Wilderness Medicine

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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

63

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

64

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]

.

75

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

77

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

78

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

79

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,

93

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

94

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 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]

1192

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]

.

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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

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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,

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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

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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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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.

189.

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.

192.

Sobsey M et al: Comparative inactivation of hepatitis A virus and other enteroviruses in water by iodine, Water Sci Technol 24:331, 1991.

193.

Sorenson S et al: Isolation and detection of Giardia cysts from water using direct immunoflourescence, Water Resources Bulletin 22:843, 1986.

194.

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.

196.

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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Suk T et al: The relation between human presence and occurrence of Giardia cysts in streams in the Sierra Nevada, California, J Freshwater Ecol 4, 1988.

198.

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200.

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201.

Thomas W et al: Effects of an iodinated water supply, Trans Am Clim Assoc 90:153, 1978.

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Thomson G et al: Evaluation of water sterilizing tablets, AR No 004-318, Scottsdale, Tasmania, 1985, Department of Defense, Armed Forces Food Science Establishment.

203.

Thraenhart O: Measures for disinfection and control of viral hepatitis, In Block S, editor: Disinfection, sterilization, and preservation, Philadelphia, 1991, Lea & Febiger.

204.

Tillet H et al: Surveillance of outbreaks of waterborne infectious disease: categorizing levels of evidence, Epidemiol Infect 120:37, 1998.

205.

Tobin R: Performance of Point-of-use water treatment devices. In Proceedings of the First Conference on Cold Regions Environmental Engineering, 1983, Fairbanks, Alaska.

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Tobin R: Testing and evaluating point-of-use treatment devices in Canada, J Am Water Works Assoc 79:42, 1987.

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231.

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233.

Zoeteman B: The suitability of iodine and iodine compounds as disinfectants for small water supplies, The Hague, 1972, WHO International Reference Centre for Community Water Supplies.

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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.

1220

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.

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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.

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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.

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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.

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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.

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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

1244

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 12 yr: 2 doses 4–8 wk apart ROUTINE FOR TRAVEL Hepatitis A

Havrix: inactive virus (720ELU)

>2 yr: 2 × 0.5 ml doses 6–12 mo apart

Vaqta (24U) Immune globulin (IgG)

Antibodies

Preferred for hepatitis A protection if over age 2 yr Protects in 4 wk after dose 1

6 yr: 1 capsule q 2 days × 4; booster q 5 yr

Meningococcal

Serogroups A, C, Y, W-135: polysaccharide

>2 years: 0.5 ml Use for central Africa, Saudi Arabia for the Hajj, SC; booster in 1 yr Nepal, and epidemic areas; minimal efficacy if 1st dose after age under age 2 yr 4 yr, otherwise in 5 yr

±

±

±

Japanese encephalitis

Inactivated virus

1–3 yr: 0.5 ml SC at Indicated for parts of India and rural Asia if stay 0, 7, 14–30 days > 1 mo; no safety data for under age 1 yr; high rate of hypersensitivity

±

±

+

±

+

+

>3 years: 1.0 ml SC at 0, 7, 14–30 days Last dose > 10 days before travel Cholera

Inactivated bacteria

>6 mo: 0.2 ml SC

Vaccine of questionable efficacy; not recommended by CDC or WHO; do not use under 6 mo

Lyme disease

LYMErix: antigenic protein

>15 yr: 0.5 ml IM at Indicated for frequent, prolonged exposure to 0, 1, 12 mo Lyme-endemic area, not brief exposures

HDCV: human diploid cell

1 ml IM in deltoid muscle at 0, 7, 21–28 days if > 1 mo stay

EXTENDED STAY Rabies

If exposed and immunized: give vaccine, 1 ml IM at 0, 3 days

If exposed and unimmunized: give rabies Ig (RIG), 20 IU/kg half at site and half IM; give vaccine, 1 ml IM at 0, 3, 7, 14, 28 days Consult Centers for Disease Control and Prevention (CDC) for current and specific vaccine recommendations for destination country. AAP, American Academy of Pediatrics; IM, intramuscularly; SC, subcutaneously; q, every; WHO, World Health Organization; +, recommended; ±, consider. *DtaP, poliovirus vaccine, and Haemophilus influenzae type b vaccine may be given at 4-week intervals if necessary to complete the recommended schedule before departure. †Measles: two additional doses given if younger than 12 months of age at first dose.

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TABLE 74-8 -- Recommended Timing and Sequence of Nonroutine Immunizations for Foreign Travel* 4–6 WEEKS BEFORE DEPARTURE 1 WEEK AFTER INITIAL VISIT WEEK OF DEPARTURE Hepatitis A (need second dose 6–12 mo later)

or Immune globulin for hepatitis A prevention

Yellow fever Typhoid-heat inactivated or ViCPS or Ty21a (oral, 1 capsule q 2 days × 4)

Typhoid: heat inactivated

Meningococcal

Meningococcal (if not given at initial visit)

Japanese encephalitis

Japanese encephalitis

Japanese encephalitis

Rabies

Rabies

Rabies

*Give only immunizations indicated for area of travel, length of stay, and age of child. Simultaneous administration of routine and travel-related vaccines is acceptable with the exception of yellow fever with cholera (yellow fever at least 3 weeks before cholera) and MMR or VZV with IgG. Administer IgG at least 3 weeks after these live virus vaccines (see Table 74-7 ).

The risk of acquiring diseases covered by many routine childhood immunizations (diphtheria, pertussis, tetanus, measles, polio, hepatitis B) is greater in developing nations. Consequently, children who have not completed their primary series of immunizations may require an acceleration of the vaccination schedule or extra doses to maximize protection before travel. Ideally, a visit to the physician to discuss travel plans and begin immunizations should be made 4–6 weeks before travel. Not all immunologic agents recommended for

travel are compatible, and some require multiple doses. Therefore the selection of immunizations to be given at any one time and the interval between immunizations are important ( Table 74-8 ). In general, all toxoid, recombinant, inactivated, and live attenuated vaccines may be given simultaneously. Exceptions are those against yellow fever and cholera, which should not be given simultaneously or within 3 weeks of each other. Alternatively, the cholera vaccine can be omitted, since its effectiveness is limited. [54] Live attenuated vaccines should be given either simultaneously or at least 30 days apart to avoid reduced immunoreactivity to each vaccine. Administration of immune globulin interferes with the humoral response to the live attenuated virus vaccines such as measles, mumps, and rubella (MMR) and varicella. If immune globulin is given first, these vaccinations should be delayed by at least 6 weeks, and preferably 3 months, to obtain an adequate immunogenic response. When both are needed for travel, it is best to give MMR or varicella vaccine first; immune globulin can be given closer to the time of travel, at least 2 weeks and preferably 4 weeks later. Immune globulin does not interfere with antibody production induced by live viral vaccines against polio (oral vaccine) or yellow fever and may be given at the same visit. Travel vaccines that require multiple doses or early administration include hepatitis A, inactivated typhoid, Japanese encephalitis, rabies, yellow fever, and MMR (if immune globulin is to be given near the time of departure). Malaria Prophylaxis The risk of acquiring malaria during visits to developing countries in the tropics is significant (see Chapter 65 ). Even areas where the overall risk is relatively low may have foci of intense transmission. Children under 5 years are particularly vulnerable and represent the largest proportion of fatalities from this disease. Of the 30,000 to 50,000 cases of malaria acquired by travelers from Europe and North America per year, most occur among visitors to sub-Saharan Africa (82%) and Asia (8%).[39] Protective measures to prevent mosquito bites help interrupt the transmission of malaria but are not fool-proof (see Box 74-2 ). Therefore chemoprophylaxis is highly recommended for travelers to countries where malaria is endemic. Plasmodium vivax and P. falciparum are the two most abundant species responsible for malaria. The most lethal species, P. falciparum, has developed widespread resistance to chloroquine and in some areas (rural Thailand, Cameroon, Indonesia) resistance to mefloquine.[6] Therefore the choice of prophylactic agent depends on the presence of resistant malaria in the area of travel. Chloroquine (Aralen) is the still the drug of choice for travelers to the few areas where chloroquine-resistant strains of P. falciparum are not a problem (Central America west of the Panama Canal, Haiti, Dominican Republic, and Middle East) or areas where falciparum malaria does not occur (Egypt). Chloroquine prophylaxis should be given weekly starting 1 week before travel and continued for 4 weeks thereafter. Chloroquine is passed through breast milk, although not in sufficient quantities to protect an infant. Therefore a breast-fed infant should receive chloroquine prophylaxis in the standard recommended doses ( Table 74-9 ). Chloroquine is not readily available in liquid form in the United States. The powder, which is extremely bitter, may be suspended in a syrup or mixed with food. Instant pudding effectively masks the bitter taste and makes the medicine more palatable. An acceptable-tasting syrup (Nivaquine) is available in most developing countries. Chloroquine should be kept out of the reach of children. As little as

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TABLE 74-9 -- Malaria Chemoprophylaxis MEDICATION

INDICATIONS

DOSING

Mefloquine (Lariam)

Travel to chloroquine-resistant areas Child > 15 kg

Given weekly: 1 wk before to 4 wk after travel

Avoid in child with epilepsy or psychiatric illness

15–19 kg: ¼ tablet 20–30 kg: ½ tablet 30–40 kg: ¾ tablet >40 kg: 1 tablet (250 mg)

Doxycycline

Alternative to mefloquine in chloroquine-resistant areas if contraindication to mefloquine

2 mg/kg/day up to 100 mg/day 1–2 days preexposure and 4 wk after exposure; photosensitivity possible

>8 yr of age only Chloroquine (Aralen) (liquid: Nivaquine)

Travel to chloroquine-sensitive areas

5 mg/kg/wk up to 500 mg for 1 wk before and 4 wk after exposure; 10 mg/ml liquid available outside United States

(Caribbean, Central America north of Panama, Middle East) Safe in children under 15 kg Proguanil (Paludrine)

Take with chloroquine when possible, particularly in Africa Not available in United States

Give daily while taking chloroquine 10 yr: 200 mg/day

Pyrimethamine-sulfadoxine (Fansidar)

Prepare for treatment if symptoms develop and medical attention > 24 hr away Contraindicated if age < 2 mo or sulfa allergy

Single dose: 2 mo-1 yr: ¼ tablet 1–3 yr: ½ tablet 4–8 yr: 1 tablet 9–14 yr: 2 tablets >14 yr: 3 tablets

Atovaquone (250 mg) + proguanil (100 mg) (Malarone)

Prepare for treatment in Fansidar-resistant areas (parts of Southeast Asia, Amazon basin) Not available in United States

Dose per day × 3 days 11–20 kg: 1 tablet 21–30 kg: 2 tablets 31–40 kg: 3 tablets >40 kg: 4 tablets

Primaquine

Prevention of relapse with Plasmodium vivax or P. ovale 0.3 mg/kg/day for 14 days after leaving area Use after prolonged stay in malaria-endemic area Avoid if glucose-6-phosphate dehydrogenase deficient

Data from Red book: report of the Committee on Infectious Disease, Elk Grove Village, Ill, 1997, American Academy of Pediatrics. 1 g may be fatal in small children.[49] If a toxic chloroquine ingestion occurs, syrup of ipecac should be administered immediately to provoke emesis, and the child should be transported promptly to a medical facility. Proguanil (Paludrine) is not available in the United States but is widely available overseas. It is recommended for use with chloroquine, particularly in chloroquine-resistant areas if mefloquine and doxycycline are contraindicated. This would include children less than 15 kg and those under age 8 years with epilepsy or psychiatric disorders. Unfortunately, this regimen is only 40% to 60% effective and should not be used unless alternative therapies are contraindicated. For children over 15 kg traveling to chloroquine-resistant areas, mefloquine (Lariam) is the preferred agent. It is started 1 week before travel and given weekly during

travel and for 4 weeks after return. Mefloquine should be avoided in children with psychiatric illnesses, epilepsy, or underlying cardiac arrhythmias. Doxycycline may be used in children over age 8 years with contraindications to mefloquine. Unlike mefloquine, however, doxycycline must be given daily. Side effects include diarrhea and photosensitivity. Since neither of these agents can be used in small children (less than 15 kg), parents should seriously consider the risks of acquiring malaria before traveling to a malaria-endemic area with an infant or toddler. If a child develops an acute febrile illness in a malaria-endemic area where medical care is not immediately available, pyrimethamine with sulfadoxine (Fansidar) may be used as standby treatment. [4] Fansidar is given as a one-time dose. Prophylaxis with this drug is not recommended because of the risk of Stevens-Johnson syndrome. Fansidar should not be given to infants less

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than 2 months old or to children allergic to sulfa medications. Atovaquone with proguanil (Malarone) is an alternative standby treatment that has been used successfully in Fansidar-resistant areas (parts of Southeast Asia and the Amazon basin).[41] [52] Studies have also demonstrated the efficacy of this preparation as prophylaxis against P. falciparum, but this use has not yet gained widespread acceptance.[37] [63] Malarone is not available in the United States. All patients who take Fansidar or Malarone for presumptive treatment of malaria should be transported to a medical facility as soon as possible for definitive care. Primaquine is an antimalarial drug used to prevent emergence of P. vivax and P. ovale after heavy exposure or prolonged (many months) exposure to mosquitoes. Routine chemoprophylaxis does not kill the exoerythrocytic stages of these Plasmodium species. Primaquine is taken daily for 2 weeks after leaving a malarial area. Primaquine should not be given to anyone with glucose-6-phosphate dehydrogenase (G6PD) deficiency.

TRAVEL-RELATED PROBLEMS After boredom and restlessness, motion sickness and eustachian tube dysfunction are the most common problems of children during travel. Parents can minimize the first two problems by preparing small activity packs or bags with paper, pencils, crayons, cards, travel puzzles, or small toys. Motion Sickness Motion sickness can occur with air, land, or sea travel, particularly in children ages 2 through 12 years. Emotional upset, noxious odors, and ear infections can make the symptoms worse. Children experiencing motion sickness are often pale and diaphoretic and feel nauseated and weak. They may vomit, but unfortunately this does not provide prolonged relief. Children known to be susceptible to motion sickness should be seated in the middle or near the front of the boat, plane, or car, where motion is minimized. They should be encouraged to look at objects far away and avoid focusing on close objects, such as books. Some children obtain significant relief from using headphones to listen to music or stories. Dimenhydrinate (Dramamine, 1 to 1.5 mg/kg) administered 1 hour before departure and repeated every 6 hours can help children known to be prone to motion sickness. If dimenhydrinate is not available, diphenhydramine (Benadryl, 1.25 mg/kg every 6 hours) may also be effective. Both medications may cause drowsiness, and diphenhydramine occasionally causes paradoxical hyperexcitability in children. Scopolamine patches should not be used because children are particularly susceptible to the side effects of belladonna alkaloids. Whether patches release too much scopolamine and consequently produce serious side effects in children is not known.[49] Eustachian Tube Dysfunction Eustachian tube dysfunction causes discomfort that results from a pressure disequilibrium between the eustachian tube and the surrounding atmospheric pressure. About 15% of children have this problem, particularly during airplane descent. Swallowing often helps relieve the pressure disequilibrium and may be facilitated by drinking or, for the breast-fed infant, by nursing. Older children may chew gum or yawn to equalize middle ear and atmospheric pressure. Contrary to popular belief, decongestants are not useful with eustachian tube dysfunction in children and may cause paradoxical drowsiness.[9] Most airline cabins are pressurized to provide an oxygen concentration of 17% to 18%, not the 21% of sea-level air. Supplemental oxygen may be necessary for children with congenital heart disease or pulmonary disease (asthma, bronchopulmonary dysplasia) if cyanosis or respiratory distress develops. Traveler's Diarrhea Traveling to wilderness areas or developing countries requires leaving behind modern sanitation and reliably disinfected tap water (see Chapter 52 ). Unfortunately, this places travelers at increased risk for diarrheal illness. Traveler's diarrhea affects 25% to 50% of adult travelers from low-risk to high-risk countries. In one pediatric study, 40% of children under age 2 years developed prolonged diarrhea during travel in tropical or subtropical areas.[50] Young children are at greater risk for traveler's diarrhea and its complications because of relatively poor hygiene, immature immune systems, lower gastric pH, more rapid gastric emptying, and difficulties with adequate hydration.[16] Traveler's diarrhea has been defined as greater than three unformed stools in a day or any number of such stools when accompanied by symptoms such as fever, abdominal cramping, vomiting, or blood or mucus in the stools.[50] In small children the course tends to be more severe and prolonged, lasting from 3 days to 3 weeks. Traveler's diarrhea can be caused by preformed toxins, viruses, invasive bacteria, or parasites ( Table 74-10 ). Enterotoxigenic Escherichia coli is responsible for 50% of traveler's diarrhea. Rotavirus and Norwalk-like viruses account for another 30%.[5] Shigella remains the most common cause of invasive diarrhea. Prevention.

Standard recommendations for prevention of traveler's diarrhea are based primarily on known potential vehicles for transmission of the illness (see Box 74-4 ). Transmission is through fecal-oral contamination, with water, food, and fingers the most common sources. Careful selection and preparation of food and beverages can decrease the risk of acquiring traveler's diarrhea. Washing hands thoroughly before eating decreases bacterial carriage and also reminds children about the need for precautions. According to the

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AGENT

TABLE 74-10 -- Causes of Traveler's Diarrhea in Children EXAMPLES

Preformed toxin

Enterotoxigenic Escherichia coli* Staphylococcus aureus Bacillus cereus

Viral

Rotavirus* Norwalk agent* Adenovirus Enterovirus Influenza Hepatitis

Bacterial

Shigella* Campylobacter Salmonella Enteroinvasive Escherichia coli Yersinia enterocolitica Vibrio cholera

Parasitic

Giardia lamblia Entamoeba histolytica Cryptosporidium

Modified from Bonadio WA: Emerg Med Clin North Am 13:457, 1995. *Most common.

"boil it, cook it, peel it, or forget it" rule, all raw vegetables and salads should be avoided, meats and seafood well cooked, and fruits properly peeled (see Chapter 51 ). Box 74-5. SIGNS OF DEHYDRATION IN CHILDREN

MILD-MODERATE (5%–10%) Irritability Sunken eyes Dry mucous membranes Extreme thirst

SEVERE (>10%) Lethargy Extremely sunken eyes Extremely dry mucous membranes Inability to consume oral liquids Cool, mottled extremities Rapid thready pulse Tachypnea

Modified from Treatment of diarrhoea: manual for physicians and other senior health workers, Geneva, 1995, World Health Organization.

Treatment.

The major cause of morbidity and mortality in infants and small children with diarrhea is dehydration[1] ( Box 74-5 ). According to the World Health Organization (WHO), dehydration is best categorized as mild-moderate or severe.[72] This distinction is based on changes in behavior and mental state, quality of mucous membranes, oliguria or anuria, changes in vital signs, and decreasing peripheral perfusion. Children young enough to be wearing diapers should have some urine output at least every 8 hours. If not, they are probably dehydrated.

Box 74-6. HOMEMADE ORAL REHYDRATION SOLUTION 1 teaspoon (5 g) salt 1 cup (50 g) rice cereal 1 quart (1 L) disinfected water

Data from World Health Organization.

The cornerstone of therapy is oral rehydration therapy (ORT), which can be used alone successfully in 90% to 95% of cases, especially if instituted early.[23] ORT is as effective as intravenous hydration in mild-moderate dehydration from diarrhea. Parents traveling to developing countries or wilderness areas with children should carry a prepared powdered oral rehydration solution (ORS) or a recipe for a homemade solution ( Box 74-6 ). Powdered ORS is readily available in most developing countries through WHO and may be obtained in the United States from Jianas Brothers, Kansas City, Missouri (816-421-2880). Although earlier studies reported rice-based ORS as more effective in reducing stool output than standard glucose-based ORS,[46] [53] more recent studies demonstrated that any advantage from rice-based ORS is lost after 6 hours of rehydration.[18] [45] Rice ORS has lower osmolality and higher concentration of organic solutes; therefore the osmotic gradient across the intestinal lumen is lower and intestinal sodium transport decreased, theoretically resulting in less stool water. Because of hydrolysis of its starches, however, rice-based ORS is stable only for 12 hours, after which it must be discarded and a new solution made.[58] For rapid treatment of mild-moderate dehydration, 50 to 100 ml/kg of ORS should be administered over the first 4-hour period, followed by maintenance solution to provide for basic fluid requirements and to replace ongoing losses.[5] [58] Ideal ORS should contain 75 to 90 mEq/L of sodium, 2% to 2.5% carbohydrate, and 20 mEq/L of potassium (Table 74-11 (Table Not Available) ). If a solution with more than 3% glucose is used, the osmotic pressure exerted by glucose in the intestinal lumen produces fluid losses greater than fluid absorption, thereby exacerbating diarrhea. Most colas and juices contain nearly 10% to 15% glucose or carbohydrate and are not appropriate rehydration solutions. [25] [42] The high sodium concentration in the ORS poses a risk for hypernatremia if the solution is used for maintenance fluids or to prevent dehydration. For maintaining hydration, alternating ORS with a fluid that has less sodium, such as water or breast milk, will avert hypernatremia.

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TABLE 74-11 -- Field Treatment of Dehydration in Children (Not Available) Modified from Goepp J, Santosham M: Principles Pract Pediatr Updates 1:1, 1993. Alternatively, a separate solution containing 50 to 60 mEq/L sodium can be used. Maintenance fluid volumes are 75 to 150 ml/kg/day. An additional 10 ml/kg, or 4 ounces, can be given for each diarrheal stool and 5 ml/kg, or 2 ounces, for each episode of emesis.[35] If vomiting develops, most children will still tolerate ORS if given in small volumes (5 to 10 ml) every 5 minutes. Feeding of solid food, particularly complex carbohydrates, should be continued during and after diarrhea because it promotes enterocyte regeneration.[9] [19] [57] Severe dehydration requires prompt medical attention and administration of intravenous fluids for rehydration. Although oral hydration should be the cornerstone of therapy for diarrhea and dehydration, medications may be helpful. Antimotility agents such as loperamide and diphenoxylate are of no proven efficacy, according to the American Academy of Pediatrics (AAP) guidelines for acute gastroenteritis.[1] In general, they should be

avoided; however, loperamide may be used with older children if fever, bloody stool, and abdominal distention are absent[17] (see Table 74-12 ). Other antidiarrheal agents (e.g., bismuth) have not been shown to be effective in children and should be avoided, particularly in those under 2 years. Antibiotic chemoprophylaxis remains controversial for adults and is not recommended for children.[1] The use of antibiotics should be limited to children with fever, bloody stools, or abdominal distention in whom invasive bacterial diarrhea is suspected.[27] Under age 3 to 6 months, the risk of bacteremia with Salmonella infection is significant, so antibiotic treatment is also indicated. With increasing bacterial resistance to trimethoprim-sulfamethoxazole, azithromycin is now the drug of choice for treatment of bacterial diarrhea.[29] [67] The dose is 10 mg/kg on day 1, then 5 mg/kg once daily for 5 days. Although quinolones (e.g., ciprofloxacin) can be used in children over age 12 years and perhaps younger, increasing bacterial resistance to quinolones makes azithromycin an even better choice. If symptoms do not improve rapidly, parents should seek immediate medical attention for their children. Salmonella typhi infection, or typhoid fever, if suspected, should be managed immediately in a hospital setting with quinolones or third-generation cephalosporins. Respiratory Infections Respiratory tract infections are common in the pediatric population. Most infections, such as acute otitis media (AOM), sinusitis, pharyngitis, croup, bronchiolitis, and bronchitis, involve the upper respiratory tract. The majority of these infections are viral in etiology; the remainder are usually the result of infections with Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. Since definitive diagnoses based on otoscopy and auscultation of the lungs often cannot be made during wilderness travel, parents must rely on symptoms and the presence of fever to determine whether treatment is necessary. The presence of high fever, otalgia, facial pain, sore throat without cough or rhinorrhea, or mucopurulent nasal discharge lasting longer than 10 days likely merits both antimicrobial and symptomatic treatment. However, 20% to 80% of AOM and 50% of streptococcal pharyngitis cases resolve without intervention. [12] [13] Furthermore, antibiotic treatment of certain upper respiratory infections, such as bronchitis, bronchiolitis, croup, and most pharyngitis, does not shorten the course, minimize symptoms, or decrease complications.[43] With increasing use of antibiotics, bacterial resistance to these agents has risen dramatically. From 10% to 30% of S. pneumoniae infections are resistant to penicillin and 5% to 20% to macrolides such as erythromycin. [11] Up to 20% of H. influenzae and 70% of M. catarrhalis infections are resistant to amoxicillin. However, testing has demonstrated sensitivity to high-dose amoxicillin, even among resistant strains. First-line therapy for these infections is therefore high-dose amoxicillin at 60 to 80 mg/kg.[67] Second-line therapy is high-dose amoxicillin-clavulanate (same amoxicillin component dosing), cefuroxime, or ceftriaxone.[43] Uncomplicated AOM in children over 2 years may be treated for 5 to 7 days; otherwise the standard treatment for AOM is 10 days and, for sinusitis, 14 days. Exudative pharyngitis with fever and lymphadenopathy but without cough can be treated for 10 days with penicillin or amoxicillin, or for 5 days with azithromycin. Fever of Undetermined Origin High fever that develops in a child during the course of foreign travel may be the result of a common infection (e.g., AOM, pharyngitis) or the manifestation of a

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tropical disease. If malaria is suspected, the child should immediately be taken to the closest medical facility. If this cannot occur within 24 hours, any child over 2 months old should be given Fansidar as standby treatment (see Table 74-9 ). Salmonella typhi infection, more commonly known as typhoid fever, can also present with high fever, paradoxical bradycardia, and at least initially, without diarrhea. Children who appear ill with high fevers may have invasive typhoidal disease and should be treated in a medical facility. Salmonella resistance is rising in developing countries, but strains are typically susceptible to quinolones (over age 12 years) and third-generation cephalosporins (e.g., cefixime, ceftriaxone). Dengue fever, caused by a mosquito-borne arbovirus, can also cause high fever, headaches, and severe myalgias (see Chapter 66 ). With the exception of recurrent dengue, which can result in hemorrhagic complications, the treatment of dengue fever is purely symptomatic. Rashes Identification of rashes in the pediatric population is an art. Although parents cannot be expected to become familiar with all types of rashes, they should learn to distinguish common rashes from potentially dangerous exanthems. Petechial, purpuric, or mucosal lesions are markers for potentially serious disease and should prompt parents to seek medical attention immediately. Standard dermatologic textbooks with photographs can be used to instruct parents to recognize common viral exanthems and rashes caused by varicella, scabies, and contact dermatitides (poison oak, poison ivy). Scabies can be abolished safely with permethrin. Contact dermatitis can be treated with 1% hydrocortisone cream. Soft Tissue Injuries Soft tissue injuries are extremely common among children, particularly as they become more ambulatory (see Chapter 18 ). All wounds sustained in the wilderness should be thoroughly irrigated with clean water and explored to ensure that no foreign bodies remain. In general, lacerations should not be sutured in the backcountry due to the risk of infection. They should be covered with a water-resistant dressing, splinted if located over a joint, and observed. If no evidence of infection develops over 4 to 5 days, the laceration may be repaired by delayed primary closure.

PEDIATRIC WILDERNESS MEDICAL KITS When a family travels in remote areas, any medical kit must be adapted to meet the special needs of children. Actual items carried vary depending on the ages of the children, preexisting medical conditions, length of travel, specific environmental conditions encountered, and medical sophistication of the adults. Although individual preference plays a role in assembling a medical kit, certain items are essential for management of common problems during wilderness travel with children ( Box 74-7 ).

Box 74-7. PEDIATRIC WILDERNESS MEDICAL KIT: BASIC SUPPLIES 1. Identification and basic health information for child: past medical history, medications, allergies, blood type, weight 2. First-aid supplies: adhesive bandages, gauze pads, gauze roll, tape, nonadherent dressings, moleskin/Spenco 2nd skin/Nu Skin, benzoin, alcohol wipes, povidone-iodine solution for dilution and disinfection, safety pins, tweezers, lightweight malleable splint (SAM splint), syringe (20–35 ml), 18-gauge plastic catheter for wound irrigation 3. Oral rehydration salts 4. Sunscreen: SPF of 15 or greater 5. Insect repellent: DEET 30 kg: 2 mg tid

Appropriate malaria prophylaxis if indicated† Pyrimethamine-sulfadoxine (Fansidar)†

See Table 74-9 Standby treatment for malaria if immediate medical attention unavailable

See Table 74-9

Recurrent acute mountain sickness (AMS) despite graded ascent

5 mg/kg/day divided bid up to 250 mg/day

Nausea and vomiting associated with AMS

0.25–0.5 mg/kg/dose every 6 hr up to 25 mg/dose

Poisonous snakebites

Apply per instructions within 3 min of bite

TRAVEL TO HIGH ALTITUDE Acetazolamide (Diamox)† 30 or 50 mg/ml suspension 125-mg tabs Promethazine (Phenergan)† 12.5 or 25 mg/suppository SNAKE-INFESTED AREAS Extractor (negative-pressure suction device)‡

qd, Every day; bid, twice daily; tid, three time daily; SC, subcutaneously. *Administration of this medication by other than trained medical personnel is strongly discouraged given the risk of overuse and subsequent worsening of eye injury; if significant eye irritation persists, medical attention must be sought to evaluate for corneal injury. †Available by prescription only. ‡Sawyer Products, Safety Harbor, Fla.

Ibuprofen is available in many forms: infant drops (40 mg/1 ml), children's elixir (100 mg/5 ml), 50- or 100-mg chewable tablets, and 100- or 200-mg caplets. Tylenol with codeine combines a centrally acting agent, codeine, with a peripherally acting analgesic, acetaminophen. It is indicated for treatment of moderate to severe pain. Acetaminophen has the added effect of fever control, and codeine has antitussive properties. Codeine can cause respiratory depression, particularly in children under 12 months of age, and may elevate intracranial pressure, especially in the presence of head injury; its use should be avoided in these situations. Dosing is based on the codeine component: both the liquid formulation (12 mg/5 ml) and tablets (10, 20, or 30 mg of codeine per tablet) are given at 0.5 to 1 mg/kg up to every 6 hours. Two or three antibiotics will cover most bacterial infections in children. Age, allergies, intolerance, and past experience must be taken into account when antibiotics are selected. Given increasing bacterial resistance to common antibiotics, antimicrobial choices should be reevaluated periodically to ensure that infections likely to be encountered can be successfully treated with these agents. All oral antibiotics require a prescription. Amoxicillin is available in pleasant-tasting chewable tablets (125 and 250 mg) and in powdered form for suspension (125 and 250 mg/5 ml) Given current resistance patterns, high-dose therapy with 60 to 80 mg/kg divided three times daily is indicated. Amoxicillin is well tolerated by most children. Amoxicillin-clavulanate (Augmentin) provides excellent coverage for recurrent pharyngitis, soft tissue infections, animal bites, and infections when a resistant organism is anticipated. The most common side effect is diarrhea, but this has been reduced with newer formulations, available in 200- and 400-mg (amoxicillin component) chewable tablets and in 200 and 400 mg/5 ml liquid. Dosing is 60 to 80 mg/kg divided twice a day. Azithromycin (Zithromax) is a long-acting macrolide without the gastrointestinal side effects of erythromycin. It is effective for treatment of AOM, sinusitis, pharyngitis, lower respiratory infections, traveler's diarrhea, and common animal bites. It is particularly useful in children with penicillin allergy. Dosing is extremely convenient because of azithromycin's long half-life: a 10 mg/kg initial dose

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on day 1 is followed by 5 mg/kg/day for 5 days. Ciprofloxacin (Cipro) has a broad spectrum of coverage and is useful for treatment of bacterial diarrhea, complex urinary tract infections, and wounds acquired in an aquatic environment. Its use has been discouraged in children under 12 years because of a potential problem with arthropathic effects on weight-bearing joints. However, a study involving more than 600 children found only a 1.3% rate of reversible arthralgia and no evidence of arthropathy.[60] Nonetheless, ciprofloxacin should not be routinely recommended for children under 12 years unless a special situation arises in which the benefits of its use outweight the risks.

Syrup of ipecac should also be included in every pediatric medical kit. Small children tend to explore their environment with hands and mouths. If toxic ingestions are recognized within 30 minutes and there is no contraindication to induced emesis (caustic agent or solvent, altered mental status, less than 1 year of age), ipecac should be administered immediately. One tablespoon or 15 ml should be given with one or two glasses of water; this dose may be repeated in 20 minutes if emesis does not occur. Parents of children with special medical conditions should carry a pertinent medical summary and have resources to access specialty physicians in destination countries. A generous supply of necessary medications with instructions for worsening symptoms must be included in the medical kit. An extra supply of all essential medications should be kept with either parents or patient in case the medical kit is lost or separated from the patient when the medication is needed. Some travelers in endemic areas for hepatitis B and acquired immunodeficiency syndrome (AIDS) carry their own needles and syringes for emergency use. The International Association for Medical Assistance to Travelers (417 Center St., Lewiston, NY 14692; 716-754-4883) has a directory of qualified physicians worldwide who speak English.

INFANTS AND YOUNG CHILDREN A family traveling with an infant must be particularly vigilant in monitoring their child's state of health. Infants become hypothermic, hyperthermic, septic, and dehydrated more rapidly than adults or older children. A thermometer and appropriate lubricant should be included in the medical kit for monitoring rectal temperature. A temperature greater than 38° C (100.4° F) in a child less than 3 months of age requires evacuation for medical evaluation. Digital thermometers are recommended, since they are less likely to break, are easy to read, and are three to four times faster than a glass thermometer. Some emit an audio alarm when the reading is ready. Infants are less tolerant of problems with excess mucus; a bulb syringe is handy for suctioning mucus from the oropharynx and nasal passages. A few drops of saline solution (¼ tsp of salt in 1 cup of water) instilled into the nares a few minutes before aspiration help to loosen mucus. Nasal aspiration should be reserved for times of most need, such as before feeding and sleep, since the procedure is irritating to the child. Other uses for a clean bulb syringe include flushing foreign bodies from ears and administering enemas. Away from the conveniences of home, diapers tend to be changed less frequently; consequently, diaper rash may become a problem. A good barrier cream (e.g., Desitin) may be helpful and should be started at the first signs of irritation. If the rash progresses despite appropriate treatment, an antifungal cream (e.g., miconazole, clotrimazole) may be used. Lost Children Lost children in the wilderness is a common, preventable problem. Children should be taught to recognize landmarks and to turn around and look backward periodically to familiarize themselves with the terrain. Those who are capable of reading a compass and topographic map should carry these at all times. Young children should wear brightly colored clothing to facilitate a search should they become lost. They should carry a whistle around their necks and should be taught the universal signal for help: three blows in a row. It should be emphasized to the child that the whistle is intended for emergency use only. All children should either know or carry with them a piece of paper with their parents' name, address, and phone number. Older children who venture without their parents should always inform an adult where they are going, with whom, and when they expect to return. Programs such as "Hug a Tree" instruct children in the basics of survival and orienteering when lost: stay in one place to facilitate any search, take advantage of the natural shelter provided by a tree, and feel the security of a large natural protector. By "hugging a tree" and not wandering, children can make signals from rocks or branches to indicate their location. Children should be taught to avoid becoming wet, to wear a hat, and to stuff pine needles or dry grasses into their clothes to insulate themselves if they are cold. Children can practice making temporary shelters out of logs, branches, and leaves to experience the warmth and protection of these natural features. Homesickness Most children will experience some degree of distress when faced with separation from home, particularly when they will not be accompanied by a parent. Predisposing factors to the depression and anxiety referred

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to as "homesickness" include young age, little prior separation experience, high parental separation anxiety, great perceived distance from home, few initial positive experiences after separation, preexisting anxiety or depression, and little perceived control over the situation.[71] Parents should introduce short periods of separation from home and family that lead up to longer periods. They should discuss the exciting aspects of the adventure to come and encourage active decision making regarding activities and destination. Parents should also alleviate their own separation anxiety and ensure positive early postseparation experiences for their child. The presence of familiar faces, such as friends or favorite playmates, can significantly reduce a child's feeling of homesickness. The child will remember favorite games and meals as fun experiences.

References 1.

American Academy of Pediatrics: The management of acute gastroenteritis in young children, Pediatrics 97:424, 1996.

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AAP Guidelines: Prevention of rotavirus disease: guidelines for use of rotavirus vaccine, Pediatrics 102:1483, 1998.

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Banks B et al: Attitudes of teenagers toward sun exposure and sunscreen use, Pediatrics 89:40, 1992.

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Barry M: Medical considerations for international travel with infants and older children, Infect Dis Clin North Am 6:389, 1992.

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Bonadio WA: Acute infectious enteritis in children, Emerg Med Clin North Am 13:457, 1995.

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Brasseur P et al: Multi-drug resistant falciparum malaria. In Cameroon 1987–88, Am J Trop Med Hyg 46:8, 1992.

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Bronstein AC, Russell FE, Sullivan JB: Negative pressure suction in the field treatment of rattlesnake bite victims, Vet Hum Toxicol 28:485, 1986.

Buchanan BJ, Hoagland J, Fischer PR: Pseudoephedrine and air travel-associated ear pain in children. In Program and abstracts of the 5th International Conference on Travel Medicine, Geneva, 1997. 8.

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Claeson M, Merson MH: Global progress in the control of diarrheal diseases, Pediatr Infect Dis J 9:345, 1990.

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Dexter W: Hypothermia, Postgrad Med 88:55, 1990.

Doern GV et al: Prevalence of antimicrobial resistance among respiratory tract isolates of Streptococcus pneumoniae in North America: 1997 results from SENTRY antimicrobial surveillance program, Clin Infect Dis 27:764, 1998. 11.

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Dowell SF, Schwartz B, Phillips WR: Appropriate use of antibiotics for URIs in children. Part I. Otitis media and acute sinusitis, Am Fam Physician 58:1113, 1998.

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Dowell SF, Schwartz B, Phillips WR: Appropriate use of antibiotics for URIs in children. Part II. Cough, pharyngitis and the common cold, Am Fam Physician 58:133, 1998.

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Downey D, Omer G, Moheb M: New Mexico rattlesnake bites: demographic review and guidelines for treatment, J Trauma 31:1380, 1991.

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Duggan C et al: How valid are clinical signs of dehydration in infants? J Pediatr Gastroenterol Nutr 22:56, 1996.

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DuPont HL: Diarrheal disease in the developing world, Infect Dis Clin North Am 9:313, 1995.

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Ericsson CD et al: Treatment of travelers' diarrhea with sulfamethoxazole and trimethoprim and loperamide, JAMA 263:257, 1990.

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Faruque ASG et al: Randomized, controlled, clinical trial of rice versus glucose oral rehydration solutions in infants and young children with acute watery diarrhoea, Acta Paediatr 86:1308, 1997.

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Fayad IM et al: Comparative efficacy of rice-based and glucose-based oral rehydration salts plus early reintroduction of food, Lancet 342:772, 1993.

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Fischer PR: Travel with infants and children, Infect Dis Clin North Am 12:355, 1998.

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Foster JA, Watson B, Bell LM: Travel with infants and children, Emerg Med Clin North Am 15:71, 1997.

22.

Gallagher R: Suntan, sunburn, and pigmentation factors and the frequency of acquired melanocytic nevi in children, Arch Dermatol 126:770, 1990.

23.

Gavin N, Merrick N, Davidson B: Efficacy of glucose-based rehydration therapy, Pediatrics 98:45, 1996.

24.

Gentile DA, Kennedy BC: Wilderness medicine for children, Pediatrics 88:967, 1991.

25.

Goepp J, Santosham M: Oral rehydration therapy, Principles Pract Pediatr Updates 1:1, 1993.

Grissom CK et al: Acetazolamide in the treatment of acute mountain sickness: clinical efficacy and effect on gas exchange. Abstract from Sixth Annual Scientific Meeting of the Wilderness Medical Society, 1990, Snowbird, Utah. 26.

27.

Guarino A et al: Oral bacterial therapy reduces the duration of symptoms and of viral excretion in children with mild diarrhea, J Pediatr Gastroenterol Nutr 25:516, 1997.

28.

Guidelines for cardiopulmonary resuscitation and emergency cardiac care, JAMA 268:2199, 1992.

29.

Hoge CW et al: Trends in antibiotic resistance among diarrheal pathogen isolates in Thailand over fifteen years, Clin Infect Dis 26:341, 1998.

30.

Hughes G: Synergistic effects of oral nonsteroidal drugs and topical corticosteroids in the therapy of sunburn in humans, Dermatology 184:54, 1992.

31.

Kaidbey K: The photoprotective potential of the new superpotent sunscreens, J Am Acad Dermatol 22:449, 1990.

32.

Kaplan LA: Wilderness dermatology: an overview. Abstract from Third Annual Winter Meeting on Wilderness Medicine, 1993, Sun Valley, Idaho.

33.

Katsambas A, Nicolaidou E: Cutaneous malignant melanoma and sun exposure: recent developments in epidemiology, Arch Dermatol 132:444, 1996.

34.

Kelly K et al: Profound accidental hypothermia and freeze injury of the extremities in a child, Crit Care Med 18:679, 1990.

35.

Kleinman R: We have the solution: now what's the problem? Pediatrics 90:113, 1992.

36.

Klocke DL, Decker WW, Stepanek J: Altitude-related illness, Mayo Clin Proc 73:988, 1998.

37.

Lell B et al: Randomised placebo-controlled study of atovaquone plus proguanil for malaria prophylaxis in children, Lancet 351:709, 1998.

38.

Litovitz TL et al: 1995 annual report of the American Association of Poison Control Centers toxic exposure surveillance systems, Am J Emerg Med 14:487, 1996.

39.

Lobel HO, Kozarsky PE: Update on the prevention of malaria for travelers, JAMA 278:1767, 1997.

40.

Longworth DL: Drug-resistant malaria in children and in travelers, Pediatr Clin North Am 42:649, 1995.

Looareesuwan S et al: Clinical studies of atovaquone alone or in combination with other antimalaria drugs, for treatment of acute uncomplicated malaria in Thailand, Am J Trop Med Hyg 54:62, 1996. 41.

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The management of acute diarrhea in children: oral rehydration, maintenance, and nutritional therapy, MMWR 41, 1992.

43.

Mason WH: The management of common infections in ambulatory children, Pediatr Ann 25:620, 1996.

44.

Meyer F et al: Drink composition and the electrolyte balance of children exercising in the heat, Med Sci Sport Exerc 27:882, 1995.

Molina S et al: Clinical trial of glucose-oral rehydration solution (ORS), rice-dextrin ORS, and rice flour ORS of the management of children with acute diarrhea and mild or moderate dehydration, Pediatrics 95:191, 1995. 45.

46.

Mota-Hernandez F: Rice solution and World Health Organization solution by gastric infusion for high stool output diarrhea, Am J Dis Child 145:937, 1991.

47.

Newman LM et al: Pediatric wilderness recreational deaths in western Washington state, Ann Emerg Med 32:687, 1998.

48.

Pertussis: report of the Committee on Infectious Disease, Elk Grove Village, Ill, 1991, American Academy of Pediatrics.

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Physicians' desk reference, ed 46, Montvale, NJ, 1992, Medical Economics Data.

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Pitzinger B: Incidence and clinical features of traveler's diarrhea in infants and children, Pediatr Infect Dis J 10:719, 1991.

51.

Pope D et al: Benign pigmented nevi in children, Arch Dermatol 128:1201, 1992.

52.

Radloff PD et al: Atovaquone and proguanil for Plasmodium falciparum malaria, Lancet 347:1511, 1996.

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Rahnan A: Rice-ORS shortens the duration of watery diarrhoeas, Trop Geogr Med, 1990, p 230.

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Red book: report of the Committee on Infectious Disease, Elk Grove Village, Ill, 1997, American Academy of Pediatrics.

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55.

Reyes I, Shoff WH: General medical advice for travelers, Emerg Med Clin North Am 15:1, 1997.

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Rivara FP, Aitken M: Prevention of injuries to children and adolescents, Adv Pediatr 45:37, 1998.

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Salahuddin S: A traditional diet as part of oral rehydration therapy in severe acute diarrhoea in young children, J Diarrhoeal Dis Res 9:258, 1991.

58.

Santosham M: A comparison of rice-based oral rehydration solution and "early feeding" for the treatment of acute diarrhea in infants, J Pediatr 166:868, 1990.

Santosham M et al: A double-blind clinical trial comparing World Health Organization oral rehydration solution with a reduced osmolarity solution containing equal amounts of sodium and glucose, Pediatrics 128:45, 1996. 59.

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Schaad U: Role of the new quinolones in pediatric practice, Pediatr Infect Dis J 11:1043, 1992.

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Schaad UB et al: Use of fluoroquinolones in pediatrics: consensus report of the International Society of Chemotherapy commission, Pediatr Infect Dis J 14:1, 1995.

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Schumacher MJ, Tveten MS, Egen NB: Rate and quantity of delivery of venom from honeybee stings, J Allergy Clin Immunol 93:831, 1994.

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Shanks GD, Gordon DM, Klotz FW: Efficacy and safety of atovaquone plus proguanil as suppressive prophylaxis for Plasmodium falciparum malaria, Clin Infect Dis 27:494, 1998.

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Sood SK et al: Duration of tick attachment as a predictor of the risk of Lyme disease in an area in which Lyme disease is endemic, J Infect Dis 175:996, 1997.

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66.

Squire DL: Heat illness: fluid and electrolyte issues for pediatric and adolescent athletes, Pediatr Clin North Am 37:1085, 1990.

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Talan DA: Update on antibiotic treatment of emergency department and outpatient infections. Abstract from Stanford Symposium on Emergency Medicine and Acute Care, 1999, Maui, Hawaii.

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Talan DA, Citron DM, Abrahamian FM: Bacteriological analysis of infected dog and cat bites: emergency medicine animal bite infection study group, N Engl J Med 340:85, 1999.

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Thanassi WT, Weiss EL: Immunizations and travel, Emerg Med Clin North Am 15:43, 1997.

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Theis MK et al: Acute mountain sickness in children at 2835 meters, Am J Dis Child 147:143, 1993.

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Thurber CA, Sigman MD: Preliminary models of risk and protective factors for childhood homesickness: review and empirical synthesis, Child Dev 69:903, 1998.

72.

Treatment of diarrhoea: manual for physicians and other senior health workers, Geneva, 1995, World Health Organization.

73.

Visscher PK, Vetter RS, Camazine S: Removing bee stings, Lancet 348:301, 1996.

74.

White R, Weber R: Poisonous snakebite in Central Texas, Ann Surg 213:466, 1991.

75.

Wyler D: Malaria chemoprophylaxis for the traveler, N Engl J Med 329:31, 1993.

76.

Zanetti R: Cutaneous melanoma and sunburns in childhood in a southern European population, Eur J Cancer 28A:1172, 1992.

77.

Zinman R et al: Predictors of sunscreen use in childhood, Arch Pediatr Adolesc Med 149:804, 1995.

Suggested Readings Brody J: Jane Brody's good food book, New York, 1987, Bantam. Castle S: The complete new guide to preparing baby foods, New York, 1992, Bantam. Foster L: Take a hike! San Francisco, 1991, Sierra Club. Hodgson M: Wilderness with children, Harrisburg, Pa, 1992, Stackpole Books. Ross C, Gladfelter T: Kids in the wild, Seattle, 1995, Mountaineers. Silverman G: Backpacking with babies and small children, Berkeley, Calif, 1986, Wilderness Press.

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Chapter 75 - Women in the Wilderness Kenneth F. Trofatter Jr. Barbara D. Dahl

Problems common and unique to a woman might diminish the wilderness experience or place her at risk. This chapter emphasizes a practical approach to the evaluation, management, and impact assessment of gynecologic and obstetric conditions of women undertaking short-term or long-term wilderness activities. A framework is provided for the diagnosis and the selection of empiric therapy, based on historical and physical observations, under circumstances in which limited medical care and resources are available. Preexisting conditions are also addressed, with consideration of access to a medical facility in the field.

PREPARATION FOR THE WILDERNESS EXPERIENCE The goal of preparation is to anticipate and recognize problems rather than to address them for the first time under suboptimal circumstances. A high priority is to identify medical problems that could be exacerbated by physical demands and the wilderness setting. These must be evaluated in relation to characteristics of the environment, length of the excursion, additional conditioning and acclimation, and difficulty in accessing more sophisticated medical care. For physically challenging conditions and prolonged stays, women should undergo thorough medical assessment ( Box 75-1 ). After historical information is collected, a comprehensive physical examination is performed, with special attention to the cardiovascular and respiratory systems, musculoskeletal system, genitourinary tract, and breasts. Other recommended tests include: Pap smear, vaginitis screening, pregnancy test, urinalysis, hemoglobin/hematocrit (Hgb/Hct), and urine culture and screening for sexually transmitted infections (STIs) and hepatitis. Additional screening, as indicated by age, medical status, and risk factors, include electrocardiogram (ECG) with stress testing, pulmonary function tests, mammogram if over age 40 or with strong family history of breast cancer, and thyroid panel. Bone densitometry should be considered in perimenopausal and postmenopausal women and in young women with a history of fractures or abnormal menses consistent with a hypoestrogenic state. In anticipation of a wilderness trip, supplemental iron, vitamins, and calcium are recommended ( Table 75-1 ). Maintenance medications should provide optimal control of medical conditions and cover planned time, emergency needs, and expected dose adjustments. Contraceptive needs should be reviewed and options explored. Hormonal replacement therapy should be discussed with postmenopausal women at risk for osteoporosis. Box 75-2 lists basic supplies for hygienic and anticipated therapeutic needs. Special considerations for pregnancy are discussed in a separate section.

PHYSIOLOGIC ADAPTATIONS Women at Altitude Recent studies have found no difference in the incidence of acute mountain sickness (AMS) in women and men.[57] Differences in how men and women respond to altitude may be hormonally mediated. Adaptation to high altitude involves a series of physiologic responses triggered by hypoxemia. The sigmoidal shape of the oxyhemoglobin dissociation curve prevents a drop in the oxygen saturation below 90% until an altitude of about 2400 m (8000 feet) in healthy individuals. At higher altitudes, hypoxia stimulates respiratory, cardiovascular, and hematologic changes that depend on both degree of hypoxia and time. The earliest and probably most important response to altitude is an increase in minute ventilation caused by increases in tidal volume and respiratory rate. This hypoxic ventilatory response (HVR) is mediated by chemoreceptors in the carotid bodies, which respond to a decrease in arterial oxygen pressure (PaO2 ) and signal the respiratory center in the medulla to increase ventilation.[141] HVR has been closely related to adequacy of acclimatization and the risk of developing AMS.[58] [83] [135] The degree of HVR to a given PaO2 varies among individuals and is genetically influenced. The HVR is inhibited by respiratory depressants, such as alcohol and sedatives and stimulated by respiratory stimulants, such as caffeine and cocoa. Progesterone is a potent respiratory stimulant and acts primarily through activation of peripheral arterial chemoreceptors.[26] [60] [61] Progesterone is produced by all steroid-forming glands, including the ovaries, testes, and adrenal cortex, and by the corpus luteum and placenta in the pregnant female. Ovariectomy in female cats lowers the carotid sinus nerve response to hypoxia and likewise decreases HVR, although translation of carotid nerve activity in the central nervous system (CNS) into ventilation was similar in ovariectomized and intact animals.[152] Exogenous progesterone and estrogen administration to male rats living at 3600 m (12000 feet)

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INDICATION Nutritional supplements

TABLE 75-1 -- Examples of Medications for Women's Health MEDICATION*

DOSE

Ferrous sulfate

300 mg qd-tid

Calcium carbonate

1250 mg qd

Multivitamin

1 tablet qd

Headache/pain

Acetaminophen

325 mg, 1 or 2 q3-4h

Dysmenorrhea/pain

Ibuprofen

200 mg, 1–4 q4-6h

Nausea/vomiting

Promethazine (tablet or suppository)

25 mg q4-6h

Urinary tract infection

Ampicillin

250–500 mg qid

Trimethoprim/sulfamethoxazole

160 mg/800 mg bid

Miconazole (cream or suppository)

One applicator hs × 3–7 days

Fluconazole

150 mg single dose

Metronidazole (tablets)

250–500 mg bid-tid

Metronidazole or clindamycin (vaginal gel)

One applicator hs × 3–7 days

Yeast vulvovaginitis Bacterial vaginosis Urine pregnancy test kit

As needed

Menstrual regulation or breakthrough bleeding

Conjugated estrogen (Premarin)

2.5 mg qd

Medroxyprogesterone acetate

5–10 mg qd

qd, Daily; bid, twice daily; tid, three times daily; qid, four times daily; q, every; h, hour; hs, at bedtime. *Suggested medications or equivalent depending on tolerance, allergy history, and patient preferences.

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significantly inhibited norepinephrine and dopamine turnover in the carotid sinus, thus stimulating the afferent chemoreflex.[44] In pregnant females, HVR is enhanced and most likely driven by higher progesterone levels. Mean PO2 value at 4,400 m (14,500 feet) in nonpregnant women is 51 mm Hg (carbon dioxide pressure [PCO2 ] 28 mm Hg) vs. 59 mm Hg (P CO2 23 mm Hg) in pregnant women.[64] Increased ventilation is a key factor in adapting to altitude in pregnancy, as evidenced by the linear correlation between birth weight and maternal ventilatory rate.[110] Despite higher levels of progesterone in women, particularly in the luteal phase of the menstrual cycle, when progesterone levels increase approximately tenfold, no difference has been observed between males and nonpregnant females in the incidence of AMS, although one study has reported a lower incidence of gastrointestinal (GI) and cardiovascular symptoms in females vs. males at altitude.[57] [62] To date, no study has been done comparing HVR and the incidence of AMS in premenopausal women in follicular vs. luteal phases.

Box 75-1. ASSESSMENT OF A WOMAN'S HEALTH: SCREENING HIGHLIGHTS Menstrual history: age of menarche, regularity, characteristics, timing, extent of blood flow (length, amount), intermenstrual bleeding, perimenstrual symptoms (e.g., dysmenorrhea, headache, premenstrual syndrome), plans for managing periods (hygienic, therapeutic) Sexual history: age of coitarche, number of partners, sexual orientation, sexually transmitted infections, contraceptive history, plans for sexual activity in the wilderness, dyspareunia Gynecologic history: ovarian cysts, uterine fibroids, endometriosis, cervical dysplasia, surgical history, pelvic pain, vaginal discharge, vaginal infections and treatment, pregnancy and complications Breast: galactorrhea, discharge, masses, surgery Gastrointestinal/urinary tract: ulcers, irritable bowel syndrome, gallbladder disease, constipation, urinary tract infections, kidney stones, stress incontinence, urgency incontinence Musculoskeletal/skin: injuries (exercise related and accidents), limitations, muscle cramps, joint pain and swelling, arthritis, rashes, acne, sun sensitivity, hirsutism, hair loss Exposure to abuse: battering, sexual harassment, sexual assault Habits: smoking, alcohol, illicit drug use Current problems: condition, medications, status of control, complications Immunizations: measles, mumps, rubella, polio, diphtheria, tetanus, hepatitis, others Family history: thyroid disease, hypertension, autoimmune disorders, diabetes, breast and gynecologic malignancies, osteoporosis Allergies: general, drug related, bite and sting sensitivity Nutritional: eating disorders, weight changes, food sensitivities, dietary preference (e.g., vegetarianism), caloric intake, assessment of mineral and vitamin intake in diet, supplements (e.g., iron, vitamins, calcium) including homeopathic compounds

Box 75-2. BASIC SUPPLIES FOR WOMEN'S HYGIENE

STANDARD Sanitary napkins or tampons (store in plastic bag) Toilet paper (store in plastic bag) Cotton underwear Matches or cigarette lighter (to burn toilet paper after use) Plastic trowel (to bury feces) Toiletries (soap, small towel, toothbrush and paste, dental floss, comb) Moisturizing lotion (unscented, to prevent skin chapping/cracking)

OPTIONAL Urinal guide (if long periods of poor weather are anticipated) Vaginal speculum and gloves (if trained medical professional accompanies expedition) Premoistened towelettes (convenient for cleaning/washing when water is limited or weather precludes bathing)

Cardiovascular adaptations to altitude also occur early and are mediated by release of catecholamines. Hypoxia stimulates a sympathoadrenal release of epinephrine and norepinephrine, resulting in elevated heart rate, cardiac output, and mean arterial pressure (MAP). This catecholamine-mediated response was studied in females at 4300 m (14,000 feet). Norepinephrine levels rose steadily during the initial days at altitude, reached a plateau at 4 to 6 days, and remained elevated for the duration at altitude.[97] Norepinephrine levels correlated with increased heart rate and MAP. This response, previously demonstrated in males, reflects elevation in whole body sympathetic nerve activity at altitude. [95] [96] No difference was found in the sympathetic response to hypoxia between follicular-phase and luteal-phase subjects; however, for a given norepinephrine level, heart rates and MAPs were lower for follicular vs. luteal subjects, possibly reflecting effects of hypoxia and ovarian hormones on adrenergic receptors. Other circulatory changes at altitude include decreased plasma volume from dehydration, increased insensible water loss, and fluid shifts into the extravascular space. Euvolemia is usually regained with adequate hydration and acclimatization. [52] Also, hypoxic pulmonary vasoconstriction results in increased pulmonary vascular resistance and increased pulmonary artery pressure. Cerebral blood flow (CBF) also increases at altitude. Although hypoxic vasodilation and hypocapnic vasoconstriction both contribute to regulating CBF, the hypoxic response is thought to dominate at altitudes over 3800 m (12,500 feet).[71] [125] Hematologic changes occur at altitude in response to hypoxia. Within hours, erythropoietin levels increase, with red blood cell mass increasing a few days later. The higher the altitude, the greater the increase in Hct and blood viscosity, which may actually be detrimental to oxygen transport despite an increase in O2 -carrying capacity.[70] This hypoxia-induced polycythemia is associated with chronic mountain sickness.[150] Recent animal studies suggest that, under hypoxic conditions, female ovarian hormones reduce erythropoietin levels and hypoxic-induced polycythemia.[44] It is not known whether this hormonally mediated effect is significant in human females at altitude. Hot and Cold Environments Because of the lower sweat rate in females compared with males, women rely more heavily on dimensional characteristics and circulatory mechanisms for heat dissipation in hot environments.[137] [138] Females adapt more easily to hot, wet environments than do males because of this lower sweat rate and decreased risk of dehydration.[9] [98] In hot, dry environments, however, a higher sweat rate is advantageous because perspiration decreases the risk of hyperthermia, provided adequate fluid replacement is available. With acclimation to dry heat, women are able to increase the sudorific response to equal that of men.[165] With similar acclimatization and physical training, women tolerate physical activity in hot environments at least as well as men.[51] [63] [69] Thus women planning wilderness expeditions to hot, dry

destinations are advised to plan a 1- to 2-week acclimation period in a hot environment.[10] Adaptation of females to hot temperatures may also depend on menstrual phases. Some evidence suggests that women in the follicular phase of the menstrual cycle may adapt better to hot environments than women in the luteal phase. The resting core temperature in women is approximately 0.4° C higher during the luteal phase than during the follicular phase.[49] Also, the threshold core temperature for the onset of thermoregulatory responses, such as sweating and vasodilation, is increased during the luteal phase. Therefore women in the luteal phase may have more difficulty in reaching thermal equilibrium in hot environments. [29] [122] In moderately cold environments, women on average adapt better than men, partly because of thicker subcutaneous fat. At extreme cold temperatures, however, women may be at a disadvantage because of the decrease in insulation from lower muscle mass. Although adaptation to cold environments depends more on body size, physical fitness, and degree of acclimation than on gender, exercise performed during cold exposure may be more effective in maintaining body heat in women than men.[55] [99]

CONTRACEPTION Women of reproductive age who anticipate having a heterosexual relationship while in the wilderness should strongly consider a reliable and convenient form of contraception, especially for extended excursions ( Box 75-3 ). Pregnancy is a relative contraindication

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to both brief and prolonged wilderness experiences because of the frequent, inconvenient, and life-threatening complications that can occur. Any form of hormonal contraception or an intrauterine device should be used for at least 3 months before departure to minimize risk of complications. Box 75-3. CONTRACEPTIVE OPTIONS

HORMONAL Oral contraceptives Monophasic combination pills Multiphasic combination pills Monophasic progestin-only pills Injectable Depo-Provera (medroxyprogesterone), 150 mg intramuscularly every 3 months Implantable Norplant system (levonorgestrel), six Silastic implants subcutaneously

BARRIER Condom and spermicide Diaphragm and spermicide Contraceptive sponge Cervical cap and spermicide Female condom

INTRAUTERINE DEVICE (IUD) ParaGard-T (copper enveloped) Progestasert system (IUD containing progesterone)

EMERGENCY CONTRACEPTION Preven (0.05 mg ethinyl estradiol + 0.25 mg levonorgestrel/tablet), two tablets within 72 hours postexposure; repeat dose in 12 hours

Hormonal Contraceptives Combination (estrogen and progestin) oral contraceptives (OCs), either monophasic or multiphasic, offer the most reliable, convenient, cost-effective, and sensible risk/benefit ratio for the healthy reproductive-age woman. Brand selection should be done with a qualified health care professional. Previous experience of use, complications of therapy, menstrual history, and skin type should be considered. For example, women with histories of irregular cycles and polycystic ovary syndrome may be better suited to brands with low androgenic side effects. Failure rates with optimal use are extremely low (1%), but may be worsened by concomitant drug therapy, substance abuse, chronic GI disturbance, and changes in dietary habits or weight. [160] Common side effects include nausea, vomiting, weight gain, and breakthrough bleeding. Other potential benefits include normalization of cycles, fewer midcycle ovulatory (i.e., mittelschmerz) and perimenstrual (e.g., dysmenorrhea, headaches) symptoms, lighter menstrual flow, suppression of ovarian cyst formation, reduced risk for endometrial cancer, prevention of osteoporosis, and increased bone mass. OCs may decrease the risk of acquiring certain STIs but cannot be relied on for this. Major contraindications include history of thromboembolic disease, certain autoimmune disorders with thromboembolic risk factors, uncontrolled hypertension, hepatic dysfunction, and cigarette smoking.[50] [105] [164] If a thrombotic or thromboembolic event is suspected in the field, OC use should be suspended and aspirin taken while awaiting evacuation. High altitude is a potential risk factor for thromboembolic events, but increased risk from use of OCs or hormonal replacement therapy has not been systematically studied. As a precaution, women planning high-altitude excursions should consider a combination pill containing the lowest dose of ethinyl estradiol (20 µg) or its equivalent. Progestin-only OCs are not generally recommended for the wilderness traveler because of higher failure rates (4% to 9%), increased frequency of irregular and unpredictable bleeding, and potentially deleterious effects on bone density over time from suppression of ovarian estrogen production. The progestin-only injectable Depo-Provera (medroxyprogesterone) and the implantable Norplant system (six Silastic capsules containing levonorgestrel, 36 mg/capsule) have similar drawbacks. Although extremely convenient for maintenance contraception, problems include weight gain, irregular bleeding, headache, fatigue, and abdominal pain, especially early in therapy. [129] [140] Prolonged use of progestin-only methods may be associated with reduced bone mass, which could be hazardous for women involved in strenuous physical activities.[151] Depo-Provera (150 mg intramuscularly) is administered every 3 months, so extended wilderness experiences would necessitate transport and storage of the drug in its

glass container and syringes for administration. Once Depo-Provera is injected, it cannot be removed. Side effects and complications, such as irregular bleeding, must be dealt with for an indefinite period, possibly a year or longer, until its effects on the hypothalamic-pituitary axis have dissipated. Similarly, once the Norplant system is placed, it cannot be readily removed in a wilderness setting unless a trained health care provider and adequate surgical supplies are available. Furthermore, subcutaneous location of the 34-mm capsules, usually on the inner aspects of the upper arm, could be traumatized by certain strenuous wilderness activities. Once implants are removed, however, cyclic hormonal activity and menstruation return almost immediately. Irregular bleeding with a long-term progestin-only OC can usually be managed with oral estrogen (e.g., Premarin,

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2.5 mg daily) for 21 to 25 days sequentially. Estrogen administration results in rapid cessation of bleeding. Within days after discontinuation, a menstrual-like withdrawal bleed should occur in the continued presence of the progestin. If the withdrawal bleed persists beyond the length of a normal period, or if irregular bleeding recurs and persists, the course of estrogen therapy is simply repeated for another cycle. No withdrawal bleed indicates that progestin has fallen below biologically active levels, with unreliable contraceptive activity. Barrier Contraceptives The barrier contraceptive methods have the widest safety profile, excluding latex allergy and method failure resulting in pregnancy, but all have the same disadvantages for regular use in a wilderness setting. Failure rates even under ideal use with a spermicidal foam or gel are relatively high, estimated at 20% with "typical use" and 6% to 9% with "perfect use." The compounds in barrier devices are variably susceptible to extremes of heat or cold, which may compromise their tensile strength and effectiveness. Some couples find these methods inconvenient and messy which might discourage compliance in an environment not conducive to cleanup. Bulk and weight complicate transport of sufficient spermicidal compound. Barrier methods decrease risk of gonorrhea, chlamydial infection, and human immunodeficiency virus (HIV) but offer minimal protection against human papillomavirus (HPV) or genital herpes simplex virus (HSV). Intrauterine Devices An intrauterine device (IUD) is a highly effective and convenient form of contraception, especially for the parous woman in a stable relationship. [38] [47] Ideally it should be inserted at least 3 months before departure. Complications occur most often within the first month after initial insertion and when the device is replaced. IUDs are occasionally associated with increased menstrual flow, dysmenorrhea, intermenstrual spotting, and expulsion. However, the ParaGard-T copper-enveloped IUD and the Progestasert system, which has a reservoir with 36 mg of progesterone and conforms to the endometrial cavity, carry minimal risk for these side effects. Once inserted, the ParaGard-T is effective for 10 years or longer. The Progestasert system requires annual replacement. The most serious risk, affecting 1% of IUD users, is acute or indolent pelvic infection that might become clinically significant and even life threatening in the wilderness. The risk for this is greatest within the first month after insertion or replacement and among women at increased risk for STIs. Women with multiple partners, previous pelvic infections, unrecognized chlamydial infection or gonorrhea, recurrent episodes of bacterial vaginosis, or tobacco use are at highest risk.[113] When acute pelvic inflammatory disease (PID) occurs, with lower abdominopelvic pain, peritoneal signs, purulent vaginal discharge, and fever, the IUD should be removed immediately by simple traction on the string protruding from the external cervical os. Broad-spectrum antibiotics should be started. Evacuation is mandatory when the device cannot be removed. Pelvic infection should be suspected, even without fever and peritoneal signs, if irregular bleeding occurs, particularly when accompanied by pelvic discomfort and discharge. When the IUD is removed at this stage, the infection may respond to therapy with oral or simple parenteral antibiotics (see later discussion). Another potentially serious risk for IUD users is pregnancy, occurring in approximately one of 100 users per year. Both intrauterine and extrauterine (ectopic) pregnancies can occur with an IUD in place. Unfortunately, the latter is more common, but the risk is still only half that in women who use no contraception. Confirmed or suspected pregnancy in a woman with an IUD is an indication for immediate evacuation. Emergency Contraception In the event of unanticipated or careless sexual activity, suspected contraceptive failure, or sexual assault, consideration should be given to emergency post-coital contraception.[53] [54] In the wilderness setting the only practical approach is hormonal therapy, ideally starting within 72 hours after exposure. Preven and several combination OCs reduce the risk of pregnancy by at least 75%.[157] [158] Treatment regimens with standard OC formulations include Ovral (0.05 mg ethinyl estradiol and 0.50 mg norgestrel), two tablets; Lo-Ovral (0.03 mg ethinyl estradiol and 0.30 mg norgestrel), four tablets; and Nordette or Levlen (0.03 mg ethinyl estradiol and 0.15 mg levonorgestrel), four tablets. The dose is repeated 12 hours later. Common side effects include nausea, vomiting, irregular bleeding, cramping, and headache, but these are usually transient and can be managed symptomatically. Administering an antiemetic 1 hour before each dose is recommended.[7]

SEXUAL ASSAULT Sexual assault of women in the wilderness is fortunately a rare occurrence. Wilderness morbidity and mortality statistics are limited, but one study of eight National Park Service areas in California over 3 years reported only one incident of sexual assault.[108] Many incidents are probably not reported, however, since only 7% of all rapes are reported.[35] The best defense against sexual assault is not going into the wilderness with unfamiliar people. The chance of meeting an assailant is quite low. A woman traveling into the wilderness alone or with someone she does

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not know well is advised to tell friends or family exactly where and with whom she is traveling and when she anticipates returning. If sexually assaulted, the woman is advised to seek medical attention as soon as possible. Most emergency departments are prepared to handle the evaluation and treatment of sexual assault victims. It may be impossible to reach a medical facility for many hours or even days, but an attempt should be made to preserve potential evidence. If a medical facility can be reached in a few hours, the woman should try not to eat, drink, urinate, or defecate. Women are also advised to avoid douching, gargling, brushing teeth, or changing clothes. If clothes are removed, clothes should be placed in a paper bag and brought to the medical facility.

VAGINITIS Vaginitis is a frequent indication for seeking medical care and a common incidental finding at gynecologic evaluation. Although rarely dangerous in healthy women, vaginitis can compromise the wilderness experience. Environmental conditions and constraints on hygiene can contribute to vaginitis and diminish the efficacy of therapy. Self-diagnosis of vaginitis is often incorrect, leading to inappropriate treatment selection. In premenopausal women, more than 90% of infectious causes of vaginitis are bacterial vaginosis (40% to 50%), candidiasis (20% to 25%), and trichomoniasis (15% to 20%). Symptoms include vaginal discharge, itching, erythema, and irritation of the vagina, introitus, TABLE 75-2 -- Differential Diagnosis of Vulvovaginitis VULVOVAGINAL TRICHOMONIASIS CANDIDIASIS

FACTORS

NORMAL

BACTERIAL VAGINOSIS

Discharge

White, clear, finely granular

Gray-white, thin, homogenous, adherent, frothy

White, thick, curdlike, adherent

pH

3.8 to 4.2

>4.5

Amine odor

Absent

Present

Primary complaints

None

Microscopic appearance

Normal epithelial cells, lactobacilli

Other findings and None diagnostic features

ATROPHIC VAGINITIS

OTHER

Gray to yellow-green, occasionally frothy, adherent

Thin, clear to serosanguineous

Normal

=4.5

>4.5

>4.5

3.8 to 4.2

Absent

Variably present

Usually absent

Absent

Malodorous discharge Pruritus, irritation

Severe pruritus, discharge, dyspareunia, dysuria

Burning, soreness, dyspareunia

Burning, irritation, swelling, soreness

"Clue cells," no WBCs Budding yeast, hyphae, spores

Trichomonads, many WBCs (PMNs)

Small, round (parabasal) epithelial cells, many PMNs

Normal

Minimal vulvar involvement

Intense vulvovaginal Atrophy of vulva and erythema, "strawberry cervix," vaginal epithelium other STIs

Vulvar and vaginal erythema, predisposing medical conditions

Highly variable

WBCs, White blood cells; PMNs, polymorphonuclear neutrophil leukocytes; STIs, sexually transmitted infections. and vulva. Therefore most vaginitis of clinical significance is more accurately described as vulvovaginitis. Severe manifestations are intense discomfort, swelling, dyspareunia, dysuria, and urinary retention. The medical history, pelvic examination, and evaluation of vaginal fluid provide the diagnosis of vaginitis ( Table 75-2 ). Recent evidence suggests that accurate diagnosis of the most common causes of vaginitis can often be done without a vaginal speculum.[22] Because diagnostic capabilities in the wilderness are limited, clinical features can help guide diagnosis and treatment of vaginitis and improve the chance of therapeutic success. Bacterial Vaginosis Bacterial vaginosis (BV) is the most prevalent cause of vaginitis, affecting as many as two thirds of women attending sexually transmitted disease (STD) clinics and 12% to 25% of premenopausal women undergoing gynecologic evaluation. The most common complaints of women with BV are discharge and odor, itching, and irritation of the vulva and vagina. More than 50% of women with BV do not complain of symptoms or are unaware that symptoms result from a treatable condition. The cause of BV is uncertain and may be multifactorial. BV is characterized by an overgrowth (100 to 1000-fold) of bacterial species in the vagina and GI tract and a dramatic reduction in lactobacilli, especially the predominant hydrogen peroxide-producing species.[155] The organisms implicated in BV are risk factors for upper genital tract infection, premature labor and delivery, and postoperative wound infections in women.[30]

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Local defects in host immunity may contribute to recurrent and persistent cases. [31] The discharge accompanying BV is typically thin, watery, grayish white, frothy, and homogenous (not flocculent), uniformly coating the vaginal walls and introitus. More than 50% of women with BV complain of a fishy odor, particularly during menstruation and immediately after unprotected sexual intercourse. Blood and semen can alkalinize the vagina and volatilize a variety of amines (e.g., cadaverine) produced by anaerobic organisms. The diagnosis of BV is confirmed by the presence of three of the following: (1) discharge, (2) pH greater than 4.5, (3) release of amines (fishy odor) when discharge is exposed to 10% potassium hydroxide (KOH) ("whiff test"), and (4) microscopic detection of "clue cells" (epithelial cells coated with bacteria) in saline solution. Microscopic appearance of pure BV is characterized by few if any leukocytes and few motile, curved rods (lactobacilli). The antimicrobial agent most successful in treating BV is metronidazole, which can be administered orally (500 mg 2 or 3 times daily for 5 to 7 days) or as a 0.75% vaginal gel (once or twice daily for 5 days).[75] These regimens have initial response rates in excess of 90%. Single-dose oral treatment with metronidazole (2.0 g) yields initial response rates of 80% to 90% but is accompanied by higher recurrence rates within 1 month of treatment. This regimen should be considered when drug supplies are limited or when the GI side effects of oral metronidazole are not well tolerated. Clindamycin (300 to 600 mg orally twice daily for 5 to 7 days or 2% vaginal gel daily for 7 days) has comparable efficacy, but disadvantages are expense, deleterious effects on normal vaginal lactobacilli, and increased risk for pseudomembranous enterocolitis, which could be life-threatening in the wilderness. Cure rates of 67% have been achieved with ampicillin (250 to 500 mg 4 times daily for 7 days) and amoxicillin (250 to 500 four times daily for 7 days), but again, deleterious effects on the normal vaginal flora often are followed by an overgrowth of yeast organisms. Yeast (Candida) Vaginitis Symptomatic yeast infections, more often referred to as vulvovaginal candidiasis (VVC), are the second most frequent cause of vaginitis and account for about 25% of cases. From 80% to 90% of these result from overgrowth of Candida albicans. C. glabrata and C. tropicalis account for most of the remainder and are of growing concern because of increased resistance to over-the-counter (OTC) antifungal preparations used to treat presumed "yeast infections," an incorrect presumption more than half the time. Risk factors for yeast infections include pregnancy, hormonal therapy, recent antibiotic use, corticosteroid therapy, postovulatory phase of menstrual cycle, frequent coitus, condom use, and intravaginal use of spermicidal compounds.[41] [128] [142] The presence of gonorrhea, chlamydial infection, and BV are negative risk factors. Recurrent or recalcitrant yeast infections should suggest depressed cell-mediated immunity and frequently affect women with undiagnosed or poorly controlled diabetes, pregnancy, HIV infection, lymphoproliferative disorders, and autoimmune diseases. The most common complaint of women with VVC is vulvar pruritus or burning, not vaginal discharge.[131] In more severe cases, redness, irritation, burning, soreness, swelling, and external dysuria are variably present. The characteristic white, flocculent ("cottage cheese"), adherent discharge is often diagnostic but is not consistently present or visible externally. The yeast discharge is thicker than that seen with BV or trichomoniasis, is usually not frothy or malodorous, and often has a pH of 4.5 or less, unless a mixed infection is present. About 50% of yeast infections are confirmed by direct microscopic examination of the discharge diluted in saline; however, diagnosis is most reliably accomplished by detection of budding yeast, hyphae, or spores using a slide preparation with 10% KOH added to lyse background epithelial cells and bacteria. The foundation of treatment for VVC is a variety of azole derivatives, many of which (e.g., butoconazole, clotrimazole, miconazole, tioconazole) are available OTC as topical creams, vaginal tablets, and suppositories. Prescription compounds for local application do not provide a significant advantage over these in most cases. Therapy periods range from 1 to 14 days, depending on the formulation and severity of the infection. Generally a treatment regimen of at least 3 days results in a

greater initial response rate and a lesser chance of immediate recurrence. Symptoms related to inflammatory vulvar involvement will respond most rapidly to the topical creams, although their application at first may be accompanied by burning pain. Oral fluconazole (150 mg, single dose) has been approved for VVC and is a convenient therapeutic agent to include in the basic pharmacopoeia of a wilderness expedition. Women with frequent recurrences or predictable outbreaks at specific times in their cycle, most often premenstrually, should consider prophylactic suppressive therapy with fluconazole (150 mg orally) or clotrimazole (500 mg vaginal tablet) weekly. Trichomonas Vaginitis Trichomonas vaginalis is a single-celled parasite that causes vaginitis in 2 to 3 million women annually in the United States. [67] It is predominantly sexually transmitted and is found most often in individuals with multiple sexual partners and those with a history of or current STIs. Diagnosis and treatment of a woman and her sexual partner are best accomplished at a screening visit before departure on a wilderness excursion. Unlike BV and yeast vaginitis, detection of Trichomonas, even in asymptomatic women, is an indication for treatment and for more complete STI screening.

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Symptoms and physical findings accompanying Trichomonas infections are highly variable. The organism can be carried asymptomatically for extended periods, but most women will develop clinically significant disease over time, often during or immediately after menstruation. The most common complaints include severe vulvovaginal pruritus, dyspareunia, and dysuria. Physical examination often reveals intense erythema of the vagina and introitus and petechial lesions of the cervix ("strawberry cervix"). The vaginal discharge is typically gray or yellow-green, somewhat cloudy, and variably frothy and malodorous. The presence of the latter two findings frequently indicates a mixed infection with the amine-producing organisms seen in BV.[91] The pH of vaginal fluid is usually above 5.0 and frequently exceeds 6.0. The clinical features of trichomoniasis overlap sufficiently with those of BV and yeast vaginitis to make them impractical alone for even presumptive diagnosis.[59] The diagnosis is confirmed by microscopic detection of the motile parasites on simple saline wet mount. Polymorphonuclear neutrophil leukocytes (PMNs) are usually present in high concentration and can interfere with microscopic diagnosis when the organisms are nonmotile. Under these circumstances, culture is now recognized as the most sensitive diagnostic technique, although not likely to be available in a wilderness setting. Because of the diagnostic difficulties, empiric therapy is justified in the wilderness. Metronidazole is the only drug approved for trichomoniasis in the United States. It is administered in a single oral dose (2 g) and in severe cases or single-dose failures for a week (500 mg bid) or longer. For optimal results, sexual partners should be treated simultaneously and sexual activity curtailed during therapy. To minimize GI side effects, metronidazole should be taken with plenty of water. This may not reduce the unpleasant metallic taste but may reduce the risk of nausea, vomiting, and gastric irritation. Because a disulfiram-like effect is possible, alcohol should be avoided while taking metronidazole. At present, metronidazole 0.75% vaginal gel is not appropriate for treatment of trichomoniasis. Atrophic Vaginitis Atrophic vaginitis occurs in postmenopausal and hypoestrogenized premenopausal women, such as some amenorrheic athletes and women on ovarian suppressive therapy with gonadotropin-releasing hormone (GnRH) agonists. The presumed etiology is lost estrogen effect on the vaginal epithelium, accompanied by reduction in epithelial cell glycogen, an important substrate for lactobacilli, with subsequent overgrowth of nonacidophilic organisms. Symptoms include burning or soreness, dyspareunia, and vaginal discharge that is often watery or even serosanguineous.[21] [120] It should be suspected in women of any age with vulvovaginal atrophy. Typically the vagina is uniformly erythematous and may have areas of petechial changes. The pH of the vagina usually exceeds 5 (often 6 to 7) and microscopic evaluation of the discharge reveals small, round, immature epithelial cells (parabasal cells), increased PMNs, and a paucity of lactobacilli. Treatment includes the use of topical or oral estrogen replacement therapy. Noninfectious Vulvovaginitis Certain noninfectious causes of vulvovaginitis result from environmental exposures that cause local irritative or allergic reactions. These may be of greater significance when attention to personal hygiene is limited.[59] Common causative agents include latex condoms, spermicidal compounds, soaps, detergents, fabric softeners, deodorant products, menstrual pads and tampons, and topical medications such as antimycotics and povidoneiodine. Exclusion of an infectious etiology and identification of the source of the reaction usually make the diagnosis. Once a potentially offending cause, such as a recent change in laundry detergent, is identified, the first step in management is removal from exposure. Treatment is usually symptomatic (pain relief, antihistamines, Sitz baths). Topical corticosteroids are rarely indicated and may initially exacerbate symptoms.

URINARY TRACT INFECTIONS In sexually active adolescent and adult women, bacterial bladder infections (cystitis) are the most common manifestation of urinary tract infection (UTI) and a frequent source of medical complaints.[16] They occur more frequently in women than men, presumably because of the shorter length of the urethra, its location in proximity to the vagina and enclosed within the introitus, and trauma secondary to sexual activity. Women with recurrent vaginitis, particularly BV; congenital or acquired genitourinary tract abnormalities; diaphragm use and use of spermicidal compounds; poor hygiene; and cigarette abuse are at increased risk for developing UTIs, as are pregnant women.[45] [56] [120] [153] About 5% of pregnant women develop asymptomatic bacteriuria, 20% of whom progress to upper tract disease. Wilderness conditions, with restricted access to fluid, deferred voiding, and less attention to personal hygiene, increase the potential for development of UTIs. Attention to maintenance of urinary tract health should be a primary goal of the female wilderness traveler. Common symptoms of cystitis include urinary frequency, urgency, dysuria, hematuria, foul-smelling or cloudy urine, and low back discomfort.[68] [90] Some women develop UTIs in relation to phase of the menstrual cycle or after sexual activity. Upper tract involvement, or pyelonephritis, should be suspected with accompanying fever, chills, malaise, flank pain, and occasionally, nausea and vomiting. Under wilderness conditions, symptoms, elevated urine pH (7 to 8), and indirect evidence of

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TABLE 75-3 -- Antibiotic Regimens for Urinary Tract Infections TYPE OF INFECTION

SELECTED ANTIBIOTICS

LENGTH OF TREATMENT

Cystitis (acute)

Ampicillin, 250 to 500 mg qid

3–7 days

Amoxicillin, 500 mg tid Cephalexin, 500 mg qid Nitrofurantoin,* 100 mg qid Sulfamethoxazole/trimethoprim,* 1 or 2 tablets bid Prophylaxis

Any of the above: 1 pill/day or 1 pill after coitus

Indefinitely

Pyelonephritis† (outpatient care)

Amoxicillin, 500 mg tid

10–14 days

Cephalexin, 500 mg qid Ciprofloxacin,‡ 500 mg bid Sulfamethoxazole/trimethoprim,* 1 or 2 tablets bid bid, Twice daily; tid, three times daily; qid, four times daily. *Contraindicated for use near term in pregnancy. †Serious infections require parenteral antibiotics. ‡Contraindicated during pregnancy and lactation.

pyuria (leukocyte esterase) or bacteria (nitrites) on urine dipstick test suggest UTI. Under ideal conditions, microscopic confirmation of pyuria and culture of organisms from a clean urine specimen are still the best methods for confirming the diagnosis and assessing the antibiotic sensitivity of etiologic bacteria. Management of UTIs includes both prophylactic and therapeutic measures. Women should drink at least six to eight glasses (48 to 64 oz) of noncarbonated fluid per day. Under dehydrating conditions, sufficient fluid should be ingested to generate voiding at least every 3 to 4 hours while awake.[116] [145] Women should void when the urge arises or on a regular schedule and not risk bladder overdistention. They should be reminded to wipe from front to back after urination and defecation and to void after sexual intercourse. Treatment of symptomatic cystitis usually requires a 3- to 7-day course of antibiotics ( Table 75-3 ). [73] Treatment of pyelonephritis usually requires a 10- to 14-day course of oral therapy or, when indicated, parenteral antibiotics until symptoms have resolved for 24 hours, followed by oral therapy to complete the 10 to 14 days.[136] Recurrent cystitis should be treated for longer than 3 days, and prophylactic therapy should be considered on an ongoing basis or after precipitating events such as coitus. Persistent problems eventually warrant urologic evaluation.[43] Pregnant women often require longer courses of therapy; pyelonephritis in pregnancy warrants suppressive therapy throughout gestation.

MENSTRUATION Normal Cycle Menstrual cycle disturbances are among the most frequent indications for which women seek medical care. Among highly trained female athletes and in environments that impose extreme physical and psychologic demands, such disturbances can be found in as many as 50% of women not taking OCs. Understanding bleeding abnormalities requires a basic understanding of the normal menstrual cycle ( Figure 75-1 ). Normal cycles occur at regular intervals, require ovulation, and typically average 28 days (range 21 to 35 days). By convention the first day of the menstrual cycle corresponds to the first day of the menstrual period, which usually lasts about 4 days (range 3 to 7 days). The onset of menstrual bleeding represents desquamation of the functional endometrium, resulting from progesterone withdrawal in the absence of conception during the previous cycle, and coincides with recruitment of a new group of primordial follicles for maturation. The first stage of the menstrual cycle, up to the time of ovulation, is referred to as the follicular phase, or endometrial proliferative phase. The second stage is the luteal phase, or endometrial secretory phase. Follicular recruitment depends on the presence of follicle-stimulating hormone (FSH) released from the pituitary as the consequence of pulsatile release of GnRH by the hypothalamus.[46] [124] FSH stimulates transformation of a primordial follicle into a primary follicle with a primary oocyte surrounded by a layer of granulosa cells.[88] Under the mitogenic influence of FSH, granulosa cells replicate to several layers, producing the secondary or preantral follicle. The granulosa cell layer is surrounded by a basement membrane that provides clear separation from the stromal theca cells. The theca cells are the primary source of androgens, predominantly androstenedione and testosterone, which are converted to the estrogens estrone and estradiol, respectively, by aromatization in the granulosa cells, an event also stimulated by FSH. Estrogens in turn enhance production of their own receptors and receptors for FSH, further stimulating granulosa cell division, aromatase activity, and more estrogen production.

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Figure 75-1 Normal human ovarian and endometrial (menstrual) cycle. (Modified from Shaw ST Jr, Roche PC: Menstruation. In Finn CA, editor: Oxford reviews of reproduction and endocrinology, vol 2, Oxford, UK, 1980, Oxford University Press.)

With adequate estrogen the follicle secretes and accumulates fluid, displacing the oocyte and surrounding granulosa cells eccentrically, forming the tertiary (antral) or mature follicle.[108] Without sufficient estrogen, androgens arrest maturation of the follicle at the preantral stage and promote its atresia.[66] In addition to their mitogenic and aromatase-enhancing effects, estrogen and FSH stimulate production of receptors for luteinizing hormone (LH) on the theca cells and on the granulosa cells in the late follicular phase. LH, which is also released from the pituitary in response to pulsatile hypothalamic GnRH, stimulates uptake of cholesterol, a primary precursor of androgens, by the theca cells and is essential for adequate estrogen production. Significant expression of LH receptor on the granulosa cells is not achieved until late in the follicular phase and prepares the dominant follicle to respond to a midcycle surge in release of LH from the pituitary and the subsequent rupture of the follicle and release of the oocyte (ovulation). The

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events leading up to ovulation itself are complex.[80] [89] [160] Elevated circulating levels of estrogen, predominantly estradiol, trigger release of both LH and FSH by direct effect on the pituitary, with a rapid drop in circulating estrogen. This event precedes ovulation by 26 to 32 hours, resulting in resumption of meiosis by the oocyte and weakening of the follicular wall. The preovulatory presence of sufficient LH receptors on the granulosa cell is essential for their next steroidogenic role, the production of progesterone, in the second phase of the menstrual cycle. Their readiness for this role is anticipated by the rise in production of 17-hydoxyprogesterone (17-OHP) just before ovulation. [128] After ovulation, LH stimulates 3ß-hydroxysteroid dehydrogenase activity, resulting in production of progesterone from cholesterol-derived pregnenolone at the ovulatory site, now the corpus luteum (CL). This luteinization results in progesterone production that peaks 7 to 8 days after ovulation. Progesterone induces the secretory phase of endometrial development, preparing for implantation of the embryo. With conception and the production of adequate human chorionic gonadotropin (hCG) by embryonic trophoblasts, the CL persists, enlarges, and increases its production of progesterone and estrogen.[2] With no conception the CL loses its sensitivity to LH and FSH, degenerates (luteolysis), and decreases production of progesterone and estrogen.[101] Without hormonal support the functional endometrium degenerates and is again shed with menstruation. The drop in these hormones is also a signal to resume release of FSH and LH from the pituitary with recruitment of more follicles. In normal menstrual cycles the luteal phase (from ovulation to menses) is 14 days (± 2 days). Although the primary feedback loop for production of reproductive hormones is directly between ovary and pituitary, the hypothalamus plays an integral role in maintaining responsiveness of the pituitary by the pulsatile release of GnRH. Pulsatility maintains pituitary GnRH receptors. Loss of pulsatility results in down-regulation of these receptors, with inhibited secretion of FSH and LH. The pulse generator for the rhythmic release of GnRH is located in the arcuate nucleus of the hypothalamus.[32] It is influenced by numerous neurotransmitters and steroid hormones. During the menstrual cycle, pulsatile release of GnRH occurs hourly during the follicular phase and every hour and a half during the luteal phase. Factors that disrupt the normal pulsatile release of GnRH or reduce the ability of the pituitary to respond to it are the major contributors to menstrual cycle abnormalities in premenopausal women.[24] Abnormal Uterine Bleeding Abnormal uterine bleeding (AUB) can be loosely defined as any aberration in the normal menstrual bleeding pattern in premenopausal women and as any bleeding episode in postmenopausal women. The most common causes of AUB are problems related to pregnancy and hormonal contraceptive therapy. Initial evaluation of AUB in any premenopausal woman includes a urine or serum screen for hCG, regardless of contraceptive history. Nonpregnancy-related causes of abnormal bleeding can be divided into episodes in ovulatory women, in anovulatory women, and from extrauterine causes, either ovulatory or anovulatory. Historical information is useful in developing a presumptive etiology and empiric therapeutic approach for AUB, particularly in the absence of laboratory resources. Past history includes age at onset of menses, regularity of menses, usual length of period and blood flow, perimenstrual symptoms, medical problems, pregnancy history, STI history, surgical history, and basic endocrinologic review of systems. [72] The current problem is then characterized by changes in the frequency of bleeding, amount of flow, new symptoms, relationship to activities, recent sexual history, systemic symptoms, weight change, change in medications or use of other health-related products, and change in exercise patterns. Ovulatory Women.

When the premenopausal woman who has consistently had regular cyclic menses presents with a history of progressively increasing amount and duration of menstrual flow, the most common causes are uterine fibroids, particularly submucosal (just beneath the endometrium) fibroids, endometriosis, and adenomyosis (endometriosis of the uterine muscle wall). These conditions are frequently associated with progressive dysmenorrhea and are more likely to occur with advancing age. Occasionally an endometrial polyp or IUD, either of which can be accompanied by endometritis, results in a similar presentation. The use of certain medications (e.g., estrogens, warfarin, non-steroidal antiinflammatory drugs [NSAIDs]) or homeopathic compounds should always be part of the evaluation of AUB, as well as clues to an acquired blood dyscrasia such as idiopathic thrombocytopenic purpura or leukemia. Otherwise healthy women with a history of heavy menstrual bleeding from the time of

menarche should be evaluated for inborn coagulation disorders, most often von Willebrand's disease. An abrupt change in the duration or amount of blood flow should suggest a corpus luteal cyst, often associated with unilateral lower abdominal discomfort, or acute PID, often accompanied by more diffuse abdominal pain and systemic symptoms. Hyperplasia of the endometrium is unusual in ovulating women, and malignancies of the uterus or ovaries (estrogen secreting) are rare. Perimenopausal women who are still ovulatory may have progressively more periods, which may be accompanied by changes in flow and duration, with or without the underlying causes noted. A regularly cyclic woman with intermenstrual or postcoital bleeding should also be evaluated for cervicovaginal

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infections, such as BV, yeast, Trichomonas, and condylomata. Endocervical polyps, cervical dysplasia, and even invasive cervical carcinoma can occur in this group. When precipitated by coitus, profuse bleeding and dyspareunia can result. Acute pelvic or abdominal pain that accompanies bleeding with coitus should suggest penetrating trauma, an uncommon but potentially life-threatening emergency. Acute pain with coitus and not usually accompanied by bleeding is more likely to be the result of PID, rupture of an ovarian cyst, or torsion of the adnexa. A clear history and the supportive physical findings limit the differential diagnosis and therapy, although codependent conditions may be present. A synergistic relationship between bleeding and infection is often found in women with prolonged bleeding or short intervals between bleeding episodes. Endometritis can develop from loss of protective cervical mucus and ascending infection by pathogenic organisms that have proliferated in a more alkaline (blood-induced) vaginal environment. Endometritis in turn can precipitate heavier, more frequent, and more symptomatic bleeding. Unfortunately, many women with AUB first present for medical care at this stage. Unless they have been attentive to abnormalities from the onset, a diagnosis based on history alone is difficult. For example, an ovulatory woman with menorrhagia from uterine fibroids may suddenly develop intermenstrual bleeding (from the fibroids or endometritis), which is difficult to distinguish from accompanying chronic anovulation. Anovulatory Women.

Anovulatory AUB is more common than ovulatory abnormalities among women who partake in wilderness experiences. Anovulatory bleeding problems can be divided into those occurring with adequate estrogen production and those accompanied by low estrogen production. The former, often characterized by hypersecretion of gonadotropins and frequent heavy bleeding, is usually seen in women with polycystic ovary syndrome (PCOS). In contrast, anovulation in the absence of normal estrogen production usually results from inadequate release of gonadotropins from the pituitary, often presents with complete amenorrhea, and may result from physical conditioning. Hypoestrogenism can have significant effects on a woman's participation in strenuous wilderness experiences. Female Athletic Triad.

The American College of Sports Medicine first coined the term female athletic triad in 1992, but the interrelated components of the triad—disordered eating, amenorrhea, and osteoporosis—had been recognized for many years.[117] The disorder usually begins with either weight control for participation in activities that emphasize physical appearance, such as cheerleading and dance, or weight loss precipitated by excessive exercise without sufficient caloric or nutritional intake. The eating disorder may evolve into frank anorexia or bulimia and may worsen with starvation, limited variety of nutritional intake, overeating and purging (vomiting, laxatives, enemas), and use of diet pills, appetite suppressants, and diuretics.[36] Unless the syndrome begins before menarche, as usually occurs in female gymnasts or ballet dancers, it is usually preceded by menstrual irregularity before frank amenorrhea. Prolonged amenorrhea usually signals inadequate ovarian estrogen production secondary to deficient gonadotropin secretion. Since estrogen plays an integral role in promoting bone growth, loss of bone density (osteoporosis) can evolve rapidly at this point, particularly if the diet is also deficient in the minerals and vitamins necessary for skeletal integrity and if the exercise program is vigorous. Skeletal stress accompanying physical exertion is usually characterized by high rates of bone turnover. The consequences of the triad range from impaired performance to life-threatening conditions. Electrolyte imbalances, vitamin and mineral deficiencies, and loss of bone and muscle mass result in loss of strength and endurance. This sets the stage for multiple or recurrent stress fractures and major musculoskeletal injury. Reduced net bone formation can result in failure to achieve optimal growth and peak bone mass, scoliosis, and increased risk for serious osteoporotic complications later in life. Electrolyte imbalances, combined with weight-reducing drugs, can result in lethal arrhythmias and cardiomyopathies. Depression, coupled with an uncompromising and distorted body image, may lead to suicide attempts. Management of young women with the female athletic triad may be difficult because many of its characteristics are valued and encouraged in the athlete: competitive nature, high self-expectations, obsessive-compulsive or perfectionist tendencies, and self-critical attitudes. The woman must understand the balance between healthy and unhealthy expression of these characteristics in terms of her goals, current well-being, and long-term health consequences. Those at risk for the triad can often be identified by a vigilant health care provider or physical trainer and offered help before full manifestation of the condition.[40] Unfortunately, the condition often goes unrecognized or is ignored until a serious complication has occurred and mandates intervention. Physically active women and individuals involved in their training and health care should be educated about the female athletic triad. Athletic training should include ongoing assessment of weight, growth, and menstrual history. Women involved in high-risk activities, such as dancing, figure skating, gymnastics, and running, should be considered for baseline and periodic assessment of bone density. [19]

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The steps in reversing the condition include temporary reduction in exercise, increased and balanced caloric intake, and a diet rich in calcium (1200 to 1500 mg/day) and vitamins. Counseling should be offered to deal with obstacles to physical and long-term rehabilitation. To reduce their risk of skeletal injury, amenorrheic women with osteoporosis who are unwilling to reduce their physical activity should receive nutritional counseling and hormonal replacement therapy at levels currently recommended to treat postmenopausal women.[34] Recent studies have indicated that the bis-phosphonates, such as alendronate (5 to 10 mg daily), and to a lesser degree, selective estrogen receptor modulators (SERMs), such as raloxifene (30 to 150 mg daily), can improve bone density and decrease fracture risks in women not receiving estrogen replacement therapy.[37] [42] Wilderness Risks.

The major risks of AUB to the wilderness participant depend on the etiology, severity, and chronicity of the process. Heavy and prolonged bleeding can result in significant blood loss, chronic iron deficiency, and infectious morbidity. These can impair endurance, prolong acclimatization, particularly at altitude, and increase susceptibility to acute cardiopulmonary decompensation. As an aesthetic measure, efforts should be made to maintain personal hygiene, thoroughly wash or not wear bloody clothing, and either store tampons or sanitary napkins in sealed containers or dispose of them away from camp and supply sites. There is no evidence that menstrual blood is an olfactory attractant to bears and sharks. In amenorrheic hypoestrogenized women, nutritional deficiency and osteoporosis can result in impaired endurance and prolonged acclimatization, susceptibility to acute deterioration in electrolyte status, particularly in high temperature and humid or aquatic environments, cardiac decompensation, and complicated musculoskeletal injury at exertional levels below the threshold expected by training.

PREGNANCY AND CHILDBIRTH Pregnancy is considered a relative contraindication to wilderness activities unless access to medical care is available in the field or provisions are made for rapid evacuation. Even though prior pregnancy experience is a relatively good predictor of outcome after the first trimester, pregnancy is still characterized by its unpredictability. No interval during pregnancy is considered absolutely safe. Mortality rates are currently less than eight per 100,000 live births. Many women with infertility and "high-risk" medical problems (e.g., diabetes, hypertension, autoimmune disorders) are conceiving and carrying pregnancies to viability. These women have become more active wilderness participants, appreciating the benefits of regular exercise in their medical management. Women with chronic medical conditions should discuss the potential consequences of pregnancy in a wilderness setting with their health care providers. Physiologic Changes Accompanying Pregnancy Hormonal changes accompanying pregnancy result in physiologic adaptations affecting every organ system within weeks of conception. For example, progesterone has smooth muscle relaxation effects that help to maintain uterine quiescence, but these also contribute to vasomotor instability, hypotension, gastric reflux, and constipation. Estrogens stimulate hepatic production of many hormone binding globulins and of coagulation factors II, V, VII, VIII, IX, X, XII, and fibrinogen, which contribute to the hypercoagulable state of pregnancy. Both estrogen and progesterone stimulate rapid uterine hypertrophy, as well as pancreatic ß-cell hyperplasia that leads to hyperinsulinemia, increased peripheral glucose utilization, and susceptibility to hypoglycemia in early pregnancy. During pregnancy, cardiac output increases 30% to 50%, much by the end of the first trimester, from an increase in stroke volume secondary to an increase in preload. The balance comes from a gradual increase in maternal heart rate that usually peaks between 24 and 28 weeks' gestation. Uterine blood flow increases from 50 to more than 500 ml/min, corresponding to an increase from about 1% to 15% to 20% of total cardiac output. Systemic vascular resistance (SVR) decreases, primarily from the low-resistance placental vascular bed, the equivalent of a large arteriovenous shunt, and also from the peripheral vasodilatory effects of progesterone, estrogen, and other factors. Decreased SVR is reflected by a fall in MAP, with a nadir in the midtrimester. Without this midtrimester pressure drop, placental abnormalities may be manifested later in pregnancy as fetal growth restriction and preeclampsia. Because of the dramatic hemodynamic changes, women with known or unrecognized cardiovascular disease may decompensate under the stress of pregnancy. This is particularly true during labor and in the immediate postpartum period, when cardiac output can increase an additional 20% to 60% because of exertion, pain, and fear. Sudden increases in SVR and intravascular volume resulting from uterine involution and autotransfusion immediately after delivery place further demands on the cardiovascular system. Healthy women who regularly participate in moderate exercise during pregnancy are usually able to meet cardiovascular demands. The benefits of regular exercise outweigh the risks, except in women who have predisposing risk factors or contraindications, such as incompetent cervix; history of preterm labor, delivery, or premature rupture of membranes; bleeding; cardiac

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disease; or preeclampsia.[11] Because of the incursions on cardiac reserves demanded by the pregnancy, however, even well-conditioned athletes have limits on strenuous activity.[74] [82] Exceeding this limit could have deleterious effects on fetal status because of decreased uterine perfusion, increased uterine contractions, maternal acidosis, and hypoglycemia. [12] [143] Total blood volume increases 40% to 50% during normal pregnancy, most during the first half of pregnancy, from a rapid expansion of plasma volume. Plasma volume peaks at about 32 weeks' gestation, despite high levels of renin, angiotensin, and aldosterone, findings usually associated with hypertension and decreased intravascular volume in the nonpregnant state. The compensatory mechanism appears to be pregnancy-related refractoriness to the vasoconstrictor effects of angiotensin II, an effect mediated by progesterone, perhaps placental-derived prostaglandins, and atrial natriuretic peptide. By 20 weeks' gestation, in response to an increase in plasma erythropoietin, red cell mass continues to expand until term and eventually reaches levels one-third higher than in the nonpregnant state. A disproportionate increase in plasma volume over red cell mass results in the so-called physiologic anemia of pregnancy. Fetal demands in the second half of pregnancy are an additional drain on iron stores and often produce true iron deficiency. Trained athletes may be at greater risk for this because of iron losses from mechanical hemolysis, intestinal bleeding, hematuria, sweating, low intake, or poor intestinal absorption.[33] Respiratory system changes in normal pregnancy more than compensate for the physiologic anemia to maintain fetal and maternal homeostasis. Progesterone directly stimulates the respiratory center and increases its sensitivity to CO2 , resulting in a 30% to 40% increase in tidal volume (TV). Respiratory rate (RR) does not change significantly, but as a result of TV changes, minute ventilation (TV × RR) increases 25% to 30%, despite a slight decrease in total lung capacity. A 20% reduction of functional residual capacity, resulting from decreases in both expiratory reserve volume and residual volume, completes the picture of relative hyperventilation with a compensated respiratory alkalosis. Many of these changes are completed by the end of the first trimester; their sum is a dramatic 50% increase in alveolar ventilation, increased PaO2 , 30% increase in minute O2 uptake, and significant decrease in PCO2 . The overall effect is to increase the O2 -carrying capacity of maternal blood to accommodate fetal and maternal metabolic needs, while facilitating diffusion of CO2 from the fetus. For the wilderness traveler, these changes lead to higher O2 saturation under hypoxic conditions, such as at altitude. Significant changes in the urinary system account for many of the complaints and complications of pregnancy. Beginning in the first trimester, the ureters become dilated, elongated, and more tortuous, presumably under the influence of progesterone. Further dilation of the proximal ureters occurs when the uterus reaches the level of the pelvic brim at about 20 weeks' gestation and compresses the ureters. Frequently at this stage, women present for the first time with pyelonephritis, more often on the right than on the left due to dextrorotation of the uterus by the descending colon. Contributing to the risk of upper tract infection, vesicoureteral reflux occurs secondary to decreased competency of the ureterovesical junction. This is exacerbated by a progressive decrease in bladder capacity and doubling of intravesicular pressures (from 10 to 20 cm H2 O) during gestation. These factors also contribute to frequent complaints of urinary incontinence that plague pregnant women. Integumentary and musculoskeletal changes can have a significant impact on the well-being of the pregnant wilderness traveler. Under the influence of estrogen, proliferation and dilation of small arterioles in the skin helps to compensate for increased demands to remove heat generated by maternal and fetal metabolism. Because of these inherent changes, pregnant women have a limited capacity to respond further to heat stress and are at increased risk for hyperthermia in hot and humid environments. Estrogen and other pregnancy-associated hormones also increase sensitivity of the skin to damage by sun exposure, particularly in fair-skinned individuals, and to the risk of pyogenic granulomata of extremities and gums resulting from trauma and inflammation. Some pregnant women have a predisposition to develop skin hyperpigmentation in a nonuniform distribution because of excessive melanin deposition in the dermis and epidermis. This is enhanced by sun exposure; often affects the face (melasma), midline abdomen (linea nigra), nipples, axillae, and perineum; and may require a prolonged period for resolution after delivery. It may never resolve completely. Striae gravidarum, or "stretch marks," may be the most notorious superficial effects of pregnancy. These result from breaks in dermal collagen and frequently occur on the abdomen, buttocks, thighs, and breasts. Striae are not necessarily associated with skin stretching and may be found before significant uterine growth or weight gain has occurred, reflecting their underlying hormonal basis. Hair loss during pregnancy, as well as nail brittleness and loss of adhesiveness between the nail and nail bed, may also increase the risk of sun exposure and trauma, respectively, for the pregnant wilderness traveler. Weight gain, weight redistribution, and ligamentous relaxation may pose the greatest risks, even to the well-conditioned pregnant woman.[6] Overall weight gain during pregnancy is usually about 20 to 35 pounds. Some weight gain is important during pregnancy to

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avoid a catabolic state and may be more important to the highly conditioned athlete who enters pregnancy with limited fat stores. This weight increases stress on the weight-bearing skeleton and ligaments throughout the body and may accumulate more rapidly than conditioning can handle. Much of the weight gain is contributed by uterine and fetal growth, resulting in forward displacement of the center of gravity. This is usually accompanied by progressive lordosis of the lower spine and increased strain on spinal ligaments, disks, and paravertebral muscles. When lumbar lordosis is exaggerated, traction and compression on the sciatic nerves can cause

significant pain and weakness in the buttocks and lower extremities. Changes in the lower spine are frequently followed by compensatory flexion of the cervical spine. This in turn can place traction on the median and ulnar nerves, resulting in pain, paresthesias, and weakness of the upper extremities. The challenges of weight gain are accompanied by dramatic changes in ligamentous support throughout the body. Under the influence of relaxin and other hormones, ligaments become more compliant and hydrophilic. Benefits of this include relaxation in the sacroiliac joints and symphysis pubis to facilitate delivery, but hormonal effects on other ligaments can lead to complications. For example, fluid retention by the flexor retinaculum in the wrist can cause compression of the median nerve, resulting in carpal tunnel syndrome, a common complaint of pregnancy. This may be more than just a nuisance to the wilderness traveler, because pain and hand weakness can compromise activities, such as climbing and canoeing, that require hand strength and endurance. Even more troublesome, pelvic girdle instability, accompanied by weight gain, shift in center of gravity, and spinal lordosis, usually leads to gait and balance disturbances. These not only predispose to more frequent falls during pregnancy under far less strenuous conditions than those encountered in many wilderness settings, but also lead to an increase in the severity of trauma accompanying these falls. The anterior cruciate ligament is especially prone to severe trauma, accounts for 3 to 4 times more injuries in women than men, and is especially susceptible to trauma in the active pregnant woman.[166] Difficult terrain also poses a risk to the pregnant wilderness traveler. Unless there are other medical or pregnancy-related contraindications (e.g., risk for premature labor, incompetent cervix, multiple gestation, bleeding), exercise and specialized training should be encouraged throughout pregnancy, taking precautions to avoid prolonged exposure to extremes in temperature, dehydration, hypoglycemia, prolonged anaerobic conditions, and excessive skeletal stress.[79] [147] Active and physically fit women tolerate labor better than inactive women. A program specifically designed for pregnant women, including exercises to strengthen the abdominal and back muscles, and careful attention to posture may reduce the risks related to changes in skeletal support. Wilderness Participation.

Pregnant women are more susceptible to altitude sickness, more likely to develop severe symptoms, and may require longer periods of adjustment before exertional activities can be undertaken. Gradual progression to higher altitudes and limited activity until completely comfortable will minimize symptoms and allow for fetal compensation. A pregnant woman must maintain adequate fluid intake throughout this process, since reduced O2 saturation combined with decreased uterine perfusion secondary to dehydration could endanger the fetus. Depending on the altitude, gestational age, maternal Hgb levels, and degree of training, even the well-acclimated pregnant woman may find that endurance and ability to participate in strenuous activity at altitude are limited.[13] When a trip is planned, frequent rest periods should be scheduled. A higher incidence of preeclampsia and fetal growth restriction has been found among women at higher elevations and may reflect the limits of the placenta and fetus to extract O2 even from well-conditioned individuals.[119] [171] Although swimming is considered an excellent form of exercise for pregnant women, scuba diving is potentially hazardous. The fetus is at risk from nitrogen bubbles in the fetal-placental circulation during decompression on ascent. Most authorities consider pregnancy a contraindication to diving.[23] Diving is compromised by increased abdominal girth, difficulty breathing due to engorgement of the mucous membranes of the nose and oropharynx, and increased buoyancy secondary to fat deposition. Higher levels of body fat also increase the risk of decompression sickness, since nitrogen tends to be retained in these tissues. Dyspnea may be exaggerated and lead to panic, even in the experienced diver who is pregnant. [113] As with exertion at high altitude, the pregnant woman may have limited ability to maintain anaerobic metabolism for prolonged periods because of fetal needs. The pregnant woman should also limit prolonged nondiving immersion in cold water that might lead to hypoventilation and hypothermia. Acclimation to environments characterized by high temperatures, particularly with high humidity, may be especially difficult for the pregnant woman and even dangerous to the fetus. Hyperthermia has been shown to be teratogenic in various animal models and a higher incidence of birth defects, particularly neural tube defects, have been found among offspring of women who experienced hyperthermia by environmental exposure or febrile illness in the first trimester.[132] 210 Later in pregnancy the fetus depends on the woman to eliminate excess heat. Elevation of ambient temperature decreases

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the heat gradient and the ability of the pregnant woman to dissipate heat. Elevated humidity exacerbates this situation by decreasing the contribution of perspiration to heat loss. This increases the risk of elevated maternal core temperature, which further raises fetal metabolic activity and heat generation. Hyperthermia increases the risk of premature labor, particularly with dehydration and loss of electrolytes. Fetal stress, resulting from decreased uterine perfusion secondary to compensatory peripheral vasodilation and depletion of intravascular volume, further increases the likelihood of preterm labor. Preparation for Pregnancy The woman who is pregnant and plans to participate in wilderness activities or who anticipates a wilderness delivery needs thorough medical evaluation and counseling before departure. The evaluation begins with the obstetric history and complications for which she is at high risk for recurrence, including preterm labor, premature rupture of membranes, preeclampsia, gestational diabetes, fetal growth restriction, group B ß-hemolytic streptococcal colonization, UTIs, chorioamnionitis, blood group isoimmunization, thromboembolic events, surgical delivery, and postdelivery complications. A complete physical examination should be conducted. Laboratory evaluation before departure includes standard blood work recommended by the American College of Obstetricians and Gynecologists: complete blood count, blood type and antibody screen (and screen of partner if the woman is Rh negative or isoimmunized), and basic serology (rapid plasma reagin, rubella, hepatitis B, HIV). Serologic screening for HSV-2 should be considered in the woman with no history of genital herpes because of the potential for first-time outbreaks during pregnancy in women with unrecognized infection.[14] [104] Individuals at risk and those not previously evaluated should also be offered Hgb electrophoresis to assess for hemoglobinopathies. Urinalysis and urine culture are performed because of the high frequency of asymptomatic infections during pregnancy that complicate outcome. Vaginal fluid should be assessed for BV, since treatment early in pregnancy may prevent premature rupture of membranes and preterm labor. A Pap smear is often done as well. A woman beyond 15 weeks' gestation before departing should be offered biochemical screening (e.g., maternal serum a-fetoprotein, estriol, hCG) to assess for certain congenital and chromosomal abnormalities. Abnormal biochemical markers may indicate complications such as fetal growth restriction and preeclampsia, resulting primarily from early abnormalities in placentation that can become clinically significant later in gestation. These conditions also increase the risk for premature delivery, as well as for maternal and fetal morbidity and mortality. Since diabetes arises as a complication of the hormonal milieu in at least 3% of all pregnancies, routine screening is indicated in any woman who is not diabetic before pregnancy. Oral administration of a 50-g glucose challenge in the nonfasting state is usually done at 24 to 28 weeks' gestation, followed by a plasma glucose determination 1 hour later. Values of 140 mg/dl or greater (but less than 200 mg/dl) warrant further evaluation with a fasting 3-hour oral glucose tolerance test using a 100-g glucose challenge. If the fasting value before administration of the glucose load is 120 mg/dl or greater, or if the 1-hour challenge is 200 mg/dl or more, the woman is considered diabetic and should not have the 3-hour test done. Otherwise, values of 90 mg/dl or greater while fasting, 190 mg/dl or more at 1 hour, 165 mg/dl or greater at 2 hours, and 145 mg/dl or more at 3 hours are considered abnormal. Two abnormal values or persistent elevation of the fasting level indicate diabetes. If departure is planned before 24 to 28 weeks' gestation, the 1-hour challenge can be done using a portable plasma glucose meter. If the woman has significant risk factors (age 35 or older, obesity, family history, steroid use, PCOS, other endocrinopathy such as thyroid disease) the 1-hour and possibly the 3-hour tests should be administered early, regardless of gestational age.[100] If the woman had gestational diabetes with a previous pregnancy, it is best to assume she will have it again. Proper dietary counseling and regular blood sugar monitoring with a portable plasma glucose monitor should be conducted throughout the pregnancy. Insulin, sufficient syringes, and alcohol wipes should be included with the basic medical supplies in the event glycemic control deteriorates. The goal is to maintain fasting plasma glucose levels at 90 mg/dl or less and lower than 120 mg/dl 2 hours after meals. Physical conditioning reduces but does not eliminate the risk of developing diabetes during pregnancy. Women with pregestational diabetes of any duration should have a baseline ECG and possibly an echocardiogram before participation in any wilderness-related activities. The pregnant wilderness traveler should have an obstetric sonogram before departure for additional risk assessment. Early in the pregnancy, sonography can accurately confirm gestational age, viability, intrauterine location, and number of babies. It is also useful in ruling out the presence of an ectopic pregnancy, adnexal mass, or molar pregnancy that could lead to life-threatening complications. In midtrimester an ultrasound is useful not only in estimating gestational age, but also in determining the presence of major fetal abnormalities, the location of the placenta in relationship to the cervix, and the cervical length and integrity of the internal cervical os. Beyond 20 weeks' gestation, normal fetal growth and blood flow patterns in the umbilical and middle cerebral arteries can be assessed by

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Doppler velocimetry. Normal results indicate lower risk for complications, such as intrauterine growth restriction, preeclampsia, and preterm labor.[38] Any findings that significantly increase maternal or fetal risk are contraindications to elective wilderness travel during pregnancy.

Prolonged wilderness excursions during pregnancy, particularly those extending into late second and third trimesters, should include preparations for ongoing assessment and even emergency delivery. Routine antepartum care usually includes visits to a health care provider at least monthly until 26 to 28 weeks, every 2 weeks thereafter until 36 weeks, then weekly until delivery. Beyond the due date, more frequent visits are often recommended. Routine visits focus on uterine activity, vaginal discharge, abdominopelvic pain, bleeding, headaches, symptoms of UTI, current medications, and fetal activity. The basic antepartum examination includes measurements of blood pressure, weight, and uterine size (height of uterine fundus above symphysis) and subjective assessments of peripheral edema and reflexes. Urine is tested at each visit with a multitest strip that provides estimates of glycosuria, proteinuria, pH, and presence of nitrites. For the wilderness traveler, elevated pH and presence of nitrites may be associated with UTIs under circumstances that might preclude culture capabilities.[156] In Rh-negative women with Rh-positive partners the antibody screen is often repeated at 26 to 28 weeks, before the administration of Rh-immune globulin for prophylaxis against third-trimester sensitization. If an antibody screen cannot be done, Rh-immune globulin should be administered empirically. Maternal Hgb and Hct are frequently done in each trimester to assess need for iron supplementation. Since many women require supplemental iron during pregnancy, this should be taken prophylactically under circumstances that obviate determination of Hgb levels, unless the woman has a contraindication, such as hemochromatosis. Basic supplies for the pregnant wilderness traveler might include a diary to record progress, reminders of scheduled testing, and complications; tape measure; stethoscope; sphygmomanometer; urine test strips; and prenatal vitamins and iron. Other supplies include a glucometer with test strips, Rh-immune globulin, a calcium supplement, and basic medications for the most common pregnancy complaints: an antiemetic such as promethazine, prochlorperazine, or chlorpromazine for nausea and vomiting; acetaminophen for headaches and pain; stool softener for constipation; and antibiotics to cover UTIs and vaginitis. In addition to the basic medical supplies, the pregnant woman should have changes in clothing size and possibly shoe size. When delivery in the wilderness is planned or a strong possibility, special preparations need to be made ( Box 75-4 ).

Box 75-4. SUPPLIES FOR MANAGEMENT OF WILDERNESS DELIVERY

STANDARD Clean towels Surgical sponges Surgical gloves Umbilical cord clamps Suction bulb Suture kit Scalpel Scissors Syringes and needles Local anesthetic Injectable oxytocin Injectable and oral methylergonovine Oral analgesics (e.g., ibuprofen, acetaminophen with codeine) Oral broad-spectrum antibiotic Sanitary napkins

OPTIONAL Injectable magnesium sulfate Intravenous fluids and administration supplies Injectable narcotic Naloxone Misoprostol Prostaglandin F2a Injectable antibiotic Neonatal mask and Ambu bag

Complications Miscarriage.

Women who are pregnant or become pregnant for the first time while in the wilderness are at high risk for complications. Approximately 15% to 25% of all pregnancies abort spontaneously during the first trimester, and this number may exceed 60% to 70% in the true primigravida.[134] Reasons may be related to immunologic naivete to paternal antigens expressed by the fetal tissues. In contrast, isolated miscarriages in women who have successfully carried pregnancies are often the result of chromosomal abnormalities. Pending miscarriage in the first trimester is usually preceded by embryonic demise and accompanied by a reduction or loss in early pregnancy-related symptoms, such as breast tenderness and nausea. Bleeding and uterine contractions eventually occur and accompany expulsion of the products of conception. Under most circumstances, hemorrhage during miscarriage is self-limited and not life-threatening but at times can be heavy, especially if fetal death does not precede the event and occurs late in the first trimester or during the second trimester, or if the expulsion process is prolonged or incomplete. Spontaneous abortion after the first trimester is

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much riskier but less common. It also can result from chromosomal abnormalities or fetal anomalies but is more likely to be caused by chorioamnionitis, UTIs, severe abnormalities of placentation, poorly controlled maternal medical conditions, or cervical incompetence. Any acute and significant blood loss in a physiologically hostile environment can compromise the endurance of the most highly trained individual. Under wilderness conditions, control of significant maternal hemorrhage accompanying miscarriage may be difficult unless provisions, facilities, and medicinal supplies are available. Uterine curettage is the method most often used to complete evacuation of the uterus when medical facilities are available. Once empty, uterine involution, spontaneous or aided by uterine massage, is usually sufficient to impede bleeding from the implantation site. In the absence of the ability to perform curettage, treatment with methylergonovine (0.2 mg orally or intramuscularly) can enhance uterine contractions, accelerate expulsion of products of conception, and promote uterine involution to maintain hemostasis. Methylergonovine should not be used in patients with hypertensive disorders, underlying vascular disease, and certain cardiac abnormalities unless the benefits clearly outweigh the risks of acute generalized vasoconstriction. As an alternative, prostaglandin F2a (250 µg intramuscularly) or misoprostol (100 µg orally or vaginally) can be administered with less risk of cardiovascular compromise. Ectopic Pregnancy.

Far more dangerous than miscarriage, ectopic pregnancy must always be considered a life-threatening emergency that requires immediate medical attention. Ectopic pregnancy refers to implantation at any location outside the uterine cavity, most often (more than 95%) the fallopian tube. Hemorrhage resulting from ectopic pregnancy is still the leading cause of death in the first trimester. The incidence of ectopic pregnancy has tripled over the past 30 years and now exceeds one of every 100 pregnancies.[121] This increase is directly proportional to the rise in incidence of acute and chronic PID. The most common predisposing risk factors include a history of infections, multiple sexual partners, early age of onset of sexual activity, delayed childbearing, and previous IUD use. Independent risk factors are a history of abdominal and tubal surgery, including previous tubal sterilization procedures, endometriosis, DES exposure, and pregnancy by assisted reproductive interventions. Regardless of the etiology, an ectopic pregnancy increases the risk for another ectopic pregnancy approximately tenfold. A woman with a history of ectopic pregnancy should not intentionally plan to conceive again in the wilderness and should have her intrauterine pregnancy confirmed sonographically before departure. Most women with a tubal ectopic pregnancy become symptomatic before 12 weeks' gestation and present with complaints of abdominal pain and altered menses. Early pregnancy symptoms may be minimal or absent. The pain often begins unilaterally with sudden onset and is usually severe, distinguishable from the cramping, intermittent pain accompanying miscarriage by its persistence and intensity. Clinical findings include a tender adnexal mass, nontender cervix, small to slightly enlarged nontender uterus, and absence of high-grade fever. Low-grade temperature elevation to 38° C (100.4° F) may occur in as many as 20% of women with ectopic pregnancy. When intraperitoneal hemorrhage accompanies rupture of the tube, the pain becomes diffuse with peritoneal signs of tenderness, guarding, and rebound. Shoulder pain from diaphragmatic irritation may be present as well. Pelvic examination at this point usually elicits discomfort with movement of the cervix and uterus. Fullness of the cul de sac posterior to the uterus and abdominal distention suggest significant intraperitoneal blood loss. Vaginal bleeding accompanying an ectopic pregnancy usually follows a variable period of amenorrhea. It often begins with minimal flow of blood darker than that seen during miscarriage and results from inadequate progestational support of the decidualized endometrium. Uterine cramping may ensue, with passage of organized clot and tissue in the form of a decidual cast resembling products of conception, leading to the mistaken diagnosis of spontaneous abortion. However, cessation of pain is typical with completion of miscarriage and quite atypical with passage of a decidual cast concurrent to an ectopic pregnancy. With rupture of an ectopic pregnancy, heavier, bright-red bleeding may occur vaginally and if accompanied by significant intraperitoneal hemorrhage, may rapidly result in hemodynamic decompensation that only can be controlled surgically. The differential diagnosis of ectopic pregnancy includes normal intrauterine pregnancy with a corpus luteal cyst or hemorrhagic corpus luteum, threatened or incomplete abortion, PID, adnexal torsion (usually associated with adnexal enlargement from a benign or neoplastic process), endometriosis, UTI or ureteral stone, degenerating fibroid, and appendicitis. Although simultaneous intrauterine and ectopic pregnancies were once considered to be extremely rare, the incidence is now estimated at one in 6000 in the general population and greater than one in 100 among recipients of assisted reproductive techniques. The diagnosis of ectopic pregnancy is considered presumptively in any woman with a positive pregnancy test, abnormal bleeding, and abdominal pain. In a full-service medical care facility the first step in management is to assess serum hCG levels and ascertain location of the pregnancy. An intrauterine pregnancy can usually be confirmed by transvaginal sonography once the serum hCG exceeds 1000 mIU/ml, corresponding

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to 2 to 3 weeks after conception or 4 to 5 weeks from the last normal menstrual period (LMP). In contrast, absence of an intrauterine pregnancy at hCG levels of 1000 mIU/ml or greater suggests ectopic pregnancy. In the absence of sonography, serum progesterone level greater than 25 ng/ml indicates a viable intrauterine pregnancy, greatly reducing the chance of an ectopic pregnancy.[149] Progesterone level less than 25 ng/ml is not diagnostic under these circumstances because it cannot differentiate nonviable intrauterine pregnancy from ectopic pregnancy. In a wilderness setting that precludes the ability to perform a sonogram and quantitative determinations of hCG and progesterone, plans for evacuation must be made at first suspicion of the diagnosis. In extraordinary circumstances when the diagnosis is questionable, evacuation is not readily possible, and an experienced health care provider is available, the only technique that might offer some reassurance is culdocentesis. Needle aspiration of serous fluid from the posterior cul de sac argues against but does not exclude an ectopic pregnancy, since more than 75% of symptomatic cases with an ectopic pregnancy will have some degree of intraperitoneal hemorrhage. The presence of nonclotting blood confirms intraperitoneal hemorrhage and in approximately 95% of cases indicates ectopic pregnancy. The remainder usually result from bleeding of the corpus luteum. Treatment options for ectopic pregnancy are not usually available in the wilderness. In the past, management of ectopic pregnancy has been exclusively surgical. Once an ectopic pregnancy is symptomatic, and when peritoneal signs or evidence of hemodynamic instability are present, laparoscopic or open abdominal procedures are still necessary. In recent years, however, medical therapy with methotrexate has proved useful in management of early, unruptured ectopic pregnancies.[148] Women with known risk factors who are attempting to become pregnant are encouraged to be followed proactively. They can often have the diagnosis of ectopic pregnancy confirmed by hCG and transvaginal sonography within 35 days from the LMP and before significant symptoms and tubal rupture. If the adnexal mass is less than 4 cm and the patient is minimally symptomatic and hemodynamically stable, single-dose methotrexate therapy (50 mg/m2 intramuscularly) is effective and reduces the need for surgical intervention, thereby maximizing the opportunity for preservation of the fallopian tube. The quantitative hCG is followed serially until undetectable. If there is a slow fall or plateau in hCG levels and the woman is still stable, the dose can be repeated, usually no sooner than 1 week after the initial dose. Methotrexate is less likely to be effective when the ectopic mass is more than 4 cm, there is fetal cardiac activity, the woman is symptomatic, or significant free peritoneal fluid is present. Methotrexate is contraindicated when the woman is hemodynamically unstable, has active pulmonary disease, or is not willing to return for follow-up.

Box 75-5. LATER COMPLICATIONS OF PREGNANCY REQUIRING EVACUATION Placenta previa Placental abruption Preterm labor Premature rupture of membranes Chorioamnionitis Preeclampsia/eclampsia/HELLP syndrome

HELLP, Hemolysis, elevated liver function enzymes, and low platelets.

Later Pregnancy.

Common conditions that do not cause problems until 20 weeks' gestation or later cannot be optimally managed in most wilderness settings ( Box 75-5 ). The safest course of action is to make plans for immediate evacuation. Second- and third-trimester bleeding could simply be the result of cervical effacement, labor, cervical polyps, coital trauma, or vaginitis, but it could also be much more dangerous if the source is placenta previa or placental abruption. Historical information and physical findings may suggest an etiology, but a definitive diagnosis is not possible without verification. PLACENTA PREVIA.

When evaluating bleeding, placenta previa always must be given primary consideration. Placenta previa results from implantation of the placenta in the lower uterine segment over or near the internal cervical os. It occurs in approximately one of 200 births. Risk increases with age and parity, multiple gestations, women who have submucosal fibroids or have had multiple dilation and curettage procedures (D&Cs) or cesarean sections, and in cigarette smokers.[1] [65] The classic presentation of placenta previa is painless, sudden, heavy, and bright-red vaginal bleeding.[17] It may occur with exertional activity, straining on the toilet, or intercourse but also occurs at rest with no obvious precipitating factor. Many women report awakening at night in a pool of blood as the initial manifestation of a placenta previa, probably the result of stretching of the lower uterine segment and implantation site by a bladder that has become distended while sleeping. Uterine contractions may accompany the bleeding and may be the precipitating cause if they have been significant enough to initiate cervical effacement. Physical examination is limited until the placental location has been ascertained by sonography. The uterus is usually nontender, and the baby is often in a lie well out of the pelvis because the placenta displaces the presenting

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part. Digital examination of the cervix and simple speculum examination of the vagina are contraindicated, unless capabilities are available for immediate delivery, because they could disrupt the placental interface from the lower uterine segment, resulting in catastrophic hemorrhage. Interestingly, women who bleed for the first time with a placenta previa may have significant blood loss, but the bleeding is often self-limited and rarely compromises fetal well-being. The course of subsequent bleeds is much less predictable. Once a woman with a complete placenta previa has bled significantly, she should probably be hospitalized until delivery. In most instances, cesarean section is required for safe delivery. PLACENTAL ABRUPTION.

Placental abruption is defined as separation of the placenta from the maternal interface before delivery. Risk factors include hypertensive disorders (e.g., preeclampsia, chronic hypertension), other chronic diseases with vascular compromise (e.g., diabetes, renal disease, certain autoimmune disorders), coagulation disorders (presence of lupus anticoagulants or anticardiolipin antibodies, protein S or C deficiencies, factor V Leiden, antithrombin III deficiency), trauma, chorioamnionitis, advanced maternal age, multiparity, and cigarette abuse.[106] [123] One of the most common causes of placental abruption in recent years has been cocaine use. Placental abruption is highly variable in presentation, depending on the location and the extent of the separation and hemorrhage. About 80% of placental abruptions result in visible bleeding accompanying the onset of other symptoms. Twenty percent result in concealed subchorionic hemorrhage that may not become apparent until many days after the event. Unlike placenta previa, abruption is usually accompanied by sudden onset of sharp pain. The pain may be focal and continuous, intermittently intensifying with the frequent uterine contractions and irritability that usually accompany and can extend the placental separation. Severe abruptions may be accompanied by prolonged tetanic contractions with extravasation of hemorrhage into the myometrium (Couvelaire uterus); these may compromise uterine involution after delivery. Fetal compromise is much more common with placental abruption than with placenta previa. Traumatic separation of the placenta results in a greater likelihood of disrupted placental vasculature, resulting in fetal blood loss into the subchorionic clot or into the maternal circulation as a fetal-maternal hemorrhage. This can be a major cause of blood group isoimmunization that can affect future pregnancies. Diagnosis of placental abruption is usually based on clinical signs and symptoms and maternal history. Standard sonography is not as useful a diagnostic tool as it is with placenta previa, because small abruptions may be difficult to differentiate from placental tissue and normal placental vascular channels. Magnetic resonance imaging (MRI) and Doppler modalities are more useful but are rarely necessary as diagnostic tools. No laboratory tests are diagnostic for placental abruption, but abnormalities of coagulation studies may suggest small abruptions and may help ascertain the extent of consumptive coagulopathy in large abruptions. A Kleihauer-Betke screen should also be done to assess fetal cells in the maternal circulation. Rh-negative unsensitized women should be given Rh-immune globulin when an abruption is suspected or confirmed. In view of the association with cocaine use, urine toxicologic screens are almost routine in the absence of other causes of placental abruption. If delivery is necessary or deemed inevitable, route of delivery is determined by the degree of fetal or maternal compromise and the prospects for vaginal delivery. PREMATURE LABOR.

Despite the advances that have been made in obstetric and neonatal care in the past 50 years, rates of preterm delivery, defined as delivery before 37 completed weeks' gestation, have not changed, persisting in the range of 8% to 10% of all pregnancies in the United States. It is still the leading cause of perinatal morbidity and mortality. Preterm labor, defined as regular uterine contractions resulting in progressive cervical change, as assessed by effacement, dilation, and softening, complicates twice as many pregnancies as actually progress to preterm delivery. Symptoms of preterm labor include mild and menstrual-like to painful uterine contractions, intermittent low back pain or pressure, pelvic pressure, increase in vaginal discharge resulting from effacement with compression of endocervical glands or leaking of amniotic fluid, and bloody "show." The more common risk factors for preterm labor and delivery include premature rupture of membranes, subclinical or overt chorioamnionitis, UTI, substance abuse (tobacco, cocaine, amphetamines), preeclampsia, multiple gestation, hydramnios, dehydration, constipation, chronic stress, and incompetent cervix.[102] The pregnant wilderness traveler is at risk for several of these factors and should strive to reduce their occurrence. Thorough evaluation and management of preterm labor cannot be done in most wilderness settings. Some empiric measures can be taken, however, based on the woman's symptoms and palpation of uterine contractions alone, while awaiting evacuation or to prepare for delivery if evacuation is delayed or impossible. Pelvic examination should be avoided unless placenta previa has been previously excluded and sterile supplies are available. If done by an experienced person, cervical examination should determine dilation, effacement, and consistency, as well as the station and presentation of

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the baby. Once it has been concluded that the woman is in preterm labor and evacuation is required, examinations should not be repeated unless delivery appears imminent. If she clearly has ruptured membranes, characteristics of the fluid should be noted (clear, bloody, meconium stained), but no internal vaginal examination should be performed initially to minimize risks of introducing infection. Interim measures for managing preterm labor include the following: encourage the woman to empty her bladder and rectum; place her at rest on her side; make sure she is kept warm and comfortable; and provide oral hydration with 32 to 64 ounces of fluid over an hour. These measures alone will decrease uterine activity in as many as one third of women having preterm contractions. If available, a broad-spectrum antibiotic, preferably one with coverage of both group B ß-hemolytic streptococci and anaerobic organisms, should be given orally or parenterally.[126] Parenteral corticosteroids, if available, are useful in accelerating fetal lung maturity in anticipation of premature delivery. Administration of ß-methasone (12 mg intramuscularly; repeat dose in 12 to 24 hours) or dexamethasone (6 mg intramuscularly every 6 hours for four doses) has become an accepted part of empiric therapy when the estimated gestational age is less than 34 weeks. Many common medications have tocolytic activity, but each should be administered only after careful consideration of their potential risks and side effects ( Box 75-6 ). Of these, the prostaglandin synthetase inhibitors are most likely to be part of the routine supplies on a wilderness excursion and are also probably the safest to use in combination with initial measures of rest and hydration. If preterm labor cannot be stopped before evacuation, guidelines exist for management of delivery, as detailed later.

Box 75-6. MEDICATIONS IN COMMON USE FOR TOCOLYSIS

MAGNESIUM SULFATE Calcium antagonist (MgSO4 ), 4–6 g IV over 20–30 min (or IM in split doses to buttocks), followed by continuous infusion of 2–4 g/hr × 12–24 hr. Interrupt or decrease infusion if deep tendon reflexes cannot be elicited or respiratory compromise develops. Effects are readily reversible by calcium gluconate in emergency circumstances. Do not use in combination with nifedipine.

TERBUTALINE SULFATE ß-Sympathomimetic, 0.25 mg SC initially, then every 1–4 hr. Repeat dosing should be withheld in the presence of maternal hypotension, tachycardia, or chest pain. Before administration, the woman should be well hydrated, but care must be taken not to fluid overload once therapy has begun because of risk for pulmonary edema.

NIFEDIPINE Calcium channel blocker, 10 mg SL every 20 min × 1 to 4 doses, then 10–20 mg PO q6h. Decrease dose or frequency for maternal hypotension. Do not use in combination with MgSO4 .

INDOMETHACIN Prostaglandin synthetase inhibitor, 50–100 mg per rectum initially, then 25–50 mg PO q6h. Do not use for more than 24 to 48 hours because of effects on fetal urine output (decreased production of amniotic fluid), potential for masking fever, and possible premature closure of the fetal ductus arteriosus. Safe for use in combination with magnesium, terbutaline, and nifedipine.

IBUPROFEN Prostaglandin synthetase inhibitor, 600–800 mg PO initially, then 400–800 mg PO q6h. Appears to have much less effect on fetal urine output and ductus arteriosus than terbutaline but can mask fever. Safe for use in combination with magnesium, terbutaline, and nifedipine.

IM, Intramuscularly; IV, intravenously; SC, subcutaneously; SL, sublingually; PO, orally; q6h, every 6 hours.

HYPERTENSIVE DISORDERS.

Pregnancy-induced hypertensive disorders include preeclampsia, eclampsia, and HELLP syndrome. These disorders complicate 10% or more of all pregnancies and are responsible for 15% to 20% of maternal mortality in the United States. Although guidelines have been put forth for their definition, the etiology of these conditions and the differences between them are unknown. Variability in presentation and unpredictability in course characterize these disorders. All are specific to pregnancy, despite mimicking nonpregnancy-related diseases, and do not begin to resolve until the baby and placenta are delivered. Generalized vasospasm and hypersensitivity to vasoconstrictors are typically present.[86] [162] Major risk factors for preeclampsia include nulliparity, obesity, previous history of preeclampsia, underlying hypertension or chronic renal disease, pregestational diabetes, autoimmune

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disorders, antiphospholipid antibody syndrome, maternal age over 40, multiple gestation, molar pregnancy, hydrops fetalis, intrauterine growth restriction, and oligohydramnios. [20] [39] [115] [161] Genetic predisposition for preeclampsia is supported by the strong association of family history and identification of certain genetic markers, such as angiotensinogen gene T235, associated with disease expression. [77] [111] [112] The diagnosis of preeclampsia is based on the triad of hypertension, proteinuria, and edema. Hypertension is defined as systolic blood pressure of 140 mm Hg and higher or diastolic blood pressure of 90 mm Hg or higher measured on two separate occasions 6 or more hours apart. Proteinuria is defined as 300 mg or greater in 24 hours or the presence of 0.1 g/L (1 + or greater) by dipstick on at least two random urine specimens 6 hours apart. Edema is considered significant to the diagnosis of preeclampsia only if it generalized or if the woman has gained 5 pounds in a week. The strict diagnosis of preeclampsia requires the presence of hypertension with proteinuria, edema, or both. Women meeting these criteria have at least mild preeclampsia. Diagnostic criteria for severe preeclampsia require only one of the following: blood pressure of 160 mm Hg systolic and higher or 110 mm Hg diastolic and higher on two occasions at least 6 hours apart; proteinuria (5 g/24 hours or higher); oliguria (400 ml/24 hours or higher); persistent epigastric pain; pulmonary edema or cyanosis; impaired liver function of unclear etiology; thrombocytopenia (less than 100,000/mm3 ); and eclampsia (grand mal seizures). Most cases of severe preeclampsia are associated with intrauterine growth restriction or abnormalities of fetal umbilical (increased resistance) and middle cerebral (decreased resistance) arterial flow consistent with relative placental insufficiency.[18] Eclampsia, as a subset of severe preeclampsia, is a major cause of maternal and fetal morbidity and mortality worldwide, occurring in about one of 2000 pregnancies in the United States. Although difficult to anticipate, the presence of visual disturbances, severe headache, irritability, epigastric or right upper quadrant pain, nausea and vomiting, and cerebral dysfunction must be considered predictors of eclampsia.[92] [169] Only about half of women complain of these symptoms before seizure, and as many as one third will not have a seizure until the postpartum period, sometimes as the first significant event suggesting preeclampsia. [15] The most serious subset of severe preeclampsia, occurring in about 10% of cases, is HELLP syndrome, or hemolysis, elevated liver function enzymes, and low platelets.[93] [133] Hemolysis is defined as an abnormal peripheral smear consistent with a microangiopathic process, total bilirubin greater than 1.2 mg/dl, and lactic dehydrogenase (LDH) greater than 600 U/L. Elevated liver enzymes include aspartate aminotransaminase greater than 70 U/L and LDH greater than 600 U/L. Low platelets generally refer to levels less than 100,000/mm3 , although some women with the other manifestations of the syndrome will maintain platelet counts above

100,000/mm3 .[76] Unlike severe preeclampsia/eclampsia, HELLP syndrome tends to affect older, white, and multiparous women. Onset of most cases of HELLP syndrome is before 37 weeks' gestation; as many as 15% of cases present before 26 weeks. Although 80% of women will have the diagnosis of preeclampsia made before delivery, more than 50% will not develop the most severe manifestations of HELLP syndrome until 1 to 2 days postpartum. During this time, mobilization of extracellular tissue fluid can suddenly precipitate pulmonary edema because of delayed renal recovery. Renal failure, disseminated intravascular coagulation, sepsis, hepatic hematoma and rupture, adult respiratory distress syndrome, and retinal detachment have been reported.[139] If preeclampsia is suspected, plans should be made for immediate evacuation from the wilderness setting. While awaiting evacuation, the woman should be placed at rest and have free access to fluids. If magnesium sulfate is available, it should be administered in the same manner as described for preterm labor (see Box 75-6 ) to decrease the risk for seizures.[169] Because of the increased likelihood of renal compromise with preeclampsia, magnesium toxicity must be carefully monitored by assessment of deep tendon reflexes. Antihypertensive medications should be administered with great caution or not at all, since preeclampsia is often accompanied by intravascular volume depletion (even with an excess of total body water) by the time the condition is recognized. Antihypertensive agents that cause vasodilation can greatly reduce MAP, placing the baby at risk for acute placental insufficiency when the placental perfusion may already be compromised. Indications for administration of an antihypertensive drug include persistent blood pressure greater than 160 mm Hg systolic or 110 mm Hg diastolic. The goal should not be to normalize blood pressure, but to maintain it in the range of 140/90 mm Hg. The a/ß blocking agent labetalol administered in incremental doses (20, 40, and 80 mg intravenously at 10to 20-minute intervals, up 300 mg) is widely used for this purpose. If a pregnant woman has a seizure, the airway should be maintained, oral cavity protected, woman positioned on her side, and no efforts made to restrain the myoclonic activity. If magnesium sulfate is available, it is still the treatment of choice for eclamptic seizures and should be administered as previously described. Alternatively, a loading dose of diphenylhydantoin (20 mg/kg intravenously no faster than 50 mg/min) or lorazepam (1 to 2 mg intravenously) can be given.

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Management Delivery.

For many reasons, a wilderness delivery at term should rarely be "planned." If it is planned, only multiparous women who have had uncomplicated pregnancies, labor and delivery, and postpartum courses and who are willing to accept the risks of unexpected fetal and maternal complications should consider this as an option. A pregnant woman planning a wilderness experience of any duration that will carry beyond 20 weeks' gestation should include emergency provisions and plans. The location, duration of stay, and distance will dictate the extent of these plans from medical care facilities, convenience of evacuation routes, and ease of communication with and availability of evacuation support. When the woman is in labor preparing for delivery, either a health care provider or the person with the most childbirth experience who is willing to assist in the delivery should be identified as team leader and "midwife." Participatory roles for other members of the party should be defined in cooperation with the pregnant woman. Requests for privacy and intimacy should be respected to the extent possible. By necessity and practicality, delivery in the wilderness dictates a laissez-faire approach. Excessive intervention (e.g., repeated cervical examinations, artificial rupture of membranes, augmentation of uterine contractions by oxytocin or nipple stimulation, manual cervical dilation) is neither warranted nor appropriate, since delivery cannot be expedited for concerns of fetal distress, and such intervention may increase maternal and fetal risks. To the extent possible, a clean, comfortable, and quiet site is prepared for the delivery. If clean and sterile supplies and medications are available, these should be brought to this location and inventoried by the team leader (see Box 75-3 ). Otherwise, clean towels, clothing, bedding, soap, and water should be made readily accessible.

Figure 75-2 Ascertaining fetal position by Leopold's maneuvers. A, First maneuver. Assess part of fetus in upper uterus. B, Ascertain location of fetal back. C, Identify presenting part. D, Determine descent of presenting part.

Fetal position should be determined. In late third-trimester pregnancies, this can be accomplished by external abdominal palpation using Leopold's maneuvers ( Figure 75-2 ). In preterm pregnancies this may first require internal digital examination, but fetal position is extremely important because the risk of malpresentation (breech, transverse, or compound lie) is inversely proportional to gestational age, as is the disparity between fetal head and abdominal circumferences. At term the incidence of breech presentation is approximately 3%, whereas it may exceed 25% under 30 weeks' gestation. If the woman reports fetal activity, or if this is visible or palpable on abdominal examination, evaluation of fetal heart activity is usually unnecessary. If the woman or the examiner cannot detect fetal activity, and since fetal activity frequently diminishes with onset of labor, viability is assessed by auscultation. A stethoscope or the ear can be positioned over the location of the baby's back and shoulder. A stethoscope bell placed on the abdomen with minimal pressure is usually more sensitive than the diaphragm. Normal fetal heart rate at term usually falls to between 120 and 160 beats/min. Under most wilderness situations, once viability is confirmed, further auscultation is probably unnecessary and may even provoke anxiety because of the inherent difficulties of fetal heart rate detection with unamplified methods, subtle changes in fetal position, descent of the presenting part, and the increasing discomfort of labor as it progresses. If facilities are available to perform an emergency cesarean section in the wilderness, intermittent fetal heart rate monitoring is done for 1 or 2 minutes every 20 to 30 minutes during the first stage of labor and every 10 to 15 minutes during the second stage. However, even under these highly unlikely circumstances, cesarean section should be considered only with persistent fetal bradycardia or with failure to progress in labor.

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In the early stages of labor or with spontaneous rupture of membranes in the absence of regular uterine contractions, rest interspersed with brief periods of ambulation, fluid intake, and frequent light meals should be encouraged. Prophylactic antibiotics should be started, especially when there has been premature rupture of membranes. Antibiotic coverage is the same as that recommended for preterm labor. Digital cervical examination is usually not necessary at this point and is contraindicated with rupture. As labor becomes more active, as gauged by increased frequency, regularity, and strength of uterine contractions, pelvic pressure, and discomfort level, the safest approach is to limit oral intake to clear liquids only. The GI tract becomes quiescent with active labor, and any stomach contents present at the outset will likely be present at the end. Since vomiting is not unusual, especially during the "transition" phase of labor, clear liquids minimize discomfort and decrease risk of aspiration. Intermittent ambulation may also decrease the discomfort associated with contractions and can be continued, if the woman desires, until she feels the need to push. During this time she should also be reminded to empty her bladder because she may not be able to differentiate the sensation to void from that of pressure from the presenting fetal part. A full bladder not only adds to the discomfort of labor but can also impede descent of the baby into the pelvis, prolonging the process. Although some women become irritable as labor intensifies before complete dilation and do not want to be touched, others appreciate low back or extremity massage between contractions. Assistance with breathing and relaxation techniques to distract, maintain composure, and preserve the energy that will be required during the second stage of labor are also beneficial. During labor, no oral pain medication should be given, and parenteral narcotics, although acceptable, should be administered sparingly (ideally, intravenously with the onset of a contraction) unless naloxone is available to manage the fetal depression that may result. If a skilled health care provider is managing the delivery and pain is intolerable, a paracervical block can be considered once the cervix has reached 7 to 8 cm of dilation. This should only be done if the provider has performed the procedure previously. The cervix is usually completely effaced at this point, so care must be taken not to inject the baby or inject the anesthetic agent intravenously. When the woman begins to feel involuntary efforts to push with contractions, cervical examination should be performed with a clean or sterile glove or freshly washed hands. At the same time that cervical dilation and effacement are assessed, the presenting fetal body part should be identified, determining its station in relation to the ischial spines in midpelvis. If the cervix is completely dilated and effaced so that no cervical tissue is palpable between the presenting part and the vaginal wall, the first stage of labor is complete, and the woman can begin pushing with contractions. If the cervix is not completely dilated, the woman should be encouraged not to push with contractions so that she does not become exhausted. She also risks entrapping the cervix between the presenting part and the pelvis, which can lead to cervical edema and thickening, although this usually results from cephalopelvic disproportion. If membranes have ruptured, presence or absence of meconium should be noted. If membranes have not ruptured, they should not be ruptured intentionally, particularly if the baby is premature or in a breech presentation. Usually, once the cervix is completely dilated, the desire to push is involuntary, and pain is less of an issue until the moment of delivery. Pushing is done only with uterine contractions. At the onset of a contraction the woman takes in a deep breath, expels this, and then taking in another deep breath and holding this, bears down without releasing air as if straining to have a bowel movement. Most contractions are long enough to permit two or three attempts at this maneuver. Proper pushing is

evident by expansion of the introitus and rectum during the effort and should not be accompanied by tensing of the extremities. Once the contraction is over, she should expel any held air and begin restful breathing, trying to relax completely to conserve energy and recover for the next contraction. The woman may push in any position in which she feels comfortable. However, she should avoid laying flat on her back because uterine compression of the inferior vena cava can lead to hypotension and decreased uterine perfusion. Common positions include semirecumbent, with back and head elevated and legs drawn up or supported at the knees during contractions; lateral recumbent, with superior leg flexed and supported during contractions; squatting; sitting; kneeling on all fours; and standing while being supported from behind around the torso. These positions can also be used for the actual delivery, as long as the attendant has adequate access. Once the presenting part reaches, distends, and remains at the vaginal introitus between contractions, final preparations are made for the delivery. A delivery position should be selected that allows control of the presenting part, protection of the perineum, and room to accomplish completion of the birth with as little trauma to the baby as possible. Delivery should be performed during a contraction. Vertex Delivery.

The most common fetal presentation is the cephalic (or vertex) presentation, with the fetal head facing the perineum (occiput anterior) (Figure 75-3 (Figure Not Available) ). When the perineum begins to distend with a contraction, the woman should be instructed to bear down. Intentional cutting of an episiotomy in a wilderness setting is not recommended. Spontaneous lacerations are

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Figure 75-3 (Figure Not Available) Management of vaginal vertex delivery. A, Control delivery of fetal head by upward pressure on chin with countertraction on occiput until symphysis is cleared. B, Delivery of anterior shoulder by downward traction on fetal head. C, Delivery of posterior shoulder by upward traction on fetal head. (Modified from Pritchard JA, MacDonald PC: Williams obstetrics, ed 16, New York, 1980, Appleton-Century-Crofts.)

more likely to occur along tissue planes that are less vascular and less likely to extend into the rectum. The perineum should be supported between the rectum and the introitus by the index finger and thumb of the nondominant hand while the fetal head is maintained in flexion until the crown has just begun to clear the symphysis. The woman stops pushing while the attendant exerts steady inward and upward pressure at the perineum against the fetal chin, thereby extending the head and completing its delivery while protecting the perineum. Once delivered, the fetal head will usually rotate laterally to align itself with the shoulders. The infant's mouth and nose should be cleaned by bulb aspiration or simple swabbing with a clean gauze or cloth. This step is especially important when meconium is present to prevent aspiration of this fluid when the baby is free to take its first breaths. Once the oropharynx is cleaned, the fetal neck should be palpated to ascertain the presence of a nuchal cord. If present, one or more loops of umbilical cord are often loose enough to be slipped over the baby's head before completion of the delivery. If they cannot be slipped over the head but are not tight, the baby can frequently be delivered through the loops. If the cord is tightly applied around the neck, the attendant should doubly clamp or tie a section of one loop, cut between the clamps, and then deliver the baby. In the final stages of delivery the woman resumes pushing while steady downward (toward the maternal sacrum) traction is applied with hands cupping both sides of the fetal head. When the anterior shoulder has cleared the symphysis, the perineum should again be supported while the head is elevated and the posterior shoulder delivered. The rest of the baby's body usually

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follows without effort. The baby is held below the perineum (to prevent loss of blood to the placenta from the baby) while the oropharynx is again cleaned and the baby dried. Usually, rubbing the baby dry is sufficient to stimulate breathing and crying. The umbilical cord should then be doubly clamped or tied and then severed. The baby should be thoroughly dried, wrapped in clean, dry, and warm fabric with its head covered and given to the mother if she desires. If the baby does not cry within 10 to 15 seconds after delivery, has obvious airway obstruction, or is premature, the umbilical cord should be cut immediately and resuscitative efforts begun. Shoulder Dystocia.

If there is difficulty delivering the anterior shoulder (shoulder dystocia) by the method outlined, immediate steps should be taken to accomplish this. True shoulder dystocia occurs in less than 1% of deliveries, is rare in uncomplicated labors, but is a substantial cause of fetal and maternal morbidity.[144] Shoulder dystocia is often anticipated when the fetal head snaps back tightly and fails to rotate after its delivery. If available, other individuals can assist. Throughout the steps necessary to accomplish delivery, excessive traction on the fetal head is avoided because it may stretch the brachial plexus, resulting in an Erb's or Klumpke's palsy. The first step is to position the woman so that the buttocks are elevated to allow at least 12 inches of free space beneath the perineum to maneuver. Both legs should then be flexed upward to the chest (McRobert's maneuver) while the woman is supported in a semirecumbent position behind her back. Delivery should then be attempted again by downward traction on the fetal head. If the shoulder is still impacted against the symphysis, pressure applied with the fist or heel of the hand just above the symphysis in the midline may reduce it sufficiently to accomplish the delivery. The assistants should not push on the uterine fundus because this can further impact the shoulder. If these maneuvers fail, an episiotomy should be cut to admit several fingers or the hand beneath the posterior shoulder. Once the hand has been inserted, the baby should be rotated by applying pressure to the shoulder and scapula (Wood's maneuver). The corkscrew rotation will deliver the posterior shoulder as it turns anteriorly, the anterior shoulder will dislodge, and the baby can be delivered without further difficulty. If this rotational maneuver fails, the posterior arm is delivered by grasping it along the forearm and sweeping it across the chest and out the vagina. This technique may fracture the humerus or the clavicle but is preferable to losing the baby because of inability to complete a delivery. Once the posterior arm is out, the anterior shoulder can usually be displaced downward, or the baby can then be rotated, allowing completion of the delivery. This approach is preferable to intentionally fracturing the clavicle, which can be technically difficult and does not provide as much room for the delivery. If the baby is in a vertex presentation but facing the symphysis (occiput posterior), the labor is often more prolonged and uncomfortable, particularly in the lower back. The delivery is basically accomplished as described, however, except the final maneuvers to deliver the fetal head are extension first, then flexion. Perineal and introital trauma is a greater risk with an occiput posterior delivery. Management of this fetal presentation by the wilderness birth attendant should be a minor challenge compared with delivery of a breech baby. Breech Delivery.

Since most wilderness deliveries will be "unexpected" and more likely to be premature, the baby also will more likely be in a breech lie. Other than chance and prematurity, the greatest risk factors for a baby to be in a breech presentation are unsuspected congenital fetal anomalies, chromosomal abnormalities, and maternal uterine abnormalities. Each of these adds a new level of challenge to the birth attendant. Under the best of circumstances, delivery of a breech carries a threefold to fourfold greater risk than a vertex presentation for morbidity resulting from prematurity, congenital abnormalities, and trauma at delivery. The trauma often results from disproportion between the larger fetal head and the smaller body circumference of a premature infant. This disproportion can lead to entrapment of the head and is especially problematic when the fetal body has negotiated an incompletely dilated cervix. Breech babies come in many forms: frank breech (hips flexed, knees extended, buttocks presenting), complete breech (both hips and both knees flexed, buttocks and feet presenting), incomplete breech (one hip flexed, one hip partially extended, both knees flexed, buttocks and feet presenting), and footling breech (hips and knees extended, feet presenting). Regardless of the form, the approach in a wilderness setting demands patience. No effort should be made to deliver a breech baby until the presenting part is visible at the introitus and the cervix is completely dilated. Membranes should not be artificially ruptured in breech presentations. As the amniotic sac balloons into the birth canal, it helps to dilate the cervix completely. This facilitates descent of the baby, providing a lubricated smooth surface against which the body can freely move, and cushions the umbilical cord against compression in the birth canal. When the cervix is completely dilated, the woman is instructed to push. Regardless of the type of breech presentation, the safest course is to allow the body to be extruded to at least the level of the umbilicus by maternal efforts alone (Figure 75-4 (Figure Not Available) ). This increases the

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Figure 75-4 (Figure Not Available) Management of vaginal breech delivery. A, Downward traction at ankles until buttocks clear the introitus. B, Traction on pelvic girdle until an axilla becomes visible. C, Delivery of posterior shoulder and arm. D, Delivery of anterior shoulder and arm with downward traction. E, Cradling the baby on forearm, finger is inserted into mouth or against chin. F, Delivery completed by outward traction while maintaining fetal head in flexed position. (Modified from Pritchard JA, MacDonald PC: Williams obstetrics, ed 16, New York, 1980, Appleton-Century-Crofts.)

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chance that the fetal head has begun to pass through the pelvic inlet. A baby in a frank or complete breech lie should have the posterior leg delivered by gently grasping the thigh and flexing the leg at the knee as it is rotated medially and toward the introitus. The baby should then be rotated to the sacrum anterior position, then another 45 degrees in the same direction to facilitate delivery of the other leg using the technique described for the first. The legs and buttocks can be wrapped in a clean towel to provide a firmer grip and decrease trauma to the baby. The delivery from this point is the same as for footling breech presentations. The upper legs should be grasped on each side with the index fingers crossing the infant's pelvic girdle and both thumbs positioned just above the crease of the buttocks. Using gentle side-to-side rotational motion over an arc of 90 degrees outward and downward, traction should be applied while the mother pushes, until the upper portion of a scapula is visible at the introitus. With the baby's body rotated 45 degrees toward the opposite side, the arm is delivered by flexion and medial rotation across the chest. The baby is rotated to the opposite side in the same position, and the other arm is then delivered. If assistants are present, the woman should be helped into the McRobert's position, with hyperflexion at the hips to maximize the space between the symphysis and the sacrum. Maintaining the baby in the same plane as the vagina, the birth attendant reaches palm up between the baby's legs and into the vagina, supporting the baby's entire body on the forearm while placing the second and fourth fingers over the infant's maxillae and placing the middle finger into the mouth or on the chin. The other hand is positioned over the infant's upper back so those fingers are overlying each shoulder. If there is sufficient room, the middle fingers can be applied to the fetal occiput. Then with the woman pushing, the baby's head is flexed downward, completing the delivery. Firm suprapubic pressure can help to maintain the head in flexion. During this final stage the baby's body should not be elevated more than 45 degrees above the plane of the vagina to avoid hyperextension of the head. If the fetal head cannot be delivered because the cervix is incompletely dilated, the cervix can be cut at the 2 and 10 o'clock positions (Duhrssen's incisions) to provide sufficient room to complete the delivery. Once delivered, if the baby breathes and cries spontaneously or with minimal stimulation, cutting the umbilical cord can be delayed while the baby is dried. This allows some of the blood retained in the placenta from umbilical vein compression (common with breech deliveries) to return to the baby. On the contrary, if the baby is clearly depressed, the umbilical cord should be immediately clamped and cut and neonatal resuscitation begun. Neonatal Resuscitation The first steps in neonatal resuscitation are to dry the baby thoroughly, keep the baby warm, and clear the nose and mouth of excess fluid. Respiratory effort and heart rate (by auscultation or palpation at the base of the umbilical cord) are then assessed. If breathing spontaneously with pulse greater than 100 beats/min, the baby should be kept warm and observed. If the pulse falls below 100 beats/min and respiratory effort is poor, the next step is to improve ventilation. If further stimulation of the baby by rubbing with a towel or flicking the heels fails to elicit improvement in respiratory effort and pulse, the next step is to provide ventilatory support, ideally by applying positive-pressure ventilation with a neonatal mask and Ambu bag (preferably with oxygen). If this is available, gentle (15 to 30 cm H2 O) and rapid (40 to 60 breaths/min) ventilation should be performed for 30 seconds and the heart rate reassessed. If no equipment is available, the resuscitator's mouth is placed over the infant's nose and mouth, and rapid shallow breaths are delivered at a rate of 30–40/min. If this restores heart rate and respiratory effort, the baby should be observed for deterioration in status and the maneuvers repeated as necessary until support is available. If the baby's heart rate falls below 60 beats/min, full infant cardiopulmonary resuscitation (CPR) should be started. Cardiac compression is performed by (1) placing both thumbs on the sternum just above the xiphoid and facing the fetal head, (2) gently stabilizing this position with the other fingers around the chest, and (3) supplying compressions to a depth of ½ to ¾ inch at a rate of approximately 90/min. Care should be taken not to deliver compression to the baby's ribs. Ventilation should be continued simultaneously as described. If the heart rate after 30 seconds of chest compression is 80 to 100 beats/min, the resuscitator continues with ventilatory support only. If the heart rate is over 100 beats/min, the person discontinues CPR and observes. If the heart rate is still less than 80 beats/min, CPR is continued. Delivery of Placenta Once the baby is delivered and stabilized, attention is redirected to the mother. The first step is to assess the status of placental separation. The heel of the non-dominant hand is placed just above the symphysis to hold the uterus in position, then the fingers are cupped to apply pressure to the uterine fundus while providing gentle, steady downward traction on the umbilical cord. If this maneuver does not promote placental separation, as indicated by a gush of bleeding, lengthening of the cord, and descent of the placenta into the vagina, efforts should be interrupted until these signs ensue. When the placenta does descend, the mother should be instructed to push once again to complete

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the third stage of labor. Rotating the placenta several times once it has passed through the introitus will usually result in complete extrusion of the attached chorioamnionic membranes. With signs of placental separation but resistance to extraction, the hand should be placed through the vagina and into the cervix. If the placenta is filling the cervix, it should be grasped and gently extracted. If the placenta does not separate spontaneously or is adherent to the uterine wall (placenta accreta), no effort should be made to separate it manually in a wilderness setting, since this could precipitate uncontrollable hemorrhage. Excessive traction on the umbilical cord also could result in uterine inversion, causing vasomotor collapse and hemodynamic decompensation. Once placental expulsion has occurred, the uterus can be gently massaged abdominally to promote contraction and involution. Usually this is sufficient to control hemorrhage from the placental bed. If this is ineffective, it may be necessary to explore the uterus manually for retained placenta while compressing the fundus externally until it contracts. Additional measures to aid uterine involution and control bleeding include administration of oxytocin (10 to 40 U intramuscularly), nipple massage to promote endogenous release of oxytocin, methylergonovine (0.2 mg intramuscularly or orally every 2 to 4 hours), prostaglandin F2a (250 µg intramuscularly), misoprostol (100 to 200 µg orally every 4 to 6 hours), and prostaglandin E2 (20-mg suppository every 2 hours).[6] If none of these measures is successful, and if bleeding from a laceration has been eliminated as a source, the uterus can be packed with clean sponges or towels until additional medical assistance arrives. Once the placenta is removed and uterine bleeding controlled, maternal damage is assessed and repaired. The most common sites of lacerations are the perineum, periurethral tissues surrounding the external meatus, lower vagina, and cervix. Significant cervical lacerations in unhurried deliveries are rare unless uncontrollable pushing has occurred before complete dilation. Other lacerations from a spontaneous delivery usually occur along tissue planes that do not disrupt vital areas; they will heal naturally or can be repaired later. Significant bleeding at any of these sites can usually be easily controlled by direct pressure. If available, application of ice packs to the perineum for the first 12 to 24 hours after delivery provides relief. During the postpartum period the woman should be encouraged to drink fluids and void frequently. Bladder overdistention resulting from impaired sensation and pain after delivery is a common cause of permanent bladder dysfunction. It may also contribute to uterine subinvolution and continued blood loss. Once the baby has stabilized after delivery, the mother should begin breast-feeding, which also helps control excessive postpartum blood loss. After a wilderness delivery a broad-spectrum antibiotic, if available, should be continued for 24 to 48 hours. If the mother is Rh negative and the baby's blood type is Rh positive or unknown, Rh-immune globulin should be given within 48 to 72 hours after delivery. Perimortem Cesarean Section In the rare event that a pregnant woman with a viable baby sustains a lethal injury while partaking in a wilderness trip, performing a perimortem cesarean section should be considered.[84] Ordinarily this procedure is done in a full-service medical facility when death is imminent and while CPR is being performed on the woman or when skilled medical personnel deem that the pregnancy is interfering with resuscitative efforts. In the wilderness, cesarean section should only be considered at the moment of maternal death, when surgical technique is irrelevant and speed is of the essence. In skilled hands the entire procedure can be performed in 30 seconds or less. A vertical incision is made in the midline abdomen from the umbilicus to the symphysis. The incision is rapidly extended through subcutaneous tissues and fascia. The rectus muscles are bluntly separated in the midline and the peritoneum entered. The uterus is then incised vertically from fundus to bladder reflection. Once a site of entry into the uterine cavity is obtained, two fingers are inserted and the incision extended by blunt dissection to avoid sharp injury to the baby. Membranes are ruptured, the baby is delivered, and neonatal resuscitative efforts are initiated. Breast-Feeding Unless the baby is too premature or too unstable to nurse, breast-feeding should be encouraged as soon as possible after birth. Benefits include promotion of uterine contractions that control hemorrhage at the placental insertion site, encouragement of maternal-newborn bonding, provision of easily digestible and balanced nutritional support for the baby, and transmission of antibodies (IgA) that protect the enteric mucosa against invasion by colonizing bacteria.[94] [146] Long-term benefits for the baby

include decreased incidence of allergies, enteric infections, UTIs, otitis media, childhood obesity, and diabetes, as well as psychologic and perhaps cognitive advantages.* Benefits for the mother include more rapid return to prepregnancy weight, enhanced bone remineralization, and reduced risk of ovarian cancer and premenopausal breast cancer.[5] *References [ 85]

[ 87] [ 130] [ 132] [ 154] [ 167]

.

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During the first 24 hours after delivery, frequent brief feedings are recommended (every 2 to 3 hours; 5 minutes on each breast, alternating first breast). Although a small amount of breast fluid (colostrum) is present initially, it contains electrolytes, minerals, and a high concentration of protein and protective IgA antibodies. The length of time spent at nursing and the interval between feedings can be increased as milk production is established over the next 2 to 3 days. The feeding schedule is typically 10- to 15-minute periods on each breast 8 to 12 times per day. It should be made clear to the mother that babies are not restricted to this regimen. Because babies have an innate urge and ability to suck, and mothers have an innate urge to mother, breast-feeding should require little formal education. However, first-time mothers often think they will not be able to breast-feed, will not provide sufficient nutrition to their babies, or will encounter frustrations and difficulties. Patience, relaxation, simple modifications in technique, and reinforcement of the benefits of nursing are beneficial. Mothers are reassured when they see that their baby is gaining weight and voiding five or six times daily and thus is receiving adequate nutritional and fluid support. Nursing women should be instructed to drink plenty of fluids (2 L/day); increase their caloric intake by 500 to 600 kcal/day, including a total protein intake of 60 to 70 g/day; and consume foods rich in calcium (1200 mg/day). Several conditions can interfere with breast-feeding or cause maternal frustration. Breast engorgement 48 to 72 hours after delivery, signifying the onset of milk production accompanied by lymphatic obstruction, can cause pain and low-grade fever, interfere with the baby latching on, and inhibit milk letdown. Frequent feedings and warm compresses just before nursing help to stimulate milk letdown. Cool compresses after nursing, a supportive nursing bra, and acetaminophen usually provide symptomatic relief until milk production and newborn consumption are in equilibrium and lymphatic obstruction is resolving. Engorgement usually resolves within 24 to 48 hours. Sore and cracked nipples are a frequent complaint of woman nursing for the first time.[25] [27] Short frequent feedings with several rotations between breasts at each sitting can be beneficial. After each feeding, gently cleansing with water and then applying a small amount of milk, expressed from the breast and spread around the areola to dry, help protect the nipples. Lanolin formulations designed for breast-feeding women can be used as well. Dry absorbent nursing pads should be placed over the nipples between feedings. If contact with clothing or even the nursing pads creates discomfort, breast shells can be used to prevent surface contact. Occasionally, nipple shields can be beneficial, as well as for the infant who has difficulty latching on to the breast.[168] Mastitis occurs in 2% to 3% of lactating women and should not be confused with breast engorgement since it rarely occurs until at least 3 to 4 weeks postpartum.[81] Unlike breast engorgement, mastitis is usually unilateral and accompanied by localized pain, erythema, brawny edema, fever, and malaise. It is more common among women who report painful and cracked nipples and who participate in vigorous exercise- and work-related upper body activities.[48] These women should be encouraged to empty their breasts by nursing or pumping before these activities and to wear a properly fitting and supportive bra as preventive measures for mastitis. Women who develop mastitis should continue to nurse from the affected breast and may benefit from warm compresses and pumping between nursings. They should be placed on a course of antibiotics (e.g., dicloxacillin 500 mg or cephalexin 500 mg four times daily) for 10 to 14 days, with coverage for Staphylococcus, Streptococcus, and Escherichia coli, the most common isolates from affected breasts. Failure to improve or worsening while on this regimen, as determined by consolidation, widening of erythema and induration, and abscess formation, occurs in 10% to 15% of women. Incision and drainage may be required.[136] Certain substances, prescription drugs, and maternal medical conditions may affect breast-feeding. Excessive alcohol consumption and cigarette smoking should be avoided because of the deleterious effects on lactation and toxic effects on the baby. Street drugs should always be avoided because of the potentially harmful effects on mother and baby and the unknown chemicals used to prepare the drugs or enhance their effects. Infectious diseases (e.g., HIV, hepatitis B) acquired through intravenous drug use are transmitted in body fluids, including breast milk, and can have devastating effects in a newborn during the first year of life. Women with active tuberculosis should not breast-feed until they have received at least 2 months of therapy. Few data address the safety of most prescription and OTC drugs in lactating women and their babies. Many new drugs become available each year, but few of these have been systematically evaluated in women, with even fewer tested in pregnant or lactating women because of ethical and liability concerns. In 1994 the American Academy of Pediatrics published a summary of recommendations for the use of drugs by lactating women ( Box 75-7 ). [4] Despite some controversy, this list is an excellent general guideline for drug use in lactating women. When given a choice of agents to prescribe or recommend in pregnancy or during lactation, health care providers should always consider those products with which there is the most clinical experience.

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Box 75-7. CATEGORIZATION OF DRUG USE BY LACTATING WOMEN

CONTRAINDICATED Amphetamines Aspirin (high dose) Bromocriptine Cytotoxic agents Ergotamine Lithium Radiopharmaceuticals

EFFECTS UNKNOWN BUT OF CONCERN Antianxiety drugs Antidepressants Antipsychotics Metronidazole Psychotropics

AFFECTING MILK SUPPLY Decongestants Diuretics Combination oral contraceptives

USUALLY CONSIDERED COMPATIBLE WITH BREAST-FEEDING Analgesics Antiasthmatics Antibiotics Anticoagulants Anticonvulsants Antiemetics Antihistamines Antihypertensives Antithyroids Corticosteroids Digoxin Narcotics Oral contraceptives Sedatives

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Suggested Readings Arroyo A et al: Inappropriate gonadotropin secretion in polycystic ovary syndrome: influence of adiposity, J Clin Endocrinol Metab 82:3728, 1997. Augenbraun MH, Rolfs R: Treatment of syphilis, 1998: nonpregnant adults, Clin Infect Dis 28(suppl 1):S21, 1999. Baker DA: Antiviral therapy for genital herpes in nonpregnant and pregnant women, Int J Fertil Womens Med 43:243, 1998. Baker DA, Blythe JG, Miller JM: Once-daily valacyclovir hydrochloride for suppression of recurrent genital herpes, Obstet Gynecol 94:103, 1999. Balen AH et al: Polycystic ovary syndrome: the spectrum of the disorder in 1714 patients, Hum Reprod 10:2701, 1995. Benedetti JK. Zeh J, Corey L: Clinical reactivation of genital herpes simplex virus infection decreases in frequency over time, Ann Intern Med 131:14, 1999. Bernardes J: The Jarisch-Herxheimer reaction and fetal monitoring changes in pregnant women treated for syphilis, Obstet Gynecol 93:631-632, 1999. Beutner KR et al: External genital warts: report of the American Medical Association Consensus Conference, AMA Expert Panel on External Genital Warts, Clin Infect Dis 27:796, 1998. Beutner KR et al: Imiquimod, a patient-applied immune-response modifier for treatment of external genital warts, Antimicrob Agents Chemother 42:789, 1998. Beutner KR et al: Genital warts and their treatment, Clin Infect Dis 28(suppl 1):S37, 1999. Bohmer JT et al: Cervical wet mount as a negative predictor for gonococci- and Chlamydia trachomatis-induced cervicitis in a gravid population, Am J Obstet Gynecol 181:283, 1999. Centers for Disease Control and Prevention: 1998 guidelines for treatment of sexually transmitted diseases, MMWR 47(RR-1):1, 1998. Chrousos GP, Torpy DJ, Gold PW: Interactions between the hypothalamic-pituitary-adrenal axis and the female reproductive system: clinical implications, Ann Intern Med 129:229, 1998. Crave JC et al: Effects of diet and metformin administration on sex hormone-binding globulin, androgens, and insulin in hirsute and obese women, J Clin Endocrinol Metab 80:2057, 1995. Diamond C et al: Clinical course of patients with serologic evidence of recurrent genital herpes presenting with signs and symptoms of first episode disease, Sex Transm Dis 26:221, 1999. Diaz-Mitoma F et al: Oral famciclovir for the suppression of recurrent genital herpes: a randomized controlled trial. Collaborative Famciclovir Genital Herpes Research Group, JAMA 280:887, 1998. Douchi T et al: Body fat distribution in women with polycystic ovary syndrome, Obstet Gynecol 86:516, 1995. Dunaif A: Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis, Endocr Rev 18:774, 1997. Dunaif A et al: The insulin-sensitizing agent troglitazone improves metabolic and reproductive abnormalities in the polycystic ovary syndrome, J Clin Endocrinol Metab 81:3299, 1996. Ehrmann DA et al: Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis in women with polycystic ovary syndrome, J Clin Endocrinol Metab 82:2108, 1997. Falsetti L et al: Treatment of hirsutism by finasteride and flutamide in women with polycystic ovary syndrome, Gynecol Endocrinol 11:251, 1997. Habel LA et al: Risk factors for incident and recurrent condylomata acuminata among women, Sex Transm Dis 25:285, 1998. Kiddy DS et al: Diet-induced changes in sex hormone binding globulin and free testosterone in women with normal or polycystic ovaries: correlation with serum insulin and insulin-like growth factor-I, Clin Endocrinol 31:757, 1989. Knochenhauer ES et al: Prevalence of the polycystic ovarian syndrome in unselected black and white women of the southeastern United States: a prospective study, J Clin Endocrinol Metab 83:3078, 1998. Koutras DA: Disturbances of menstruation in thyroid disease, Ann NY Acad Sci 816:280, 1997. Langley PC, Tyring SK, Smith MH: The cost effectiveness of patient-applied versus provider-administered intervention strategies for the treatment of external genital warts, Am J Manag Care 5:69, 1999. Legro RS et al: Evidence for a genetic basis for hyperandrogenemia in polycystic ovary syndrome, Proc Natl Acad Sci USA 95:14956, 1998. Legro RS, Finegood D, Dunaif A: A fasting glucose to insulin ratio is a useful measure of insulin sensitivity in women with polycystic ovary syndrome, J Clin Endocrinol Metab 83:2694, 1998. Mardh PA, Arvidson M, Hellberg D: Sexually transmitted diseases and reproductive history in women with experience of casual travel sex abroad, J Travel Med 3:138, 1996. Nelson DB et al: Factors predicting upper genital tract inflammation among women with lower genital tract infection, J Womens Health 7:1033, 1998. Nestler JE et al: Insulin stimulates testosterone biosynthesis by human thecal cells from women with polycystic ovary syndrome by activating its own receptor and using inositol glycan mediators as the signal transduction system, J Clin Endocrinol Metab 83:2001, 1998. Nestler JE et al: Ovulatory and metabolic effects of D-chiro-inositol in the polycystic ovary syndrome, N Engl J Med 340:1314, 1999. Nestler JE et al: A direct effect of hyperinsulinemia on serum sex hormone-binding globulin levels in obese women with the polycystic ovary syndrome, J Clin Endocrinol Metab 72:83, 1991. Rosen T, Brown TJ: Cutaneous manifestations of sexually transmitted diseases, Med Clin North Am 82:1081, 1998. Scott LL: Prevention of perinatal herpes: prophylactic antiviral therapy? Clin Obstet Gynecol 42:134, 1999. Sheffield JS, Wendel GD Jr: Syphilis in pregnancy, Clin Obstet Gynecol 42:97, 1999. Singh AE, Romanowski B: Syphilis: review with emphasis on clinical, epidemiologic, and some biologic features, Clin Microbiol Rev 12:187, 1999. Stanberry L et al: New developments in the epidemiology, natural history and management of genital herpes, Antiviral Res 42:1, 1999. Stanley M: The immunology of genital human papilloma virus infection, Eur J Dermatol 8(7 suppl):8, 1998. Tulppala M et al: Polycystic ovaries and levels of gonadotropins and androgens in recurrent miscarriage: preliminary experience of 500 consecutive cases, Hum Reprod 9:1328, 1994. Van Voorst Vader PC: Syphilis management and treatment, Dermatol Clin 16:699, 1998. Velazquez E, Acosta A, Mendoza SG: Menstrual cyclicity after metformin therapy in polycystic ovary syndrome, Obstet Gynecol 90:392, 1997. Velazquez EM et al: Metformin therapy in polycystic ovary syndrome reduced hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure, while facilitating normal menses and pregnancy, Metabolism 43:647, 1994.

Wald A: Herpes: transmission and viral shedding, Dermatol Clin 16:795, 1998. West RV: The female athlete: the triad of disordered eating, amenorrhea, and osteoporosis, Sports Med 26:63, 1998. Xiao E, Ferin M: Stress-related disturbances of the menstrual cycle, Ann Med 29:215, 1997. Yoshimura Y: Insulin-like growth factors and ovarian physiology, J Obstet Gynaecol Res 24:305, 1998. Young H: Syphilis: serology, Dermatol Clin 16:691, 1998. Zawadzki JK, Dunaif A: Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In Dunaif A et al., editors: Polycystic ovary syndrome, Boston, 1992, Blackwell Scientific. Zenilman JM: Update of the CDC STD treatment guidelines: changes and policy, Sex Transm Infect 74:89, 1998.

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Chapter 76 - Elders in the Wilderness Blair Dillard Erb

Too many people live their lives by the calendar. John Glenn, senior astronaut[22]

Seniors in our society are encouraged to remain mentally, physically, and socially active. They perceive this recommendation as a welcome invitation to live life to its fullest. In response, elders in increasing numbers have come to enjoy the fellowship, camaraderie, and adventure of wilderness activities. Unfortunately, health risk associated with high-performance activities increases with age because of altered physiologic function, unrecognized impairments, or effects of illnesses and their treatment. To reduce risk, seniors should be advised to temper their enthusiasm with the caution derived from the wisdom of experience. John Glenn made his second space flight safely at age 77 because of thoughtful planning and training. A maxim from his aeronautical colleagues reminds us, "There are old pilots, and there are bold pilots, but there are no old, bold pilots." This review examines the risks, pathology, treatment, and, most important, prevention of health problems of elders as they venture into the wilderness.

THE AGING PROCESS Aging is a natural consequence of life's continuum. It results in anatomic, biochemical, and physiologic alterations in function. Degenerative disorders and diseases occur that include a variety of problems, such as atherosclerotic and cerebrovascular diseases; chronic obstructive pulmonary disease; emphysema; diabetes mellitus; arthritis; emotional, mood, and memory disorders (e.g., depression, Alzheimer's disease); impaired thermoregulation; and increase in medication intake. These may affect individual performance and increase medical risk in the wilderness. The cumulative effect of these changes on elders subjected to stressful environmental factors results in a major increase in health risk and health care demand.[9] Every organ system of the body is affected to some degree by the aging process. Anatomic changes are usually organ specific, occurring in a way that is unique to the organ and the disease. Organs appear to age independently of each other and not necessarily in a parallel fashion. For example, glomerular filtration rate (GFR) and renal blood flow (RBF) decrease with age, but many elders have normal serum creatinine levels because there is a concomitant loss of muscle mass and creatinine production. Physical and physiologic alterations may evolve so slowly that they may not be apparent for many years, yet result in functional and anatomic changes. The degree of loss of function in various physiologic systems can be approximated by using the "1% rule," which states that "most organ systems lose function at roughly 1% per year after the age of 30 years."[18] Some age-related morphologic changes and their resulting functional changes include the following: Cardiovascular system: elongation and tortuosity of aorta and arteries, thickening of arterial intima, fibrosis of arterial media, sclerosis of cardiac valves, especially aortic and mitral Functional results: decreased cardiac output of 20% to 30% by age 70 years; decreased maximal heart rate of 6 to 10 beats/min/decade Lung: decreased elasticity, decreased activity of cilia, and reduced volume Functional results: decreased vital capacity of roughly 30 ml/year after age 30 years Kidney: increase in number of abnormal glomeruli Functional results: compensatory reduction in muscle mass neutralizing creatinine elevation; proteinuria Gastrointestinal tract: decreased gastric hydrochloric acid, reduced salivary flow, and decreased number of taste buds Functional results: modified appetite, food intake, and motility Musculoskeletal system: decreased height and weight, loss of skeletal calcium, sarcopenia, increased ratio of fat to muscle mass, reduced elasticity in connective tissue, decreased viscosity of synovial fluid, loss of cartilaginous surfaces, and hypertrophic changes in joints Functional results: osteoporosis, degenerative joint disease, failure to thrive (FTT) syndrome, loss of muscle mass and strength of 20% by age 65 years Central nervous system: reduced brain mass, brain weight, decreased cortical cell count Functional results: impaired cerebral function; decreased nerve conduction; loss of agility; and sensory impairment, including taste, smell, and touch Eyes: decreased translucency of the lens and decreased size of the pupil, potential increase in intraocular pressure, and arcus senilis

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Functional results: decreased vision, including color and night vision, and impaired accommodation Ears: loss of auditory neurons and atrophy of cochlear hair cells. Functional results: decrease in hearing, primarily affecting high tones, especially frequencies greater than 2000 Hz Skin: flattening and atrophy, attenuation of undulations in the dermal rete pegs, loss of cytoplasm of basal keratinocytes, and loss of dermal collagen Functional results: decreased skin thickness, risk of dermoepidermal separation, decreased resistance to tear, and loss of elasticity

Inasmuch as aging reflects a time dimension, injuries and illnesses that occur along the path of life may produce cumulative anatomic scars, which, when combined with the degenerative changes of aging, may result in a functionally impaired elderly person. The risk may be greatly exaggerated by wilderness ventures. The challenge to health professionals is to determine the extent of that risk and to take appropriate action.

CLASSIFICATIONS OF ELDERS For purposes of identifying elderly individuals at risk, it is useful to divide them into groups. Barry and Eathorne[3] suggest classifying elders as the hale and the frail. This is a clever play on words but not very useful from a medical perspective. Smith,[27] as reported by Howley, recommends classifying individuals according to chronologic age: (1) athletic old (less than 55 years of age, (2) young old (55 to 75 years of age), and (3) old old (greater than 75 years). However, this scheme focuses only on chronologic age and implies from a limited perspective that there is uniform functional change that may be quantified by age in years. I prefer a comprehensive classification that defines three factors: (1) chronologic: simple time-based classification in years, (2) pathologic: describing morphologic and anatomic changes, and (3) functional: defining functional changes that may modify or impair an individual.

ETIOLOGY OF THE AGING PROCESS Why do some individuals age faster than others? Lifestyle and genetic predisposition are the most commonly incriminated "causes," but this does not explain the biologic basis for aging.[13] Somehow, and often indirectly, genetic events may determine longevity. For example, there is an increased risk of development of Alzheimer's disease in the presence of an allele of apolipoprotein E (ApoE) gene, which encodes a carrier of cholesterol.[2] Support for genetic determination of tissue longevity is scant. Most biologists believe that the processes of aging are multifactorial. Stochastic theories suggest that deoxyribonucleic acid (DNA) damage and damage to proteins occurs from a variety of sources, such as reactive oxygen species including superoxide, the hydroxyl radical, and hydrogen peroxide. Mitochondria are an important source of reactive oxygen species and a major site of damage. Other theories on the aging process include cellular changes, autoimmune mechanisms, neuroendocrine factors, and even a "biological clock," but Strehler[30] feels that the cause should explain the progressive deleterious and intrinsic changes universal within the species. For example, some animals, usually cold-blooded fish or amphibians, which may grow to an indeterminate size, may have an indeterminate lifespan, whereas warm-blooded animals with a limited or fixed size after maturation may die at a more predictable time and at an actuarially determined rate.[31] Questions concerning the nature and cause of aging include the following: • Does aging affect everybody? Yes, but with considerable variation. • Is aging a disease? Are there decrements in or natural losses of function and anatomic content representing "normal aging"? If so, there must be such a thing as "abnormal aging." • Is aging genetically programmed as a sequence of events? Evidence suggests that genetic events may influence longevity, especially by modifying various influences such as cholesterol and blood sugar. • Is aging a result of natural selection? Darwin's laws of natural selection and evolution have been considered, but in the 2 to 3 million years of human existence, there have been too few old humans in any generation until recently to provide proof of a selective advantage favoring genetic expressions related to aging. • Is there a finite number of population doublings of human fibroblasts? Hayflick suggested that there are 50 doublings of fibroblasts during their lifespan. If, for example, the lifespan of fibroblasts is 18 months, 50 doublings would result in a predicted lifespan of approximately 75 years. • Is an individual responsible for personal longevity? Lifestyle factors, such as lack of exercise, dietary habits, tobacco use, and drug and alcohol use, not only influence anatomic and functional characteristics but may have deleterious effects on health and length of life. In perhaps the clearest summation of these theories, Hayflick suggests that the ultimate effect from the many factors influencing and affecting human life is that we simply exceed our reserve capacity. This lends support to the mountaineering dictum, "Always keep your reserve," which is particularly appropriate for elders.

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DEMOGRAPHY OF ELDERS AND THE WILDERNESS Extended lifespans during the twentieth century have resulted in changes in the composition by age of the populations of Western civilizations. The median age in the United States in 1900 was 23 years, rose to 30 years in 1950, and reached 33 years in 1990. Predictions for changes in life expectancy forecast a median age of 36 years in the year 2000, and 41 years by 2025. Persons over 65 years were the fastest growing segment (22.3%) of the U.S. population between 1980 and 1990, when the total persons over 65 years of age was 35.1 million.[6] Estimates predict that by the year 2030, the number of individuals 65 years and over will reach 70 million in the United States alone.[1] It is not simply the size and growth of this group of seniors that is responsible for its changing medical needs, but rather changes in the characteristics of the lifestyle and activities adopted by them. Of the 18 million persons between ages 65 and 74, most are retirees, and many devote their new leisure time to outdoor activities. The largest increases in elders between 1980 and 1990 occurred in regions of the United States most commonly associated with an active outdoor lifestyle: mountain states 44%, Pacific states 31%, and southern Atlantic states 34%. By contrast, the population of elders in the north central area increased only 11.4%.[6] [11] Leaf[21] reported three locations in the world, all in relatively remote mountainous areas (the Caucasus Mountains in Georgia, the Andes in Equador, and the Karakoram range in Pakistani-controlled Kashmir), where individuals frequently live to ages beyond 100 years. Speculation suggests that this is due to a combination of factors, including genetic selection and a physically active lifestyle.

Figure 76-1 President George Bush celebrating his 75th birthday with a parachute jump. He remarked, "Even old guys can still do stuff." (Newsweek, June 21, 1999. Photo courtesy George Bush Presidential Library.)

WHY ELDERS VENTURE INTO THE WILDERNESS Most members of Western industrialized cultures adhere to principles of hard work, family and fiscal responsibility, and delayed gratification. As retirement years approach, seniors begin to collect their "rewards." These include the pleasures and benefits of recreational activities. Nash[24] suggests that the personal reasons for elders to venture into the wilderness are for enjoyment of nature, for physical fitness, for tension reduction, for tranquility and solitude away from noise and crowds, for experiences with friends, for enhancement of skill and competency, and for excitement or even risk-taking ( Figure 76-1 ). As a result, outdoor recreational activities selected in the U.S. National Park System in order of decreasing frequency include: driving for pleasure, sightseeing, walking for pleasure, picnicking, stream/lake/ocean/pool swimming, and motorboating. Less common recreational activities include backpacking, off-road motorcycling, exploration, kayaking, and cross-country skiing.[5] Although the venture frequency of the latter group is much less than the former, the risk per venture is much greater. These ventures often take place in difficult and inaccessible areas under extraordinary environmental circumstances and, in the event of an emergency, may invoke search and rescue services and/or a medical intervention.

ENVIRONMENTAL STRESSES AND ELDERS Potential physiologic stresses encountered in the great diversity of outdoor wilderness activities are legion. They include extremes of heat and cold, high altitude, water immersion, tropical humidity, and desert aridity. The common denominator in nearly all of these ventures

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is physical activity, often at extreme levels. To compound the complexity, with any environmental stress, the physician may be dealing with an elder afflicted with subclinical disease or manifest disease. When the physiologic demands from environmental stresses are added to the increase and prevalence of disease associated with aging, risk for illness and injury is multiplied. The complete package of age, conditioning, environment, and nature of the activity must be considered when an elder is advised or treated in the wilderness. Heat (see Chapter 10 ) Tolerance to heat depends on physiologic factors: (1) characteristics of the host, including health status and medications, frequency and duration of exposure, and history of recent acclimatization; and (2) additional environmental factors. Industry has considered levels for permissible exposure limits (PEL), threshold limit values (TLV), and standards for maximal exposure, but there has been no consensus on an exact environmental stress index for heat. Elders in a hot wilderness setting may have personal host characteristics, in addition to the environment, that further limit tolerance and safety. Weight; fractionated body mass; cardiovascular, renal, or pulmonary problems; and the presence of various medications may influence individual response to heat. Regulation of body heat may be affected by altered function of the thermoregulatory center located in the anterior preoptic hypothalamic nuclei, by deranged skin sensors, or by medications used to treat various diseases, including anticholinergics, ß-blockers, antipsychotic medications, and major tranquilizers. Side effects influence adaptation of sweat mechanisms to thermal stress. Diuretics may produce hypovolemia with loss of adequate subcutaneous circulation for heat dissipation. Because elders as a rule consume more medications than younger persons, it is very important to approach heat injury preventatively rather than after hyperthermia occurs. The cardiovascular system plays a major role in heat regulation through heat dissipation. Circulatory abnormalities, peripherovascular disease, hypertension, and reduced cardiac output may modify heat dissipation, resulting in vulnerability to heat injury. Functional capacity as measured by maximal O2 consumption (V?O2 max) decreases 5% to 15% per decade after age 25 years. ß-Blockers and calcium channel blockers may also influence cardiac output by modifying heart rate and myocardial contractility. To prevent heat-related illness in the elderly, it is prudent to suggest a regular exercise program in heat. A regular program of physical activity consisting of 60 to 100 minutes of low-intensity exercise per day for 7 to 14 days at tolerable heat levels before the planned exposure should result in significant adaptation in normal individuals. The exercise level should require an oxygen consumption of less than 50% of the individual's V?O2 max. Experience teaches us that a degree of adaptation results from frequent and extended periods of exposure. Acclimatization to heat yields a more beneficial response to concomitant exercise. This includes lower heart rate, enhanced tolerance to physical activity, predictable core temperature in response to heat stress, increased sweat rate, and decreased sodium loss through sweating. Additional environmental factors, such as high humidity, high winds, and infrared and ultraviolet radiation exposure, may modify levels of individual tolerance to heat, partly through skin changes. It is valuable to teach individuals to be aware of the environment and whether the skin feels warm, cold, or damp. It also is helpful to advise the prospective wilderness venturer that, as a general rule, it takes a breeze of greater than 5 knots (5.75 mph) to be appreciated against the skin of the face. This may serve as a body signal reflecting one of the features that may add to the process of heat dissipation (see Body Signals, Box 76-2 ). Characteristics of Elders Vulnerable to Heat Exposure

1. 2. 3. 4. 5. 6. 7. 8.

Host characteristics: obesity, decreased physical functional capacity Infrequent heat exposure Altered thermoregulatory center in the hypothalamus or insensitive skin sensors Metabolic and serum electrolyte abnormalities Heart disease, coronary artery disease, pulmonary disease, diabetes, and renal disease Peripheral vascular disease Multiple medications, often in combination: anticholinergics, antipsychotics, tranquilizers, and ß-blockers Alcohol

Prevention of Heat Injury in the Elderly

1. 2. 3. 4. 5. 6.

Maintain adequate hydration. Assess the health status, with particular emphasis on history, cardiovascular status, obesity, and previous history of problems associated with heat exposure. Maintain adequate nutritional status—food, fluid, and electrolyte intake. Use estrogen replacement therapy where indicated (see Clinical Medicine, Menopause). Participate in a proper acclimatization program. Avoid the use of superfluous medication.

Cold (see Chapter 6 ) Cold exposure is poorly tolerated among the elderly, and body temperature is more difficult to control in elders than in younger people. Peripheral vasoconstrictive response to cold is diminished. Systolic hypertension

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through stimulation of the sympathetic nervous system is exaggerated in a cold environment. Cardiac workload is increased, and consequently, in the presence of coronary artery disease, angina is frequently precipitated by exertion and cold. Four avoidance factors for persons with coronary artery disease are exertion, exposure to cold, eating excessively, and emotional extremes, any one of which can precipitate angina. These factors are referred to as "the four Es of angina." An elder individual should remember that any one of these can induce angina and should be particularly careful not to combine any two of these potential ischemia-producing factors. With aging, diminished metabolic rate occurs. When associated with age-related reduction in muscle mass, the shivering response is blunted and there is reduced capacity for heat generation. Exhaustion added to hypoglycemia and dehydration compounds the problem of impaired metabolic function, making the elder individual more vulnerable to the effects of cold. Adequate food intake is essential for maintaining body heat and may become critical. Other physical environmental influences, such as wind, humidity, ultraviolet and infrared radiation, and altitude, should be factored into the exposure equation. The wind chill index provides a useful teaching device for reminding the

explorer about the hazards of combining cold and wind. The classic combination of cold, dampness, wind, and exhaustion may prove fatal, especially in an elder with decreased physical reserve. Medical conditions may contribute to hypothermia. Cardiovascular disease, metabolic diseases such as hypothyroidism and diabetes, compromised nutritional status, and modified thermoregulatory responses resulting from central nervous system disease or medication may influence heat conservation. Heat loss may also be increased by damp, wet clothing. All persons should be cautioned to carry ample clothing for changes after saturation with moisture. The fundamental mechanism for heat conservation, peripheral vasoconstriction, may be enhanced to some small degree by long-term adaptation to cold, resulting in more effective protective function. When an elder recognizes intolerance to cold, he or she may begin a program of gradual increase in exposure to cold. However, prevention of cold injury is best achieved through a learning process derived from experience. Elders should never venture unaccompanied into the cold wilderness. Judgment and independent responsibility may be impaired by elders who find themselves lost or in a rescue situation. Characteristics of Elders Vulnerable to Cold Exposure, Cold Injury, and Frostbite

1. 2. 3. 4. 5. 6. 7. 8.

Peripheral vascular disease (impaired vasoconstriction) Hypertension (cold-induced) Heart disease, including coronary artery disease, decreased cardiac output, congestive heart failure Metabolic diseases (diabetes, obesity, hypothyroidism) Hematologic disorders (anemia, dysproteinemias) Pulmonary disease (cold-induced asthma, chronic obstructive pulmonary disease) Drugs and alcohol Medications, particularly ß-blockers and tranquilizers

Prevention of Cold Injury in the Elderly

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Avoid exhaustion during wilderness ventures. Limit exposure. Carry and wear adequate clothing, including rain gear. Stay dry and avoid damp undergarments from excessive sweating. Maintain adequate nutrition with high carbohydrates and fat. Carry adequate food for the trip. Maintain adequate fluid intake. Do not consume cold ice or snow! Participate in a preexpedition physical training program. Avoid exhaustion. Pay attention to medication effects. Avoid alcohol and illicit drugs. Always maintain access to an adequate shelter.

Altitude Demographic data for altitude illness among the elderly are limited. Most studies have been on healthy, vigorous young males. However, Houston,[15] Honigman,[14] and others studied the general population at moderate altitude (2000 to 3000 m [6562 to 9843 feet]) elevation at ski resorts in Colorado. Predictors of mountain sickness included chronic residence at altitude greater than 1000 m (3281 feet) before a high-altitude venture, underlying lung problems, previous history of acute mountain sickness (p