbreaks, but the western mountain regions (Rocky Mountains, Cascades, Sierra Nevada) have reported the majority, where giardiasis must be considered endemic.[67] [131] [148] Giardia accounts for a small percentage of TD. [60] [158] It has been identified in a large percentage of cases among travelers to St. Petersburg, Russia, where tap water is the usual source. Because of the relatively long incubation period and persistent symptoms, Giardia is more likely to be found as the cause of diarrhea that occurs or persists after returning home from travels to any developing region.[42] [60] [158]
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The pathophysiologic mechanisms of diarrhea and malabsorption in giardiasis are poorly understood.[148] Reversible malabsorption of fats, vitamins A and B, folate, and
disaccharides has been demonstrated in some patients with diarrhea. Malabsorption may result from (1) physical blockade by large numbers of trophozoites blanketing the intestinal mucosa; (2) deconjugation of bile acids; (3) bacterial or fungal overgrowth in the small intestine; (4) increased turnover of cells on the mucosa of the villi, which do not absorb normally; and (5) epithelial damage. Altered gut motility and hypersecretion of fluids, perhaps through increased adenylate cyclase activity, may play a role. Histologic changes of villous atrophy and inflammatory infiltrates with epithelial cell destruction have been observed. In some series, these changes correlated with degree of malabsorption and reverted to normal after treatment. However, most small bowel biopsies in human patients demonstrate minimal or no changes, with only occasional mucosal invasion (with trophozoites found intracellularly and extracellularly) and no local inflammatory response.[67] Enterotoxins have not been found. More than one mechanism is probably involved. Infectivity apparently depends on both host and parasite factors.[148] Most infections are asymptomatic, and in endemic areas, Giardia is found in healthy people. The attack rate for symptomatic infection in the natural setting varies from 5% to 70%.[148] Asymptomatic carrier states with high numbers of cysts excreted in stools are common. Correlation between inoculum size and infection rates has been noted, but not with numbers of cysts passed or severity of symptoms. Hypochlorhydria, certain immunodeficiencies, blood group A, and malnutrition apparently predispose to symptomatic infection.[67] [148] The incubation period averages 1 to 2 weeks, with a mean of 9 days and a wide clinical presentation. A few people experience abrupt onset of explosive watery diarrhea accompanied by abdominal cramps, foul flatus, vomiting, low-grade fever, and malaise. This typically lasts 3 to 4 days before transition into the more common subacute syndrome. In most patients the onset is more insidious and symptoms are persistent or recurrent. Stools become mushy, greasy, and malodorous. Watery diarrhea may alternate with soft stools and even constipation. Upper GI symptoms, typically exacerbated postprandially, accompany stool changes but may be present in the absence of soft stool. These include mid-abdominal and upper abdominal cramping, substernal burning, acid indigestion, sulfurous belching, nausea, distention, early satiety, and foul flatus. Constitutional symptoms of anorexia, fatigue, and weight loss are common.[67] [148] Unusual presentations include allergic manifestations, such as urticaria, erythema multiforme, and bronchospasm. Some Giardia infections are associated with a chronic illness. Adults may have a longstanding malabsorption syndrome and marked weight loss, and children may have a failure-to-thrive syndrome. [44] [148] Laboratory confirmation of giardiasis can be difficult. Stool examination remains the primary means of diagnosis ( Figure 52-2 ) but is being replaced by newer immunodiagnostic tests. Trophozoites may be found in fresh, watery stools but disintegrate rapidly. Although trophozoites remain in fresh stools for at least 24 hours, stools should be preserved in a fixative such as polyvinyl alcohol or a formalin preparation if not immediately examined. Cyst passage is extremely variable and not related to clinical symptoms.[148] In the office, fresh stool can be mixed with an iodine solution (e.g., Gram's iodine) or methylene blue and examined for cysts on a wet mount. Many antibiotics, enemas, laxatives, and barium studies mask or eliminate parasites from the stools, so examinations should be delayed for 5 to 10 days after these interventions. Trichrome stain is better than the formalin-ether concentration technique for identification of protozoal cysts and trophozoites.[75] The current recommendation is to examine three samples taken at intervals of 2 days. Another noninvasive office test is duodenal mucus sampling, using a string test (Enterotest), which has a reported sensitivity of 10% to 80%. [75] [148] Duodenal biopsy is rarely necessary but may be the most sensitive test.[75] A commercial enzyme immunoassay (EIA) has shown the same sensitivity as microscopic examination, but has 100% specificity, making it a convenient screening method. EIA is much easier and requires less experience than microscopy, but can not differentiate between cysts and trophozoites.[5] Immunofluorescent techniques using monoclonal antibodies can detect low numbers of organisms in short time but require centrifugation of the sample.[74] Molecular techniques need further development.[148] [199]
Figure 52-2 Giardia lamblia trophozoite seen by methylene blue wet mount staining under oil (1000×). The finding of cysts or trophozoites in a patient with diarrhea is sufficient to make a tentative diagnosis of giardiasis.
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Immunologic responses to Giardia infection are complex. Epidemiologic studies show acquired resistance, with lower rates of infection and illness (1) among residents of endemically infected areas compared with visitors and (2) among adults compared with children. However, reinfection does occur. Levels of IgG antitrophozoite antibodies rise with both symptomatic and asymptomatic infections, helping to clear the infection. Hypogammaglobulinemic patients have a higher incidence of symptomatic giardiasis, implying an important protective function of immunoglobulins.[67] [148] Effects of mucosal secretory antibodies in humans have not been clearly demonstrated, although mouse studies show a protective effect of IgA secretory antibodies. Both cellular and humoral responses to Giardia have been demonstrated. Immunologic responses are effective in the majority of infections because spontaneous clinical recovery is common with or without the disappearance of organisms. Average duration of symptoms in all ages ranges from 3 to 10 weeks. [44] [148] Given the difficulty and expense of confirming the diagnosis in some patients, a therapeutic trial of drugs may be attempted when suspicion is high. Imidazole derivatives, (e.g., metronidazole) affect bacterial flora as well, so they are less specific but still better for empiric (unproven diagnosis) therapy because of their wide activity. Symptomatic patients should be treated for comfort and to prevent the development of chronic illness. Asymptomatic carriers in nonendemic areas should be treated when identified because they may transmit the infection or develop symptomatic illness. No drug is effective in all cases. In resistant cases, longer courses of two drugs taken concurrently have been suggested. Relapses occur up to several weeks after treatment, necessitating a second course of the same medication or an alternative drug. Malabsorption usually resolves with treatment, but persistent diarrhea may result from lactose intolerance or a syndrome resembling celiac disease rather than treatment failure.[148] Three groups of drugs are currently being used: nitroimidazoles (metronidazole, tinidazole, albendazole, ornidazole, nimorazole), nitrofuran derivatives (furazolidone), and acridine compounds (mepacrine, quinacrine). Metronidazole (Flagyl, 250 mg three times a day for 5 days for adults) is often used in the United States. Cure rates of 85% to 90% are comparable to those with quinacrine, but with better tolerance. Tinidazole (Fasigyn, 2000 mg single dose) has the same success rate with better compliance but is not available in the United States. Quinacrine (Atabrine, 100 mg three times a day for 5 days for adults and 7 mg/kg/day in three divided doses for children for 5 days), with cure rates of about 95%, has been considered the drug of choice in adults. Unfortunately, quinacrine is no longer available in the United States because it produces more frequent side effects, especially in children. No pediatric liquid form is always available. In severely symptomatic individuals, paromomycin (Humatin, 25 to 30 mg/kg in three divided doses for 5 to 10 days) has been effective.[67] [123] [148] Entamoeba Lösch described the trophozoite form of Entamoeba in 1875 and Quincke and Ross the cyst form in 1893. Recently molecular biologic studies confirmed the existence of an invasive parasite (Entamoeba histolytica) and a noninvasive, commensal organism (E. dispar).[100] [124] Isoenzyme analysis has recognized 22 different zymodemes of E. histolytica, which may explain the pathogenic and commensal strains and the geographic differences in rates of invasive disease.[22] [124] [163] The life cycle of E. histolytica involves two forms and one host. The reproductive form is the trophozoite, which resides in the large intestine of the host and can cause illness. Encystment occurs in the gut, and cysts pass in the stool. The early cyst matures within the host or externally by undergoing two nuclear divisions. Usually the cysts are infectious when passed. Although sensitive to boiling, adequate chlorination, and complete desiccation, cysts may survive drying or freezing and persist for months in a moist environment. After cysts are ingested, they undergo nuclear division in the small intestine, resulting in eight trophozoites per cyst.[22] [124] Humans are the primary reservoir of E. histolytica. Infected individuals may pass up to 45 million cysts per day. E. histolytica is found worldwide. Approximately 12% of the world's population is infected.[163] The higher prevalence in tropical countries (30% to 50%) is related to increased risk of fecal-oral contamination, which depends on sanitation, cultural habits, crowding, and socioeconomic status.[22] [124] It is the third most important cause of death by parasitic infection worldwide. Similar conditions create pockets of endemic infection in the United States among institutional inmates, Native Americans on reservations, and homosexuals. Importation of infections by travelers and immigrants accounts for most cases in the United States and other temperature countries.[117] Attack rate and prevalence are difficult to determine because the majority of infections are asymptomatic, and screening with single stool samples is likely to identify only 20% to 50%.[22] [124] The 10% to 15% of the U.S. population once infected with E. histolytica has decreased to 1% to 5% overall, primarily because of adequate water and sewage treatment.[109] [117] Between 1946 and 1980, six waterborne outbreaks of amebiasis were reported in the United States.[131] [125] Amebiasis accounts for less than 1% of TD.[60] [124] [158] Pathogenicity of E. histolytica is not well understood.[124] Invasion may be a function of motility or lytic
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enzymes. The cecum and ascending colon are most frequently involved, followed by the rectum and sigmoid colon. Five different lesions of increasing severity can be distinguished in the colon: (1) diffuse inflammation with cellular infiltrate and an intact epithelium, (2) superficial erosions, (3) early invasion followed by shallow ulceration, (4) late invasive lesions forming the classic flask ulcers with skip lesions, and (5) loss of mucosa and muscularis, resulting in exposure of underlying granulation tissue. Extraintestinal spread is hematogenous. Abscesses containing acellular debris develop primarily in the liver but may involve the brain and lung. [124] Although 80% to 99% of infections result in asymptomatic carriers, a spectrum of GI diseases may result. The incubation period ranges from 1 to 4 months, depending on the area of endemicity. Most often, colonic inflammation without dysentery causes lower abdominal cramping and altered stools, sometimes containing mucus and blood.[124] [163] Weight loss, anorexia, and nausea may be present. Symptoms commonly fluctuate and continue for months. The subacute infection may evolve into a chronic, nondysenteric bowel syndrome, with intermittent diarrhea, abdominal pain, weight loss, and flatulence. Dysentery may develop suddenly after an incubation period of 8 to 10 days or a period of mild symptoms. Affected persons may have frequent passage of bloody stools, tenesmus, moderate to severe abdominal pain and tenderness, and fever. There is considerable variation in severity.[124] Humoral antibodies increase with invasive disease and persist for long periods. Although they do not protect against reinfection or bowel invasion, they show antiamebic action in vitro and may prevent recurrent liver infection, which is uncommon. Once the infection is cleared, recurrence is unusual, but asymptomatic cyst shedding and active GI illness may persist for years, indicating lack of consistent immune response in the intestinal lumen.[124] [163] The fatality rate for amebic dysentery and its complications is about 2%. Complications of intestinal involvement develop in 2% to 20% of cases and include perforation, toxic megacolon, and ameboma. An ameboma is an annular inflammatory lesion of the ascending colon containing live trophozoites. It may be improperly diagnosed as a pyogenic abscess or a carcinoma. A postdysenteric syndrome can occur in patients with acute amebic dysentery and can be confused with ulcerative colitis. The diagnosis of intestinal amebiasis is made by identification of cysts or trophozoites in stool. Mucus from fresh stools or sigmoidoscopic scrapings and aspirates mixed with a drop of saline may show trophozoites if examined within an hour. For delayed examination, stool must be preserved in polyvinyl alcohol or other fixative and may later be examined with trichrome stain.[75] [124] The same limitations and problems discussed with Giardia apply to E. histolytica. Fecal shedding of cysts is irregular. Three stools on alternate days identify most infections. Overdiagnosis may result from misidentification of leukocytes. Sigmoidoscopy or colonoscopy is useful for viewing the pathologic lesions and obtaining selective samples of mucus and biopsies of mucosal ulcers, which usually contain organisms. [75] Finding cysts does not confirm the diagnosis of symptomatic intestinal amebiasis. The key to establish the diagnosis is finding motile trophozoites with ingested red blood cells. Culture techniques have been developed that identify infection in some cases when small numbers of cysts are missed in stool examinations, but culture techniques are expensive and time-consuming.[75] Serologic tests are not useful for identifying asymptomatic carriers but are positive in 85% to 95% of patients with dysentery and 90% to 100% of patients with liver abscess. [75] [91] [157] Also, new antigen detection techniques can differentiate between E. histolytica and E. dispar.[100] [111] Recently, PCR techniques have been developed, showing greater than 95% sensitivity and specificity.[2] [199] Treatment of amebiasis is based on the location of infection and degree of symptoms. Medications are divided into tissue amebicides, which are well-absorbed drugs that combat invasive amebiasis in the bowel and liver (e.g., metronidazole, tinidazole, emetine, dehydroemetine, chloroquine), and poorly absorbed drugs for luminal infections (e.g., iodoquinol, paromomycin, diloxanide furoate). In general, treatment is effective for invasive infections but disappointing for intestinal colonization. U.S. guidelines suggest that asymptomatic carriers should be treated, since a cyst passer represents a potential health hazard to others and reinfection in the United States is uncommon. Routine screening of asymptomatic persons of high-risk groups is not cost-effective, except perhaps for food handlers.[124] The current drug of choice for asymptomatic carriers is iodoquinol (650 mg 3 times a day for adults and 40 mg/kg/day in three divided doses for children for 20 days). Side effects are mild and consist of abdominal pain, diarrhea, and rash. Diloxanide furoate (Furamide) is another drug of choice (500 mg 3 times a day for adults and 20 mg/kg/day in three divided doses for children for 10 days), but in the United States it is classified as an investigational drug, available only through the CDC. Side effects are limited to flatulence and other mild GI symptoms. [124] Paromomycin is also effective (500 mg 3 times a day for adults and 30 mg/kg/day in three divided doses for children for 7 days). Although metronidazole has been used in asymptomatic carriers with 90% success, most reserve this drug for invasive and symptomatic infections. Invasive disease is treated with a tissue-active drug, followed by a luminal agent (in the same doses as just
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listed). For oral therapy, metronidazole is the drug of choice (750 mg 3 times a day for adults and 50 mg/kg/day in three divided doses for children for 5 to 10 days), followed by iodoquinol. Tinidazole (1000 mg twice daily for 3 days), is not available in the United States but appears to be effective and is well tolerated for intestinal and hepatic amebiasis. Emetine and dehydroemetine (1 mg/kg/day, maximum 90 mg/day) are used parenterally in severe cases of amebiasis, primarily extraintestinal, followed by iodoquinol for 20 days. These two drugs have frequent systemic side effects, including the development of cardiac arrhythmias requiring hospitalization for cardiac monitoring. Since this class of drugs is related to ipecac, they also cause vomiting. [23] [124] Another species, Entamoeba polecki, although usually nonpathogenic, has been suspected of causing lower intestinal symptoms in sporadic cases involving heavy infection.[167] Cysts are passed in stool and may be confused with E. histolytica, which they closely resemble. Successful resolution of symptoms has been reported with metronidazole followed by diloxanide furoate in the same doses as for amebiasis and balantidiasis. Cryptosporidium Cryptosporidium is a coccidian parasite that belongs to the phyla Sporozoa. It is a reemergent enteric pathogen in humans. Cryptosporidium parvum, the only human pathogen of this genus, was originally described in 1912 but first identified in humans in 1976.[34] [35] [86] Ingested thick-walled oocysts release sporozoites, which invade small bowel enterocytes, then develop into trophozoites that reside intracellularly but are extracytoplasmic (beneath the host cell membrane, similar to a vacuole). Trophozoites divide by asexual multiplication into merozoites (type I meront), with each one containing six to eight nuclei. From this stage they continue with asexual multiplication as type I meronts, which can infect other enterocytes (merogonic or schizogonic stage), or they develop into a type II meront and initiate sexual multiplication and oocyst development (sporogonic or gametogonic stage). About 80% of zygotes develop into thick-walled oocysts (each with four sporozoites) that are released in the stool, while the rest develop into thin-walled oocysts that participate in autoinfection of the host.[82] C. parvum is a ubiquitous zoonosis with a worldwide distribution. Cryptosporidium infects a wide variety of young animals, including domestic calves, birds, piglets, horses, pigs, kittens, puppies, and wild mammals, such as raccoons, beavers, squirrels, and coyotes.[86] Prevalence of infection in human populations varies from 0.1% to 3% in cooler, developed countries (Europe, North America) to 0.5% to 10% in warmer areas (Africa, Asia). The infection has been described in those who have contact with animals, such as veterinarians and farmers; infants in day-care centers; travelers to endemic areas; and AIDS or other immunocompromised patients. It may infect large numbers of individuals in community-wide waterborne outbreaks.[35] [86] [131] The infective dose of Cryptosporidium for humans is low, similar to Giardia species. Sporulated oocysts are infective as passed in the stool, so fecal-oral contamination is the mode of transmission.[86] The different routes of transmission are waterborne, especially in large community outbreaks; person to person, especially in day-care centers, custodial institutions, and hospitals; food-borne disease, through apple cider, uncooked sausage, and raw milk; sexual, with no association with specific behavior; and zoonotic.[73] [86] [121] [122] In 1993 in Milwaukee, Cryptosporidium caused the largest waterborne outbreak of protozoal parasites in the United States.[127] The pathophysiologic mechanisms of diarrhea and malabsorption are not completely understood. The initial invasion of parasites may activate cellular and humoral immune and inflammatory responses, leading to cell damage with villi atrophy and crypt hyperplasia, ultimately producing malabsorption and osmotic diarrhea.[82] [86] The clinical manifestations depend on immune status, but asymptomatic infection occurs in both normal and immunocompromised hosts.[86] In immunocompetent persons the usual incubation period of Cryptosporidium is from 5 to 28 days. Symptoms consist of watery diarrhea associated with cramps, nausea, flatulence, and at times, vomiting and low-grade fever. The syndrome is generally mild and self-limited, with a duration of 5 to 6 days in some groups (range 2 to 26 days). In contrast, immunocompromised hosts experience more frequent and prolonged infections, with profuse chronic watery diarrhea, malabsorption, and weight loss lasting months to years. Fluid losses can be overwhelming in a fulminant cholera-like illness, with high mortality. Cyst passage in stool usually ends within 1 week of symptom resolution but may persist for up to 2 months after recovery. Reinfection of an immunocompetent person has been documented. Rarely, Cryptosporidium can infect the respiratory system, which may be fatal in the immunocompromised host. The other extraintestinal manifestations relate to involvement of the liver and biliary system, particularly in immunocompromised persons. Cholangitis may not respond to common luminal agents used to treat intestinal
cryptosporidiasis, requiring sphincterotomy for therapy.[86] Diagnosis in initial case descriptions was made by small bowel biopsy, but oocysts can be found in the stools routinely in intestinal infections, even though shedding may be intermittent. Concentration techniques, such as formalin-ether or sucrose flotation, and subsequent staining with modified acid-fast, Giemsa, or Ziehl-Neelsen techniques facilitate identification of
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Cryptosporidium oocysts. The Enterotest is also useful in the diagnosis of cryptosporidiosis. Newer immunologic techniques are faster and have adequate sensitivity and excellent specificity. Several other methods (flow cytometry using monoclonal antibodies, PCR, RFLP analysis) have been developed, but their efficacy in the clinical setting is not yet known.[25] [74] [86] [114] No clearly effective treatment has been found for cryptosporidiosis. Because this disease is usually mild and self-limited in immunocompetent hosts, only supportive care is needed. Anticryptosporidial agents, such as paromomycin (500 to 750 mg 3 or 4 times a day for 2 weeks) and azithromycin (1200 mg daily for 4 weeks) may be used in immunocompetent persons with persistent infection and in immunocompromised patients. Paromomycin, azithromycin, roxithromycin, ionophores, sulfonamides, mefloquine, and nitazoxanide have been tested against cryptosporidiosis, especially in AIDS patients with chronic diarrheal disease, with variable but generally positive effects.[86] [180] [201] Further studies with these and other new agents, including clinical trials using immunotherapy options, are in progress.[33] [86] Isospora belli I. belli is also a coccidian protozoal parasite. The first description of Isospora was in 1915. More recently, I. belli was identified as the pathogenic species for humans. It is an uncommon cause of diarrhea in humans, but as with Cryptosporidium, its prevalence has been increasing in immunocompromised patients.[33] [82] [129] [131] [200] Humans are the only host, and infections are transmitted by fecal-oral contamination through direct contact of food and water. I. belli is endemic in areas of South America, Africa, and Asia. The prevalence is not precisely known but it ranges from 0.2% to 3% in United States AIDS patients and 8% to 20% in Haitian and African AIDS patients. This parasite has also been associated with outbreaks in custodial institutions, in day-care centers, and among immigrants. Infection rates in otherwise healthy persons with diarrhea are usually low. Most cases have been identified in tropical regions among natives, travelers, and the military.[82] [131] Life cycle and pathogenesis of I. belli are similar to Cryptosporidium. The organism invades mucosal cells of the small intestine, causing an inflammatory response in the submucosa and variable destruction of the brush border.[82] In immunocompetent persons, the I. belli infection may be asymptomatic or cause mild transient diarrhea and abdominal cramps. Other symptoms include profuse watery diarrhea, flatulence, anorexia, weight loss, low-grade fever, and malabsorption.[82] Generally infection is self-limited, ending in 2 to 3 weeks, but some persons have symptoms lasting months to years, clinically similar to giardiasis. Recurrences are common. Infections in immunocompromised patients tend to be more severe and follow a more protracted course.[129] Rarely, acalculous cholecystitis or reactive arthritis has been reported in isosporiasis.[12] Diagnosis can be made by identification of immature oocysts in fresh stool. However, excretion may occur sporadically and in small numbers, so concentration techniques are usually required. Staining with modified Ziehl-Neelsen and auramine-rhodamine are also useful. When stools are negative, the organism can be recovered from the jejunum through a biopsy or string test. Unlike the other intestinal protozoa, I. belli may cause eosinophilia. [75] Successful treatment has been reported with TMP/SMX (160/800 mg 4 times a day for 10 days, then 2 times a day for 3 weeks in normal hosts). Other options are pyrimethamine (75 mg daily for 14 days) with folinic acid, and metronidazole (for patients allergic to sulfonamides). In HIV patients, chronic lifetime suppression therapy is indicated with either TMP/SMX (160/800 mg 3 times a week) or pyrimethamine (25 mg) plus folinic acid (5 mg) daily.[82] [129] Cyclospora Cayetanensis Cyclospora species were first discovered in moles in 1870 and were identified as human pathogens in 1979. They were initially thought to be blue-green algae (cyanobacteria-like organism).[149] [182] [202] The life cycle and pathogenesis of C. cayetanensis are not completely understood. The organism has shown to be an important cause of acute and protracted diarrhea. C. cayetanensis is endemic in many developing countries in all continents, with the highest rates occurring in Nepal, Haiti, and Peru. In the United States, most of the native outbreaks have been from areas east of Rocky Mountains, usually associated with ingestion of contaminated imported raspberries. [27] [82] Fecal-oral transmission also occurs through water and soil.[182] Cyclospora infection is closely associated with diarrhea in travelers to endemic areas.[82] [95] [131] [202] The onset of diarrhea is usually abrupt with symptoms lasting up to 7 weeks or even longer.[82] In AIDS patients the duration may be longer and the severity greater.[129] Small spheric organisms can be detected in fresh or concentrated stool, and they show variable staining with acid-fast methods. C cayetanensis stains best with carbolfuchsin.[202] Phase-contrast microscopy and autofluorescence are also useful in the diagnosis.[75] A PCR method is still used only for research.[131] The treatment of choice is TMP/SMX (160/800 mg 4 times a day for 10 days). This treatment provides more rapid clinical and parasitologic cure, with fewer recurrences.[82] [182] In AIDS patients, chronic suppression with TMP/SMX may be required.[129] Miscellaneous Parasitic Agents Microsporidia.
More than 100 genera and 1000 species of microsporidia exist in the phylum Microspora. Most
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species infect insects, birds, and fish. Since the first description in humans in 1985, only 12 species have been reported to infect humans: Enterocytozoon bieneusi, three Encephalitozoon species, three Nosema species, two Trachipleistophora species, Pleistophora, Vittaforma corneae, and Microsporida species. Microsporidians cause a wide spectrum of disease, but only two, E. bieneusi and E. intestinalis, have been found to cause diarrhea.[38] [82] [198] [200] Transmission is thought to be fecal-oral or urinary-oral[38] and the infection zoonotic. Waterborne transmission also occurs.[131] Prevalence of microsporidiosis in AIDS patients with chronic diarrhea is 7% to 50%. [9] [198] The clinical manifestations of intestinal microsporidiosis are chronic diarrhea, loss of appetite, weight loss, malabsorption and fever.[9] [198] Acute self-limited diarrhea has been reported in immunocompetent hosts. Other infections include keratoconjunctivitis, hepatitis, peritonitis, myositis, CNS infection, urinary tract infections, sinusitis and disseminated disease. Diagnosis involves trichrome staining of concentrated stools or intestinal biopsy sampling, but electron microscopy is considered the gold standard. Immunologic and molecular biologic techniques are still under evaluation.[69] [198] The most effective drug is albendazole (400 mg twice a day for 2 to 4 weeks). It is effective against most species, but results are variable with diarrhea from E. bieneusi.[39] Other drugs show different efficacy and include thalidomide, fumagillin, atovaquone, metronidazole, furazolidone, azithromycin, itraconazole, and sulfonamides.[38] Sarcocystis.
Few human infections with Sarcocystis have been reported. Infection may be asymptomatic or associated with diarrhea, abdominal pain, nausea, and bloating. Symptoms typically improve within 48 hours of onset of illness. Diagnosis is based on identification of cysts in concentrated feces. No specific treatment has been established, but TMP/SMX and furazolidone have had variable efficacy.[200]
Balantidium.
Balantidium coli is a rare pathogen in humans.[186] [200] Although many aspects of the epidemiology are unclear, pigs appear to be the primary reservoir and source of human infection. Clinical features also resemble amebiasis, with a spectrum including asymptomatic infection, chronic intermittent diarrhea of variable intensity, acute dysentery with mucosal invasion, and rarely, metastatic abscesses. Diagnosis is made by observing the organism in stool. Trophozoites are seen much more often than are cysts. Recommended treatment is tetracycline (500 mg 4 times a day for 10 days) or metronidazole (750 mg 3 times a day for 10 days). [200] Blastocystis.
The role of Blastocystis hominis in diarrheal disease is still controversial, although it is often identified in stool samples. B. hominis has not been directly correlated with symptoms,[200] which could be caused by other undetected pathogens. When found in large numbers as the sole pathogen, B. hominis is suspected as the potential etiologic agent of diarrheal illness. Dientamoeba.
Dientamoeba fragilis occasionally causes diarrhea, occurring characteristically in residents of or visitors to developing tropical regions. It may be found in stools of persons without enteric symptoms. Because cyst forms have not been identified, the mode of transmission remains unknown. Illness caused by the parasite typically resembles giardiasis, but treatment of these two parasitic infections is different. Iodoquinol and tetracyclines are effective against D. fragilis.[200]
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Chapter 53 - Nutrition, Malnutrition, and Starvation E. Wayne Askew
How does it feel to starve? A test subject in the Minnesota Starvation Study made the following observation after 24 weeks of semistarvation (1570 kcal/day, 24% weight loss)[35] : I am hungry. I am always hungry ... at times I can almost forget about it but there is nothing that can hold my interest for long ... I am cold ... my body flame is burning as low as possible to conserve precious fuel and still maintain my life processes ... I am weak. I can walk miles at my own pace in order to satisfy laboratory requirements, but often I trip on cracks in the sidewalk. To open a heavy door it is necessary to brace myself and push or pull with all my might. I wouldn't think of throwing a baseball and I couldn't jump over a twelve inch railing if I tried. This lack of strength is a great frustration. It is often a greater frustration than the hunger ... And now I have edema. When I wake up in the morning my face is puffy ... Sometimes my ankles swell and my knees are puffy ... Social graces, interests, spontaneous activity and responsibility take second place to concerns about food ... I lick my plate unashamedly at each meal even when guests are present ... I can talk intellectually, my mental ability has not decreased, but my will to use my ability has. Nutrition is essential to proper human physiology and daily functioning but is often unappreciated in wilderness expedition planning. Many enthusiasts do not consider food as critical as gear and equipment, medical supplies, physical fitness, and other logistical considerations. In temperate environments, where food and water are plentiful and resupply is feasible, the importance of nutrition diminishes. When a stressful physical environment is superimposed on physically demanding wilderness tasks, however, the role of nutrition becomes crucial to maintain performance and prevent disease and injury, as evidenced from the description of Napoleon's disastrous 1812 winter retreat from Moscow by Baron D.J. Larrey[50] : The ice and deep snow with which the plains of Russia were covered, impeded ... calorification in the capillaries and pulmonary organs. The snow and cold water, which the sol- diers swallowed for the purpose of allaying their hunger or satisfying their thirst ... contributed greatly to the destruction of these individuals by absorbing the small portion of heat remaining in the viscera. The agents produced the death of those particularly who had been deprived of nutriment. Although they usually have food, misfortune can strike the best-prepared adventurers. A wrong turn on the trail, injury, unanticipated terrain, an unexpected storm, or a downed airplane can isolate a victim from anticipated food sources. Food is often the most important item in a survival situation, particularly as the supply is exhausted. Although a concern, a shortage of food does not necessarily mean disaster. Humans are remarkably adaptable and can subsist on non-ideal dietary patterns for prolonged periods without disastrous effects on health and performance. A baseline level of energy intake ensures a minimal intake of vitamins and minerals, forestalling malnutrition and nutrient deficiency states. Hunger is uncomfortable and may hinder performance, but a food-deprived individual can still function for an extended time. This chapter discusses three nutritional states or situations in terms of wilderness environments: (1) nutrition for optimal or effective functioning in environmental extremes; (2) malnutrition or suboptimal nutrition; and (3) starvation, or lack of nutrition. Preventive dietary planning for wilderness expeditions and emergency nutrition measures after rescue from starvation will be discussed.
ENVIRONMENTAL STRESS AND NUTRIENT REQUIREMENTS The physical environment plays a significant role in determining survival time in the absence of food or water. The most important nutrient is water. [9] If an adequate supply of water is not available, death occurs from dehydration before depletion of energy stores. Humans can survive complete food deprivation for weeks or even months depending on body fat. A nonobese adult fasting in a clinical setting can live as long as 60 to 70 days, with loss of all their body fat and one-third their lean body mass.[32] One climber survived 43 days and was near death when rescued from a cave in the Himalayas with water but no food.[55] Time to death after complete water deprivation is 6 to 14 days, depending on the rate of water loss. Death from starvation in nonobese individuals is imminent if approximately 50% of body weight has been lost. This discussion on energy restriction assumes an adequate supply of water (see Chapter 10 and Chapter 11 ). Modern camping foods and military field rations can support health and performance in a variety of temperate environments.[41] The situation may change rapidly, however, in wilderness environments characterized by more extreme temperatures and terrain.[40] [42]
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Figure 53-1 (Figure Not Available) Influence of extreme wilderness environments on food and fluid intake and physical and mental performance. (From Askew EW: Nutrition and performance under adverse environmental conditions. In Hickson JF Jr, Wolinski I, editors: Nutrition in exercise and sport, Boca Raton, Fla, 1989, CRC Press.)
Stress, whether heat, cold, altitude, level of exertion, or food restriction, influences nutrient requirements.[7] [53] Superimposed stressors, such as extreme altitude or sleep deprivation, jeopardize both physical and mental performance[10] [26] [40] [42] [43] (Figure 53-1 (Figure Not Available) ). Energy and fluid deficits arising from the interaction of environment and nutrition can potentially negatively impact both physical[27] and mental[43] performance. Energy Needs Cold and altitude stress and its influence on macronutrient and vitamin requirements have been a major focus of military and civilian research.[8] Vitamin and mineral requirements are not significantly increased by cold exposure, although caloric requirements for thermogenesis may be elevated.[42] Work in cold environments can be adequately supported by combinations of fat, carbohydrate, and protein, although certain macronutrients may be more beneficial.[4] The macronutrient source is not as important as consuming enough total calories to support activity and thermogenesis. When wilderness activities shift from sea-level cold weather to moderate or high altitude, however, the importance of the macronutrient mixture should be reconsidered. Fat is an efficient energy source during cold weather activities at sea level but is not as well tolerated at altitude.[5] The substitution of carbohydrate for fat and partly for protein can help an individual's oxygen economy while working at altitude.[3] Carbohydrate is more efficient fuel at altitude than fat because it is already partially oxidized and requires less oxygen to combust its carbon skeleton to CO2 . The metabolism of carbohydrate for energy requires approximately 8% to 10% less inspired oxygen than that required to process a similar amount of calories from fat. A high-carbohydrate diet can reduce the symptoms of acute mountain sickness, enhance short-term high-intensity work as well as long-term submaximal efforts,[3] [11] [24] and "lower the effective elevation" as much as 300 to 600 m (about 1000 to 2000 feet) by requiring less oxygen for metabolism. Initial altitude exposure results in anorexia and subsequently reduces energy and carbohydrate intake.[20] Food intakes usually improve with time and acclimatization but, depending on the altitude, may never match those at sea level. Weight loss and performance decrements are common under these conditions. Carbohydrate supplementation of the diet at elevations exceeding 2200 m (7218 feet) is usually an effective method to increase carbohydrate and total energy intakes.[3] [20] [25] Carbohydrate supplementation at altitude may reduce symptoms caused by acute altitude exposure,[24] but not all studies have demonstrated this benefit.[62] The most effective form of carbohydrate supplementation is usually liquid beverages; people will drink even when they are reluctant to eat.[20] [25] Also, increasing fluid intake is beneficial at high altitudes, where increased fluid losses occur with diuresis and respiration in the dry atmosphere.[9] Nutritional requirements for males in environmental extremes are well studied, but little research has been done on female requirements.[36] Studies in the late 1960s reported that female soldiers deployed to moderate to high altitude would require supplemental dietary iron for optimal support of the hematopoietic response to hypoxia.[30] Subsequent research on iron requirements and the thermogenic response to cold identified iron as a key micronutrient for females in a cold environment.[17] [39] Females usually consume less total food calories
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than males because of their reduced body size and therefore are at increased risk for reduced vitamin and mineral intakes. Fortunately, the need for these vitamins and minerals (except iron) is related to lean body mass, and females usually have less lean body mass than males. Performance across a broad spectrum of backcountry tasks is not always severely degraded by suboptimal energy and carbohydrate intakes. Soldiers can maintain relatively normal work capacities for short periods (less than 10 days) of food restriction.[26] The Minnesota starvation studies conducted during World War II demonstrated that energy deficits resulting in less than 10% body weight loss did not impair physical performance; however, underconsumption of calories for longer periods with continued body weight loss produced significant deficits in physical performance.[63] Restricted energy and dietary carbohydrate content over 30 days supported light to moderate activity level without evidence of greatly impaired physical performance capabilities.[12] On the other hand, longer periods of caloric restriction (8 weeks) and higher levels of energy expenditure have been associated with significantly reduced physical performance capacity.[48] It is difficult to derive a closely predictable relationship between energy deficit and performance. Some indicators of performance, such as grip strength, appear to be well preserved until nutritional status is severely compromised, whereas other measures, such as the maximal lift test, maximal jump height, isometric leg extension, and maximal oxygen uptake, appear to be more sensitive predictors of impaired performance.[34] Nonobese individuals seem to maintain strength with up to 5% body weight loss. Aerobic capacity and strength are reduced when body weight loss exceeds 10%. Friedl[26] concluded that changes in oxygen capacity in response to modest caloric restriction influence performance less than reductions in muscle strength in response to weight loss. The primary concern with weight loss from inadequate energy during extended wilderness activities may be loss of muscle strength, which is significant with 5% to 10% body weight loss. Significant declines in aerobic capacity can also occur after weight losses of this magnitude, but the decline in aerobic capacity appears to have relatively little effect on individual performance at moderate (less than 50% oxygen capacity) sustainable workload levels.[26] Thus a prior food restriction with significant loss of body weight may not preclude a gradual trek to the summit, but a short-term rigorous push for the summit to avoid impending bad weather might be compromised. The effects of energy restriction on performance involve other factors besides strength and aerobic capacity. Weight losses up to 6% over 10 to 45 days generally do not significantly impair cognitive performance, but habitual or forced consumption resulting in a 50% loss of energy requirements may degrade cognition.[43] Reduced food intake coupled with other stressors, such as high rates of energy expenditure and sleep deprivation, can also impair immune function.[37] [45] Carbohydrate Both the time provided for dietary adaptation to carbohydrate restriction and the level of carbohydrate in the diet can influence the level of aerobic endurance.[2] Performance can be reduced by 40% after only 4 days on a calorie-adequate but low-carbohydrate (10% of kcal) diet.[29] Another calorie-adequate low-carbohydrate (5% of kcal) diet for 2 weeks also reduced performance, but only by 15%, presumably because of metabolic adaptations to the shift in energy sources.[52] More than any macronutrient other than water, reduced carbohydrate intake can negatively influence muscle glycogen levels and endurance.[2] Certain types of performance, such as backpacking, cross-country skiing, and climbing, may be influenced by an acute shortage of carbohydrate in the diet, depending on the intensity of the workload. Inadequate carbohydrate and successive days of intense prolonged exercise may result in gradual reduction of glycogen stores, deterioration of
performance, and perception of fatigue. Furthermore, perceived exertion for certain wilderness activities, such as load bearing, may be assumed to be a function of the dietary carbohydrate and its effect on muscle glycogen levels. Carbohydrates may extend or enhance performance when ingested before, during, and after moderate to intense aerobic exercise.[33] This requires daily consumption of approximately 500 to 550 g of carbohydrate. Typical dietary carbohydrate intakes of male soldiers fed a variety of rations during 18 field studies in temperate, hot, and cold environments ranged from 244 to 467 g/day.[15] It is also probable that daily carbohydrate intakes for wilderness activities would be less than the 500 to 550 g/day recommended for optimal physical performance, since total caloric intake during outdoor work is often less than that required to maintain energy balance.[41] Most people do not selectively consume low-carbohydrate diets during wilderness activities; however, total carbohydrate intake is often low because of its relationship to total energy intake and to limited food choices. In the short term, lack of energy (calories) is not as significant to performance as lack of carbohydrate.[26] Definitive field studies demonstrating a positive effect of dietary carbohydrate supplements on performance are lacking.[6] When field conditions can be modeled under well-controlled laboratory settings, results suggest that carbohydrate supplementation benefits performance. One study tested the concept that soldiers would benefit from carbohydrate supplementation under conditions simulating field operations.[47]
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Supplemental carbohydrate permitted a higher level of physical performance or aerobic power. Run times to exhaustion were increased approximately 6% with single carbohydrate feeding and 17% with divided doses. The ingestion pattern influenced performance, indicating that a supply of easily consumed carbohydrate supplement or food item ingested before, during, and after field activities is an effective method to sustain or boost physical performance. Protein Considerable discussion of the proper amount of protein to maintain muscle mass, prevent "wasting," and maintain performance under conditions of physical stress exists in the literature. However, despite all the controversies, recommendations concerning the amount of protein in the diet have changed little since World War I, as evidenced by reviewing a 1919 report by Murlin and Miller[46] : "The amount of protein ... sufficient to repair all of the wastes of the body and to supply an adequate reserve is 13% of the total energy intake. It seems a matter of indifference to the muscles whether they receive their energy from carbohydrate or from fat ... Hard muscular work, therefore can be done on a diet high in carbohydrate or upon a high fat diet. It is of general experience, however, that muscular work is done with less effort if there is a plentiful supply of carbohydrate." "Thirteen percent" of the energy intake translates to an intake of 65 g of protein on an energy-restricted intake of 2000 kcal/day, or 130 g of protein for a 4000-kcal diet. This quantity of dietary protein is easy to obtain (e.g., one stick of beef jerky or one serving of peanut butter contains 6 to 8 g of protein). Although dietary protein is important, the quantity of carbohydrate in a food-restricted diet is more closely related to nitrogen balance or the preservation of lean body mass than to the absolute amount of protein. Carbohydrates apparently "spare" amino acids derived from dietary protein from subsequent deamination and oxidation for energy. Approximately 40 g of dietary protein seems to be a minimum daily amount required to prevent excessive nitrogen loss under food restriction. Vitamins Vitamins are coenzymes of important biochemical reactions in energy metabolism. Vitamins E and C and the precursor of vitamin A (ß-carotene) also exert important protective actions as antioxidants. Oxidative stress may be significant during work in environmental extremes.[7] Prevention of vitamin deficiencies is poorly understood in short-term and long-range nutrition planning. Body stores of some vitamins (primarily the water-soluble vitamins) are limited, and, vitamin deficiencies
Figure 53-2 Impact of restricted vitamin intake on functional performance. Experimental conditions: diet, 3070 kcal; % U.S. RDA: thiamin 28%, riboflavin 31%, vitamin B 6 16%, vitamin C 10%; performance test—incremental cycle ergometer. (Data from van der Beek EJ: Marginal deficiencies of thiamin, riboflavin, vitamin B6 , and vitamin C: prevalence and functional consequences in man, Amsterdam, 1992, TNO.)
can occur with prolonged periods of dietary restriction. Tissue depletion of thiamin, riboflavin, and pyridoxine can occur in 11 weeks with a calorie-adequate but vitamin deficient, experimental diet composed of common food products.[66] Van der Beek et al[65] [66] [67] studied the maintenance of human physical performance with varying degrees of vitamin restriction. With vitamin intakes significantly less than the recommended dietary allowances (RDAs), vitamin deficiencies manifested slowly in terms of physical performance impairments. Restricted intakes (percent U.S. RDA) of thiamin (28%), riboflavin (31%), pyridoxal phosphate (16%), and ascorbate (vitamin C, 10%) resulted in less than a 20% decrease in cycle ergometer performance (maximum workload) after 8 weeks at this level of restriction ( Figure 53-2 ). The effect of vitamin restriction on performance contrasts with the more immediate effects of acute or long-term dietary carbohydrate restriction. Physical performance impairment is much more sensitive to the amount of dietary carbohydrate in the short term (1 to 3 days) than to dietary vitamin, protein, or fat in the long term (6 to 8 weeks).[2] A vitamin deficiency is a progressive process with four stages and a spectrum of physiologic manifestations ( Box 53-1 ). The possibility that certain nutrients might help people "adapt" or in some manner function more efficiently in stressful environments has intrigued explorers and scientists for years. Perhaps the most thorough exploration of this possibility was conducted in 1953 in the "Medical Nutrition Laboratory Army Winter Project: Vitamin Supplementation of Army Rations Under Stress Conditions in a Cold Environment—The Pole
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Mountain Study." The objective of this study was to determine if supplementation with large quantities of ascorbic acid and B-complex vitamins would influence the physical performance of soldiers engaged in high levels of physical activity in a cold environment, both with and without caloric restriction.[8] The investigators concluded that supplementing the diet of men engaged in high levels of physical activity in the cold, with or without caloric restriction, did not result in significantly better physical performance.[8]
Box 53-1. FOUR STAGES IN DEVELOPMENT OF A VITAMIN DEFICIENCY 1. PRELIMINARY STAGE Inadequate amount from poor dietary patterns or altered availability in the diet Often occurs after short-duration wilderness activities (160
>200
40–54
50–64
160
>150
70
5
200–300
2
65
5
3.5 (>1 mo)
6
3–3.5
1
Respiratory rate (breaths/min)
PaO2 /FIO2
*
PaCO2 † (mm Hg) Glasgow Coma Score Pupillary reactions
Potassium (mEq/L)
‡
4
6.5–7.5 7.5
5
Calcium (mg/dl)
7–8
2
12–15 15 Glucose (mg/dl)
40–60
4
250–400 400 Bicarbonate§ (mEq/L)
32 Modified from Pollack MM et al: Crit Care Med 16:1113, 1998. BP, Blood pressure; HR, heart rate; Pao2 /PaCO2 , arterial oxygen/carbon dioxide pressure; FIO2 , fraction of inspired air; PT/PTT, prothrombin/partial thromboplastin time. *Cannot be assessed in patients with intracardiac shunts or chronic respiratory insufficiency; requires arterial blood sampling. †May be assessed with capillary blood gases. ‡Assessed only if there is known or suspected CNS dysfunction; cannot be assessed in patients during iatrogenic sedation, paralysis, anesthesia, etc. Scores 240 mg/dl). Human immunodeficiency virus (HIV) infection should not preclude outdoor travel so long as an HIV-positive person pays meticulous attention to water disinfection and receives immunizations against pneumonia, influenza, hepatitis A, and hepatitis B. Many prescription drugs predispose to heat, cold, and altitude-related illnesses. Diuretics contract intravascular volume and may thus impair heat transfer to the skin or may exacerbate dehydration and hypokalemia resulting from fluid loss from exertion or diarrhea. Such persons should carry a packaged electrolyte replacement (oral rehydration solution) and a source of potassium (dried orange slices or bananas). The anticholinergic action of antihistamines, phenothiazines, and tricyclic antidepressants may result in hypothalamic dysfunction and diminished sweating. Whenever possible, alternative preparations should be considered for use during wilderness travel. Alcohol should generally be avoided because it induces peripheral vasodilation and may lead to net heat gain in hot environments and excessive heat losses in cool, windy, or wet conditions. In addition, alcohol's effects on judgment and sensory perception may result in failure to acknowledge early symptoms of environmental illness. Patients with serious medical allergies or active illnesses should have an appropriate medical identification bracelet, anklet, medallion, or wallet card and store their personal medications in a protected but accessible location in their pack. Persons with cardiac disease should carry a copy of their most recent electrocardiogram. Everyone should carry a complete medicine list in some form during foreign travel.
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Oral Hygiene and Health.
Mild sore throat and a foul taste are common when traveling in the mountains and in cool weather, probably because of mouth breathing and enhanced loss of moisture from the upper respiratory tract. Carry a supply of hard candies or medicated lozenges (e.g., Cepacol, Chloraseptic). Saline spray may be used to keep nasal passages hydrated. Since treatment of early caries and loose fillings (which may trap expanding air) can prevent this, each party member should have a dental examinations before the trip. On the trail, frequent brushing may be impractical; flossing after meals, rinsing well with water, and chewing sugar-free gum will help maintain oral hygiene en route. Toothache is common at high altitude. Temporary filling materials, such as Cavit (see Chapter 23 ), can be obtained in small squeeze tubes and applied to a tooth with a wet cotton applicator to prevent sticking. Urine containers may be appropriate if prolonged adverse weather is a possibility. Funnel-like devices that connect to urine containers (e.g., Lady-J, available from Campmor; see Appendix B ) are helpful for women. Groups camping in a delicate ecology or when close to a lake or river should use a lightweight, portable commode with disposable plastic holding bags. Hikers whose feet sweat excessively may benefit from talc or medicated powder (e.g., tolnaftate; see Table 69-2 ). Keeping feet and socks dry minimizes the tendency to blister formation and reduces heat loss in the cold. Travelers to cold and aquatic environments are especially prone to dry skin. Regular application of a lubricating lotion such as Eucerin, Lubriderm, or Keri lotion may help forestall microtrauma and epidermal cracking. Education in First Aid and Wilderness Safety.
Participants should be encouraged to take general courses in first aid and wilderness safety. Agencies that offer general and specialized training in skiing, mountaineering, river-rafting, and other types of wilderness medicine are listed in Appendix C . Locally organized programs may be found through the American Red Cross, sporting goods stores, and continuing education departments of local colleges. Before departure, the trip coordinator should review the emergency supplies with the rest of the group. The proper use of mechanical devices should be demonstrated, and indications for the use of medications should be discussed. Groups planning an extended or high-risk outing may wish to conduct an exercise of mock injury evaluation and management. Factors in Trip Planning The primary considerations in planning a trip relate to: (1) the maximum anticipated delay in obtaining medical assistance, (2) duration of an outing, (3) risks imposed by environmental extremes, and (4) hazardous recreational activities that require use of specialized equipment and supplies. Availability of Medical Care.
The longer the maximum anticipated delay in obtaining advanced medical assistance, the more likely the irreversible loss of neurologic function, limb, or life. The anticipated delay must take into account that in very rural areas, the nearest physician or hospital may not be equipped to handle a major wilderness injury or illness. An extreme case example is the planning of emergency access to a recompression chamber for members of a deep-sea diving expedition. A more typical example is a deeply penetrating arm laceration. As the hours pass, the likelihood of infection grows. If the victim can reach advanced medical help within an hour, it will suffice to control bleeding and apply a sterile dressing held in place by improvised cravats or tape. If definitive care is several hours away, irrigation with water containing a topical disinfectant is desirable. If the delay in care will be over 6 hours, a decision will have to be made whether to close the wound in the field or to evacuate the victim to medical care (see Chapter 18 ). The estimate of the anticipated delay depends on the type of rescue services, method of contact, terrain and weather, and number of able (carrying) persons. Party members should agree in advance on simple emergency distress signals, such as whistle or flashlight bursts in groups of three. Usually, uninjured party members have to make contact with outside agencies. Manually evacuating the victim is an option but requires a relatively mobile victim or at least six carriers if the victim is immobilized. In this regard, it is important to know whether other groups might be trekking in the same vicinity. If access is controlled by permit, the administering agency should be asked about the itinerary of neighboring parties. The decision to carry a victim out must be based on a realistic appraisal of the hours it would take messengers to reach aid vs. a manual evacuation effort to traverse the greatest distance or worst foreseeable weather and terrain. Trip Duration.
The likelihood of mishap rises as the trip duration increases. This is partly attributable to unpredictable weather and the cumulative effects of fatigue and overuse syndromes. In addition, long trips usually involve extensive planning, significant financial investment, and time away from work. Party members are therefore reluctant to cut the trip short and are more willing to continue in the face of mild medical disability and equipment failure. Groups planning to be away from civilization for more than a week should have a maximally diversified list of medical and contingency items.
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Environment and Risk of Activities.
Weather, terrain, and activity interact and increase the risk of illness or injury. Particularly hazardous combinations include winter climbing, mountaineering, skiing, and white-water kayaking. The anticipated ranges of weather and terrain must be figured into estimates of the maximum delay to medical assistance (see earlier discussion). U.S. and global historical summary data indicating temperature ranges, winds, and duration, type, and amount of precipitation can be obtained from the National Climatic Data Center (see Box 69-1 and Appendix C ). State and national park services and state climatology offices are also sources of such information about their territories. The National Weather Service office nearest the travel site can provide short-term forecasts and in many regions broadcasts weather information between 162.40 and 162.55 MHz VHF (see Appendix C ). Expedition Travel: Special Equipment and Supplies for High-Risk Groups.
Medically trained individuals traveling with a group at high risk of trauma or illness may wish to carry supplies requiring special expertise for proper use ( Box 69-4 and Box 69-5 ). Some of the necessary skills may be acquired in advanced first aid, paramedic, or nursing classes. Intramuscular and intravenous (IV) medications should be administered only by those with formal training in the indications, dosing, and risks of those drugs. Inclusion of a limited supply of emergency oxygen or IV saline may be reasonable to carry for a high-risk expedition. Adequate rehydration can generally be accomplished in a conscious person with a motile bowel using commercially available oral rehydration packets. Thus a comprehensive supply and variety of IV solutions (e.g., antibiotics, pain medicines, dextrose in saline) is predominantly a component of either a medical base support camp or for situations of search and rescue (see Chapter 25 ). Items such as surgical tools, chest tubes, and mechanical suction devices would be appropriate only for extremely high-risk expeditions and military excursions.
Box 69-4. CHECKLIST FOR HIGH-RISK OUTINGS: DEVICES REQUIRING SPECIAL MEDICAL TRAINING Airway, nasopharyngeal (impaired mental status; resuscitation) Cricothyrotomy cannula or catheter (e.g., Abelson cannula—see Appendix B ) Chest tube set (chest trauma; empyema—practical only on major expeditions) Glucose testing strips and buccally absorbed glucose preparation (if diabetic on trip; strips must be protected from freezing) Ophthalmoscope with blue filter and fluorescein strips to stain corneal lesions (retinal hemorrhages; anterior eye examination—practical only on expeditions) Oxygen (hypoxemia, shock, cerebral/pulmonary edema, impaired mental status) Sphygmomanometer (aneroid, plastic housing—practical only on expeditions) Stethoscope Suction device (mechanical) (clearing oral cavity; chest tube drainage—practical only on expeditions) Surgical tools (practical only on remote expeditions)
Box 69-5. CHECKLIST FOR HIGH-RISK OUTINGS: MEDICATION REQUIRING SPECIAL MEDICAL TRAINING
GENERAL USE Intravenous (IV) solutions (isotonic) and tubing (for hydration, route for IV medications) Needles and syringes (for IV hydration and emergency injectables) Antibiotic, potent oral with wide-spectrum coverage (e.g., ciprofloxacin)* or injectable (ceftriaxone)* ß-Agonist metered-dose inhaler (for asthma, anaphylactic reaction)* Ophthalmic anesthetic*
HIGH RISK OF INSECT BITES/ALLERGIES EpiPen* Diphenhydramine oral (for allergic reaction, mild sedation/insomnia) Oral corticosteroid*
HIGH RISK OF TRAUMA Fentanyl patch (Duragesic) applied to skin on chest when mental status precludes oral narcotics* Alprazolam (Xanax) for sedation*
HIGH RISK OF ALTITUDE ILLNESS Acetazolamide for mountain sickness* Corticosteroid oral or injection (e.g., dexamethasone) (cerebral edema)* Furosemide tablets for pulmonary edema* Nifedipine for pulmonary edema*
HIGH RISK OF SNOWBLINDNESS Ophthalmic cycloplegic (e.g., cyclopentolate 1%) (for pain from snowblindness)* Ophthalmic corticosteroid-antibiotic combination (e.g., Maxitrol) (recommended for short-term use in snowblindness only if blue filter ophthalmoscopic examination using fluorescein stain rules out herpetic keratitis)*
*See Table 69-2 and Table 69-3 for comments on considerations of dispensing medication.
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A host of recreational activities have inherent risks that may dictate specialized equipment beyond a basic medical kit. Mountain climbing not only poses a risk from traumatic injury but also subjects the climber to high-altitude illness, thus requiring portable oxygen or a pressure (Gamow) bag for treatment of victims suffering the ill effects of extreme altitude. Extreme cold exposure might dictate the need for technical devices to provide warmed IV fluids and humidified oxygen. Adventures in white-water sports place the participants at risk from freshwater drowning, and such expeditions might consider carrying adjuncts for airway management. Cycling poses soft tissue injuries from abrasions that require occlusive water-based gel dressings for optimal wound care. Travel to underdeveloped nations in which mosquitoes transmit deadly infectious diseases requires specialized equipment, such as protective netting for sleeping and chemical insecticides or repellents. Table 69-1 lists common recreational activities and identifies specialized equipment that may be considered for high-risk expeditions (see Box 69-8 ).
ASSEMBLING THE MEDICAL KIT Organizational Levels The emergency kit may be broken down into five components (see Box 69-6 , Box 69-7 , Box 69-8 , Box 69-9 , Box 69-10 ): (1) a personal medical kit, (2) a more comprehensive community medical kit, (3) medical kits for expeditions and the medically trained, (4) specialized equipment and supplies to deal with environmental and recreational hazards, and (5) items stored in the vehicle. The components TABLE 69-1 -- Recreational Activities Requiring Specialized Equipment SPECIALIZED EQUIPMENT RECREATIONAL ACTIVITY
HIGH ALTITUDE COLD EXPOSURE WATER SPORTS BICYCLING CLIMBING AND HIKING THIRD WORLD TRAVEL
Backpacking Mountain climbing and expeditions
X
X
X
X
X
X
X
Rock climbing Winter backcountry camping and skiing
X
X X
X
Cycling
X
Water sports
X
X
Fishing
X
X
Hunting
X
X
X
Search and rescue
X
X
X
X
X
International travel and trekking
X
Recommended specialized equipment for each recreational activity is denoted by an X in the appropriate column and itemized in Box 69-8 . Lists are comprehensive and intended for groups at a distance from medical help or involved in a high-risk adventure; not all items may be needed for low-risk travel. Purchase of specialized equipment should be based on the foundation of a comprehensive medical kit as highlighted in Box 69-6 . of a well-equipped first-aid medical kit designed for the management of trauma and common medical problems are itemized in Box 69-6 . Such a kit consists of nontechnical items that promote wound management and permit stabilization of extremity injuries, while including useful over-the-counter medicines to deal with common medical complaints. For persons without the time or desire to create such a comprehensive medical kit, consideration can be given to a host of commercially packaged wilderness first-aid kits (see Figure 69-1 and Appendix B ). Experienced groups involved in high-risk expedition travel having participants with medical knowledge may wish to consider carrying the basics recommended in Box 69-7 . Further tailoring of this medical kit may be achieved via the index for expedition travel ( Figure 69-2 ) that helps guide selection of prescription medicines as a function of trip duration and remoteness from medical care. Items Carried on the Person.
The purpose of carrying a minimum amount of items on one's person relates to the ever-present danger of separation from travel partners. A sudden fall, avalanche, or swamping can quickly separate victim and gear. In anticipation of this, experienced wilderness travelers need to carry a bare minimum of items on their person at all times (see Box 69-9 ). Such supplies provide protection from the elements, permit self-treatment of minor traumatic injuries, and help signal for help for purposes of search and rescue. These typically include assorted adhesive compress strips, knife or razor blade, butane lighter or matches (preferably the waterproof, strike-anywhere type), plastic whistle, small reflective mirror, length of thin nylon
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1669
Figure 69-1 Prepackaged wilderness first-aid kits are available from many manufacturers. Kits are neatly organized and rugged, with detachable inner pouches that are useful for day trips. Bags are water resistant to allow for white-water use. A surprisingly large amount of first-aid material can be carried, as shown in the illustration.
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Figure 69-2 Recommendations for prescription medicines for expedition travel based on the duration of outing (vertical columns) and the maximum interval to medical care (horizontal rows). Itemized numbers refer to recommended topical and systemic medicines found in Table 69-2 and Table 69-3 , respectively.
cord, and bandanna (which can double as a cravat or sling). A nonperishable source of quick high-energy food may be of value during isolation to maintain strength. These items can be compactly stored inside a plastic bag or small stuff sack and may be carried in either a pocket or a small fannypack (zippered, passport-size waist belts are comfortable and inexpensive). As noted previously, all travelers should carry some form of identification, and those with serious medical allergies or active illnesses should have an appropriate medical alert bracelet, anklet, medallion, or wallet card. Those with a history of bee, wasp, or other anaphylactic allergy should carry at least two preloaded syringes of 1:1000 aqueous epinephrine solution (EpiPen; Ana-Kit) in a cool dark compartment and should inform others in the party of the medicine's location and proper usage.
Box 69-6. CONTENTS OF A COMPREHENSIVE MEDICAL KIT
WOUND MANAGEMENT Irrigation syringe with 18-gauge needle Povidone-iodine solution USP 10% Wound closure strips Butterfly closures Tincture of benzoin Alcohol pads Moleskin Antiseptic towelettes Scalpel with no. 11 or 15 blade Latex or non-latex surgical gloves
OVER-THE-COUNTER MEDICATIONS Acetaminophen (Extra Strength Tylenol) Ibuprofen 200 mg (Nuprin) Diphenhydramine (Benadryl) Pseudoephedrine (Sudafed) Ranitidine (Zantac 75) Simethicone (Mylanta II antacid) Loperamide (Imodium AD) Rectal glycerine suppositories Saline eye wash Glutose paste Hydrocortisone cream 1% Tinactin antifungal cream High-SPF sunscreen and lip balm Aloe vera gel Neosporin ointment
BANDAGING MATERIALS Lamino Trauma Dressing 4 × 4 sterile dressing pads Eye pad Cotton-tipped applicators Nonadherent sterile dressing Elastic bandage wrap with Velcro closure Adhesive cloth tape Band-Aids 3-inch sterile gauze bandage
MISCELLANEOUS EQUIPMENT Folding scissors Forceps for removal of splinters and ticks Thermometer Cavit temporary dental filling SAM splint Triangular bandage and safety pins Plastic resealable (Zip-Lock) bags
SAM splint Triangular bandage and safety pins Plastic resealable (Zip-Lock) bags
PRESCRIPTION MEDICINES* Selection function of trip duration/interval to care
*See Table 69-2 and Table 69-3 .
Box 69-7. CONTENTS OF A MEDICAL KIT FOR EXPEDITIONS AND THE MEDICALLY TRAINED Comprehensive first-aid kit for the management of trauma (see Box 69-6 ) Medical devices requiring specialized training (see Box 69-4 ) Appropriate prescription medications for general illness (see Table 69-2 and Table 69-3 ) Prescription medications for specific injuries/illness (see Box 69-5 ) Repair materials (see Table 69-4 ) Indicated equipment based on recreational and environmental hazards (see Box 69-8 )
Box 69-8. SPECIALIZED EQUIPMENT FOR RECREATIONAL AND ENVIRONMENTAL ACTIVITIES
HIGH ALTITUDE Gamow Bag and accessories Gamow Tent Breathing Bladder Portable air compressor EPAP mask with headstrap Sportstat portable pulse oximeter
COLD EXPOSURE External thermal stabilizer bag Res-Q-Air Hot-Sack IV Warmer Grabber Warmers Hotronic Foot Warmers Space Thermal Reflective Survival Bag Low-reading thermometer Adhesive climbing skins Life-link adjustable ski/probe pole AvaLung avalanche vest Tracker DTS (digital transceiving system) avalanche beacon
WATER SPORTS CPR Microshield Katadyn or MSR WaterWorks filter
BICYCLING All-Terrain Cyclist Kit Hydrogel occlusive dressing
MOUNTAIN CLIMBING AND HIKING SAM Splint Air-Stirrup ankle brace
MOUNTAIN CLIMBING AND HIKING SAM Splint Air-Stirrup ankle brace
TROPICAL AND THIRD WORLD TRAVEL Sawyer Extractor Permethrin repellent TropicScreen mosquito net Oral rehydration salts packets
Box 69-9. CONTENTS OF A PERSONAL MEDICAL KIT
ON-PERSON ITEMS Identification/pencil and notepad Hat and sunglasses Topographical map/compass Swiss Army knife or razor blade Nylon cord Whistle and small reflective mirror Lighter or waterproof matches Poncho and space blanket Adhesive compress and tape Bandanna Nonperishable high-carbohydrate energy bar
IN-PACK ITEMS Personal first-aid and hygiene material Survival guide/first-aid booklet Prescription medications, labeled (in plastic or water-proof aluminum box) Over-the-counter medications noted in the comprehensive first-aid kit (see Box 69-6 )
Box 69-10. CHECKLIST: RECOMMENDED IN-VEHICLE EMERGENCY SUPPLIES
FIRST-AID KIT As for trail, but include large burn dressings Boards for splint construction Backboard, short or folding long (e.g., Junkin—see Appendix B )
RESCUE AND SURVIVAL Avalanche probe poles, collapsing* Bags, large plastic Blankets, wool and "space" blankets Climbing rope and hardware† Candles, long-burning Flashlight Food and water (in canteen) Ice ax† Matches (waterproof) or lighter Radio, citizens band Rope Saw with metal-cutting blade Small stove, pot or coffee can, and utensils Ski climbing skins, snowshoes* Tarp, plastic Toilet paper
AUTOMOTIVE Aluminum foil to cover windows (minimizes heat loss or gain) Cables to jump battery Chains with tighteners (with repair links and special pliers)* Fire extinguisher Flares, 10-minute (at least six) (can also serve as fire starter) Gloves Oil, extra can Shovel, metal or Lexan with short or collapsing handle Tool kit (consider inclusion of a small ax) Tow chain or cable Wheel chock or wedgeblocks
*Winter weather supplies. †Mountain terrain supplies (special training needed).
Personal Items Carried in the Pack.
Certain basic contingency "essentials" should be carried on virtually every venture. In addition to one's personal first-aid, hygiene, and clothing items, a flashlight, coins for telephone calls, and extra pair of sunglasses are recommended. Extra clothing, food, and water should be carried in proportion to the risk associated with the trip. A host of over-the-counter medications may be useful for wilderness travel, especially for low-risk outings of short duration. Some commonly required nonprescription items that may be of value are listed in Box 69-6 . Of prime importance is the control of pain associated with trauma. For mild to moderate pain, aspirin, acetaminophen, or a nonsteroidal antiinflammatory drug is effective. Decongestants are helpful in treating symptoms associated with upper respiratory infections, and their antihistaminic effects are useful for the treatment of allergies and insomnia. Gastrointestinal complaints necessitate antacids and an antidiarrheal agent. Saline eyewash is helpful for irritated eyes and in removing foreign objects. Antiseptic cream or ointment is useful in treating superficial infections of the skin, and a steroid ointment is of value for treatment of certain rashes or contact dermatitis. Aloe vera gel is useful for treatment of frostbite and injuries from burns or excessive sun exposure. Frequently needed first-aid material and personal medications are carried in stuff sacks or plastic box containers. Medication containers should be stored in an accessible but thermally and physically protected location in each individual's pack because capsules and suppositories may melt if exposed to extreme heat. Dressings, bandages, and adhesive materials should be kept in a plastic bag within their container to protect them from moisture.
Medications should be stored in unit dose sheets or screw-top plastic bottles labeled with the patient's and physician's names, generic and trade drug names, dispensing information, and expiration date. Medications
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requiring a prescription with directions for their use ( Table 69-2 and Table 69-3 ) should be secured in a watertight plastic or aluminum box. The trip coordinator should ask each member of the party to check that any expired medications are replaced and that capsules and suppositories are intact. Community Supplies Carried in the Pack.
As mentioned previously, traumatic injuries represent the greatest concern during wilderness travel. A comprehensive medical kit is the most important community item (see Box 69-6 ). Emphasis is placed on the management of wounds and stabilization of injuries through appropriate bandaging. Suture material is not recommended on the list of items because of the likelihood of subsequent infection. Large wounds are best treated with sterile pressure dressings. Bulky and heavy items, including most stock first-aid and contingency supplies, should be labeled and distributed among the members of the group for storage and transport. A cross made from strips of tape or cloth should be placed on the pack overlying the compartment containing the first-aid items. This allows ready access by any member of the party in an emergency situation. Repair materials are best kept in clearly labeled stuff sacks, or aluminum or plastic boxes independent of the first-aid and medical supplies. Items Stored in the Vehicle.
A complete emergency kit in the vehicle (see Box 69-10 ) is highly recommended. It will facilitate further stabilization of an injured person evacuated to a trailhead. The vehicle kit should also provide material necessary to deal with accidents encountered along the highway and to cope with the environment if the occupants are stranded by automotive trouble or natural disaster. Several large burn dressings and a neckboard with strapping will fit in a standard trunk or other recess. Although only large vehicles can accommodate the usual full-length backboard, a folding backboard is now available from Junkin Safety Appliance Co. (see Appendix B ). The remaining contents of an emergency kit will fit in a medium (6 inches W × 12 inches L × 9 inches H) or large (8 inches W × 18 inches L × 14 inches H) war surplus ammunition box or a toolbox of similar size. Selecting Contingency Supplies: Advanced Expedition Planning Individuals with medical training involved with risky wilderness travel may opt to tailor their own medical kit. Adventurous expeditions may wish to include a host of prescription medications that require advanced knowledge (see Box 69-5 ) and carry special devices requiring medical training (see Box 69-4 ). In addition, specialized equipment to handle expected environmental and recreational hazards should be considered (see Box 69-8 ). An appropriate emergency kit is adequate in content but not too heavy or bulky. Attempting to carry all possible medical supplies and equipment to handle any conceivable emergency is not practical. An alternative approach is as follows: Assess the group's trip risk on the basis of proximity to support (a function of interval to medical care) and comfort level of handling unanticipated traumatic injury or medical illness (cumulative probability related to trip duration). Figure 69-2 itemizes recommended prescription medicines as highlighted in boxes formed by the intersection of the latter two factors in bold. Specialized equipment purchases ( Box 69-8 ) are then added on as dictated by unique recreational activities ( Table 69-1 ). Using a Wilderness Index.
The wilderness index for expedition travel serves to assist group participants with advanced first aid or medical training in the selection of appropriate prescription medications. The latter serve to augment the contents of the comprehensive medical kit that includes only over-the-counter medicines. In Figure 69-2 a unique "square" of recommended prescription medicines is found at the intersection of the horizontal row "Duration of Outing" and the vertical column "Maximum Interval to Medical Care." Numbers refer to specific medical items, topical and systemic, found in Table 69-2 and Table 69-3 , respectively. The drug doses listed in Table 69-3 are intended for nonpregnant, young, or middle-aged adults in good health. Reduced doses are often necessary for children, the elderly, and those with end-organ disease (especially renal, hepatic, and cardiac). The personal physician should modify the doses appropriately. The rationale for medicine selection among a host of prescribed items is based on one's expected time frame for support and rescue in the event of unexpected injury and the cumulative likelihood of experiencing a medical illness as trip duration increases. A low-risk outing (e.g., a day hike) is one in which the interval to medical care is short (24 hr) painful disorder or injury
Respiratory depression, constipation (D); sinus bradycardia and hypotension, nausea/vomiting, itching (O)
1–2 patches 4 patches applied every (individual) 3 days to a nonirritated, clean and dry area on the upper torso
16. Antibiotic for giardiasis and amebiasis
Metronidazole 500 mg
Flagyl
Profuse None for short-term use in diarrhea indicated setting delayed >2 weeks (Giardia suspected), or dysentery in areas endemic for Entamoeba histolytica (amebiasis suspected)
Nausea; vomiting, metallic taste (C) abdominal discomfort (O)
Giardiasis: 1 15–90 tablet 3 times tablets daily for 5 (individual) days
Bowel obstruction, preexisting respiratory depression or difficulty breathing, head injury with impaired consciousness
Amebiasis: 750 mg 3 times daily for 10 days (followed by 3 weeks of iodoquinol 650 mg 3 times daily) C, Common,