Wilderness Medicine: Expert Consult Premium Edition, 6th Edition

WILDERNESS MEDICINE

WILDERNESS MEDICINE Sixth Edition Paul S. Auerbach, MD, MS, FACEP, FAWM Redlich Family Professor of Surgery Division of Emergency Medicine Department of Surgery Stanford University School of Medicine Stanford, California

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

WILDERNESS MEDICINE

ISBN: 978-1-4377-1678-8

Copyright © 2012, 2007, 2001, 1995, 1989, 1983 by Mosby, an imprint of Elsevier Inc. Chapter 83 © 2012 by Michael E. Jacobs and Charles G. Hawley Chapter 3 all figures, tables, and photographs © Dr. Mary Ann Cooper Chapter 29 photographs © Dr. Grant S. Lipman, Elsevier granted non-exclusive license to publish Chapter 20 © Swaminatha Mahadevan No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of product liability, negligence, or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Wilderness medicine / [edited by] Paul S. Auerbach.—6th ed.     p. ; cm.   Includes bibliographical references and index.   ISBN 978-1-4377-1678-8 (hardcover : alk. paper)   I.  Auerbach, Paul S.   [DNLM:  1.  Wilderness Medicine.  2.  Emergency Treatment—methods.  3.  Environmental Exposure.  4.  Recreation.  5.  Rescue Work.  6.  Survival.  WB 107]   LC classification  not assigned   616.9′8—dc23                      2011032078 Acquisitions Editors: Dolores Meloni and Stefanie Jewell-Thomas Developmental Editor: Lucia Gunzel Publishing Services Manager: Anne Altepeter Associate Project Manager: Jessica Becher Design Direction: Steve Stave Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1 

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Contributors Javier A. Adachi, MD, FIDSA, FACP

Associate Professor, Department of Infectious Diseases, Infection Control, and Employee Health, The University of Texas MD Anderson Cancer Center; Adjunct Professor, The University of Texas Health Science Center at Houston, Medical School and School of Public Health; Adjunct Professor, Baylor College of Medicine, Houston, Texas; Visiting Professor, Universidad Peruana Cayetano Heredia, Lima, Peru

Martin E. Alexander, BScF, MSc, PhD, RPF

Adjunct Professor, Wildland Fire Science and Management, Department of Renewable Resources, Alberta School of Forest Science and Management, University of Alberta; Honorary Research Associate, Faculty of Forestry and Environmental Management, University of New Brunswick, Fredericton, New Brunswick, Canada; Senior Fire Behavior Research Officer (Retired), Canadian Forest Service, Northern Forestry Centre, Edmonton, Alberta, Canada

Robert C. Allen, DO, FACEP

Colonel, United States Air Force MC CFS (Retired), Contingency Operations Division, United States Air Force School of Aerospace Medicine, Brooks City, Texas

Susan Anderson, MD, MS

Clinical Associate Professor, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California; Travel, Tropical, and Wilderness Medicine Consultant, Travel Medicine and Emergency/Urgent Care, Palo Alto Medical Foundation, Palo Alto, California

Aaron L. Baggish

Associate Director, Cardiovascular Performance Program, Division of Cardiology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts

Jennifer G. Baine, MD

Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Buddha Basnyat, MD, MSc, FACP, FRCP(E)

Medical Director, Nepal International Clinic, Himalayan Rescue Association; Principal Investigator, Oxford University Clinical Research Unit, Patan Academy of Health Sciences, Kathmandu, Nepal

Ryan P. Bayley, MD

Resident Physician, Emergency Medicine, New York-Presbyterian Weill Cornell Medical Center and Columbia University Medical Center, New York, New York

Greta J. Binford, PhD

Associate Professor of Biology, Lewis and Clark College, Portland, Oregon

Nicholas H. Bird, BA, MD, DABFM, DABPM

CEO and Chief Medical Officer, Divers Alert Network, Durham, North Carolina

Christopher J. Andrews, BE, MBBS, MEngSc, PhD, JD, EDIC, DipCSc, GDLP

Ryan Blumenthal, MBChB (Pret), MMed (Med Forens) Pret, FC for Path (SA), Dip For Med (SA)

E. Wayne Askew, PhD

Jolie Bookspan, MEd, PhD, FAWM

Mt Ommaney Family Clinic, Australia

Colonel, United States Army MSC (Retired), Professor and Chair, Division of Nutrition, University of Utah, Salt Lake City, Utah

Dale Atkins, BA

Forensic Pathologist, Department of Forensic Medicine, University of Pretoria, Pretoria, Gauteng, South Africa

Medical Director, Neck and Back Pain Sports Medicine, Academy of Functional Exercise Medicine, Temple University, Philadelphia, Pennsylvania

President, American Avalanche Association; Vice President, Avalanche Rescue Commission; International Commission for Alpine Rescue, North America Training and Education Manager, RECCO, AB, Boulder, Colorado

Ralph S. Bovard, MD, MPH, FACSM

Paul S. Auerbach, MD, MS, FACEP, FAWM

Warren D. Bowman, MD, FACP

Redlich Family Professor of Surgery, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Kira Bacal, MD, PhD, MPH, FACEP

Phase 2 Director, Medical Programme Directorate, University of Auckland, Auckland, New Zealand

Howard D. Backer, MD, MPH

Director, California Emergency Medical Services Authority

Department of Occupational and Environmental Medicine, HealthPartners, St. Paul, Minnesota

Clinical Associate Professor Emeritus, Department of Internal Medicine, University of Washington School of Medicine, Seattle, Washington; Staff Physician (Retired), Department of Internal Medicine, Division of Hematology-Oncology, The Billings Clinic, Billings, Montana

Leslie V. Boyer, MD

Director, Venom Immunochemistry, Pharmacology, and Emergency Response Institute; Associate Professor of Pathology, University of Arizona, Tucson, Arizona

v

CONTRIBUTORS

John E. Bradford, RN, MPAS, PA-C

Charles Clarke, MA, MBBCh, FRCP

Mark A. Brandenburg, MD

Kenneth S. Cohen, MA, MSTh

Peace Corps Medical Officer, United States Peace Corps, Malawi, Lilongwe, Malawi, Africa; Clinical Adjunct Professor, University of Utah Physician Assistant Program, Salt Lake City, Utah

Medical Director, Emergency Department, Bristow Medical Center, Bristow, Oklahoma; Medical Director, Emergency Medical Services, Tulsa Technology Center, Tulsa, Oklahoma

Beau Briese, MD

Resident Physician, Division of Emergency Medicine, Stanford/ Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California

Colin M. Bucks, MD

Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

George H. Burgess

Florida Program for Shark Research, Florida Museum of Natural History, University of Florida, Gainesville, Florida

Sean P. Bush, MD, FACEP

Honorary Consultant Neurologist, National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom

Independent Scholar, Traditional Healer, Nederland, Colorado

Stephen D. Coleman, MD

Clinical Assistant Professor, Department of Anesthesia, Pain Management Division, Stanford University School of Medicine, Stanford, California

Bryan R. Collier, DO, FACS, CNSP

Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Shon Compton, MPAS, PA-C

Major, Specialty Corps (Retired), Chief Instructor, Center for Predeployment Medicine, United States Army Medical Department Center and School, Fort Sam Houston, Texas

Benjamin B. Constance, MD

Professor of Emergency Medicine, Loma Linda University School of Medicine, Loma Linda, California

Chief Resident Physician, Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California

Frank K. Butler Jr., BS, MD

Donald C. Cooper, PhD, MBA, EMT-P

Dale J. Butterwick, ATC(C), BA, MSc

Jimmy L. Cooper, MD, FACEP

Chairman, Committee on Tactical Combat Casualty Care, Defense Health Board, Pensacola, Florida

Associate Professor, Faculty of Kinesiology, University of Calgary; Former President, Canadian Pro Rodeo Sport Medicine Team, Calgary, Alberta, Canada

Steven C. Carleton, MD, PhD

Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio

Betty Carlisle, MD

Adjunct Assistant Professor, Department of Public Health and Preventive Medicine, State University of New York Upstate Medical University; Staff Physician, Emergency Department, St. Joseph’s Hospital, Syracuse, New York

Scott P. Carroll, PhD

Department of Entomology, University of California, Davis, California

John W. Castellani, PhD

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Samuel N. Cheuvront, PhD

Research Physiologist, Division of Thermal and Mountain Medicine, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Richard F. Clark, MD

Professor of Clinical Medicine, Director, Division of Medical Toxicology, University of California, San Diego, San Diego, California

vi

State Fire Marshal, Department of Commerce, State of Ohio, Columbus, Ohio

Staff Physician, Department of Emergency Medicine, Director, Center for Predeployment Medicine, San Antonio, Texas

Mary Ann Cooper, MD, FAMS, FAAEM

Emerita Professor, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois

Kevin Coppock, BSc, MSc

Head of Mission, Northern Sudan, Médecins Sans Frontières, Khartoum, Sudan

Larry I. Crawshaw, PhD

Professor Emeritus, Department of Biology, Portland State University, Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon

Joy E. Crook, MD, MPH

Instructor, Department of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland

Gregory A. Cummins, DO, MS

Assistant Clinical Instructor, Department of Internal Medicine, Kansas University of Medicine and Biosciences; Hospitalist, Department of Medicine, North Kansas City Hospital, Kansas City, Missouri

Tracy A. Cushing, MD, MPH, FACEP, FAWM

Assistant Professor, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado; Attending Physician, Fellowship Director, Denver Health Wilderness Medicine Fellowship, Department of Emergency Medicine, Denver Health Medical Center, Denver, Colorado

Specialty Doctor, Emergency Department, Bristol Royal Infirmary, Bristol, United Kingdom

Daniel F. Danzl, MD

Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky

Ian Davis, MBBCH, BSc (Hons)

Herbert L. DuPont, MD

Professor and Director, Center for Infectious Diseases, University of Texas School of Public Health and Medical School; Chief of Internal Medicine, St. Luke’s Episcopal Hospital; Vice Chairman, Department of Medicine, Baylor College of Medicine, Houston, Texas

Blair Dillard Erb, BS, MD, FACP, FACC

Past President, Wilderness Medical Society, The Study Center, Townsend, Tennessee

Resident Medical Officer, Department of Accident and Emergency, Cirencester Hospital, Gloucestershire; Polar Medicine, Medical Cell, Royal Geographical Society, London; Chief Medical Officer, Polar Challenge, Venture Group, Cirencester, England, United Kingdom

Timothy B. Erickson, MD

Kathleen Mary Davis, BScF, MSc

Charles D. Ericsson, MD

Kevin Davison, ND, Lac

Peter J. Fagenholz, MD

Superintendent, Montezuma Castle and Tuzigoot National Monument, National Park Service, Camp Verde, Arizona

Director, Maui Prolotherapy Clinic, Hamakuapoko, Peahi, Haiku, Maui, Hawaii

Chad P. Dawson, BS, MPS, PhD

Professor, Forest and Natural Resources Management, State University of New York College of Environmental Science and Forestry, Syracuse, New York

Janice A. Degan, RN, MS

Senior Research Nurse, Venom Immunochemistry, Pharmacology, and Emergency Response Institute, Arizona Health Sciences Center, University of Arizona, Tucson, Arizona

Thomas G. DeLoughery, MD, FACP

Professor, Department of Emergency Medicine, Division of Medical Toxicology; Director, Center for Global Health, University of Illinois College of Medicine, Chicago, Illinois

Professor of Medicine, Head, Clinical Infectious Disease, Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas

Department of Surgery, Division of Trauma, Emergency Surgery, and Critical Care, Massachusetts General Hospital; Instructor in Surgery, Harvard Medical School, Boston, Massachusetts

Joanne N. Feldman, MD, MS

Clinical Faculty, Division of Emergency Medicine, University of California, Los Angeles, Los Angeles, California

D. Nelun Fernando, BA, MA, PhD

Department of Geography, Rutgers University, New Brunswick, New Jersey

Murray E. Fowler, BS, DVM

Professor of Medicine, Pathology, and Pediatrics, Head, Benign Hematology Section, Oregon Health and Science University, Portland, Oregon

Professor Emeritus, Veterinary Medicine and Epidemiology, University of California, Davis, California

Arlene E. Dent, MD, PhD

Assistant Professor, Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio

Clinical Associate Professor, Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina

Thomas F. Ditzler, PhD, MA, FRSPH, FRAI

Michael E. Franco, Major, MSM, MPAS, PA-C

Director of Research, Department of Psychiatry, Tripler Army Medical Center, Honolulu, Hawaii

Mark Donnelly, MD

Salem Emergency Department, Salem, Oregon

Howard J. Donner, MD

Wilderness Medicine Instructor, Mountain Medical Seminars, Bozeman, Montana; Adventure Training Coordinator, The Finer Points of Flying, San Francisco, California

Mark S. Fradin, MD

Chief, Plans and Operations, United States Army Environmental Management Systems Programs Office, United States Army Medical Department Center and School, Fort Sam Houston, Texas

Luanne Freer, MD, FACEP, FAWM

Medical Director, Medcor, Yellowstone National Park, Wyoming; Founder and Director, Everest Base Camp Medical Clinic, Himalayan Rescue Association, Kathmandu, Nepal

Eric Douglas, BA, EMT, DMT

Steven P. French, MD, BS, MS, IUCN, ASNE, SFW

Jennifer Dow, MD, FACEP, FAWM

Nathan K. Friedline, MD

Director, Education, Divers Alert Network, Durham, North Carolina

Medical Director, Denali National Park and Preserve; Medical Director, National Park Service, Alaska Region, Department of Emergency Medicine, Alaska Regional Hospital, Anchorage, Alaska

Co-founder and Research Director, Yellowstone Grizzly Foundation, Jackson Hole, Wyoming

Resident, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah; Captain, United States Army, 32nd Medical Brigade, Fort Sam Houston, Texas

vii

CONTRIBUTORS

Jon Dallimore, MB, BS, MSc, MRCGP, MCEM, FFTM RCPS (Glasg), DCH, DRCOG

CONTRIBUTORS

Raymond R. Gaeta, MD

Charles G. Hawley, BS

Tom Garrison, BS, MA, PhD

David M. Heimbach, MD

Associate Professor, Department of Anesthesiology, Medical Director, Pain Management Service, Stanford University School of Medicine, Stanford, California

Professor, Department of Oceanography, Orange Coast College, Costa Mesa, California; Adjunct Professor, Higher Education, University of Southern California, Los Angeles, California

Daniel Garza, MD

Assistant Professor, Department of Orthopaedic Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Alan Gianotti, MS, MD

Clinical Assistant Professor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Gordon G. Giesbrecht, BPE, BTh, MPE, PhD

Professor of Thermophysiology, Health Leisure and Human Performance Research Institute, University of Manitoba; Professor, Department of Anesthesia, University of Manitoba, Winnipeg, Manitoba, Canada

Kimberlie A. Graeme, BS, MD

Division of Emergency Medicine, Naval Medical Center San Diego, San Diego, California

Colin K. Grissom, MD

Associate Professor of Medicine, University of Utah School of Medicine; Associate Medical Director, Shock Trauma Intensive Care Unit, Intermountain Medical Center, Murray, Utah

Kirby R. Gross, MD, FACS

Trauma Services, United States Army Medical Department, Walter Reed Army Medical Center, Washington, DC

Peter H. Hackett, MD

Clinical Professor of Surgery, Department of Emergency Medicine, Altitude Research Center, University of Colorado Denver School of Medicine, Denver, Colorado; Director, Institute for Altitude Medicine, Telluride, Colorado

N. Stuart Harris, MD

Chief, Division of Wilderness Medicine, Director, Wilderness Medicine Fellowship, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School, Boston, Massachusetts

Patricia R. Hastings, DO, MPH, FACEP, RN, NREMT

Colonel, Medical Corps, United States Army; MEDCOM Liaison, Department of Homeland Security, Washington, DC, Department of Emergency Medicine, Brooke Army Medical Center, San Antonio, Texas

Seth C. Hawkins, MD, FACEP, FAWM

Director, Mountain Emergency Physicians; Medical Director, Burke Emergency Medical Services Special Operations Team; Executive Director, Appalachian Center for Wilderness Medicine, Morganton, North Carolina; Assistant Professor, Emergency Medical Care Program, Western Carolina University, Cullowhee, North Carolina

viii

Vice President, West Marine, Safety at Sea Moderator, United States Sailing Technical Board Member, American Boat and Yacht Council, Santa Cruz, California

Professor of Surgery, University of Washington School of Medicine, Seattle, Washington

Carlton E. Heine, MD, PhD, FACEP, FAWM

Clinical Instructor, University of Washington School of Medicine, Seattle, Washington; Attending Physician, Emergency Department, Bartlett Regional Hospital, Juneau, Alaska

Lawrence E. Heiskell, MD, FACEP, FAAFP

International School of Tactical Medicine, Palm Springs, California

John C. Hendee, PhD

Emeritus Professor and Dean (Retired), University of Idaho, College of Natural Resources, Moscow, Idaho

Henry J. Herrmann, DMD, FAGD Dentist, Falls Church, Virginia

Ronald L. Holle, BS, MS

Meteorologist, Holle Meteorology and Photography, Oro Valley, Arizona

Renee Y. Hsia, MD, MSc

Assistant Professor, Department of Emergency Medicine, University of California, San Francisco; Attending Physician, Department of Emergency Services, San Francisco General Hospital, San Francisco, California

Franklin R. Hubbell, DO

Physician and Director, Urgent Care and Spine Center, Saco River Medical Group; Physician, Director of Education, Stonehearth Open Learning Opportunities Schools; Author, Wilderness Medicine Newsletter, TMC Books, Conway, New Hampshire

Stephen E. Hudson, CEO, NTC

National Training Coordinator, National Cave Rescue Commission, National Speleological Society, Huntsville, Alabama; President, Pigeon Mountain Industries, Lafayette, Georgia

Cynthia L. Idzik-Starr, DDS

Assistant Professor, Director of Urgent Care, Department of Oral and Maxillofacial Surgery, University of Maryland Dental School, Baltimore, Maryland

Christopher H.E. Imray, PhD, MB, BS, DiMM, Clin Med Sci, FRCS, FRCP

Professor of Surgery, Warwick Medical School, Department of Vascular Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, United Kingdom

Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, FIFEM

Professor Emeritus, Department of Emergency Medicine, The University of Arizona, Tucson, Arizona

United States Coast Guard Licensed Captain; Founder and Program Director, MedSail (Medicine for Mariners and Safety at Sea); Medical Director, Vineyard Medical Services, Martha’s Vineyard, Massachusetts

Ramin Jamshidi, MD

Fellow, Department of Pediatric Surgery, Children’s Hospital of Wisconsin; Clinical Instructor, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; Adjunct Professor, Physics Department, University of California, San Francisco, San Francisco, California

James M. Jeffers, BA, LLB, LLM, MPhil

PhD Candidate, Department of Geography, Rutgers University, New Brunswick, New Jersey

Jamie G. Jenkins, MD

Brian J. Krabak, MD, MBA

Clinical Associate Professor, Department of Rehabilitation, Orthopedics, and Sports Medicine; Team Physician, Seattle Children’s Sports Medicine, Seattle University Athletics, University of Washington; Team Physician, USA Swimming; Medical Director, RacingThePlanet: 4 Deserts Ultra Marathon Series, Seattle, Washington

Andrew C. Krakowski, MD

Pediatrician and Dermatologist, Rady Children’s Hospital of San Diego, University of California, San Diego, San Diego, California; Founder and Director, boonDOCS Wilderness and Travel Medicine, La Jolla, California

Peter Kummerfeldt, AD

President, OutdoorSafe, Former Survival Training Director, United States Air Force Academy, Colorado Springs, Colorado

Ultrasound Fellow, Department of Emergency Medicine, Washington Hospital Center, Georgetown University Hospital, Union Memorial Hospital, Washington, DC

Ashley R. Laird, MD

Kirsten Johnson, MD, MPH, CCFP-EM

Carolyn S. Langer, MD, JD, MPH

Assistant Professor, Department of Family Medicine; Director, University Humanitarian Studies Initiative; Affiliated Faculty, Institute for Health and Social Policy, McGill University, Montreal, Canada; Affiliated Faculty, Harvard Humanitarian Initiative, Harvard University, Cambridge, Massachusetts

Hemal K. Kanzaria, MD

Resident Physician, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California

Emergency Physician, Sonora Regional Medical Center, Sonora, California

Instructor, Harvard Massachusetts

School

of

Public

Health,

Boston,

Patrick H. LaValla

CEO, ERI International; Operations Chief, All Hands Consulting; Former President, National Association for Search and Rescue, Olympia, Washington

Jay Lemery, MD, FACEP, FAWM

Lee A. Kaplan, MD

Clinical Professor, Department of Dermatology, University of California, San Diego Health System, La Jolla, California

Assistant Professor, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital; President-Elect, Wilderness Medical Society; Visiting Scientist, François-Xavier Bagnoud Center for Health and Human Rights, Harvard School of Public Health, Boston, Massachusetts

Misha R. Kassel, MD

Lisa R. Leon, PhD

Stephanie Kayden, MD, MPH

Benjamin D. Levine, MD, FACC, FACSM

Clinical Instructor, Departments of Emergency Medicine and Orthopaedic Surgery, Stanford University School of Medicine, Stanford, California

Director, Harvard International Emergency Medicine Fellowship; Attending Physician, Brigham and Women’s Hospital; Instructor, Harvard Medical School; Faculty, Harvard Humanitarian Initiative, Boston, Massachusetts

James W. Kazura, MD

Professor of International Health and Medicine, Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio

Robert W. Kenefick, PhD

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Alexa B. Kimball, MD, MPH

Vice Chair, Department of Dermatology, Massachusetts General Hospital; Associate Professor, Harvard Medical School, Boston, Massachusetts

Judith R. Klein, MD, FACEP

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Director, Institute for Exercise and Environmental Medicine; S. Finley Ewing Jr., Chair for Wellness, Texas Health Presbyterian Dallas; Harry S. Moss Heart Chair for Cardiovascular Research; Professor of Medicine and Cardiology, Distinguished Professorship in Exercise Science, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas

Matthew R. Lewin, MD, PhD, FACEP

Director, Center for Exploration and Travel Heath, California Academy of Sciences, San Francisco, California

James R. Liffrig, MD, MPH, FAAFP

Chair, Department of Family Medicine, Womack Army Medical Center, Fort Bragg, North Carolina; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland

Grant S. Lipman, MD, FACEP

Clinical Assistant Professor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Assistant Professor, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California ix

CONTRIBUTORS

Michael Jacobs, MD, FAWM

CONTRIBUTORS

Joanne Liu, MDCM, FRCPC

Board of Directors, Médecins Sans Frontières-Switzerland, Assistant Professor, Sainte-Justine Hospital, Montreal, Canada

Vicki Mazzorana, MD, FACEP, FAAEM, FAWM

Andrew M. Luks, MD

Assistant Professor, Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington

Associate Clinical Professor, Department of Emergency Medicine, University of Nevada School of Medicine; Codirector, Wilderness Medicine Clerkship; Co-medical Director, Death Valley, Joshua Tree National Park, Mojave National Reserve; Ringside Physician, Nevada Athletic Commission, Las Vegas, Nevada

Binh T. Ly, MD, FACMT

Loui H. McCurley, RAT, TRS

Professor, Director, Medical Toxicology Fellowship, Division of Medical Toxicology; Director, Emergency Medicine Residency, Department of Emergency Medicine, University of California San Diego, California Poison Control System, San Diego, California

Edgar Maeyens Jr., MD

Board of Visitors, Nicholas School of the Environment, Duke University, Durham, North Carolina; Private Practice Dermatology, Dermatopathology and Mohs Surgery, Coos Bay, Oregon

Swaminatha V. Mahadevan, MD, FACEP, FAAEM

Associate Professor of Surgery and Associate Chief, Division of Emergency Medicine, Stanford University School of Medicine; Emergency Department Medical Director, Stanford University Medical Center, Stanford, California

Rick Marinelli, ND, MAcOM

Clinical Professor, National College of Natural Medicine, Doctoral Faculty, Division of Biomedicine, Oregon College of Oriental Medicine, Portland, Oregon

David S. Markenson, MD, FAAP, FACEP

Medical Director, Disaster Medicine and Regional Emergency Services, Westchester Medical Center, Maria Fareri Children’s Hospital; Professor of Pediatrics, New York Medical College; Director, Center for Disaster Medicine and Professor of Clinical Public Health, New York Medical College School of Health Sciences and Practice, Valhalla, New York

Millicent Marmer, BA, MS

Graduate Student, Alden March Bioethics Institute, Albany Medical College, Albany, New York

Armando Márquez Jr., MD, FACEP

Assistant Clinical Professor, Director, Emergency Medical Services, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois

Denise Martinez, MS, RD

Adjunct Faculty, Division of Nutrition, University of Utah, Salt Lake City, Utah

Nicholas P. Mason, MB, ChB, FRCA

Consultant in Intensive Care Medicine, Royal Gwent Hospital, Newport, United Kingdom

Michael J. Matteucci, MD, FAAEM

Assistant Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Director, Emergency Medicine Residency Program, Emergency Medicine Department, Naval Medical Center San Diego, San Diego, California

x

Technical Rescue Specialist, Alpine Rescue Team, Evergreen, Colorado; Technical Director, Vertical Rescue Solutions; Vice President, Pigeon Mountain Industries, Denver, Colorado

Marion C. McDevitt, DO, MPH

Associate Director, Wilderness Medicine Emergency Medical Services Fellowship; Associate Director, Global Health Fellowship; Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah

Marilyn McHarg, MSc (A), LLD (Hon)

Executive Director, Médecins Sans Frontières-Canada, Toronto, Ontario, Canada

Scott E. McIntosh, MD, MPH

Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah

Christopher M. McStay, MD, FACEP, FAWM

Assistant Professor of Emergency Medicine, Chief of Service, Bellevue Hospital Center Emergency Department, Department of Emergency Medicine, New York University School of Medicine, New York, New York

Timothy P. Mier, BA, EMT-P

Deputy Fire Marshal, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio

Alicia B. Minns, MD

Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Division of Medical Toxicology, University of California, San Diego, San Diego, California

John Mioduszewski, BA, MA

Department of Geography, Rutgers University, New Brunswick, New Jersey

James K. Mitchell, PhD

Professor of Geography, Rutgers University, New Brunswick, New Jersey

James Moore, RN, BSc (Hons), Dip TravMed, MFTM, RCPS (Glasg), FRGS

Director, Travel Health Consultancy, Exeter, Devon, United Kingdom

Larry A. Moore, MD

Department of Emergency Medicine, Penrose-St. Francis Hospital, Wilderness Medicine Instructor, WildernessWise, Colorado Springs, Colorado

Barry Morenz, MD

Associate Professor of Psychiatry, Department of Psychiatry, College of Medicine, University of Arizona, Tucson, Arizona

Professor of Surgery and Biomedical Informatics, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Roger B. Mortimer, MD

Health Sciences Associate Clinical Professor, Department of Family and Community Medicine, University of California, San Francisco; Fresno Medical Education Program, Western Region Coordinator, National Cave Rescue Commission, Fresno, California

Michael J. Mosier, MD

Assistant Professor of Surgery, Loyola University Medical Center, Maywood, Illinois

Parveen K. Parmar, MD, MPH

Associate Director, International Emergency Medicine Fellowship, Brigham and Women’s Hospital; Associate Faculty, Harvard Humanitarian Initiative, Harvard Medical School, Boston, Massachusetts

Naresh J. Patel, DO

Private Practice, Fort Wayne Allergy and Asthma Consultants, Fort Wayne, Indiana

Sheral S. Patel, MD, FAAP

Consultant, Pediatrics and Pediatric Infectious Diseases, Hartford, Connecticut

Martin I. Radwin, MD

Robert W. Mutch, BA, MScF, DF (Honorary) Consultant, Fire Management Applications, Darby, Montana

Department of Medicine, Granger Medical Clinic, Chief of Gastrointestinal Endoscopy, Department of Medicine, Pioneer Valley Hospital, Salt Lake City, Utah

Kei Nagashima, MBSS, DMSci

Sheila B. Reed, MS

Professor, Laboratory of Integrative Physiology (Body Temperature and Fluid Laboratory), School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Mayumi Nakamura, PhD

Consultant, Disaster Risk Reduction and Development, Middleton, Wisconsin

William P. Riordan Jr., MD, MS†

Visiting Researcher, Faculty of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Eric K. Noji, MD, MPH

Robert C. Roach, PhD

Chairman and CEO, Noji Global Health and Security LLC, Director (Retired), International Emergency and Refugee Health Program, Centers for Disease Control and Prevention, Washington, DC

Robert L. Norris Jr., MD

Professor of Surgery, Stanford University School of Medicine; Chief, Division of Emergency Medicine, Stanford University Medical Center, Stanford, California

Director, Altitude Research Center; Co-Chair, International Hypoxia Symposia, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado

David A. Robinson, PhD

Professor and New Jersey State Climatologist, Department of Geography, Rutgers University, New Brunswick, New Jersey

Eloy Rodriguez, PhD

Command Surgeon, United States Army Training and Doctrine Command, Fort Monroe, Virginia

James A. Perkins Endowed Professor of Environmental and Toxicology Studies, Institute of Comparative Environmental Toxicology, Department of Plant Biology, Cornell University, Ithaca, New York

Lesley J. Ogden, MD, MBA, FACEP

Nancy V. Rodway, MD, MPH, MS

Karen K. O’Brien, MD

Staff Physician and Assistant Emergency Room Director, Department of Emergency Medicine, Samaritan North Lincoln Hos­ pital, Lincoln City, Oregon; Clinical Faculty, Department of Emergency Medicine, Western University of Health Sciences, Pomona, California; Affiliate Assistant Professor, School of Medicine, Oregon Health and Science University, Portland, Oregon

Bohdan T. Olesnicky, MD

Medical Director of Occupational Medicine and Ambulatory Care, Lake Health Hospital System, Painesville, Ohio; Adjunct Faculty, Department of Occupational Medicine, Ohio State University College of Medicine, Columbus, Ohio

Richard S. Salkowe, DPM, FACFAS, FAWM

PhD Candidate, Department of Geography, Environmental Science, and Policy, University of South Florida, Tampa, Florida

SWAT Team Physician, Palm Springs Police Department, Palm Springs, California; Partner, Global Protection Medical Group, Indian Wells, California; Director of EMS, Eisenhower Medical Center, Rancho Mirage, California

Sandra M. Schneider, MD

Sheryl Olson, BSN, RN, FAWM, CCRN

Robert B. Schoene, MD, FACP

Outdoor Survival and Navigation Instructor, Flight Nurse, Wilderness Safety Instructor, Colorado Springs, Colorado

Edward J. Otten, MD

Professor of Emergency Medicine and Pediatrics, Director, Division of Toxicology, University of Cincinnati, Cincinnati, Ohio

Professor and Chair Emeritus, Department of Emergency Medicine, University of Rochester, Rochester, New York

Clinical Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of Washington School of Medicine, Seattle, Washington, Bozeman Deaconess Hospital, Bozeman, Montana

Justin Sempsrott, MD, EMT

Emergency Medicine Resident, University of Nevada School of Medicine, Las Vegas, Nevada †

Deceased.

xi

CONTRIBUTORS

John A. Morris Jr., MD, FACS

CONTRIBUTORS

Jamie R. Shandro, MD, MPH

Assistant Professor, Division of Emergency Medicine, University of Washington School of Medicine, Seattle, Washington

Charley Shimanski

Education Director and Past President, Mountain Rescue Association; Senior Vice President, Disaster Services, American Red Cross, Washington, DC

Uta S. Shimizu, MD

Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

David R. Shlim, MD

Jackson Hole Travel and Tropical Medicine, Jackson, Wyoming

Joshua D. Shofner, MD

Resident, Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts

Julie A. Switzer, MD

Assistant Professor, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, Minnesota; Director, Geriatric Orthopaedic Trauma Program, Regions Hospital, St. Paul, Minnesota

Robert I. Tilling, BA, MS, PhD

Senior Research Volcanologist, Volcano Science Center, U.S. Geological Survey, Menlo Park, California

Ken Tokizawa, PhD

Assistant Professor, Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan

Joseph E. Tonna, MD

Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University School of Medicine, Stanford, California

David A. Townes, MD, MPH, DTM&H

Eunice Singletary, MD, FACEP

Clinical Associate Professor, Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia

Associate Professor of Medicine, Division of Emergency Medicine; Adjunct Associate Professor of Global Health, Department of Global Health, University of Washington School of Medicine, Seattle, Washington

Kieran Smart, MBChB, MSc, MPH, MRCGP

Stephen J. Traub, MD

Physician, Florida FL-3 Disaster Medical Assistance Team, Florida State Medical Response Team Region 4; Advisor, Space Medicine Associates; Adjunct Clinical Assistant Professor, Department of Community Health and Family Medicine, University of Florida College of Medicine, Gainesville, Florida

Jennifer Cohen Smith, MD

Medical Toxicologist, Banner Good Samaritan Medical Center, Phoenix, Arizona

Will Smith, MD, EMT-P

Clinical Faculty, Division of Emergency Medicine, WWAMI, University of Washington School of Medicine, Seattle, Washington; Medical Director, Teton County Search and Rescue, Jackson Hole Fire/EMS, Grand Teton National Park; President and Medical Director, Wilderness and Emergency Medicine Consulting, LLC; Faculty, Student/Resident Rotation Coordinator, Department of Emergency Medicine, St. John’s Medical Center, Jackson, Wyoming

Matthew C. Spitzer, MD, DTMH

Chairman, Department of Emergency Medicine, Mayo Clinic Arizona, Phoenix, Arizona; Assistant Professor of Emergency Medicine, Mayo Medical School, Rochester, Minnesota

Yuki Uchida, MS

PhD Student, Laboratory of Integrative Physiology (Body Temperature and Fluid Lab), Graduate School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Sydney J. Vail, MD, FACS

Director of Trauma Surgery, Medical Director, Tactical Medicine Program, Trauma Center, Maricopa Medical Center, Phoenix, Arizona

Karen B. Van Hoesen, MD

Clinical Professor, Department of Emergency Medicine, University of California, San Diego; Director, University of California San Diego Diving Medicine Center; Director, Undersea and Hyperbaric Medicine Fellowship, University of California San Diego, San Diego, California

President, Doctors Without Borders/Médecins Sans Frontières, Member, International Council and International Council Board, Médecins Sans Frontières; Assistant Clinical Professor of Medicine, Director, Predoctoral Education, Center for Family and Community Medicine, College of Physicians and Surgeons of Columbia University, New York, New York

Michael VanRooyen, MD, MPH, FACEP

Alan M. Steinman, MD, MPH, FACPM

Raghu Venugopal, MD, MPH, FRCPC

Rear Admiral (Retired), United States Public Health Service, Director of Health and Safety, United States Coast Guard, Olympia, Washington

Robert C. Stoffel

CEO, Emergency Response International; Prime Survival Training Contractor, Department of Homeland Security; Customs and Border Protection, United States Coast Guard Aviation Survival Technician Program, Cashmere, Washington

Jeffrey Suchard, MD

Professor of Clinical Emergency Medicine, Director of Medical Toxicology, Department of Emergency Medicine, University of California, Irvine Medical Center, Orange, California xii

Chief, International Division, Department of Emergency Medicine, Brigham and Women’s Hospital; Director, Harvard Humanitarian Initiative, Harvard University; Associate Professor, Department of Emergency Medicine, Harvard Medical School, Boston, Massachusetts

Assistant Professor of Medicine, University of Toronto; Attending Physician, Department of Emergency Medicine, University Health Network, Toronto, Ontario, Canada

Brandee L. Waite, MD

Medical Director, Racing The Planet: 100, Ultra Marathon Series; Assistant Professor, Physical Medicine and Rehabilitation, Sports Medicine, University of California, Davis Medical Center, Sacramento, California

John Walden, MD, DTM&H

Professor and Chairman, Department of Family and Community Health, Marshall University Joan C. Edwards School of Medicine, Huntington, West Virginia

Emeritus Professor of Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom

Eric A. Weiss, MD, FACEP

Associate Professor of Surgery, Director, Wilderness Medicine Fellowship, Division of Emergency Medicine, Stanford University School of Medicine; Medical Director, Office of Emergency Management, Stanford University Medical Center, Lucile Packard Children’s Hospital, Stanford, California

Jan West, PhD

Visiting Professor of Biology, Soka University of America, Aliso Viejo, California

James A. Wilkerson III, MD

Merced Pathology Medical Group (Retired), Merced, California

Tamae Yoda, PhD

Associate Professor, Department of Interdisciplinary Studies, Faculty of International Liberal Arts, Dokkyo University, Soka, Saitama, Japan

Lynn E. Yonge, MD, FAAFP, FAWM

Chairman, Environmental Council, Wilderness Medical Society, Director, Wilderness Medicine Training, Outward Bound, Assistant Clinical Professor, The University of South Alabama College of Medicine, Mobile, Alabama

Ken Zafren, MD, FAAEM, FACEP, FAWM

Clinical Associate Professor of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California; Staff Emergency Physician, Alaska Native Medical Center, Alaska Mountain Rescue Group, Anchorage, Alaska; Vice President, International Commission for Mountain Emergency Medicine; Associate Medical Director, Himalayan Rescue Association, Kathmandu, Nepal.

xiii

CONTRIBUTORS

David A. Warrell, MA, DM, DSc, FRCP, FRCPE, FMedSci, HonFZS, FRGS

Foreword Two hours into my first trans-Pacific flight to Hong Kong (on my way to Nepal), a flight attendant put out a call to see if there was a physician on board. I raised my hand and was taken to see a 22-year-old American soldier who was suffering a moderately severe allergic reaction to peanuts. The young man was flushed, had a diffuse urticarial rash, and felt some swelling in his throat. He was so itchy he could not sit still. The reaction had been going on for 45 minutes. As I looked him over, the captain of the plane came down the aisle to talk to me. “We’re as close as we’re going to be to Anchorage,” he said. “We can dump the entire trans-Pacific load of fuel and land there, if you say so.” I greeted this with disbelief. A few hours into my first trip to Asia, and suddenly I was in charge of the plane. I did not want to land in Anchorage if we did not have to (apart from not wanting to dump 40,000 gallons of fuel into the ocean). I asked the flight attendants to bring me the first-aid kit from the plane. I would give the soldier a shot of epinephrine and an antihistamine tablet, and we could keep going. “We don’t carry a first-aid kit,” came the reply. “We have a few bandages, that’s it.” I looked at the soldier. I did not think he was in danger of dying, but it would be a long flight for him with itchy skin and a swollen face. On the other hand, hundreds of people would be delayed a day or more, at a cost of hundreds of thousands of dollars, if we diverted to Anchorage. It occurred to me that someone on a Boeing 747 with 400 passengers might be carrying a bee sting kit. I asked the flight attendant to make an announcement, and three people raised their hands. I accepted one of the kits, injected the soldier, gave him some diphenhydramine, and watched him quickly improve. I told the captain that we could continue flying to Hong Kong. Solving problems with what you have at hand is one of the main themes of wilderness medicine, a discipline that had yet to evolve in 1979 when I was on that flight. Ten days later, I was trekking on my way to the Himalayan Rescue Association Aid Post at Pheriche, a yak-herding village at 14,000 feet, near the base of Mt Everest. Eating dinner at a teahouse next to the Thyangboche monastery, I was asked if I could help an 84-yearold Sherpa man just up the valley in Pangboche. He had fallen down his stairs and sustained a scalp laceration the day before. I was not carrying suture supplies, but I had just visited the Kunde Hospital and was familiar with the staff, so I wrote a note to request instruments and suture material. A Sherpa runner carried the note and would return with the supplies the next morning. In the morning, I walked a couple of hours to Pangboche, where I was led to the house of the man who had fallen down. He lay inside, moaning, and his hair was densely matted with blood. We carried him outside into the sun, where it was warm enough to work and there was good light. I put the instruments in a pot of water and boiled them on the hearth inside. I had no gloves and no sterile field. I poured povidone-iodine into the bowl that held the instruments and used the bowl as my sterile field, reaching into the disinfectant each time I needed to use an instrument. This kept both my hands and the instruments relatively sterile as I worked. The laceration was truly major. It split the old man’s right eyebrow and extended across his forehead and over the crown of his head to the back of his neck. A huge skin flap had been created, so I lifted it up and irrigated underneath it with copious quantities of water I had boiled earlier. I began to sew. The man moaned and muttered as I worked. I asked one of the Sherpas what he was saying. “He’s saying, ‘Leave me alone. I just want to die.’ ”

I finished the repair and placed a padded dressing on his head. I gave instructions to his son and continued my journey to the Pheriche aid post. Three days later in Pheriche, the defining case in my wilderness medicine education arrived on the back of a yak. The patient being carried down the valley was a young New Zealand nurse named Barbara. She had not been feeling well for 2 days at 16,000 feet and was no longer able to descend under her own power. Barbara was alert and oriented, although she appeared very tired. She denied having a headache, nausea, or shortness of breath over the past 2 days, and she had just descended 2000 feet. I gave her a cup of tea. She drank half the cup and then lay down and fell asleep. I sat in a chair across the room and watched her. I half-convinced myself that she looked a little blue, then talked myself out of it. She had just descended a considerable distance, with only mild symptoms of possible altitude illness. She could not have high-altitude cerebral edema (HACE). I continued this internal debate for about an hour, until I felt like I needed to know if she was okay. I touched her shoulder and spoke her name. She did not respond. I shook her gently, and she shifted slightly and made unintelligible sounds. I shook her more vigorously, but she was unable to wake up. She was no longer just sleeping—she was unconscious. There was no radio at the aid post. I sent a written note to the park ranger in Namche, requesting a helicopter rescue for early the next morning. I gave her intravenous dexamethasone and put an oxygen mask over her mouth and nose running at 2 liters per minute, trying to conserve the only two small bottles of oxygen that we had on hand. A little while later, she suddenly stirred and vomited all over her sleeping bag. Over the course of the night, she deteriorated steadily. I observed the effects of every additional drop of fluid that leaked into her brain. She became decerebrate, then flaccid, then unresponsive to deep pain. She was clearly dying. It was now just a matter of whether the helicopter would arrive in time. I felt very alone, wondering if there was anything more that I could do. The night had been completely clear when I had stepped outside before taking a short nap. When I awoke at 6:00 A.M., it was snowing. I did not think a helicopter could fly through the mountains in a snowstorm. I had kept up my hope for rescue all night long, but at that moment I began to feel that she might not make it. When that thought hit me, I found myself emotionally unprepared to watch her die. Alone in a remote aid post, with one Sherpa helper and the patient’s best friend, the circumstances were too intimate, the patient too like myself. I realized what it meant to do medicine in a wilderness setting. You are on your own. There is no one to call, no one to help. You just have to do the best you can with whatever limited resources you have. At 10:00 A.M., a Sherpa arrived carrying a portable radio. This enabled me to tell the park ranger how desperate the situation had become. His response was not encouraging. He informed me that he had been unable to reach Kathmandu by radio to request a helicopter. Later in the day, he was finally able to contact Kathmandu, but the trekking company refused to guarantee payment for a helicopter evacuation. The park ranger offered to guarantee the money himself. It got worse from there. A helicopter was ready at the airport, but the pilot had gone home for the day. When they tried to telephone him, they found that the phone lines had just gone dead. By this point, Barbara was completely unresponsive to deep pain and barely breathing at a rate of 4 times per minute. She had even lost her corneal reflexes. xv

FOREWORD

At least it had stopped snowing. I sat near the radio, waiting. The park ranger called again. “Maybe we should just try to organize the helicopter for tomorrow,” he told me. “She’s going to die this afternoon if we don’t rescue her,” I replied. “If you can’t get a helicopter this afternoon, there won’t be any point in sending one tomorrow.” “Got that,” said the ranger. Another hour went by. Finally, I heard the ranger’s voice. “Pheriche, Pheriche, Pheriche. This is Namche. The pilot has landed here and set off fuel. He’s on his way up the valley, but the weather is bad and he wants the patient ready to go.” I pulled out the intravenous line, and we secured Barbara in her sleeping bag. Her friend would fly out with her. I stepped outside the clinic and looked down the valley. Clouds whipped past the peaks. I spotted the Alouette III helicopter emerging from the clouds. I had never before been involved in a helicopter rescue, and the miraculous appearance of the aircraft seemed like an angel descending from heaven. The helicopter flew past the clinic, made an abrupt turn, and landed. The pilot shut down the rotors, but left the engine running. He waved impatiently for us to bring the patient. We carried her outside with the help of some trekkers and slid her onto the floor in the back of the helicopter, which immediately took off. We turned our faces away from the dust as the chopper disappeared down the valley, back into the clouds. It was 3 days before we got word about Barbara. She had arrived in the emergency room at Patan Hospital in Kathmandu an hour and a half after leaving us, having descended 10,000 feet. On arrival at the hospital, she was breathing 18 times per minute and was already responding to pain. Twenty-four hours later, she was sitting up in bed and eating. Thirty years later, I recognize that the key things I have learned about wilderness medicine were introduced during my experience of caring for Barbara. I was on my own, with no expert to whom I could turn for advice. I had to care for a patient in ways that I had never done in a hospital setting. I had to clean her up, turn her, catheterize her—all by candlelight, in addition to trying to figure out how to medically treat and evacuate her. Although her presentation of HACE remains the most atypical I have ever encountered, I still had to make a diagnosis and act on it, with no further tests or opinions to rely on. As I reflect back on these events, I still recall the depth of my fear that she would die despite my efforts. I have since witnessed on a number of occasions that this is a not-uncommon feeling among rescuers, who often feel devastated when the person they have tried to rescue ends up dying. Barbara’s illness taught me the value of personal experience. After this episode, the lectures I gave every day that season at the aid post on the prevention of altitude illness carried a sense of personal authority that I could not otherwise have evoked. Symptoms can be subtle. Altitude illness really can be fatal. Descent really is lifesaving. My career in medicine ran parallel to the development of the field of wilderness medicine. In the mid-1970s, physicians and mountain guides began to meet to discuss what was then called “mountain medicine.” The topics included altitude illness, first aid, frostbite, hypothermia, and evacuation. Lectures and handson workshops were included. Gradually the gatherings expanded to include topics of hiking and rafting and the skills that supported those activities, such as water disinfection, treatment of traveler’s diarrhea, and heat and cold injury. Because we were no longer talking only about the mountains, this new field was dubbed wilderness medicine. Lecturers shared their anecdotal experiences and opinions, but soon they mined the research literature and carried out investigations of their own. In 1983, the first edition of Wilderness Medicine was published. It was also in 1983 that I moved to Kathmandu to begin a 15-year stint working at the CIWEC Clinic Travel Medicine Center and started carrying out my own research into the diseases and injuries that affect travelers in Nepal. Wilderness Medicine now appears in its sixth edition. Rather than wilderness medicine defining what should be in the textbook, the textbook has helped define what is in the field of wilderness medicine. Instead of focusing solely on traditional xvi

areas, the editor has opted for inclusiveness, covering topics that include such stalwarts as lightning and frostbite, but also volcanic eruptions, combat casualty care, alligator and crocodile attacks, global humanitarian medicine, and space travel. Despite this wide range of knowledge, the specialty of wilderness medicine still has a common denominator: when something bad happens in the field, immediacy and bonding lead to an increased emotional requirement from the rescuers. In addition to diagnosis and treatment of the patient, one is confronted with limited resources and the compounding factors of weather, terrain, and isolation. Not infrequently, rescuers have to place themselves in harm’s way. At the very least, they may have to endure their own discomfort and exhaustion. Although these factors create a different dynamic of medical care, ultimately the goal is the same—to ease or prevent suffering in the patient. The quest for adventure may take travelers to countries with little or no available medical care. Many adventurers think only of their personal medical situation or of the risks that they are taking in a remote environment. They may give little or no thought to the thousands of people along their routes who can live entire lives without access to even basic medical care. The plight of the world’s poorest people may only briefly come to light at those times when a major disaster strikes. Wilderness medicine aficionados have frequently been rescuers in these extreme situations. Their experiences have sometimes taught the physicians what it really means to try to practice medicine on behalf of people who have no resources. They often return with a newly discovered desire to share medical knowledge and skills around the planet on an ongoing basis. They have come to recognize that all human beings are the same in wanting to be happy and free from suffering. Seen in this light, there is no difference between a mountaineer with altitude illness, the traveler with diarrhea, a Tibetan refugee with frostbite, the woman in an African village in the midst of a difficult birth, or a child shivering with the fever of malaria. My initial attraction to high-altitude medicine had far-reaching consequences in my personal life that I could never have foreseen. After three trekking seasons in the mountains, I moved to Kathmandu, and within a year I had volunteered to be the doctor for a Tibetan Buddhist monastery. The head of the monastery, Chokyi Nyima Rinpoche, became my teacher and close personal friend. By applying his teachings on Buddhist philosophy to my medical practice, I became more the physician I wanted to be— calmer, kinder, clear thinking, and willing to help. Our friendship led to collaboration on a book about how to train in compassion. I strongly believe that there is a way to connect wilderness medicine to conventional medicine, and even further, to our personal lives. This advice can be condensed into three key principles. First, there is competence. We should be advocates of learning and apprenticeship in the backcountry and not be satisfied with merely attaining just enough fitness to be guided on an adventure. Although one can take pleasure from achieving a distinct goal, one’s satisfaction is greatly enhanced by the cultivation of skills gained through lectures, practice in the field, and extensive personal experience. When one starts to plan a journey or an adventure, one needs to do research and fully understand the limitations imposed by that activity. Are there hazards of weather and terrain that could result in being stranded for long periods? Is there the possibility of rescue? Where is the closest medical care? To what degree are we prepared to accept the situation? Commitment means accepting the risks and limitations of a given adventure before facing the challenge, so that one can deal with it realistically. Ideally one would like to avoid having to say, “If I had known it was going to be like this, I would never have gone.” Finally, no matter what happens, one should always make decisions with full consideration of compassion. This could involve abandoning one’s own goals to help someone else or modifying the trip so that everyone can succeed. There is a famous Tibetan Buddhist saying that is true in all aspects of our lives, including our wilderness adventures:

Adventures in the wilderness, by occasionally taking us close to our limits, can teach us a great deal about our true nature. A well-known mountaineer, after living through a major rescue drama on Mt Everest, once said, “The person I wanted to be met the person I actually was.” In such defining moments, I have observed that those who abandoned their own ambitions in order to help others have always ended up happier than those who pursued only their own goals.

The wilderness is a proving ground that draws us in with its physical splendor, then tests us with hardship. We are often changed by these encounters. Whether we perceive these changes as positive or not may depend less on whether we have succeeded in our adventurous goals and more on how we learned to conduct ourselves in pursuit of those goals. The elderly Sherpa with the head laceration healed without infection and lived for 3 more years, before dying of old age. David R. Shlim, MD Author, Medicine and Compassion: A Tibetan Lama’s Guidance for Caregivers Jackson Hole, Wyoming

xvii

FOREWORD

All the joy the world contains Has come through wishing happiness for others. All the misery the world contains Has come through wanting pleasure for oneself.

Preface The sixth edition of Wilderness Medicine arrives at an exciting juncture for the field and its practitioners. Except at the time of the origin of the practice of medicine, when one might argue that perhaps all of medicine was “wilderness medicine,” there has never been greater need for people to heal in austere settings. With each natural disaster, adventure into uncharted territory, and global humanitarian relief effort, medical professionals and amateurs alike must make diagnoses with their eyes, ears, fingertips, and noses; better understand the unique physiology and pathophysiology of extreme environments; and recognize the limitations of technology in the deepest jungles and on the most remote mountaintops. More than any other specialty of medicine, wilderness medicine engages humans with Planet Earth, as it constantly calls the question, “What can we do to help?” We should help our fellow humans, while we always seek to preserve the planet. On the eve of the sixth edition, it is fair for an editor to reminisce. I suspect that many readers of this book were not born when the first edition of Wilderness Medicine (then titled Management of Wilderness and Environmental Emergencies) was published. I owe so much to the contributors to each and every edition, who in the beginning ranged from savvy clinicians and hardy explorers to youthful (and upstart) innovators. Without the collaboration of my best friend, Edward Geehr, and inspiration from the legendary professors Charlie Houston and Dave Sabiston, this book would have never exited my typewriter. In the beginning, it was no more complicated than the fact that Ed and I loved the outdoors. We had been medical students together at Duke, where we camped and hit the beach, and then enjoyed what little free time we had as interns at Dartmouth hiking and cross-country skiing. During medical school, I had been an extern on the prairie for the Indian Health Service at Fort Belknap in Montana and Ed an instructor in the mountains of New Hampshire for Outward Bound. When we were emergency medicine residents at the University of California, Los Angeles, we attended one particular mountain medicine symposium at the Yosemite Institute and listened to Charlie Houston, Herb Hultgren, John Dill, and other experts spin tales of intertwined adventure and medicine. There was no book for physicians that covered what we had heard and what more we wished to learn, so we proposed the first edition of what became Wilderness Medicine. After more than a few turndowns, the book was published as a title in the Nursing Division at Macmillan, because even though we were young and unknown, an acquisitions editor believed in us. We endured a tempestuous relationship with our senior editor, so we eagerly moved to Mosby for the second edition. The book has remained here through a series of mergers with Saunders and Elsevier. It has been a blessing to have a publisher with a vision for the vitality and relevance of wilderness medicine, and the imagination to understand that this field crosses into uncharted territory. In this edition, Dolores Meloni, Lucia Gunzel, and Jessica Becher have put forth their wonderful Elsevier spirit. My lifelong wilderness medicine buddies are too numerous to count, sustaining me for more than three decades. Each generation has raised the bar. With every edition, we used the book to push the envelope. As the content of Wilderness Medicine expanded, so did the training, practice, research, and education. It was not my intention to define the specialty, but it happened. Somewhere around the third edition, numerous aspects of a thriving specialty emerged, eminently capable leaders arose, and I could put the cart behind the horse. Now, we run to catch up, and I suspect that it will be that way forever. As change abounds, we daily appreciate novel interrelationships that are integral to a complete understanding of wilderness

medicine. High altitude is not just about hypoxia. It is about exercise physiology, genetics, ventilatory response during sleep, and much more. Understanding frostbite requires superb knowledge of anatomy, cell membrane function, reperfusion injury, and much more. To comprehend the field management of trauma, one must integrate all of the complexities related to hemorrhage, shock, hypoxia, and pain. The entire field of wilderness medicine does much more than overlap with military medicine, disaster medicine, sports medicine, environmental medicine, and travel medicine—it defines many of their most important features. Wilderness medicine is much more holistic than I would ever have imagined. Yet as robust as it has become, it will continue to expand, because we have only scratched the surface and our need is so great to know more. In recognition of venues in which wilderness medicine has been applied, to support a continuing effort to deliver credible information about the wilderness environment, and based upon requests from readers, much has been added to this sixth edition. Some of the chapters, such as Expedition Medicine, Global Humanitarian Medicine and Disaster Relief, and Ultrasound and Telemedicine in the Wilderness, are completely new, whereas others are refinements derived from wanting to leave no stone unturned. Because wilderness medicine volunteers are so capable under difficult circumstances, such as while providing disaster or global humanitarian relief, I have invited experts to broaden the coverage and better meet the information needs of the readers. Wilderness Medicine is affected by an accelerating sea change in the publishing world. Electronic publishing—words, images, and multimedia presentations—will one day render paper pages obsolete, except for collectors. Information is available instantly and disseminates at light speed, so the obligations of authors and editors have multiplied and deepened. This edition of Wilderness Medicine occurs at a watershed, when the contributors have provided much more material than can be economically offered in printed volumes. As a result, the traditional book contains the information one must be able to retrieve even when the power fails (… and if you are willing to carry 20 pounds of textbook with you); the entire electronic offering with its additional features will be there when your Internet connection is good or the power for your tablet or e-reader is plentiful. For authors, all of this takes a bit of acclimation. For readers, I suspect the transition will be welcome. There is much discussion these days about the future of medicine and in particular, if it is headed in a good direction. The camaraderie of the wilderness medicine community negates any doubts about whether or not medicine is still a desirable career path. In the days immediately after the January 2010 earthquake in Haiti, I stood side by side in Port-au-Prince with wilderness medicine colleagues from around the globe—pediatric surgeons from Switzerland, logistics experts from Norway, mountaineers from the United States, ocean divers from Spain— to put our collective skills to the most difficult challenge of our careers. Time and time again, military medical personnel make essential use of research and practice advances generated by wilderness medicine specialists that decrease morbidity and improve survival in extreme environmental settings. During global humanitarian relief efforts, when there are scarce resources, physicians, nurses, and other health care professionals who have learned how to make do with what is at hand through wilderness medicine education programs are vital to their adopted communities. The doctor who accompanies climbers to the base camp at Mt Everest also builds clinics in rural Nepal, and a nurse who leads adventure treks is moved to staff a refugee camp in the Sudan. Wilderness medicine resides at the core of what it means to be a healer. xix

PREFACE

Wilderness is at the center of wilderness medicine. To a certain degree and appropriately so, wilderness will always remain enigmatic and mysterious. Its verdant landscapes and abundant wildlife should be approached with the explicit understanding that human intrusion on its current scale is a recent phenomenon. The best that our collective environmental efforts have been able to do for wilderness is limit its destruction. We speak and write of managing wilderness, but that activity really means that we are trying to protect it from humansponsored consumption and devastation. Humans are a force of nature, so if wilderness is to cease shrinking and unimpeded fulfill its destiny, without wholesale alteration of patterns and disruption of natural cycles, then our behaviors must change. Today wilderness is considered austere because it is remote and not defined by modern technology. Our appreciation for it grows greater because breathtaking scenery is becoming more elusive. If we are not proactive, then tomorrow’s wilderness will be desolate because it has become used up and bleak. For heaven’s sake, we cannot let that happen. For the rest of my career, I am going to try to give something back. My wife, Sherry, and I began doing that with three wonderful children—Brian, Lauren, and Danny. By helping to establish a specialty, a research tradition, the Wilderness Medical Society, a peer-reviewed journal, education programs, affinity groups, clubs, and an ethos of service and multiple goals to which wilderness medicine enthusiasts can aspire, this book has accomplished its mission. Wilderness medicine in the modern

xx

age has passed its infancy and is now into childhood. There is still so much to be done. Let us together go forward with integrity and optimism.

Paul S. Auerbach, MD, MS, FACEP, FAWM

Photo credits for cover images and part openers Cover: Photographs on the cover are provided courtesy of fine art landscape photographer Elizabeth Carmel from Truckee, California. Her wonderful images may be viewed at www.ElizabethCarmel.com and www.TheCarmelGallery.com. (All images copyright ElizabethCarmel.com.) Back Cover: For cover photos and other outdoor images, visit www.TheCarmelGallery.com. Part 1: Upper: Courtesy Paul S. Auerbach, MD; Middle and Lower: Courtesy Mathias Schar, MD Part 2: Upper: Courtesy Mathias Schar, MD; Lower: Courtesy Paul S. Auerbach, MD Part 3: Upper: Courtesy R.W. Halsey, California Chaparral Field Institute; Middle: Courtesy NASA; Lower: Courtesy Michael Poland, U.S. Geological Survey Part 4: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Sheri Trbovich and Weber County Sheriff’s Department; Lower: Courtesy Jack Putnam, Maridocs Part 5: Upper: Courtesy Will Smith; Middle: Courtesy Kris H. Green; Lower: Courtesy Mathias Schar, MD Part 6: Upper: Courtesy Timothy Floyd; Middle: Courtesy Jan Ove Rein; Lower: Courtesy Michael Cardwell Part 7: Upper: Provided by K. Davison and R. Marinelli; Middle: Courtesy asimulator via flickr.com; Lower: Courtesy Daniel Ryan Part 8: Upper: Courtesy Brenda Tiernan, RN; Middle and Lower: Courtesy Paul S. Auerbach, MD Part 9: Upper and Lower: Courtesy Carl Roessler; Middle: Courtesy Marty Snyderman Part 10: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Francesco Zizola, Médecins Sans Frontiéres; Lower: Courtesy N. Stuart Harris, MD Part 11: Upper: Courtesy N. Stuart Harris, MD; Middle: Courtesy Mathias Schar, MD; Lower: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Part 12: Upper: Courtesy Corbis; Middle: Courtesy Craig Gray; Lower: Courtesy Paul S. Auerbach, MD Part 13: Upper: Courtesy Arius Hopman; Middle: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal; Lower: Courtesy Paul S. Auerbach, MD Index: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Preface: Courtesy Chuck Liddy, The News & Observer, 2010

xxv

CHAPTER 1 

High-Altitude Medicine and Physiology PETER H. HACKETT AND ROBERT C. ROACH

The Population More than 40 million tourists 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 above 4000 m (13,123 feet). In addition, millions live in large cities above 3000 m (9843 feet) in South America and Asia. The population in the Rocky Mountains of North America has doubled in the past decade; 700,000 live above 2500 m (8202 feet) in Colorado alone. 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. Altitude illness should be considered a public health problem. In this chapter, we emphasize clinical issues likely to be encountered in lowlanders visiting high-altitude locations by reviewing basic phy­siology of ascent and the pathophysiology, recognition, and management of medical problems for both visitors and residents of high altitudes (see Box 1-1).

Definitions HIGH ALTITUDE (1500 to 3500 M [4921 to 11,483 FEET]) The onset of physiologic effects of diminished partial pressure of inspired oxygen (PIO2) includes decreased exercise performance and increased ventilation (lower PaCO2) (Box 1-2). Minor impairment exists in arterial oxygen transport (arterial oxygen saturation [SaO2] at least 90%), but PaO2 is significantly diminished. Because of the large number of people who ascend rapidly to 2500 to 3500 m (8202 to 11,483 feet), high-altitude illness is common in this range (Table 1-2; see Table 1-1).

VERY HIGH ALTITUDE (3500 to 5500 M [11,483 to 18,045 FEET]) Maximum arterial oxygen saturation falls below 90% as PaO2 falls below 50 mm Hg (Figure 1-1; see Table 1-2). Extreme hypoxemia may occur during exercise, sleep, and high-altitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.

EXTREME ALTITUDE (HIGHER THAN 5500 M [18,045 FEET]) Marked hypoxemia, hypocapnia, and alkalosis characterize 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.

The Environment of High Altitude Barometric pressure falls with increasing altitude in a logarithmic fashion (Table 1-3). Therefore the partial pressure of oxygen 2

(21% of barometric pressure) also decreases, resulting in the primary insult of high altitude: hypoxia. At approximately 5800 m (19,029 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 1-3). The relationship of barometric pressure to altitude changes with distance from the equator. Thus, polar regions afford greater hypoxia at high altitude in addition to extreme cold. West565 has calculated that barometric pressure on the summit of Mt Everest (27 degrees N latitude) would be about 222 mm Hg instead of 253 mm Hg if Mt Everest were located at the latitude of Mt McKinley (62 degrees N). Such a difference, he claims, would be sufficient to render impossible an ascent without supplemental oxygen. In addition to the role of latitude, fluctuations related to season, weather, and temperature affect the pressure-altitude relationship. Pressure is lower in winter than in summer. A lowpressure trough can reduce pressure 10 mm Hg in one night on Mt McKinley, making climbers awaken “physiologically higher” by 200 m (656 feet). The degree of hypoxia is thus directly related to barometric pressure, not solely to geographic altitude.565 Temperature decreases with altitude (average of 6.5° C [11.7° F] per 1000 m [3281 feet]), and the effects of cold and hypoxia are generally additive in provoking both cold injuries and highaltitude pulmonary edema.419,559 Ultraviolet light penetration increases approximately 4% per 300-m (984-foot) gain in altitude, increasing the risks for sunburn, skin cancer, and snowblindness. Reflection of sunlight in glacial cirques and on flat glaciers can cause intense radiation of heat in the absence of wind. We have observed temperatures of 40° to 42° C (104° to 107.6° F) in tents on both Mt Everest and 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 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.

Acclimatization to High Altitude Although rapid exposure from sea level to the altitude at the summit of Mt Everest (8848 m [29,029 feet]) causes loss of consciousness in a few minutes and death shortly thereafter, climbers can ascend Mt Everest over a period of weeks, without supplemental oxygen, because of a process termed acclimatization. A complex series of physiologic adjustments increases oxygen delivery to cells and also improves their hypoxic tolerance. The severity of hypoxic stress, rate of onset, and individual physiology determine whether the body successfully acclimatizes or is overwhelmed. Recently, a revolution has taken place in our understanding of the molecular mechanisms of human responses to hypoxia. At the center of this rapidly changing field is hypoxia-inducible factor (HIF), a transcription factor that modulates the expression

BOX 1-2  Glossary of Physiologic Terms

Lowlanders on Ascent to Altitude • Acute hypoxia • High-altitude headache • Acute mountain sickness • High-altitude cerebral edema • Cerebrovascular syndromes • High-altitude pulmonary edema • Symptomatic pulmonary hypertension • High-altitude deterioration • Organic brain syndrome (extreme altitude) • Peripheral edema • Retinopathy • Disordered sleep • Sleep periodic breathing • High-altitude pharyngitis, bronchitis, and cough • Ultraviolet keratitis (snowblindness) • Exacerbation of preexisting conditions

PB P O2 PIO2 PAO2 PACO2 PaO2 PaCO2 SaO2 RQ Alveolar gas equation

Barometric pressure* Partial pressure of oxygen Inspired PO2 (0.21 × [PB − 47 mm Hg] (47 mm Hg = vapor pressure of H2O at 37° C [98.6° F]) PO2 in alveolus PCO2 in alveolus PO2 in arterial blood PCO2 in arterial blood Arterial oxygen saturation (HbO2 ÷ total Hb × 100) Respiratory quotient (CO2 produced ÷ O2 consumed) PAO2 = PIO2 − (PACO2/RQ)

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

on repeated exposure if rate of ascent and altitude gained are similar, supporting the notion of important genetic factors. Successful initial acclimatization protects against altitude illness and improves sleep. Longer-term acclimatization (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.317 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.365

Life or Long-Term Residents of Altitude • Chronic mountain sickness (chronic mountain polycythemia) • Symptomatic high-altitude pulmonary hypertension with or without right heart failure • Problems of pregnancy: preeclampsia, hypertension, and low-birth-weight infants • Exacerbation of lung disease and congenital heart disease

of hundreds of genes, including those involved in apoptosis, angiogenesis, metabolism, cell proliferation, and permeability processes.90,423,484-487,503,504 In chronic hypoxia, HIF activation by hypoxia has the positive effect of elevating oxygen delivery by boosting hemoglobin mass. But HIF also plays a role in carotid body sensitivity to hypoxia, which in turn largely determines the ventilatory response to hypoxia. As a master regulator of the hypoxia response in humans, HIF has some beneficial and harmful effects at different stages in the time course of human exposure to hypoxia, and in different cells in the body. See Figure 1-2 for an overview of some of the hundreds of processes in which the response to hypoxia is modulated by HIF. Individuals vary in their ability to acclimatize, no doubt reflecting certain genetic polymorphisms, including HIF. Some adjust quickly, without discomfort, whereas acute mountain sickness (AMS) develops in others, who go on to recover. A small percentage fails to acclimatize even with gradual exposure over weeks. The tendency to acclimatize well or to become ill is consistent

VENTILATION By reducing alveolar carbon dioxide, increased ventilation raises alveolar oxygen, improving oxygen delivery (Figure 1-3; see Figure 1-1). This response starts as low as 1500 m (4921 feet) (PIO2 = 124.3 mm Hg; see Table 1-3) and within the first few minutes to hours of high-altitude exposure. The carotid body, sensing a decrease in PaO2, through a HIF-mediated process, signals the central respiratory center in the medulla to increase ventilation.153,281 This carotid body function (hypoxic ventilatory response [HVR]) is genetically determined562 but influenced by a number of extrinsic factors. Respiratory depressants such as alcohol and soporifics, as well as fragmented sleep, depress HVR. Agents that increase general metabolism, such as caffeine and coca, as well as specific respiratory stimulants, such as progesterone277 and almitrine,192 increase HVR. (Acetazolamide, a respiratory stimulant, acts on the central respiratory center rather than

TABLE 1-1  Incidence of Altitude Illness in Various Groups

Study Group

Number at Risk per Year

Western state visitors

30 million

Mt Everest trekkers

12,000

Mt McKinley climbers Mt Rainier climbers Mt Rosa, Swiss Alps

1200 10,000 †

Indian soldiers Aconcagua climbers Kilimanjaro hikers

Unknown 4200 2500

Maximum Altitude Reached (m [ft])

Average Rate of Ascent*

~2000 (6562) ~2500 (8202) ~≥3000 (9843) 3000-5200 (9843-17,060)

3500 (11,483)

1-2

5500(18,045)

3000-5300 (9843-17,388) 3000 (9843) 2850 (9350) 4559 (14,957) 3000-5500 (9843-18,045) 3300-5800 (10,827-19,029) 2700-4700 (8858-15,420)

6194 4392 2850 4559 5500 6962 5895

1-2 (fly in) 10-13 (walk in) 3-7 1-2 1-2 2-3 1-2 2-8 2-6

Sleeping Altitude (m [ft])

(20,322) (14,409) (9350) (14,957) (18,045) (22,841) (19,341)

Percent With AMS 18-20 22 27-42 47 23 30-50 30 67 7 27 † 39 (LLS >4) 50-83

Percent With HAPE and/or HACE

Reference

0.01

214

1.6 0.05 2-3 — — 5 2.3-15.5 2.2 †

376 181 286 323 99, 323, 475 499, 500 405 106, 242

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

3

CHAPTER 1  High-Altitude Medicine and Physiology

BOX 1-1  Medical Problems of High Altitude

PART 1  MOUNTAIN MEDICINE

TABLE 1-2  Arterial Blood Gases and Altitude* Population

Altitude Meters †

Altitude residents Acute exposure

Subacute exposure

1646 2810‡ 3660‡ 4700‡ 5340‡ 6140‡ 6500§ 7000§ 8000§ 8400|| 8848§ 8848¶

Feet

PB (mm Hg)

5400 9219 12,008 15,420 17,520 20,144 21,325 22,966 26,247 27,559 29,029 29,029

630 543 489 429 401 356 346 324 284 272 253 253

PaO2 (mm Hg)

SaO2 (%)

PaCO2 (mm Hg)

73.0 60.0 47.6 44.6 43.1 35.0 41.1

(65.0-83.0) (47.4-73.6) (42.2-53.0) (36.4-47.5) (37.6-50.4) (26.9-40.1) ± 3.3

95.1 91.0 84.5 78.0 76.2 65.6 75.2

35.6 (30.7-41.8) 33.9 (31.3-36.5) 29.5 (23.5-34.3) 27.1 (22.9-34.0) 25.7 (21.7-29.7) 22.0 (19.2-24.8) 20 ± 2.8

36.6 24.6 30.3 30.6

± ± ± ±

67.8 ± 5 54 58 ± 4.5

2.2 5.3 2.1 1.4

(93.0-97.0) (86.6-95.2) (80.5-89.0) (70.8-85.0) (65.4-81.6) (55.5-73.0) ±6

12.5 ± 1.1 13.3 11.2 ± 1.7 11.9 ± 1.4

PB, Barometric pressure; PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen; SaO2, arterial oxygen saturation. *Data are mean values and (range) or ± SD, where available. All values are for subjects age 20 to 40 years who were acclimatizing well. † Data from reference 302. ‡ Data from reference 343. § Data for chronic exposure during Operation Everest II from reference 526. || Data from near the summit of Mt Everest from reference 172. ¶ Data from the simulated summit of Mt Everest from reference 430.

SaO2

160

100

140

90

PIO2

120

80

100 80

70

PaO2

60

SaO2 (%)

Partial pressure oxygen (mm Hg)

on the carotid body.) Physical conditioning apparently has no effect on HVR. Numerous studies have shown that a good ventilatory response enhances acclimatization and performance and that a very low HVR may contribute to illness433 (see Acute Mountain Sickness and High-Altitude Pulmonary Edema, later). However, over a normal range of values, HVR is not a reliable predictor of susceptibility to altitude illness. Other factors influence ventilation on ascent to high altitude. As ventilation increases, hypocapnia produces alkalosis, which acts as a braking mechanism on the central respiratory center and limits a further increase in ventilation. To compensate for the alkalosis, within 24 to 48 hours of ascent the kidneys excrete bicarbonate, decreasing the pH toward normal; ventilation increases as the braking effect of the alkalosis is removed. Ventilation continues to increase slowly, reaching a maximum only after 4 to 7 days at the same altitude (see Figure 1-3). The plasma bicarbonate concentration continues to drop and ventilation to increase with each successive increase in altitude. Persons with

60

40 20 0

2000

4000

6000

50 8000 10,000

Altitude (m) FIGURE 1-1  Increasing altitude results in decreasing inspired PO2 (PIO2), arterial PO2 (PaO2), and arterial oxygen saturation (SaO2). Note that the difference between PIO2 and PaO2 narrows at high altitude because of increased ventilation and that SaO2 is well maintained while awake until over 3000 m (9843 feet). (Data from Morris A: Clinical pulmonary function tests: A manual of uniform lab procedures, Salt Lake City, 1984, Intermountain Thoracic Society; and Sutton JR, Reeves JT, Wagner PD, et al: Operation Everest II: Oxygen transport during exercise at extreme simulated altitude, J Appl Physiol 64:1309, 1988.)

4

lower oxygen saturation at altitude have higher serum bicarbonate values; whether the kidneys might be limiting acclimatization or whether this reflects poor respiratory drive is not clear.102 This process is greatly facilitated by acetazolamide (see Acetazolamide Prophylaxis, later). The paramount importance of hyperventilation is readily apparent from the following calculation: the alveolar PO2 on the summit of Mt Everest (about 33 mm Hg) would be reached at only 5000 m (16,404 feet) if alveolar PCO2 stayed at 40 mm Hg, limiting an ascent without supplemental oxygen to near this altitude. Table 1-2 gives the measured arterial blood gas levels resulting from acclimatization to various altitudes.

CIRCULATION The circulatory pump is the next step in the transfer of oxygen, moving oxygenated blood from the lungs to the tissues. Systemic Circulation Increased sympathetic activity on ascent causes an initial mild increase in blood pressure, moderate increases 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 hours577 as a result of the bicarbonate diuresis, a fluid shift from the intravascular space, and suppression of aldosterone.35 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.417,518 Interestingly, myocardial ischemia at high altitude has not been reported in healthy persons, despite extreme hypoxemia. This is partly because of reduction in myocardial oxygen demand from reduced maximal heart rate and cardiac output. Pulmonary capillary wedge pressure is low, and catheter studies have shown no evidence of left ventricular dysfunction or abnormal filling pressures in humans at rest.174,236 On echocardiography, the left ventricle is smaller than normal because of decreased stroke volume, whereas the right ventricle may become enlarged.518 The abrupt increase in pulmonary artery pressure can cause a change in left ventricular diastolic function, but because of compensatory increased atrial contraction, no overt diastolic dysfunction results.7 In trained athletes doing an ultramarathon, the strenuous exercise at high altitude did not result in left ventricular damage; however, wheezing, reversible pulmonary hypertension, and right ventricular dysfunction occurred in one-third of those completing the race and resolved within 24 hours.107

Pressure, Estimated Partial Pressure of Inspired Oxygen, and the Equivalent Oxygen Fraction at Sea Level*

m

ft

PB

PIO2

FIO2 at SL

Sea level 1000 1219 1500 1524 1829 2000 2134 2438 2500 2743 3000 3048 3353 3500 3658 3962 4000 4267 4500 4572 4877 5000 5182 5486 5500 5791 6000 6096 6401 6500 6706 7000 7010 7315 7500 7620 7925 8000 8230 8500 8534 8839 8848 9000 9144 9500 10,000

Sea level 3281 4000 4921 5000 6000 6562 7000 8000 8202 9000 9843 10,000 11,000 11,483 12,000 13,000 13,123 14,000 14,764 15,000 16,000 16,404 17,000 18,000 18,045 19,000 19,685 20,000 21,000 21,325 22,000 22,966 23,000 24,000 24,606 25,000 26,000 26,247 27,000 27,887 28,000 29,000 29,029 29,528 30,000 31,168 32,808

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

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

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

Exp, Exponent; FIO2, fraction of inspired oxygen; PB, barometric pressure; PIO2, partial pressure of inspired oxygen; SL, sea level. *Barometric pressure is approximated by the equation PB = Exp (6.6328 − {0.1112 × altitude − [0.00149 × (altitude2)]}), where altitude = terrestrial altitude in meters/1000 or km. PIO2 is calculated as the PB − 47 (where 47 = water vapor pressure at body temperature) × fraction of O2 in inspired air. The equivalent FIO2 at sea level for a given altitude is calculated as PIO2 ÷ (760 − 47). Substituting ambient PB for 760 in the equation allows similar calculations for FIO2 at different altitudes.

Pulmonary Circulation On ascent to high altitude, a prompt but variable increase in pulmonary vascular resistance from hypoxic pulmonary vasoconstriction increases pulmonary artery pressure. Mild pulmonary hypertension is greatly augmented by exercise, with pulmonary pressure reaching near-systemic values,174 especially in persons with a previous history of high-altitude pulmonary edema.32,110 During OEII, Groves and colleagues174 demonstrated that even with a mean pulmonary artery pressure of 60 mm Hg, cardiac output remained appropriate and right atrial pressure did not rise above sea level values. Thus, right ventricular function was intact

in spite of extreme hypoxemia and pulmonary hypertension in these well-acclimatized subjects. Administration of oxygen does not completely restore pulmonary artery pressure to sea level values,324 likely because of vascular remodeling with medial hypertrophy. See Stenmark and associates509 for an excellent review of molecular and cellular mechanisms of the pulmonary vascular response to hypoxia, including remodeling. Pulmonary vascular resistance returns to normal within a few weeks after descent to low altitude. Cerebral Circulation Cerebral oxygen delivery, the product of arterial oxygen content and cerebral blood flow (CBF), depends on the net balance between hypoxic vasodilation and hypocapnia-induced vasoconstriction. CBF increases, despite hypocapnia, when PaO2 is less than 60 mm Hg (altitude greater than 2800 m [9186 feet]). In a classic study, CBF increased 24% on abrupt ascent to 3810 m (12,500 feet) and returned to normal over 3 to 5 days.491 These findings have been confirmed by positron emission tomography and brain magnetic resonance imaging (MRI) studies showing both elevations in CBF in hypoxia in humans and striking heterogeneity of the CBF, with CBF rising up to 33% in the hypothalamus and 20% in the thalamus, with other areas without significant changes.66,396 Cerebral autoregulation, the process by which cerebral perfusion is maintained as blood pressure varies, is impaired in hypoxia. Interestingly, this occurs both in newcomers, with acute246,296,521,547 and prolonged hypoxia,522 and in natives to high altitude.246 This observation raises questions about the importance of this process in AMS and acclimatization, because it appears to be a uniform response in all humans made hypoxemic. Overall, global cerebral metabolism seems well maintained with moderate hypoxia.103,356

BLOOD Hematopoietic Responses to Altitude Ever since the observation in 1890 by Viault550 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 values apparently have no relationship to susceptibility to high-altitude illness. In response to hypoxemia, erythropoietin is secreted by the kidneys and stimulates bone marrow production of red blood cells.483 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 altitude202 (Figure 1-4). The increase in hemoglobin 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. Overshoot of the hematopoietic response causes excessive polycythemia, which may 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 increased cerebral functioning.465 Oxyhemoglobin Dissociation Curve The oxygen dissociation curve (ODC) plays a crucial role in oxygen transport. The sigmoidal shape of the curve allows wellmaintained SaO2 up to 3000 m (9843 feet), despite significant 5

CHAPTER 1  High-Altitude Medicine and Physiology

TABLE 1-3  Altitude Conversion: Barometric

PART 1  MOUNTAIN MEDICINE

Ub Ub

A Normoxia

PHD2

HIF-1α

Fe2+ 2-OG Ascorbate

PHD1 O2

Ub

PHD3

HIF-1α

HIF-1α

OH OH OAc

OH OH OAc

VHL

VHL

B Hypoxia HIF-1α HIF-1α

Ub Ub

Ub

26s Proteasome

Proteolytic degradation

HIF-1α HIF-1α p300/CBP HIF-1α

Nucleus

HIF-1β

HIF-1β HRE

Angiogenesis Erythropoiesis Apoptosis

Cell proliferation and survival

HIF-1 target genes

Proteolysis pH regulation Glucose metabolism

FIGURE 1-2  Regulation of oxygen sensing by hypoxia-inducible factor (HIF). The HIF is produced constitutively, but in normoxia the α subunit is degraded by the proteasome in an oxygen-dependent manner. Hypoxic conditions prevent hydroxylation of the α subunit, enabling the active HIF transcription complex to form at the hypoxia-response element (HRE) associated with HIF-regulated genes. A range of cell functions are regulated by the target genes, as indicated. CBP, CREB binding protein; OAc, acetylation of HIF-1α; 2-OG, 2-oxoglutarate; PHD, prolyl hydroxylase; Ub, ubiquitin; VHL, von Hippel–Lindau tumor suppressor. (Reprinted from Carroll VA, Ashcroft M: Targeting the molecular basis for tumour hypoxia, Expert Rev Mol Med 7:1, 2005.)

decreases in PaO2 (see Figure 1-1). Above 3000 m (9843 feet), small changes in PaO2 cause large changes in SaO2 (Figure 1-5). Because PaO2 determines diffusion of oxygen from capillary to cell, small changes in PaO2 can have clinically significant effects. This is often confusing for clinicians because SaO2 appears relatively well preserved. At high altitude, small changes in PaO2 lead to lower O2 uptake that can have a large effect on systemic hypoxemia, and thus on clinical status, while the SaO2 may appear relatively unchanged. In 1936, Ansel Keys and colleagues266 demonstrated an in vitro right shift in position of the ODC at high altitude, favoring release of oxygen from blood to tissues. This change, due to increased 2,3-diphosphoglycerate, is proportional to the severity of hypoxemia. In vivo, however, the alkalosis at moderate altitude offsets this, and no net change occurs. In contrast, the marked alkalosis of extreme hyperventilation, as measured on the summit and simulated summit of Mt Everest (PaCO2 8 to 10 mm Hg, pH greater than 7.5), shifts the ODC to the left, facilitating oxygen-hemoglobin binding in the lung that raises SaO2 and is advantageous.462 Persons with a very left-shifted ODC, caused by an abnormal hemoglobin (Andrew-Minneapolis), when taken to moderate (3100 m [10,171 feet]) altitude, had less tachycardia and dyspnea and remarkably had no decrease in exercise performance.208 Highaltitude adapted animals also have a left-shifted ODC.

TISSUE CHANGES The next link in the oxygen transport chain is tissue oxygen transfer, which depends on capillary perfusion, diffusion distance, and driving pressure of oxygen from the capillary to the cell. Banchero20 has shown that capillary density in dog skeletal muscle doubled in 3 weeks at a barometric pressure of 435 mm Hg. A recent study in humans noted no change in 6

capillary density or in gene expression thought to enhance muscle vascularity.316 Ou and Tenney395 revealed a 40% increase in mitochondrial number but no change in mitochondrial size, whereas the study of Oelz and colleagues392 showed that highaltitude climbers had normal mitochondrial density. A significant drop in muscle size is often noted after high-altitude expeditions because of net energy deficit,316,319 resulting in increased capillary density and ratio of mitochondrial volume to contractile protein fraction as a result of the atrophy. Although there is no de novo synthesis of capillaries or mitochondria, the net result is a shortening of diffusion distance for oxygen.316,319

SLEEP AT HIGH ALTITUDE Disturbed sleep is common at high altitude. There are multiple causes. Reflecting the great interest in sleep, more than 160 papers in the last 10 years have addressed sleep at altitude. The interested reader is referred to recent reviews.67,308,551,561,569 Nearly all subjects complain of disturbed sleep at high altitude, with severity increasing with the altitude. At moderate altitude, sleep architecture is changed, with a reduction in stages 3 and 4 sleep, stage 1 time increased, and little change in stage 2. Overall, there is a shift from deeper sleep to lighter sleep. In addition, more time is spent awake, with significantly increased arousals. Clinicians have reported either slightly less rapid eye movement (REM) time or no change in REM compared with what occurs at low altitude. REM sleep may improve over time at altitude.268 The subjective complaints of poor sleep are out of proportion to the small reduction (if any) in total sleep time and appear to be due to sleep fragmentation. With more extreme hypoxia, sleep time was dramatically shortened and arousals increased, without a change in ratio of sleep stages but with a reduction in REM sleep.10 The mechanisms of this change in sleep architecture and

~10% decrease

80 10 8 40

PACO2 (mm Hg)

~ No change

12

SaO2 (%)

· VE (L/min, BTPS)

100

CHAPTER 1  High-Altitude Medicine and Physiology

14

60

40

35

B

20

30 25

A

0 0

100

20

40

60

80

100

120

SaO2 (%)

PaO2 (mm Hg) FIGURE 1-5  Oxygen-hemoglobin dissociation curve showing effect of 10-mm Hg decrement in arterial partial pressure of oxygen (PaO2) on arterial oxygen saturation (SaO2) at sea level (A) and near 4400 m (14,436 feet) (B). Note the much larger drop in SaO2 at high altitude. (Modified from Severinghaus JW, Chiodi H, Eger EI, et al: Cerebral blood flow in man at high altitude: Role of cerebrospinal fluid pH in normalization of flow in chronic hypoxia, Circ Res 19:274, 1966.)

90

80 0 1 Denver

2

3

4

5 Placebo

Days at 4300 m FIGURE 1-3  Change in minute ventilation ( V E ), end-tidal carbon dioxide (PACO2), and arterial oxygen saturation (SaO2) during 5 days’ acclimatization to 4300 m (14,108 feet). BTPS, Body temperature pressure saturated. (Modified from Huang SY, Alexander JK, Grover RF, et al: Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude, J Appl Physiol 56:602, 1984.)

50

Hematocrit (%)

100 80 SaO2 (%) 60 40

Acetazolamide

Men Women (+Fe)

48 46

Women (−Fe) 44 42 40

Respiratory pattern

Sea level 1

20

40

60

Days at 4300 m

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: Effects of acute high altitude exposure on body fluids, Fed Proc 28:1178, 1969.)

fragmentation are poorly understood. Periodic breathing appears to play only a minor role in altering sleep architecture at high altitude.461 The arousals have been linked to periodic breathing in some studies but not in others. Other factors might include change in circadian rhythm and perhaps body temperature.98 Obesity may explain susceptibility to both deranged sleep and sleep-disordered breathing in some individuals.155 Recent studies

Respiratory pattern 100 80 60 40

SaO2 (%)

FIGURE 1-6  Respiratory patterns and arterial oxygen saturation (SaO2) with placebo and acetazolamide in two sleep studies of a subject at 4200 m (13,780 feet). Note pattern of hyperpnea followed by apnea during placebo treatment, which is changed with acetazolamide. (Modified from Hackett PH, Roach RC, Harrison GL, et al: Respiratory stimulants and sleep periodic breathing at high altitude: Almitrine versus acetazolamide, Am Rev Respir Dis 135:896, 1987.)

of infants and children590 and athletes in simulated altitude devices used for training also revealed deranged sleep quality in these groups.269,270,401 Although deranged sleep is a frequent complaint in high-altitude visitors, it seems to have little relation to susceptibility to altitude illness or other serious problems. Symptomatic treatment that avoids respiratory depression is safe (see Treatment under Acute Mountain Sickness, later). Periodic Breathing Periodic breathing is most common in early and light sleep, may occur during wakefulness when drowsy, and does not occur in REM sleep. The pattern is characterized by hyperpnea followed by apnea (Figure 1-6) and is caused by a battle for control of 7

100

SaO2 (%)

80 60 40 Arrival Acclimatized

20

0

50

100 150 200 250 300 350 400 450 500 Time asleep (min)

FIGURE 1-7  Sleep oxygenation improves with acclimatization to same altitude. Top line is maximum, and bottom line is minimum arterial oxygen saturation (SaO2) in an acclimatized person. Shaded area is maximum and minimum SaO2 values for new arrival at 5360 m (17,585 feet). (Modified from Sutton JR, Gray GW, Houston CS, et al: Effects of acclimatization on sleep hypoxemia at altitude. In West JB, Lahiri S, editors: High altitude man, Bethesda, Md, 1984, American Physiological Society, pp 141-146.)

breathing between peripheral chemoreceptors (carotid body) and the central respiratory center. Respiratory alkalosis during hyperpnea acts on the central respiratory center, causing apnea. During apnea, SaO2 decreases, carbon dioxide increases, and the carotid body is stimulated, causing a recurrent hyperpnea and apnea cycle. The apnea is central, not associated with snoring, and occurs with absence of rib cage movement. Persons with high hypoxic ventilatory response have more periodic breathing,55 with mild oscillations in SaO2,282 whereas persons with low hypoxic ventilatory response have more regular breathing overall but may suffer periods of apnea with extreme hypoxemia distinct from periodic breathing.192 As acclimatization progresses, periodic breathing lessens but does not disappear, especially over 5000 m (16,404 feet), and sleep SaO2 increases (Figure 1-7; see Figure 1-6).10,55,524 Periodic breathing has not been implicated in the etiology of highaltitude illness, but nocturnal oxygen desaturation has been implicated.55,133,150 Eichenberger and colleagues130 have also reported greater periodic breathing in persons with HAPE, secondary to lower SaO2. As with fragmented sleep, intensity of periodic breathing is quite variable. Total sleep time with periodic breathing can vary from 1% to over 90%.598 Most studies report no association between periodic breathing and AMS.55 This may relate to the fact that persons with periodic breathing tend to have higher HVR and greater average ventilation and oxygenation.561 Pharmaceutical Aids Acetazolamide, 125 mg at bedtime, diminishes periodic breathing and awakenings, improves oxygenation and sleep quality, and is a safe and superior agent to use as a sleeping aid (see Figure 1-6). It has the added benefit of diminishing symptoms of AMS. Other agents include diphenhydramine (Benadryl, 50 to 75 mg) or the short-acting benzodiazepines such as triazolam (Halcion, 0.125 to 0.25 mg) and temazepam (Restoril, 15 mg).308 Although caution is warranted for any agent that might reduce ventilation at high altitude, some studies have suggested that benzodiazepines in low doses are generally safe in this situation.124,164,384 Another option is to use both acetazolamide and a benzodiazepine. Bradwell and colleagues63 showed that acetazolamide (500 mg slow-release orally) given with temazepam (10 mg orally) improved sleep and maintained SaO2, counteracting a 20% decrease in SaO2 when temazepam was given alone. The nonbenzodiazepine hypnotic zolpidem (Ambien, 10 mg) was shown to improve sleep at 4000 m (13,123 feet) without adversely affecting ventilation.45

EXERCISE Maximal oxygen consumption drops dramatically on ascent to  2 max ) falls from high altitude.151,434 Maximal oxygen uptake ( VO 8

sea level by approximately 10% for each 1000 m (3281 feet) of altitude gained above 1500 m (4921 feet). Persons with the  2 max values have the largest decrement in highest sea level VO  2 max at high altitude, but overall performance at high altitude VO  2 max .392,428,566 In fact, is not consistently related to sea level VO many of the world’s elite mountaineers have quite average  2 max values, in contrast with other endurance athletes.392 VO Acclimatization at moderate altitudes enhances submaximal  2 max (Figure 1-8).151 endurance time but does not enhance VO 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.347 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).417 Recent work has attributed the  2 max to the lower PIO2, impairment altitude-induced drop in VO of pulmonary gas exchange, and reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third  2 max .76 However, mechanisms to explain the of the loss in VO impairment of gas exchange and the lower blood flow remain elusive. Wagner556 proposes 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.91,241,356,519,520 Mountaineers, for example, become lightheaded and their vision dims when they move too quickly at extreme altitude (Figure 1-9).564 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.104 For events

180 Endurance time · VO2max

160 Sea level performance (%)

PART 1  MOUNTAIN MEDICINE

SLEEP SATURATION AT 5360 m

140 120 100 80 60 40 0

2

4

6

8

10

12

Days at altitude FIGURE 1-8  On ascent to altitude, maximum oxygen consumption  2max ) decreases and remains suppressed. In contrast, endurance ( VO  2max ) time (minutes to exhaustion at 75% of altitude-specific VO increases with acclimatization. (Modified from Maher JT, Jones LG, Hartley LH: Effects of high altitude exposure on submaximal endurance capacity of men, J Appl Physiol 37:895, 1974.)

Alveolar

Arterial

PO2 (torr)

30

20

Mixed venous

Assumed critical PO2

NEUROLOGIC SYNDROMES

Loss of consciousness · VO2max

10 Man on summit PB 253 torr DMO2 100 mL/min/torr 0 0

200

400

600

800

1000

1200

Oxygen uptake (mL O2/min) FIGURE 1-9  Calculated changes in the PO2 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 mm Hg. PB, Barometric pressure; DMO2, muscle dif 2max , maximum oxygen consumption. (Modified fusing capacity; VO from West JB: Climbing Mt. Everest without oxygen: An analysis of maximal exercise during extreme hypoxia, Respir Physiol 52:265, 1983.)

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. Also, intermittent exposures to hypoxia seem to have no benefit.251,540 Runners returning to sea level after 10 days’ training at 2000 m (6562 feet) had faster running times and an increase in aerobic power, plasma volume, and hemoglobin concentration.19 Today the “live high–train low” approach pioneered by Levine and Stray-Gundersen294,513 has been adopted by many endurance athletes. The optimal dose for specific sports is still being worked out,570 but overall, endurance athletes believe and the science supports a small, but significant improvement in sea level performance after participating in a live high–train low training camp.514 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.328,443,512 Some individuals do not respond to live high–train low, perhaps related to genetic polymorphisms and the inability to increase erythropoietin levels sufficiently to raise red cell mass and thus increase oxygen-carrying capacity.79,247

High-Altitude Syndromes High-altitude syndromes are illnesses attributed directly to hypobaric hypoxia, even if exact mechanisms are unclear. Clinically and pathophysiologically these syndromes overlap. Rapidity of onset of hypoxia is crucial; for example, sudden exposure to extreme altitude may result in death from acute hypoxia (asphyxia), whereas more gradual ascent to the same altitude may result in AMS or no illness at all. Where symptoms of acute hypoxia end and AMS begins is vague, as reflected in the classic

Neurologic syndromes reflect both nervous system sensitivity to hypoxia and effects of compensatory mechanisms. Although brain adenosine triphosphate (ATP) production and overall metabolism remain intact during moderate hypoxia, impaired synthesis of neurotransmitters can produce cerebral symptoms such as lassitude, malaise, and cognitive defects. Compensatory cerebral vasodilation at altitude appears to be the trigger for altitude headache and contributes to development of AMS and HACE. However, much of the pathophysiology of AMS and HACE remains a mystery. Focal neurologic deficits without cerebral edema are also difficult to explain; cerebral artery spasm and watershed hypoxia have both been invoked. Understanding the exact etiology of these neurologic syndromes will parallel advances in neuroscience; the emphasis in altitude illness is finally and appropriately on the brain.438

ACUTE CEREBRAL HYPOXIA Acute, profound hypoxia, although of greatest interest in aviation medicine, may also occur on terra firma when ascent is too rapid or when hypoxia abruptly worsens. Carbon monoxide poisoning, pulmonary edema, sudden overexertion, sleep apnea, or a failed oxygen delivery system may rapidly exaggerate hypoxemia. Unacclimatized persons will lose consciousness from acute hypoxia at SaO2 of 40% to 60% or a PaO2 of less than about 30 mm Hg or mixed venous PO2 of 15 mm Hg. Tissandier, the sole survivor of the flight of the balloon Zenith in 1875, gave a graphic description of the effects of acute hypoxia: But soon I was keeping absolutely motionless, without suspecting that perhaps I had already lost use of my movements. Towards 7500 m [24,606 feet], the numbness one experiences is extraordinary. The body and the mind weaken little by little, gradually, unconsciously, without one’s knowledge. One does not suffer at all; on the contrary. One experiences inner joy, as if it were an effect of the inundating flood of light. One becomes indifferent; one no longer thinks of the perilous situation or of the danger; one rises and is happy to rise. Vertigo of the lofty regions is not a vain word. But as far as I can judge by my personal impression, this vertigo appears at the last moment; it immediately precedes annihilation—sudden, unexpected, irresistible. I wanted to seize the oxygen tube, but could not raise my arm. My mind, however, was still very lucid. I was still looking at the barometer; my eyes were fixed on the needle which soon reached the pressure number of 280, beyond which it passed. I wanted to cry out “We are at 8,000 meters.” But my tongue was paralyzed. Suddenly I closed my eyes and fell inert, completely losing consciousness.54 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 9

CHAPTER 1  High-Altitude Medicine and Physiology

experiments of Bert.54 In terms of altitude illness, the general concept of a spectrum of illness with a common underlying pathogenesis is well accepted and provides a useful framework for discussion. For the neurologic syndromes, the spectrum progresses from high-altitude headache to AMS to high-altitude cerebral edema (HACE). In the lungs, 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/or oxygen. Longer-term problems of altitude exposure include high-altitude deterioration in sojourners and chronic mountain sickness in high-altitude residents.

40

PART 1  MOUNTAIN MEDICINE

progressive diminution of pressure to the point of death, while the other breathes, also to the point of death, under normal pressure, an air that grows weaker and weaker in oxygen. Both will die after having presented the same symptoms.54 Bert goes on to describe the symptoms of acute exposure to hypoxia: It is the nervous system which reacts first. The sensation of fatigue, the weakening of the sense perceptions, the cerebral symptoms, vertigo, sleepiness, hallucinations, buzzing in the ears, dizziness, pricklings … are the signs of insufficient oxygenation of central and peripheral nervous organs. … The symptoms … disappear very quickly when the balloon descends from the higher altitudes, very quickly also … the normal proportion of oxygen reappears in the blood. There is an unfailing connection here.54 Bert was also able to both prevent and immediately resolve symptoms by breathing oxygen. Modern studies of acute hypoxic exposure use the measurement of time of useful consciousness; that is, the time until a subject can no longer take corrective measures, such as putting on an oxygen mask. With exposure to 8500 m (27,887 feet), that time is 60 seconds during moderate activity and 90 seconds at rest. Acute hypoxia can be quickly reversed by immediate administration of oxygen, rapid pressurization or descent, or 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 during severe hypoxia.

HIGH-ALTITUDE HEADACHE The term high-altitude headache (HAH) has been used in the literature for decades, and studies directed toward the pathophysiology and treatment of HAH have been reported. Obviously these are to an extent also studies of AMS. Headache lends itself to investigation better than do some other symptoms, because headache scores have been well validated.244 Headache is generally the first unpleasant symptom consequent to altitude exposure and is sometimes the only symptom.214 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.435 One could even argue that it is the headache itself that causes other symptoms such as anorexia, nausea, lassitude, and insomnia, as is commonly seen in migraine or tension headaches, and that mild AMS is essentially due to headache. The International Headache Society206 has defined high-altitude headache as headache with at least two of the following characteristics: (1) bilateral; (2) frontal or frontotemporal; (3) dull or pressing quality; (4) mild or moderate intensity; and (5) aggravated by exertion, movement, straining, coughing, or bending. In addition, the headache must occur with an ascent to altitude greater than 2500 m (8202 feet), develop within 24 hours after ascent, and resolve within 8 hours after descent. Recent studies have attempted to characterize the clinical features and incidence of headache at altitude (Table 1-4). Silber and co-workers496 found that 50 of 60 trekkers (83%) in Nepal up to 5100 m (16,732 feet) developed at least one headache when over 3000 m (9843 feet). Older persons were less susceptible; women and those with headaches in daily life had more severe headaches, but no more headaches than others. Of those with headache, 52% did not have AMS by the Lake Louise criteria. The clinical features were widely variable. In general, the headaches were bilateral, generalized, dull, exacerbated by exertion or movement, often occurring at night, and resolved within 24 hours. Thus the headaches had some features of increased intracranial pressure (ICP). Persons with history of migraine did not have a higher incidence of headache. Various medications alleviated the headaches, especially mild ones, 70% of the time. Serrano-Duenas489 also described in detail HAH in 98 climbers in the Andes. Persons with history of primary headache were excluded. He found the following characteristics: holocranial, 65.6%; pulsatile-burst type quality, 75.3%; oscillating evolution, 10

TABLE 1-4  Clinical Characteristics of Headache Characteristic Location Global Frontal Hemi-cranial Occipital Change side Quality Pulsatile-burst Pressing/tightening Burning Dull Evolution Oscillate Disappear Diminish Increase Equal Break out in Elements Worsening Exercise Sudden movements Valsalva maneuver Light Elements Relieving Rest Analgesics Darkness Activity Concurrent Symptoms Anorexia Irritability Nausea Vomiting Apathy Gastric Malaise Somnolence Dysphasia Feelings Pessimism Anxiety Fear Isolation Strangeness

Percent Reporting 65.6 18.9 8.7 3.6 3.2 75.3 14.8 5.1 4.8 36.7 18.1 17.8 10.4 10.4 6.6 49.5 30.2 13.8 6.5 41.8 39 10.2 9 26.8 26.5 16.3 9.7 7.1 6.1 5.7 1.8 33.2 29.5 23.4 11.2 2.7

Modified from Serrano-Duenas M: High-altitude headache: A prospective study of its clinical characteristics, Cephalalgia 25:1110, 2005.

36.7%; increasing with exercise, 49.5%; relieved by rest, 41.8%; concurrent symptoms referred to: anorexia, 26.8%, irritability, 26.5%, and finally pessimism and anxiety feelings, 33.2% and 29.5%, respectively. Headaches were worse after a night’s sleep, more common in men, were of moderate intensity, and responded to analgesics. In general, the literature suggests that HAH can be prevented by the use of nonsteroidal antiinflammatory drugs65,72,157 and acetaminophen204 as well as the drugs commonly used for prophylaxis of AMS, acetazolamide and dexamethasone. Some agents appear more effective than do others, with ibuprofen and aspirin apparently superior to naproxen.65,70,73 A serotonin agonist (sumatriptan, a 5-HT1 [serotonin type 1] receptor agonist) was reported to be effective for HAH prevention and/or treatment in some studies,69,243,544 but not in others.28 Flunarizine, a specific calcium antagonist used for treatment of migraine, was not effective in one study.44 Interestingly, oxygen is often immediately effective for HAH (within 20 minutes) in subjects with and without AMS, indicating a rapidly reversible mechanism of the headache.26,191 The response to many different agents might reflect multiple components of the pathophysiology, or merely the nonspecific nature of analgesics. As Sanchez del Rio and Moskowitz463 have

Hypothalamus Brainstem

Autonomic response

CNS processing

High-altitude headache

Lower threshold for pain Trigeminovascular system activation

Hypoxia

eNOS upregulation

ACUTE MOUNTAIN SICKNESS Epidemiology and Risk Factors Although the syndrome of AMS has been recognized for centuries, modern rapid transport and proliferation of participants in mountain sports have increased the number of victims and therefore public awareness (see Table 1-1). The incidence and severity of AMS depend on the rate of ascent and the altitude attained (especially the sleeping altitude), duration of altitude exposure, level of exertion, recent altitude exposure, and inherent physiologic (genetic) susceptibility.440,475 For example, AMS is more common on Mt Rainier because of the rapid ascent, whereas high-altitude pulmonary or cerebral edema is uncommon because of the short stay (less than 36 hours). Persons with a demonstrated susceptibility to AMS had twice the incidence of AMS compared with nonsusceptibles, and this was independent of rate of ascent.475 The basis for inherent susceptibility is still unknown, but obviously depends on genetic factors. Acclimatization induced by recent altitude exposure can be protective; 4 days or more in the previous 2 months above 3000 m (9843 feet) reduced susceptibility to AMS on ascent to 4559 m (14,957 feet) by one-half, which was as effective as slow ascent475 (Figure 1-11). It also appears that protective effects of acclimatization persist after descent to low altitude. AMS was essentially absent in those who acclimatized to high altitude, returned to low altitude for 7 days, and were then reexposed to 4300 m (14,108 feet) in a hypobaric chamber.317 In addition, ventilation, SaO2, and exercise performance at altitude were maintained for at least 7 days,46,317,377 with some enhanced physical performance retained for several weeks.59,60,141,273,274 Recent epidemiologic studies suggest that protection from AMS may persist for months.475,586 Retention of the HVR might explain these results;305,433 yet studies showed that HVR returned to preascent values 7 days after descent.377 Compared with persons living at a lower altitude, residents at 900 m (2953 feet) or above reduced the incidence of AMS from 27% to 8% when ascending to between 2000 and 3000 m (6562 and 9843 feet) in Colorado.214 Age has an influence on incidence, with those over 50 years old somewhat less vulnerable.439,496 In a large study in Colorado, those over 60 had one-half the

incidence of AMS as those under 60 years of age. In contrast, a study of 827 mountaineers in Europe showed no influence of age on susceptibility.475 Perhaps different populations and physical activity explain the differing results. No study has ever shown older people to be more susceptible. Children from 3 months to puberty studied in Colorado had the same incidence as did young adults.534,592 A small study of tourists in Chile, however, found lower oxygen saturation and higher AMS in the 6- to 48-month age-group at 4440 m (14,567 feet).369 The largest study of children to date, of Han Chinese after ascent to Tibet, showed essentially the same incidence of AMS in 464 children as in 5335 adults, 34% and 38%, respectively.580 Women apparently have the same442,464,475 or a slightly greater incidence of AMS,214,546 but may be less susceptible to pulmonary edema.99,506 There appears to be no relation between AMS and the menstrual cycle.424 Most studies show no relation between physical fitness and susceptibility to AMS. However, obesity seems to increase the odds of developing AMS.154,214 Neither smoking nor the use of oral contraceptives increases risk for AMS.214,259,391 In summary, the most important variables related to AMS susceptibly are genetic predisposition, altitude of residence, altitude reached, rate of ascent, and prior recent altitude exposure. 70% 60%

Prevalence of AMS

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 have provided a useful multifactorial concept of the pathogenesis of HAH, based on current understanding of headaches in general.463 They suggest that the trigeminovascular system is activated at altitude by both mechanical and chemical stimuli (vasodilation, nitric oxide [NO] and other noxious agents), and in addition, the threshold for pain is likely altered at high altitude (Figure 1-10).463 If AMS and especially HACE ensue, then altered intracranial dynamics may also play a role, via compression or distension of pain-sensitive structures. A recent study provided evidence against sustained trigeminovascular activity,14 but more study will hopefully bring better understanding of the pathophysiology of these often debilitating headaches, and new treatments as well.

↑ NO

Nonsusceptible Susceptible

50% 40% 30% 20% 10% 0% Either ascent Ascent 3 days or and preexposure preexposure 3 days and preexposure ≥5 days

FIGURE 1-11  The prevalence of acute mountain sickness (AMS) and 95% confidence intervals in nonsusceptible (blue bars) and susceptible (red bars) mountaineers in relation to the state of acclimatization defined as slow ascent (more than 3 days), fast ascent (3 days or less), preexposed (5 days or more above 3000 m [9843 feet] in the preceding 2 months), and not preexposed (4 days or less above 3000 m [9843 feet] in the preceding 2 months). (Reprinted from Schneider M, Bernasch D, Weymann J, et al: Acute mountain sickness: Influence of susceptibility, preexposure, and ascent rate, Med Sci Sports Exerc 34:1886, 2002.)

11

CHAPTER 1  High-Altitude Medicine and Physiology

FIGURE 1-10  Proposed pathophysiology of high-altitude headache. CNS, Central nervous system; eNOS, endothelial nitric oxide synthase; NO, nitric oxide. (Modified from Sanchez del Rio M, Moskowitz MA: High altitude headache. In Roach RC, Wagner PD, Hackett PH, editors: Hypoxia: Into the next millennium, New York, 1999, Plenum/Kluwer Academic Publishing, pp 145-153.)

PART 1  MOUNTAIN MEDICINE

TABLE 1-5  Clinical Characteristics of High-Altitude Illnesses Clinical Classification HAH

Mild AMS

Moderate to Severe AMS

HACE

Symptoms

Headache only

Headache plus one or more symptoms (nausea/vomiting, fatigue/lassitude, dizziness or difficulty sleeping) Symptoms of moderate to severe intensity

±Headache Worsening of symptoms seen in moderate to severe AMS

LL-AMS score* Physical signs

1-3, headache only None

Headache plus one more symptom (nausea/ vomiting, fatigue/ lassitude, dizziness or difficulty sleeping) All symptoms of mild severity 2-4 None

Findings

None

None

Pathophysiology

Unknown; cerebral vasodilation, trigeminovascular system?†

Unknown; same as HAH?

Antidiuresis Slightly increased body temperature Slight desaturation Widened A-a gradient Elevated ICP White matter edema (CT, MRI) Vasogenic edema; cytotoxic edema?

5-15 None

Ataxia Altered mental status HAPE common: positive chest radiograph, rales, dyspnea at rest Elevated ICP White matter edema (CT, MRI) Advanced vasogenic cerebral edema; cytotoxic edema?

AMS, Acute mountain sickness; CT, computed tomography; HACE, high-altitude cerebral edema; HAH, high-altitude headache; HAPE, high-altitude pulmonary edema; ICP, intracranial pressure; MRI, magnetic resonance imaging. *The self-reported Lake Louise AMS score. † See Figures 1-10 and 1-12.

Diagnosis Diagnosis of AMS is based on the setting, symptoms, physical findings, and exclusion of other illnesses. The setting is generally rapid ascent of unacclimatized persons to 2500 m (8202 feet) or higher from altitudes below 1000 m (3281 feet). For partially acclimatized persons, abrupt ascent to a higher altitude, overexertion, use of respiratory depressants, and perhaps onset of infectious illness376 are common contributing factors. The cardinal symptom of early AMS is headache, followed in incidence by fatigue, dizziness, and anorexia.214,500 The headache is usually throbbing, bitemporal, typically worse during the night and on awakening, and made worse by the Valsalva maneuver or stooping over (see High Altitude Headache, earlier). A good appetite is unusual, and nausea is common. These initial symptoms are strikingly similar to an alcohol hangover. Frequent awakening may fragment sleep, and periodic breathing often produces a feeling of suffocation. Although sleep disorder is nearly universal at high altitude, also affecting those without AMS, these symptoms may be exaggerated during AMS. Affected persons commonly complain of a deep inner chill, unlike mere exposure to cold temperature, accompanied by facial pallor. Other symptoms may include vomiting, dyspnea on exertion, and irritability. Lassitude can be disabling, with the victim too apathetic to contribute to his or her own basic needs. Pulmonary symptoms vary considerably. Everyone experiences dyspnea on exertion at high altitude; dyspnea at rest is distinctly abnormal, however, and presages HAPE rather than AMS. Cough is also extremely common at high altitude and not associated with AMS. Recent work suggests that altitude hypoxia actually lowers the cough threshold, as measured with an inhaled citric acid stimulus.333 However, any pulmonary symptom mandates careful examination for pulmonary edema. Specific physical findings are lacking in mild AMS. A higher heart rate has been noted in those with AMS,34,391 but Singh and associates500 noted bradycardia (heart rate less than 66 beats/min) in two-thirds of 1975 soldiers with AMS. Blood pressure is normal, but postural hypotension may be present. Occasionally, localized rales may be present,323 but this has also been observed in those without AMS.187 A slight increased body temperature with AMS may be present but is not diagnostic.321 Peripheral oxygen saturation as measured by pulse oximetry correlated poorly with presence of AMS during rapid ascent391,439,450 but was related to AMS during trekking.39 SaO2 at altitude on Denali was predictive of developing AMS on further ascent.436 Overall, pulse oximetry is 12

of limited usefulness in diagnosing AMS. Funduscopic examination reveals venous tortuosity and dilation; retinal hemorrhages may or may not be present and are not diagnostic. They are more common in AMS than non-AMS subjects at 4243 m (13,921 feet).187 Absence of the normal altitude diuresis, evidenced by lack of increased urine output and retention of fluid, is an early finding in AMS, although not always present.35,188,442,500,528 More obvious physical findings develop if AMS progresses to HACE. AMS displays no neurologic findings, whereas HACE is an encephalopathy (see High-Altitude Cerebral Edema, later). It is clinically useful to classify AMS as mild or moderate to severe on the basis of symptoms (Table 1-5). Importantly, AMS can herald the beginning of life-threatening cerebral edema. Differential Diagnosis Given the nonspecific nature of the symptoms, AMS is commonly confused with other conditions (Box 1-3). 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 myalgias. Hangover is excluded by the history. Exhaustion may cause lassitude, weakness, irritability, and headache and may therefore be difficult to distinguish from AMS. Dehydration, which causes weakness, decreased urine output, headache, and nausea, is commonly confused with AMS. Response to fluids BOX 1-3  Differential Diagnosis of High-Altitude

Illnesses

Acute mountain sickness and high-altitude cerebral edema

High-altitude pulmonary   edema

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

CNS, Central nervous system.

↓O2 vasodilation

Acute hypoxic ventilatory ↓CO2 response vasoconstriction ←→

Ca2+

sensitivity NO→impaired →relaxation/vasodilation

↑Ca2+ No release

Endothelium Elastic lamina Smooth muscle

Other molecules that may be involved: Acetylcholine Substance P Prostaglandins

Microhemorrhage

↑K+

Raised hydrostatic pressure

Venous

Capillary and blood-brain barrier

Arteriole

CHAPTER 1  High-Altitude Medicine and Physiology

Artery

NO

HIF-1α not broken down

Hypoxemia

Raised venous pressure

Free radical formation

Basement membrane damage Na+/K+ Upregulation ATPase failure of VEGF →intracellular Edema→↑ICP edema Adenosine →hypoxic vasodilation

Headache

Capillary basement membrane damage and angiogenesis Mechanical mediator PO2/PCO2 mediator Chemical mediator

Vasodilation→pain Pain fibers of trigeminal nerve→trigeminovascular system

FIGURE 1-12  Proposed pathophysiology of acute mountain sickness. HIF, Hypoxia-inducible factor; ICP, intracranial pressure; NO, nitric oxide; VEGF, vascular endothelial growth factor. (Modified from Wilson MH, Newman S, Imray CH: The cerebral effects of ascent to high altitudes, Lancet Neurol 8:175, 2009.)

helps to differentiate the two. AMS is not improved by fluid administration alone, and body hydration does not influence susceptibility to AMS (contrary to conventional wisdom).11 Hypothermia may manifest as ataxia and mental changes. Sleeping medication can cause ataxia and mental changes, but soporifics may also precipitate high-altitude illness because of increased hypoxemia during sleep. Migraine may be very difficult to distinguish from AMS. A trial of oxygen breathing or descent can be helpful to discriminate these other conditions from AMS. Pathophysiology The basic cause of AMS is hypoxemia, but the syndrome is different from acute hypoxia. Because symptoms are somewhat worse with hypobaric hypoxia than with normobaric hypoxia, hypobaria apparently also plays a minor role, most likely through its effect on fluid retention.240,261,303,304,441 Because of a time lag in onset of symptoms after ascent and lack of immediate or complete reversal of all symptoms with oxygen, AMS is thought to be secondary to the body’s responses to modest hypoxia. In addition, even though an altitude of 2500 to 2700 m (8202 to 8858 feet) presents only a minor decrement in arterial oxygen transport (SaO2 is still above 90%), AMS is common and some individuals may become desperately ill. Some aspects of AMS pathophysiology are clear. Findings documented in mild to moderate AMS include relative hypoventilation,336,366 impaired gas exchange (interstitial edema),171,286 fluid retention and redistribution,35,442,528 and increased sympathetic

drive.31,34 In mild to moderate AMS, limited data show that ICP or cerebrospinal fluid (CSF) pressure is not elevated at rest.17,205,579 In contrast, increased ICP and cerebral edema are documented in severe AMS, reflecting the continuum from advanced AMS to HACE.220,276,337,500,573 The known, well-established findings in AMS are reviewed extensively elsewhere.179,233,240 The remainder of this section focuses on remaining questions and new work in the quest to find the cause of AMS. We proposed more than a decade ago that moderate to severe AMS was caused by brain swelling leading to elevated ICP via a compromised buffering capacity. This hypothesis has not yet been directly tested. We now examine the data on brain swelling, ICP, and cranial buffering capacity in AMS. Brain Swelling in AMS.  For decades, clinicians have postulated that AMS is a mild form of cerebral edema. Although this appears true for moderate to severe AMS, it now seems unlikely that mild AMS, or the headache alone, is due to edema (see High-Altitude Headache, earlier). Persons with moderate to severe AMS or HACE display elevated ICP and white matter edema on brain imaging in most but not all studies,144 whereas those with mild AMS do not.* Recent MRI studies have demonstrated that brain swelling occurs in all subjects ascending rapidly to moderate altitude, regardless

*References 197, 220, 276, 295, 337, 500.

13

PART 1  MOUNTAIN MEDICINE

of the presence of AMS, and is due to both vasodilation and minor vasogenic edema. In addition, there may be an intracellular fluid shift as evidenced by low apparent diffusion coefficient. Although this was greater in those with AMS, the volumetric changes were minor and unlikely to result in increased ICP without contributing factors.144,239,252,372,481 In summary, no gross elevation in brain volume has been found yet in mild AMS or headache alone, but elevated brain volume is almost universally observed in moderate to severe AMS and HACE. Intracranial Pressure and AMS.  A fascinating story was recently reported in which a neurosurgeon measured ICP changes from a self-implanted ICP monitoring bolt in himself and in two others.572 They demonstrated that ICP remained normal at rest at all altitudes (studied from sea level to 5030 m [16,503 feet]); however, in the single subject with AMS, there was a dramatic increase in ICP even on minimal exertion. This study is consistent with recent indirect assessment of elevated ICP in AMS based on optic nerve sheath diameter.138,523 In addition, a study that measured opening lumbar pressure revealed significant elevations in AMS subjects compared with control or after AMS resolved.500 In contrast, one recent study in normobaric hypoxia reported no elevation of ICP in AMS when measured indirectly by repeat lumbar puncture.252 The evidence that ICP is elevated in mild AMS is limited and not compelling. Stronger evidence suggests that perhaps intracranial compliance is altered,275 and that although ICP might not be elevated at rest, it rises abruptly with isometric maneuvers such as lifting a pack, with Valsalva, or even with turning the head, which slightly elevates venous pressure.205,572 Altered compliance is consistent with the tight-fit hypothesis (see below). The Tight-Fit Hypothesis and AMS.  Ross457 hypothesized in 1985 that persons with smaller intracranial and intraspinal CSF capacity would be disposed to develop AMS, because they would not tolerate brain swelling as well as those with more “room” in the craniospinal axis. It is displacement of CSF through the foramen magnum into the spinal canal that is the first compensatory response to increased brain volume, followed by increased CSF absorption and decreased CSF formation. Studies have shown that the increase in ICP for a given increase in brain volume is directly related to the “tightness” of the brain in the cranium (the brain volume: intracranial volume ratio) and to the volume of the spinal canal.492 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 still 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,182,252,572,593 as do the studies showing elevated ICP in moderate to severe AMS.220,276,337,500,573 The idea deserves further study. New Concepts.  New, potentially important work is under way to understand the potential role of inflammatory mediators, free radicals, and even HIF-modulated reactions in the pathophysiology of AMS.14,16 Progress is hampered by the technical difficulty of some of these approaches, by lack of an animal model, and by the unresolved status of the basic pathophysiology. A potentially unifying hypothesis, with several novel ideas, is presented in Figure 1-12. In this schema, mechanical factors increase intravascular pressure and hence can cause vasogenic edema and vessel wall damage. This pressure can act in the artery (increased hydrostatic pressure associated with increased flow) or vein (if there is venous outflow obstruction, as in benign intracranial hypertension, for example). The partial pressures of oxygen and carbon dioxide are thought to have direct vasoactive properties, with hypoxemia causing vasodilation and hypocarbia causing vasoconstriction. A balance between these is mediated by the hypoxic and CO2 ventilatory responses. Cytotoxic edema is attributed to direct hypoxia-induced Na+/K+ ATPase failure. Many chemical mediators have been implicated. Free radical formation could directly damage the blood–brain barrier, causing vasogenic edema. Accumulation of HIF-1α and subsequent upregulation of 14

vascular endothelial growth factor (VEGF) could contribute to further blood–brain barrier damage and edema. Neuronally mediated adenosine release also causes vasodilation. Vessel dilation has been implicated in activating the trigeminovascular system, causing headache. An important element of HACE is microhemorrhage formation, caused by vessel damage from chemical mediators or cytokines or by damage through increased hydrostatic pressure.253 Natural Course of Acute Mountain Sickness The natural history of AMS varies with initial altitude, rate of ascent, and clinical severity. Symptoms can start within 2 hours after arrival and rarely if ever start after 36 hours at a given altitude. AMS usually resolves over the next 24 to 48 hours. The more rapid the ascent, and the higher the altitude, the more likely that symptoms will appear sooner and be worse. Singh and associates500 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.500 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.583 Persistent anorexia, nausea, and headache may afflict climbers at extreme altitude for weeks and can be considered a form of persistent AMS. The natural history of AMS in tourists who sleep at more moderate altitudes is much more benign. Duration of symptoms at 2700 m was 15 hours, with a range of 6 to 94 hours.361 Most individuals treat or tolerate their symptoms as the illness resolves over 1 to 3 days while 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 (3.4% at 4243 m [13,921 feet]) go on to develop cerebral edema, especially if ascent continues in spite of illness. Although 50% of persons with HAPE have AMS, no study has documented how many with AMS develop HAPE. Treatment Management of AMS is based on severity of illness at presentation, logistics, terrain, and experience of the caregiver. Early diagnosis is key, because treatment in the early stages of illness is easier and more successful (Box 1-4). Proceeding to a higher sleeping altitude in the presence of symptoms is contraindicated. The victim must be carefully monitored for progression of illness. If symptoms worsen despite 24 hours of acclimatization or treatment, descent is indicated. The two indications for immediate descent are neurologic findings (ataxia or change in consciousness) and pulmonary edema. Mild AMS can be treated by halting the ascent and waiting for acclimatization to improve, which can take from 12 hours to 3 or 4 days. Acetazolamide (250 mg twice a day orally, or as a single dose) speeds acclimatization and thus terminates the illness if given early.171,326 Symptomatic therapy includes analgesics such as aspirin (500 or 650 mg), acetaminophen (650 to 1000 mg), ibuprofen65 or other nonsteroidal antiinflammatory drugs, or codeine (30 mg) for headache. Ondansetron 4 mg orally disintegrating tablets every 4 hours as necessary is useful for nausea and vomiting. Persons with AMS should avoid alcohol and other respiratory depressants because of possible exaggerated hypoxemia during sleep. Descent to an altitude lower than where symptoms began effectively reverses AMS. Although descent should be as far as necessary for improvement, 500 to 1000 m (1640 to 3281 feet) is usually sufficient. Exertion should be minimized. 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 1-13). An inflation of 2 psi is roughly equivalent to a drop in altitude of 1600 m (5249 feet); the exact equivalent depends on initial altitude.257,437 A few hours of pressurization

High-Altitude Headache and Mild Acute Mountain Sickness • Stop ascent, rest, acclimatize at same altitude • Symptomatic treatment as necessary with analgesics and antiemetics • Consider acetazolamide, 125 to 250 mg bid, to speed acclimatization • OR descend 500 m (1640 feet) 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, 8 mg PO, IM, or IV, then 4 mg q6h • Hyperbaric therapy High-Altitude Pulmonary Edema • Minimize exertion and keep warm • Immediate descent or hyperbaric therapy • Oxygen, 4 to 6 L/min until improving, then 2 to 4 L/min • If above unavailable, one of the following: • Nifedipine, 30 mg extended release q12h • Sildenafil 50 mg q8h • Tadalafil 10 mg q12h • Consider inhaled β-agonist Periodic Breathing • Acetazolamide, 62.5 to 125 mg at bedtime as needed

hydrochlorothiazide, and other diuretics have not yet been evaluated for treatment (see Prevention, later). The steroid betamethasone was initially reported by Singh and co-workers500 to improve symptoms of soldiers with severe AMS. Subsequent studies have found dexamethasone to be effective for treatment of all degrees of AMS.140,196,262 Hackett and colleagues196 used 4 mg orally or intramuscularly every 6 hours, and Ferrazinni and associates140 gave 8 mg initially, followed by 4 mg every 6 hours. Both studies reported marked improvement within 12 hours, which was the first postdrug assessment, but clinical experience suggests improvement of AMS within 4 hours. There were no significant side effects. Symptoms increased when dexamethasone was discontinued after 24 hours.196 Clinicians debate whether the use of dexamethasone should also mandate descent. Is it safe to continue to ascend after treatment with dexamethasone or while taking the medication? In reality, people do, and problems seem to be few. In our opinion, dexamethasone use should be limited to less than 72 hours to minimize side effects. This generally is sufficient time to descend, or to better acclimatize, with or without acetazolamide. The mechanism of action of dexamethasone is unknown; it does not affect oxygen saturation, fluid balance, or periodic breathing.295 The drug blocks the action of VEGF,476 diminishes the interaction of endothelium and leukocytes (thus reducing inflammation),167 and may also reduce cerebral blood flow.250 Dexamethasone seems to not improve acclimatization, because some symptoms recur when the drug is withdrawn. Therefore an argument could be made for using dexamethasone to relieve symptoms and acetazolamide to speed acclimatization.52 Prevention Prevention strategy is based on risk assessment311 (Table 1-6). Graded ascent is the surest and safest method of prevention, although particularly susceptible individuals may still become ill. TABLE 1-6  Risk Categories for Acute Mountain

Sickness

IM, Intramuscularly; IV, intravenously; PO, orally.

result in symptomatic improvement and can be an effective temporizing measure while awaiting descent or the benefit of medical therapy.257,375,398,444,532 Long-term (12 hours or more) use of these portable devices is necessary to resolve AMS completely. Acetazolamide is of unquestionable prophylactic value and is now commonly and successfully used to treat AMS as well, although data supporting this are minimal.171,326 Singh and colleagues500 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.500 Spironolactone,

Risk Category Low

Moderate

High

FIGURE 1-13  A fabric hyperbaric pressure bag being used on Mt Everest for treatment of severe altitude illness. Two psi pressure is equivalent to a drop of approximately 1600 m (5249 feet) in altitude.

Description Individuals with no prior history of altitude illness and ascending to 2 days to arrive at 2500-3000 m (8202-9843 feet) with subsequent increases in sleeping elevation 2800 m (9186 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) at altitudes above 3000 m (9843 feet) but with an extra day for acclimatization every 1000 m (3281 feet) History of AMS and ascending to >2800 m (3281 feet) in 1 day All individuals with a prior history of HAPE or HACE All individuals ascending to >3500 m (11,483 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) above >3000 m (9843 feet) without extra days for acclimatization Very rapid ascents (e.g., 400 >500 >750 >1000

Flash scale April 12, 1995 – December 31, 1999

NASA/MSFC

FIGURE 3-10  Total flashes per square kilometer per year for the world from April 12, 1995, to December 31, 1999 from the Optical Transient Detector. (http://thunder.nsstc.nasa.gov/data/OTDsummaries/gifs/mission_world.gif )

LIGHTNING AROUND THE WORLD Over 60 cloud-to-ground lightning detection systems using commercial instrumentation in the very low frequency (VLF) and low frequency (LF) range have been installed in more than 45 countries on every continent except Antarctica.86 Some have operated for longer than two decades. However, the only formally published compilation of flash data from more than one country at a time is for the United States and Canada.226 The ability to detect the full horizontal and sometimes vertical extent of flashes in cloud has been developed in recent years.86,193 These cloud lightning or total lightning flashes are detected in the VHF range over regions as large as metropolitan areas. Total lightning networks detect three to five cloud flashes for every cloud-to-ground flash, although some storms have much higher ratios. The longest detected cloud flash stretched horizontally across 190 km (118 miles) over the Dallas-Fort Worth area and was connected with two cloud-to-ground flashes during its 2-second lifetime.92 Cloud flashes do not directly affect people on the ground. However, their association with cloud-to-ground flashes helps to understand the location and timing of ground strikes. No maps of total lightning have been developed to date, although there is a general view of worldwide total lightning detected by the satellite-borne Optical Transient Detector and Lightning Imaging Sensor that measure both cloud-to-ground and cloud flashes as shown in Figure 3-10.59 The highest rates of all types of lightning occur over tropical and subtropical continents. Maxima have been found in central Africa and northwest South America.2 Lightning frequencies in these areas far exceed those over Florida and the Gulf Coast. The uncertainty concerning the portion of these maxima that are cloud-to-ground flashes is being resolved by the recent deployment of the Global Lightning Dataset GLD360.93

TIME OF U.S. LIGHTNING* During the year, lightning is by far most common during summer months. Two-thirds of U.S. cloud-to-ground flashes occur in June, July, and August (Figure 3-11, online). The maximum during the warmer months of the year, especially in the southeastern states,

*References 141, 191, 194, 277.

is due primarily to daytime heating of the lower and middle levels of the atmosphere. An equally critical ingredient is the large amount of moisture in the lower and middle levels of the atmosphere that provides fuel for the daily thunderstorm cycle. The concentration of U.S. cloud-to-ground lightning in June, July, and August is present over nearly all of the United States.141 During the day, cloud-to-ground lightning is most common in the afternoon (Figure 3-12, online). Nearly one-half of all lightning occurs between noon and 18:00 local standard time (LST). Lightning is at a maximum in the afternoon because updrafts necessary for thunderstorm formation are strongest during the warmest times of the day when surface temperatures are highest, resulting in the greatest vertical instability. Other factors can extend the maximum into the evening hours, especially in the plains and southeastern states, because of outflows and other propagating features that usually originate with the afternoon convection.

U.S. LIGHTNING CASUALTIES Each month, NWS offices compile a list of damaging or notable weather phenomena that occurred in the office’s area of responsibility. These lists are combined into a monthly national report issued by the National Oceanic and Atmospheric Administration (NOAA) titled Storm Data. During the last 20 years, U.S. lightning fatalities have averaged 51 per year. Lightning deaths have equaled or exceeded those from tornadoes in 11 years and equaled or exceeded those from hurricanes in 18 of the 20 years (Figure 3-13). Flood deaths exceeded lightning fatalities during 16 of these 20 years. Males (84%) make up a much higher number of fatalities in the United States than females.87 This male majority has been found in every region of the world over the last two centuries, although some subsets can have less dominance of males than this typical value. The most common situation is for one victim to be involved in a lightning incident. The largest single death total in one U.S. event resulted from a 1963 airliner crash that killed 81, and the largest U.S. injury total was 90 at a Michigan campground. Although single-incident cases dominate the more developed countries’ data sets, very large numbers of deaths and injuries often occur in developing countries.140 Lightning-related casualties and damages are often less spectacular and more dispersed in time and space than are those from other storm phenomena. As a result, lightning deaths, 65

PART 1  MOUNTAIN MEDICINE

+

150 125 100 75 50 25 0 1989

1991

1993

1997

1995

1999

2001

2003

2005

2007 2008

Lightning Tornado Flood Hurricane FIGURE 3-13  U.S. storm-related fatalities from 1989 through 2008 from the National Oceanic and Atmospheric Administration publication Storm Data. The + sign indicates that hurricane Katrina had 1016 fatalities in 2005.

injuries, and damages have been found to be underreported in Storm Data.19,144,196,258 The following factors contribute to this underreporting: most casualties occur to one person or object at a time, Storm Data collection is not entirely consistent among offices, there are some differences in the definitions of lightning versus secondary lightning-related deaths, and there is inconsistency in listing medical diagnoses.1,19,239,258 Nonfatal injuries are underreported to a greater extent than are fatalities. A thorough search of Colorado hospital and emergency department visits found a ratio of 10 injuries to every death.53 Although this ratio of injuries to fatalities is generally applicable, there may be additional injuries that are not reported. Damage reports in Storm Data are an extremely small portion of the estimated total damages, direct or indirect, of several billion dollars per year in the United States.19,144 Despite its underreporting and sometimes incomplete nature, Storm Data has been a consistent national database for lightning impacts since 1959 and is likely the best system in the world for such information. Data drive change. It would be highly desirable for similar data to be collected and made available in many other areas of the world, both to have a baseline of damage and injuries to measure changes and to spur governments and other organizations to address injury prevention.

DISTRIBUTION OF U.S. LIGHTNING DEATHS BY STATE Lightning casualty deaths in the United States by state for the decade from 1999 to 2009 are shown in Figures 3-14 and 3-15. The general pattern is somewhat similar to the distribution of lightning in Figure 3-9. In general, there are more fatalities in the Southeast, but the more populous states also have larger totals. Note that Florida has had more than twice as many deaths as Colorado, the next state in terms of frequency. Fatality information is used for these maps, rather than injuries, because of the greater uncertainty due to injury underreporting, as mentioned previously. The lightning hazard is shown more clearly when population is taken into account in Figure 3-15. There are two maxima with this approach, one in the southeast and the other in the northern Rocky Mountain states. Most populous states, such as Illinois, no longer have high ranks. The only states in the top 10 of both lightning fatality and fatality rates are Florida, Colorado, Alabama, and South Carolina. Similar tabulations were recently made by Ashley and Gilson,19 and earlier maps for single U.S. states are listed by Curran and colleagues.87 Outside the United States, the distributions of fatalities by political boundaries have been developed for Canada,207

FATALITIES 2000-2009 0

0

2

0

7

3

1

3 9

27

8 7

66

9 3

7

27

9

11

14

10

5

10 0

24

17

11

6 11

1

5 4

13

13

4

12 4

3

Source: Storm Data Alaska: 0 Hawaii: 0 American Samoa: 1 D.C.: 0 Guam: 1 Puerto Rico: 3 Virgin Islands: 1

8

4

2 1

2 0

3

20

14

70

Rank 1-10 11-20 21-30 31-52

FIGURE 3-14  Rank and number of lightning fatalities in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)

CHAPTER 3  Lightning Injuries

FIGURE 3-15  Rank of population-weighted lightning fatality rate in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)

FATALITY RATE 2000-2009

Source: Storm Data Ranks include 50 states, D.C., and Puerto Rico

Singapore,228 Australia,61 and France.116 Many additional studies have included national casualty totals, but not maps, over periods from several to many years.138

time series in the plains and Midwest.87 At night between 18:00 and 06:00, the relatively few fatalities occur mostly in the plains, upper Midwest and some populous eastern states, because of outflows and other propagating features that usually begin with afternoon convection. More than one-half of the deaths after midnight occurred when people were in a house set on fire by lightning,139 whereas some fatalities were campers.

TIME OF U.S. FATALITIES During the course of the year, lightning fatalities are nearly symmetric around the most frequent month of July (Figure 3-16, online). This annual casualty cycle is quite similar to the cloud-toground lightning variation by month in Figure 3-11, online. Because summer dominates the sample size, summer fatality maps are very similar to Figures 3-11 and 3-12, online for the entire year.87 On the West Coast, fatality rates are highest during autumn and winter, and these rates are also higher in the southern states than elsewhere in months other than summer. Outside the United States and away from the tropics, summer also accounts for the largest number of fatalities, such as that shown by the January peak in Australia because of the reversal of seasons from the northern hemisphere.61 In the equatorial location of Singapore, fatality maxima in November and April are similar to the annual maxima in local thunderstorms.228 During the hours of the day, most lightning fatalities occur during the afternoon (Figure 3-17, online). About two-thirds of U.S. fatalities occur between noon and 18:00 LST.87 There is a somewhat faster rise up to the maximum then a slower decrease afterward. This general cycle is very similar to cloud-to-ground lightning in Figure 3-12, online. However, there is a somewhat narrower concentration of fatalities in the afternoon in the Rockies, southeast, and northeast compared with the broader

FIGURE 3-18  Annual reported U.S. lightning fatalities from 1900 to 2007. (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)

Rank 1-10 11-20 21-30 31-52

TRENDS IN U.S. LIGHTNING FATALITIES During the early years of the 20th century, U.S. lightning deaths were much more frequent than at present (Figure 3-18). Not all states participated in lightning fatality data collection systems in the early years of the period shown in Figure 3-18. However, once all states reported, the peak was reached in 1921, when 459 lightning fatalities were reported.195 Since then, there has been a steady decline in the number of fatalities listed in Storm Data. In recent years, there have been less than 50 fatalities annually. The steady downward trend is made more noticeable by population weighting, shown in Figure 3-19. Although the U.S. population has increased greatly since 1900, the weighted rate has decreased from as high as 6 fatalities per million people per year in the early 20th century to about 0.3 in recent years. Paralleling this decrease is a shift from a mainly rural to a mostly urban population in the United States during the same years (see Figure 3-19). Other significant factors that contribute to this downward trend are improved grounding of home and building electrical and plumbing systems, ready access to fully enclosed metal-topped vehicles, improved medical treatment, and greater

500

300 200 100 0

19 00 19 07 19 14 19 21 19 28 19 35 19 42 19 49 19 56 19 63 19 70 19 77 19 84 19 91 19 98 20 05

Reported fatalities

400

67

PART 1  MOUNTAIN MEDICINE

Deaths per million Percent rural

Deaths per million

6 5

70 60 50

4 3

40

2

30

1

20

0 1900

10 1920

1940

1960

1980

Percent rural to total population

7

2000

meteorologic and lightning awareness and warnings. The potential effects of changing fatality data collection rules and methods are difficult to identify but may account for some variations in all data sets. The net effect of these changes is apparent in a comparison of fatality data from the 1890s to 1990s in Figure 3-20.195 Agricultural cases have decreased from 26% to 10%, while indoor cases went from 40% to 5%. The latter may be due to the introduction of grounding into buildings, often on a farm or ranch, which has greatly reduced the lighting threat in recent years. There has been a large increase in recreational and sports incidents during that century and in the general category of outdoors, often in the yard of a dwelling and other everyday situations.

WORLDWIDE LIGHTNING FATALITIES

Lightning deaths (per million)

The weighted U.S. lightning fatality rate dropped during the 20th century by more than a factor of 10, from 6 deaths per million in some early years to under 0.3 in most recent years, as shown in Figure 3-19. Three apparently dominant factors are reduction in the rural population involved in labor-intensive agriculture, substantial grounding of most buildings where people live and work, and ready availability of fully enclosed metal-topped vehicles. Other more developed countries, such as Australia, Canada, England and Wales, France, Japan, and Sweden, have seen very similar reductions. All show current rates of less than 0.5, although some had rates exceeding 2 a century ago in areas where the lightning frequency is not as high as in the United States.138 Many people continue to participate in labor-intensive agriculture and live in ungrounded buildings in areas of the world where lightning frequency is high.163,164 The rates a century ago in the United States and other more developed countries can be considered for estimating fatalities and injuries in locations where lightning injury statistics are not readily available. Populous regions of Africa, South America, and Southeast Asia have as many as 4 billion people who are vulnerable to the lightning

Australia Canada India Japan

Agriculture

0

FIGURE 3-19  Annual lightning fatalities weighted by population ( ) from 1900 to 2007 for the United States and rural percentage ( ). (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)

10 9 8 7 6 5 4 3 2 1 0

1890s 0

25%

Indoors

25%

Outdoors

50%

75%

Recreation

100%

Small Sports structures

75%

100%

1990s FIGURE 3-20  Types of U.S. lightning fatalities from 1891 to 1894 compared with 1991 to 1994. (From Holle RL: Lightning-caused recreation deaths and injuries. Preprints, 14th Symposium on Education, January 9-13, San Diego, Cali. Boston, 2005, American Meteorological Society.)

threat, although urbanization makes it difficult to know the number of agriculturally dependent people living in unsafe structures. If the annual rate of 6 fatalities per million is used for 4 billion people, a total of 24,000 lightning deaths per year is obtained. If there are 10 injuries for every death,54 then 240,000 injuries occur per year in these areas. Holle138 lists all known published estimates of the lightning totals and converts them to fatality rates per population. Some of the countries indeed reach the rate of 6 per million per year, whereas other less developed countries have much lower rates (Figure 3-21). There is such a dearth of reliable data in regions such as Africa and Southeast Asia that it is very difficult to know whether these estimates are generally correct. However, a study of lightning casualties in and near dwellings and other buildings showed that large losses of life occur in schools, huts, and agricultural field shelters in these regions.139 Also in these countries, people spend less time inside the safety of fully enclosed metal-topped vehicles while working or traveling between school, work, and home than in more developed regions.137 Better systematic and reliable lightning fatality collection in these regions is needed to determine the validity of the global estimate of 24,000 deaths and 240,000 injuries per year from lightning.

Forensic Investigation An unwitnessed lightning event can be one of the most difficult clinical presentations to diagnose.50,111 The forensic examination of a critical lightning event can be divided into the following five stages:33,197,253,282 1. Case history 2. Scene investigation 3. Physical and/or autopsy examination 4. Special investigations 5. Collation

Singapore S. Africa U.S. Zimbabwe

1900-9 1910-9 1920-9 1930-9 1940-9 1950-9 1960-9 1970-9 1980-9 1990-9

68

50%

FIGURE 3-21  Lightning deaths per million people per year for eight countries outside Europe by decade during the 20th century. Note that the 1990s Zimbabwe value is 17.8. (From Holle RL: Annual rates of lightning fatalities by country. Preprints, International lightning detection conference, April 21-23, 2008, Tucson, Ariz., Vaisala.).

If a witness is available, it is important to ascertain the following: • Was there a storm? • Was there lightning? • Did the witness actually see the lightning strike the victim? • Was death immediate or not? • Where was the deceased at the time of the strike (e.g., under a tree, on an open golf course)? • Was any attempted resuscitation applied? • What was the activity of the deceased before death? • A meticulous description of the lightning event must be given. • How many people were involved? • Were there any survivors? If so, where are they? • What was the medical history of the deceased? Specifically, were there any cardiac problems? • A history of electrical storm activity should be ascertained from the weather service, because lightning network detection and location systems should be able to assist with the exact time and location of the strike.103

SCENE INVESTIGATION Attending a critical lightning incident is a very specialized activity that crosses many disciplines. Insurance investigators, electrical engineers, scene reconstruction experts, and/or investigating officers will be called to review the scene of a lightning strike. Signs of lightning strike on the scene can be subtle or blatant.154 Lightning scene investigation can be divided into the following: • Environmental signs of direct lightning strike • Structural signs of direct lightning strike • Trace evidence signs of direct lightning strike Environmental Signs of Direct Lightning Strike • At the scene there may be damage to nearby trees, such as splitting or removal of bark. • Arc marks may be present on the walls or nearby structures. • The ground may display a fern pattern.

A

CHAPTER 3  Lightning Injuries

CASE HISTORY

FIGURE 3-22  Damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural damage to the clubhouse. (Copyright Ian R. Jandrell.)

• Soil may show fulgurite formation—bore or tube-like structures formed in sand or rock by lightning. • Often a crater will be exposed in the earth, with rock and sand being flung far afield. Craters of up to 2 meters (6.6 feet) in diameter have been reported. • To preserve the case history for scientific purposes, a relevant academic institution or other expert in the field should if possible be advised of the incident, more specifically should there be any suggestion of litigation by a surviving party. Structural Signs of Direct Lightning Strike Jandrell and associates described the effects of direct lightning strike to housing structures in southern Africa.118,203,204 Figure 3-22 shows damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural and internal damage (Figure 3-23). Figure 3-24 shows damage to curtaining material covering the window. Thatched structures have been known to ignite as a result of lightning strike. Thatch is very combustible, so inhabitants are at greater risk for severe injury and burns.118,139

B

FIGURE 3-23  Damage to the ceiling (A) and internal wall (B) of the clubhouse in Figure 3-22 with resultant damage to the electrical and electronic devices connected to the electrical system. (Copyright Ian R. Jandrell.)

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PART 1  MOUNTAIN MEDICINE

Trace Evidence Signs of Direct Lightning Strike This can be very difficult to prove. Cindering on clothing or arc marks on metallic structures may be seen. In “zincification” and/ or “cuprification” metal with a lower melting point vaporizes, leaving the other metal behind. Magnetization of metallic objects has been mentioned in the literature, although current thinking is that this could possibly be a myth. Reports of metallic chains being magnetized and “sticking” to metallic postmortem trays have yet to be verified.

PHYSICAL AND/OR AUTOPSY EXAMINATION A complete postmortem examination should be performed. • The external examination should include a meticulous description of clothing and any evidence of resuscitation (Figures 3-25 and 3-26; Figure 3-25, online). • Metal objects may have burned underlying skin or may have been marked by the heat of electrical arcing. Figure 3-27 shows damage to clothing and underlying burns. Figure 3-28 shows permanent tattooing from a metal necklace burned into skin in a nonfatal injury.159

FIGURE 3-24  Damage to curtaining material covering a window of the clubhouse in Figure 3-22. (Copyright Ian R. Jandrell.)

A

B

FIGURE 3-26  Damage to the socks of a fatally injured farmer. (Copyright Mary Ann Cooper.)

A

B

FIGURE 3-27  A, Melting of synthetic clothing material from lightning damage. B, Underlying damage to skin from zipper and melted material. (Copyright Ryan Blumenthal.)

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CHAPTER 3  Lightning Injuries

A FIGURE 3-28  Metal necklace burned into skin by lightning with permanent tattooing (nonfatal injury). (Copyright Mary Ann Cooper; courtesy R. Washington.)

• Metal objects may show signs of fusing, zincification, or cuprification. Always check for magnetization. Metallic objects, such as tooth fillings, spectacles, belt, buckles, coins, and pacemakers, should be specifically described. • The type, pattern, and distribution of any cutaneous thermal injuries, including clusters of punctuate burns, blisters, or charred burns, should be noted. Figure 3-29 shows damage to a hiking shoe with underlying damage to the skin of the foot.15 • Determine if there has been rupture of tympanic membranes. Barotrauma has been cited as one of the injuring mechanisms of lightning. Pneumomediastinum has been cited in the literature.124 Burst eardrums and pneumomediastinum are signs suggestive of barotrauma. • Singed or scorched hair should be noted. • Ocular injuries, such as retinal detachment, should be determined. Cataracts may be difficult to demonstrate postmortem. • Unique arborescent or fern-like injuries (Lichtenberg figures) (Figure 3-30) should be noted. • Determine if there are lightning wounds on the bases of the feet—the “tiptoe” sign typically on the base of the foot.213 • The procedure for internal examination is identical to that for any forensic autopsy. • In female victims, ascertain whether or not the victim was pregnant, and if so, carefully examine the fetus macroscopically and microscopically for any injuries.112

SPECIAL PROCEDURES • Diagrams: Where possible, diagrams of the pattern and distribution of the lightning injury to the body should be constructed to provide graphic documentation of the nature and extent of the electrothermal injury patterns. • Photographs: Close-up and distance photographs should be taken to document all injuries. • Radiographs: Radiographic examination may be helpful. Certain fractures, dislocations, and subluxations may be missed at autopsy examination.155 Computed tomography (CT) or magnetic resonance imaging (MRI) might add to the body of knowledge that constitutes postmortem, noninvasive, and virtual analyses. Certain keraunopathologic findings, such as pneumomediastinum, may be missed at autopsy examination.124 • Histologic examination:155,159 The skin burn wounds should always be microscopically examined for signs of electrothermal injury patterns such as vacuolation in the epidermis, eosinophilia, and elongation and streaming of the nuclei of the lower epidermis. Histologic staining of the heart with hematoxylin and eosin may prove useful. The heart should also be carefully examined under the

B FIGURE 3-29  The heat from a lightning strike caused water in the wet boot to instantaneously turn to steam, exploding the boot off the foot (A) and causing burns (B). (Courtesy Sheryl Olson, RN.)

microscope for signs such as “waviness” of the myofibers,155 necrosis, and contraction bands.286 Special staining of the heart with Mallory, Weigert elastic, Movat pentachrome, acid fuchsin orange, and immunohistochemical staining with monoclonal anti–complement C9 antibodies may help in the diagnosis of myofiber breakup—an antemortem change that may be a distinct finding in electrothermal injury cases.105 Any neuropathologic condition should also be specifically investigated and commented on. • Toxicologic studies: Ethanol, recreational drugs, and carbon monoxide levels would be justified as the minimum toxicologic investigations required in such cases. From a mitigating-circumstance point of view, ethanol and recreational drugs are always important to know. Carbon monoxide levels will be valuable, especially if there is a thermal component to the injuries.

FIGURE 3-30  Lichtenberg figures in a teenager who survived. (Courtesy/copyright Mary Ann Cooper.)

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• Collection of evidence: Collect and preserve evidence or specimens, because equivocal cases may require electrical testing of equipment by an electrical expert. Nearby damaged electrical equipment should be sent to an electrical engineer for testing. Unwitnessed lightning cases are typically complex, and unusual situations may arise from time to time. The approach to all these cases should be multidisciplinary. Only by means of a careful forensic investigation, with strict adherence to guidelines, will the truth be revealed. This becomes even more important in determining whether or not a lightning strike was the cause of a later medical condition.

COLLATION If the fresh facts which come to our knowledge all fit themselves into the scheme, then our hypothesis may gradually become a solution. SHERLOCK HOLMES

The Adventures of Wisteria Lodge

Data become information, which becomes knowledge, which becomes scientific opinion. Scientific opinion depends on experience, cognitive ability, and facts. At the end of the investigation, one should collate one’s findings with the known physics and effects of lightning.234

Early Scientific Studies and Invention of the Lightning Rod* The study of electrical 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 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.60,234 Before his work, it was thought that two distinct types of electric phenomena existed. Franklin’s work111 unified these two aspects and is responsible for renaming them positive and negative. He went on to prove that lightning was an electrical phenomenon and that thunderclouds are electrically charged, as demonstrated by the famous kite and key experiment.110 Because of the damage he saw to buildings, he invented the lightning rod and announced its use in 1753 in Poor Richard’s Almanack: It has pleased God in his Goodness to Mankind, at length to discover to them the Means of securing their Habitation and other Buildings from Mischief by Thunder and Lightning. The Method is this: Provide a small Iron Rod (It may be made of the Rod-iron used by the Nailers) but of such a Length, that one End being three or four Feet in the moist Ground, the other may be six or eight Feet above the highest Part of the Building. To the upper End of the Rod fasten a Foot of brass Wire the Size of a common Knitting-needle, sharpened to a fine Point; the Rod may be secured to the House by a few small Staples. If the House or Barn be long, there may be a Rod and Point at each End, and a middling Wire along the Ridge from one to the other. A House thus furnished will not be damaged by Lightning, it being attracted to the Points, and passing thro the Metal into the Ground without hurting any Thing. Vessels also, having a sharp pointed rod fix’d on the Tops of their Masts, with a Wire from the Foot of the Rod reaching down, round one of *References 60, 110, 111, 234.

72

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 the protection of buildings and ships. Some scientists in Europe urged installation of lightning rods on government buildings, churches, and other tall buildings. Religious advocates at the time, unfortunately, maintained that it would be blasphemy to install such devices on church steeples, which received “divine protection.” Some groups chose to store munitions in churches, leading on more than one occasion to significant destruction and loss of life when the buildings were struck by lightning. Part of the delay in installing lightning rods in England has been attributed to distrust of scientific theories originating in the upstart, newly independent United States. Years and numerous unsuccessful trials with English designs were required before the Franklin rod became accepted on Her Majesty’s ships and buildings.40 At one time (and still believed by some laymen today), lightning rods were theorized to diffuse electric charge, neutralizing storm clouds and averting lightning. This may have been an outgrowth of the observation of St Elmo’s fire, an aura appearing around the tip of lightning rods, noses of airplanes, and ships’ masts during a thunderstorm, caused by an electron discharge that results from the strong electromagnetic field induced around the glowing object. Properly installed lightning rods and lightning protection systems neither “diffuse” nor “attract” lightning, but rather protect a building by allowing the current from a lightning strike to be harmlessly directed through the system to the ground.34,215,217 Lightning otherwise can travel into or through the building and cause extensive damage (see Figures 3-22 to 3-24) Around the late 1800s and 1900s, it was not uncommon for charlatans to take advantage of the fear of lightning and the danger of lightning-caused fires. They drove from farm to farm, offering to “discharge” the lightning rods on buildings for a fee. The first Lightning Rod Conference was held in London in 1882. Recommendations from this conference were published that year and again in 1905. Several countries developed codes of practice for lightning protection (Germany, 1924; United States, 1929; Britain, 1943; British colonies, 1965).87 In the past decade, NFPA 780 (U.S. National Fire Protection Act) has been accepted worldwide as a reliable standard.215 Building codes and industrial standards may require particular structures to have lightning protection systems.34,215 Including a system in the initial design and construction is always easier and less expensive than modifying a completed building. Other factors to be considered include relative frequency of strikes in an area; height, construction, and design of the building; and degree of protection desired, depending on whether the building is a storage shed, house, school, hospital, or munitions factory. In instances not covered by code, a lightning protection system, despite high exposure to lightning, may not be worth the expense, such as for a mountain cabin that is seldom visited.170,216 Today the most important economic impacts from lightning include electrical utility interruption; interruptions at airports and other outdoor locations; loss or corruption of financial, security, and other databases and control systems; and down time of industrial equipment. Lightning may pose significant danger not just to individuals, but to larger groups, such as when hundreds of miners are trapped deep underground after lightning has made elevators, ventilation systems, and water pumps nonoperational.216 At home the most reliable way to protect electronic equipment is to unplug it from the wall before the arrival of a thunder­ storm. Surge protectors, which may be effective for minor household electrical surges, are seldom effective with lightning, despite manufacturers’ claims. The best source of information on lightning risk for people is the NWS Lightning Safety website (http://www.lightningsafety.noaa.gov) and for more general risk, the National Lightning Safety Institute (http:// www.lightningsafety.com).132,216,217

CHAPTER 3  Lightning Injuries

High-altitude winds

40,000

30,000

–36

Snow

–16 Snow

25,000 20,000

10,000

18

air

Freezing

W ar m

15,000

–3

32

level

Rain

46

Temperature (° F)

Altitude (feet)

35,000

–60

Ice

63

5000

A

Heavy surface rain

B

Downward leader

Return stroke

Upward streamer

C

D

E

F

FIGURE 3-31  A, Air rises and condenses into a cumulonimbus cloud. B, Typical anvil-shaped thundercloud. C, Water droplets within the cloud accumulate and layer charges. D, Stepped downward leader initiates the lightning strike. E, Positive upward streamer releases from the ground to meet the stepped leader. F, Return stroke travels back up the channel made by the stepped leader.

Physics of Lightning Stroke* LIGHTNING DISCHARGE The study of lightning discharge and formation is complex and has led to development of a separate specialization within physics and meteorology Here we describe the simplified and most common mechanisms of thundercloud formation and lightning strike. Thunderstorms can be formed by a number of methods to produce the necessary vertical updrafts. These ingredients are afternoon heating of warm moist air, large-scale upward motions (Figure 3-31, A), sea and lake breezes, lifting of deep layers of the atmosphere by mountains, and cold fronts.141,269 As warm air rises, turbulence and induced friction cause a complex redistribution of charges within the cloud (Figure 3-31, B). Although the ground temperature may be very warm to hot, thunderstorms are tall enough that their highest parts are colder than freezing. In fact, all lightning comes from clouds that have ice aloft at temperatures colder than freezing. At temperatures colder than freezing, water droplets and ice particles of several types within the cloud acquire and increase their individual charges as they interact and transfer charge. The varying sizes and shapes of the frozen snow and ice crystals, supercooled water droplets, and hail are moving vertically at different speeds because of their different fall speeds. The result is separation of charge into several layers. A large potential difference develops *Reference 230.

between layers as a result of the interaction of charged water and ice particles, updrafts that vary in time and space, and internal and external electric fields within the cloud. Lower layers of the cumulonimbus generally become negatively charged relative to the earth. The earth, which normally is negatively charged relative to the atmosphere, has a strong positive induced charge as the negatively charged thunderstorm passes overhead. The induced positive charge tends to flow as an upward current from trees, tall buildings, poles, people, or sometimes very small objects or flat open ground beneath the overhead thunderstorm cloud and may move up in upwardpropagating leaders.234 Normally the discharge of the potential difference is discouraged by the strong insulating nature of air. However, when the potential difference between charges within the clouds or between the cumulonimbus cloud and the ground becomes too strong, the molecular structure of the intervening air may break down under the influence of the electric field that has developed, and the charge is then dissipated as lightning. A downward stroke begins as a relatively weak and slow downward leader from the cloud (Figure 3-31, C ). Although the tip of the leader may be luminous, the stepped leader itself is barely discernible with the unassisted eye. Recent very high-speed video has shown this bright tip and more faint trailing leader as it travels to the ground.249,251 The leader travels at about one-third the speed of light (1 × 108 m/sec), and the potential difference between the leader’s lower tip and the earth ranges from 10 to 200 million volts. The leader ionizes a pathway that contains superheated ions, both positive and negative, and forms a plasma column of very low resistance. The leader travels in relatively short 73

PART 1  MOUNTAIN MEDICINE

branched steps downward about 50 m (164 feet), and then retreats upward. The next time the leader goes downward toward the ground, it fills the original ionized path but branches at the end to go down another 50 m (164 feet) and then retreats again. This up-and-down multiple-branching process continues until the leader comes to within 30 to 50 m (98 to 164 feet) of the ground. Because lightning follows this ionized path, its lower tip only can sense the existence of nearby objects within a radius of about 30 to 50 m (98 to 164 feet), meaning that lightning will not be affected by the existence of a hill or tower farther away. For human safety, being within 50 m (164 feet) of the lowest tip of a cloud-to-ground lightning flash as it comes to ground is very unsafe.

DIAMETER AND TEMPERATURE OF LIGHTNING* Although many techniques have been used to measure the diameter and temperature of lightning, all measurement techniques have artifact problems. Visual measurements of the lightning stroke using standard photography usually show the diameter of the main body of the stroke to be about 2 to 3 cm (0.8 to 1.2 inches). The diameter of the channel is sometimes measured indirectly, using measurements of holes and strips of damage that lightning produces when it hits aircraft wings, buildings, or trees. Measurements vary from 0.003 to 8 cm (0.001 to 3.15 inches), depending on the material that was destroyed. Hard metallic structures sustain smaller punctures than relatively softer objects such as trees. The ionized sheath around the tip of the bright leader stroke has not been measured but is estimated to have a diameter of 3 to 20 m (9.8 to 6.6 feet). The temperature of the lightning stroke varies with the diameter of the stroke and has been calculated to be about 8000° C (14,400° F). Other estimates of the temperature are as high as 50,000° C (90,000° F). After a few milliseconds the temperature falls to 2000° to 3000° C (3600° to 5400° F), similar to the temperature of a high-voltage electric arc.

FORMS OF LIGHTNING Lightning can be divided into cloud-to-ground and cloud (intracloud) flashes (Figure 3-32). Cloud-to-ground flashes contain one or more return strokes. The flickering often seen in a cloudto-ground flash is due to the return strokes, which average three to four per flash. Cloud-to-ground flashes contact the surface of the earth at one or more locations, because one of the subsequent return strokes often takes a different path to the surface, *Reference 230.

FIGURE 3-32  Cloud-to-ground flash (right) and cloud flash (center). (Copyright Ronald L. Holle.)

74

up to a few kilometers from the first return stroke; the average is 1.47 ground contact points per flash.262 The term total lightning describes the sum of cloud-to-ground and cloud flashes. An extremely small portion (less than 0.01 of 1%) of all lightning travels from ground to cloud, when this is induced by the special circumstances of high towers or mountains. Cloud flashes can travel between clouds, within clouds, from cloud to cloud, and in all combinations of these paths. The same flash can simultaneously strike ground at one or more locations and travel a long distance in cloud (see Figure 3-32). There are several times as many cloud flashes as those that reach the ground. Cloud flashes have been measured to exceed 190 km (118 miles) in horizontal length and last up to 2 seconds.92 From the point of view of a person on the ground, cloud flashes may appear to travel in long streaks across the sky, or the channels may be obscured and visible only by the brightening within clouds along their paths. Such cloud flashes are seen more often in regions with low cloud bases in humid areas. This effect was one of the reasons for the phenomenon to be originally called “lightening.” The most unusual and least understood type of lightning is ball lightning. It is usually described as an orange, blue, or white globe between the size of a softball and a basketball. It has been observed to enter planes, ships, or houses and travel down narrow spaces such as hallways. Ball lightning very infrequently injures people and objects and often exits through a door, chimney, or window.257 It may explode with a loud bang or exhibit other bizarre behavior. Cloud-to-ground lightning flashes usually lower negative charge to the ground.234 The less frequent (5% to 10%) positive cloud-to-ground flashes tend to occur during the winter, at the end of thunderstorms, on the U.S. high plains, and in relatively shallow thunderstorms. Positive flashes usually have one return stroke. It is not known if positive cloud-to-ground flashes cause a different injury profile, although they have a tendency to have long continuing current that may impart more energy to a person than do the usually shorter-pulsing negative cloud-to-ground flashes.

THUNDER Thunder is formed when shock waves result from the almost explosive expansion of air heated and ionized by the lightning channel. Understanding some basic features of thunder is important because of its usefulness in many lightning safety recommendations.114,217 The following are accepted features of thunder: • Cloud-to-ground lightning flashes produce the loudest thunder. • Thunder is seldom heard more than 16 km (10 miles) away, except under extremely quiet conditions. • The time interval between the perception of lightning and the first sound of thunder can be used to estimate the distance from the lightning channel, at a rate of 3 sec/km (5 sec/mile). • Wind, rain, man-made noise such as traffic, and vegetation, as well as intervening buildings, hills, and mountains, reduce the audibility of thunder. • The pitch of thunder deepens as the rumble persists, because only lower frequency sounds remain at greater distances. • Atmospheric turbulence reduces the audibility of thunder. The thunderclap from a close lightning flash is heard as a sharp crack. Distant thunder rumbles as the sound waves are refracted and modified by the thunderstorm’s turbulence.269 Because there is a large difference between the speed of light and the speed of sound, the distance to lightning can be estimated by a person on the ground. The estimation is made by the flash-to-bang method of counting the seconds between seeing a flash and hearing thunder from the same flash, when the two can be matched. The time interval between lightning and thunder is 3 sec/km (5 sec/mile). For example, if the difference is 30 seconds between when a flash is seen until its thunder is heard, the flash is 10 km (6.2 miles) away. This time interval is part of the basis for the 30-30 rule described in Precautions for Avoiding Lightning Injury.

BOX 3-3  Mechanisms of Lightning Injury

CONCEPTS IN ELECTRICAL MECHANISMS— DIFFERENCES BETWEEN LIGHTNING AND INDUSTRIAL ELECTRICITY

Electrothermal Effects 1. Direct strike 2. Contact potential 3. Side flash, sometimes called “splash” (1 to 3 may include surface arcs over the body surface) 4. Step voltage (also termed “Earth potential rise” or “ground current”) a. Transmitted through the ground b. Surface arcing 5. Upward streamer current1,53 (also called “fifth mechanism”)

A voltage can be applied to a body. It can be regarded as the pressure applied to a body to force it to conduct electric current, like water pressure applied at one end of a pipe to cause water flow. It is an external force, and after it is applied, a current (measured in amperes) flows through the conductor (i.e., body), like water in the pipe. The amount of current is inversely proportional to the resistance of the body. That is, for a given applied voltage, the higher the resistance of the body, the smaller the resulting current. For technical or generated electrical injuries, the voltage is externally selected, and the resistance of a body is a given. The current is the result. Resistance is a given property of a body. A piece of metal has a predictable and exact resistance, for our purposes invariable. It might be thought of as analogous to the diameter of the water pipe, or friction within the pipe. It is the property that determines how easy it is to force current through the body. Resistances of various tissues have been measured and characterized as properties. If it is assumed that resistance is predictable, then resistance, voltage, and current can be linearly related, making modeling, and therefore prediction, possible. Voltage, current, and resistance are related by Ohm’s law (Voltage = Resistance × Current). However, tissue resistance is not constant but affected by a number of factors that do not depart from principles of linear analysis. Alterations in tissue resistance are predictable, so analysis can proceed on a “piecewise linear” basis. Unlike generated electricity that is voltage driven, lightning is a “current” phenomenon. If a current is forced to flow through a body of a given resistance, as is the case with lightning, a voltage directly proportional to the resistance of the body can be measured across the body. That is, for a given current forced through a body, the higher its resistance, the higher will be the measured voltage. The relationship is, once again, governed by Ohm’s law. The terms voltage and potential tend to be used interchangeably. In the case of lightning, current and resistance are the external variables. The resulting voltage is derived. The remaining concept is that of an electric field. When a voltage is applied to a distance (for instance, the “gap” between a cloud and the ground), an electric field results. Air generally has a high resistance and is a very good insulator, conducting very little current under normal circumstances. The electric field is defined as the voltage across the gap divided by the width of the gap. If the magnitude of the field is increased, it reaches a size where the intervening insulator will “break down.” Before this point, a degree of current will be conducted under the influence of the field. After this point, entirely new processes come into play, causing the physical structure of the conducting medium to be disrupted, resulting in an avalanche of current—“breakdown.” The actual moment that this event occurs varies with the voltage applied and the width of the gap. The voltage that is necessary to flash over an air gap is about 4000 V/cm (10,000 V/inch), depending on humidity and other factors, and is also referred to as the “dielectric” constant of air. A large noisy flashover (thunder) may be observed if the gap is sufficiently large. By definition, fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured by an electric field, explaining why lightning injury is a primarily a neurologic injury rather than a burn injury as one might otherwise expect from the high voltages associated with lightning.

CHAPTER 3  Lightning Injuries

Mechanisms of Injury by Lightning*

Blunt Force Trauma Effects 6. Barotrauma 7. Concussive injury 8. Musculoskeletal injury from muscle contraction, falls

Lightning is dangerous to humans because of the effects caused by electricity, heat, and concussive force. In addition, lightning may injure indirectly via forest fires, house fires, explosions, or falling objects. Only injuries directly caused by lightning are

discussed here. The later discussion on pathophysiology states that when lightning current is injected into an individual, the current is initially transmitted directly through the individual. Then, as internal structures (capacitances) charge, flashover occurs over the surface of the individual, and internal current reduces dramatically.225 Lightning current may initially be inflicted on a person in one of several ways, described in more detail later (Box 3-3 and Figure 3-33). In each of these mechanisms, the following processes can occur:169 1. The internal current phase may be the most causative for development of cardiac and respiratory arrest, particularly if the pathway directly includes the heart. 2. As the body’s electric potential builds up in response to the internal current, it produces an electric field over the surface of the body. At a certain level (about one-half the air breakdown field of 4000 V/cm [10,000 V/inch]), current can emerge or escape the body at various points on the body’s surface. Because of the very fast rise time and high current associated with lightning, this occurs after only a few microseconds. In wood, current travels over the surface of wood or internally to it, but not both.89 The consistency and resistance of wood are much closer to the human body than one would initially expect. Metal pieces inserted into wood enhanced “swapping” from internal to external flow. It is unknown if metal pieces on the body may trigger, enhance, or reroute surface discharges and flashovers. However, there is no evidence that metal “attracts” a lightning attachment, regardless of where it may be on or near the body, including whether one is using a mobile phone or other personal digital device* 3. As the current continues to increase, the surface flashover bridges the strike point and the ground. At this level, most of the lightning current flows as an arc current through the air outside the body (flashover effect). Only a very tiny fraction flows through the body at this point and may be too little to cause cardiac and respiratory arrest. A direct strike occurs when the lightning stroke attaches directly to the victim (see Figure 3-33, A). This is most likely in the open when a person has been unable to find a more safe location and probably occurs no more often than in 3% to 5% of injuries. Even though it seems intuitive that direct strike might be the most likely to cause fatalities, there are no studies on the relative fatality rate for each strike mechanism. This low rate of occurrence is estimated on the basis of the examination of thousands of cases by the authors (Figure 3-34).77 Contact, or touch potential, injury occurs when the person is touching or holding onto an object to which lightning attaches. A voltage gradient is set up on that object from strike point to ground, and the individual in contact with the object is subject

*References 4, 6, 7, 15, 25, 43, 53, 68-73, 77.

*References 3, 14, 104, 126, 127, 206, 217.

MECHANISMS OF INJURY

75

PART 1  MOUNTAIN MEDICINE

Contact voltage

Side flash

A

Direct strike

B

C

Upward streamer Ground current

D2

Step voltage

Step voltage

D1 D3

E

FIGURE 3-33  Illustrations of mechanisms of injury. A, Direct. B, Contact. C, Side splash/flash. D1, Ground current through the earth. D2, Ground arcing. D3, Ground arcing cave. E, Upward streamer.

76

Upward streamer 10–15% Side splash/flash 30–35%

Ground current 50–55%

FIGURE 3-34  This chart shows the frequencies of primary lightning fatality mechanisms. (From Cooper MA, Holle RL: Mechanisms of lightning injury should affect lightning safety messages, 2010, University of Illinois at Chicago.)

to the voltage between his or her contact point and the earth (see Figure 3-33, B). A current therefore flows through them. Contact injury probably occurs in about 3% to 5% of injuries. A more frequent cause of injury, perhaps as much as 30% to 35%, is a side flash, also termed “splash.” Side flashes occur when lightning that has hit an object such as a tree or building travels partly down that object before a portion “jumps” to a nearby victim (see Figure 3-33, C). Standing under or close to trees and other tall objects is a very common way in which people are splashed and is the reason safety instructions stress keeping away from trees or other tall or overhanging objects. Current divides itself between the two paths in inverse proportion to their resistances. The resistance of the “jump” path represents an additional path separate from the path to the earth through the originally stricken object. Side flash may also occur from person to person. Earth potential rise (EPR) occurs because the earth, modeled ideally as a perfect conductor, is not so in reality. When lightning current is injected into the earth, it travels through the earth just as it would in any other conductor. Earth has a finite resistance, and so voltages are set up in the ground, decreasing in size with distance from the strike point. The voltage (or potential) of the earth is raised, hence the term EPR. EPR may account for 50% or more of lightning injuries. There are several consequences of EPR. If a person is standing in an area where EPR is active, that is, near the base of a strike, a voltage will appear between their feet and current will flow via the legs into the lower part of the body. This is more significant between the front and back legs of animals, where the path may involve the heart (see Figure 3-33, Dl and D2). A special case occurs on those relatively rare occasions when a person is injured inside a building as lightning hits nearby and is transmitted through the land line of the telephone, pipes of plumbing and faucet handles, or electrical wiring as one uses a computer or attempts to dispatch an ambulance.8,16,95 This is caused, for example, when the person, along with the environment around the person, is raised in potential via EPR. If the telephone line is not locally earthed (grounded), it is at the same voltage as the environment. The fact that the line is earthed remotely away from the local EPR environment causes the person to be subjected to a shock with current flowing between the local Earth at high potential and the distant unaffected Earth. This highlights that local electrical apparatus, including telephones, should be well grounded locally. The grounds of all local structures (power, telephone, plumbing, structural steel) should have a common grounding point (i.e., be bonded) to eliminate any voltage differences developing between separated ground points for each system. For the special case of indoor or telephone

injury, EPR may account for 80% or more of the injuries. It should be noted that all of these refer to hard-wired phones. Cell phones, not being hard wired or distantly grounded, provide no connection or EPR effect to a person during a lightning strike. Static electrical discharges may occur when a person reaches for a car door or stands close to a metal window or door frame in a thunderstorm, because the surrounding electric field induces static electrical charges. These are not lightning injuries. Although people may be startled when this happens, these discharges are unlikely to be any more dangerous than static discharges experienced in the winter months from shuffling across the carpet and reaching for a door handle. Kitagawa and colleagues169 have identified further subdivisions of the EPR phenomenon. They note that not only can EPR occur as discussed, but it can also occur in a manner similar to the surface flashes over a body, with arcs developing over a ground surface (Figure 3-35). Despite modeling that assumes the contrary for mathematical reasons, the grounding Earth is not homogeneous and provides arc generation points. Ground current effects are possibly more likely to be temporary and less likely to produce fatalities. However, multiple victims and injuries are frequent. Large groups have been injured on baseball fields, at racetracks, while hiking, and during military maneuvers.40,41,188 Shocks via telephones can produce significant long-term problems, and the majority of these are via EPR.16,95,212 Irregularities occur on mountainsides. If the terrain is markedly irregular, spreading lightning current may reach the surface. A surface arc discharge may develop together with flow of the conduction current in the ground. Because arcs carry considerable energy, a person exposed to a surface arc discharge is more likely to have a more severe effect, including thermal injuries, temporary

A

B FIGURE 3-35  A, Lightning injury and ground current effect to a golfing green—photographed a few days after the strike when the grass had died. B, Laboratory lightning onto a pool surface.

77

CHAPTER 3  Lightning Injuries

Contact Direct Blunt injury strike injury 3–5% 3–5% ?

PART 1  MOUNTAIN MEDICINE

FIGURE 3-36  Example of contact injury.

paralysis, or even death. This mechanism of injury makes it particularly dangerous for someone on a mountainside to shelter inside a shallow cave or under a small cliff or outcropping of terrain where surface arcing is much more likely to occur, injuring the person just as they feel some degree of safety has been achieved (see Figure 3-33, D3). All these factors point to the danger of being anywhere outside in the presence of lightning. The danger of upward streamers has been documented.4,41,68 Injury may occur when a victim serves as the conduit for one of the usually multiple upward leaders induced by a downward stepped leader and its field (see Figure 3-33, E). Streamers occur even when there is no attachment between them and the stepped leader. Although one might think that these are weak in energy compared with the full lightning strike, they may carry several hundred amperes of current to be transmitted through the victim. Upward streamer injury is probably a much underestimated mechanism of injury and may account for as much as 10% to 15% of injury cases, but needs substantial additional study and documentation. Finally, persons may suffer from (nonelectrical) 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 a person struck by lightning may suffer from explosive and implosive forces created by the thunderclap, with resulting contusions and pressure injuries, including tympanic membrane rupture (barotrauma—see Lightning Explosive Barotrauma, later). Another mechanism of blunt injury is blast injury resulting from vaporization of water on the body surface from a surface flashover spark. Lightning blast injury to the skull, brain, and viscera has been elegantly demonstrated in animals.224 Many cases of multiple injuries are likely a combination of many of these effects, with the majority of them from EPR and upward streamers, sometimes complicated by side flashes if people or animals are standing too close together (Figures 3-36 and 3-37).

medical literature. Figure 3-38 shows 20 kV applied to a 1.8-m (6-foot) man, causing current to ground. This produces an internal electric field strength of approximately 10 kV/m. When a child chews on an electric cord and suffers a lip burn, the field strength is approximately the same: 110 V applied to 1 cm of a child’s lip generates a field strength of 11 kV/m. Even though no one would classify the child’s injury as “high” voltage, it is a high electric field strength and produces the same tissue destruction in a small localized area, much as would a high-voltage injury. Electric fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured, explaining why lightning injury is a primarily a neurologic injury. Although Lee184 has discussed the importance of internal electric field calculations in describing electroporation damage, this has not been studied for lightning injury. A similar inconsistency involves the breakdown strength of air (the force needed to cause a spark of electricity to cross a gap), which is roughly 4000 V/cm, or 10,000 V/inch. Most people are familiar with the shock experienced from walking across a carpet in the winter, although few appreciate this phenomenon would be classified as “high-voltage” injury by the 500- to 1000-V criterion used in medical literature. Thus terms used in the medical literature to categorize electrical injuries, such as high versus low voltage and exit versus entry in alternating current injuries, as well as the simplistic application of Kouwenhoven’s six factors, do not reflect either medical or engineering reality and are poor predictors of injury.

LIGHTNING INJURY PHYSICS It is necessary to distinguish between lightning and generatorproduced high-voltage electrical injuries, in that there are significant differences between the mechanisms of injuries and their treatment.65 Although lightning is an electrical phenomenon and is governed by the laws of physics, it accounts for a unique spectrum of induced signs and symptoms that are best understood relative to specific physical properties of lightning.

FREQUENCY, VOLTAGE, AMPERAGE, AND RESISTANCE Lightning is neither a direct nor an alternating current. At best description, 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

Pathophysiology of Lightning Injury* ELECTRICAL INJURY PHYSICS REVISITED Kouwenhoven determined six factors that affect the type and severity of injury encountered with electrical accidents: frequency, duration of exposure, voltage, amperage, resistance of the tissues, and pathway of the current. However, several inconsistencies appear when these are applied too literally. Electric field strength, not listed as one of the factors, is a more useful and accurate concept in explaining and predicting injuries from technical or man-made electricity than are the classic Kouwenhoven factors that have traditionally been cited in the

*References 15, 64, 72, 153.

78

FIGURE 3-37  Example of side flash or “splash.”

Energy ( heat ) = Current 2 × Resistance × Time

20 kV

6 feet

= Electric field approx. 10 kV/m 20 kV 2m

A

= 10 kV/m

PATHWAY, DURATION OF CURRENT, FLASHOVER EFFECT, AND TIME

110 V

1 cm

1 cm = 11 kV/m

B

where a current flows through a resistance for a time T. As resistance goes up, so does the heat generated by passage of the same 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 what appear to be discrete entry and exit wounds, these are rare. Lightning more commonly causes only superficial streaking burns. Burns are discussed later and are a most important distinction between lightning and technical electric shocks. The exception to this is when there occurs long continuing current. This is a prolonged stroke lasting up to 0.5 second that delivers a tremendous amount of energy, capable of exploding trees and setting fires. Other poorly understood factors may contribute to the formation of deep burns, although deep burns similar to those of high-voltage electrical injuries generally are quite rare with lightning.

110 v/1 cm = 11 kV/m

C FIGURE 3-38  A, If 20 kV is applied to a 1.8-m (6-foot) man source to ground, an electric field strength of approximately 10 kV/m is produced. B, When a child chews on the end of an extension cord, the applied voltage of 110 V across 1 cm produces an electric field strength of 11 kV/m—higher than the classic “high-voltage” injury.  C, This explains the deep full-thickness burns the child receives, which one would not predict given the “low-voltage” source.

It takes a finite amount of time for the skin to break down when exposed to heat or energy. Generally lightning is not present long enough to cause this skin breakdown. Probably a large portion travels along the outside of the skin as “flashover.” There is some experimental evidence that a portion of the current may enter the cranial orifices—the eyes, ears, nose, and mouth.10 This pathway would help explain the myriad eye and ear symptoms that have been reported with lightning injury. Andrews 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 respiratory control centers. It is postulated that current travels via cerebrospinal fluid (CSF) and blood vessel pathways to impinge directly on the myocardium. Andrews also showed histologic damage to the myocardium, consistent with a number of autopsy reports of inferior myocardial necrosis.9,17 An alternative hypothesis can be tested with mathematical modeling.15 Certain assumptions are made in any model, usually based on principles accepted in the literature.31 Figure 3-39, A shows a model for skin resistance, and its connection to the internal body milieu is shown in Figure 3-39, B. Note that the internal body structures are regarded as purely resistive, whereas the skin contains significant elements of capacitance.31 In the model, the sequence of events during the strike starts with the postulate that the stroke attached initially to the head of the victim. From our knowledge now that “direct strike” occurs in probably only 3% to 5% of lightning injuries, it seems that this is an uncommon point of attachment, but the model is still useful in illustrating lightning energy flow. For a small fraction of time, current flows internally as the skin capacitance elements become charged. At a voltage taken as 5 kV, the skin was assumed to break down. (A lightning stroke is modeled as a current wave, building to a maximum value in around 8 msec, although this may be “modulated lightning,” that is, 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 the earth built up, and external flashover across the body occurred when the field reached the breakdown strength of air. 79

CHAPTER 3  Lightning Injuries

their effects on the human body, is not well advanced. Lightning is said to be a “current” phenomenon rather than a “voltage” phenomenon. Examining the particular voltage in these equations becomes difficult because the voltage between cloud and ground disappears after lightning attachment, and equations such as Ohm’s law (V = I × R) and power calculation (P = V × I) cannot be accurately applied. 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:

PART 1  MOUNTAIN MEDICINE

10 k

0.25 µ 10 k

10 kΩ

200 0.25 µF

200 0.25 µ

Key

A

300

300

10 k

0.25 µ

300

10 k

0.25 µ

B FIGURE 3-39  A, Electrical model for human skin impedance. B, Model of human body for the purpose of examining current flow during lightning strike.

The results of mathematical modeling of these events are shown in Figure 3-40, 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. Andrews9 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, although this has not been corroborated in clinical studies.169 Experimental evidence suggests that “a fast flashover appreciably diminishes the energy dissipation within the body and results in survival.”225 In addition, Ishikawa obtained experimental results with rabbits similar to the human data found by Cooper’s study.64,153 Cooper has carried her studies to animals in developing a 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.80-82 As current flashes over the outside of the body, it may vaporize moisture on the skin and blast apart clothes and shoes, leaving the victim nearly naked, as noted by Hegner128 in 1917: The clothing may not be affected in any way. It may be stripped or burned in part or entirely shredded to ribbons. Either warp or woof may be destroyed leaving the outer garments and the skin intact.… Metallic objects in or on the clothing are bent, broken, more or less fused or not affected. The shoes most constantly show the effects of the current. People are usually standing when struck, the current then enters or leaves the body through the feet. The shoes, especially when dry or only partially damp, interpose a substance of increased resistance. One or both shoes may be affected. They may be gently removed, or violently thrown many feet, be punctured or have a large hole torn in any part, shredded, split, reduced to lint or disappear entirely. 80

The soles may disappear with or without the heels. Any of the foregoing may occur and the person not injured or only slightly shocked. The amount of damage to clothing or 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, Cooper and others have found that forensic evidence of damage to shoes and clothing may be the most important and reliable indicator in determining whether lightning caused a person’s death, in addition to ruptured tympanic membrane when no other cause is apparent.32,162,279 The factor that seems most important in separating the effects of lightning from high-voltage electrical injuries is the duration of exposure to the current, both because lightning is not present long enough to cause tissue breakdown in the classic burn sense and because of the results of the mathematical modeling describing the path of the energy and how long it is in contact with the body.

ESTIMATES OF STREAMER CURRENTS A fifth mechanism of current impingement on an individual has been described.4-6,68 This mechanism recognizes that as a stepped leader steps toward the earth from a cloud, an upward leader will emanate from several objects that are possible points of attachment. Of these, a return stroke will evolve perhaps from only one. Alternatively stated, there will be several upward leaders that dissipate without attachment. The current needed to establish and maintain any upward leader nonetheless must be supplied from the earth, and if a person is the source of an upward leader, then current must flow through the person as a first approximation. Becerra and Cooray25 have studied the amount of current to which a victim of upward leader current may be exposed. They identify two processes that are important to model. First, current flows through a victim to establish the upward streamer and the space charge around the victim’s head, under the influence of the electric field resulting from the stepped leader’s downward

Response

No flashover 5 MV

G4

VAC VAB

4 MV

CHAPTER 3  Lightning Injuries

A

5 kV

F

5 kA VAF VEB,DB

IFH

1.11.7

50

G1 500 kV

Time (µsec)

H

5 kA peak 8/20 µsec wave

With flashover E

D VAB

500 kV

IFH

800A

G2

5 kV

150

VDB 340 nsec

B

Physical Earth

261,467

— — 18,000 10,000 — — — — — — — — — — — — — — — — — — — — — — — — — — — — — 28,000

Posteruption Starvation — — — — — — — — — — 9340 — — — 48,000 — — — — — — — — — — — — — — — — — — >57,340

Modified from Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; and Tanguy J-C, Ribière C, Scarth A, et al: Victims from volcanic eruptions: A revised database, Bull Volcanol 60:137, 1998.

Younger. In two letters written to the Roman historian Tacitus, Pliny wrote that the first explosion began in the early afternoon and ended in the evening of the following day. At first, Vesuvius produced an enormous eruption cloud that ejected ash, pumice, and volcanic gases vertically up to 30 km (19 miles) high. Then, from a darkened sky, ash and pumice rained down on the towns of Pompeii and Straide, causing roofs to collapse under the weight of the ash fall and burying the towns (Figure 15-6, online). The town of Herculaneum, lying at the foot of Mt Vesuvius on a cliff overlooking the sea, was initially spared from burial. The prevailing wind blew away from the town and toward TABLE 15-3  Fatalities From Volcanic Eruptions,

1783-2000

Fatalities Volcanic Hazard Posteruption famine and disease epidemics Pyroclastic flows Lahars Volcanogenic tsunamis Debris avalanches Volcanic ash Volcanic gases Lava flows TOTAL

No. 75,000 67,500 42,500 42,500 10,000 10,000 1750 750 250,000

TABLE 15-4  Fatalities From Volcanic Eruptions by

Region, 1600-1982

% 30 27 17 17 4 4 1,250 m [4101 feet]) of tropical Africa, Central America, and North India.17-19,49,71,74 Fluoride leached from volcanic rocks into drinking water can also cause disease. In eastern Turkey near Tendurek Volcano, mottled enamel from high levels of fluoride, called endemic dental fluorosis, has been observed in humans and livestock since the 1950s.52

PART 3  BURNS, FIRE, AND RADIATION

TABLE 15-5  Casualties Caused by Pyroclastic Flows in 20th-Century Explosive Eruptions Eruption

Year

Deaths (N)

Ratio of Dead to Injured

Montagne Pelée, Martinique La Soufrière, St Vincent Taal, Philippines Lamington, Papua New Guinea Mount St Helens, United States Unzen, Japan Merapi, Indonesia Soufrière Hills, Montserrat

1902 1902 1911 1958 1980 1991 1994 1997

28,000 1565 1335 2942 58 43 63 19

230 : 1 11 : 1 10 : 1 44 : 1 16 : 1 5 : 1 3 : 1 4 : 1

Survivors After Treatment 163 treated, 123 survived 194 treated, 120 survived Not known 70 treated, 67 survived 130 airlifted, 9 treated, 7 survived 17 treated, 4 survived (minor burns) 86 treated, 11 dead on arrival 7 treated, all survived

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

areas and river valley regions, is of utmost importance. Goggles and masks should be distributed, especially to individuals who must work in dusty conditions.

EMERGENCY MEDICAL RESPONSE Emergency medical care plays a small role in severe volcanic eruptions. The number of injured who could benefit from treatment is much smaller than the number of victims killed within minutes of a catastrophic eruption (Table 15-5).5 Therefore prevention is of utmost importance, and evacuation is the key to decreasing morbidity and mortality.5 Health care professionals should be prepared to treat a variety of medical problems in persons who survive (Box 15-2), and they must be aware that access to victims will be limited by high ash conditions, burial beneath volcanic debris, and ongoing hazards. Transient increases in emergency department visits and hospital admissions will require additional resources.8

GEOTOURISM With the increased interest in visiting volcanic environments, the numbers of injuries and illnesses are increasing. Areas like Hawaii Volcanoes National Park have experienced a high rate of injuries and illness because of inexperienced hikers entering high-risk environments and disregarding warning signs.26 People working or traveling near an active volcano or volcanic environment should heed these safety recommendations: • Read about the volcanic environment, including past eruptions and accidents. • Know the current volcano warning level, and obey local authorities.

BOX 15-2  Summary of Health Effects From Volcanic

Eruptions

Physical • Blunt trauma from pyroclastic material, lahars, debris avalanches, tsunamis, and tephra • Burns, wounds, and gangrene complications • Asphyxiation from lack of oxygen or inhaled ash • Acute irritation of the respiratory tract caused by ash • Exacerbation of prior respiratory disease caused by inhaled particles • Respiratory tract and lung burns caused by inhalation of hot steam • Conjunctivitis and corneal abrasions • Toxic effects of gases such as CO2, H2S, SO2, HF, CO, and radon • Gastroenteritis • Skin irritation from acid water • Drowning in lahars or tsunamis Psychological • Depression • Anxiety • Nightmares • Psychomotor disorders • Irritability • Insomnia • Confusion • Neurosis • Stress Modified from Zeballos JL, Meli R, Vilchis A, et al: The effects of volcanoes on health: Preparedness in Mexico, World Health Stat Q 49:204, 1996. CO2, Carbon dioxide; CO, carbon monoxide; HF, hydrogen fluoride; H2S, hydrogen sulfide; SO2, sulfur dioxide.

• Travel with a guide experienced in local conditions. • Leave travel details with a responsible person. • Wear a hard hat and take a gas mask, if appropriate. • Beware of the sources of danger on a volcano: • Rock falls • Avalanches • Hazardous gases • Look for warning signs of an eruption. • Immediately leave the area if it becomes dangerous. • Do not approach lava flowing through vegetation. FIGURE 15-40  First of a series of powerful explosions beginning on June 12, 1991, Pinatubo Volcano, Philippines (see text); note within the yellow oval a farmer and buffalo plowing. (Courtesy David Harlow, U.S. Geological Survey.)

332

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 16 

Injury Prevention: Decision Making, Safety, and Accident Avoidance EUNICE SINGLETARY AND DAVID S. MARKENSON

For many, it is the wild in wilderness that fuels a passion for the wilderness experience. Wilderness areas are considered the last areas that humans do not control and have not developed. This lack of human control in undeveloped terrain, combined with the enthusiasm of wilderness explorers, is an ideal recipe for unintentional injury. Managing the risk through sound decisions and efforts to improve safety and reduce accidents is a critical component of wilderness medicine and the focus of this chapter. Contributing to overall risk for injury is the growing feasibility of exploration by wilderness novices, children, elders, and persons with disabilities or chronic health issues by using offroad vehicles, watercraft, and aircraft or via improved access. For persons who venture into the wilderness, there are growing technologic advances in communications equipment, global positioning systems, sporting equipment design, water purification and disinfection, and food processing and preservation techniques, all of which extend the duration of expeditions and permit exploration of remote wilderness once accessed by only the most skilled and experienced persons. Environmental hazards, such as exposure to cold, heat, snow, or altitude, can be minimized through proper planning and training. Wilderness sports activities, such as hunting, snowmobiling, and backcountry ski touring, are safer today not only because of advances in technologic and safety equipment, but because of efforts to educate the public about associated risks and how to manage or reduce these risks and efforts to train the public in wilderness first-aid and medicine (Figure 16-1, online). Despite the growth in numbers of practitioners of wilderness medicine and improved ability to provide care for many injuries and illnesses in remote settings, evacuation of injured victims from the wilderness remains daunting and can turn a minor problem into a major medical situation with a protracted rescue. There are 78 million hectares (193 million acres) of land in the U.S. National Forests and Grasslands. Thousands of rivers and lakes are parts of the National Forests, and there are 247,000 km (153,000 miles) of trails, primarily for nonmotorized use. It is estimated that 178 million people recreate each year in the national forests.152 Sixty-four percent of 446 million visits to national parks in 2009 were considered recreational, with 1.9 million categorized as backcountry overnight visits.97 The National Sporting Goods Association estimates that between 1994 and 2004, the number of Americans involved in backpacking and wilderness camping climbed from 10.2 million to 13.3 million. During the same time period, the number of hikers increased from 25 million to 29.8 million.98 With increased access comes the potential for higher numbers of injuries, illnesses, and fatalities. According to the Centers for Disease Control and Prevention (CDC), in 2005 a total of 173,753 injury-related deaths occurred in the United States, and during 2006 an estimated 29,821,159 persons with nonfatal injuries were treated in U.S. hospital emergency departments.26 The number of injuries and injury-related deaths as a result of wilderness activities is unknown and can only be extrapolated, particularly from National Park Service (NPS) data. Between 2003 and 2006, there were 12,337 search and rescue (SAR) operations in national parks, involving 15,537 visitors and involving 522 fatalities and 4860 ill or injured visitors.60 From a public health point of view, the physical, financial, and emotional consequences of injury can 334

be wide ranging, devastating, and long lasting. The CDC’s National Center for Injury Prevention and Control (Injury Center) was formed partially as a result of a recommendation of the 1985 Institute of Medicine report Injury in America, which concluded that supporting injury research is necessary to substantially reduce injury rates.30 The Injury Center strives to prevent injury and reduce its consequences, using a public health approach that describes the problem, identifies risk and protective factors, develops and tests prevention interventions and strategies, and promotes widespread adoption of effective interventions and strategies. Although the Injury Center includes intentional as well as unintentional injuries in its focus on injury prevention, their efforts and approach may prove to be a model for future research and methods for injury reduction in the wilderness setting. This chapter reviews basic principles of injury applied to the wilderness environment. Individual (human/host) factors and behavior and how they apply to injury risk and prevention are detailed, including preparation, planning, anticipation of problems, and errors of omission or commission. Problems are approached from the perspective of environmental hazards, rather than from a particular activity, because many hazards are common to different wilderness activities. Throughout this chapter, prevention of injury is the focus. Details of pathophysiology and treatment are found in the referenced chapters throughout this text.

Principles of Wilderness Injury and Prevention THE INJURY FIELD: BASIC PRINCIPLES Injury prevention is a key component of public health and medical care. It is a long-held belief of physicians and public health practitioners that injury prevention is far superior to injury treatment. Underlying injury prevention is the concept that when an injury occurs it is usually the result of a series of events under specific circumstances that had they been identified in advance might have been avoided, addressed, and/or eliminated to prevent or mitigate the injury. In the field of injury prevention, accidents are defined as unpredictable acts of fate or chance events, whereas injuries are defined as damages resulting from a sequence of accidents or intentional actions. Injuries are prevented by stopping or reducing the number of accidents causing them and/or eliminating the intentional actions and situations that lead to them. By applying this principle, practitioners of injury prevention estimate that 90% of all injuries are predictable and preventable. For example, by inspecting, testing, and replacing equipment, individuals may prevent accidents related to equipment failure. The need for this approach is even greater in wilderness medicine than in many other fields of medicine. In medicine we attempt to prevent injury, but if that prevention fails, we then provide emergency care and rehabilitation to limit the lasting effects of injury and return the person to good health. In the case of wilderness injuries, which may occur in areas with limited immediate care and often with significant distance and time to reach definitive care, our ability to limit the extent of injury is less, magnifying the need for prevention.

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Injury prevention can occur at many points along the continuum, beginning before injury through rehabilitation. In classic injury prevention and epidemiology, opportunities for prevention are divided into primary, secondary, and tertiary phases. Primary prevention avoids development of a disease. Most population-based health promotion activities are primary preventive measures. In addition, many environmental or regulatory controls are primary. Secondary prevention activities are aimed at early disease detection, thereby increasing opportunities for interventions to prevent progression of disease and emergence of symptoms. In the field of injury prevention this would include early recognition of injury to limit the extent and impact of an injury should it occur. An example in wilderness medicine is early recognition of foot blisters and use of protective coverings or footwear alteration to prevent skin breakdown and further extension of blisters or infections. Wearing protective equipment is both primary and secondary if it limits the extent of injury. Interventions may cross multiple stages of prevention. Tertiary prevention reduces the negative impact of an already established disease by restoring function and reducing diseaserelated complications. In the field of injury prevention, this traditionally includes prompt and appropriate medical rehabilitation. An example is early splinting of a fracture in the field to prevent further injury and to limit swelling and associated complications. Quaternary prevention is the set of health activities that mitigate or avoid the consequences of unnecessary or excessive interventions within the health system. This stage is the latest addition to the classic three stages of prevention and is not always included in descriptions of injury prevention.

EPIDEMIOLOGIC FACTORS: HUMAN OR HOST, AGENT, AND ENVIRONMENT One of the most commonly used methods of categorizing the factors that lead to injury is “human (host), agent, and environment.” Numerous human factors can lead to injury and be used as opportunities for prevention. Examples include predisposition to injury, such as osteoporosis predisposing to fractures; behaviors that may be high risk for injury, such as alcohol consumption and intoxication; decision making, such as a choice to proceed on an icy trail; and different body habitus, ages, or conditions, such as pregnancy. The next factor is the agent. Broadly defined, the agent is what causes the injury. Although this may seem straightforward, the lines can be blurred. For example, if someone decides to strike a branch with his or her hand to break it, is the branch the agent or is the human who made the decision the agent? Most would agree the branch is the agent and the human factor was the decision to strike it. Classic descriptions of agents would be propelled objects, items that strike people, falls from heights, or malfunctioning mechanical devices. In the wilderness, the items include failing ropes or belts when climbing, branches and rocks when falling, wet ground causing a slip, a poorly positioned or inappropriately worn backpack leading to back injury, or a hot object that causes burns. The last factor is the environment, which includes the situation in which the injury occurred. This might be temperature conditions, such as extremes of heat or cold, but may also include a situation where there is only one option for moving forward through less-than-ideal terrain without the option to turn back.

CONCEPTUAL MODELS A more comprehensive conceptualization for intervention and prevention can be done by combining stages of injury prevention with the host, agent, and environment approach. This combination was proposed by Dr. William Haddon, Jr., who is widely considered the father of modern injury epidemiology. Haddon’s matrix is an injury prevention brainstorming tool originally designed for motor vehicle safety that combines the epidemiology triangle (host, agent, environment) and levels of prevention. This combination allows planning for injury interventions and prevention strategies by phases in time of the event.

In addition to planning interventions, this matrix can also be used to collect data to determine the factors that cause injuries. The following are the steps to complete Haddon’s matrix: 1. Assess the contributing factors or characteristics of an injury from the perspective of the following: • Host or human factors • Agent of energy or vehicle (such as crashworthiness of a vehicle) • Physical environment (such as roadway design or safety features) • Social environment (such as passage and enforcement of seat belt laws) 2. Then combine them with time phases: • Pre-event: What factors affect the host before the event occurs? • Event: What are factors related to the crash phase? • Postevent: What are factors related to the postevent crash phase? 3. Place the items with the possible intervention in the appropriate location in Haddon’s matrix. Haddon’s 10 Strategies for Reducing Injuries In addition to developing the matrix, Haddon also proposed strategies for reducing injuries. These strategies have been grouped into 10 specific approaches, commonly known as Haddon’s 10 Strategies (with examples): 1. Prevent creation of the hazard. • Perform preparticipation musculoskeletal physical examination to identify underlying pathologic problems of the knee joints. • Provide treatment and rehabilitation before sports participation. • Provide warm-up programs involving neuromuscular and proprioceptive training to stabilize the knee. 2. Reduce the amount of the hazard. • Limit the physical areas for activities. Provide limitations on activities or exposure to the environment. 3. Prevent the release of the existing hazard. • Ensure that waste is kept properly distant from potable water sources. 4. Modify the rate or partial distribution of release of the hazard from its source. • Limit activity to an individual’s ability. • Substitute individuals as necessary during a specific activity. 5. Separate, in time or space, the hazard and that which is to be protected. • Limit climbing to certain weather conditions. • Perform strenuous activity only when ambient conditions are appropriate. 6. Separate the hazard and that which is to be protected by interposition of a material barrier. • Use well-fitted gear. • Employ protective gear. 7. Modify basic relevant qualities of the hazard. • Avoid surfaces that increase the potential for injury. 8. Make what is to be protected more resistant to damage. • Provide fitness training, including stretching, strengthening, and improving balance and movement. 9. Begin to counter the damage already done by the hazard. • Seek and receive prompt medical care as soon as the injury is noted. 10. Stabilize, repair, and rehabilitate the object of the damage. • Provide rehabilitation, and use stabilization devices, such as knee braces.

ENVIRONMENTAL, EDUCATIONAL, AND ENFORCEMENT APPROACHES TO INJURY PREVENTION In addition to describing possible interventions using Haddon’s matrix approach, it may be helpful to characterize the type of intervention. One way to categorize injury prevention efforts is by the three E’s: 335

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• Environment makes the environment or product safer. • Education provides information to individuals. • Enforcement relies on change through laws. Comprehensive injury prevention projects employ strategies that include all of these. Environmental Approach The environment includes physical surroundings (e.g., roadway), products (e.g., vehicles), and the social environment (e.g., societal attitudes toward drinking and driving). The environmental approach is a strategy that does not depend on action by those being protected; it is passive, automatic, and constant in its protective effects. As a result, this approach is considered the most effective strategy. In some cases, there is the technology available to make products safer, but industry has not adopted it, often because of economic disincentives. In classic injury epidemiology, environmental interventions refer to the following: • Physical surroundings • Product design, protocols, and practices • Social environment The following are key concepts for environmental modifi­ cation: • Design safer surroundings • Pool fencing • Handrails • Antislip surfaces • Playground surfaces • Roadways • Bike/walking paths • Design safer products • “Kill switches” • Childproof packaging • Crib slat spacing • Flame-resistant sleepwear • Vehicle design • Protocols and practices • “Traffic calming” • Walk-light timing at crosswalks • Bus stop placement • Lighting for crime reduction • Factory settings for water heaters • Social environment • Alcohol consumption and operating motorized devices while drunk • Domestic violence • Violence on television • Safety devices Educational Approach Preventive measures defined as an educational approach involve education of large populations, targeted groups, or individuals and efforts to alter specific injury-related behaviors. Many injuries result less from lack of knowledge than from failure to apply what is known. Three goals of educational interventions are as follows: 1. Provide information regarding injury risks and how to avoid them. 2. Change attitudes away from risks and toward safer practices. 3. Alter behaviors. It is not enough to know that seat belts save lives, but one must actually use the seat belt for it to be effective. An educational approach may be appropriate in the following instances: • New knowledge about a risk is needed (e.g., defective equipment, better approaches to an activity, newer and safer technology available) • No other approach exists (e.g., an activity that is inherently unsafe and avoidance is the only strategy) • To influence decision makers, lawmakers, and design engineers • To teach specific behaviors and skills (dialing 9-1-1, crawl under smoke, self-care of injuries) 336

Limitations of the educational approach include the following: • It uses an active approach. Passive approaches are pre­ ferred. • It may be an inappropriate message for the target audience. Targeted, at-risk populations are not always reached through mass-media educational campaigns. • There are variations in learning style among adults and possible language barriers. In education, “one size doesn’t necessarily fit all.” There are variations in learning styles unique to children and adults, cultures, and socioeconomic status. • There may not be cultural acceptance of the message. Messages should be tested with a focus group to be certain that they are not offensive. Enforcement Approach This approach uses a strategy that seeks to require change in behavior, the environment, or product by enacting law and policy. Enforcement initiatives and laws are directed toward individuals, products, and environmental conditions. The following are examples of laws targeted to individuals: • Requiring: • Seat belts • Child restraints • Helmet use • Prohibiting: • Drunk driving • Excessive speed The following are examples of laws targeted to products: • Requiring: • Motor vehicle standards • Helmet standards • Childproof packaging • Prohibiting: • Fully automatic weapons • Flammable fabrics The following are examples of laws targeted to the environment • Requiring: • Swimming pool fence • Smoke detectors • Prohibiting: • Firearms in airports/schools • Rigid structures on highways Characteristics of successful laws include the following: • There are few exceptions to compliance. • Detection is easy (measuring speed with radar, observing helmet use). • Punishment is certain, swift, and sure. • There is publicity about enforcement. Enforcement and laws can have a much greater impact on changing behavior when enforcement is highly visible and media are used to let the public know about enforcement campaigns. Controversies arise when legislation is perceived to restrict personal freedoms.

SOCIAL-ECOLOGIC MODEL In addition to the classic epidemiology approach of host, agent, and environment enhanced by the stages of prevention and articulated by Haddon in his matrix, another conceptual model attempts to describe injury prevention but with more focus on the interplay of different factors. The social-ecologic model has its foundation in human development and has been refined to apply to injury prevention and epidemiology. The social-ecologic framework was created by Urie Bronfenbrenner19 in the context of understanding human development and is very compatible with a broader view of public health.76 Social-ecologic theory defines various levels of the social environment, depicting the nested roles of intrapersonal factors, interpersonal factors, institutional elements, and cultural elements. This social-ecologic framework enhances the standard public health model of agent-host-environment.88,120,135 With respect to understanding injury prevention, intrapersonal factors include both developmental and sociobehavioral features

RISK AND EFFECT MODIFICATION IN INJURY PREVENTION EPIDEMIOLOGY Two basic epidemiologic concepts are risk and effect modification. Risk is the likelihood of disease occurrence and is often operationalized as relative risk to aid in decision making. This is a method to describe how one option versus another option may lead to different disease outcomes. In injury prevention, one always must consider risk. Some activities are inherently risky, and all one can do is provide interventions that protect the individual or minimize the impact of a potential injury. In other cases, there may be several options each with different risk, so that one can determine the relative risk. Major human risk factor examples are age, gender, and experience. Another basic epidemiologic concept that can be applied to injury prevention is that of effect modification. An effect modifier is a variable that lies in the pathway from independent/main explanatory variable and the dependent/outcome variable. When applying this to injury prevention, one can think of an effect modifier as something that lies in the pathway between the event and the injury, and that can alter the injury outcome from similar events. An example might be wearing a helmet, so that when thrown from a horse the injury to one’s head is less than if not wearing a helmet. Human factors can be considered from the perspective of effect modifiers. For example, when caught in bad weather, the more experienced hiker will be less likely than the novice to be injured.

ACTIVE VERSUS PASSIVE INJURY PREVENTION STRATEGIES Before proceeding to implement methods of injury prevention, it is important to recognize that injury prevention strategies are either active or passive.112 Active injury prevention strategies require change in behaviors by individuals before or when exposed to risks.145 For example, individuals must be convinced that wearing seat belts reduces the risk for injury and then must take the action of buckling up. Passive injury prevention

strategies are preferable because they require no action on the part of the individual.54,72 For example, recent advances in automotive safety have been gained by placement of air bags. A more classic passive approach has been referred to as environmental controls. An example of this is a fence placed around a pool to prevent entry of unsupervised children, thus reducing drowning incidents.

MORBIDITY AND MORTALITY STATISTICS FOR WILDERNESS INJURY The difficulties of obtaining data about injury prevention in the wilderness are the diversity of activities covered and lack of a single source for the data. As a result, data are often only for a selected activity and in a single location. Some data involve several activities. An example is a CDC study released in 2008 of nearly 213,000 people who had been treated each year in emergency departments for outdoor recreational injuries from 2004 to 2005.44 Of those injured, about 109,000 (51.5%) were young people between the ages of 10 and 24. For both men and women of all ages, the most common injuries were fractures (27.4%) and sprains (23.9%). Of these, most injuries were to the arms or legs (52%) or to the head or neck (23.3%). Overall, 6.5% of outdoor injuries treated were diagnosed as traumatic brain injury. Researchers found that snowboarding (25.5%), sledding (10.8%), and hiking (6.3%) were associated with the highest percentage of injuries requiring emergency department visits. The study points out that wilderness injury prevention begins with planning, preparation, and problem anticipation, which are discussed later in this chapter. An example of event-specific data is for backpacking and camping. Data reveal that more than 11 million people participated in backpacking or wilderness camping in 1990. The morbidity and mortality figures from eight national parks in California between 1993 and 1995 are 1708 injuries and 78 fatalities.95 Another event-specific activity for which there are data is scuba diving. There are more than 9 million certified scuba divers in the United States, with approximately 650,000 annual certifications.35 The Divers Alert Network37 at Duke University Medical Center (Durham, NC) reported approximately 1000 serious diving-related injuries and approximately 90 diving-related fatalities annually between 1995 and 2002. In addition to event-specific data, one can examine equipmentbased data, which can include data based on certain types of vehicles. For example, from 1990 through 1995, an estimated 32,954 persons were involved in injuries related to personal watercraft.18 Lastly, one may search data to learn about specific types of injuries or deaths. An example of this type of data is a western Washington study of 40 pediatric wilderness-activity related deaths between 1987 and 1996.100 Ninety percent of the victims were male, and 83% were 13 to 19 years of age. The most common cause of death was drowning (55%), followed by closed head injury (26%). Injuries or deaths resulted from lack of preparation, lack of training for wilderness activities, and inadequate basic safety equipment; alcohol use and rescue delays were contributing factors. Of note, the presence of adults did not appear to be significant in reducing the incidence of mortality.

PUTTING INJURY PREVENTION INTO PRACTICE Planning Careful planning is the foundation for a safe activity that minimizes risk and avoids injury. Planning begins by gathering all relevant data for the planned activity. This includes up-to-date information regarding weather, trail, and campground conditions, best times to travel, permit requirements, equipment needed, and special considerations unique to the activity. After gathering all available information, one develops a plan for activities. The plan may be very brief and purely a mental exercise for some activities such as brief hikes, camping trips, rock climbing, or day diving. For longer excursions, the planning phase will include a detailed, written plan. Planning activities may include activity-specific 337

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of individuals (i.e., the host), for example, a young child’s curiosity and exploratory behaviors through touching, tasting, and crawling; an adolescent’s propensity to take risks and the varied responses to parent and peer influences; or an older adult’s suicide risk due to a sense of hopelessness in the face of an incurable chronic disease, or avoidance of walking in certain locations because of fear of falling or assault. Likewise, biologic features of the host, such as a young child’s lack of balance and strength, high center of gravity, and small size, relate to some of the hazards encountered. For an older adult, biologic characteristics such as bone brittleness; reduced visual acuity, reaction time, and balance; and thinner skin all increase susceptibility to injury events such as traffic crashes, pedestrian injuries, falls, and burns. Interpersonal factors are those that result from the interactions between two persons, for example, intimate partners, parent and child, employer and employee, or adolescents. In the injury sphere, this relates to intentional injury as a result of behaviors associated with disciplinary practices or conflict resolution. Institutional elements are those that reflect organizations in which individuals function, for example, schools, places of worship, and workplaces. How these organizations promote or control activities and environments can affect injury risks. Work sites contain many hazards and adopt many types of safety practices, whereas places of worship may either encourage or discourage certain safe or unsafe practices. Prehospital trauma care and inpatient health care systems are institutions that affect injury outcomes.105 Cultural elements include broad social values and norms as well as governmental policies that guide or mandate behaviors of individuals or organizations. Examples are values placed on individual freedom; social norms about drinking or corporal punishment; and laws, policies, and regulations about producing, selling, and storing firearms. Any health problem can be viewed as resulting from and being alleviated by the interactions among these dynamic factors.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

planning that addresses unique risks or needs. For example, to plan for a climb that includes high altitude, allowance is made for ascent and descent to allow time for acclimatization. Planning may include provision of equipment specific to the activity, such as scuba gear or helmets. Two of the most important planning factors are personal limitations and required preparation. It is important to establish criteria under which the activity can be undertaken safely. The level of detail is based on the risks. For events with high risk or multiple risks, these criteria need to be detailed. There are many factors that figure into a “go” or “no-go” decision plan. Some factors, such as weather, local conditions, physical conditioning for the activity, sleep, and wellness, may apply to all activities, but others may be activity specific, such as water conditions for rafting and kayaking. Once the criteria are established, the most important thing is to adhere to them. Injuries often occur when the desire to perform an activity causes someone to participate in a situation that is either unsafe or exceeds personal abilities. At a minimum, one must address the following: • Predetermined “go” or “no-go” criteria, which may include the following: • Weather and environmental conditions at the activity site • Personal criteria such as sleep, preparation time, preexisting illness, departure time and window • Required participants • Equipment • Comprehensive equipment checklist • Timeline • Alternative plans • Communication methods, including emergency communi­ cations • Emergency procedures, including the following: • Medical emergencies • Unexpected weather or local conditions • Equipment failure Preparation After planning, the next step in a good injury prevention approach is to prepare for the activity so as to minimize risk and put into place factors that are targeted at the human, agent, and environmental issues that can lead to injury. Preparation activities can be grouped into human factors (physical and mental preparation) and material factors, such as equipment preparation. Physical Preparation.  Physical preparation includes maintaining excellent fitness and health in anticipation of the activity and the added stresses over daily activities. This may include conditioning, medical evaluation for physical abilities and health to undertake the activity, better medication adjustment for persons with chronic illness, and/or disability-specific planning for those with disabilities. In addition to general physical preparation there are unique considerations for physical preparation related to the genitourinary tract (see Injury Prevention for the Genitourinary Tract, later). Mental Preparation.  Mental preparation emphasizes thinking through the plan, ensuring that one is well rested, focusing on the activity, and being confident about the activity. Mental preparation also includes proper education and training. This should include training specific to the activity and emergency medical training. Discuss and agree on a travel route. Select a leader, and review each member’s capabilities and what equipment and supplies are necessary. Equipment Preparation.  Material preparation involves acquiring proper equipment (both routine and for emergencies and unplanned events), testing and organizing equipment, and having backup equipment. Carry sufficient equipment to survive for extended periods if unforeseen changes occur and under the worst possible environmental conditions for the season. This includes ensuring that preventive maintenance has been performed for equipment and that equipment is in good working condition. Review each person’s responsibility for equipment. Make sure that equipment and weight are properly distributed, taking into 338

account abilities. Equipment should be appropriate for the activity and the environment (e.g., waterproof, ruggedized). Selecting battery-powered items that require the same size and type of batteries minimizes items to be carried. Maintain an equipment checklist. If using specialized equipment, know its proper use and maintenance. Courses are available through retail outlets, clubs, and wilderness organizations to prepare and train participants for most outdoor activities. The minimum equipment list should include, but is not limited to the following: • Emergency equipment • Emergency blankets • Emergency bag • First-aid kit • Flashlight • Maps, compass, navigation equipment • Communication and emergency communication equipment • Footwear • Skin and eye protection • Backpack • Water, extra food • Extra clothing • Timepiece • Survival/unplanned conditions equipment may include the following: • Fire starter, matches • Shelter (e.g., emergency tube tent) • Survival whistle • Water • Water disinfection system • Avalanche beacon • Personal locator beacon, rescue laser, ground insulation Problem Anticipation Even with good planning and preparation, problems occur. For most activities and trips, major problems can be anticipated. A good exercise before undertaking any activity (and during the activity at various times) is to think through the five most likely problems and the two rare but significant problems, to both plan and prepare for them. Standard problem anticipation approaches include bringing adequate protection from environmental and recreational hazards, having all the appropriate immunizations, safe drinking and food hygiene practices, and ensuring that everyone has a working knowledge of first aid. Physical Disabilities (see Chapter 102) For persons with disabilities, it may be a great challenge to access wilderness. In federally designated wilderness areas, Congress reaffirms in the Americans with Disabilities Act that nothing in the Wilderness Act prohibits use of a wheelchair in the wilderness by a person whose disability requires its use. There are 54 million persons with disabilities in the United States, and this number is expected to grow. The challenge for the future will be ensuring that persons with disabilities have the same opportunity to participate in wilderness activities and programs as do persons without disabilities, without necessarily making wilderness access easier.153 The principles of injury prevention apply to people with disabilities who participate in wilderness activities. Their preparation, planning, and anticipation of problems must take into account the specific disability and unique physical and mental challenges of that disability.

Individual Factors and Injury Prevention SPECIFIC TOOLS FOR PLANNING AND PREPARATION IN THE WILDERNESS Maps and Orienteering People should have the ability to tell where they are and where they are going. A single wrong turn can have disastrous consequences. Maps are useful tools for planning, and the Global Positioning System (GPS) gives an accurate determination of actual location. Traditional two-dimensional maps, such as road maps, identify a sampling of features on the ground, with symbols

Global Positioning System Devices The GPS is a U.S. space-based global navigation satellite system that provides continuous positioning, navigation, and timing services to users from anywhere on Earth. Use of a GPS device requires an unobstructed view of four or more GPS satellites, each of which broadcasts signals that GPS receivers use to provide absolute locations in three dimensions (latitude, longitude, and altitude), velocity of movement and orientation, and precise time. GPS receivers have become commonplace for navigation on ground, air, and water. Modern GPS receivers often overlap graphic displays of terrain or nautical features to further assist navigation. A GPS unit can assist SAR organizations with recovery of lost or stranded travelers. Because line of sight is required for GPS receivers to function, their use may be limited in dense forests or jungles or below steep cliffs or rock overhangs. In addition, they are sensitive to extremes of temperature, moisture or humidity, and mishandling. They depend on battery power, so users should carry spare batteries. They should not be used as total replacement for traditional maps or compasses for navigation and positioning or use of natural references, such as sun position, wind, or topography. Communication Devices Traditionally, emergency communications from wilderness settings have been limited to signaling with devices such as a mirror or other reflector, whistle, fire, smoke, or flare (Figure 16-2). Newer laser devices encased in waterproof housings have been found to be very effective in identifying people during aerial searches, particularly at night. Commercially available “rescue laser flares” are small, lightweight, and rugged handheld laser devices that project a wide line, rather than the pinpoint light normally associated with a laser. They allow the user to sweep across an area with a dispersed red or green light beam that can be seen from up to 30 miles away (3 miles in daylight). The device is powered by lithium batteries that when used continuously will last for up to 72 hours, depending on the model.111 The international distress signal (SOS), which can be used with many signaling devices, consists of three short signals, followed by three long signals, and then three short signals, repeated at

intervals. Signals may communicate the general location of an injured person, but to provide more detailed information about injuries or illness, some form of vocal or written communication is needed. Vocal communication allows rescuers to obtain an accurate, on-site victim report with descriptions of injuries, mechanism of injury and the specific location of the victim. Ongoing communications with a reporting party can help guide rescuers to the victim and allow them to provide advice about first aid before their arrival. Cell phone technology is useful only when travel is within an area with cell phone relay stations, making its use limited in the wilderness. Wireless access for cell phone use is becoming more common inside U.S. national parks but is limited to the more populated areas where the park service often provides audio tours. Signals may be weak or unreliable. Cell phones in national parks are controversial: Conservationists argue that parks run the risk of becoming too civilized. Critics argue that the presence of cell phone towers in wilderness areas and national parks creates a false sense of security. Despite the controversies, cell phones are being used increasingly within national parks to notify authorities of mountaineering and recreational accidents. If a cell phone is used within a park, it is best to program in the direct number for park dispatch, because dialing 9-1-1 will often reach a county sheriff, who must then relay the call. Once dispatch is reached, state your location and call-back number early in the conversation in case of connection failure. A member of a party may need to hike to the nearest trailhead to obtain cell phone service. Completion of a standard incident report form before leaving the scene will allow the caller to provide critical information about the nature of the incident, location, and initial care provided. Cell phones with GPS (E911) technology can be useful for providing the location of an injured person. As a result of a mountaineering accident with three fatalities on Mt Hood in 2007, the Oregon state legislature proposed bills that mandate electronic signaling devices (personal locator beacons, mountain locator beacon, GPS receiver with cell phone/two-way radio) for all climbs above 3048 m (10,000 feet) on Mt Hood. Although local rescue personnel and climbers are reported to encourage the use of such equipment, they do not believe its use should be required.127 One survey of climbers found that 14% of them always carry a cell phone. Twenty-one percent of climbers who reported carrying a cell phone indicated that they had used it to report an accident.8 If a cell phone or GPS unit is carried into the wilderness, consider using a waterproof box or case to prevent damage from crushing, dropping, or water, along with a backup battery. In most cases, portable radios serve as a good choice for communication between party members. When carrying a portable radio, determine which frequencies are allowed for personal use and which frequencies are monitored in your area. Radiofrequency interference from transmitting cell phones (code division multiple access [CDMA]) or two-way radios can cause interference with some avalanche beacons. Playing an iPod at close range has also been found to cause radio frequency interference in all beacons.38 A common intermediate (processing) frequency for cell phones or digital cameras is 455 kHz, which is very close to the 457 kHz radio frequency of avalanche beacons. In addition, false signals may be produced in some beacons from cell phones cycling their transmission to “handshake” with their cell. To ensure there is no radio frequency interference, electronic equipment, including cell phones and digital cameras, should be turned off while doing an avalanche transceiver search with any brand of digital or analog transceiver.149 Satellite phones connect with orbiting satellites and have the potential to be used worldwide. The size and weight of early “sat phones” once limited their use in the wilderness, but current versions are as small as a “smartphone” or mobile PDA (Figure 16-3, online). The cost of newer satellite phones can top $1000, prohibiting their use by many wilderness adventurers. In addition, most satellite phones will only work with a corresponding network and cannot be used if the network is switched. Depending on the type of satellite phone service used, there may be a delay in transmission of voice or data. Geostationary satellite phone systems depend on line of sight for service. 339

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to represent physical objects. Topographic maps, also known as “topo” maps or contour maps, use contour lines or shaded relief to represent the shape of land surface. Contour lines connect contiguous points at the same altitude. Topo maps usually depict significant bodies of water, forest cover, or other features and are prepared using interpretation of aerial photography or remote sensing techniques. The U.S. Geological Survey (USGS) produces several series of national topographic maps, the largest and best known of which is the 7.5 minute, 1:24,000 scale, quadrangle nonmetric scale map, each of which covers an area of 0.125° latitude by 0.125° longitude spaced 7.5 minutes apart (an area of about 49 to 64 square miles). The 7.5 minute series of maps has been abandoned recently in favor of The National Map, a collaborative effort of the USGS and federal, state, and local agencies to improve topographic information in the United States and contributing to the development of a new generation of digital topographic maps.141 An accurate graphic information system (GIS), such as a digital elevation (terrain) model, allows wilderness explorers to extract and analyze additional information via three-dimensional digital representation of surface terrain or topography. An offshoot of GIS is location-based services, which allows GPS-enabled mobile devices (such as cell phones, personal digital assistants [PDAs] and laptop computers) to display their location in relation to fixed or mobile assets (such as a gas station or police car) or to relay their position back to a central server for display or other processing. This is a potentially useful future application in national parks. GIS has led to the explosion of Internet mapping services, such as Google Maps and MapQuest, which allow users access to aerial satellite imagery useful in the planning and preparation stage of wilderness travel. Whether a two-dimensional planimetric, topographic, or graphic display map is used for wilderness travel, it is essential that the user carry the map and know how to use it. In addition, ingress points, checkpoints, and egress points should be established before traveling.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

D

E

FIGURE 16-2  A, Smoke signal. B, Handheld flare. C, Marking location with flare. D, Rocket flare. E, The Rescue Laser Flare Magnum. (A to D courtesy Eunice Singletary; E copyright Greatland Laser, Anchorage, Alaska. http://www.greatlandlaser.com.)

Low-Earth-orbit systems (60% maximum oxygen consumption [ VO heat production exceeds heats loss at a temperature of 5° C (41° F) in wet clothes with wind velocity of 5 m/sec, and body temperature is maintained. With light or no exercise, heat loss exceeds heat production, and core temperature declines. Exercise in rain leads to rapid declines in core temperature.22,106,109 Wind reduces the insulating value of clothing. Wind-blocking outerwear can counter much of this effect (Figure 16-15, online).

A

WATER

B FIGURE 16-14  A and B, Plan to carry enough water and electrolytecontaining fluids to hydrate adequately in warm weather. (A courtesy Haley Buffman; B courtesy Eunice Singletary.)

Windchill is the apparent temperature felt on exposed skin and depends on wind speed and air temperature. The “windchill factor” is always lower than the ambient temperature; when apparent temperature (what it feels like) exceeds ambient temperature, a heat index is used. Windchill tables have been available through the National Weather Service since the 1970s, with the most recent revised index published in 2001. The index applies to temperatures of 10° C (50° F) or below and wind speeds above 3.0 mph, calculates wind speed at 5 feet (typical height of a human face), and assumes no impact from the sun. Figure 16-16 shows a windchill chart from the National Weather Service.99 Windchill is useful for planning wilderness travel in order to anticipate appropriate clothing and insulation. Wind

Between 2003 and 2006, there were 12,337 reported SAR operations in NPS units, involving 15,537 park visitors. The combined lake, ocean, and river environments accounted for 35% of the total SAR environments—nearly double the number within mountain environments. Motorized boating, swimming, and nonmotorized boating (e.g., canoeing, kayaking, rafting) were three of the top six activities reported by visitors at the time SAR operations were initiated.60 An evaluation of visitor fatalities at all NPS units between 2003 and 2004 found that of 356 fatalities, 16% involved boating incidents or swimming. More than one-half of the swimming fatalities involved rip currents, river currents, and large waves, whereas one-half of boating fatalities involved boats capsizing (Figure 16-18). The most significant risks associated with water immersion or recreational activities on the water are drowning, hypothermia, and trauma from striking an object. Hypothermia is a significant risk from immersion, considering that convective heat loss in water is 25 times greater than that in air, and heat loss by conduction increases as thermal gradients increase in cold water.51 The greater the surface area of a body that is immersed, the greater the heat exchange area and the faster the decline in core temperature.81 Endurance athletes and swimmers are not immune to core temperature drop but can often partially compensate by adapting through cold-water training and by use of wetsuits. When people fall from a boat, kayak, or raft, they usually do not have the advantage of prior cold-water training or a wetsuit. A recent review of U.S. Coast Guard annual boating statistics reports for 1997 to 2006 found that although canoeists and kayakers accounted for 13% of total reported recreational boating deaths, they accounted for 29% of deaths due to hypothermia and 17% of deaths due to drowning (Figure 16-19). In the canoeist/kayaker group, failure to wear a personal flotation device was the primary factor in accidental drowning, and capsizing precipitated two-thirds of injuries or fatalities.103 A

FIGURE 16-16  Windchill chart. (From National Weather Service: NWS windchill chart, 2001. http://www.weather. gov/os/windchill/index.shtml.)

Wind (mph)

Calm 5 10 15 20 25 30 35 40 45 50 55 60

40 36 34 32 30 29 28 28 27 26 26 25 25

35 31 27 25 24 23 22 21 20 19 19 18 17

30 25 21 19 17 16 15 14 13 12 12 11 10

25 19 15 13 11 9 8 7 6 5 4 4 3

20 13 9 6 4 3 1 0 -1 -2 -3 -3 -4

15 7 3 0 -2 -4 -5 -7 -8 -9 -10 -11 -11

Frostbite Times

Temperature (° F) 10 5 0 -5 -10 1 -5 -11 -16 -22 -4 -10 -16 -22 -28 -7 -13 -19 -26 -32 -9 -15 -22 -29 -35 -11 -17 -24 -31 -37 -12 -19 -26 -33 -39 -14 -21 -27 -34 -41 -15 -22 -29 -36 -43 -16 -23 -30 -37 -44 -17 -24 -31 -38 -45 -18 -25 -32 -39 -46 -19 -26 -33 -40 -48 30 minutes

-15 -28 -35 -39 -42 -44 -46 -48 -50 -51 -52 -54 -55

10 minutes

-20 -34 -41 -45 -48 -51 -53 -55 -57 -58 -60 -61 -62

-25 -40 -47 -51 -55 -58 -60 -62 -64 -65 -67 -68 -69

-30 -46 -53 -58 -61 -64 -67 -69 -71 -72 -74 -75 -76

-35 -52 -59 -64 -68 -71 -73 -76 -78 -79 -81 -82 -84

-40 -57 -66 -71 -74 -78 -80 -82 -84 -86 -88 -89 -91

-45 -63 -72 -77 -81 -84 -87 -89 -91 -93 -95 -97 -98

5 minutes

Wind chill (° F) = 35.74 + 0.6215T – 35.75(V0.16) + 0.4275T(V0.16) Where, T=Air temperature (° F) V=Wind speed (mph)

Effective 11/01/01

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speeds do not reflect man-made wind. For instance, a snowmobiler traveling 35 mph on a calm day will be exposed to wind speed of 35 mph across his or her body. In addition, wet skin exposed to wind chills faster than does dry skin. If wet skin is exposed to wind, the ambient temperature used in the windchill chart should be 10° C (18° F) lower than measured actual ambient temperature.17 When windchill temperature falls below −27° C (−17° F), frostbite can occur in 30 minutes of less. Travelers in mountain terrain should presume that wind speed would likely increase as altitude increases and natural barriers to wind (trees) become more sparse. Wind-blown snow is a potential travel hazard. Reduced visibility from blowing snow can cause a person to become disoriented, lost, and even to fall off rocky precipices or into a crevasse (Figure 16-17). Wind makes securing of shelters significantly more difficult and can turn natural and man-made objects into trauma-inflicting missiles.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Figure 16-20). If a fall is into swift water, contact with rocks or downed trees (streamers) increases the chance of additional trauma or becoming trapped underwater and drowning (Figures 16-21 and 16-22). Prevention of drowning from falls off boats or rafts begins with use of a personal flotation device. A water-activated light is useful for locating a person in a nighttime rescue. In swift-water boating activities, most wilderness excursion companies and leaders require a helmet to be worn (Figure 16-23, online). If

A

B A

C FIGURE 16-17  A, Wind from blowing snow can reduce visibility and cause climbers or hikers to become lost or fall off rocky precipices. B and C, Wind can make posing for pictures on cliff edges especially precarious. (A courtesy Haley Buffman; B and C courtesy Eunice Singletary.)

B

C FIGURE 16-18  Large waves and river currents are commonly involved in water-related fatalities. (Courtesy Haley Buffman.)

348

FIGURE 16-19  A, B, and C, Canoeists and kayakers account for 13% of the total reported recreational boating deaths in the United States. (Courtesy Haley Buffman.)

FIGURE 16-20  A fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Courtesy Eric Becker.)

people fall into swift water, they are instructed to position themselves so that they travel downstream feetfirst, which allows them to avoid hitting their head on rocks and to see and avoid objects in the water (Figure 16-24, online). Alcohol ingestion is associated with a higher relative risk for death while boating, even with lower levels of blood alcohol. The risk is the same for passengers as for operators.25,39,130 One of the greatest preventive measures for both operators and passengers engaged in watercraft activities is to abstain from drinking.

SNOW To a wilderness enthusiast, nothing can be more delightful than fresh snow, and yet nothing can be potentially more dangerous. Snow becomes a hazard when it slides (avalanches), when it accumulates in heavy snowstorms to such great depths that a person can asphyxiate following a fall, and when a wilderness adventurer becomes wet, cold, or unable to see due to blowing snow. Non–avalanche-related snow immersion death was described by Cadman20 in 1999. Asphyxiation associated with snow immersion occurs when skiers or snowboarders fall upside down into a snow bank or into a tree well around a conifer. It has been

proposed that snowboarders are at higher risk than are skiers from asphyxiation because of the lack of releasable bindings on snowboards. Preventing injury or death from non–avalanche snow immersion begins with basic precautions. Always ski or ride with a partner; in very deep snow following a snowstorm, always ski or ride a slope within eyesight or voice contact of your partner; ski or ride one at a time on slopes using a spotter; and avoid tree wells on glady slopes.142 In case of accidental submersion, attempt to release bindings; if a ski pole is available, it may be the only means of releasing a binding short of twisting out. Several products designed for surviving avalanche burials are potentially useful to backcountry and sidecountry recreationalists to improve chances of surviving snow immersion. The AvaLung (see above) and the Snow Snorkel may increase survival time under snow by diverting expired air away from the face.150 Inflatable air bag type of devices marketed for improving survival in avalanches (e.g., Snow Pulse) may help prevent snow immersion asphyxiation by allowing a skier or snowboarder to remain in a “head-on-top” position following a fall in deep snow.

HYDRATION If fluid intake is less than fluid loss, dehydration may result. Many individuals do not drink an adequate amount of fluids in the wilderness. In a cold environment, this is because when skin temperatures fall significantly, thirst is less noticeable compared with during hot weather.73 In cold temperatures, moderate fluid loss may not be as important for exercise performance as during hot weather.27 If cold-weather clothing maintains skin and core temperature to what would be expected during exercise in a temperate or hot environment, then dehydration will likely

A

B

C

FIGURE 16-22  A, B, and C, Removal of logs and branches from rivers can lessen the risk for injury or death after falling from a raft or kayak. (Courtesy Haley Buffman.)

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CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

FIGURE 16-21  Downed trees or branches (streamers) increase the chance of additional trauma or becoming trapped underwater and drowning. (Courtesy Haley Buffman.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

negatively impact performance.49 Individuals with hypohydration or hyperhydration who are exposed to intermittent exercise with normobaric hypoxia demonstrate greater physiologic-strain hypoxemia and acute mountain sickness (AMS) symptoms than do individuals with euhydration.110 Hydration status can be monitored in the wilderness by observing the color (and thus concentration), volume, and frequency of urine output. Oral fluids containing sodium have been shown to aid in fluid retention over several days of cold exposure, as well as in wildland firefighters in heat-stress conditions.32,115 During wilderness excursions, a source of water needs to be readily available and easily reached to permit frequent, ad libitum fluid intake. Severe exercise-associated hyponatremia (EAH) from overzealous hydration is a well-described problem in endurance sports participants, particularly women, individuals with low body weight, and those taking nonsteroidal antiinflammatory drugs (NSAIDs).50,65,66,101 In general, EAH is not frequently encountered in the wilderness setting, although there are reports of EAH in hikers, trekkers, climbers, cold weather endurance athletes, and long-distance cyclists.* Symptoms reflect noncardiogenic pulmonary edema and cerebral edema and include nausea, vomiting, and headache followed by neurologic symptoms such as confusion, disorientation, seizures, or coma. A recommended preventive measure to be considered, especially by those at risk (women, low body weight, planned prolonged exercise duration, extremes of heat), is to refrain from using NSAIDs while participating in sustained physical activity in the wilderness setting. In addition, moderate fluid intake is recommended based on the perceived need (ad libitum) rather than a specific amount. Any fluid intake during prolonged exercise that exceeds combined urine and sweat output (800 to 1000 mL/hr) should be considered high risk for development of EAH.114 Wilderness excursion leaders need to educate and advise their group members on appropriate fluid intake and be able to recognize early symptoms of EAH. There are many marketed hydration systems. These systems use bags (“bladders” or reservoirs) to hold water or other liquid inside an insulated carrier or are integrated into a backpack. Water is sucked through a bite valve from a dispensing tube extending from the reservoir up over the shoulder or through the inside of an insulated shoulder strap. “Wearable” hydration includes garments, such as cycling jerseys, that contain concealed reservoirs. Some hydration system manufacturers use antimicrobial compounds in the reservoir and bag to inhibit bacterial growth. Hydration systems are more difficult to clean than are water bottles but have the advantage of allowing a person to easily carry large amounts of liquids needed for maintaining hydration during prolonged physical activity.

ALTITUDE Wilderness adventurers most commonly encounter changes in altitude during travel through mountainous terrain. As travelers ascend to higher altitude, barometric pressure decreases. Although the fraction of oxygen in the atmosphere remains constant, the partial pressure of oxygen decreases with ascent. Hypoxia is the physiologic insult that is responsible for altitude illness. The altitude where symptoms of altitude illness occur varies between persons. One study of tourists in Colorado found that 71% experienced symptoms of altitude illness following arrival at altitudes of 2103 to 2957 m (6900 to 9700 feet), which represents the elevation of many ski areas.67 There is no absolute elevation where altitude illness can be predicted; rather, it is influenced by the rate of ascent, the altitude reached and where sleep occurs, duration of exposure to altitude, and level of physical activity. Individuals with a prior history of altitude illness are prone to future altitude illness,143 and adolescent girls have a higher incidence than do boys.34 Prevention begins with education. Only just over one-half of respondents on a survey at a major U.S. ski area were aware of the existence of AMS, and one-third were unaware that it could *References 9, 14, 77, 119, 134, 151.

350

be prevented. One-half the respondents preferred to receive information about AMS from the Internet. This suggests that the Internet may be an effective means of educating the public about AMS symptoms and means of prevention.57 Because slow, gradual ascent allows time for acclimatization to altitude, this is the primary means of prevention, particularly when ascending to high or extremely high altitude. If symptoms develop during ascent, additional time is needed for acclimatization before resuming ascent. If symptoms do not abate, then descent to an altitude 305 to 914 m (1000 to 3000 feet) lower, particularly for sleep, may be needed. The use of acetazolamide 125 to 250 mg twice daily beginning 1 day before travel and continuing for several days at altitude has been shown to prevent symptoms of AMS.1,28,42 While at high altitude, a dose of 250 mg every 8 hours has been shown to dramatically reduce symptoms.46 Dexamethasone has also been found to prevent symptoms of AMS.41,113 Risk factors and susceptibility for high-altitude pulmonary edema (HAPE) are similar to AMS and include a prior history of HAPE, rapid ascent, and higher altitudes. Additional risk factors include male gender, intense exercise, cold ambient temperatures, and preexisting respiratory tract infection.40,68,132 Preexisting primary pulmonary hypertension and intracardiac shunt, such as ventricular or atrial septal defect, or patent foramen ovale, may predispose to HAPE.3,74,148 As for AMS, primary prevention of HAPE is by gradual ascent. Ascent rate should be limited to no more than 300 to 350 m (984 to 1148 feet) per day above 2500 m (8202 feet) (sleeping altitude) with an additional day of acclimatization added for every 600 to 1200 m (1969 to 3937 feet) above 2500 m (8202 feet).11 Pharmacologic prophylaxis aimed at preventing altitude-induced pulmonary hypertension is most commonly achieved with the calcium channel blocker nifedipine, 30 mg extended release daily or twice daily.12 Sildenafil and tadalafil, both phosphodiesterase-5 inhibitors and pulmonary vasodilators, have been evaluated for prophylaxis and treatment of HAPE but have the potential side effect of causing significant headache. When taken beginning a day before ascent, dexamethasone reduced the incidence of HAPE by 78% and was superior to tadalafil in its efficacy. However, side effects may limit its use as a prophylactic agent.13,86 For individuals who are prone to development of HAPE, the β-agonist salmeterol 125 mcg inhaled twice a day has been found to reduce the incidence of HAPE by 50%. Side effects, notably tachycardia, are similar to those of other β-agonists. Studies do not conclusively support the use of acetazolamide for prevention of HAPE.85 Because of its safety profile and lack of serious side effects other than reflex tachycardia, nifedipine remains the prophylactic drug of choice for individuals with a prior history of HAPE.133 High-altitude cerebral edema (HACE) is the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status change and ataxia in a person without AMS.136 Symptoms typically occur at night, and after several days at altitude; many persons with HACE also have HAPE or AMS. Without rapid treatment, HACE progresses to coma, and death occurs by herniation. There are no studies showing a benefit to prophylactic treatment. However, slow ascent and prophylaxis against AMS are likely beneficial.

BITES AND STINGS The incidence of wilderness-acquired bites and stings and their fatalities is difficult to ascertain, especially because many injuries go unreported, but there is likely a resemblance to statistics maintained by the American Association of Poison Control Centers (AAPCC). Between 2001 and 2005, an annual average of over 92,000 bites or stings were reported to the AAPCC. Over three-quarters (76%) were due to insects and spiders, 7.2% were from snakes, 6.9% from mammals, and 3% from aquatic animals (Figure 16-25, online). Twenty-seven fatalities were reported for the period, with 16 from snakebites.80 A study of long-distance hikers in Vermont found 6.6% of reported injuries in 155 hikers were due to insect bites. Heggie58 found that 7% of wilderness injuries in children under 18 years and 1% of injuries in adults in Mt Rainier and Olympic National Park in Washington were due to insect stings. Just over 2% of injuries reported by NOLS over a 4-year period were due to stings.82

FIGURE 16-26  Stings from hymenoptera commonly cause pain and local allergic reactions. (Courtesy Eunice Singletary.)

A

B FIGURE 16-27  A and B, Bells are frequently worn by hikers to produce noise and avoid startling a bear. Grizzly (A) and black bear (B). (Courtesy Eunice Singletary.)

hospitalization. The vast overall majority (69%) were due to rattlesnakes.102 Preventing snakebites begins with being aware of the presence of snakes and their typical habitats. Snakes tend to hide under debris, rocks, and other objects in the outdoors, so caution is urged when lifting up fallen wood or logs. It is important to not step on or near snakes. Use a flashlight to check for snakes in dark holes, and be aware that snakes can swim. If a snake is spotted, back away from it slowly and do not attempt to capture it. One study found that up to 67% of snakebites were the result of intentional interaction, and up to 40% of snakebite victims had consumed alcohol before the bite occurred.96 Snakes have a strike zone of one-third to one-half of body length. Since snakebites are typically to the lower leg, outfitters recommend specialized snake boots. Hiking boots and several layers of pants legs also help divert bites from many snakes. Keep tents zipped closed, and check inside sleeping bags and clothing before using. Mammalian attacks in the wilderness are unusual and typically provoked. Attacks by bears are a common preoccupation of hikers and campers, although the actual incidence of attacks is believed to be very low. Herrero63 found 77 people with reported injury from 66 incidents involving grizzly bears in North American national parks between 1900 and 1970, most involving bear sows with cubs. Attacks were frequently provoked either intentionally or unintentionally (i.e., surprising/startling a bear in its habitat); only 5 fatalities were reported. Attacks by black bear sows are much less common than those by brown bears (Figure 16-27). Hikers often wear bells to create noise while hiking to prevent inadvertently startling a bear and provoking an attack. Avoiding high-risk areas, such as where carrion or bear scat is located, is a way to avoid an encounter with a bear. It is recommended to keep food out of tents and in bear-proof containers and to burn garbage at least 300 feet downwind of a campsite. In the case of an encounter with a brown bear, it is best to avoid eye contact, to avoid running or turning away, and to assume a submissive posture (“play dead”) until the bear has left the area.53 Predatory encounters by a black bear should be dealt with by standing still, by attempting to intimidate and appear larger by raising one’s arms above the head, or by fighting back with any available 351

CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

Permethrin is a repellent that helps prevent bites from many crawling and blood-sucking insects. Some permethrin clothing formulations reportedly last up to 6 weeks, even with weekly laundering.124 In the United States, ticks transmit more diseases than do any other insects. When traveling in tick-infested country, wear long pants, bloused at the ankles and tucked into shoes or boots, and a long-sleeved, buttoned or pullover shirt tucked into pants and, if possible, covered with a jacket. Use of 0.5% permethrin spray on shoes and outer clothing is a barrier to ticks. Careful daily inspection of clothing and skin and removal of crawling insects while in tick-infested areas is recommended. Other precautions include avoiding sleeping on a cabin floor, not sleeping in a bed that touches the wall, and changing and laundering all bed linens before use if a cabin has been unoccupied.10 In general, mosquitos in North America cause little problem beyond minor itching and skin irritation. However, certain mosquitos transmit forms of encephalitis. Since 1999, West Nile virus has spread throughout the United States, infecting thousands and killing hundreds of people. Use of long pants and sleeves is a measure for preventing mosquito bites. Mosquito netting is effective for sleeping areas and is used on hats to protect the face and neck. N,N-diethyl-3-methylbenzamide (DEET) is an insect repellent used to reduce mosquito bites, including the species responsible for transmission of West Nile virus in the United States. The higher the percentage of DEET in a repellent, the longer and better the insect-repelling effect. Concentrations of at least 23.8% are highly effective in reducing mosquito bites for up to 5 hours.48 Newer formulations allow a lower percentage of DEET to be as effective as a higher-percentage formulation by mixing DEET in a controlled-release lotion vehicle that can last up to 20 hours. DEET can be absorbed through skin and should not be used on children under 2 years of age. Flies, gnats, and no-see-ums are not repelled as effectively as are other insects by DEET. When traveling in areas with these bothersome insects (coastal regions, southwestern United States), use a repellant containing di-Npropyl isocinchomeronate, or R-326. Some insect repellants are combined with sunscreens, but this may decrease the effectiveness of the repellant and/or the sunscreen. Certain spider bites cause significant morbidity. Prevention includes awareness of habitat; inspection of clothing, shoes, and sleeping bags; and shaking out items before use. Stings from hymenoptera cause local and allergic reactions (Figure 16-26). Limiting exposure to these insects is not easily accomplished. Wilderness travelers with known allergy to hymenoptera may prevent serious reactions to stings by prior desensitization therapy and should carry injectable epinephrine, oral antihistamines, and a corticosteroid. Avoiding brightly colored clothing, perfume or fruity scents, and walking barefoot in areas where stinging insects may be present are maneuvers to help prevent hymenoptera stings. Between 2001 and 2004, an estimated 9873 snakebites were treated each year in emergency departments in the United States, with nearly one-third due to venomous species, 18.7% while the patient was outdoors hiking or camping, and over 25% requiring

PART 4  INJURIES AND MEDICAL INTERVENTIONS

weapon or object.45 Pepper spray (5% to 10% capsicum oleoresin) may be an effective deterrent in the event of a charge by a bear.64 For some predatory species, such as mountain lions and wolves, it may be best to display aggressive behavior or fight back in the event of an attack.15,94 Other mammals that may inflict injuries or fatalities in the wild include bison, cougars, bats, deer and elk, coyotes, wolves, moose, porcupines, foxes, raccoons, skunks, and rodents (Figure 16-28). Human attacks by foxes are usually by rabid animals. One general method of preventing attacks by wild animals includes never approaching or attempting to capture or restrain an animal.

TOXIC EXPOSURES Exposure to inhaled toxins may stem from natural or man-made sources. The most common man-made exposures are most likely smoke from campfires. Fatalities are reported not infrequently from carbon monoxide (CO) inhalation due to accumulation inside of poorly ventilated tents after using camp stoves. Injury or death is preventable by being aware of the symptoms of CO poisoning, by ventilating tents, cleaning ice or snow off tent fabric, using maximum blue flames and avoiding low flames, and avoiding prolonged simmering.84 Wilderness travelers at altitude need to be especially alert to the symptoms of possible CO poisoning, because symptoms may be similar to those of altitude illness, although no relation has been found between increased CO exposure and AMS symptoms.117,118 Climbers on descent were found to have higher carboxyhemoglobin levels and an increased risk for CO exposure with increased hours of stove operation. Volcanoes are another source of possible toxic inhalation injury in wilderness adventurers. Volcanic laze is a dense plume of concentrated hydrochloric acid and seawater mist that forms when hot lava enters the ocean waters. It has been identified as the cause of two fatalities in Hawaii and is a risk for wilderness adventurers seeking close views of active volcanos.61 Volcanoes

A

release a number of potentially toxic gases, including sulfur dioxide, hydrogen fluoride, and carbon dioxide. Injury prevention includes avoiding standing under or downwind of a laze plume, avoiding depressions where carbon dioxide may settle, avoiding proximity to volcanic fumaroles, and avoiding exposure to volcanic ash.21 Poison ivy, oak, and sumac are common sources of allergic plant contact dermatitis caused by exposure to urushiol found throughout the plant (Figure 16-29, online). Exposure may be the result of direct contact, from inhalation of smoke particles from burning plants, and from contact with contaminated clothing, shoes, or gear. A skin protectant containing 5% bentoquatam (quaternium-18 bentonite) in a lotion form has been found to be effective at preventing allergic contact dermatitis from poison oak.89 When combined with skin cleansing using isopropyl and cetyl alcohol wipes and education to recognize offending plants, it may be especially effective at preventing contact dermatitis from Toxicodendron species.126 Prevention of adverse reactions from plants begins with being aware of potentially toxic plants that may be encountered in the area of planned travel, and being able to identify and avoid them. Wearing long-sleeved shirts and pants will help decrease exposure, but contamination is still possible from clothing. If contact with a potentially toxic plant is suspected, the area of contact should be washed thoroughly with water and mild soap and sun exposure to the area avoided. The opportunity to ingest poisons in the wilderness is practically limitless. Mushrooms, berries, roots, fruits, leaves, and other vegetation are tempting to many hikers or campers. Prevention involves being able to definitely identify toxic plants and to not ingest them in a harmful form.

WATER, GERMS, AND HYGIENE Water in wilderness areas is used for drinking, cooking, cleaning, and recreation. When wilderness travelers are concerned about possible water contamination in an area where they plan to drink that water, they should use a viable option for water disinfection. Perhaps the most important means of preventing infectious diarrhea in the wilderness is fastidious hand hygiene and education on hygienic techniques for food handling and preparation. Proper disposal of human waste in high-traffic alpine climbing routes, and all wilderness areas, is encouraged. Exposure to a travel or climbing companion with diarrhea increases the risk for developing infectious diarrhea.93 A revised three-bowl system of washing eating utensils was recently recommended for cleaning and reducing bacterial contamination on expeditions where running water is not available. The first bowl contains detergent to remove food residue and grease. A second bowl contains 20 mL of 4% bleach and is used to wash utensils until visibly clean, and a third bowl of drinkable water is used as a rinse to remove the smell and taste of disinfectant.56

Unique Risks of Select Wilderness Activities BACKPACKING

B FIGURE 16-28  A and B, Attacks by mammals, such as coyotes and porcupines, are uncommon. (Courtesy Eunice Singletary.)

352

The two basic types of backpacks are those with external frames and those with internal frames (Figure 16-30, online). The frames are designed to transfer the weight of the backpack from the shoulders and back to the hips and legs. An ideal backpack weight distribution is 20% on the shoulders and 80% on the hips. This distribution lowers the body’s center of gravity, making the fit more stable and places weight on the location best suited to carrying the weight. Backpack size is an important consideration for injury prevention. Individuals need to be sure that all equipment necessary for the duration of the trip can be carried without putting excessive strain on the shoulders and back muscles. In addition to backpack design, the prime concern regarding stress on the back and muscles is the proper amount of weight an individual can carry. This is determined by the size, body weight, and fitness level of the person. For multiday trips, where there is repetitive stress, a good rule of thumb is to limit the contents to 25% of body weight. To minimize the chance of back injury

Backpacks With External Frames A backpack with an external frame may be preferred because it allows a larger amount of weight to be carried, using a ladderlike frame commonly made of aluminum or plastic. A hip belt and shoulder strap are attached to the frame, usually with clevis pins and split rings. A backpack that is adjustable to fit the length of the spine is best. One should optimally select a design that prevents injuries. Lumbar padding and increased stability via a conical hip belt allow for comfort. Recurved shoulder pads/straps and a chest compression strap improve weight distribution and increase comfort. Additional advantages of a backpack with an external frame are allowing air space between the back and the pack, thus reducing sweating and skin breakdown; and weight carried higher in the pack, allowing for more upright posture. However, the pack may wobble side to side during walking, potentially compromising balance. Backpacks With Internal Frames The advantages of an internal frame backpack are that if well designed and fitted, it will conform more to the body, allowing for better balance, and can be worn comfortably for longer periods of time. With this advantage comes the absence of airflow, leading to problems with back perspiration and possible skin breakdown. Because the weight is carried lower, one must bend more, which in turn alters proper posture and can predispose to low back strain. Backpack Lifting Proper lifting techniques are the key to minimize injury. The least injurious method for donning a backpack is to have someone hold and stabilize the pack while the carrier slips his or her arms into the shoulder straps. If a second person is not available, the backpacker can lift and rest the backpack on an object that is waist high and then slip into it. If a backpack must be donned from the ground, the wearer should lift the backpack onto a bent knee and slide one arm through the shoulder strap. After adjusting the strap so that the backpack rests on the shoulder, the carrier should lean forward and rotate the body slightly, allowing the free arm to slide through the other shoulder strap. While still leaning forward with bent knees, the backpacker adjusts the second strap and hip belt. Backpacks and Children There are specially designed child carriers. Be certain to use a well-structured carrier that provides appropriate support and weight distribution. A child-carrying device should be equipped with restraints that prevent an active child from climbing out. One should not use an ordinary backpack to carry small children. Risks include strangulation if a child becomes entangled in the carrier’s harness, and head and body injury if a child wiggles out of the harness and falls or is struck by an overhead obstruction, such as a tree branch.

HIKING Environmental hazards to be anticipated during hiking include those common to many wilderness activities, such as altitude illness, temperature extremes, UV exposure, plant and insect exposure, and hygiene and water effects. Negotiating trails and uneven and hazardous terrain, including snow, ice, and mud, can be challenging. Because a trail is marked or exists on a map does not mean it is safe, clear, and well maintained. Plan to check actual conditions on the day of travel. The key to a safe and injury-free trip is ensuring proper balance. Watch for unstable rocks and boulders. Keep body weight over feet, with knees bent, and do not lean backward. When crossing rivers and streams, remember that water is very powerful. Use predefined crossing points, safety ropes, or watercraft and flotation devices.

A common injury during hiking and backpacking is low back pain. The most common reason for back injuries is carrying excessive or poorly distributed loads. Using a properly designed backpack and proper lifting techniques can help avoid these injuries. A useful injury prevention adjunct is a hiking pole or staff to provide stability on rough ground and diminish impact on knees and ankles. A staff can support a good walking rhythm and prevent imbalance when carrying a heavy load. Hiking poles allow for probing and identifying hidden rocks and deep spots and can hold back bushes, barbed wire, stinging plants, and other trail obstructions. Although one pole can be helpful, it can often lead to uneven balance and weight shift. Using two poles takes the load off the legs and hips and redistributes part of the weight to the upper body musculature. On a steep area, hiking poles enable tripoding, which is having three points of contact with the ground.

HAMMOCK SAFETY Hammocks safety issues exist. The priorities are strong and secure attachments with clear knowledge by the user of the weight tolerances for the hammock and the hanging hardware. A slight modification to the traditional hammock is the lightweight minihammock, which is popular for camping and backpacking. These hammocks have no spreader bars and can be folded easily. The CPSC warns that children can become trapped and strangle in certain mini-hammocks; two deaths and one nonfatal incident have involved mini-hammocks or backpacker hammocks. If a hammock is rigged too high off the ground, a child will have difficulty climbing into it and may become trapped or entangled, leading to strangulation. To prevent injuries, install a mini-hammock near the ground.139

HUNTING More than 35,000 firearm fatalities have occurred in the United States each year since 1989, and it is estimated that there are three nonfatal firearm injuries for each death associated with a firearm.6 The key elements to injury prevention while hunting are at a minimum the following: • Proper training for hunting and use of firearms, focusing on safety • Hunters wearing appropriate protective clothing; wearing international orange clothing articles when traveling in areas frequented by hunters; and ear and eye protection • Hunting only in approved areas and at safe distances from residential or populated areas • Compliance with all local and state laws and regulations Hunter safety courses are available in every state and are a prerequisite in most states to obtaining a hunting license. Key recommendations include warning nonhunters of hunting season, limiting hunting to designated hunting areas, and wearing international orange clothing articles when traveling in areas frequented by hunters. Hunters should always be sure of their target before shooting. A safety harness should be worn when using a tree stand. Care should be taken to use appropriate techniques when cleaning game to prevent lacerations. Eye protection with impact-resistant lenses should always be worn to prevent injury from ricocheting fragments and shotgun pellets. Ammunition should always be stored separately from guns. The greatest potential serious injury from hunting is a gunshot wound, but this is actually uncommon. A 9-year retrospective review of illnesses and injuries in hunters found that trauma accounted for only 45% of emergency department visits by hunters, with the majority of injuries being knife injuries associated with the field dressing of game. The most common medical visits were for cardiac signs and symptoms, and all emergency department deaths were due to cardiac causes.108 Cardiac evaluation of big game hunters with risk factors for cardiac disease should be considered.

HORSEBACK RIDING In 2005, an estimated 73,576 people were treated in hospital emergency departments for horseback-riding injuries.47 Horsebackriding injuries most frequently occur to the upper extremity as 353

CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

and allow better stability, the goal is distribution of the weight via maximal use of the frame. To achieve this goal, 50% of the weight should be in the upper one-third of the pack. To accomplish this distribution, lighter and bulkier items should be packed in the bottom and heavier items should be packed in the top close to the frame.

riders try to break a fall. Serious horseback-riding injuries involve the spine, pelvis, internal organs, and head. The following precautions should be taken to prevent horseback-riding injuries: • All riders should always wear riding helmets that meet proper safety standards. • Wear properly fitted, sturdy leather boots with a minimal heel. • Inspect all riding equipment for damage. • Be sure the saddle and stirrups are appropriate for your size and are properly adjusted. • Secure all riding equipment properly. • Amateurs should ride on open, flat terrain or in monitored riding arenas. • Jumps and stunts require a higher level of riding skill. Do not attempt these without supervision.

CLIMBING Climbing is a wilderness activity that poses risks common to many other wilderness activities, such as hypothermia, dehydration, heat illness, altitude illness, trauma from falls, and avalanches (Figure 16-31, online). Hand injuries, including fractures, tendon ruptures, and digital amputations, are common in climbers.87,116 Use of stiffer ropes, reducing rope slack, and grabbing rope in a controlled manner during a fall have all been suggested as means for preventing digital injuries in climbers.69

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 17 

Principles of Pain Management STEPHEN D. COLEMAN AND RAYMOND R. GAETA

Pain is ubiquitous in daily life, and multiple treatment modalities are available under normal circumstances. However, the wilderness setting presents significant challenges when available treatments are limited to those that are included with medical supplies for travel into remote locations. Many travelers have medical conditions that may restrict or limit the use of certain therapies. Some travelers may suffer chronic pain and are already receiving treatment with medications or implanted devices. The treatment of pain in remote and extreme environments is guided by patient characteristics, type of injury, and available therapies. Optimal treatment reduces the chances of further injury, decreases suffering, and improves the likelihood of successful rescue. The International Association for the Study of Pain4 defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition indicates that pain is not simply sensory input from tissue damage; rather, it is a complex experience that depends in varying degrees on an emotional component. The emotional component can vary markedly among individuals and circumstances; however, these factors may significantly affect physiology and dramatically alter the impact of pain on an individual patient. For example, fear and anxiety associated with injury in remote areas can exacerbate the situation. The optimal management of pain often requires a multimodal approach. This approach includes treatment of ongoing tissue damage, which may include interventions locally and systemically, non-narcotic medications, opioid and adjuvant medications, and awareness and management of psychological factors that affect an individual’s perception of pain.

Anatomy and Physiology of Acute Nociceptive Pain The early understanding of the transmission of sensation was that pain perception followed nerves that were simple conduits to the brain. As a greater understanding of pain has developed, it is clear that nociceptive pain, which is defined as the pain of tissue injury or potential tissue injury, is initiated by nociceptor activation in the periphery and modulated at multiple levels in the nervous system, thereby allowing for multiple targets for therapy. This sequence of events is categorized into four processes: 354

1. Transduction: Chemical, thermal, or mechanical energy is converted into an electrochemical signal. 2. Transmission: The signal is conducted to the central nervous system via Aδ and C fibers. 3. Modulation: The signal is altered by both positive and negative feedback loops in the spinal cord and the brain. 4. Perception: The signal is finally appreciated as pain. The skin, the periosteum, and the joint surfaces are abundantly populated with nociceptors that are activated by potential or actual tissue damage. Thinly myelinated Aδ and unmyelinated C fibers terminate in the skin as nociceptors and transmit nociception to the spinal cord. Fast-conducting Aδ fibers respond to mechanical stimuli and transmit sharp sensations. Slow-conducting C fibers respond to chemical, thermal, and mechanical stimuli and transmit burning sensations. Acute injury of the skin results in simultaneous transmission through Aδ and C fibers. Cell bodies of the Aδ and C fibers are located in the dorsal root ganglion, and they project fibers to the posterior horn of the spinal cord. Aδ and C fibers synapse with second-order neurons in the dorsal horn of lamina I to lamina V. These second-order neurons cross to the contralateral side of the spinal cord and ascend in the anterolateral spinal tracts to the thalamic nuclei, brainstem, and midbrain, where they synapse with third-order neurons and project to the cerebral cortex. The simple stimulation of nociceptors without tissue damage may result in transmission of an action potential to the spinal cord and higher levels of the nervous system, and this may eventually result in a perception. However, if stimulation results in tissue damage, a host of changes can occur; these include the local release of many chemicals near the site of the injury as well as chemical changes at the spinal cord and higher levels of the central nervous system. Locally released chemicals may be excitatory or inhibitory. Substance P and neurokinin A are excitatory neuropeptides that are released locally during tissue damage that may facilitate nociceptive transmission. Release of calcitonin gene-related peptide and substance P results in tissue edema and erythema by increasing vascular permeability in peripheral vasculature, thereby contributing to inflammation. There are proinflammatory substances released during tissue damage, including bradykinin, which can initiate pain transmission and sensitize nociceptors. Glutamate, nerve growth factor, serotonin, and histamine also potentiate the response of nociceptors. In addition, low pH may reduce the threshold of nociceptors. There are many additional sensitizing chemicals that act locally at the site of tissue injury as well as at the spinal cord level. The opposing system includes

Pain Measurement The experience of pain is completely subjective. Various scales have been introduced that attempt to quantify the level of pain; these include numeric scales (e.g., 0 to 10, with 10 being the worst pain), categoric scales (i.e., none, mild, moderate, or severe), and even face scales (i.e., smile, neutral, or frown). The visual analog scale appears to be more objective because the patient makes a mark along a 100-mm horizontal line that can then be measured to give a pain score of 73 mm, for example. The usefulness of any scale is best determined when making repeated measures for the same patient with the use of the same scale, especially in an acute setting. A baseline value establishes a set point from which higher pain scores should be interpreted as “worse” and lower pain scores interpreted as “better.” Infrequent measures (e.g., for a patient with a chronic condition) are somewhat less reliable. Interpatient reliability is even more problematic, because different people may experience the same injury differently.

Types of Pain The nomenclature of acute pain versus chronic pain is familiar to many, and relies on time as a determining factor; however, it adds little else to the understanding and treatment of pain. Understanding the mechanisms of pain allows pain to be treated on a continuum, with recognition that unmitigated acute pain can become chronic on the basis of physiologic changes that may occur within the nervous system rather than just with the passage of time. With this approach, the rationale for preemptive strategies and aggressive acute strategies comes into clearer view. Coexistence of acute and chronic pain in the same patient is thus treated in an integrated model. With an understanding of the common mechanisms of pain disorders, a rational approach to initial therapy can be developed with the use of three general categories that are based on pathophysiology. Pain may be considered nociceptive, inflammatory, or neuropathic, or it may be a combination of two or all three types with certain forms of injury (Figure 17-1). The categories and initial therapies are as follows:

Nociceptive

CHAPTER 17  Principles of Pain Management

release of pain-inhibitory substances such as endogenous opioids, β-endorphins, acetylcholine, γ-aminobutyric acid, and somatostatin; these substances impede nociceptive transmission. Modulating nociceptive input can inhibit or facilitate the transmission of signals. In addition to local and spinal cord effects of these chemicals, transmission of action potentials to the spinal cord may be modulated by the transmission of signals by other fiber types. A landmark publication by Melzack and Wall3 described the gate control theory, which operates at the spinal cord level. The authors described input from Aβ fibers, which transmit light touch and pressure and have an inhibitory modulation effect on transmission of nociception to the spinal cord. This description of the gate control theory may explain the mechanism for modulating nociception at the spinal cord level when transcutaneous electrical nerve stimulation (TENS) is applied. At the level of the spinal cord, nociception and the autonomic nervous system are under descending inhibitory control from supraspinal levels. A familiar example of descending inhibitory control is found in our normal disregard for the sounds of our heartbeat and respirations. Normally these signals are suppressed, but they are easily called into consciousness by cortical mechanisms. Similarly, the nociceptive system is also under descending inhibition from supraspinal systems, allowing us to ignore our pain at times during stressful situations. Serotonin and norepinephrine appear to be the primary neurotransmitters that regulate descending inhibitory control; however, others (e.g., α2 agonists, cannabinoids) may be involved. Thus the perception of pain involves not simply the transmission of signals from peripheral sensors to the brain. It is in fact a complex system that is initiated by stimulating peripheral nociceptors in the presence of a milieu of local mediators that facilitate or inhibit signal transmission. As transmission of the signal moves centrally, modulating influences exert their influence before the perception of the sensation occurs.

Inflammatory

Neuropathic

FIGURE 17-1  Categories of pain.

1. Nociceptive. Acute pain that is initiated by tissue injury in the form of a laceration, fractured bone, or crush injury is a type of nociceptive pain. It is a consequence of activating specific nociceptors within the skin, muscle, periosteum, joints, and probably the viscera. These receptors are likely the distal terminals of Aδ and C fibers; they may respond to specific stimuli, including chemical, thermal, and mechanical insults, or they may respond to more than one of these stimuli, in which case they are called polymodal receptors. Polymodal receptors represent the majority of nociceptors. The primary medications directed toward treating nociceptive pain are opioids. Opioids have their primary effects on the opioid receptors µ, δ, and κ. Their analgesic effect is produced in the periphery, at the dorsal horn of the spinal cord, and at supraspinal sites. 2. Inflammatory. Inflammatory pain is mediated by elaborating prostaglandins via the cyclooxygenase pathway. Sensitization of peripheral nociceptors is also mediated via this mechanism, which leads to hyperalgesia around the wound. Nociceptive pain and inflammatory pain generally coexist, because the pain stimulus provokes them both. Immunemediated inflammation with or without tissue injury also falls into this category. Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids are particularly effective for treating inflammation as well as mild to moderate pain. Peripherally decreased production of prostaglandins, including prostaglandin E2 (PGE-2), is the likely mechanism for decreased pain and inflammation. In addition to their peripheral actions, NSAIDs also appear to act on the dorsal horn of the spinal cord. Prostaglandin 2 at the level of the spinal cord is thought to cause release of glutamate both pre­ synaptically and postsynaptically. Glutamate may augment pain states and hyperalgesia. Inhibition of glutamate release at the spinal cord by reduction of PGE-2 as a consequence of NSAID administration involves a centrally acting mechanism in addition to the well-known peripheral mechanism. 3. Neuropathic. Neuropathic pain results from injury to the nervous system (e.g., peripheral nerve, spinal cord) that may occur as an acute injury of the nerve. Neuropathic pain may be the result of an isolated injury to the nervous system, or it may be the result of an injury that causes nociceptive or inflammatory pain. At the dorsal horn of the spinal cord, after peripheral nerve injury, release of cytokines and growth factors results in upregulation of nociceptive neurons. Although this is considered a broad category, various mechanisms are responsible for maintaining neuropathic pain, which results in multiple agents that are used to treat it. Antidepressants, anti­convulsants, antiarrhythmics, and local anesthetics are considered first-line agents 355

PART 4 INJURIES AND MEDICAL INTERVENTIONS

for treatment of neuropathic pain, and are given empirically. Gabapentin, which is commonly prescribed, was developed for treatment of epileptic seizures and designed to bind to γ-aminobutyric acid receptors. However, its analgesic effect is thought to be related to actions at the α2-δ subunit of L-type calcium channels that block the influx of calcium.

Pretravel Preparation Optimally a pretravel evaluation should assess the individual’s suitability for the wilderness experience and include an assessment of chronic medical conditions. A thorough history and physical examination should include the individual’s use of medications as well as any allergies and intolerances. Determining the use of chronic pain medications is important, because there are common and potential side effects to these medications. Some medications may cause cognitive impairment and psychomotor changes that may increase an individual’s risk for injury. Use of opioids may be associated with side effects including cognitive changes, constipation, and tolerance as well as withdrawal if the medication dose is significantly reduced or terminated abruptly. Termination of adjuvant medications—including antide­pressants (e.g., desipramine, duloxetine), benzodiazepines (e.g., lorazepam, alprazolam), and anticonvulsants (e.g., carbamazepine, gabapentin)—can also cause withdrawal-type syndromes. Individuals who are receiving chronic opioids or adjuvants for chronic pain may not have a predictable response to acutely administered analgesic medications for acute injuries. As management of chronic pain has become more complex and as more sophisticated implanted devices have become available, it has become more likely that individuals with chronic pain will be traveling in the wilderness. These devices include spinal cord stimulators, peripheral nerve stimulators, cortical and deep brain stimulators, and implanted intrathecal infusion devices. If an individual has one of these devices, it will be important for him or her to understand how to operate the device and to have contingency plans in case the device fails. For example, individuals with implanted pumps that deliver intrathecal medication require periodic refills of the reservoir, typically every 1 to 3 months. Persons who use these devices and persons with allergies should wear identification bracelets. Device manufacturers have a worldwide network of support that is accessible by telephone or e-mail, but this may not be practical in the wilderness, so written instructions should be available. Having the device information (i.e., the name of the manufacturer and the model number) and contact information for local health care providers and manufacturers will facilitate resolving difficulties when civilization is reached. When medications are transported internationally and specifically by air carrier, the Travel Security Administration in the United States may require specific handling of medications. Because regulations change periodically, one should check for updates before traveling. Medications should be properly labeled with appropriate prescription and patient identification information.

Treatment Modalities After injury, the patient should be assessed with regard to mechanism and severity of injury. Treatment modalities are available for management of acute pain; these include local, regional, and systemic techniques. Local physical modalities (e.g., cold, heat), local anesthetics, and topical medications may be effective. Regionally, nerve blocks of the extremities or other body parts may provide excellent analgesia or even anesthesia for many hours. Systemically, medications include opioids, NSAIDs, and antineuropathics for treatment of acute pain. Preparation of a pain first-aid kit for excursions into the outdoors allows for the greatest number of options for treatment of various maladies (Box 17-1).

PHYSICAL MODALITIES Rest minimizes additional pain and inflammation. If practical, maximize rest and minimize motion until pain is fundamentally 356

BOX 17-1  Pain Management First-Aid Kit* Basics Esmarch bandage, 3 × 36 inches Hot and cold packs Oral Medications Acetylsalicylic acid, 500 mg Acetaminophen, 500 mg Carisoprodol (Soma), 350 mg, or metaxalone (Skelaxin), 500 mg Diazepam (Valium), 5 mg Hydrocodone, 5 mg Injectable Medications Naloxone, two 0.4-mg ampules Ketamine, 50 mg/mL, 5 to 10 mL Lidocaine, 1%, 30 mL Procaine, 1%, 30 mL Midazolam (Versed), 5 mg/mL, 5-mL vial Morphine, 5 mg/mL, 5-mL vial Meperidine (Demerol), 50 mg/mL, 5-mL vial Topical Therapies Capsaicin ointment, 2-g tube Lidocaine ointment, 5%, 30 to 50 g Lidocaine patches, 5% Diclofenac, 1% gel, 100 g Diclofenac, 1.3% patch (Flector Patch) Additional Supplies Intravenous cannula, 20 gauge, three Intravenous cannula, 18 gauge, three Tourniquet Intravenous tubing sets, two Normal saline, 500 mL Intravenous 5% dextrose in lactated Ringer’s solution, 500 mL Acupuncture needles, 50 *Items in this list are subject to the individual’s training and scope of practice. This pain kit should be available in addition to a regular first-aid kit.

gone and the majority of function is restored. Ice or another cold application (e.g., immersing a sprained ankle in a cold stream) can reduce inflammation and pain from an acute injury. Ice should be applied intermittently (e.g., for 20 minutes per hour; by alternating ice with no ice in 20-minute intervals to avoid the risks of decreased blood flow to the region, which could result in decreased oxygen delivery, decreased clearance of cellular by-products, or even frostbite [further ischemia of the limb or local tissue may occur with prolonged contact with ice]). A towel or a similar material should be placed between the ice and skin, and tissue status should be closely monitored. Edema and swelling result from the acute inflammatory process and may cause significant pain and loss of function. As swelling in the extremities increases, there may be compression of the veins, which results in worsening bleeding and swelling. Further swelling may compress nerves and arteries (i.e., compartment syndrome), which will result in ischemia distal to the injury. Elevation reduces swelling by increasing venous return of blood and by minimizing tissue edema. Distended tissues increase pain. If possible, the injured site should be maintained above the level of the heart. If a bandage is applied to reduce swelling, an elastic bandage rather than a tight nonelastic bandage will help to prevent overly aggressive reduction of sufficient blood flow and, potentially, ischemia. Compression Analgesia Wrapping an extremity proximal to the site of injury to compress the relevant peripheral nerves can produce distal analgesia and anesthesia. This may occur intentionally or may be the consequence of placing a compression dressing over an injured site.

Topical Therapies Topical application of analgesic medications may be effective for treatment of mild to moderate pain. The advantages of using a topical preparation include eliminating the need for oral medication administration, beneficial metabolic interactions with other medications, reduced systemic adverse events, direct access to the site of pain, and ease of termination of treatment if a side effect occurs. Topical medications include NSAID gels and patches, lidocaine ointments and patches, and capsaicin creams, lotions, and patches. Topical application of NSAIDs is generally less effective than oral therapy; in addition, there may be localized skin irritation. Any topical analgesic medication should only be used on intact skin. In the United States, the only available topical NSAID is diclofenac, either as a 1% gel or a 1.3% patch. Outside of the United States, other topical NSAIDs may be available. Topical 1% diclofenac gel is applied four times daily over the site of pain, and is indicated for relief of osteoarthritis pain in joints that are amenable to topical therapy. The diclofenac patch (i.e., Flector Patch) is applied twice daily to the site of pain, and is indicated for acute pain that results from minor strains, sprains, and contusions. Topical lidocaine is available as 5% topical ointment, 4% topical cream, and 5% patch. Ointment and cream are applied up to three times per day. Up to three patches at a time may be applied, and the patches are to remain on the skin for no more than 12 hours during any 24-hour period. Lidocaine patches are indicated for postherpetic neuralgia; however, they may be effective for any localized pain condition. Capsaicin is available as a cream, lotion, or patch. Concentrations of capsaicin cream preparations range from 0.025% to 0.25%. A recently approved 8% capsaicin patch has limited usefulness outside of the clinic or hospital setting. Capsaicin results in burning pain at the site of application. Start with the least concentrated formulation of capsaicin, and apply it with lidocaine 5% ointment three or four times a day. Initially use three parts of lidocaine ointment to one part of capsaicin. As the application becomes more tolerable, increase to a one-to-one concentration; this will eventually be followed by full-strength capsaicin. Although the evidence for efficacy of capsaicin is the best for all of the topical agents, analgesia occurs approximately 7 days after the initiation of therapy, thereby limiting its use for acute pain.2 TENS can be an effective technique for management of painful stimuli. This therapy requires special equipment that users may easily bring into the wilderness. TENS is frequently used to treat chronic back pain with placement of electrode patches over the area of pain and then connecting them to the battery and controller. Clinical studies to demonstrate efficacy have been inconclusive. There are many criticisms of these studies, including the use of heterogeneous patient populations and nonstandard lead placement and stimulation parameters. Nonetheless many individuals report significant benefit while using TENS. The proposed mechanism is explained by the gate control theory. Peripheral stimulation of large afferent Aβ fibers by TENS inhibits nociceptive transmission in the dorsal horn. Some studies have noted release of endogenous opioids and serotonin.6,7 In addition, increases in opioid agonists in cerebrospinal fluid have been noted after TENS use. At least two patches are used. Patch placement requires experimentation to find the locations that provide the best analgesia. Pulse width, frequency, and intensity may be adjusted. TENS can be applied at high frequency (>50  Hz) with an intensity that is below motor contraction (i.e., “sensory intensity”) or at low frequency (15  mL) of 0.5% bupivacaine, which is absorbed quickly from muscles.

NERVE BLOCKS Pain as a result of injuries to extremities may be amenable to placement of nerve blocks. The simplest of these is the field block, which involves local anesthetic being infiltrated around the wound. Injuries to the forearm and hand may be managed with an axillary nerve block (Figures 17-2 and 17-3). Injuries to the hand in an ulnar, radial, or median nerve distribution can be blocked at the wrist or in the forearm by blocking the respective nerves. Digital blocks may be placed for injuries to individual fingers or toes. More sophistication is required for blockade of a major nerve or plexus. With minimal training, the motivated individual can readily instill blocks, such as the femoral block near the inguinal ligament, for the lower extremities. Similarly 357

CHAPTER 17  Principles of Pain Management

In addition to providing analgesia, compression may result in loss of distal pulses, which should be monitored. Compression analgesia may result in development of paresthesias, thereby confounding the diagnosis of compartment syndrome. Therefore compression analgesia is not a recommended technique. However, it may be considered in rare circumstances, such as when a limb is not salvageable.

PART 4 INJURIES AND MEDICAL INTERVENTIONS

Median n.

Musculocutaneous n. Supraclavicular n. (lateral antebrachial (cervical plexus) cutaneous n.) Axillary n. Radial n. Radial n. (superficial br.) (inferior lateral brachial cutaneous n.) Humerus Axillary a.

(Palmar br.) Median n. Musculocutaneous n. Ulnar n. (palmar digital br.)

Median antebrachial Intercostobrachial and cutaneous n. medial brachial cutaneous n.

Radial n.

Ulnar n.

FIGURE 17-2  Ventral nerve distribution of the upper extremity. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

FIGURE 17-4  Axillary block. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

the entire foot can be blocked by placing local anesthetic at the level of the ankle joint in one of a combination of easily identifiable locations. The use of surface landmarks is adequate for anatomic localization of the appropriate nerves, because nerve stimulators and ultrasound machines are luxuries that are found only in the clinic or operating theater. Blunt-needle placement and administration of local anesthetic guided by paresthesias will usually suffice.

to the skin and then redirected inferior (medial) and deep to the artery, where the radial nerve is located; another 5 to 10 mL of local anesthetic are deposited. Finally, the needle is withdrawn to the depth of the axillary artery, where the ulnar nerve is located, and the remaining 5 to 10 mL of local anesthetic is deposited. During this procedure, the patient may experience paresthesias, which can be used to verify the location of the needle. However, this is not necessary. If the axillary artery is entered, continue to advance the needle through the artery, and then aspirate to make sure that the needle is deep to the artery (not intravascular) before depositing the local anesthetic. If the artery is entered, direct pressure should be maintained over the site for 5 minutes to limit bleeding. If 0.5% bupivacaine without epinephrine is used, the block duration will be 4 to 6 hours; with the addition of epinephrine, it may be 8 to 12 hours. Potential complications include intravascular injection of local anesthetic and vascular or nerve injury.

Axillary Block Sites distal to the elbow can be blocked by placing local anesthetic near the musculocutaneous, median, radial, and ulnar nerves at the distal axilla guided by the axillary artery pulse (Figure 17-4). This block is performed by having the patient supine with shoulder abducted to 90 degrees and externally rotated, with the elbow flexed. Stand or sit at the patient’s side caudal to the arm, and identify the axillary pulse over the proximal humerus. The site of entry is sterilized, and local anesthesia injected locally before a blunt needle is placed. (Blunt needles have a shorter bevel than do traditional hypodermic needles. These needles may be safer when performing nerve blocks, because they may be less likely to injure vascular and neural structures.) A 22-gauge blunt needle is then advanced superior to the pulse. The musculocutaneous nerve lies deep to the artery, and this is where 5 to 10 mL of local anesthetic is deposited. Superficial to the musculocutaneous nerve and the pulse of the axillary artery is the median nerve, where an additional 5 to 10 mL of local anesthetic are deposited. The needle is withdrawn Radial n. Median n.

Median antebrachial cutaneous n.

Ulnar n.

Axillary n.

(Posterior brachial (Posterior cutaneous n.) antebrachial cutaneous n.) (Inferior lateral brachial cutaneous n.)

Radial n.

Musculocutaneous n. Intercostobrachial (lateral antebrachial cutaneous n. cutaneous n.) Supraclavicular n. (cervical plexus)

FIGURE 17-3  Dorsal nerve distribution of the arm. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

358

Wrist Block To accomplish a wrist block, it may be necessary to block one or two of the three nerves that innervate the hand. To perform this nerve block, the shoulder is abducted with the arm supported and the hand in a supine position. The ulnar nerve is located medial to the ulnar pulse at the level of the ulnar styloid. A blunt-beveled needle is advanced, a paresthesia may be obtained, and then 3 to 5 mL of local anesthetic is injected. If no paresthesia is obtained, the needle can be moved in a fanlike distribution while injecting local anesthetic to ensure nerve block. The median nerve is located between the ulnar styloid process and the distal radial prominence and between the flexor carpi radialis and palmaris longus tendons. With the wrist and fingers flexed, these tendons are easily identified. A blunt-beveled needle is advanced deep to the tendons, and 3 to 5 mL of local anesthetic is injected. The radial nerve is blocked by injecting 5 mL of local anesthetic subcutaneously as a field block over the radial aspect of the wrist proximal to the anatomic “snuff box.” The use of 1% lidocaine or 0.25% bupivacaine is sufficient to achieve good analgesia at each of these nerves. Digital Block The dorsal digital and proper palmar digital nerves are located over the medial and lateral aspects of the digits. To perform this block, the hand is pronated and supported. The skin is entered on the dorsal aspect of the digit. A blunt-beveled needle is inserted at the medial and lateral aspect of the proximal phalanx (Figure 17-5), and 1 to 2 mL of local anesthetic is injected on each side of the digit. The use of 0.25% bupivacaine or 1% lidocaine without epinephrine provides good analgesia. Femoral Block The sensory distribution of the femoral nerve includes the anterior and medial thigh and knee as well as the medial lower leg

Femoral nerve Femoral artery Femoral vein

Needle entry sites

Lateral femoral cutaneous nerve Rectus femoris muscle

Dorsal digital nerves Palmar digital nerves

FIGURE 17-5  Digital nerve block. (Courtesy Bryan L. Frank.)

in the saphenous nerve distribution (Figure 17-6). A femoral nerve block can be used for a femur fracture. With the patient supine, the inguinal ligament, anterior-superior iliac spine, pubic tubercle, and femoral pulse at the level of the inguinal ligament are identified. A 4-inch, 22-gauge, blunt-bevel needle is entered through the skin 1 cm lateral to the femoral pulse and advanced in the anterior-posterior plane. As the needle is advanced, a paresthesia may be elicited, although this is variable. A total volume of 20 to 40 mL of local anesthetic is injected while redirecting the needle from the initial medial position adjacent to the femoral artery to a more lateral position, thereby achieving a field block. The use of 0.25% bupivacaine will provide good analgesia; if motor block and anesthesia are necessary, 0.5% bupivacaine should be used. Because this is a field block, it may be slower in onset than other nerve blocks. The femoral artery is in close proximity to the injection site, so arterial puncture of the artery and intravascular injection are possible (Figure 17-7).

FIGURE 17-6  Distribution of the femoral nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)

Head of femur FIGURE 17-7  Femoral nerve block.

Common Peroneal Block A common peroneal block may be helpful for distal tibia and ankle trauma (Figure 17-8). With the patient in a lateral position, the fibular head is identified. A blunt-bevel needle is introduced just below the fibular head. A paresthesia can be elicited at a depth of 0.5 to 1 cm, and 5 mL of local anesthetic is deposited (Figure 17-9). Ankle Block To achieve analgesia of the foot, five nerves are blocked at the level of the ankle (Figure 17-10). Depending on the injury, one or more of the nerves may be blocked with local anesthetic. To block the posterior tibial nerve, a 22-gauge blunt-bevel needle is advanced at the level of the superior aspect of the medial malleolus from posterior to anterior, beginning just medial to the Achilles tendon. If a paresthesia is obtained, 5 mL of local anesthetic is injected. If a paresthesia is not elicited, the needle is advanced to the malleolus, and local anesthetic is injected. The sural nerve is blocked by entering the skin lateral to the Achilles tendon at the level of the superior aspect of the lateral malleolus. The needle is advanced from posterior to anterior until a paresthesia is obtained or the needle contacts the lateral malleolus, at which point 5 mL of local anesthetic is injected. The deep peroneal nerve is blocked by entering the skin lateral to the

FIGURE 17-8  Distribution of the common peroneal nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)

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CHAPTER 17  Principles of Pain Management

Iliopsoas Sartorius muscle muscle

PART 4 INJURIES AND MEDICAL INTERVENTIONS

Semitendinosus m. Biceps femoris m.

Tibial n.

Popliteal v.

Popliteal a.

Common peroneal n. Fibular head

Tibia

FIGURE 17-9  Common peroneal block. (From Waldman SD: Atlas of interventional pain management. Philadelphia, 2009, Saunders.)

anterior tibial pulse, and then 5 mL of local anesthetic is injected. Field block of the superficial peroneal and saphenous nerves is performed by injecting 5 mL of local anesthetic medially and laterally from the point of entry for the deep peroneal block down to the malleoli.

SYSTEMIC THERAPY The use of various oral and parenteral analgesics forms the basis for the specific treatment of pain related to trauma in the

1 3 Extensor hallucis longus tendon

2

Superficial peroneal n.

Tibia

Posterior tibial a. Posterior tibial n.

Fibula

Flexor hallucis m. Peroneus brevis m. Sural n. Tendocalcaneus (Achilles tendon)

1 2

2

FIGURE 17-10  Ankle block.

360

Opioids Opioids that are effective for treatment of nociceptive acute pain are available in many forms and dosages to achieve various routes of administration. Although there can be differences in absorption of various opioids, the general rule of thumb is that titration to beneficial effect best suits the needs of patients. Oral administration remains the easiest form of delivery, and is accomplished with combination medications that contain hydrocodone and acetaminophen (e.g., Vicodin, Norco, Lortab). Care should be taken to avoid consuming more than 4 g of acetaminophen in 24 hours, because hepatic toxicity may occur above these levels. A step up from hydrocodone is oxycodone, which comes as both a sustained-release preparation (OxyContin) and as a shorter-acting agent (Roxicodone). Because there is no acetaminophen in these latter agents, the maximum dose is limited only by efficacy and side effects. Morphine remains the gold standard, and is available for both oral and parenteral use. Intravenous administration of opioids reduces variability introduced by oral administration and decreases the time to onset of analgesia. Intravenous administration can be by intermittent injection or continuous infusion. However, continuous infusion requires additional equipment, so intermittent bolus injections in remote locations are more practical. Intramuscular administration of opioids is feasible in remote areas, but drugs may have variable absorption from different muscle groups, thus making titration to effect and duration of action more difficult to determine. Management of nausea and vomiting, which are the most common side effects of these drugs, can be accomplished with antiemetics. Phenothiazines may cause undue sedation; therefore the use of a 5-hydroxytryptamine antagonist such as ondansetron (Zofran) is advised. Oversedation and respiratory depression are feared complications of opioid use. Naloxone is supplied in 1-mL vials that contain 0.4 mg/mL; when used judiciously in 40-mcg increments, naloxone can reverse many of the minor side effects, such as nausea, vomiting, pruritus, and sedation. Fulldose naloxone is still the appropriate treatment for respiratory depression. Nonsteroidal Antiinflammatory Drugs NSAIDs have both analgesic and antiinflammatory properties. Common agents such as ibuprofen and naproxen are readily available and offer first-line treatment for various minor aches and pains that may be encountered in the outdoors. They offer an inexpensive and effective means of treatment without concern about the possible adverse effects of opioids, and are generally free from regulation in foreign countries.

Deep peroneal n. Tibialis anterior tendon Saphenous n.

Ankle section

outdoors. Familiarity with multiple classes of medications is imperative. Their use should be guided initially on the basis of the mechanism of pain and whether pain is the result of nociceptive, inflammatory, or neuropathic causes (see Figure 17-1). Tables 17-1 and 17-2 list medications from various classes and doses that are calculated for a 70-kg (154-lb) man. Oral and parental doses are listed.

1

Anti-Neuropathic Drugs The efficacy of anti-neuropathic agents is variable because of the complexity of the mechanisms present within neuropathic pain states. Although antidepressants and antiarrhythmics can be effective, anticonvulsants (particularly gabapentin) offer a safe and reasonably tolerated therapy for the pain of nerve injury. Although it is sedating at higher doses, gabapentin that is started at 300 mg 3 times daily and then increased to 600 mg 3 times daily over the course of several days is usually well tolerated. Sedation is the major side effect, so dose escalation is not advised if the patient receives benefit at lower doses or cannot tolerate higher doses. Ketamine Ketamine is a powerful dissociative anesthetic that, when used in a small parenteral dose, can provide profound analgesia. As a centrally acting N-methyl-D-aspartate receptor antagonist, ketamine is effective for all types of pain in the short term. As little as 10 to 20 mg given intravenously or intramuscularly to an adult produces the desired analgesia. If needed, the dose may be

Drug

Dosage (mg)

Salicylates Acetylsalicylic acid

325-650

4-6

300-600

8-12

Gastrointestinal distress; inhibited platelet function; contraindicated in children with viral illness Similar to aspirin

300-1000

4-6

Hepatic toxicity with overdose

50 50-75 10

4-6 4-6 4-6

Similar to aspirin Similar to aspirin Similar to aspirin; use for 5 days or less because of the potential for gastrointestinal bleeding

4-6 4-6 6-8 8 6-8

Similar Similar Similar Similar Similar

Diflunisal Para-Aminophenol Acetaminophen Indoles Indomethacin Sulindac Ketorolac

Interval (hr)

Propionic Acids Fenoprofen 400-600 Ibuprofen 300-400 Ketoprofen 25-50 Dexketoprofen 25 Naproxen 200-275 Cyclooxygenase-2 Inhibitor Celecoxib 100-200 Narcotic Agonists (Oral) Codeine 15-60, with a maximum of 360 mg per 24 hr Hydrocodone 5-10 Hydromorphone 7.5 Levorphanol 4 Meperidine 300 Methadone 2.5-150 Morphine 30-60 Oxycodone 5-10 Extended release, 10

Risks and Precautions

12-24

to to to to to

aspirin aspirin aspirin aspirin, with less gastrointestinal distress aspirin

Gastrointestinal distress; skin rash

4-6

Narcotic side effects; note the cumulative acetaminophen dosage

4-6 3-4 6-8 2-3 4-12 3-4 4-6 12

Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic

side side side side side side side

effects; note the cumulative acetaminophen dosage effects effects effects effects effects effects; note the cumulative acetaminophen dosage

From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002.

repeated every 2 to 3 hours. Titration to effect or to the presence of side effects is imperative. Psychomimetic effects (e.g., hallucinations, bad dreams) are seen with higher doses and may limit the use of this drug. A calm and quiet setting with minimal stimulation is the ideal setting for use. Benzodiazepines (e.g., midazolam, 2 mg intravenously) are effective for blunting this response.

Muscle Relaxants Muscle relaxants that are centrally acting are reasonable to use to treat acute muscle spasms related to injury. Sedation is a significant side effect that may limit the use of these drugs. Baclofen is a preferred agent because of its activity at the γ-aminobutyric

TABLE 17-2  Common Parenteral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults Drug

Dosage (mg)

Narcotic Agonists Codeine 15-75 IM Fentanyl 50-100 mcg Hydromorphone 1-2 IM Levorphanol 4 10-20 IM, 2.5 IV Morphine Meperidine 50-100 IM, 25-50 IV Oxymorphone 1 Narcotic Agonists and Antagonists 0.3-0.6 IM Buprenorphine 2-4 IM Butorphanol Dezocine 5-20 IM, 5-10 IV 10-20 IM, 1-5 IV Nalbuphine Nonsteroidal Antiinflammatory Drug 15-30 IM, 2-5 IV Ketorolac Dissociative Analgesic and Anesthetic 50-75 IM, 15-30 IV Ketamine

Interval (hr) 4-6 0.5-1 3-4 6-8 3-5 2-4

Risks and Precautions

3-4

Narcotic side effects Narcotic side effects; wide range of dosages Narcotic side effects; choose over morphine for a patient with hepatic impairment Narcotic side effects Narcotic side effects Narcotic side effects; active metabolite accumulates in patients with renal impairment and may cause seizures Narcotic side effects

6-8 3-4 2-4 3-6

May May May May

4-6

Similar to aspirin

2-4

Increased intracranial pressure

precipitate precipitate precipitate precipitate

narcotic narcotic narcotic narcotic

withdrawal withdrawal withdrawal withdrawal

From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002. IM, Intramuscularly; IV, intravenously.

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CHAPTER 17  Principles of Pain Management

TABLE 17-1  Common Oral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults

PART 4 INJURIES AND MEDICAL INTERVENTIONS

acid B receptor; this makes it different from other agents that also act centrally but that have less specific sites of action, thereby resulting in less desirable side effect profiles. Carisoprodol (Soma), metaxalone (Skelaxin), and cyclobenzaprine (Flexeril) are examples of less preferred agents.

ALTERNATIVE THERAPIES Acupuncture Acupuncture has developed over the past 3 to 5 millennia in Asia, and has been practiced for the past several hundred years in the Western world. In many cases, acupuncture as an art and science was developed in geographic areas and under social and austere conditions that are familiar to wilderness travelers. The use of acupuncture by physicians to treat trauma and illness in wilderness settings has been described recently in the medical literature.1 When properly administered, acupuncture should have a very low risk of morbidity, and may be extremely effective for alleviating pain and restoring function to an injured wilderness traveler. It has been demonstrated that endorphin, enkephalin, monoamine, and adrenocorticotropic hormone are released after stimulation with acupuncture. Furthermore, the gate control theory of pain modulation and altered sympathetic activity may also apply. Clinically improved microvascular circulation may lead to decreases in tissue edema, which in turn may diminish pain and help with restoring function. Release of adrenocorticotropic hormone leads to increased circulating corticosteroids; decreased inflammation may contribute to decreased pain and improved healing. Contemporary medical acupuncturists are typically trained in a variety of styles and traditions. Many physicians make use of a combined approach of acupuncture point selections based on neuroanatomy and the points that are felt to have energetic effects within the body. In addition, acupuncture microsystems in which the entire body is represented in a small area (e.g., the ear, scalp, or hand) are often employed. These microsystems are often quite beneficial for acute pain relief. Sterile acupuncture needles are compact, lightweight, and easy to include in a daypack or a first-aid kit. Integration of acupuncture into the biomedical care of wilderness trauma, pain, and illness may dramatically enhance patient comfort and facilitate extrication from a remote setting. An energetic style of acupuncture that is especially useful for common trauma makes use of the tendinomuscular meridians of the acupuncture energetic subsystems. Indications for activation of the tendinomuscular meridians treatment include acute strains, sprains, abrasions, and hematomas. The method of activation for this style of treatment is to place a needle in the jing-well or ting point of one to three of the meridians involved in the lesion. This is followed by placing a needle in the “gathering point” of the meridians and then by placing needles around the area of induration, swelling, or bruising, approximately 1 cm (0.4 inch) out from the edge. All needles in this treatment are placed only 2 to 3 mm (0.08 to 0.12 inch) deep and are left in place for 20 to 45 minutes.

362

FIGURE 17-11  LI4 (ho gu) acupuncture site for headache.

Treatment of headaches is also amenable to acupuncture; a general point of insertion into the web space between the thumb and forefinger, known as LI4 (ho gu), is recommended (Figure 17-11).

PSYCHOLOGICAL TECHNIQUES Guided imagery or self-hypnosis is an often overlooked modality for pain management. The ability to transport the sensorium out of the painful experience into a different context is the aim of this technique. Although it is seemingly in the realm of a vaudeville show, self-hypnosis has been demonstrated to lessen the pain experience of patients with breast cancer, and is putatively felt to activate descending inhibitory pathways. Although these techniques are often thought of in the context of pain relief, their use to heighten the state of concentration has other uses in human performance, so learning the techniques before traveling is worth the investment of time. The mind is capable of extraordinary feats, as illustrated by the experience of Aron Ralston, whose arm was trapped between a rock and a canyon wall while canyon climbing alone in a remote area of Utah in 2004. Aron’s initial attempts to free himself produced excruciating pain. After reassessing his situation, relaxing, and making a plan, he touched his crushed hand and realized that it had lost sensation. This produced a sense that his arm was isolated from his body. He noted the disfigurement of this arm and observed that is was strange that he was not suffering pain. Unable to free himself and stranded alone with a limited water supply, he concluded that he needed to amputate his own arm and to focus all of his attention on this task. Not able to cut the bone, he levered the trapped arm, breaking the ulna and radius bones and thus freeing the arm. Although he felt a “blaze of pain” with the maneuver, he refocused on survival and was able to make his way to rescue.5 This is a story of an extraordinary person that illustrates the power of the human mind.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 18 



Taping and Bandaging DANIEL GARZA

Taping and bandaging are both useful skills in wilderness medicine. Taping can be used to support injured joints and soft tissues; bandaging is most often used to secure a wound dressing (Figure 18-1, online). In addition, bandaging with an elastic wrap is an alternative to taping, and, over larger joints such as the knee, it is often preferable. In general, taping requires practice and experience, but some simple techniques can be easily mastered. Taping is most often used for mild to moderate sprains and strains, with which some functional capacities (e.g., weight bearing, lifting), are maintained. Although taping offers dynamic support, it is in no way comparable with splinting, which is intended to immobilize an extremity. The most common tape that is applied is white athletic or “adhesive” tape, which is often used by athletic trainers in organized sports. Athletic tape may be applied to the skin, although it may lose adhesion if the body part is not shaved and if tape adhesive is not applied. Some keys to successful taping include the following: • Avoid leaving any gaps in the tape (i.e., allowing any skin to be visible), because these gaps will lead to blisters. Avoid excessive tension on tape strips that serve to fill such gaps. • Apply tape in a manner that follows skin contours to avoid wrinkles. • Try to overlap one-half of the width of the tape with each successive strip. Bandaging is accomplished with the use of either elastic wraps or gauze rolls of varying widths. After a dressing is applied to a wound, appropriate bandaging allows the patient to feel confident that the dressing will remain secure during reasonable amounts of activity. Regardless of the method used, it is important to remember that taping and bandaging—especially when circumferential— should not be so tight as to limit circulation.

Taping TYPES OF TAPE Athletic tape is composed of fibers that are woven into strips and that are coated with zinc oxide, which is an adhesive compound. Although athletic tape is most commonly colored white, it is available in many colors. Athletic tape is the most commonly used tape in sports and first aid for support and for the prevention of injuries. It is also available in many widths. Although the major advantage of athletic tape is versatility, its major disadvantage is the tendency of zinc oxide to lose adhesive properties with heat and moisture, thereby resulting in a loss of support when the patient sweats. A variety of techniques, which are described later in this chapter, are used to increase the durability of athletic tape under these conditions. Elastic tape (e.g., Elastikon) is cotton elastic cloth tape that incorporates a rubber-based adhesive. The elasticity of this tape allows for greater flexibility, so it is particularly useful for large joints such as the knees and shoulders.

SKIN PREPARATION Skin preparation involves measures that are intended to increase patient comfort as well as the longevity of tape adhesion. If tape is to be applied directly to skin, the area is usually first shaved to remove hair that may interfere with direct contact. Care must

be taken to avoid small abrasions in the skin when shaving, because these can serve as entry sites for infection. If the area cannot be shaved in a clean and deliberate manner, it is advisable to avoid shaving. Any obvious abrasion or other wound should be covered with a thin layer of gauze or a small adhesive bandage before taping. Some commercially available skin adhesives are available in aerosolized form. These preparations (e.g., Tuf-Skin) use benzoin as the adhesive. Skin adhesive is applied after the skin has been shaved and after all abrasions have been dressed. If the area is not shaved, a foam underwrap or prewrap is used to protect the patient’s body hair. Prewrap is available in 3-inch–wide rolls in many colors. After the application of a topical skin adherent (e.g., Tuf-Skin), prewrap is applied over the part to be taped in a simple and continuous circular wrap. The prewrap is sufficiently self-adherent and does not need to be taped. When tape is applied over bony prominences, it can create tension on the skin surface that leads to blistering. Heel-and-lace pads and foam pads are used to provide additional comfort by relieving potential pressure points. Heel-and-lace pads are prefabricated pieces of white foam that are adhered together with petroleum jelly and then applied to the anterior and posterior aspects of the talus when the ankle is taped. Pads of foam can be cut to size to fit over painful areas that need to be taped (e.g., for medial tibial stress syndrome) or used for support in special cases (e.g., for patellar subluxation).

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

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

LOWER-LEG TAPING Medial tibial stress syndrome, which is commonly referred to as shin splints, can be taped for support and comfort. Tape is brought from a lateral to a medial direction. A small foam pad can be placed to cover the area of tenderness. Underwrap should be used over a foam pad to secure the pad in place (Figure 18-4).

For online-only figures, please go to www.expertconsult.com

363

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

D

E

F

G

H

I

J

K

FIGURE 18-2  Ankle taping. A, With the ankle bent 90 degrees, apply anchors of 1.5-inch–wide tape at the lower leg and the distal foot. B, Apply three stirrups from a medial to a lateral direction in a slight fanlike projection. C, Fill in any gaps with horizontal strips. D, Begin the figure-8 technique. Apply tape across the front of the ankle in a left-to-right direction. E, Continue taping under the foot to the opposite side, and cross back over the top of the foot. F, Complete by wrapping tape around the leg, and end at the anterior aspect of the ankle. G, Apply heel locks for both feet (omit if not familiar with this technique). Start in a left-to-right direction, and apply tape across the front of the joint. H, Wrap tape around the heel (the bottom margin of the tape should be above the superior edge of the calcaneus) to form the first heel lock. I, Continue under the foot to the opposite side, and then cross back over the top of the foot. J, The tape is then brought back around the superior margin of the calcaneus and down and around the heel. K, Finish by wrapping the tape around the ankle. Repeat the figure-8 or heel-lock technique as desired.

364

Place the first anchor around IP joint of first toe with 1-inch tape. Place the second anchor around midfoot with 11/2-inch tape. 2. Apply strip of 1-inch tape from distal to proximal anchor along medial aspect.

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

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

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

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

PATELLA TAPING Subluxation of the patella is exacerbated by the stress of walking long distances across uneven terrain. Incorporating a piece of foam into the taping of the knee can help to relieve symptoms. As with all taping around the knee, underwrap should not be used (Figure 18-6).

FINGER TAPING Injuries to the fingers are common in outdoor settings. Simple fractures and sprains can be initially treated by taping. The most common scenarios involve fingers that are hyperextended or that are “jammed.” Injuries in this scenario are often to the palmar ligaments and tendons. Patients may find it difficult to flex the finger against the resistance of an examiner’s finger, or they may demonstrate tenderness over the palmar aspect of the finger. Swelling is almost always present, so the precise injury may be difficult to diagnose. This presentation is also seen after reduction of a dorsal dislocation of the proximal interphalangeal joint. In all of these cases, it is always best to splint or tape the finger in slight flexion to avoid further injury to the flexor apparatus. Fingers are buddy taped to the adjacent finger, which serves as a splint (Figure 18-7). The second and third fingers and the fourth and fifth fingers are always paired. If the third and fourth fingers are paired, this makes injury to the second and fifth fingers more likely with subsequent activity. A small piece of gauze, cotton, or cloth should be placed between the fingers to avoid blistering or pressure on a tender joint. Strips of tape should be applied around the fingers but not over the joints. Although they are not as common, injuries of the extensor tendons can occur. These typically occur with hyperflexion, but they may also occur with hyperextension and axial loading.2 “Mallet finger” results from fracturing the base of the distal phalange, which is the site of attachment for the extensor tendon. The resulting inability of the distal phalange to fully extend results in a partially flexed finger. Injuries in which the extensor mechanism is clearly disrupted should be treated with the finger taped in full extension. A straight splint (e.g., a tongue blade, a

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

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

FIGURE 18-3  Toe taping.

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

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

FIGURE 18-4  Lower-leg taping.

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CHAPTER 18  Taping and Bandaging

1. Apply two anchors:

PART 4  INJURIES AND MEDICAL INTERVENTIONS

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

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

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

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

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

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

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

5. Repeat steps 3 and 4 twice.

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

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

FIGURE 18-5  Knee taping.

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

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

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

FIGURE 18-6  Patella taping.

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

TYPES OF BANDAGES FIGURE 18-7  Buddy taping of the fingers.

smooth stick) can be placed on the dorsal or volar surface and the finger taped to it for additional extensor support (Figure 18-8). Any significant injury to the fingers or hands should be evaluated by a physician, who can determine whether radiographs are necessary. Given the importance of maintaining optimal functioning of the hands for personal and professional activities, this point cannot be overemphasized.

THUMB TAPING The thumb is frequently injured when it is placed in extreme extension or abduction, which occurs when it is caught in the strap of a ski pole when a person is falling. Taping can prevent reproducing the mechanism of injury, particularly when the individual is grasping an object (Figure 18-9).

The type of bandage depends on the intended purpose. Elastic bandages (e.g., Ace wraps) come in many widths and are used to wrap injuries such as sprains and strains. These bandages generally are accompanied by separate clips or have built-in clips for the purpose of securing the bandage. Of note is that the double-length 6-inch–wide elastic bandage is quite useful for wrapping large joints, such as the knee and the shoulder. Bandaging wounds generally involves rolled gauze or cottonbased wraps that secure a dressing in place. These wraps are more desirable than are elastic bandages for wound care, because they do not place as much tension on the dressing. A triangular bandage, which is often used to create a sling, can be folded two to three times into a strap called a cravat (Figure 18-14). Cravat dressings are useful for applying pressure to a bleeding wound to promote hemostasis. In the discussion of bandaging different parts of the body that appears later in this chapter, the method for using an elastic bandage is described. When securing a wound dressing, the same methods may be used, except that rolled gauze or cotton

WRIST TAPING Wrist sprain generally occurs during a fall. It can initially be difficult to distinguish from a fracture. Although splinting is usually the most desirable treatment, there are two basic taping approaches that can be used, depending on whether the injury occurred with the wrist in hyperextension or hyperflexion. Anchors are first placed around the palm and the distal wrist. Support strips to prevent undesirable movements are placed on the palmar aspect for hyperextension injuries or on the dorsal aspect for hyperflexion injuries (Figure 18-10).

ELBOW TAPING The two most common soft-tissue injuries to the elbow result from hyperextension or excessive valgus force. Each of these injuries can result in significant ligament and tendon injuries. Taping techniques are intended to prevent reproduction of painful movements while maintaining function. Because these techniques allow for substantial joint movement, underwrap should not be used, and tape should be applied directly to the skin to allow for maximal adhesion. Taping for a hyperextension injury involves use of a fan of elastic or tape, which is similar to that used for the wrist, to prevent excessive extension (Figure 18-11). Individuals who have suffered valgus stress injuries require reinforcement with elastic tape placed on the medial aspect of the elbow (Figure 18-12).

A

SHOULDER TAPING Taping the glenohumeral joint is rarely performed, mostly because it results in such a significant restriction of movement that the patient cannot effectively function. Thus taping offers little advantage over a sling. However, taping the acromioclavicular joint can be effective in reducing pain and maintaining adequate function at the glenohumeral joint.

B FIGURE 18-8  A and B, Extension taping of the finger with a small splint.

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Injury to the acromioclavicular joint most commonly occurs when a patient falls on the lateral aspect of the shoulder. Sufficient force is transmitted through the acromioclavicular ligament to stretch or tear it, which results in an “AC sprain” or a “separated shoulder.” For this injury, tape should be applied directly to the skin (Figure 18-13).

PART 4  INJURIES AND MEDICAL INTERVENTIONS

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FIGURE 18-9  Thumb taping. A, With the use of 1.5-inch–wide athletic tape, wrap an anchor strip around the wrist. B, With the use of 0.75-inch– wide tape, start at the volar aspect of the wrist and continue along the dorsal aspect of the thumb toward the first web space. C, Allow the patient to crimp the tape as it comes across the web space, and then continue around the base of the thumb. D, Bring the tape around to the volar aspect of the wrist, and then tape at that point. To complete a thumb spica, apply several more strips of tape in succession. To reinforce this, rather than repeating a series of strips, continue as follows. E, Apply an anchor strip from the volar to the dorsal aspect of the wrist through the first web space; note the crimping. F, Apply a strip from the dorsal to the volar aspect of the anchor strip. G, Apply successive strips until the wrist is reached. H, Add a finishing anchor strip through the first web space. I, Complete the wrapping with an anchor strip at the wrist.

bandages should be substituted. If there is a special technique for wound care, it will be described separately.

SECURING BANDAGES Because bandages are not adhesive, they must be secured with tape or clips or by tying them to the body. Two techniques for tying off a bandage are as follows: 1. As you are finishing wrapping the body part with the bandage, bend the free end of the bandage backward over your fingers to create a loop. Double back around the body part, and then tie the remaining free end to the loop to secure the bandage1 (Figure 18-15). 2. As you are finishing wrapping the body part, tear or cut the remaining portion of the bandage lengthwise down the middle. Double back with one of the resulting strips, and then tie off the bandage.

ANKLE AND FOOT BANDAGING Ankle bandaging with a 2- to 3-inch–wide elastic wrap can be used to support a sprain. The bandage can be applied over a sock or directly to the skin. It is usually the most simple to use 368

a series of figure-8 wraps. One may also use a series of heel locks, which were described in the section about ankle taping. Anchors and stirrups are not used. When bandaging the foot, the same technique should be carried out to the metatarsophalangeal joint. Circumferentially bandaging the foot by itself often results in the bandage slipping, which does not occur when the ankle is also bandaged as part of the process.

KNEE BANDAGING A double-length 6-inch–wide elastic bandage can provide support to the knee. Ask the patient to hold the knee in slight flexion by placing his or her heel on a small stone or a piece of wood (Figure 18-16, A, online). The elastic wrap is then applied circumferentially from the mid quadriceps to the mid calf (Figure 18-16, B, online). If using gauze or a smaller-width elastic wrap to secure a dressing, a series of figure-8 wraps can be applied, with the patella left exposed.

THIGH AND GROIN BANDAGING Quadriceps, hamstring, and hip-adductor (i.e., groin) strains can all be treated with an elastic bandage in a hip-spica configuration.

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

The bandaging is modified slightly for a groin strain (Figure 18-17). Although the quadriceps and hamstring can be supported by wrapping only the leg with a 6-inch–wide elastic bandage, the hip spica helps to prevent slipping and provides additional support.

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

SCALP BANDAGING WRIST AND HAND BANDAGING Support to the wrist can be supplied with the use of a 2- to 3-inch–wide elastic wrap and a continuous wrapping technique (Figure 18-18). This same technique can be used with gauze to secure a dressing to a wound that involves the palm of the hand. A hand cravat bandage can be used for wounds that continue to bleed despite manual pressure1 (Figure 18-19).

FINGER BANDAGING Finger wounds are generally easily treated with adhesive bandages. However, if the size of the wound or the degree of bleeding necessitates a larger dressing, then the following method may be used. Fold a 1-inch–wide piece of rolled gauze back and forth over the tip of the finger to cover and cushion the wound (Figure 18-20). Next, wrap the gauze around the finger until the gauze is snug. On the last turn around the finger, pull the gauze over the top of the hand so that it extends beyond the wrist. Split this gauze tail lengthwise, and then tie the ends around the wrist to secure the bandage.

THUMB BANDAGING The application of a bandage or dressing to the thumb usually involves a thumb spica, as described in the previous section about taping. The gauze or elastic bandage should be looped continuously rather than applied in individual strips.

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

EAR OR SIDE OF HEAD BANDAGING A wound to the pinna of the ear or other location on the side of the head may require a compression dressing. If the ear is involved, gauze should be placed both anterior and posterior to the ear to allow the ear to maintain its natural curvature. A cravat is used to secure the dressing (Figure 18-24). This method may be used for wounds anywhere along the side of the head or under the chin.

EYE BANDAGING When bandaging an eye, a shield is placed over the eye socket to protect the globe, and this is followed by the application of a bandage over the shield. The shield may be made of commercially available sterile pads, or it may be cut foam or felt, stacked gauze, or a shirt or cravat that has been fashioned into a doughnut shape (Figure 18-25). The bandage is fashioned from a cravat and a spare piece of 15-inch–wide cloth or a shirt. The spare cloth is placed over the top of the head from a posterior to an anterior direction so that the anterior portion lies over the unaffected eye. A cravat is then applied horizontally to hold the shield over the injured eye. To expose the uninjured eye, pull up both ends of the spare cloth, and tie it at the top of the head (Figure 18-26). 369

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

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

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

2. Apply 3-inch elastic tape that forms an X over the medial joint line.

3. Apply closure strips above and below the elbow over the original anchors.

The first strip begins at the posterior aspect of the proximal anchor and crosses to the anterior aspect of the distal anchor. The second strip begins at the anterior aspect of the proximal anchor and crosses to the posterior aspect of the distal anchor. Apply a total of four strips.

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

FIGURE 18-11  Elbow taping.

3. Apply closure strips above and below the elbow over the original anchors.

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

FIGURE 18-12  Elbow taping for a valgus stretch injury.

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

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

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

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

FIGURE 18-13  Shoulder taping.

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

2. At the groin crease, continue up and around the waist once to help anchor the bandage. FIGURE 18-14  Making a cravat from a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

3. Return to the thigh to complete the figure-8. For quadriceps and hamstring strains, concentrate on wrapping the leg, using an additional figure-8 bandage to anchor the wrap. For groin strains, concentrate on supporting the hip adductors by alternating wrapping the leg with figure-8 wraps.

A

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

4. Finish wrapping leg.

FIGURE 18-17  Thigh and groin bandaging.

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FIGURE 18-18  Wrist bandaging. A, Begin by encircling the wrist with the bandage two to three times. B, Continue bandaging across the dorsum of the hand, through the first web space, and around the base of the proximal phalanges. C, Continue down and across the dorsum of the hand. D, Circle the wrist, and bring the bandage across the dorsum of the hand to form a figure-8. E, Repeat these steps, and make alternating figure-8 patterns on the dorsum of the hand. Secure the bandage at the wrist.

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

2. Starting from the anterior aspect of the wrist, wrap one end around the dorsum of the hand, over the fingers and back to the wrist. FIGURE 18-20  To begin a finger bandage, place layers of gauze over the fingertip. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.) 3. With tension, wrap the other end around the dorsum of the hand, over the fingers and back to the wrist, creating an X.

4. Cross both ends around the wrist.

5. Tie the ends to secure the dressing.

FIGURE 18-19  Hand cravat bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy, Ski Patrol Magazine Winter:66, 2005.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

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

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

3. Repeat the figure-8 pattern as the length of the bandage allows and finish on the upper arm.

FIGURE 18-21  Shoulder bandaging.

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

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

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

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

FIGURE 18-22  Shoulder bandaging with a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

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

FIGURE 18-23  Scalp bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

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

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

FIGURE 18-25  Bandaging for the injured eye. A cravat or cloth is rolled and wrapped to make a doughnut-shaped shield, which is then fixed in place over the eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

3. Tie off the ends.

FIGURE 18-24  Ear or side of head bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

FIGURE 18-26  To hold an eye patch in place with a cravat, hang a cloth strip over the uninjured eye. Hold the patch in place with the cravat, and then tie the cloth strip to lift the cravat off of the uninjured eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

CHAPTER 19 



Splints and Slings MISHA R. KASSEL AND ALAN GIANOTTI

Splints and slings have been staples of medical care for thousands of years. For instance, orthopedic splinting was well documented in ancient Egypt more than 5000 years ago1,33 (Figure 19-1, online). First and foremost, splints and slings stabilize injuries by limiting movement (Box 19-1). Limiting movement minimizes pain and decreases potential further tissue damage. Splinting eases transportation from the field, minimizes blood loss, and aids in healing.12 In general, all fractures and dislocations should be splinted before transport unless the patient’s life is at immediate risk or the rescue scene is unsafe.13 Basic splint types include rigid, soft, anatomic, and traction. Splint choice is based on fracture type and available materials. In improvisational situations, splints can be made from just about any material. Examples include newspapers, pillows, umbrellas, and other supportive materials5 (Figure 19-2).

Spinal Immobilization Spinal cord injuries are rare, affecting 40 to 50 individuals per million annually in the United States. These injuries may result in long-term disability.22 The 5 million people each year who are placed in spinal immobilization after traffic collisions contribute

to the majority of spinal cord injuries. In one wilderness study, 3.6% of mountain trauma patients who were alive when rescued had spinal injuries.12 In an attempt to prevent further neurologic damage, prehospital spinal immobilization of urban trauma patients is the standard of care. This may not be practical in wilderness settings, but it should always be considered. Spinal stabilization is first accomplished by manual techniques, and then mechanical devices (e.g., backboards, collars, straps) are required. Indications, risks, benefits, and equipment descriptions are discussed later in this chapter.

INDICATIONS FOR SPINAL IMMOBILIZATION The most common scenario for prehospital spinal immobilization is an injury sustained during a motor vehicle collision. All-terrain vehicles, automobiles, snowmobiles, motorcycles, and other offroad vehicles are the most common causes of high-force spinal trauma in the wilderness setting. Falls and other high-force mechanisms are also concerning. Worrisome symptoms include spine pain or palpable tenderness, altered mental status, neurologic complaints, head injury, extremes of age, or an unreliable examination that involves a distracting injury, alcohol or drug use, or a communication barrier6 (Box 19-2).

For online-only figures, please go to www.expertconsult.com

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BOX 19-1  Principles of Splinting

BOX 19-2  Indications for Spinal Immobilization

Visualize the injured body part. Continually recheck the patient’s neurovascular status. Traction is indicated if the pulse is not palpable. Gentle traction involves less than 10 lbs of force. Cover open wounds with sterile dressings. Immobilize the joints above and below the injury. Padding prevents further tissue damage. Do not reset open or protruding fractures. Splint the extremity in the position in which it was found. Splint the patient before transport (if he or she is stable). Ice and elevate the injury after immobilization.

Spine pain or tenderness Traumatic mechanism of injury Altered mental status Distracting injury Unreliable examination (e.g., as a result of alcohol or drug use) Neurologic complaints Head injury Extremes of age

Modified from Bowman W, et al: Outdoor emergency care: Comprehensive prehospital care for nonurban settings, ed 4, 2003, Sudbery, Jones and Bartlett Publishers; and Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady.

Spinal immobilization is intended to prevent worsening of an existing spinal cord injury or the creation of a spinal cord injury in the case of a ligamentous disruption. The medical literature has multiple reports of worsening neurologic deficits after patients with spinal cord injuries are moved.6,34,35 Extreme settings mandate a different interpretation of “urban” recommendations to fit the survival wilderness scenario. Wilderness data are limited, so prehospital spinal immobilization is prudent when practical. Spinal immobilization is not performed without reservation. Backboards and collars may increase discomfort. Airway management may be restricted and evacuation times increased with spinal immobilization. However spinal immobilization remains the standard of care when practical in the wilderness setting.12 Further research is indicated to better classify appropriate indications and to further assess the risk-benefit ratio for spinal immobilization in the wilderness.

Modified from Brabson T, Greenfield M: Prehospital immobilization. In Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders.

CERVICAL SPINE IMMOBILIZATION High cervical spine (C-spine) injuries have great potential for morbidity and disability. The goals of C-spine immobilization are to minimize movement and maintain a “neutral” alignment. Standard C-spine immobilization is performed with a hard collar in conjunction with a backboard and lateral support devices. The modern standard cervical collar has five contact points and makes use of the head, C-spine, and thorax. The thorax contact points include the trapezius muscles (posterior), clavicle, and sternum (anterior). Hard collars alone do not adequately limit cervical motion. Backboards and lateral support devices are required in conjunction with a hard collar (Figures 19-3 and 19-4). The

FIGURE 19-3  Standard hard cervical collars. (Courtesy Laerdal Medical Corporation.)

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FIGURE 19-2  Improvised cervical spine and ankle stabilization (pillow, towels, cardboard and tape) in Port au Prince, Haiti, 2010. (Courtesy Anil Menon, MD.)

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FIGURE 19-4  A to C, Different lateral support devices. D, Complete spinal immobilization. (Courtesy Laerdal Medical Corporation.)

CERVICAL SPINE APPLICATION The application of a C-spine immobilization device depends on the position in which the patient is found and the device that is available. Universal application diagrams are generally helpful with regard to in-line stabilization, neutral neck alignment, chin positioning, and collar placement. Diagrams for application of C-spine collars on both upright and supine patients are easily referenced and generally intuitive (Figure 19-5). Diagrams for application of improvised C-spine collars or C-spine collars on patients who are found in sitting positions are also helpful (Figures 19-6 to 19-9; Figure 19-8, online).

SPECIAL CONSIDERATIONS Special populations require accurately sized equipment. This includes people with extra long or short necks for which a standard cervical hard collar is not effective. Children who are less than 8 years old are at risk for further injury when immobilized on a standard backboard because of a proportionately large head, which may cause increased flexion during a collision.36 Modifications to counter this anatomic feature include raising the shoulders to the level of the head by placing a pad underneath the shoulders (Figure 19-10). This should be considered for all children who are on backboards.28,29

IMPROVISATIONAL TECHNIQUES The key ingredients to an improvisational C-spine device include maximizing stability and fit while limiting airway compromise and allowing access for mouth opening, thus limiting aspiration risk.14 A “horse collar” technique involves a towel, blanket, or other available and malleable material rolled to the desired thickness and placed underneath the patient’s neck. The ends are then crossed over the patient’s chest and secured. As with the cervical hard collar, the patient’s C-spine is maintained in a neutral position during application and for as long as possible afterward by manual in-line stabilization2,6 (see Figure 19-6). A structural aluminum malleable (SAM) splint can also be molded into a C-spine collar. Studies have shown it to be as effective as a Philadelphia collar, with the advantage of being small, lightweight, versatile, and portable. These characteristics are advantageous in the wilderness setting26 (see Figure 19-7).

COMPLICATIONS OF CERVICAL SPINE STABILIZATION Studies have shown that C-spine collars cause increased intracranial pressure, which may be clinically significant for patients with head injuries. Therefore hard cervical collars should be removed immediately after exclusion of a C-spine injury, especially among patients with head injuries. C-spine collars may also be contraindicated in patients with penetrating neck injuries, because they may interfere with management of neck wounds or even conceal these wounds. Penetrating wounds to the spinal cord are rare. Cervical immobilization creates the real possibility of causing greater morbidity than protection.18,19

THORACOLUMBAR IMMOBILIZATION A full-length backboard best accomplishes immobilization of the thoracolumbar spine. In addition, a cervical collar, lateral neck stabilizers, and backboard straps are essential for full spinal immobilization. If the patient is already upright, standing, or lying supine, application of a full-body backboard is straightforward, as described later in this chapter. However, with the suspected cervical injury of a seated patient, an intermediate device is

required. There are many forms of this short board, such as a Kendrick Extrication Device (see Figure 19-9). Short boards are applied only after manual in-line stabilization and cervical collar placement. When the short board is in place, the patient can be safely transferred to a full backboard device.6 Strict contraindications for spinal immobilization are few but include emergency evacuation from an unsafe environment. Examples of such environments, with the risk of impending danger, include toxic spills, fire hazards, congested traffic areas, and other situations in which the application of an immobilization device would delay immediate evacuation to safety. In these dangerous situations, expedited removal with manual cervical stabilization is advised.21 When the patient is in a safe location, full spinal immobilization should be applied. Choices for full-body splints include hard backboards, scoop stretchers, and full-body vacuum splints (Figures 19-11 to 19-13). Full-body hard backboards are used for their ease of application, availability, and effectiveness. Unfortunately, their size and weight make them undesirable for backcountry use, so they are often improvised in the field. Secured straps minimize spinal movement during transport. These are especially important with vomiting patients, when the airway is potentially compromised and a quick change of position is required to allow for removal and drainage of emesis.6 Hard backboards are uncomfortable. Spinal pain that is induced by a backboard may be misinterpreted, and this can complicate and delay therapy.16 Vacuum splint devices offer certain advantages over rigid hard backboards. They can be applied more quickly, and are significantly more comfortable. They also offer a similar degree of spinal immobilization.20 During mountain rescue, vacuum splints are the preferred device for total spinal immobilization (see Figure 19-12).

FULL SPINE IMMOBILIZATION From a supine (lying) position and after the placement of a cervical collar, the patient is logrolled and placed onto a board or vacuum splint. Three people are required to transfer a patient onto a board. The first person is positioned at the head and applies in-line stabilization, the second is at chest level, and the third is at pelvis level. On the command of the person at the head, the patient is rolled onto his or her least-injured side. The board is then slid underneath the patient while the back is evaluated for injuries. Body straps and lateral neck stabilizers are then placed.6 Logrolling is not required with scoop stretchers, thereby minimizing spinal movement (see Figure 19-13). Full spinal immobilization can also be applied to a standing patient (see Figure 19-5). Complications of full spinal immobilization are listed in Box 19-3.

Upper-Extremity Splinting The most common upper-extremity injury scenario is bracing from a ground-level fall. Rigid and soft splints are used to stabilize upper-extremity injuries. It is always important to leave fingertips exposed to allow continuous assessment of neurovascular status.6 Common examples of upper-extremity splints include malleable, cardboard, air, vacuum, pillow, and sling and swathe splints. Specific splinting recommendations for upperextremity injuries are given in Table 19-1. When feasible, upperextremity injuries are splinted in a position of function (Table 19-2).

Lower-Extremity Splinting Although the principles of lower-extremity splinting are similar to those of upper-extremity splinting, the ramifications are not the same in terms of evacuation. Lower-extremity fractures are more likely to involve weight-bearing bones and thus to require rigid splinting. Specific recommendations, including positions of function, are found in Tables 19-2 and 19-3. One needs look no further than Joe Simpson’s 1985 epic selfrescue from the Peruvian Andes, which was described in Touching the Void, to appreciate the pain of an unsplinted weight-bearing fracture: 377

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patient’s neck requires manual stabilization in a neutral, in-line position until he or she is fully immobilized. Standard emergency medical services equipment includes lateral support devices (foam or plastic). In the wilderness setting, these devices can be improvised by rolling clothes, sheets, or blankets and placing them on both sides of head while securing everything in place with tape17 (see Figure 19-2).

PART 4  INJURIES AND MEDICAL INTERVENTIONS

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FIGURE 19-5  Full spinal immobilization from a standing position. A, Step 1: Manual stabilization. B, Step 2: Apply a rigid collar. C, Step 3: Insert a long backboard. D, Step 4: Center the backboard. E and F, Step 5: Rescuers grasp the board with the use of a handle that is higher than the patient’s armpit. G, Step 6: Slowly lower the patient. H, Step 7: Fully immobilize the torso and then the head and neck. (From Elling R, Politis J: Backboarding the standing patient, JEMS 12:9, 1987. Used with permission.)

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FIGURE 19-6  Improvisational “horse collar.” (Courtesy Ferno-Washington, Inc.)

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G

H

F

I

FIGURE 19-7  Improvised cervical spine collar from a SAM splint. A, Fold 36-inch splint 5 inches from the end. B, While bracing the thumbs on either side of the fold, pull the edges to create a V-shaped chin rest. C, Place the chin rest below the patient’s chin, and place the rest of the splint loosely around the patient’s neck. D, Bring the end forward and down in an oblique direction until it touches the chest. E, While supporting the chin, bring the chest portion of the splint around the chin to create a chin post. Squeeze to deepen the chin post. F, Insert the index fingers on either side of the splint and pull. G, Squeeze to create lateral posts to ensure a snug fit. H, Squeeze the back of the splint to create more stability. I, Fold up any excess splint and secure it with wrap or tape. (Courtesy SAM Medical Products.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

C

B

D

FIGURE 19-9  A, Kendrick Extrication Device (KED). B, Manual in-line stabilization of the cervical spine with the KED slid behind the patient. C, Applied KED with cervical collar in place. D, Patient transferred to long board. (Courtesy Ferno-Washington, Inc.)

BOX 19-3  Complications of Spinal Immobilization Tight straps and a rigid board may cause discomfort or distress. Tight straps may cause vascular compromise. An immobilized position may interfere with normal respiratory function. Complications from emesis include aspiration. Loose straps may be inadequate for spinal immobilization From Brabson T, Greenfield M: Prehospital immobilization. In Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders; Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady; Hamilton RS, Pons PT: The efficacy and comfort of full-body vacuum splints for cervical-spine immobilization, J Emerg Med 14:553, 1996; and Kwan I, Bunn F, Roberts I: Spinal immobilisation for trauma patients, Cochrane Database Syst Rev (2):CD002803, 2001.

380

The moment I jumped I knew I would fall…. I had lain face-down in the gravel, clenching my teeth, waiting for the pain to subside. It remained with me, burning my knee unbearably as it had never done before… I stood and fell, writhed where I fell, cried and swore, and felt sure in my heart that these were my last spastic efforts before I lay still for good.32

Rigid Splints Rigid splints can be improvised from materials such as cardboard, wood, and wire. Proprietary vacuum splints and air splints are commonly used in the field. Rigid splints are attached to the extremity with a variety of fasteners, including tape, straps, gauze, and Velcro. For all splints, ample padding is essential, especially over bony surfaces and swollen tissue to minimize pressure damage and pain.5

CHAPTER 19  Splints and Slings

A

B

C FIGURE 19-10  Backboard considerations and increased cervical flexion for children who are younger than 8 years old. A, A young child immobilized on a standard backboard. Note how the large head forces the neck into flexion. Backboards can be modified by B, an occiput cutout or C, a double mattress pad to raise the chest. The actual clinical consequences of this observation are unknown. (Modified from Herzenberg JE, Hensinger RN, Dedrick DK, et al: Emergency transport and positioning of young children who have an injury of the cervical spine, J Bone Joint Surg Am 71:15, 1989.)

Cardboard splints have the advantage of being lightweight, inexpensive, easy to apply, and radiolucent.6 They can be premade or improvised (Figures 19-2, 19-14 to 19-16; Figure 19-16, online). When improvising, it is important to cut the cardboard so that the corrugations run lengthwise to maintain the material’s intrinsic strength. Splints can be individually fitted

FIGURE 19-12  Example of a full-body vacuum splint used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department, Utah.)

using the unaffected extremity as a model and then placed on the affected extremity. They are usually secured with adhesive tape. Disadvantages include loss of integrity when wet and greater laxity as compared with other splinting options. The distorted and grossly swollen extremity is difficult to splint using this technique.12 Although they are initially malleable, vacuum splints are a type of rigid splint (Figure 19-17, online). These splints are made of many tiny plastic pellets in a closed, airtight bag. The bag is placed around the injured extremity, and then air is manually extracted via a hand pump to form a rigid “mold” of the injured extremity. The extremity is left in its position of injury to minimize pain (Figure 19-18). No external force is applied, thereby maximizing circulation.6 Unfortunately vacuum splints are expensive, moderately bulky, affected by changes in altitude, and penetrable. In addition, any perforation renders the splint nonfunctional.12 A lightweight, inexpensive, and popular rigid splint is the SAM splint (Figures 19-7, 19-8, and 19-19 to 19-33; Figure 19-8, online). Constructed of an aluminum center that is sandwiched between thin strips of foam, this splint is also malleable and versatile.6 It is very strong and pliable, and it can be used for

TABLE 19-1  Upper Extremity Splints Splint

Indication

Figure-8 splint Sling and swathe splint Sugar-tong splint   Proximal   Distal Posterior arm splint Volar splint

Medial clavicle fractures Shoulder and humeral injuries

Gutter splint Thumb spica splint Volar finger splint

FIGURE 19-11  Standard rigid splint. (Courtesy Laerdal Medical Corporation.)

Humeral fractures Wrist and distal forearm fractures Stable elbow and forearm injuries Wrist fractures and fractures of the second through fifth metacarpals Phalangeal and metacarpal fractures Scaphoid fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries Fractures of the distal phalanges and the interphalangeal joints

Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19:137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 19-2  Splinting Guidelines: Positions

of Function

Splint

Position

Volar wrist splint

Neutral forearm (thumb up) with the wrist in 20 degrees of flexion Neutral forearm with the wrist in 20 degrees of extension; metacarpophalangeal joint in 50 degrees of flexion; proximal interphalangeal joint in slight flexion (e.g., 10 degrees); distal interphalangeal joint in extension Forearm neutral with the wrist in 20 degrees of extension and the thumb slightly flexed to allow for thumb–index finger opposition and alignment of the thumb and the forearm Finger in slight flexion Elbow at 90 degrees of flexion with a neutral position of the forearm and the wrist

Ulnar and radial gutter splints

A

Thumb spica splint Finger splint Sugar-tong and posterior arm splints Posterior leg splint

Ankle at 90 degrees

Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19(2):137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, WB Saunders.

B

C Long backboard

Short backboard

Board splint

Ladder splint

D FIGURE 19-13  A, Scoop stretcher. B, Stretcher placed beside the patient. C, Stretcher slid under the patient. D, Stretcher locked in place with straps secured. (Courtesy Ferno-Washington, Inc.)

Padded board

Cardboard splint

Aluminum splint

Half ring

Air splint

FIGURE 19-14  Premade Washington, Inc.)

382

cardboard

splint.

(Courtesy

Ferno-

FIGURE 19-15  A variety of splints. (From Geiderman JM, Katz D: General principles of orthopedic injuries. In Marx J, Hockberger R, Walls R, editors: Rosen’s emergency medicine: Concepts and clinical practice, ed 7, Philadelphia, 2009, Saunders. Used with permission.)

Splint

Indication

Knee immobilizer splint Posterior ankle splint

Knee injuries Distal tibia and fibula injuries; ankle, tarsal, and metatarsal fractures Ankle fractures Toe fractures Femur fractures

Stirrup splint Buddy taping Traction splint

CHAPTER 19  Splints and Slings

TABLE 19-3  Lower-Extremity Splints

Modified from Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.

nearly all extremity requirements. Other malleable splints include ladder splints (i.e., pliable metal splints) and rolled-wire splints, both of which are readily available at most outdoor sporting goods stores5 (Figure 19-34). Given their weight, size, reliability, versatility, and cost, malleable splints have become a popular choice for the universal wilderness medical kit.12

Soft Splints A soft splint earns its name from the soft, padded material that is used to secure the injury. Soft splints include sling and swathe splints, pillow splints, and blanket-roll splints7 (see Figure 19-2). Soft splints allow for more laxity than rigid splints, but they can be combined with rigid splints for extra stability. Pillow splints are soft splints that are adapted for wrist and hand injuries. Their main advantages are ease of application and comfort.6 As with other soft splints, they allow for more movement at the fracture site, but are bulkier than other splints. Sling and swathe splinting can be used alone or in combination with other forms of splints. Shoulder, clavicle, upper arm, elbow, forearm, wrist, and even hand injuries are commonly stabilized with a sling and swathe. For a shoulder injury with which it is not possible to adduct the arm, a pillow (or similar material) can be used to bridge the empty space, with the sling supporting the arm and the swathe stabilizing it.6 This technique takes advantage of the chest wall to provide the splint foundation. Distal humeral injuries necessitate a sling and swathe splint in combination with rigid splints. Sling and swathe splinting is used alone for many clavicle, shoulder, and proximal humeral injuries. Advantages are its weight, portability, and improvisational versatility. Air splints are hybrid splints that are made from inflatable yet durable plastic. These splints are most often used for the elbow, knee, and ankle (Figure 19-35). They are placed around the injured extremity and inflated to the desired pressure and rigidity.5 They have the advantages of being lightweight and portable. Variable external pressures can be used to control hemorrhage. External pressure has the potential to limit distal perfusion. Air splints should be temporarily deflated (e.g., for 5 minutes every 90 minutes) to decrease the risk for ischemic damage.7 Air splint pressure varies with altitude and temperature. For these reasons, it is important to reevaluate neurovascular status during transport.12

FIGURE 19-18  Upper and lower body vacuum splints used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department.)

A

B

“Click”

SAM Splints Malleable splints such as SAM splints37 no longer fall into the category of improvised splinting. These splints are commonly found in the standard wilderness medical kit. They are lightweight, reusable, versatile, and padded, and they are not affected by changes in pressure or temperature. They are also radiolucent to allow radiographs to be taken with the splint in place. The malleable SAM splint is pliable in its native form yet easily strengthened with creasing. The basic SAM splint adaptations are depicted in Figure 19-22. In addition, the SAM splint can be

C FIGURE 19-19  Application of the SAM pelvic sling. A, Remove all objects from the pockets. Place the sling under the patient’s hips.  B, Place the black strap through the buckle, and pull it completely through. C, Hold the orange strap with one hand, and then pull the black strap in the opposite direction under tension until a click is heard. Maintain tension, and place the black strap against the sling surface to secure. (Courtesy SAM Medical Products.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

D

C

E

FIGURE 19-20  The Slishman femur traction splint. A, Apply the ankle strap. B, Apply the groin strap. C, Extend the middle pole from the outer side of the leg, and lock it in place for coarse adjustment. D, Pull the cord to apply traction. E, Lock the splint in place. F, Splint the injured extremity. (Courtesy Sam Slishman, MD.)

F

A

A

B

B

C FIGURE 19-22  Basic SAM splint adaptations. A, C-curve. B, Reverse C-curve. C, T-curve (maximum strength). (Courtesy SAM Medical Products.)

FIGURE 19-23  Shoulder splint. A, Fold a 36-inch splint into three equal sections. Fold the outer sections along the longitudinal axis, and leave the middle section flat. Hook the outer ends together to make a triangle splint. B, Place the triangle splint under the patient’s axilla to support the abducted arm. The splint can then be held in place by the patient or secured with wrap. (Courtesy SAM Medical Products.)

SAM

SPLINT

®

CHAPTER 19  Splints and Slings

A

B

D

C

E

FIGURE 19-24  Humeral shaft splint. A, Fold one-third of a 36-inch splint on itself. B, Curve the double-layer portion into a fishhook shape, and secure it with tape or wrap. C, Form a C-curve along the shank of the fishhook to create strength, and then mold it to the arm. D, Apply the splint to the arm. Fold any excess splint back on itself. E, Secure the splint with wrap, and apply a sling and swath splint for additional support. (Courtesy SAM Medical Products.)

B

A

D

E

C

F

G FIGURE 19-25  Dislocated elbow splint. A. Use the unaffected arm as a model, and extend a 36-inch splint from under the patient’s armpit to the knuckles. B, Fold under the portion of the splint that extends past the knuckles. C, Form a C-curve along the entire length of splint. D, Use your own arm as a template, and shape the splint. E, You may reverse the C-curve bends on the edges for more strength. F and G, Apply and secure the splint to the patient with wrap or tape. (Courtesy SAM Medical Products.)

385

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

D

B

E

C

F

G

FIGURE 19-26  Sugar-tong splint. A, Fold a 36-inch splint in one-half. B, To determine the proper length, fold the splint around the patient’s elbow to the knuckles. C, Form a C-curve in each one-half of the splint, but no more than two thirds down each one-half. D, Shape the splint to fit, using your own arm as a template. E, Pad any bony prominences around the wrist and elbow. F and G, Fit and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

molded to form an adequate C-spine collar (see Figures 19-7 and 19-8, online).

lie in less effectiveness compared with commercial splinting devices.12

Improvised Extremity Splints

Pelvic Splinting

Improvised splints can be made from branches, boards, padded pack straps, or rolled-up newspapers or magazines. Anatomic splints involve an uninjured neighboring body part, primarily a digit. Slings can also be made from unused clothes.5 In these cases, one need not pack additional materials. Disadvantages

Pelvic fractures are potentially life-threatening injuries.24 Splinting is essential for pain and hemorrhage control. Pelvic fractures are often difficult to diagnose in the field, but must be suspected with a high-force mechanism in the face of pelvic pain or altered sensorium. A pelvic compression device should be applied.12

A

B

C

D

E

F

G FIGURE 19-27  Volar wrist splint. A. Roll the end of a 9-inch splint for children or an 18-inch splint for adults over to provide comfort for the patient’s fingers. B, Apply a C-curve. C, Mold the splint into a position of function, using your own wrist as a template. D, Create a generous curve for the base of the thumb. E, Fold up the ulnar side for additional strength. F and G, Apply and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

386

B

C

D FIGURE 19-28  Ulnar gutter splint. A, Fold a 9-inch splint longitudinally. B, Mold the splint into a desired shape, using the ulnar aspect of your own wrist and hand as a template. C, Apply the splint to the patient. D, Make fine adjustments to the splint, and secure it with wrap or tape. (Courtesy SAM Medical Products.)

A

B

D

C

E

FIGURE 19-29  Thumb spica splint. A, Use a 9-inch splint. B, Use your hand and thumb to mold the splint to create a generous curve for the thumb. C, Add a reverse C-curve to strengthen the splint. D and E, Apply and secure splint with tape or wrap. (Courtesy SAM Medical Products.)

387

CHAPTER 19  Splints and Slings

A

Appropriate stabilization with such a splinting device slows hemorrhaging and stabilizes fracture fragments.6 “Open-book” fractures (i.e., diastasis of the pubic rami with posterior pelvic disruption) create a large surface area for potential hemorrhage. Circumferential compression of the pelvis is recommended for emergency stabilization.4 This can be accomplished by pelvic circumferential compression devices, a pneumatic antishock garment (PASG), or improvised techniques such as pelvic sheeting7 (see Figure 19-16, online). Optimal pelvic stabilization is achieved by applying a sling around both greater trochanters and the symphysis pubis.4 Pelvic circumferential devices are similar in function (see Figure 19-19). A pelvic compression device can be improvised in the wilderness. Sheets, jackets, and other long fabrics are readily available on most expeditions. The sheet or fabric is wrapped around the pelvis over the greater trochanters and the symphysis pubis and then pulled tight and secured to increase pressure at the wound and to decrease the potential space for hemorrhage. The PASG and the military antishock trouser, which were commonly used in the past, have generally fallen out of favor (Figure 19-36). Proponents of PASG and military antishock trouser use point to the position paper of the National Association of EMS Physicians for support. The paper states that the PASG is beneficial in the setting of a ruptured abdominal aortic aneurysm and that it is potentially beneficial in many other scenarios (e.g., hypotension from pelvic fractures, gynecologic bleeding, ruptured ectopic pregnancies, severe traumatic hypotension, and uncontrolled lower extremity hemorrhage).11 Postulated successful mechanisms for correcting hypotension include increasing peripheral vascular resistance, tamponade of local hemorrhage, and increasing blood return from the lower extremities.23 PASG disadvantages include prolonged scene time, pressure changes with altitude (e.g., potential compartment syndrome with air travel), and interference with normal pulmonary function.27 In addition, animal studies have demonstrated lactic acidosis after prolonged use. Rapid deflation may cause hypotension as a result of volume redistribution. Studies have not shown improvement in hospital duration, and others have actually shown increased mortality rates.9 PASGs are bulky and expensive. Absolute contraindications for PASG use include diaphragmatic rupture, penetrating thoracic injury, a splinted lower-extremity fracture, a gravid uterus, or abdominal evisceration.23 Thus the routine use of the PASG in the field is not recommended. In the case of isolated femur fracture, a PASG can be used, but other viable options are more readily available in the wilderness.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

FIGURE 19-30  Finger splint. A, Form a C-curve B, Place the affected finger into the curved splint, and then squeeze the tip to make a fingertip guard. C, Secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

Hip and Femur Splinting Femur fractures result from high-force trauma. These fractures can be diagnosed clinically in the appropriate wilderness setting. Deformity, swelling, and tenderness along the thigh and in the face of significant trauma are highly suggestive of a femur fracture.15 Femur fractures produce significant hemorrhage; a closed femur fracture may bleed more than 1 L into the thigh.10 Femoral shaft fractures also have a high mortality rate that ranges from 20% to 54%.25 Traction splints minimize blood loss, pain, and other adverse sequelae while achieving realignment of bone fragments.6 Contraindications to traction splint placement are fractures that involve the knee, pelvis, or ankle, or that include damage

A

B

to the sciatic nerve.25 Unfortunately, such comorbidities are common with severe wilderness injuries, which makes it impossible or dangerous to anchor the traction splint.3 Controversy exists regarding whether a traction splint should be placed with an open femur fracture, but this is not a strict contraindication. An indication for traction splint placement is any suspected femur fracture in the nonambulatory patient.6 There are many femur traction splint devices, and all are based on the same principle: a rigid frame that anchors at the proximal pelvis and that extends traction beyond the distal heel. The proximal aspect is padded against the ischial tuberosity. Traction to the fractured femur is then applied with a heel strap that is anchored off of the distal frame. The thigh, knee, and leg are also secured with soft straps.12 Traction devices that have a halfring design (e.g., Thomas or Hare splints) can cause hip flexion (i.e., up to 30 degrees). This can cause incomplete fracture realignment unless the leg is elevated to match the angle.6 Traction splints that do not have a posterior half ring (e.g., Sager) do not compress the sciatic nerve and can be used with groin injuries. They can also be used for patients with pelvic fractures or for bilateral femur fractures by making use of two splints (i.e., one applied to each leg).31 Traction splint application is not always intuitive (Figures 19-20, 19-21, 19-37, and 19-38; Figure 19-21, online). Two rescuers are needed for proper placement.5 Manual traction should be applied to reduce the fracture until the splint can be placed.1 As with any splint placement, it is important to establish pain control, to check neurovascular status both before and after splint placement, and to fully explain the process to the conscious patient. After the proximal femur splint is in place, the thigh strap is fastened. The ankle harness is then placed just above the malleoli and attached to the distal splint. Traction (6.8 kg [15 lbs]) is applied, and the remaining straps are applied. After the traction splint is in place, the patient should be logrolled onto a backboard to minimize fracture fragment movement.5 Traction splint complications result from improper strap and splint placement and include sciatic or peroneal nerve injury, pressure wounds, hemorrhage and pain.7,12,25,31

Ankle Splinting C

D FIGURE 19-31  Thomas half-ring femur splint. A, The foot support is made by cutting an 8-inch section from the ski pole. Drill or puncture two holes that are 15 cm (6 inches) apart, with the entry hole being larger. Use duct tape, cord, and safety pins to secure. Create a half-ring support by placing two ski poles, handle facing handle, on the outer thirds of a 36-inch SAM splint. B, Roll the splint tightly around each handle, and secure with duct tape. Bend the splint so that the poles are now parallel and facing down. Firmly fit the pole ends through the foot support. C, Duct tape the thigh and calf supports, and reinforce them with cloth and elastic straps. An improvised ankle strap is required for traction. (Courtesy SAM Medical Products.)

388

Ankle sprains are common orthopedic injuries incurred during expeditions and the most common sprain.2 There are literally hundreds of examples of readily available over-the-counter ankle supports, braces, and splints. These include but are not limited to leather bracing, canvas bracing, air stirrups, air bladders, air casts and air boots, plastic splints with Velcro strapping, and malleable varieties, including wire ladder splints. On the basis of the high incidence of ankle sprains, it appears prudent to have a readily available lightweight ankle splint in one’s medical kit. The goal is to offer ankle support that will fit within the size constraints of the patient’s hiking boot. The time-tested alternative is athletic tape. The taped sprained ankle has talofibular ligament support (for a limited duration), and tape does not add significant weight to the medical kit. All wilderness health care providers should be adept at taping ankles.

Shoulder Dislocation Anterior shoulder dislocation is a common injury. The arm is most comfortable in an abducted position. This can be accomplished with a rolled blanket, a pillow, a jacket, or a SAM splint that has been fashioned into a triangle (Figure 19-23).

CHAPTER 19  Splints and Slings

SAM

SPLINT

NT

SA ® M LI

B

SP

SAM®

SPLIN T

SAM®

SPLIN T

A

C SAM

SAM

SAM

SA

M®

D

E F

G

FIGURE 19-32  Knee immobilizer splint. A, Fold a 36-inch splint in the center to create two equal lengths. Fan the halves so that the splint is twice as wide at one end as compared with the other. B, Apply tape to the top and middle of the splint to keep the fan shape. C, Create a second fan-shaped splint. D, Form a C-curve in each splint. E, The C-curves should appear as shown. F, Place the splints on each side of the knee. G, Secure the splint with tape. (Courtesy SAM Medical Products.)

Humeral Shaft Injury

Thumb Injuries

Humeral shaft fracture is often treated with a sling or with a sling and swathe splint alone. For pain control, a splint is often desirable (see Figure 19-24).

A thumb spica splint is used for suspected scaphoid (navicular) fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries (see Figure 19-29).

Elbow Dislocation

Finger Injuries

A dislocated elbow can be reduced in the field with the appropriate analgesia and experience. The dislocated elbow can also be splinted in place and the patient transported for definitive care (see Figure 19-25).

Finger splints are used for finger fractures, fingertip injuries, and lacerations (see Figure 19-30).

Elbow Fracture A sugar-tong splint is useful for most elbow injuries. These most commonly include supracondylar, olecranon, and radial head fractures (see Figure 19-26).

A femur traction splint can be improvised in a variety of ways with a SAM splint. One practical wilderness example involves the use of ski poles and a SAM splint. An improvised version of a half-ring splint is made from two ski poles, a small piece of metal, and a 91.4-cm (36-inch) SAM splint (see Figure 19-31).

Wrist Fracture

Knee Injuries

The volar wrist splint is used for most wrist fractures, dislocations, sprains, lacerations, and other wrist injuries. A T-beam volar wrist splint (i.e., apply a T-curve to the folded SAM splint) can be used for greater support, when traveling over rough terrain, or when more support is desired (see Figure 19-27).

A knee immobilizer splint is used for knee injuries, patella tendon injuries, dislocations, and other severe ligamentous sprains when immobilization is required (see Figure 19-32).

Metatarsal Fractures

Long-leg splints are used for tibial and fibular fractures. Depending on the amount of stabilization needed, a single or double long-leg splint can be applied. The double long-leg splint offers more stabilization (see Figure 19-33).

Ulnar gutter splints are used for fourth and fifth metatarsal injuries and for corresponding digit injuries (see Figure 19-28).

Femur Fracture

Leg Fractures

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

B

A

SAM®

SPLINT

C

D

E

F

FIGURE 19-33  Single long-leg splint. A, Place padding around any bony prominences on both sides of the ankle. B, Make a C-curve out of 30 of the splint’s 36 inches, and leave the last 6 inches flat. C, Apply a reverse C-curve to the edges for extra strength. D, Place the splint against the outside of the leg, and fold the last 6 inches under the foot. E, Adjust the splint to fit the leg. F, Secure the splint with wrap or tape. (A double long-leg splint is made by repeating steps B to F so that the splints are on both sides of the leg.) (Courtesy SAM Medical Products.)

FIGURE 19-34  Pliable metal ladder splints. (Courtesy FernoWashington, Inc.)

FIGURE 19-36  Military antishock trouser/pneumatic garment. (Courtesy Common Cents EMS Supply.)

FIGURE 19-35  Lower-extremity air splint used for a wilderness rescue. (Courtesy Ed Gray.)

390

antishock

A

C

B

F

E

D

FIGURE 19-38  Applying the Sager traction splint. A, Position the splint between the patient’s legs, and rest the splint cushion against the ischial tuberosity. B, Fold down the number of comfort cushions needed to engage the ankle above the medial and lateral malleoli. C, Use the ankle straps to secure the splint snugly. D, Pull the control tabs to tightly engage the ankle harness against the crossbar. Grab the padded shaft of the splint with one hand and the traction handle with other, and then gently extend the inner shaft to obtain the desired traction. E, Adjust the thigh strap at the upper thigh securely. F, Firmly secure the elastic leg cravats. G, Apply the foot strap around the feet to prevent rotation. Check the patient for sensation and pulses. (Courtesy Minto Research and Development, Inc.)

CHAPTER 19  Splints and Slings

FIGURE 19-37  Ferno traction splint. A, Adjust the length of the splint to fit the patient. Use the patient’s uninjured leg to determine the desired length. B, One operator supports the injured leg and places the ankle wrap under the ankle. C, Center the foot, wrap the strap around the ankle, and secure it with the fastening strip. D, Support the leg, slide the splint under the injured leg until the pad rests against the lower pelvic bone, and then fasten the hip strap. E, Attach the S-hook to the D-ring, and apply traction. F, Reposition the splint, and then fasten the straps. (From Ferno-Washington Inc. Used with permission.)

B A

C

E

D

F

G 391

A

B

D

C

E

FIGURE 19-39  Ankle stirrup splint. A, Pad any bony prominences. B, Fold a 36-inch splint in half. C, Apply C-curves two thirds of the way down each half. Add reverse C-curves for strength. D, Fold the stirrup splint around the foot and ankle. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)

A

B

C

D

E

FIGURE 19-40  Figure-8 splint. A, Pad any bony prominences. B, Lay a 36-inch splint flat. Put the patient’s foot in middle, with the splint just in front of the heel. C, Conform one side of the splint around the ankle. D, Repeat with the other side of the splint around the opposite side of the ankle. Crimp to fit. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)

Ankle and Foot Injuries Ankle stirrup and figure-8 splints provide for the immobilization of ankle injuries. The ankle stirrup splint can also be used for fractures (Figures 19-39 and 19-40). The combination of an ankle stirrup splint and a figure-8 splint offers maximal support; this is done by first applying the figure-8 splint and then adding the ankle

stirrup splint last. The combination of the two splints provides greater stabilization and immobilization. This procedure could potentially be used for weight-bearing metatarsal fractures.30

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 20 

Emergency Airway Management SWAMINATHA V. MAHADEVAN Emergency airway management encompasses assessment, establishment, and protection of the airway in combination with effective oxygenation and ventilation. Timely and effective airway management can literally mean the difference between life and death, and it takes precedence over all other clinical considerations. Airway management in the wilderness must often be provided in austere or unusual environments under less-than-ideal circumstances. Many of the resources that are readily accessible in a hospital or emergency department setting are not available in the wilderness, so improvisation may prove invaluable. 392

Airway Anatomy Internally, the airway is composed of many structures and welldefined spaces. It originates in the nasal and oral cavities (Figure 20-1). The nasal cavity extends from the nostrils to the posterior nares or choanae. Because resistance to airflow through the nose is almost twice that of the mouth, patients who require high flow rates (e.g., during exercise) often breathe through their mouths. The nasopharynx extends from the end of the nasal cavity to the level of the soft palate. Tonsillar lymphoid structures are the primary impediments to airflow through the nasopharynx. The

For online-only figures, please go to www.expertconsult.com

Nasopharynx

Hyoid bone Thyroid membrane Thyroid notch Laryngeal prominence Thyroid cartilage Cricothyroid membrane Cricoid cartilage Tracheal rings

Oral cavity

Oropharynx Epiglottis

Thyroid gland

Vallecula Laryngeal inlet Laryngopharynx

Larynx Glottis

FIGURE 20-1  Lateral airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

oral cavity is bounded by the teeth anteriorly, hard and soft palates above, and the tongue below. The oropharynx, which communicates with the oral cavity and the nasopharynx, extends from the soft palate to the tip of the epiglottis. The tongue is the principal source of obstruction in the oropharynx. The oropharynx continues as the laryngopharynx (hypopharynx), which extends from the epiglottis to the upper border of the cricoid cartilage at the level of the C6 vertebral body. The larynx, which lies between the laryngopharynx and trachea, serves as an organ of phonation and a valve to protect the lower airway from aspiration. The larynx is made up of muscles, ligaments, and cartilages, including the thyroid, cricoid, arytenoids, corniculates, and epiglottis. The flexible epiglottis, which originates from the hyoid bone and base of the tongue, covers the glottis during swallowing and provides protection from aspiration. During laryngoscopy, the

FIGURE 20-2  External airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

epiglottis is an important landmark for airway identification and laryngoscopic positioning. The vallecula is the space at the base of the tongue that is formed posteriorly by the epiglottis and anteriorly by the anterior pharyngeal wall. The laryngeal inlet is the opening to the larynx that is bounded by the epiglottis, aryepiglottic folds, and arytenoid cartilages. The glottis is the vocal apparatus, which is made up of the true and false vocal cords and the glottic opening, which is a triangular fissure between the vocal cords and the narrowest segment of the adult larynx. Externally identifiable landmarks are also important to airway assessment and management (Figure 20-2). The mentum is the anterior aspect of the mandible that forms the tip of the chin. The hyoid bone forms the base of the floor of the mouth. The thyroid cartilage forms the laryngeal prominence (i.e., the “Adam’s apple”) and the thyroid notch. The cricoid cartilage, which lies inferior to the thyroid cartilage, forms a complete ring that provides structural support to the lower airway. The cricothyroid membrane lies between the thyroid and cricoid cartilages and serves as an important site for surgical airway management. Knowledge of the anatomic differences between adults and infants is integral to effective pediatric airway management. These important differences are summarized in Table 20-1 and Figure 20-3.

TABLE 20-1  Anatomic Airway Differences Between Children and Adults Anatomy

Clinical Significance

Large intraoral tongue that occupies a relatively large portion of the oral cavity High tracheal opening: C1 in infancy as compared with C3 or C4 at the age of 7 years and C4 or C5 in adulthood Large occiput that may cause flexion of the airway; large tongue that easily collapses against the posterior pharynx

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

Cricoid ring is the narrowest portion of the trachea as compared with the vocal cords in adults Consistent anatomic variations with age, with fewer abnormal variations related to body habitus, arthritis, or chronic disease Large tonsils and adenoids may bleed; more acute angle between the epiglottis and the laryngeal opening results in nasotracheal intubation attempt failures Small cricothyroid membrane

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

Modified from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.

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CHAPTER 20  Emergency Airway Management

Nasal cavity

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Tongue

Vocal cords

Epiglottis

Cricoid membrane Cricoid ring

Junction of chin and neck Infant

Vocal cords

Tongue

Cricoid membrane

Epiglottis

Cricoid ring Junction of chin and neck

Adult FIGURE 20-3  Anatomic airway differences between infants and adults. The anatomic differences particular to infants include the following:  (1) a higher and more anterior position for the glottic opening (note the relationship of the vocal cords to the chin–neck junction); (2) a relatively larger tongue in the infant that lies between the mouth and the glottic opening; (3) a relatively larger and more floppy epiglottis in the infant; (4) the cricoid ring is the narrowest portion of the pediatric airway; in adults, the narrowest portion is the vocal cords; (5) the position and size of the cricothyroid membrane in the infant; (6) the sharper and more difficult angle for blind nasotracheal intubation; and (7) the larger relative size of the occiput in the infant. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

Assessment of the Airway and Recognition of Airway Compromise Assessment of the airway begins with an evaluation of airway patency and respiratory function. The goal is to determine whether the airway is patent and protected and whether breathing is present and adequate. This is accomplished by inspection, auscultation, and palpation, which is commonly known as the “look, listen, and feel” approach. Visual signs of airway compromise include agitation, obtundation, and cyanosis. Blue, gray, or ashen skin—especially around the eyes, lips, and nail beds—is a worrisome finding. Significant airway compromise may manifest without cyanosis; examples include an allergic reaction with upper airway edema and vasodilation (causing flushed red skin) and unconsciousness as a result of carbon monoxide poisoning. Bradypnea, tachypnea, and irregular respirations may be signs of impending respiratory compromise. Breathing that is shallow, 394

deep, or labored may indicate respiratory insufficiency. Respiratory muscle fatigue may result in recruitment of the accessory muscles of respiration; this is clinically manifested as suprasternal, supraclavicular, or intercostal retractions. Traumatic injury to the chest (e.g., flail chest) or an aspirated foreign body may result in paradoxic or discordant chest wall movement. In children, visual signs of airway compromise and respiratory distress include tachypnea, cyanosis, drooling, nasal flaring, and intercostal retractions. A child with severe upper airway obstruction may sit upright with the head tilted back (i.e., “sniffing” position) to straighten the airway and reduce occlusion. A child with severe lower airway obstruction may sit up and lean forward on outstretched arms (i.e., “tripod” position) to augment accessory muscle function. Under most circumstances, hearing the victim speak with a normal voice suggests that the airway is adequate at that moment. Unusual sounds or noisy respirations may be present with partial airway obstruction. Snoring indicates partial airway obstruction at the pharyngeal level; gurgling may be heard with blood or secretions in the airway; stridor may be associated with partial airway obstruction at the level of the larynx (inspiratory stridor) or at the level of the trachea (expiratory stridor); hoarseness suggests a laryngeal process. The central face and mandible should be assessed for structural integrity, because injuries to these structures may lead to airway distortion and compromise. The anterior neck should be carefully inspected for penetrating wounds, asymmetry, or swelling that may herald impending airway compromise. The palpation of subcutaneous air suggests direct airway injury. In the unconscious victim, feel for air movement at the mouth and nose. Open the mouth to inspect the upper airway, taking care not to extend or rotate the neck. Identify and remove any vomitus, blood, or other foreign bodies. Look for swelling, bleeding, or other abnormalities of the oropharynx. The gentle use of a tongue blade may facilitate this task. The victim’s ability to spontaneously swallow and handle secretions is an important indicator of intact airway protective mechanisms. In the unconscious victim, absence of a gag reflex has traditionally been linked with loss of protective airway reflexes. Auscultation of the lung fields should demonstrate clear and equal breath sounds. Diminished breath sounds may result from a pneumothorax, hemothorax, or pleural effusion. Wheezing and dyspnea are often associated with lower airway obstruction.

Opening the Airway Opening the airway and ensuring airway patency are essential for adequate oxygenation and ventilation; these are the first priorities of airway management. The conscious victim uses protective reflexes and the musculature of the upper airway to maintain a patent airway and to protect against aspiration of foreign substances, gastric contents, or secretions. In the severely ill, compromised, or unconscious victim, these protective airway mechanisms may be impaired or absent. Upper airway obstruction in the unconscious victim most commonly results from posterior displacement of the tongue and the epiglottis at the level of the pharynx and the larynx. Head positioning, manual airway techniques, and mechanical airway adjuncts may be employed to alleviate upper airway obstruction.

HEAD POSITIONING If the mechanism of injury or physical examination raises concern for cervical spine injury, the head and neck should be stabilized in the neutral position. Care should be taken to not flex, extend, or rotate the victim’s head. After cervical spine immobilization, the airway should be reevaluated for obstruction. The optimal head position for airway alignment and patency varies with age. A supine infant’s large occiput contributes to flexion of the head and neck and resultant airway obstruction; this may be alleviated by elevating the shoulders with a small towel (Figure 20-4). In children, slightly extending the head into the sniffing position helps to relieve airway obstruction. In adults,

Infant

Small child

CHAPTER 20  Emergency Airway Management

A

Older child/adult

B FIGURE 20-4  A, The clinical determination of optimal airway alignment with the use of a line passing through the external auditory canal and anterior to the shoulder. B, The application of the line to determine the optimal position. In this small child, the occiput obviates the need for head support, yet the occiput is not so large as to require support of the shoulders. Note that the line traversing the external auditory canal passes anterior to the shoulders. With only slight extension of the head on the atlanto-occipital joint, the sniffing position is achieved. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

placing a folded towel or article of clothing under the occiput, which flexes the neck at the torso, followed by gentle hype­r­ extension of the head at the atlanto-occipital joint, provides for the optimal alignment of the airway axes.

MANUAL AIRWAY TECHNIQUES Manual airway techniques are effective but often require con­ tinuous involvement of a single provider to maintain airway patency.

FIGURE 20-5  Head tilt with chin lift. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

An alternative to piercing the patient’s lower lip is to pass a string through the safety pins and then secure the end of the string to the victim’s shirt button or jacket zipper (Figure 20-8), thereby exerting traction on the tongue.

MECHANICAL AIRWAY ADJUNCTS Several airway adjuncts are available to maintain airway patency while freeing up the health care provider to perform other duties. Oropharyngeal Airway The oropharyngeal airway (OPA) is an S-shaped device that is designed to hold the tongue away from the posterior pharyngeal wall (Figure 20-9). When the OPA is properly placed, it prevents the tongue from obstructing the glottis, and also provides an air

Head Tilt With Chin Lift The head tilt with chin lift (Figure 20-5) is a simple and effective technique for opening the airway. The palm of one hand is placed on the victim’s forehead and applies firm backward pressure to tilt the head back. Simultaneously, the fingers of the other hand are placed under the bony part of the chin and lifted to bring the chin forward. These fingers support the jaw and maintain the head-tilt position. This maneuver extends the neck and should not be used if cervical spine injury is a concern. Jaw Thrust With Head Tilt If a cervical spine injury is not suspected, the jaw thrust with head tilt maneuver may be used to gain additional forward displacement of the mandible. Position yourself at the top of the victim’s head, and then grasp the angles of the mandible with both hands and lift to displace the jaw forward while tilting the head back. Jaw Thrust Without Head Tilt If a cervical spine injury is suspected or cannot be excluded, the jaw thrust without head tilt (Figure 20-6) can be performed while maintaining neutral cervical spine alignment. With this maneuver, the jaw thrust is performed without extending or rotating the neck. Tongue Traction If the patient is unconscious or in extremis, the airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins (Figure 20-7).

FIGURE 20-6  Jaw thrust without head tilt. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 20-7  Tongue traction. The airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins.

channel and suction conduit through the mouth. These devices are most effective for unconscious and semiconscious victims who lack a gag reflex or cough. Use of an OPA in a victim with a gag reflex or cough is contraindicated, because the OPA may stimulate retching, vomiting, or laryngospasm. OPAs are made of disposable plastic, and come in varying sizes to accommodate children and adults. The size is based on the distance in millimeters from the flange to the distal tip. The proper OPA size is estimated by placing the OPA’s flange at the corner of the mouth so that the bite-block segment is parallel with the victim’s hard palate; the distal tip of the airway should reach the angle of the jaw. Two types of OPAs are commonly employed. The Guedel makes use of a tubular design, whereas the Berman is distinguished by having airway channels on each side. Technique for insertion: 1. Open the mouth and clear the pharynx of any secretions, blood, or vomitus. Remove dentures or partial dental plates, if present. 2. In an adult or older child, insert the OPA upside down or at a 90-degree angle to avoid pushing the tongue posteriorly during insertion. Slide it gently along the roof of the mouth. As the OPA is inserted past the uvula or the crest

FIGURE 20-8  Tongue traction. An alternative to piercing the lower lip is to pass a string through the safety pins and then exert traction on the tongue by securing the end of the string to the victim’s shirt button or jacket zipper.

396

FIGURE 20-9  Oropharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

of the tongue, rotate it so that the tip points down the victim’s throat. 3. In a child, grasp the tongue and gently pull it forward or use a tongue blade to displace it inferiorly and anteriorly. Insert the OPA with the tip pointing toward the tongue and throat (i.e., the intended position after placement). 4. The OPA flange should rest against the victim’s lips, and the distal portion should rest on the posterior pharyngeal wall. If the OPA is too short, it may displace the tongue into the hypopharynx and occlude the airway. If the OPA is too long, it may displace the epiglottis and thereby cause an airway obstruction. Nasopharyngeal Airway The nasopharyngeal airway (NPA) is an uncuffed trumpet-like tube that provides a conduit for airflow between the nares and the pharynx (Figure 20-10). The NPA is inserted through the nose rather than the mouth, and it has a flange at the outer end to prevent displacement or slippage beyond the nostril. These devices are better tolerated than are OPAs, and they are commonly used with intoxicated or semiconscious victims. They are also effective when trauma, trismus (i.e., clenched teeth), or other obstacles (e.g., wiring of the teeth) preclude OPA placement. NPAs are contraindicated in victims with basilar skull or facial fractures, because inadvertent intracranial placement may occur.

FIGURE 20-10  Nasopharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

Technique for insertion: 1. Lubricate the nasopharyngeal airway with a water-soluble lubricant to minimize resistance in the nasal cavity. Do not use petroleum jelly or a non–water-based lubricant. 2. If the NPA has a beveled (angled) edge, place the airway in the nostril with the bevel directed toward the nasal septum. 3. Gently insert the NPA straight back along the floor of the nasal passage (i.e., perpendicular to the coronal plane of the face). 4. If resistance is met, rotate the tube slightly, reattempt insertion through the other nostril, or try a smaller-diameter tube. Do not force insertion of the tube, because injury to the nasal mucosa can result in bleeding. 5. After insertion, the NPA flange should rest on the victim’s nostril, and the distal portion of the airway should rest in the posterior pharynx, behind the tongue. Any flexible tube of appropriate diameter and length can be used as an improvisational substitute for the NPA. Examples include a Foley catheter, radiator hose, solar shower hose, siphon tubing, or an inflation hose from a kayak flotation bag or sport pouch. An endotracheal tube (ETT) can be shortened and then softened in warm water to substitute for a commercial nasal trumpet. The flange can be improvised with the use of a safety pin through the nostril end of the tube (Figure 20-11). Although OPAs and NPAs help to establish artificial airways, they do not provide definitive airway protection from aspiration.

RECOVERY POSITION In the spontaneously breathing unconscious victim who is not at risk for cervical spine injury, the recovery position (Figure 20-12) allows for airway patency while reducing the risk of aspiration. In the recovery position, the tongue is less likely to fall back and occlude the airway, and vomitus is more likely to be expelled than inhaled. Even a diminutive rescuer can place a large person in the recovery position if the proper technique is employed.

Foreign-Body Airway Obstruction Foreign bodies—most commonly a piece of meat—may cause partial or complete airway obstruction. A victim with partial airway obstruction can usually phonate or produce a forceful

FIGURE 20-11  Improvised nasal trumpet.

CHAPTER 20  Emergency Airway Management

NPAs made of soft and pliable rubber or plastic come in varying sizes to accommodate children and adults. Sizes (as indicated by internal diameter) range from 12 to 36 Fr. Proper NPA length is determined by measuring the distance from the tip of the patient’s nose to the tragus of the patient’s ear.

FIGURE 20-12  Recovery position.

cough in an attempt to expel the foreign body. When encountering a victim with a partially obstructed airway, if air exchange is adequate, do not interfere with the person’s attempts to clear the airway. Encourage forceful coughing, and closely monitor the victim’s condition. If the obstruction persists or if air exchange worsens or becomes inadequate, the victim should be managed as if a complete airway obstruction exists. Worrisome findings that should prompt immediate aggressive airway management include a weak or ineffective cough, increased respiratory difficulty, decreased air movement, and cyanosis. A person with a complete airway obstruction cannot speak (aphonia), exchange air, or cough. The person will often grasp the neck (i.e., the universal distress signal for choking) and open the mouth widely. The unconscious victim with complete airway obstruction will not demonstrate any typical chest movements or other signs of adequate air exchange. Individuals with complete airway obstruction from a foreign body require immediate medical attention. Failure to rapidly relieve the obstruction can lead to cardiac arrest. A complete summary of the treatment for complete airway obstruction caused by foreign bodies in adults and children is provided in Table 20-2.

Suction All sick or injured victims are at risk for airway obstruction and pulmonary aspiration, typically of gastric contents or blood. Lifesaving interventions, such as bag-mask ventilation (BMV), may increase this risk. Suction is essential for removal of vomitus, secretions, blood, and foreign bodies that may occlude the airway or increase the risk for pulmonary aspiration. Portable suction devices, which are available from a number of manufacturers, are ideal for the wilderness setting. These portable units should provide enough vacuum flow for adequate pharyngeal suction. Portable devices may be powered by oxygen, air, or electricity, or they may be manually powered (Figure 20-13, online). Hand-operated units are popular because they are lightweight, compact, reliable, and inexpensive. All units should have large-bore, nonkinking suction tubing, an unbreakable collection container, and a sterile disposable suction catheter. Flexible (i.e., “French”) suction catheters are used to suction the nose, mouth, and oropharynx, whereas rigid suction catheters are used to suction the mouth and the oropharynx. These suction catheters should not be inserted beyond the base of the tongue. Adults should not be suctioned for more than 10 to 15 sec to prevent oxygen deprivation; children should be suctioned for less time. Care should be taken when using rigid suction catheters in children, because stimulation of the oropharynx may 397

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 20-2  Relief of Choking Adults and Children >1 Year Old

Children 40 >140 Decreased Decreased >35 Negligible Confused, lethargic Crystalloid and blood

B

C

FIGURE 21-1  A, FAST1 intraosseous infusion system. B, Bone Injection Gun (BIG). C, EZ-IO.

crystalloid, and its use has been associated with hypokalemia, pulmonary edema, and dramatic increases in serum sodium and osmolarity.6 The significance of these reported complications in trained hands is questionable, and hypertonic fluids may have a future role in resuscitation. Further study is warranted on the use of hypertonic saline, but its use in the wilderness setting is not recommended at this time. Based on the current literature, it is clear that both colloids (including hetastarches and albumin) and crystalloids are efficient volume expanders.80 Larger volumes of crystalloids than of colloids are needed to achieve similar resuscitative end points, usually in a ratio of 3 to 1. However, no benefit in survival by using colloids has been demonstrated, and recent studies indicate that their use in critically ill patients may increase mortality.18,71 In addition, no proved detriment, including increased extravascular lung water, impaired wound healing, or decreased tissue oxygen diffusion, has been demonstrated with the use of large volumes of crystalloids. Crystalloids are safe, nonantigenic, easily stored and transported, effective, and inexpensive. Most experts in trauma care agree that crystalloid is preferable to colloid infusion in the prehospital, early resuscitative phase of trauma care. Accordingly, the resuscitative fluid recommended by ATLS protocol is normal saline. In expeditions in which weight and space are considerations, colloids may have an advantage. “Colloid fluids will achieve a given increment in plasma volume with only one-quarter to onethird the volume required of crystalloid fluids.”58 To restore circulating volume, colloids provide greater efficacy per weight/ volume trekked into the austere environment. For the expeditionist carrying resuscitation fluids in a backpack, 1 lb of colloid will provide about three times the volume expansion of 1 lb of crystalloid. Several animal studies and recent human clinical trials in trauma victims have found that treatment with IV fluids before control of hemorrhage resulted in increased mortality rates.8,60 Although these data are compelling, they have been accumulated in victims with penetrating injuries and short prehospital times, and the definition of prehospital resuscitation in these studies comprised widely varying volumes. Prehospital resuscitative protocols remain in evolution. However, application of these data to the wilderness setting at the current time is dangerous, for a number of reasons. First, the leading cause of death in wilderness trauma is head injury. Many multiple-trauma victims have a head injury, and it may be impossible to discern whether an intracranial lesion is present. Although under continued study, the current approach to management of head injury is aggressive maintenance of cerebral perfusion pressure to control intracranial pressure (ICP). Underresuscitation in the context of an intracranial injury could be catastrophic. Second, the multisystem-injured victim frequently presents with associated orthopedic injuries. A victim with closed extremity fractures with significant contained hemorrhage benefits from fluid resuscitation. Third, a victim with significant external hemorrhage that can be controlled before evacuation benefits from intravascular repletion.

In summary, resuscitation with IV fluids should be initiated in the field, particularly in victims with head injury and unquantified multiple trauma. Victims should have vascular access secured and resuscitative fluids given in the form of normal saline as dictated by severity of injuries and hemodynamics. In patients in whom urinary catheterization can be performed, a target of 30 mL/hr is a good target. In those patients in whom hourly urine output cannot be determined, other measures of perfusion, such as heart rate, blood pressure, and mental status, can determine the efficacy of resuscitation.

SECONDARY SURVEY The secondary survey is an extension of the primary survey and should not be undertaken until the primary survey is complete and the victim has been stabilized. In addition, resuscitative regimens, if available, should have been initiated. The secondary survey is a head-to-toe assessment of the victim, including history and physical examination. The face, neck, chest, abdomen, pelvis, extremities, and skin should be examined in sequence. A more detailed neurologic examination should be completed, including reassessment of the GCS. The neck should be examined independently of the thoracolumbar spinal cord. Examination of the pelvis should not include the traditional “rocking” to determine stability, because in the presence of pelvic fractures, this action may exacerbate existing comminution. The detailed secondary survey should not delay evacuation packaging. As in the nonwilderness setting, it is imperative to repeat the primary survey as the victim’s condition warrants. Specific examinations are discussed in the sections covering regional injuries. History The victim’s history should be assessed during the secondary survey. Knowledge of the mechanism of injury and any comorbid medical conditions or allergies may enhance understanding the victim’s physiologic state. The ATLS “AMPLE” history is a useful and rapid mnemonic for this purpose: Allergies Medications currently used Past medical history/Pregnancy Last meal Event or Environment related to the injury Adjuncts Resuscitation should be initiated simultaneously with the primary survey. The degree of resuscitation depends on available resources, experience of the rescuer(s), and environmental conditions. Under the best circumstances, initial management of the wilderness trauma victim provides for airway control, adequate oxygenation and ventilation, appropriate fluid resuscitation, and stabilization of cardiac function while continuing to monitor and reassess the patient’s vital signs. As adjuncts to the secondary survey, it also 415

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

A

PART 4  INJURIES AND MEDICAL INTERVENTIONS

includes placement of a urinary catheter and nasogastric (NG) tube. This degree of resuscitation will be almost universally unavailable in the wilderness setting. Here, resuscitation may be limited to oral administration of warm, high-calorie fluids and maintenance of victim comfort and body temperature. An NG tube and indwelling urinary (Foley) catheter should be placed if available and appropriate. Aspiration of gastric contents can be catastrophic in terms of patient survival after trauma. Gastric decompression with an NG tube may help prevent this type of adverse event in patients with a depressed level of consciousness. It should be remembered that children can exhibit significant hemodynamic consequences secondary to massive gastric distention. In this setting, decompression becomes critical. If possible, NG tubes should be placed in persons who are endotracheally intubated in the field. The tube can be aspirated sequentially with a syringe or left open to gravity drainage. Any suspicion of facial fracture should deter attempts to place an NG tube, and orogastric decompression should be chosen instead. A Foley catheter can assist in volume assessment and hemodynamic status determination in a critically injured victim. Hourly urine output typically does not decrease until the onset of class III hemorrhagic shock, with loss of 30% to 40% of blood volume. Contraindications to urinary catheter placement in the field are blood at the urethral meatus, high-riding prostate, scrotal hematoma, and personnel not experienced in placement. Injuries to the Head, Face, and Neck The secondary survey begins with examination of the entire head and scalp for evidence of skull or facial fractures, ocular trauma, lacerations, and contusions. The scalp is thoroughly palpated for tenderness, depressions, and lacerations. The bones of the face, including the zygomatic arch, maxilla, and mandible, are palpated for fractures. Elements of the GCS are repeated. The wilderness eye is discussed in detail in Chapter 28, but general examination principles are simple. Significant periorbital edema may preclude examination of the globe, so assessment should be carried out early. The globe should be evaluated for visual acuity, pupillary size, conjunctival hemorrhage, lens dislocation, and entrapment. Persons with significant facial trauma have a high incidence of associated ocular or orbital injuries.77 Recent studies of ocular injuries in trauma victims have emphasized underappreciation by many disciplines of ocular and periocular signs indicative of significant underlying injury.73

HEAD INJURIES Approximately 500,000 to 2 million cases of head injury occur in the United States yearly.34 Of these, approximately 10% result in the patient’s prehospital death.3 Long-term disability associated with head injury is significant, with more than 100,000 persons suffering varying degrees of permanent impairment. Because of the high-risk nature of traumatic brain injury (TBI) and the impact of initial management on disability and survival, clinical management objectives must address both immediate survival and longterm outcome. Management guidelines for head injuries in a wilderness do not exist, and a wide range of clinical approaches are used in hospital settings.34 However, the literature suggests that morbidity and mortality can be reduced by means of a protocol that includes early airway control with optimization of ventilation,40 prompt cardiopulmonary resuscitation, and rapid evacuation to a trauma care facility. Initial management of head injury in the wilderness should follow established ATLS protocols. Prompt attention must then be given to victim triage, evacuation strategies, and ongoing resuscitative needs to prevent or minimize secondary brain injury. Expeditious evacuation to a neurosurgery-capable trauma center is essential. Multiple clinical and experimental studies have demonstrated the detrimental effects of hypoxia on the injured brain. A definitive airway should be established if any degree of neurologic or respiratory compromise exists. Cervical spine injuries are common in patients with TBI. Therefore cervical spine immobilization is paramount in the prevention of further devastating neurologic injury. 416

After immobilization, attention is directed to the prevention of secondary brain injury. The purpose of the wilderness head injury protocol is to allow individuals with widely varying levels of experience and expertise to identify signs of significant head injury, begin proper resuscitation in the context of prevention of secondary brain injury through airway maintenance and hemodynamic support, and evacuate appropriately. Anatomy The scalp comprises five layers of tissue that cover the calvaria: skin, connective tissue, galea aponeurotica, loose areolar tissue, and periosteum of the skull. The galea is a fibrous tissue layer with important ramifications in closure of scalp wounds, discussed later in this chapter. Loose areolar tissue beneath the galea represents the site of accumulation of blood in scalp hematomas. A rich vascular network located between the dermis and the galea supplies the scalp. When lacerated, these vessels can be a significant source of hemorrhage, which may be important if evacuation is impossible or delayed. The skull is composed of two groups of bones that form the face and cranium. Cranial bones are divided into the calvaria and skull base. The calvaria is composed of frontal, ethmoid, sphenoid, parietal, and occipital bones. Within the skull, the brain is covered by three membranous layers that may be of pathophysiologic importance after injury. However, in the wilderness environment, these layers have little clinical relevance (except in terms of defining an open versus closed brain injury). Pathophysiology of Traumatic Brain Injury TBI can be divided into primary and secondary brain injuries. Primary injury consists of the physical or mechanical insult at the moment of impact, and the immediate and permanent damage to brain tissue. Little can be done in the wilderness setting relative to primary brain injury. Secondary brain injury is the biochemical and cellular response to the initial mechanical trauma and includes physiologic derangements that may exacerbate effects of the primary trauma. Such pathophysiologic alterations include hypoxia, hypotension, and hypothermia. Compounding these pathophysiologic alterations is elevation of ICP after TBI. Increased ICP increases cerebral ischemia and exacerbates secondary brain injury. Many forms of head injury result in elevated ICP, the duration of which is significantly correlated with poor outcome. The Monro-Kellie doctrine states that the volume of intracranial contents must remain constant because the cranium is a rigid container. The normal compensatory response to increased intracranial volume is to decrease venous blood and cerebrospinal fluid (CSF) volume within the brain. If this normal response is overwhelmed, small increases in intracranial volume result in exponential increases in ICP. A rigid bony cranium cannot expand to accommodate increases in brain volume and the resultant increase in ICP. Brain parenchyma becomes compressed and eventually displaced from its anatomic location. In the most devastating circumstances, the brain parenchyma herniates toward the brainstem through the largest cranial opening (the foramen magnum) and death rapidly follows. The volume– pressure curve in Figure 21-2 relates the small, but critical, time period between neurologic symptoms, hemodynamic decompensation, and brainstem herniation. Elevation in ICP directly correlates with secondary brain injury. Therefore the field provider must attempt to minimize ICP of head-injured patients to the greatest extent possible. The most important priority in minimizing secondary brain injury in the field is optimizing cerebral perfusion pressure (CPP). CPP is related to ICP and mean arterial pressure (MAP) as follows: CPP = MAP − ICP A CPP less than 70 mm Hg after head injury correlates with increased morbidity and mortality.3,39 Cerebral blood flow (CBF) should be maintained at approximately 50 mL/100 g brain tissue per minute.57 At 5 mL/100 g per minute, irreversible damage and potential cell death occur.3 Study data have shown a correlation between low CBF and poor outcome.57 At a MAP between 50 and 160 mm Hg, cerebral autoregulation maintains CBF at relatively constant levels. Not only is autoregulation disturbed in

Herniation

60 55 50 ICP (mm Hg)

45 40 35 30 25 20 15 10 5

Point of hemodynamic decompensation Volume of mass

FIGURE 21-2  Critical time period between decompensation and brainstem herniation after traumatic brain injury.

injured regions of the brain, but a precipitous fall in MAP can further impair autoregulatory function, decreasing CBF and exacerbating ischemia-induced secondary injury. The field provider is able to combat a rise in ICP by simply optimizing MAP through aggressive IV fluid resuscitation. Diagnosis The three useful descriptions of head injury that may be applied to field recognition are history, severity, and morphology. History includes mechanism of injury, timing of the event, and related circumstances. This knowledge assists in the decision-making process with regard to resuscitation and evacuation.3 Mechanism of injury is identified as blunt or penetrating trauma. The anatomic demarcation between blunt and penetrating injury is traditionally defined by violation of the outer covering of the brain (dura mater). Blunt injuries in the wilderness setting most often result from falls, falling objects, or assaults. Penetrating injuries are most commonly gunshot or other projectile wounds. Severity of injury can be estimated by quantifying the GCS and pupillary response. The generally accepted definition of coma is a GCS score less than or equal to 8; these patients often require endotracheal intubation. Although GCS score does not directly correlate with the need for intubation, it is essential that all head-injured patients be provided a stable, secure airway by the most appropriate means available. It is important to note the TBI victim’s best initial motor response because this is most predictive of long-term neurologic outcome. Any victim with a GCS score less than 15 who has sustained a head injury should be evacuated if possible. A low or declining GCS score suggests increasing ICP. Abnormal pupil size or asymmetric pupillary responses suggest increased ICP. These clinical deteriorations demand the rapid attention of rescue or evacuation personnel to optimize MAP and CPP, minimize secondary brain injury, and prevent brainstem herniation. Injury morphology may be difficult to assess in the wilderness setting and relies on level of suspicion and clinical signs and symptoms. After attention to the primary survey, including airway provision and spinal immobilization, the physical examination component of the secondary survey is imperative and can provide information about the presence of a TBI. Injury Classification Intracranial injuries range from concussion to massive subdural hematoma. Subdural hematomas are more common than are epidural hematomas, constituting 20% to 30% of mass lesions. “Subdurals” result from torn bridging veins between the cerebral cortex and draining venous sinuses. Their prognosis is worse than that of “epidurals,” although prompt recognition and drainage improve patient outcome. Epidural hematomas are most commonly located in the temporal region and result from injury to the middle meningeal artery, often associated with a fracture.

These patients may present with loss of consciousness, followed by a lucid interval and subsequent rapid neurologic deterioration. This sequence, however, is not frequently observed. Hemorrhagic contusion is also quite frequent, constituting 35% of traumatic injuries, and has the propensity to significantly increase ICP. Diffuse axonal injury (DAI) is the term used to describe prolonged post-traumatic coma not resulting from a mass lesion or ischemic insult. Similar to hemorrhagic contusion, diffuse axonal injury may result in elevated ICP. Physical Examination After the primary survey and initial attempts to resuscitate the victim, a more complete physical examination should be done. However, this examination should not delay patient evacuation. A hallmark of TBI is altered level of consciousness. Determination of the GCS score aids in recognition of TBI and should be regularly reassessed to provide a mechanism for quantifying neurologic deterioration. Physical signs that may denote underlying brain injury include significant scalp lacerations or hematomas, contusions, facial trauma, and signs of skull fracture. Findings specific for basilar skull fracture include ecchymosis behind the ears (Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood behind the tympanic membrane on otoscopic examination (hemotympanum), frank bleeding from the ears, and CSF rhinorrhea/otorrhea also suggest skull fracture and underlying TBI. The pupillary examination may provide valuable data in assessing underlying TBI. Herniation of the temporal lobe of the brain may be heralded by mild dilation of the ipsilateral pupil with sluggish response to light. Further dilation of the pupil followed by ptosis (drooping of the upper eyelid below its normal level), or paresis of the medial rectus or other ocular muscle, may indicate third cranial nerve compression by a mass lesion or herniation. Table 21-2 relates pupillary examinations to possible underlying brain lesions. Most dilated pupils (mydriasis) are on the ipsilateral side to the mass lesion. With direct globe injury, traumatic mydriasis may result, making evaluation of TBI more difficult. In addition, 5% to 10% of the population has congenital anisocoria (a normal difference in pupillary size between the eyes). Casual inspection may overlook a prosthetic eye, which is mistaken for a fixed pupil. Neither direct trauma nor congenital anisocoria should be assumed in a head-injured victim exhibiting mental status change in the wilderness. After quantification of GCS score, pupillary examination, and examination of the head and face for signs of external trauma, a concise neurologic examination should be performed. The goal of the field neurologic examination is to identify motor or sensory focal deficits suggestive of intracranial injury. Sensory deficits follow the general dermatome patterns shown in Figure 21-3. Unilateral hemiplegia may signify uncal herniation resulting from mass effect in the contralateral cortex because of compression of the corticospinal tract in the midbrain. Ipsilateral pupillary dilation associated with contralateral hemiplegia is a classic and ominous sign of tentorial herniation. Deep tendon reflex changes in the absence of altered mental status are not indicative of TBI. TABLE 21-2  Interpretation of Pupillary Findings in

Head-Injured Victims

Pupil Size

Light Response

Interpretation

Unilaterally dilated

Sluggish or fixed

Bilaterally dilated

Sluggish or fixed

Unilaterally dilated or equal Bilaterally constricted

Cross-reactive (Marcus Gunn) Difficult to determine; pontine lesion Preserved

Third nerve compression secondary to tentorial herniation Inadequate brain perfusion; bilateral third nerve palsy Optic nerve injury

Bilaterally constricted

Opiates Injured sympathetic pathway

417

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

VOLUME-PRESSURE CURVE

PART 4  INJURIES AND MEDICAL INTERVENTIONS

C2 C2 C3 C4 C5 T1 T2 T3 T4 T5

C6

Posterior cervical rami Posterior thoracic rami Supraclavicular (C3,4) Axillary (C5,6) Medial brachial cutaneous (C8–T1) Radial (C5,8) Anterior thoracic rami Lateral thoracic rami

T6 T7 T8 T9 T10 T11 T12 L1 L2 L3

L4

Musculocutaneous (C5,6) Medial antebrachial cutaneous (C8, T1) Iliohypogastric (L1) Posterior sacral rami Radial (C6–8) Ulnar (C8,T1)

S2 Ilioinguinal (L1)

Median (C5–8)

Lateral femoral cutaneous (L2,3) Obturator (L2,3,4) Anterior femoral cutaneous (L2,3)

C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3

L3 Posterior lumbar rami

S2 L1 L2

Posterior femoral cutaneous (S1,2,3)

L5

Common peroneal (L4,5,S1) Saphenous (L3,4)

S1 Superficial peroneal (L4,5,S1)

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

Dermatomes–anterior

CUTANEOUS NERVES

Dermatomes–posterior

FIGURE 21-3  Dermatome pattern, showing the skin area stimulated by spinal cord elements. Sensory deficits follow general dermatome patterns.

Detailed evaluation of brainstem function cannot be undertaken in the wilderness setting. Performance of gag and corneal reflex evaluations may provide some information helpful in triage and evacuation planning, but their presence would not automatically obviate the need for prompt evacuation. Resuscitation Resources and circumstances permitting, resuscitation should be initiated as an adjunct to the primary survey. The primary focus for the head-injured victim, similar to any traumatized victim, is the airway. During the primary survey and performance of the ABCDE sequence, IV access should be established. If IV resuscitation is impossible, it is not advisable to administer fluids orally to the victim with head injury because of the likelihood of vomiting, airway compromise, and aspiration. Individuals sustaining head trauma have a high incidence of concomitant injuries. Up to 32% of persons with severe head injury have a long bone or pelvic fracture, 20% to 25% a chest injury, and 10% an abdominal injury. A victim who does not have a palpable femoral pulse or presents with other signs of hypotension in the context of suspected head injury must not be assumed to have a neurogenic etiology of shock, so other etiologies must be thoroughly and aggressively investigated. Resuscitation is critical in the setting of head injury for multiple reasons. Management of a head injury should be secondary to other life-threatening injuries, which, if not addressed, may preclude survival. As previously discussed, maintenance of MAP (and thus CPP) is critical in preventing secondary brain injury. The type of resuscitative fluid administered to trauma victims continues to be controversial. Previously, recommendations warning of the dangers of overhydration in head injury led to 418

recommendations restricting fluids. Restriction of fluid has not been shown to reduce ICP or edema formation in laboratory models of TBI. Theories about limiting cortical free water content in TBI by using hypotonic IV solutions have not been borne out in animal studies.88 The need for resuscitation and intravascular volume support has been well established. Possible resuscitative fluids include isotonic crystalloids, hypertonic crystalloids, or colloid solutions. There is convincing evidence that hypotonic fluids are not appropriate in TBI secondary to an increase in whole-brain water content and subsequent elevation in ICP. Recent data from animal studies of TBI suggest that colloid solutions offer no advantage over isotonic crystalloids, such as lactated Ringer’s solution, in terms of augmenting CBF or preventing cerebral edema.97 As previously noted, no prospective trial has clearly documented an advantage of colloid over crystalloid administration in the victim with multiple systemic injuries. Evidence is accumulating that hypertonic solutions, particularly hypertonic saline, may be beneficial in TBI.90,94 However, an advantage has not been demonstrated in trauma victims overall, and expertise is necessary for their use. The recommended resuscitative fluid for the head-injured victim in the wilderness setting is isotonic crystalloid, with a target MAP of 85 to 95 mm Hg based on cuff blood pressure determinations or extrapolation from distal pulses evaluation. Further Management Numerous adjuncts exist in the management of the head-injured victim, few of which are applicable in the wilderness setting. Once the primary and secondary surveys are complete, the airway is secured, resuscitation has been initiated, and spine immobilization has been achieved, the victim should be placed

Skull Fracture Skull fracture in the wilderness mandates evacuation. Therapeutic options in the field are few, with intervention limited to identifying the injury and arranging rapid transport. Skull fractures may be open or closed, linear or stellate, and may occur in the vault or skull base. These fractures are associated with a high incidence of underlying intracranial injury. Skull fractures with depression greater than the thickness of the skull may require elevation. No attempt at elevation should be made in the field. Any exposed brain surface should quickly be covered with the most sterile covering available, preferably moistened with crystalloid solution. Loose bone or brain fragments should not be manipulated. If a broad-spectrum antibiotic is available, it should be administered. After attention to the wound and stabilization of associated injuries, the victim should be rapidly evacuated. Penetrating Head Injuries The majority of penetrating head injuries in the wilderness are gunshot wounds, although knives and arrows may penetrate the cranium. Such penetrating injuries are usually catastrophic. However, examples of survival exist with small-caliber, lowvelocity injuries and tangential wounds.59 As with closed head injury, management priorities consist of maintenance of airway, prevention of secondary brain injury, and rapid evacuation. If the cranium has been violated, the victim should receive antibiotics and tetanus immunization in the same manner as for open skull fracture. In the rare instance that the projectile is embedded

in the skull, no attempt at removal should be undertaken. If the length of the projectile makes immobilization or transport cumbersome, excess length may be removed, but only if this can be done without displacement of the intracranial segment. Evacuation Survival and outcome of head injury in the wilderness correlate directly with rapidity of evacuation. Certain situations dictate immediate evacuation. Any person with evidence of an open or closed skull fracture should be evacuated. The incidence of TBI associated with skull fracture is variable but significant throughout the literature. Recent data predict that 30% to 90% of persons with raccoon eyes or Battle’s sign will show abnormalities on computed tomography (CT) scan.11,17 Similarly, any person who sustains a penetrating injury should be evacuated. Decisions concerning evacuation of victims who have sustained closed head injuries can be simplified by dividing the victims into three groups based on probability of injury. A high-risk group, defined as patients with a GCS score of 13 or less, focal neurologic signs, or evidence of decreasing level of consciousness, requires evacuation. The low-risk group includes persons who have suffered a blow to the head but are asymptomatic, did not lose consciousness, and complain only of mild headache or dizziness. Data from recent studies suggest that persons who meet low-risk criteria (including a GCS of 15, no loss of consciousness, minimal symptomatology, and unlikely mechanism) have a minimal chance of having significant TBI and may be closely observed.11,17 This group includes patients who have suffered a concussion. The Quality Standards Subcommittee of the American Academy of Neurology78 defines concussion as a trauma-induced alteration in mental status that may or may not involve the loss of consciousness. The neurologic impairment is short-lived and resolves spontaneously without any structural injury to the brain. Close observation includes awakening the patient from sleep every 2 hours and avoidance of strenuous activity for at least 24 hours. The following signs indicate more advanced medical care is necessary: (1) inability to awaken the patient; (2) severe or worsening headaches; (3) somnolence or confusion; (4) restlessness, unsteadiness, or seizures; (5) difficulties with vision; (6) vomiting, fever, or stiff neck; (7) urinary or bowel incontinence; and (8) weakness or numbness involving any part of the body.51 No prospective validated guidelines for return to activity have been established. Generally, one should not return to an environment in which concussion is a risk (e.g., contact sports) until symptoms have been absent for 7 days. Patients with a predisposition to bleeding need a much more aggressive approach requiring evacuation and evaluation at a higher level of care. The group for which the evacuation decision is most difficult is the moderate-risk group. These persons have a history of brief loss of consciousness or change in consciousness at the time of injury, or a history of progressive headache, vomiting, or posttraumatic amnesia. If any of these signs is present in the face of concurrent systemic injury, the victim should be evacuated immediately. Studies associating clinical variables and abnormal results on CT scan have demonstrated the significance of decreased GCS score, symptoms, and loss of consciousness. If these signs are present in isolation and the evacuation can be completed in less than 12 hours, the evacuation should proceed. If the evacuation is impossible or will require longer than 12 hours, the victim should be closely observed for 4 to 6 hours. If the examination improves to normality during the observation period, it is reasonable to continue observation.

NECK INJURIES Blunt Neck Injuries Injuries to the neck may be classified as blunt or penetrating. Significant blunt injuries include cervical spine injuries and laryngotracheal injuries. Seventy-five percent of injuries to the trachea are confined to the cervical region.72 Fracture of the larynx and disruption of the trachea usually require surgical intervention unavailable in the wilderness. The sooner laryngeal repair is accomplished, the better the outcome with respect to phonation.20 Victims present with a history of a significant blow to the 419

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

in a 30-degree head-up position. This position assists in control of ICP, and thus CPP, through augmentation of venous outflow. This maneuver should not be attempted if the spine cannot be adequately immobilized. If endotracheal intubation is possible, ventilation should be optimized without hyperventilating the victim. Hyperventilation has been used aggressively in the past to promote hypocarbiainduced cerebral vasoconstriction, theoretically to decrease brain swelling. However, if the PaCO2 falls below 25 mm Hg, severe vasoconstriction ensues, effectively reducing CBF, promoting ischemia, and possibly augmenting secondary brain injury. Studies have demonstrated worse outcomes in victims with severe head injury who were hyperventilated.67 Inability to measure or titrate PaCO2 in the wilderness mandates that res­ piration be controlled to approximate near-normal minute ventilation. All bleeding from the scalp or face should be controlled with direct pressure. Scalp hematomas, regardless of size, should not be decompressed. Open wounds, particularly skull fractures, should be irrigated and covered with the most sterile dressing available. Fragments of displaced cranium overlying exposed brain tissue should not be replaced. If signs of skull fracture are present, broad-spectrum antibiotic prophylaxis and immunization against tetanus are recommended as soon as possible. Although diuretics have been widely used in the intensive care management of intracranial hypertension, no rationale exists for their use in the field. The wilderness trauma victim may have many injuries that are impossible to evaluate fully in the field. In this setting, particularly in the presence of hemorrhagic shock, attempts to induce osmotic diuresis to decrease ICP may be lifethreatening. Diuretics such as furosemide or mannitol may exacerbate hypotension, cause metabolic alkalosis, and induce renal complications in the absence of physiologic monitoring.2 Corticosteroids have no role in head injury in the field or intensive care unit. Studies have documented no beneficial impact on ICP or survival. Attempts at brain preservation by slowing metabolic rate and oxygen consumption have no role in the wilderness setting. Barbiturates have been used for elevated ICP refractory to other measures, but may induce hypotension, depress myocardial function, and confound the neurologic examination.2 Compared with minimizing ICP, these interventions offer no significant benefit.39 Approximately 15% of persons with severe head injury experience post-traumatic seizures. Phenytoin, if available, can be safely administered in the field, but only after a witnessed seizure. Prophylactic administration has not been shown to decrease long-term seizure activity.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

anterior neck. Physical examination findings include difficulty with phonation, subcutaneous emphysema that may extend as far inferiorly as the abdominal wall, stridor, odynophagia, and often acute respiratory distress. Treatment is focused on establishing and maintaining an airway until evacuation can occur. Frequently the airway is in jeopardy. Because of the propensity for injuries of this type to result in significant and progressive edema, endotracheal or nasotracheal intubation is often necessary. If these options are unavailable, airway maintenance techniques, as described in the Primary Survey section, should be used. In the event of intubation failure or lack of availability with impending hypoxic death, a surgical cricothyrotomy may be needed. A recent study of prehospital cricothyrotomy demonstrated that success rates were high regardless of medical specialty as long as previous training had been accomplished.53 For further descriptions of airway management, refer to Chapter 20. Background.  Vertebral column injury, with or without neurologic deficits, must be identified in any wilderness multipletrauma victim. Fifteen percent of victims sustaining an injury above the clavicles and 5% to 10% of persons with a significant head injury have a cervical spine injury. In addition, 55% of spinal injuries occur in the cervical region.59 In the wilderness setting, fractures or dislocations of the cervical spine are a result of falls from significant heights or of high-velocity ski or vehicular injuries. Twenty-eight percent of persons with cervical spine fractures have fractures elsewhere in the spine.10 Anatomy.  The cervical spine consists of seven vertebrae. The anteriorly placed vertebral bodies form the weight-bearing structure of the column. The bodies are separated by intervertebral disks and held in place anteriorly and posteriorly by longitudinal ligaments. The paraspinal muscles, facet joints, and interspinous ligaments contribute as a whole to the stability of the spine. The cervical spine, based on its anatomy, is more susceptible to injury than are the thoracic and lumbar spine. The cervical canal is wide from the foramen magnum to C2, with only 33% of the canal constituting the spinal cord itself. The clinically relevant tracts in the spinal cord include the corticospinal tract, spinothalamic tract, and posterior columns. Classification and Recognition.  Fractures of the cervical spine may result in neurologic deficit, with total loss of function below the level of injury.49 Spinal cord injuries should be classified according to level, severity of neurologic deficit, and spinal cord syndrome. Fractures of the C1-C2 complex generally result from axial loading (a C1 ring fracture, or Jefferson’s fracture) or an acute flexion injury (a C2 posterior element fracture, or hangman’s fracture). Approximately 40% of atlas (first cervical vertebra) fractures have an associated fracture of the axis (second cervical vertebra). The atlas fracture, if survived, is rarely associated with cord injury but is unstable and requires strict immobilization. Usually a complete neurologic injury at this level is unsurvivable owing to paralysis of respiratory muscle function. One-third of victims sustaining a severe upper cervical spine injury die at the scene. The severity of cervical spine fractures is a result of the neurologic compromise incurred. The most common mechanism of injury is flexion, and the most common level of injury is C5-C6.10 Fractures and dislocations may result in partial or complete neurologic injury distal to the fracture or in no neurologic injury at all. Partial injuries to the spinal cord result from typical patterns of injury. Because flexion injuries are the most common type of injury to the cervical spine, the anterior cord syndrome (see later) is the most commonly seen serious neurologic picture. A careful neurologic examination in the field to grade motor strength and document sensory response to light touch and pinprick yields important information that should be documented and reported to the treating physician at the definitive care facility. When appropriate resources are available, a rectal examination should be performed. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicate the presence of spinal cord injury. 420

When individuals with cervical spine fractures or dislocations are transported, the neck must be stabilized to prevent further injury to the spinal cord or nerve roots at the level of the fracture or dislocation. Approximately 28% of persons with cervical spine fractures have fractures elsewhere in the spine10; therefore the entire spine must be protected during transport. Occasionally a pure flexion event can result in dislocation of one or both of the posterior facets without fracture or neurologic injury. The victim may complain only of neck pain and limitation of motion. If so, the victim should be transported with the neck rigidly immobilized. With this injury, posterior instability is present (because the interspinous ligament is ruptured), and any further flexion stress could produce a spinal cord injury. Physical Examination.  A thorough neurologic examination should be performed. Initial documentation of deficits and frequent repeat examinations are critical to follow-up care. The classification of injury in the field begins with determination of the level of injury. Knowledge of sensory dermatomes (see Figure 21-3) and motor myotomes is invaluable. The sensory level is the lowest dermatome with normal sensation and may differ on each side of the body. C1 to C4 are variable in their cutaneous distribution, so assessment should begin at C5. The examiner should not be confused by the occasional innervation of the pectoral skin by C1 to C4, known as the “cervical cape.” Light touch and pinprick should be assessed. Motor function should be assessed by the myotomal distribution listed in Box 21-2. Each muscle should be graded on a sixpoint scale: 0—Total paralysis 1—Palpable or visible contraction 2—Full range of motion without gravity 3—Full range of motion against gravity 4—Full range of motion with decreased strength 5—Normal strength Each muscle must be tested bilaterally and documented. The reflexes alluded to in the classification section, as well as anal sphincter tone, must be tested. Syndromes.  There are three clinically useful spinal cord syndromes: Central cord syndrome is characterized by a disproportionate loss of motor power between the upper and lower extremities, with greater strength retained in the lower extremities. Sensory loss is variable. The mechanism of injury usually involves a forward fall with facial impact and hyperextension of the spine. Anterior cord syndrome is characterized by paraplegia and loss of pain and temperature sensation. It is the most common manifesting syndrome caused by cervical spine injury and carries a poor prognosis. Brown-Séquard syndrome results from hemisection of the cord. It consists of ipsilateral motor loss and position sense with contralateral sensory loss two levels below the level of injury. It is usually secondary to penetrating injury. Immobilization.  After identification of injury, the caregiver faces a critical decision with important ramifications—whether to immobilize.29 Victims who would as a matter of course be immobilized in an urban setting might not be appropriate candidates for immobilization in the wilderness. The decision to immobilize converts an otherwise ambulatory victim who can actively participate in his or her own evacuation to one requiring more involved evacuation procedures. The subsequent evacuation can be dangerous to the victim and rescuers and demands significant expense and resource utilization. Risk criteria for cervical spine injury and the need for immobilization have been defined.43,56 All criteria for the exclusion of immobilization must be satisfied. These include normal mental status without chemical influence; lack of distracting injury; normal neurologic examination; and a reliable neck examination without midline neck pain, deformity, or tenderness. Figure 21-4 presents an evidence-based algorithm for determining need for immobilization. Although the need for immobilization poses hazards for the evacuation process, if criteria are met, immobilization takes

Sensory C5: Area over deltoid C6: Thumb C7: Middle finger C8: Little finger T4: Nipple T8: Xiphisternum T10: Umbilicus T12: Symphysis pubis L3: Medial aspect of thigh L4: Medial aspect of leg L5: First toe web space S1: Lateral foot S4 and S5: Perianal skin FIGURE 21-5  Proper spine immobilization.

Motor C5: Deltoid C6: Wrist extensors C7: Elbow extensors C8: Finger flexors, middle finger T1: Small finger abductors L2: Hip flexors L3: Knee extensors L4: Ankle dorsiflexors L5: Great toe extensors S1: Plantar flexors

precedence over ease of evacuation.63 A difficult balance must be struck in the wilderness between the likelihood of true injury and the danger to the expedition members and rescuers that may ensue when the victim is immobilized. If a rigid litter is not available, the victim should be maintained on the flattest surface possible. A rigid cervical collar should be placed. All collars allow some degree of movement, particularly rotation. Soft collars offer the least immobilization.28 The Philadelphia collar has been shown to allow 44% of normal rotation and 66% of normal lateral bending.59 To achieve 95% immobilization, a halo and vest are necessary. Any number of materials may be used to improvise an immobilizing device (see Chapter 23). Restriction of flexion, extension, and rotation must be achieved to the greatest degree possible. Optimal immobilization consists of a long spine board or litter, rigid collar, bolsters to the sides of the head, and tape or straps restricting movement (Figure 21-5). Treatment.  The issue of pharmacotherapy for spinal cord injury is under continuous study. Currently, based on data accumulated by the National Acute Spinal Cord Injury Study Group,

documented blunt spinal cord injury should be treated with a bolus of 30 mg/kg of methylprednisolone within 8 hours of injury followed by a continuous infusion of 5.4 mg/kg/hr over the next 23 hours.14 Corticosteroids are not recommended in the field unless a victim clearly presents with a spinal cord injury in the absence of head injury. Because little definitive treatment for cervical spine injury can be accomplished in the field, survival and outcome depend on speed of transport and maintenance of airway. This is particularly true considering the association of cervical spine injury with head injury and major systemic trauma. Transport all victims with proven or suspected cervical spine injury to a definitive care facility. Penetrating Neck Injuries Similar to penetrating head injury, penetrating neck injury is usually due to gun or knife wounds. Most penetrating injuries do not confer bony instability; however, stability should not be assumed. Neurologic deficits, if present, can progress with further movement of an unstable spine. Projectiles should not be removed if embedded in the neck. Penetrating injuries to the neck may not directly injure the spine, but neurologic sequelae may result from blast effect. The same immobilization criteria should be implemented as when dealing with blunt injuries. Penetrating injuries to the neck are classified according to anatomic zones of injury (Figure 21-6). Zone I injuries extend from the clavicles to the cricoid cartilage. Zone II injuries occur between the cricoid cartilage and the angle of the mandible. Zone III injuries occur superior to the angle of the mandible. Historically, treatment has been based on penetration of the platysma muscle. In the wilderness setting, if the examiner is confident that platysmal penetration has not occurred, the victim may be observed and the wound considered a laceration. Much

Mechanism of injury suggestive of cervical spine injury? Yes/unknown Alert and oriented, no distracting injury, not intoxicated? Yes

III

II

Tenderness, pain spontaneously or with movement? No

I

Normal neurologic exam? Yes Immobilization unnecessary? FIGURE 21-4  Clinical assessment of cervical spine stability. Failure of any criterion suggests need for immobilization.

FIGURE 21-6  Zones in penetrating neck trauma (see text).

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BOX 21-2  Sensory and Motor Deficit Assessment

PART 4  INJURIES AND MEDICAL INTERVENTIONS

debate has occurred over management of platysmal penetration within respective topographic zones, with treatment arms con­ sisting of surgical exploration versus radiographic evaluation. In the wilderness setting, such considerations remain relevant. A penetrating injury violating the platysma muscle indicates the possibility of significant neurovascular, esophageal, or tracheal injuries, so the victim should be evacuated with close attention to the airway.

INJURIES TO THE THORAX Background The mortality rate from thoracic trauma is approximately 10%. Approximately 25% of all trauma deaths in the United States are attributable to chest injury.3 However, only 15% of persons with penetrating thoracic trauma require thoracotomy. In the wilderness environment, blunt thoracic injuries usually result from falls or direct blows to the chest. Penetrating injuries result from gun, knife, or arrow wounds, or from impalement after a fall. Immediate, life-threatening thoracic injuries include airway obstruction, tension pneumothorax, flail chest, and cardiac tamponade. Pathophysiology Chest injuries often result in hypoxia, hypercarbia, and acidosis. The tissue hypoxia of thoracic trauma can be multifactorial. Inadequate delivery of oxygen can be from hemorrhagic shock, direct lung injury with ventilation–perfusion mismatch (pulmonary contusion, atelectasis, hematoma), or changes in normal intrathoracic pressure dynamics (tension or open pneumothorax). Hemodynamic instability and inadequate oxygen delivery may also result from cardiac tamponade or contusion. The expedition team member should report to any air crew the consideration of pneumothorax in the evacuated patient. Many wilderness expeditions involve travel to different altitudes. Flight medics are well trained in the impact of altitude on air in closed spaces. Flight medics may be better equipped and prepared to deal with chest injuries than is the expedition team. The air crew will also know the flight path and anticipated elevations to traverse to reach the next level of care. Physical Examination Thorough physical examination begins with visualization and inspection of the chest. Exposure of the chest should be completed in the primary survey. The airway is assessed for patency and air exchange, and the pattern of breathing is noted. In the immediate postinjury period, most trauma victims are tachypneic, partly from pain and anxiety. Dyspnea, cyanosis, the use of accessory muscles of respiration, and intercostal muscular retraction are abnormal and may give clues to the underlying injury. Chest wall movement during respiration should be symmetric. Paradoxical chest wall movement is associated with flail chest. The chest wall should be inspected for contusions and abrasions, which may herald underlying bony or visceral injury. Distention of the external neck veins in a person who has just suffered thoracic trauma and is hypotensive or tachycardic (heart rate greater than 130 beats/min) suggests impaired venous return to the heart. This finding may be seen in situations of increased intrathoracic or intrapericardial pressure and is associated with tension pneumothorax and pericardial tamponade. In tension pneumothorax, deviation of the trachea is in a direction opposite the lesion. One technique to identify the deviated trachea is to place the index finger in the suprasternal notch. Dyssymmetry of the space between the trachea and the lateral margins of the suprasternal notch facilitates identification of tracheal deviation. However, a recent review suggests the tracheal deviation should be de-emphasized as an indicator of tension pneumothorax because tracheal deviation was observed in less than 5% of two series of patients with pneumothorax.54 Significant sternal bruising may herald fracture or cardiac contusion. The thorax should be palpated systematically for bony tenderness, starting at the distal clavicles and working medially toward the sternum. The sternum is divided into the manubrium, 422

gladiolus (body), and xiphoid cartilage. The manubrium is joined to the gladiolus by fibrocartilage, but mobility at this joint is minimal. Each rib should be palpated individually. Ribs 1 to 7 are vertebrosternal; their costal cartilages join the sternum. Ribs 8 through 10 are vertebrochondral, with each costal cartilage commonly joining the cartilage of the rib above. Ribs 11 and 12 are vertebral ribs without attachment to the sternum. Point tenderness over a rib can be associated with contusion or fracture. Displaced fractures can be palpated; occasionally, bone grating can be palpated during respiration. Subcutaneous emphysema may extend up into the neck and down to the level of the inguinal ligaments. In the trauma situation, subcutaneous emphysema is invariably associated with pneumothorax. Vocal fremitus describes palpation of vibrations transmitted through the chest wall. During speech, the victim’s vocal cords emit vibrations in the bronchial air column that are conducted to the chest wall. Diminished vocal fremitus is associated with pneumothorax or hemothorax. To test for vocal fremitus, the examiner applies the palmar arch of the examining hand against the person’s anterior chest wall. The person is asked to repeat “one, two, three,” using the same pitch and intensity of voice with each repetition. If the vibrations are not well perceived, the patient is asked to lower the pitch of the voice. The chest should be symmetric, left to right. Percussion is used to detect changes in the normal density of an organ. Percussion of the chest is performed by placing the examining fingertips on the chest wall and sequentially striking the fingertips with the tip of the index or middle finger of the other hand. In the trauma victim, dullness replacing resonance in the lower lung suggests hemothorax. Hyperresonance or tympani replacing resonance occurs only with a large pneumothorax or tension pneumothorax. If a stethoscope is not available, primitive chest auscultation can be performed using a rolled piece of cardboard or paper. Any cylinder that can transmit sound through a column of air accentuates breath sounds when placed against the chest wall. The absence of sounds normally produced by the tracheobronchial air column indicates blockage in the airways or abnormal filtering of sound by fluid in the pleural cavity. In the trauma victim, this is invariably associated with pneumothorax or hemothorax. Ultrasound may be considered as an extension of the physical examination. Portable ultrasound systems are lightweight and durable. Ultrasound can be used to identify pneumothorax with greater sensitivity than physical examination. A pneumothorax can be identified by loss of the “comet tails” or pleural sliding. In a study using CT as the gold standard for identification of pneumothorax in 176 victims of blunt trauma, the sensitivity and specificity for ultrasound were 98.1% and 99.2%, respectively. This compared with the sensitivity and specificity for chest radiography of 75.5% and 100%, respectively.9 Six articles on the use of ultrasound to identify hemothorax concluded that ultrasound is a sensitive and specific method to identify hemothorax in trauma patients.61 Chapter 92 addresses the use of ultrasound and telemedicine in the wilderness. Blunt Chest Trauma Blunt chest trauma in the wilderness is most often associated with either a direct blow or a deceleration injury. The mechanism usually relates to a fall from a height. Compression of the chest wall by moving or falling debris may also contribute to intrathoracic injuries, as may be seen in traumatic asphyxia associated with burial in an avalanche or earthquake. Rib Fractures.  Rib fractures range in severity from an isolated nondisplaced single fracture, which causes minor discomfort, to a major flail segment, which can be associated with an underlying hemopneumothorax and pulmonary contusion. Rib fractures are characterized by painful respiration, most severe on inspiration. Victims often breathe in a characteristically rapid, shallow pattern. Point tenderness is palpated over the fracture, and displacement can occasionally be detected. Rib fractures are detected with a compression test, in which pressure is exerted on the sternum

Costochondral Separation.  It is difficult to distinguish between a rib fracture and costochondral separation. With the latter, pain is more likely to be predominantly anterior over the costochondral junction. Pain increases with inspiration and worsens with direct palpation. Costochondral separation also responds to intercostal nerve block and oral and IV analgesics. Sternal Fracture.  A sternal fracture is usually associated with a direct blow to the anterior chest wall. The injury is characterized by severe, constant chest pain that worsens with direct palpation. Sternal instability is unusual and can be associated with a significant underlying visceral injury, including pulmonary or myocardial contusion. If the sternum is unstable, the victim should immediately be evacuated by litter or helicopter. Pneumothorax.  Simple pneumothorax can occur from an injury that allows air to enter through the thoracic wall or, more frequently, from an injury to the lung that permits air to escape into the pleural space. Symptoms include tachypnea, dyspnea, resonant hemithorax, absence of breath sounds, and tactile fremitus. A person with chest pain after a blunt blow to the chest, particularly with accompanying rib fracture, should be suspected of having a pneumothorax. Treatment of pneumothorax involves decompression of the pleural space. In the wilderness environment, tube thoracostomy is rarely possible. Fortunately, although victims with isolated pneumothorax may complain of chest pain or dyspnea, they are not completely disabled. With analgesia to control pain, ambulation facilitates evacuation. It may be easier and more prudent to set a slow pace with frequent rest periods than to perform an unnecessary litter evacuation. If resources and expertise allow placement of a thoracostomy tube, it should be performed only when clinically indicated. Considering possible morbidity in a remote area, prophylactic decompression should never be undertaken. Suspicion of a pneumothorax alone on physical examination does not warrant a catheter or chest tube. When a high index of clinical suspicion is accompanied by incapacitating symptoms, such as shortness of breath, decompression should be considered. The key to saving a victim’s life is understanding that a condition exists that can rapidly progress from a nondisabling condition to a lifethreatening condition. Once the diagnosis of pneumothorax is entertained, vigilant observation and a high index of clinical suspicion are necessary in the event of progression to a tension pneumothorax. Symptoms should be closely monitored, and frequent repeat examinations should be performed. Tension Pneumothorax.  A tension pneumothorax develops when a one-way air leak follows lung rupture or chest wall penetration. Air is forced into the thoracic cavity with no means of escape, and pressure mounts within the hemithorax. With sufficient increases in intrathoracic pressure, the mediastinum is shifted to the contralateral side, which impedes venous return from both the superior and inferior venae cavae. Cardiac output is diminished, and the victim soon exhibits signs and symptoms

of shock. Victims with tension pneumothorax present with distended neck veins and tracheal deviation away from the side of the lesion. There is unilateral absence of breath sounds, and the hemithorax is hyperresonant or tympanitic. Respiratory distress, cyanosis, and frank cardiovascular collapse may occur. Tension pneumothorax is life threatening and frequently associated with additional serious injuries. It mandates rapid chest decompression, followed by evacuation to a medical facility. Decompression is performed by inserting a needle or catheter into the chest and converting the tension into an open pneumothorax. Ideally, a 14-gauge catheter is inserted percutaneously over the second rib in the midclavicular or over the fifth or sixth intercostal space along the anterior axillary line (Figure 21-7). Once the rib is identified with the tip of the needle, the needle is marched over the anterior superior surface of the rib and inserted through the intercostal muscles and pleura into the thoracic cavity. As the pressure within the hemithorax is released, a distinct rush of air is heard. The plastic catheter is advanced over the tip of the needle, the needle withdrawn, and the catheter left in place to ensure continued decompression. The needle should not be reintroduced into the catheter because it may damage or sever the catheter. Because tension pneumothorax is commonly associated with severe injury, the victim should be evacuated to a medical facility as rapidly as possible. A rubber glove or a finger cot can be attached to the external catheter opening to create a unidirectional flutter valve that allows egress of air from the pleural space. The Asherman chest seal (Figure 21-8) can be applied directly over the 14-gauge catheter and serves as a one-way valve to permit evacuation of pleural air. The Asherman chest seal can also be applied to sucking chest wounds to permit more normal chest dynamics (see Penetrating Chest Trauma). If resources are limited and treatment is needed, any number of devices can be used to decompress the chest. A sharp instrument and hollow tube sterilized as well as possible are all that is needed. Rapid cleansing of the skin surface is accomplished with antiseptic, alcohol, or water. A Heimlich valve kit is ideal for decompression and represents a valuable addition to the expedition first-aid arsenal. If resources permit placement of a thoracostomy tube, adequate anesthesia and expertise are required. The skin should be sterilized if possible, and local anesthetic should be infiltrated

Fifth rib Intercostal vessels and nerves Air escaping from pleural space

Lung

Sixth rib

Parietal pleura

Pleural space

Visceral pleura

FIGURE 21-7  Needle decompression of tension pneumothorax. This procedure is performed only for tension pneumothorax in patients with hemodynamic instability.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

while the victim lies supine. This will elicit pain over the fracture site. Most patients with rib fractures can be managed with oral analgesics and rest. Thoracic taping and splinting are contraindicated. Multiple rib fractures are significant because of the potential seriousness of associated injuries and increased pain. However, if extreme and compromising respirations, this pain responds well to an intercostal nerve block. Victims with multiple rib fractures need to be evacuated as conditions permit. After administration of an intercostal block, a person may regain the ability to hike out of the wilderness. The morbidity of rib fractures relates to decreased inspiratory tidal volume secondary to pain and splinting. In the wilderness setting, management must focus on pain control and pulmonary toilet. If oral analgesia is insufficient to control pain, an intercostal block is ideal. Depending on the anesthetic used, varying durations of analgesia can be attained, perhaps allowing transient ambulation for evacuation. Deep breathing should be encouraged at a rate of 10 times hourly to help prevent atelectasis.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

flail segment only to control unnecessary motion and pain may provide minimal relief from the discomfort.

FIGURE 21-8  Asherman chest seal.

into the skin and periosteum of the rib. Insertion is most effectively accomplished through the fifth intercostal space at the anterior axillary line. A small incision is made and the subcutaneous tissue bluntly separated with a finger or clamp. A blunt instrument, preferably a clamp, is forcefully inserted into the pleural space closely adhering to the superior surface of the rib to avoid the inferiorly located intercostal neurovascular bundle. Once the pleural space is entered, a tube (36F or greater in size) is inserted apically and posteriorly. The tube should then be secured with suture or tape and 10 to 20 cm H2O suction or underwater seal applied. A tube open to the atmosphere can accomplish decompression. The end of the tube can be covered with a rubber glove, finger cot, or plastic bag modified to permit unidirectional flow of air. One-way flow evacuating the chest is the goal. This procedure is not without morbidity and should be used only by trained personnel under optimal conditions. Antibiotics with grampositive coverage should be initiated if the pleural space is penetrated with an indwelling catheter or tube. Hemothorax.  Hemothorax is usually associated with multiple rib fractures resulting from a direct blow to the chest. The primary cause of a hemothorax is laceration of the lung, intercostal vessel, or internal mammary artery. The victim complains of chest pain, tenderness associated with rib fractures, inspiratory pain, and dyspnea. Vocal fremitus is absent, percussion may be flat or dull, and breath sounds are diminished or absent. A chest tube for hemothorax is rarely required in the wilderness setting but may be placed if proper equipment is available, the patient is symptomatic, and evacuation will be prolonged. Needle aspiration of a hemothorax is unnecessary in the immediate postinjury period and may precipitate a pneumothorax. Flail Chest.  When a series of three or more ribs is fractured in both the anterior and posterior planes, a portion of the chest wall may be mechanically unstable. As negative intrathoracic pressure develops during inspiration, the unstable segment paradoxically moves inward and inhibits ventilation. A flail segment indicates a severe direct blow to the chest wall with associated multiple rib fractures and decreased tidal volumes, often with associated underlying pulmonary contusion. The contusion can be expected to progressively impair ventilation and oxygenation over the succeeding 48 hours. Victims often tolerate a flail segment for the first 24 to 48 hours, after which they require mechanical ventilation. Any victim with a flail segment should be rapidly evacuated. Because the victim is usually incapable of participating in evacuation, a litter should be prepared or aeromedical evacuation considered. Intercostal nerve block may assist in short-term management of pain and pulmonary toilet. Restrictive (to chest wall expansion during inhalation) external chest wall supports, including taping or extensive stabilization with sandbags, are contraindicated. These measures hinder chest wall movement, decrease vital capacity, and are less effective than intercostal nerve block in pain control. However, focal stabilization or cushioning of the 424

Blunt Cardiac Injuries.  Blunt cardiac injuries leading to pericardial tamponade or cardiac contusion are rare. Pericardial tamponade is life threatening. The pericardial sac is fibrous and expands little. A small amount of intrapericardial blood can severely restrict diastolic function. Blunt injury resulting in tamponade is usually from chamber rupture and rarely survivable, particularly in a remote setting. The diagnosis of tamponade can be difficult, particularly in the wilderness. Beck’s triad, which consists of distended neck veins, hypotension, and muffled heart sounds, is present in less than 33% of cases of tamponade and is particularly difficult to ascertain under nonoptimal conditions. Pulsus paradoxus, an increase in the normal physiologic decrease in blood pressure with inspiration, may be indicative of tamponade. Kussmaul’s sign, or a rise in venous pressure with spontaneous inspiration, is possible to assess outdoors. Once pericardial tamponade is diagnosed, immediate evacuation is required. Treatment consists of median sternotomy in a hospital operating room. The only temporizing measure pending evacuation is pericardiocentesis. This procedure can be lifesaving, particularly if a cardiac injury with a slow leak exists. However, its application in the wilderness setting should occur only if there is a high index of suspicion, coupled with shock and impending death unresponsive to resuscitative efforts. A long (approximately 15 cm [6 inches]), 16- to 18-gauge needle with an overlying catheter is introduced through the skin 1 to 2 cm (0.5 to 0.75 inches) below and to the left of the xiphoid. The needle is advanced at a 45-degree angle with the tip directed at the tip of the left scapula. When the pericardial sac is entered, aspiration with a syringe follows. The catheter is left in place and secured for possible repeat aspirations as the victim’s condition warrants. Immediate evacuation should follow. Cardiac contusion is a rare condition resulting from a severe blow to the precordium. An overlying sternal contusion or fracture may be present. The diagnosis should be suspected in an isolated high-velocity blow to the precordium with unexplained evidence of increased venous pressure, arrhythmias, and hemodynamic instability. Chest pain is invariably present, usually resulting from musculoskeletal contusion. Morbidity results from ensuing arrhythmias. Diagnosis can be definitively made only at autopsy. Electrocardiographic abnormalities after injury have correlated with subsequent arrhythmias.55 In the wilderness setting, any person who is unstable or symptomatic from an arrhythmia should be evacuated. If evacuation is not possible, it is noteworthy that fatal arrhythmia potential decreases significantly after 24 hours. Traumatic Asphyxia.  Traumatic asphyxia is a rare syndrome of craniocervical cyanosis, facial edema, petechiae, subconjunctival hemorrhage, and occasional hypoxemia-related neurologic symptoms that results from severe thoracic crush injury. In the wilderness environment, it is associated with landslides or mud slides, avalanches, or falling debris. Any significant blunt compressive force to the thorax can result in the syndrome. Children are particularly susceptible because of high compliance of the chest wall.15 Traumatic asphyxia is associated with a high incidence of serious associated injuries,1,70 and the mortality rate in natural disasters is consequently high.32 A significant crush injury component may accompany traumatic asphyxia.32 Crush injuries and rhabdomyolysis are discussed later in the Extremity Trauma section of this chapter. The pathophysiology of traumatic asphyxia involves two elements. The crush injury results in acute increases in intrathoracic pressure and thus inferior and superior vena caval pressures. Venous flow is reversed in the veins of the head, which contain no valves. Venous hypertension leads to capillary rupture and the characteristic facial edema and petechiae. Recognition of the physical findings is imperative in diagnosing the syndrome and identifying concomitant injuries (Figure 21-9). Treatment consists of carefully extracting and, if necessary, immobilizing the victim. Rapid extrication is the single most important factor in improving survival. Establishment and

FIGURE 21-9  Typical clinical facial appearance of traumatic asphyxia.

maintenance of an airway is critical because significant facial and laryngeal edema may rapidly develop. Associated injuries should then be addressed in the primary survey. Subsequent care is supportive, consisting of airway control, administration of oxygen, head elevation of 30 degrees, treatment of associated injuries, and possible evacuation. The mortality rate is low in civilian environments but higher in wilderness disaster settings. Mortality is due to pulmonary dysfunction and associated injuries. Morbidity is secondary to neurologic damage; however, the majority of neurologic sequelae clear within 24 to 48 hours. If the victim survives, long-term sequelae are rare. Penetrating Chest Trauma Penetrating chest trauma above the nipple line is associated with hemopneumothorax and may also be associated with significant visceral injury. A victim with penetrating chest trauma below the nipple line often has intra-abdominal penetration in addition to possible thoracic injury. Such a victim requires immediate rapid evacuation. The open (“sucking”) chest wound produces profound intrathoracic physiologic alterations. Normal chest expansion creates negative intrathoracic pressure, which pulls air into the trachea and allows the lungs to expand. When the diaphragm and chest wall relax, positive pressure creates expiration. If the chest wall sustains an injury approximately two-thirds the tracheal diameter, negative intrathoracic pressure for inspiration is lost, the ipsilateral lung collapses, and loss of negative intrathoracic pressure affects the good lung. Consequently, it is important to rapidly reconstruct chest wall integrity. Initially this is most easily done by placing a hand over the sucking chest wound. Field treatment includes placing petrolatum gauze on top of the wound, covering it with a 4 × 4 gauze pad, and taping it on three sides (Figure 21-10). The untaped fourth side serves as a relief mechanism to prevent tension pneumothorax. Persons with sucking chest wounds should be rapidly evacuated to sophisticated medical care. Alternatively, an Asherman chest seal could be applied over the wound.

Anatomy.  For descriptive purposes, the abdomen may be divided into thoracic, true, and retroperitoneal compartments. The thoracic abdomen contains the liver, spleen, stomach, and diaphragm. The liver, spleen, and, more rarely, stomach may be injured by direct blows to the ribs or sternum. Twenty percent of persons with multiple left lower rib fractures have a ruptured spleen. A direct blow to the epigastrium may result in increased intra-abdominal pressure with subsequent rupture of the liver or diaphragm. The true abdomen contains the small bowel, large bowel, and bladder. Isolated bowel injuries are rare in the wilderness setting. Blunt bladder or rectal injury usually occurs in conjunction with severe pelvic fracture and carries high mortality. The retroperitoneal abdomen contains the kidneys, ureters, pancreas, and great vessels. It is notoriously difficult to evaluate by physical examination. Life-threatening hemorrhage can occur into the true abdomen or retroperitoneal space. Diagnosis.  The wilderness physician must have a high index of suspicion and perform a superlative history and physical examination. Physical Examination.  The physician should look for signs of early shock: tachycardia, tachypnea, delayed capillary refill, weak or thready pulse, and cool or clammy skin. Physical examination of the abdomen begins with visualization and inspection. Contusions and abrasions may be the only harbingers of occult visceral injury. Periumbilical ecchymosis associated with abdominal hemorrhage (Cullen’s sign) is virtually never present in a victim with acute abdominal trauma. Abdominal distention secondary to hemorrhage is a very late sign and never present before shock and cardiovascular collapse. Abdominal inspection should survey the flanks, lower chest, and back. Inspection of the back should follow palpation of the spine while the victim is supine. The victim should be very carefully logrolled if there is any suspicion of spinal injury. Looking for muscle guarding, the examiner gently palpates the abdomen in all four quadrants. Any persistent guarding or tenderness after wilderness trauma mandates rapid evacuation. Percussion tenderness is an indicator of peritoneal irritation, also mandating evacuation. The presence or absence of bowel sounds has little prognostic significance. Bowel sounds may be present in the face of significant intra-abdominal hemorrhage or, conversely, absent in victims when extra-abdominal injuries induce ileus. Referred pain to the left shoulder (Kehr’s sign) strongly suggests the presence of a ruptured spleen. This pain is often exaggerated by placing the victim in the Trendelenburg position,

INJURIES TO THE ABDOMEN Intra-abdominal injuries in the wilderness setting are difficult to recognize. However, if recognized, all intra-abdominal injuries require rapid resuscitation and immediate evacuation. The abdomen represents the most frequent site of life-threatening hemorrhagic shock; however, in the wilderness setting, few diagnostic and treatment options exist. Blunt Abdominal Trauma Blunt intra-abdominal injury is commonly associated with falls. Abdominal injuries are often associated with fractures or closed head injuries. Often the decision for evacuation is made on the basis of other injuries; however, the wilderness physician must

Petrolatum gauze and 4˝ x 4˝ gauzepad

FIGURE 21-10  Treatment of a sucking chest wound. Sealing the wound with a gel defibrillator pad works best because this pad adheres to wet or dry skin. Petrolatum gauze or plastic wrap also works well. Note that one side is not sealed to allow egress of air.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

be attuned to the potential for intra-abdominal hemorrhage as an occult injury.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

increasing the amount of left upper quadrant blood irritating the diaphragm. Pain from the retroperitoneal abdomen associated with injuries to the kidneys or pancreas may be referred to the back. However, referred pain is usually a late finding and not helpful in the evaluation of acute trauma. Gross hematuria that does not clear immediately or is coupled with an associated injury, such as pelvic fracture or abdominal or back pain, requires immediate evacuation. To minimize blood loss, the victim should be kept stationary and the evacuation team brought as close to the victim as possible. In a wilderness setting, rectal and vaginal examinations add little to the evacuation decision when evaluating for abdominal trauma. The unstable pelvic fracture associated with rectal and vaginal injuries is usually the determinant for evacuation. Diagnostic modalities in the austere environment are limited. Plain imaging, CT scans, and diagnostic peritoneal lavage have a very limited role. Ultrasound can be used to identify fluid in the peritoneum. Penetrating Abdominal Trauma Penetrating intra-abdominal injuries may result from gunshot, stab, or arrow wounds. The social context in which these injuries occur (accidental, intentional, or self-inflicted) makes little difference in the wilderness setting. Recrimination, guilt, and blame only interfere with the paramount goal of immediate evacuation. Gunshot Wounds.  Low-caliber gunshot injuries often manifest with small entrance and no exit wounds. High-caliber, highvelocity gunshot injuries may have relatively innocuous entrance wounds but may be associated with large, disfiguring exit wounds and extensive internal injuries. No matter what the caliber or trajectory and no matter where the entrance and exit, all gunshot wounds from the nipple line to the inguinal ligament should be presumed to have penetrated the abdominal cavity and created an intra-abdominal injury. These injuries mandate immediate surgical intervention. A victim of gunshot wounds to the head, neck, chest, abdomen, or groin should undergo immediate evacuation accompanied by the administration of a single-agent broad-spectrum antibiotic, such as an oral fluoroquinolone (e.g., ciprofloxacin, 750 mg orally [PO]). Hunting injuries are discussed in Chapter 24. Shotgun Injuries.  Shotgun injuries to the torso are managed in the same manner as gunshot wounds. Shotgun injuries have a potentially lower incidence of underlying visceral injury than gunshot wounds, but there is often extensive soft tissue damage requiring surgical debridement. The potential exists for delayed development of peritonitis from a single penetrating pellet to the viscera. Consequently, shotgun injuries should also be treated with emergency evacuation and a broad-spectrum antibiotic, as recommended previously for gunshot wounds. Occasionally, a close-range shotgun blast results in a soft tissue defect large enough for the injured bowel to extrude through the wound. The injured bowel should not be placed back into the abdomen. Injured bowel displaced from the abdominal cavity conceptually should be treated as though it were an enterocutaneous fistula. Because evacuation is often delayed in the wilderness, it is better to have fecal contents outside, rather than inside, the peritoneal cavity. The exteriorized bowel should be kept moist and covered at all times. Uncovered bowel outside the peritoneal cavity rapidly desiccates and becomes nonviable, mandating later surgical resection. Exposed bowel should be covered with an abdominal pack or cloth moistened with sterile saline at best, or at worst with potable water. The dressing should be checked and remoistened at least every 2 hours. Stab Wounds.  The penetrating object is usually a knife but may be as varied as a piton, ski pole, or tree limb. Any deep skin laceration from the nipple line to the groin should be considered to have damaged an intra-abdominal organ. Whereas the odds of an abdominal gunshot wound injuring a visceral organ exceed 85%, the odds of a stab wound injuring a visceral organ are less than 50%. 426

In certain urban hospitals, the high incidence of negative surgical explorations for stab wounds had led to a more selective approach toward patients with abdominal stab wounds.68 This approach uses local wound exploration and frequent physical examination. Although there are no data addressing the management of stab wounds in the wilderness environment, the following approach is practical and reasonable. If the wound extends into the subcutaneous tissue, the evacuation decision depends on local wound exploration. This procedure is simple to perform, even in the wilderness environment. The skin and subcutaneous tissue are infiltrated with local anesthetic, and the laceration is extended several centimeters to clearly visualize the underlying anterior fascia. It is helpful to use lidocaine (Xylocaine) 1% with epinephrine to minimize slight but annoying bleeding that can impair visualization. The wound should never be probed with any instruments, particularly if overlying the ribs. Wound exploration is confined to the area from the costal margin to the inguinal ligament. Local wound exploration is contraindicated in wounds that extend above the costal margin, because it is possible for such exploration to communicate with a small pneumothorax, potentially exacerbating respiratory distress. If thorough exploration of the wound shows no evidence of anterior fascial penetration, and if the victim demonstrates no evidence of peritoneal irritation, the wound can be closed with tape (Steri-Strips) or adhesive bandages, dressed, and the evacuation process delayed. Physical examination should be performed every few hours for the next 24 hours. If no peritoneal signs develop and the victim feels constitutionally strong, a remote expedition may resume with caution and an eye to evacuation should the victim become ill. In the wilderness environment, it is prudent to have a low threshold for evacuation because of technical difficulties in performing wound exploration, such as insufficient light and inadequate instruments. Persons who have been impaled by long objects, such as tree limbs or ski poles, should have the object left in place and carefully shortened, if possible, to facilitate transport.

PELVIC TRAUMA In the wilderness setting, fractures of the pelvis are generally associated with falls from significant heights, high-velocity ski accidents, or vehicular trauma. Pelvic fractures can be lethal. With opening of the pelvic ring, there may be hemorrhage from the posterior pelvic venous complex and occasionally from branches of the internal iliac artery. For hemodynamically unstable victims with severe pelvic fractures, resuscitative efforts should be instituted. In addition, simple techniques to reduce increased pelvic volume through the application of sheets or slings may slow bleeding. Several pelvic binders are available commercially and all provide circumferential pressure to minimize the pelvic volume (e.g., T POD [www. pyng.com], SAM Pelvic Sling II [www.sammedical.com]). The key factor in initial management of pelvic fractures is identification of posterior injury to the pelvic ring. Posterior ring fractures or dislocations are associated with a greater incidence of significant hemorrhage, neurologic injury, and mortality than are other pelvic fractures. The diagnosis of a posterior ring fracture is based on instability of the pelvis associated with posterior pain, swelling, ecchymosis, and motion at the sacroiliac joints with application of manual pressure at the anterior superior iliac spines. Persons with posterior ring fractures must be immediately evacuated on backboards, with care taken to minimize leg and torso motion. The flank, scrotum, and perianal areas should be inspected for blood at the urethral meatus, swelling or bruising, or a laceration in the perineum, vagina, rectum, or buttocks suggestive of an open pelvic fracture. The pelvis should be examined carefully once, without any aggressive rocking motion. The first indication of mechanical disruption is leg length discrepancy or rotational deformity in the absence of an obvious leg fracture or hip location. For more information on pelvic fracture, see Chapter 27.

BOX 21-3  Vascular “Hard Signs”

The majority of wilderness-related extremity injuries involve fractures and sprains, which are discussed in Chapter 27. This section focuses on the general field management of significant extremity vascular injury, traumatic amputation, and recognition and treatment of rhabdomyolysis.

Pulsatile bleeding Palpable thrill Audible bruit Expanding hematoma Six “P’s” of regional ischemia Pain Pulselessness Pallor Paralysis Paresthesia Poikilothermia

Vascular Injuries Injury to the major vessels supplying the limbs can occur with penetrating or blunt trauma. Fractures can produce injury to the vessels by direct laceration (rarely) or by stretching, which produces intimal flaps. Penetrating injuries can be devastating if transection of a vessel occurs. Significant vascular injuries, from both penetrating and blunt causes, can result in multiple vessel injury subtypes, each of which may be limb-threatening. Injury subtypes include laceration, transection, contusion with spasm, thrombosis, or aneurysm formation (true and false), external compression, and arteriovenous fistula. An accurate history, expeditious physical examination, and prompt evacuation are the keys to life and limb salvage. Significant vascular injuries result in one of two clinical presentations—hemorrhage or ischemia. The greatest priority is cessation of hemorrhage. The victim of trauma may die in short order from a major vascular injury. Stop the bleeding. Ideally, control of hemorrhage can be accomplished without resultant ischemia of the distal extremity. The vast majority of times, hemorrhage from an extremity wound can be controlled with pressure dressings and direct pressure. These measures permit circulation to and from the extremity outside the area of pressure application. In the very rare circumstance, a tourniquet may be required. History.  A complete history of the time and mechanism of injury is invaluable in planning further management. Although no absolute ischemia time has been established, a goal of less than 6 hours to reperfusion is prudent.28 The amount of blood present at the scene should be quantified. A history of bright pulsatile blood that abates suggests arterial injury. Thirty-three percent of victims with arterial injuries have intact distal pulses. Physical Examination.  Vascular examination in the field can be highly variable. Hypovolemia, hypothermia, and hostile conditions make accurate examination challenging. Skin color and extremity warmth should be first assessed. Distal pallor and asymmetric hypothermia suggest vascular injury. Pulses should be palpated. In the upper extremity, the axillary, brachial, radial, and ulnar pulses should be assessed. In the lower extremity, the femoral, popliteal, posterior tibial, and dorsalis pedis pulses should be assessed. Location and direction of the wound, amount of hemorrhage, and presence of hematomas or palpable thrill should be noted. A neurologic examination that quantifies motor and sensory deficits is critical. Because of the high metabolic demands of peripheral nerves, disruption of oxygen delivery makes neuronal cells highly susceptible to ischemic death. Conversely, skeletal muscle is relatively resistant to ischemia. Loss of sensation or limb paralysis is an alarming sign of impending anoxic necrosis. Treatment of Vascular Injuries.  All external hemorrhage should be identified during the primary survey and controlled with direct pressure at the site of injury. Tourniquets should be applied only when direct pressure fails to control bleeding or when direct pressure cannot be applied (such as while a casualty is being evacuated by hoist to an aircraft). In the civilian experience, the need for tourniquets should be uncommon, because direct pressure is the preferred technique. Tourniquets should be released every 5 to 10 minutes to attempt to limit ischemia, unless severe hemorrhage continues when the tourniquet is loosened. In this case, it should be left tightened. Efforts to control bleeding with pressure should be undertaken. Direct pressure permits collateral flow to provide some perfusion to the distal extremity. Hematomas should never be explored or manually expressed without surgical capability readily available. Attempts to clamp or ligate vessels are not recommended. Frequent repeat neurovascular examinations are mandatory.

Once bleeding is controlled and the wound is covered with a sterile but nonconstrictive dressing, completion of the primary survey, identification and stabilization of associated injuries, and appropriate resuscitation with normal saline should follow. After hemostasis is achieved, a nonconstrictive dressing will obviate the chance for unintended venous outflow obstruction. The extremity should be splinted to prevent movement. The need for evacuation depends directly on the results of the physical examination. Examination results can be grouped into “hard signs,” indicative of ischemia or continued hemorrhage, and “soft signs” that are suggestive but not indicative of ischemia (Boxes 21-3 and 21-4). All victims with hard signs should be evacuated emergently. Based on current data, an isolated soft sign may warrant observation alone, depending on the remoteness of the expedition and the risks of evacuation. The data for observation of soft signs have emerged from hospital settings and must be applied with great caution in the wilderness. If soft signs are present, clinical suspicion is high, and evacuation can be accomplished safely, the victim should be transported and observed in a medical facility. Traumatic Amputation In the wilderness environment, amputation victims require immediate evacuation. Hemorrhage is controlled during the primary survey with direct pressure, and resuscitation is instituted. Tourniquets are rarely required. The victim should be kept warm and calm. Reassurance and analgesics should be administered. Amputations should be completed only if minimal tissue bridges exist and it is clear that the neurovascular supply has been interrupted. Amputation of a mangled extremity, defined as an extremity with high-grade open fracture and soft tissue injury, should not be carried out in the wilderness except to free a trapped victim to avoid further severe injury or even death, or in the case of uncontrollable hemorrhage threatening the life of the victim, and then only by experienced surgical personnel. All other severely injured extremities should be wrapped in available sterile materials, splinted, and kept moist. Amputated extremities should be cooled if possible, optimally in a plastic bag in ice or ice water. Avoid placing the extremity in direct contact with ice. Without cooling, the amputated extremity remains viable for only 4 to 6 hours; with cooling, viability may extend to 18 hours. The amputated extremity should accompany the victim throughout the course of the evacuation. Crush Injuries and Rhabdomyolysis Rhabdomyolysis is a potentially fatal syndrome that results from lysis of skeletal muscle cells. In its fulminant form, BOX 21-4  Vascular “Soft Signs” Injury in proximity to major vessel Diminished but palpable pulses Isolated peripheral nerve deficit History of minimal hemorrhage

427

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

EXTREMITY TRAUMA

PART 4  INJURIES AND MEDICAL INTERVENTIONS

rhabdomyolysis can affect multiple organ systems. Compartment syndrome, renal failure, and cardiac arrest represent the major complications. Any condition resulting in significant acute or subacute striated muscle damage can precipitate rhabdomyolysis. Crush injuries of the extremities and pelvis, revascularization of ischemic tissue, ischemic extremities, animal bite and snakebite,16,22 frostbite, and traumatic asphyxia32 can all result in rhabdomyolysis in a wilderness setting. Crush injuries are frequently results of avalanches, falls from heights, or rock slides. The pathophysiology of rhabdomyolysis remains controversial. The exact mechanism of muscle injury appears not to be simple direct force or isolated ischemia and is probably multifactorial.32 The common cellular derangement is interference of the normal function of muscle cell membrane sodium-potassium adenosine triphosphatase (ATPase) with intracellular calcium influx and cell death.76 After cell death, multiple intracellular constituents, including myoglobin, creatine kinase, potassium, calcium, and phosphate, are released into the systemic circulation. The metabolic derangements of rhabdomyolysis depend directly on release of intracellular muscle constituents. Myoglobinemia, hypercalcemia, hyperphosphatemia, hyperkalemia, hyperuricemia, metabolic acidosis, coagulation defects, and contracted intravascular volume result. The clinical presentation of rhabdomyolysis may include muscle weakness, malaise, fever, tachycardia, abdominal pain, nausea and vomiting, or encephalopathy. Symptoms may mimic those of persons with spinal cord injury.7 The danger of the syndrome lies in the cardiovascular effects of electrolyte disturbances and renal failure69 secondary to changes in renal perfusion and direct toxicity of myoglobin to tubular cells. Successful treatment relies on prompt diagnosis based on clinical signs and urinalysis, aggressive hydration, and forced diuresis. Myoglobin turns urine tea-colored, which is an important indicator of significant muscle death and need for aggressive treatment. Normal saline should be administered IV at 1 to 2 L/hr to achieve a urine output of 100 to 300 mL/hr. Signs for fluid overload should be monitored. Victims who are trapped in rubble should have resuscitation initiated before extrication, if possible. The addition of agents to alkalinize the urine and promote diuresis has been shown to improve clearance of myoglobin but not to alter survival. In addition, diuretics may be detrimental in multisystem trauma victims who are hypovolemic. All victims demonstrating myoglobinuria should be evacuated.

Wilderness Surgical Emergencies THE ACUTE ABDOMEN In the wilderness, the critical distinction between the surgical and nonsurgical abdomen determines whether the victim should be evacuated. A myriad of nonsurgical conditions mimic a surgical abdomen. It has been extensively reported that the bite of the black widow spider, Latrodectus mactans, can induce abdominal pain indistinguishable from a surgical acute abdomen,48 and mushroom ingestion can cause severe gastroenteritis.83 Pain, anorexia, nausea, vomiting, and fever are characteristic manifestations of an acute abdominal disorder. Tenderness and guarding are the hallmarks of peritoneal irritation and suggest that surgery is indicated. The approach to someone with abdominal pain begins with a detailed history that includes age, gender, systemic symptoms, and past medical history. This information provides a framework for more detailed questioning about the character of the pain, its mode and time of onset, severity, and precipitating and palliating factors. In persons 15 to 40 years of age, women are more likely to have abdominal pain, but men have a higher incidence of surgical disease. Common genitourinary causes for abdominal pain in men include epididymitis, renal colic, urinary retention, and testicular torsion. Common causes in women include pelvic inflammatory disease (PID), urinary tract infection (UTI), dysmenorrhea, ruptured ovarian cyst, and ectopic pregnancy. Pain is the hallmark of a surgical abdomen (Table 21-3). It can be characterized by nature of onset, severity, location, and precipitating factors. The onset of abdominal pain can be explosive, rapid, or gradual. The person who is suddenly seized with explosive, agonizing pain is most likely to have rupture of a hollow viscus into the free peritoneal cavity. Colic of renal or biliary origin may also be sudden in onset, but seldom causes pain severe enough to prostrate the victim. If someone has rapid onset of pain that quickly worsens, acute pancreatitis, mesenteric thrombosis, or small bowel strangulation should be suspected. The person with gradual onset of pain is likely to have peritoneal inflammation, such as that accompanying appendicitis or diverticulitis. Severity of the pain may be characterized as excruciating, severe, dull, or colicky. Excruciating pain unresponsive to narcotics suggests an acute vascular lesion, such as rupture of an abdominal aneurysm or intestinal infarction. Both conditions are

TABLE 21-3  Differential Diagnostic Features of Abdominal Pain Disease Acute appendicitis Intestinal obstruction Perforated duodenal ulcer Diverticulitis Acute cholecystitis Renal colic Acute pancreatitis Acute salpingitis

Ectopic pregnancy

428

Location of Pain and Prior Attacks

Mode of Onset and Type of Pain

Associated Gastrointestinal Problems

Periumbilical or localized generally to right lower abdominal quadrant Diffuse

Insidious to acute and persistent

Anorexia common; nausea and vomiting in some

Sudden; crampy

Vomiting common

Abrupt; steady

Anorexia; nausea and vomiting Diarrhea common

Epigastric; history of ulcer in many Left lower quadrant; history of previous attacks

Gradual; steady or crampy

Epigastric or right upper quadrant; may be referred to right shoulder Costovertebral or along course of ureter Epigastric penetrating to back Bilateral adnexal; later, may be generalized

Insidious to acute

Anorexia; nausea and vomiting

Sudden; severe and sharp Acute; persistent, dull, severe Gradually becomes worse

Frequently nausea and vomiting Anorexia; nausea and vomiting common Nausea and vomiting may be present

Unilateral early; may have shoulder pain after rupture

Sudden or intermittently vague to sharp

Frequently none

Physical Examination Low-grade fever; epigastric tenderness initially; later, right lower quadrant Abdominal distention; high-pitched rushes Epigastric tenderness; involuntary guarding Fever common; mass and tenderness in left lower quadrant Right upper quadrant pain Flank tenderness Epigastric tenderness Cervical motion elicits tenderness; mass if tubo-ovarian abscess is present Adnexal mass; tenderness

General Field Treatment Principles When evaluating someone with a possible emergent surgical condition in the wilderness, correctly identifying the etiology of a given condition is less important than identifying peritoneal inflammation and the need for operation. When dealing with a surgical abdomen or other condition requiring evacuation, adjuncts to definitive hospital treatment can be initiated in the field. Dehydration and intravascular volume depletion accompany many surgical conditions, particularly when the disease process has progressed and evacuation is delayed. Crystalloid resuscitation in the field is beneficial for patients who have developed or have the potential to develop septic or hypovolemic shock. Dehydration is common in the wilderness, and frank hypovolemia can result from vomiting associated with gastroenteritis, appendicitis, renal colic, and small bowel obstruction. Perforated viscus, pancreatitis, cholecystitis, small bowel obstruction, PID, and necrotizing soft tissue infections all may feature volume depletion. The goal in the wilderness setting is to recognize the signs of hypovolemia and initiate resuscitation to decrease perioperative morbidity. Nasogastric tube decompression of the stomach may help alleviate emesis secondary to abdominal pain or obstruction. Large-bore (i.e., 18F) catheters are best and can be easily aspirated with a syringe. Placement should be confirmed by aspiration of gastric contents or auscultation of gastric air on insufflation of the stomach. Foley catheters are becoming increasingly more available in wilderness first-aid kits (Figure 21-11). Recording urine output provides an effective estimate of intravascular volume status. Foley catheter placement should never hinder the possibility of ambulatory evacuation. Radiographic imaging techniques will not be available. Some expeditions will have the availability of portable ultrasound and the professional expertise to use this modality. A team of three emergency medicine physicians described their application of ultrasound in the austere environment following mud slides in Guatemala. In a series of 99 patients, ultrasound was used to identify an emergent problem in 6% of patients and rule out an emergent problem in 42% of patients.19 Appendicitis Acute appendicitis is the most common cause of a surgical abdomen in persons younger than 30 years of age. Acute appendicitis is more than a single disease entity. In terms of physical signs and symptoms, appendicitis proceeds from inflammation to obstruction to ischemia to perforation, all within approximately 36 hours. Symptoms reflect the stage of the disease. Unfortunately, the time frame for the progression of clinical events is highly variable.

The differential diagnosis of appendicitis includes gastroenteritis and mesenteric adenitis, the most common inflammatory disorders in adults. The first symptom of gastroenteritis is typically vomiting, which precedes the onset of pain and is often associated with diarrhea; it is rarely associated with localizing signs or muscular spasm. Bowel sounds are usually hyperactive. A rectal examination rarely shows abnormalities in gastroenteritis but frequently does in adults with appendicitis. Mesenteric adenitis is often preceded by an upper respiratory infection and is associated with vague abdominal discomfort that often begins in the right lower quadrant. Abdominal examination reveals only mild right lower quadrant tenderness that is often poorly localized. The incidence of PID in young women with abdominal pain confounds the diagnosis of appendicitis. Some clinicians have documented a connection between menses and onset of pain. If abdominal pain occurs within 7 days of menses, the incidence of PID is twice that of appendicitis. If onset of pain occurs greater than 8 days from menses, appendicitis is twice as likely as PID. This history with a pelvic examination may enable the examiner to differentiate between the two entities. Acute appendicitis mandates evacuation, because untreated perforation is associated with significant mortality. Recent literature has supported nonoperative management of acute appendicitis.5,41,92 However, in these series, patients who do not improve promptly with antibiotics proceed to appendectomy. The prudent medical director of an expedition would seek to evacuate the patient with presumed appendicitis to ensure surgical capability is available. Broad-spectrum antibiotics (if IV capability, cefotetan [Cefotan] 2 g IV every 12 hours, or as an alternative, piperacillin/ tazobactam [Zosyn] 3.375 g IV every 6 hours; if only oral antibiotic capabilities, a fluoroquinolone, such as ciprofloxacin [Cipro] 750 mg PO twice a day) should be initiated, attempting coverage against gram-negative and anaerobic organisms. IV crystalloid resuscitation should be initiated, particularly if the victim is older or perforation is suspected, and the victim should be placed on bowel rest. Acute Cholecystitis and Biliary Colic Biliary colic refers to pain induced by obstruction of the cystic duct, usually by gallstones. The label of this condition as “colic” is a misnomer because the pain is usually constant. The condition is rarely seen before adulthood and is several times more common in women than in men. A sufferer often relates a past history of gallstones and previous episodes of similar pain, which is described as constant right upper quadrant or epigastric pain, radiating to the right scapula and back. Onset ranges from insidious to acute and frequently follows a meal. The episode usually lasts 15 minutes to 1 hour and then abates.66 If pain is severe, nausea and vomiting may be present (60% to 70%). Acute cholecystitis is an infection of the gallbladder secondary to cystic duct obstruction, usually from gallstones. In the wilderness setting, it is useful to think of these interrelated conditions as a continuum of one unified disease process. Both biliary colic and cholecystitis manifest with right upper quadrant pain; however, biliary colic has the potential to be self-limited and may not require evacuation. Not all persons with biliary colic develop cholecystitis, and signs of infection should be excluded. Cholecystitis symptoms typically escalate in severity. Pain that persists for more than 1 to 2 hours is suspect for cholecystitis, particularly when accompanied by fever, more significant nausea and vomiting, and right upper quadrant tenderness. Studies have shown that fever may be an unreliable predictor of severity of infection.38 Acute cholecystitis mandates hospitalization, and evacuation plans should be instituted. The disease can progress to gangrenous changes in the gallbladder wall, leading to perforation and death if untreated. The definitive treatment of cholecystitis is cholecystectomy. In the field, IV antibiotics (ampicillin/sulbactam [Unasyn] 3 g IV every 6 hours) or an oral alternative (ciprofloxacin 750 mg PO twice a day) should be given, directed at common biliary organisms, including Escherichia coli and Klebsiella, Bacteroides, Enterobacter, Streptococcus, and Proteus species. Oral antibiotics with optimal bioavailability should be initiated in the absence of parenteral forms, ensuring the broadest spectrum of coverage 429

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

unusual in the wilderness environment. Severe pain readily controlled by medication is characteristic of peritonitis from a ruptured viscus or acute pancreatitis. Dull, vague, and poorly localized pain suggests an inflammatory process and is a common initial presentation of appendicitis. Colicky pain characterized as cramps and rushes is suggestive of gastroenteritis. The pain from mechanical small bowel obstruction is also colicky but has a rhythmic pattern, with pain-free intervals alternating with severe colic. The peristaltic rushes associated with gastroenteritis are not necessarily coordinated with colicky pain. Physical examination of the abdomen is initiated by inspection. Valuable clues to the underlying condition that may be obtained in this manner include stigmata of cirrhosis, distention, hyperperistalsis, or incarcerated hernia. The victim may not be able lie still, which is indicative of renal or biliary colic. Persons lying perfectly still frequently have peritoneal inflammation. Auscultation is helpful if the classic “rushes and tinkles” of small bowel obstruction are present. Palpation in the wilderness setting is most helpful in documenting the presence or absence of peritoneal signs. Shake or percussive tenderness, particularly in the context of fever, nausea, and/or vomiting, indicates a need for evacuation. Rectal and vaginal examinations should be performed as dictated by the clinical presentation and setting.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

available. As with most abdominal infections, IV hydration should be started in the field. If significant nausea and vomiting are present, NG decompression may improve comfort and prevent aspiration. Peptic Ulcer Disease The incidence of peptic ulcer disease (PUD) is decreasing in the United States. With the advent of treatment of Helicobacter pylori infections and the variety of acid-reducing agents available, PUD is now rarely seen by surgeons. The exception is perforation of a gastric or duodenal ulcer, which should be considered in the differential diagnosis of acute abdomen in the wilderness. Victims frequently relate a history of PUD and need for medication. This history, in combination with acute onset of unrelenting epigastric pain radiating to the back, is suspect for perforation of an ulcer. The physical examination greatly assists in differentiation between simple ulcer disease symptoms and perforation. Pain may be severe. Gastric secretions are caustic to the peritoneum and, as a result, the abdomen frequently displays a rigid, boardlike character with associated diffuse peritoneal signs. History and examination consistent with gastric or duodenal perforation mandate evacuation. Dehydration may be significant. IV resuscitation should be started and the victim placed on bowel rest. Diverticulitis Diverticulitis is localized infection of a colonic diverticulum. Impacted material in the diverticulum, usually feces, leads to a localized inflammatory process that can lead to abscess formation and perforation. Diverticulitis manifests over a wide range of severity, from mild, localized infection to an intra-abdominal catastrophe. It is more common in middle age; one-third of the population older than 45 years of age has diverticula, 20% of whom will develop diverticulitis.81 Victims often relate a history of previous attacks. Pain is typically described as gradual in onset and localized in the left lower quadrant of the abdomen, although right-sided diverticulitis can occur. Diarrhea and fever are frequently associated complaints. Examination findings range from mild left lower quadrant abdominal tenderness to frank peritonitis, depending on the severity of the underlying infection. Treatment in the wilderness setting consists of hydration, bowel rest, antibiotics, and evacuation. If evacuation is impossible or significantly delayed, oral broad-spectrum antibiotics may be effective. Mild cases of diverticulitis are frequently treated on an outpatient basis with broad-spectrum oral antibiotics,81 such as ciprofloxacin 750 mg PO twice a day. Antibiotic therapy is directed primarily at gram-negative aerobic and anaerobic bacteria, and single-agent therapy covering these organisms has been demonstrated to be as effective as multiple-agent regimens.47 Because of unpredictability of response to antibiotic treatment, evacuation is indicated. Mechanical Small Bowel Obstruction Small bowel obstruction is a true emergency in the wilderness. When the obstruction is complete, expedient surgery is the only treatment. Small bowel obstruction in the United States is almost invariably the result of adhesions from previous laparotomy or incarceration of abdominal hernias. Victims complain of sudden onset of diffuse, crampy abdominal pain associated with vomiting and obstipation. With progression of the process to strangulation and infarction of bowel, fever and tachycardia develop. Late physical examination findings reveal a distended, tympanitic abdomen. Although variable, high-pitched tinkling bowel sounds suggest obstruction. A thorough inspection for hernias should be performed. Progression of examination findings to frank peritonitis is alarming and suggests ischemic bowel. The adage, “Don’t let the sun set on a small bowel obstruction,” is sound advice in the wilderness setting. All persons suspected of having a small bowel obstruction should be evacuated immediately. In the interim, the stomach should be decompressed with an NG tube to relieve vomiting and abdominal distention, and aggressive IV hydration should be started. 430

Incarcerated Abdominal Wall Hernias Abdominal wall hernias are common. Hernias can become incarcerated or strangulated, which constitutes a surgical emergency. Seventy-five percent of hernias occur in the groin84; the majority of incarcerated hernias manifesting in the wilderness setting are inguinal hernias. Other common hernias with the capacity for incarceration are incisional and umbilical hernias. Many people live with bulging asymptomatic hernias. Others manually reduce symptomatic hernias. New painful hernias or known hernias that can no longer be reduced are concerning. The pain of inguinal hernias is usually intermittent. A description of constant pain is suspect for incarceration. Associated symptoms of fever, tachycardia, nausea, and vomiting are indicative of possible incarceration or strangulation. On physical examination, a mass should be sought along the course of the spermatic cord. Masses may manifest from the external inguinal ring to the scrotum. The differential diagnosis for painful inguinal or scrotal masses includes lymphadenopathy, testicular torsion, and epididymitis. Associated tenderness of the spermatic cord may be present. A painful mass at the umbilicus, a previous incision site, or below the inguinal ring could represent an incarcerated umbilical, incisional, or femoral hernia, respectively. Bowel within an incarcerated hernia sac can become gangrenous in as little as 4 to 5 hours64; therefore it is important to determine the time of incarceration. The decision to evacuate is influenced by the presence of contraindications to manual reduction (see later), which are essentially physical signs that suggest progression to strangulation. Femoral hernias should not be reduced. The danger is en masse reduction of compromised or gangrenous bowel. Contraindications to reduction include associated signs of toxicity, such as fever, tachycardia, or evidence of bowel obstruction in association with a painful, irreducible mass. If the hernia itself is exquisitely tender to palpation and the overlying skin is erythematous and warm, the hernia should not be reduced. Victims with incarcerated hernias with signs of systemic or local toxicity should be evacuated. Similarly, victims with irreducible hernias—which require emergent surgery—should be evacuated. A newly incarcerated hernia without contraindications to reduction may be reduced by personnel experienced in such techniques. Gentle pressure is exerted on the hernia mass toward the inguinal ring, optimally with the victim flat and hips elevated. Analgesia and sedation may aid in reduction. Gangrenous bowel can rarely be reduced by this method.64 If successful, the victim should be closely observed for signs of recurrence or abdominal pain.

UROLOGIC EMERGENCIES Renal colic describes a symptom complex resulting from acute obstruction of the urinary tract secondary to calculus formation. The goal of the wilderness physician is to recognize the symptom complex and institute treatment. After obstruction of the urinary tract, the pain crescendo of renal colic begins in the flank. The pain progresses anteriorly over the abdomen and radiates to the groin and testes in men and the labia in women. Because the autonomic nervous system transmits visceral pain, many abdominal complaints may manifest. Nausea and vomiting are common. With severe colic, the victim writhes in pain and is unable to find a comfortable position. Physical findings are less revealing than is the review of systems. Tenderness to deep palpation of the region of obstruction or to percussion of the flank is present. Diagnosis in the wilderness is assisted by the presence of gross hematuria. Management of ureteral colic is pain control. Although almost universally deployed, forced diuresis may reduce ureteral peristalsis. Thus, forced oral fluids or aggressive IV hydration are of questionable benefit.96 The majority of calculi pass spontaneously in 4 to 6 hours. The goal of management is to control pain until passage of the stone has occurred. A number of pharmacologic approaches may be used. Nonsteroidal antiinflammatory drugs, such as ibuprofen and ketorolac, have been shown to be effective in the management of renal colic.96 For symptoms

Urinary Retention Urinary retention is a painful experience that requires immediate medical, and often surgical, intervention.13 The etiology of urinary retention ranges from prostatism45 in men to atonic bladder in women. In general, causes have been broadly divided into four groups: obstructive, neurologic, pharmacologic, and psychogenic.95 Twenty-five percent of men reaching 80 years of age will experience acute retention,13 which has been shown to increase prostate surgery perioperative mortality rates.75 Acute urinary retention can lead to incapacitating symptoms in the wilderness; prompt recognition and intervention are necessary. Principal symptoms are bladder distention and pain that may mimic acute abdomen, overflow incontinence, dribbling, and hesitancy. Physical examination findings include prostatic enlargement in men and lower midline abdominal tenderness and distention. If painful distention of the bladder is present, decompression should be undertaken. Medical therapy may be considered before complete obstruction to urinary flow. Tamsulosin (Flomax CR) is a third-generation α-blocker that may provide some relief. The α-blockers promote bladder neck and prostatic urethral relaxation.35 Bladder decompression should be initially attempted with a standard Foley catheter. In men with prostatic hypertrophy, passage of the catheter may be challenging, and a large catheter or coudé catheter should be used if a standard Foley catheter cannot be passed. Instrumentation of the urethra with hemostats or dilators is dangerous and should not be attempted in the field. The OPTION-vf (female) (see Figure 21-11, A) and OPTIONvm (male) (see Figure 21-11, B) are valved urinary catheters

A

B FIGURE 21-11  A, OPTION-vf (female) catheter. B, OPTION-vm (male) catheter. (Courtesy Opticon Medical, Dublin, Ohio.)

that eliminate the need for urine drainage bags and connecting tubes normally required with Foley catheters. These catheters incorporate a manually activated valve at the end of the catheter that allows the patient to store urine in the bladder and to mimic normal voiding behavior. The catheters may be used with a continuous drainage adapter when appropriate, so that a bag may be placed and urination rate and volume assessed. If multiple attempts are unsuccessful and symptoms are severe, needle decompression is indicated. The skin of the suprapubic region should be anesthetized, if possible. The distended bladder is palpated to guide aspiration. A 22-gauge needle attached to a syringe is introduced through the skin of the lower abdomen two finger breadths above the pubic symphysis and directed at the anus. The needle is advanced with simultaneous aspiration of the syringe until free-flowing urine is visualized. Palpation of the bladder in combination with adherence to this technique should lead to successful decompression. Complications related to decompression can occur.82 Drainage of greater than 300 mL/hr can induce mucosal hemorrhage. In addition, 10% of victims develop postobstructive diuresis that may lead to dehydration, in which case aggressive oral hydration or crystalloid repletion should be undertaken. Finally, surgical decompression is temporizing, and retention will recur. Treatment may need to be continued or repeated. Drainage of the bladder acutely relieves symptoms and may allow ambulatory evacuation, but the underlying etiology must be addressed in a medical facility. The Acute Scrotum Acute onset of scrotal pain and swelling requires immediate attention. Etiologies are multiple, but incarcerated hernia and testicular torsion are the most clinically significant in the field. Although any one aspect of the history and physical examination may not be diagnostic, when taken as a whole, they frequently suggest the etiology of the scrotal pathology.46 Testicular torsion can occur at any age, but it is more likely near puberty. The likelihood of testicular salvage is inversely proportional to elapsed time from torsion; this is a true surgical emergency. Acute onset of severe testicular pain is the hallmark. Mild to moderate pain is more suggestive of torsion of a testicular appendage or epididymitis. It has been stated that victims who can ambulate with minimal pain are less likely to have testicular torsion. In addition, nausea and vomiting may accompany torsion, whereas fever, dysuria, and frequency are associated with epididymitis. Physical examination reveals a patient in extreme discomfort with a swollen scrotum and a tender testicle; the affected testicle may be higher than normal and have a horizontal lie.46 Scrotal skin may be edematous and discolored. Unilateral scrotal swelling without skin changes is more indicative of a hernia or hydrocele. In testicular torsion, the affected testis is often larger than the unaffected testis. Testicular torsion can be somewhat differentiated from acute epididymitis by Prehn’s sign,86 which is relief of pain accomplished by elevation of the testicle. Because torsion twists the spermatic cord and elevates the testicle, pain is not relieved by elevation (negative Prehn’s sign). Conversely, pain is relieved in epididymitis with elevation (positive Prehn’s sign). This maneuver has low sensitivity in distinguishing the two conditions, but may be helpful in conjunction with other findings.86 Treatment consists of surgical detorsion, which should be accomplished within 12 hours of torsion.46 Manual detorsion is not the treatment of choice; however, remoteness of the wilderness environment may mandate manual attempts. Studies of manual detorsion are scant and the cohorts small.42 If manual detorsion is necessitated, the victim should be placed supine. Because testicular torsion typically occurs in the medial direction, detorsion is initially attempted with outward rotation of the testis (toward the ipsilateral thigh). Simultaneous rotation in the caudal to cranial direction may be necessary to release the cremasteric muscle.31 The surgical treatment of testicular torsion includes pexing the testis to prevent recurrent torsion. Thus, although detorsion may temporize an acute situation in the field, all victims must be evacuated for definitive treatment. 431

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

uncontrolled by antiinflammatory agents, narcotics may be added. Narcotic analgesics are most effective given parenterally; however, agents such as meperidine (Demerol), codeine, and hydromorphone (Dilaudid) may be given orally. Antiinflammatory agents and analgesics can be combined. An antiemetic may be added to relieve nausea. When administering pain medication in the field, particular attention should be given to airway maintenance and induced nausea and vomiting. Any person whose symptom complex cannot be controlled must be evacuated. Additional indications for evacuation include calculus anuria and evidence of obstruction-induced infection.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Prostatitis A number of forms of prostatitis have been defined, including viral, bacterial, nonbacterial, and chronic forms. The acute bacterial form may potentially lead to severe infection. Bacterial prostatitis is an infection of the prostate caused primarily by gram-negative bacteria, with 80% attributable to E. coli. It is an acute, febrile illness characterized by perineal pain radiating to the low back, chills, malaise, and voiding symptoms, such as urgency, frequency, and dysuria. Urinary retention is common, and cystitis frequently accompanies the infection. On rectal examination, the prostate gland is usually boggy, warm, and tender and enlargement is variable. In an ideal situation, treatment is individualized to the cause, which may be difficult to discern in the wilderness. The infection may respond to an oral antibiotic such as ciprofloxacin (750 mg PO twice a day), ampicillin (500 mg PO 4 times a day), or tri­ methoprim (160 mg with sulfamethoxazole 800 mg PO twice a day). Penetration of prostatic secretions has been shown to be best achieved by trimethoprim/sulfamethoxazole (TMP/SMX). The chosen antibiotic should be administered for 30 days. If retention is present, catheterization or suprapubic aspiration should be undertaken. Acute bacterial prostatitis can escalate in severity to systemic toxicity. Persons with evidence of systemic toxicity unresponsive to a trial of oral or parenteral antibiotic therapy should be evacuated. Urinary Tract Infection UTIs are extremely common and include episodes of acute cystitis and pyelonephritis occurring in otherwise healthy individuals. These infections predominate in women; approximately 25% to 35% of women 20 to 40 years of age report having had a UTI.44 Conversely, men between the ages of 15 and 50 years rarely develop a UTI. Despite the striking difference in prevalence, symptoms are similar between men and women. The symptoms may represent urethritis, cystitis, or an upper UTI; the distinction is often difficult. Common symptoms include frequency, urgency, dysuria, suprapubic pain, flank pain, and hematuria. Flank pain with tenderness to percussion suggests pyelonephritis. On urinalysis, pyuria is nearly invariably present, and hematuria may assist in the diagnosis. Definitive diagnosis is based on significant bacteriuria. The leukocyte esterase test has a screening sensitivity of 75% to 96% and a specificity of 94% to 98% in detecting greater than 10 leukocytes per high-power field.44 Treatment in the wilderness setting for both men and women should be directed at the most common causative agents, although 50% to 70% of cases resolve spontaneously if untreated. Causative bacteria include E. coli (70% to 95%); Staphylococcus species (5% to 20%); and, less frequently, Klebsiella, Proteus, and Enterococcus. Fortunately, oral antibiotics are highly effective. Although resistant E. coli strains are being reported, trimethoprim/ sulfamethoxazole (Bactrim DS) is an excellent first-line drug. Alternative regimens include nitrofurantoin, a fluoroquinolone, or a third-generation cephalosporin. A 3-day course of therapy has been shown to be more effective than single-dose therapy.44 For pyelonephritis, a similar antibiotic in a 10- to 14-day course is an acceptable initial treatment. Evacuation should be reserved for systemic toxicity unresponsive to oral antibiotics.

SKIN AND SOFT TISSUE INFECTIONS Poor hygiene, superficial skin wounds, blisters, dermatologically significant plants, and insect bites contribute to disruption of the skin barrier. Most often seen are superficial pyodermas that do not extend beyond the level of the skin. These include erysipelas, impetigo, folliculitis, furunculosis, and carbunculosis. The majority of superficial skin infections are self-limited. However, with less than optimal hygiene and limited resources, skin infections may progress to deep soft tissue infections. Cellulitis Cellulitis is acute infection of the skin involving subcutaneous tissue. The superficial form of cellulitis, erysipelas, is identified 432

by well-demarcated, warm, and erythematous plaques with raised borders. The face, scalp, hands, and lower extremities are most often affected. Cellulitis is frequently preceded by a superficial wound. In the wilderness setting, there are ongoing infection risk factors. Members of expeditions may be physically stressed and nutritionally depleted. High altitude is associated with immunosuppression. Clostridium species and other pathogens are ubiquitous in the soil, and proper initial wound care may be suboptimal. Under such conditions, cellulitis can progress to abscess formation and tissue necrosis, leading to septicemia. Wounds that develop erythematous, warm, and boggy margins should be treated with antibiotics and closely observed. The margins of erythema should be marked to gauge progression. Treatment consists of proper wound hygiene and antibiotic therapy. Local wound measures include elevation, application of moist heat every 4 to 6 hours, and immobilization. Antibiotic therapy is directed at common causative pathogens. Group A streptococci and Staphylococcus aureus are most commonly implicated. If complications occur and the cellulitis appears to be progressing, a mixed infection is likely. Because Gram’s stain and culture-directed therapy are not possible, the most broad-spectrum antibiotic available should be administered. Parenteral antibiotics are indicated for serious or mixed infections. Penicillin G (1 to 2 million units every 4 to 6 hours) is recommended, with first-generation cephalosporins as an alternative. Because oral antibiotics may be the only available therapy, they should be initiated early in the field. Suggested agents include erythromycin (for the penicillin-allergic victim); cephalexin; a macrolide, such as clarithromycin; or a fluoro­ quinolone, such as ciprofloxacin or levofloxacin. Methicillinresistant S. aureus is present in wilderness settings. If infection with this organism is suspected, appropriate antibiotics should be used. Lymphangitis Acute lymphangitis is an infectious process involving subcutaneous lymphatic channels. Its recognition in the wilderness setting is important relative to its propensity to follow puncture wounds, hand wounds, infected blisters, and animal bite wounds. Clinical presentation involves linear erythematous streaks that originate in the lymphatic drainage basin of the wound and “point” to the draining nodal group. Causative agents are similar to those common for cellulitis, with the addition of Pasteurella multocida from animal bite wounds. Treatment consists of antibiotics; warm, moist soaks every 4 to 6 hours; and immobilization and elevation of the extremity. Optimal treatment consists of parenteral antibiotics, but as with cellulitis, oral agents should be initiated if parenteral drugs are not available. Broad-spectrum agents with good oral bioavailability and gram-positive coverage are recommended.85 Abscess Formation When untreated, many superficial skin infections convert to abscesses. Development of a raised, fluctuant mass with overlying warmth and erythema should raise suspicion that surgical drainage is necessary. Frequently, the lesion will “point” when purulent fluid has amassed below the dermis and rupture is impending. Warm soaks and observation are recommended by some clinicians, particularly if the presence of drainable pus is uncertain. However, the definitive treatment is drainage. Antibiotics are recommended if significant associated cellulitis is present, but penetration may be poor. Local anesthesia should be administered before incision. The lesion should be incised in line with tissue planes over the point of maximum fluctuance. The value of cruciate incisions over linear incisions is debatable; the important feature is assurance of adequate drainage to prevent recurrence. If drainage is undertaken, the incision must be large enough to adequately drain the cavity. All purulent material should be evacuated and the cavity copiously irrigated with saline or water. Packing is unnecessary if continued drainage is ensured. The wound should be covered with a sterile dressing, changed two to three times per day with concurrent irrigation, and closely observed for reaccumulation of purulence.

Necrotizing skin and soft tissue infections are life-threatening conditions caused by virulent, toxin-producing bacteria. Depth of tissue involvement is variable and may involve skin, fascia, or muscle. The etiology of necrotizing infections is related to breaks in normal cutaneous defenses associated with some form of injury. Although rare, such infections are of importance to the wilderness physician because of the array of documented inciting injuries and the reduction in mortality possible if diagnosis and treatment are rapid.27 Necrotizing infections have developed after innocuous-appearing injuries, including simple scratches, insect bites, ankle sprains, and sore throats.37 The incidence of necrotizing soft tissue infections is unknown, and there is no age or gender predilection. They most commonly occur on the extremities, abdominal wall, and perineum, within 1 week of the inciting event. Common pathogens include Streptococcus species, Staphylococcus, Vibrio species, Clostridium, Pseudomonas, Aeromonas, Enterobacter, and fungi. Many infections become polymicrobial. The clinical manifestations can be subtle. An area of cellulitis is commonly the first indication of infection. Pain is often excruciating, and fever is usually present. The infection then progresses to spreading erythema, induration, blue-black discoloration, and blister formation. Necrosis of skin, subcutaneous fat, muscle, or fascia follows, depending on the organism involved. Necrotic tissue exudes a foul-smelling, watery “dishwater” fluid. Subcutaneous emphysema may be present, particularly with clostridial infections, although enteric organisms may also produce air in tissues. Unfortunately, treatment is limited in the wilderness environment. Debridement of infected tissue should be carried out to the greatest degree humanely possible, but further debridement in a hospital setting is invariably necessary. The extent of debridement necessary is often striking. After debridement, parenteral antibiotics are necessary. Vancomycin and gentamicin are appropriate first-line agents. The most broad-spectrum oral antibiotic available should be initiated, and the victim expeditiously evacuated. Time is of the essence because the infection can be halted only by aggressive surgical intervention.

FIELD OPERATING ENVIRONMENT On a rare occasion, surgical procedures must be performed in the austere environment. By definition, the austere environment is not the ideal situation in which to conduct any invasive procedure. Site security is a consideration. The circumstances responsible for the injury must not continue to exist. Otherwise, the caregivers may be at risk for suffering the same fate as the casualty. The medical expeditionist will need to select a location that provides optimal illumination, yet protection from the elements. Sterility in the Austere Environment One of the major disadvantages of operative procedures in the austere environment is the inability to establish a sterile field. The goal will be to decrease the risk for bacterial contamination to as little as possible. Antiseptics are agents that are used to decontaminate the skin. Chlorhexidine is an antiseptic with excellent antimicrobial activity and prolonged length of activity. In many health care facilities, chlorhexidine has replaced iodophors as the antiseptic of choice. Isopropyl alcohol may be used if no other antiseptics are available. Isopropyl alcohol is commonly available, but it is particularly ineffective on dirty skin and it has little persistent activity. If nothing is available, soap and water may be of benefit. Soaps

will remove the bacteria on the surface of the skin that are not attached, but will do nothing for adherent bacteria. Sterile irrigation may not be available for wound irrigation. If no sterile fluid is available, potable water may be used. Water could be boiled before irrigation, but boiling does not rid the water of spores. If water is to be treated by boiling, the boiling should be at a rolling boil for 20 minutes to be effective. Any irrigation that is used should be removed from the wound as best possible. Wounds should be managed to ensure that no devitalized tissue or foreign bodies remain to minimize the chance of infection. Should an expedition make preparations for the possibility of surgical procedures, instruments taken into the field should be packed sterile in durable containers. Paper wrappers can become perforated, permitting contamination. The term disinfectant means an agent to decontaminate inanimate objects. If surgical instruments are not sterile, disinfectants can be used to decrease the bacterial count on the surface. Of course, all instruments should be clean of debris. Unfortunately, many of the disinfectants used in health care facilities are not practical for the austere environment. Ortho-phthalaldehyde (Cidex OPA), peracetic (Nu-Cidex, Perasafe), and glutaraldehyde (Cidex) are agents that are effective disinfectants, but hazardous for personnel and the environment and impractical in the field environment.24 The antiseptic chosen for skin preparation may be applied to the instruments in the absence of a disinfectant. Placing the instruments into boiling water will decrease the bacterial count, but will not completely eliminate bacterial spores. Applying flame to the instruments may kill bacteria but may leave products of combustion on the instruments that are then left in the wound as foreign material. The U.S. Army has developed a field sterilization system that is lightweight and does not require an external energy source. The system is the size of a suitcase and has the capacity to accommodate a surgical tray. A mixture of water and dry reagents controllably generates chlorine dioxide. The chlorine dioxide kills all vegetative cells and bacterial spores within one-half hour.24 Anesthesia Local and regional anesthesia will be the techniques of choice to provide comfort during minor operative procedures. General anesthesia should not be considered without a full complement of trained personnel and equipment. Procedural sedation and analgesia may be used with the availability of adequate monitoring, and the capability to establish a definitive airway should be immediately available. Common agents to supplement local or regional anesthesia are opioids and benzodiazepines. Should these agents be used, reversal agents of naloxone and flumazenil should be available. Another consideration would be the use of ketamine to provide dissociative sedation.4 Chapter 17 discusses pain management more specifically. Any operative interventions performed in the wilderness should keep in mind “damage control” principles. The general concept of damage control is to manage immediately lifethreatening problems, such as hemorrhage and gross contamination. Definitive management is delayed. Resuscitation continues during this period of time.87 Damage control principles should be kept in mind before considering any procedure in the austere environment. Generally, the approach in the wilderness should be temporizing with resuscitation or lifesaving or limb-saving procedures before contemplating definitive management.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

Necrotizing Infections

CHAPTER 22 

Wound Management RAMIN JAMSHIDI

Management of wounds sustained in remote and wilderness environments requires special preparation and knowledge. The basic elements of wound care can be outlined so that a provider in a remote, austere, or wilderness environment can safely manage the immediate wound and thereby limit secondary injury. In the care of acute injuries, attention is frequently focused on wound closure. In truth, most traumatic wounds would fare well if left open to heal by secondary intention.17 However, open wounds incur prolonged time to complete healing, discomfort of wound care, vulnerability to further injury, and larger scars. The critical goals of immediate wound care are to stop hemorrhage and limit morbidity related to infection. Secondary goals are to promote rapid healing and optimize cosmetic outcome.44

Types of Wounds and Definitions Abrasions result from tangential (shearing) forces. Although abrasions are most commonly superficial, they can be extensive and involve deep tissues. Superficial abrasions pose no threat to the patient but may require use of analgesics. Deep abrasions that have completely obliterated skin and denuded underlying fascia are at increased risk for infection and must be kept clean. By virtue of the mechanism of injury, abrasions involve more surface area than they do depth. As a consequence, they are not amenable to suture closure. Abrasions are treated by extensive irrigation to remove all debris (often dirt or gravel) and application of nonadherent dressings. Topical antiseptic solutions are not necessary but are useful adjuncts in preventing gauze dressings from adhering to raw tissue. Such dressings should be changed once daily or more frequently as needed for soiling or adherence (“drying out”). Abrasions do not form abscesses because they have no deep spaces to contain infection. They may become superinfected and develop cellulitis; although this is generally rare, the possibility is more real in the exposed wilderness environment. Diagnosis and management of cellulitis are discussed later in this chapter. Burns (see Chapter 13) may result from thermal or chemical insults. These injuries span a spectrum from trivial sunburn to deep tissue necrosis. The first principle of management is to limit further injury by extinguishing the source, seeking shade, washing out chemicals, and so on. For chemical exposures, voluminous irrigation is the key to limiting further injury. This should be done with clean (not necessarily sterile) water, and the run-off irrigant should be prevented from injuring more skin.7,15,34 Chemical quenchers (i.e., alkaline solution for an acid burn) should never be used because the resulting exothermic reaction will cause secondary injury. Once the burning process is arrested, burn care must focus on antisepsis because infection poses the single most important immediate threat. Burn wounds should be fastidiously cleaned to remove all foreign material and devitalized skin. Depth was formerly described as first, second, or third degree, but modern description relies on the descriptors partial thickness and full thickness (Figure 22-1). Blisters should be left intact unless they interfere with function. There is some debate about the management of blisters, but in a wilderness environment, the “biologic bandage” provided by an intact blister supersedes any academic debate about the presence of inflammatory mediators in the blister fluid. Blisters over the palms or joints are exceptions to this rule, because their presence will significantly limit motion and potentially engender contraction or decrement in function. One school of thought is that these blisters should be unroofed and gently scrubbed away with a moistened gauze or trimmed with scissors. 434

Once cleaned, burns should be dressed and kept clean. Topical antiseptic agents should be applied to burns with invasion deep enough to result in blistering or erosion through the skin to white tissue or burned muscle underneath. Silver sulfadiazine is an excellent agent, and can be reapplied once or twice daily to prevent the wound from desiccating. In the absence of silver sulfadiazine (and for burns 90%). Sucking chest wounds should be treated with petroleum gauze applied during expiration, covering it with tape or a field dressing, placing the victim in the sitting position, and monitoring for development of a tension pneumothorax. Asherman seals are also ideal for quickly securing chest tubes and for sucking chest wounds. 3. Bleeding: Same as for tactical field care. 4. IV line: Same as for tactical field care. 5. Fluid resuscitation: Same as for tactical field care, with blood and/or lactated Ringer’s solution possibly available. 6. Monitoring, wound care, reinspection for additional wounds, analgesia, reassessment of fractures, antibiotics: All the same as for tactical field care. A main precept of TCCC is to move medical care from being the sole responsibility of the combat medic, to involve each operator and each level of leadership. Each fighter carries a tourniquet that can be self-placed. Each fighter is trained in basic combat lifesaving skills so that the effects of wounds can be minimized (within defined limits) and fire can be returned until the medic can arrive and perform the appropriate advanced medical care. Each leader, from the squad level up, is trained to evaluate medical concerns as an integral part of the mission execution and is able to decide when to abort the mission, when to continue, and when to alter the plan, based on the mission objective and the issues that the injured team member or members bring to the fight.

Principles of Tactical Medicine The tactical environment presents unique challenges to law enforcement officers, and the same is true for personnel 494

FIGURE 25-13  Tactical medics discuss placing a suspect under arrest during a tactical operation operational preplan during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

providing EMS medical support in that environment. Tactical medical care providers must have an understanding of and consideration for law enforcement tactics and mission-specific objectives when planning and providing medical support (Figure 25-13).52 Most comprehensive law enforcement tactical medicine programs require medical providers to attend some formal law enforcement training. Before deployment, further training in SWAT school will most likely also be required to familiarize the tactical medic with basic and advanced tactics. This extensive training may result in reserve police officer status for the medical provider if there is a reserve program in existence at the law enforcement agency where the program is based. The operator then enters a true hybrid role between medicine and law enforcement. Traditional EMS doctrine maintains that rescuer and scene safety are first priorities, and that patient care is a secondary concern.76 The nature of tactical operations requires that law enforcement officers and tactical medical personnel operate in unsecured environments and situations with significant potential for violence and injury (Figure 25-14).72 Tactical scenes are rarely safe from the civilian standpoint, but tactical medical personnel are trained to conduct concise and limited medical evaluations and interventions in potentially threatening areas.82 What sets tactical EMS apart from standard EMS is the ability to render immediate care in an environment that may not be completely secured from threats (Figure 25-15). When a SWAT

FIGURE 25-14  At the International School of Tactical Medicine, law enforcement tactical medics train for high-risk vehicle assault situation treating a tactical officer with massive blood loss during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

team relies on traditional EMS to provide medical care and an operator or civilian is acutely injured during the mission, the EMS unit must either wait until the victim is brought out to the safe (“cold”) zone (Figure 25-16) or wait for the entire scene to be secured by law enforcement before evaluating and moving the victim. The Columbine School shooting illustrated how victims will die if medical aid is not rendered in a timely manner. When a tactical medical unit is present, care can generally be rendered to the victim swiftly, and when the injuries involve acute airway issues or life-threatening hemorrhage, lives may be saved by faster access to care. Other differences between tactical EMS and conventional EMS include limitations in medical equipment at hand, performing in adverse or austere environments (e.g., while maintaining light or sound discipline), and performing patient assessment from remote locations.87 “Medicine across the barricade” involves remote evaluation and management of patients, such as when a hostage has become ill or injured and the provider attempts to assist the victim by using the eyes, ears, and hands of someone closer to the situation.34 The tactical medical provider must use skills not unlike those of an EMS dispatcher handling an

Hot zone • Highest threat of gunfire, Level of care injury, etc. • Limited to stopping major hemorrhage and extricating the victim to a safer location

Cold zone • Secured area, safe for civilian EMS responders

Warm zone • Lower risk of gunfire or injury, but not secured Level of care • Standard care available in the prehospital environment using any equipment available on an ambulance or medical helicopter

Level of care • Limited to that which can be rendered with the equipment carried by the tactical medical provider (largely focused on the ABC’s)

FIGURE 25-16  The zones-of-care concept of tactical emergency medical services. ABC, Airway, breathing, and circulation; EMS, emergency medical services. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

495

CHAPTER 25  Tactical Medicine

FIGURE 25-15  Tactical medics perform advanced airway management in a tactical training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

emergency over the radio. In addition, standard EMS medical care performed in specific clinical scenarios may require a different approach when the same situation is encountered under tactical conditions.33 Tactical medicine can be provided by EMTs, paramedics, registered nurses, midlevel providers (physician assistants, nurse practitioners), or physicians who serve on law enforcement tactical teams.47 Midlevel providers and physicians traditionally have training in advanced surgical and medical procedures beyond what is normally allowed for traditional EMS personnel.22 The primary goal of tactical medicine is to assist a tactical team in accomplishing its mission. This is achieved through a comprehensive program outlined first by the California Commission on Peace Officer Standards and Training (POST) and the California Emergency Medical Services Authority (EMSA). State Regulation 1084 established operational programs and standardized training recommendations for tactical medicine programs in California. This produced the first tactical medicine operational and standardized training recommendations set forth by a state regulatory body in the United States. Its seven elements are medical oversight, medical contingency planning, operational support, quality improvement, team health management, training and education, and medical equipment acquisition and maintenance. A tactical medicine program cannot be effective with only the operational component in place. It must include other elements, such as team health management—keeping the tactical team members healthy before, during, and after special operationss.20,59 A full tactical medicine program encompasses provision of preventive and acute medical and dental care and for some teams, even canine support veterinary care.49 Ready access to such care has a positive effect on team morale (Figure 25-17). One of the most important roles of the provider is to create a formal medical threat assessment for each training and operational deployment. This includes consideration of issues such as environmental conditions (heat, cold, wind), low-light conditions (Figure 25-18, A),41,42 operator fatigue (and the possible need for rotating operators), nutritional issues,21 plant and animal threats, and a plan for extrication and transport of patients.10 When operational, this medical plan should include any medical intelligence that can be gathered before or during the mission, including issues such as who is involved, ages of persons involved, medical history and background, preexisting medical conditions, geographic location, and weather19 (Figure 25-18, B). Predetermining evacuation routes to ensure timely transport to the

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Medical equipment acquisition and maintenance

Medical oversight Medical contingency planning

Tactical medicine Training and education

Team health management

Operational support (TEMS)

Quality improvement

FIGURE 25-17  California tactical medicine diagram.

appropriate medical facility is also part of the medical threat assessment. This should include both ground and air evacuation plans, or water transportation where necessary. Aeromedical evacuation planning includes predetermined landing zone coordinates that are cleared for approach before the start of the mission if possible. Day and night landing zone requirements

differ, so both need to be considered, depending on the time of day. SWAT teams and their tactical medical teams are important community resources not only for responding to major emergencies but also in planning for the community response. Tactical medical operators, in conjunction with local medical control, EMS, and public health officials, should take a leadership role to ensure that aggressive, proactive planning for future threats is completed before resources are needed.16,100 Although no one doubts that some terrorists, outlaw states, and organized criminals have the capability to produce or access chemical and biologic agents, the question is whether they will use them.38 The use of explosive devices is on the rise worldwide. The potential for terrorist acts against the United States is immeasurable. As a result, domestic preparedness and proper training for blast injuries are essential.26,31,37,73,95 Any terrorist incident is a large crime scene by definition. Initially it is unsecured, and additional threats, such as bombers, gunmen, or secondary devices, may present themselves. Tactical medics are trained to deal with such a situation. Knowing how not to disturb evidence, take care of a patient, and provide security are a combination of skills needed at any terrorist incident. It is advantageous to have more than one provider as part of a tactical team, particularly in the event of a serious injury or when multiple casualties are involved (e.g., in a school shooting or an act of community violence).46,60 Team medical personnel can lessen the agency’s liability exposure with adequate written, photographic, diagrammatic, or video documentation of the injuries.64 Another benefit of having multiple providers is the ability to send a provider to the hospital with an officer who becomes ill or injured during a mission. This provider can serve as a concerned advocate for the officer and as a liaison with hospital personnel. This provides significant reassurance to the entire tactical team.40,45,69

A

B

C

D

FIGURE 25-18  A, Tactical medic trainees for low-light situations. B, Tactical medic trainees discuss their operation plan with an instructor at the International School of Tactical Medicine. C, Tactical medic trainees apply a tourniquet to an injured officer who is suffering from massive blood loss. D, Tactical medics must prepare for the unexpected, including evaluating and treating pediatric patients injured during tactical operations. (Courtesy International School of Tactical Medicine.)

496

Tactical medical providers ensure that everyone on the team is healthy and optimally fit for duty.48 The team’s medical officer is responsible for the team’s physical fitness, diet, exercise, sleep, stress management, and preventive medicine. The tactical unit can be viewed as a group of elite operators who are “occupational athletes.” Strength training for many tactical operators consists of traditional bodybuilding exercises. However, this type of physical conditioning does not duplicate the actions needed to perform as a tactical operator. Tactical operators, like professional athletes, need a broad-based program of training and physical conditioning tailored to the specific actions they will perform. The team’s medical officer should stress regular physical conditioning. A comprehensive plan of proper nutrition and exercise must be established and maintained. This should include a balance of aerobic and anaerobic exercises and stretching. Cardiovascular fitness workouts, such as running or swimming, are excellent for the tactical team. Full-body or resistance circuit weight training is excellent for strength training, but it must be a total body workout. Training some parts of the body but ignoring others can lead to costly injuries and a lower level of fitness.90 Flexibility training is one of the best ways to prevent injuries in the field. Unfortunately, it is frequently ignored. Regular stretching or yoga has been long recognized as beneficial in athletic physical conditioning. In this respect, the tactical unit is no different from any other group of athletes. When the physical conditioning program encompasses all these points, the team operates at its peak potential with fewer injuries. A sound diet should be stressed and maintained, but diet is often a controversial topic. In response to the obesity problem in the United States, the Food and Drug Administration (FDA) and many other researchers have looked at diets worldwide and their effects on the human body. Randomized clinical trials studying the risks and benefits of various individual diets are recent.9,27,80,97 The FDA studied the traditional food pyramid (which is based on four food groups and is now no longer considered a valid nutritional program).70 Many other diets have been extensively studied.24 Based on these and other studies, the FDA revised the food pyramid to a more balanced program designed for variations in age, gender, and level of physical activity. It now contains five food groups: grains, vegetables, fruits, milk, and meat and beans. Fats, sugars, sodium, and total caloric intake are restricted. The FDA has an interactive website for the new food pyramid (http://www.foodpyramid.gov). Although our knowledge of diet and exercise has improved, data continue to be gathered, and the perfect dietary program for the tactical operator is not yet known. Nonetheless, fast foods and simple sugars should be deemphasized or eliminated from the tactical operator’s diet. Smart nutrition, coupled with physical training, are the keys to the fitness level necessary to perform at the expected level for a SWAT operator. Preventive medicine should be stressed with regular physical examinations, weight loss programs, and treatment where appropriate. Smoking cessation, alcohol and drug counseling, and stress management are the responsibilities of every team medical officer.

OPERATIONAL CASUALTY CARE Education from military medical operations has helped civilian law enforcement medical providers recognize injury patterns coupled with appropriate treatments, as well as identify equipment that can be used during SWAT operations. The typical ABCs cannot be directly extrapolated to a hostile environment. Extrication to a place where appropriate medical care can be provided is a priority that may be unfamiliar to normal urban EMS. Hemorrhage control is paramount; saving as much of the victim’s own blood as possible has more value than trying to replace blood volume with IV fluid. Tourniquets are a first-line treatment modality in tactical medical support, whereas they may be seen as a last resort in routine EMS (Figure 25-18, C ). Tactical medical personnel are aware that tactics come first, followed by appropriate medical care. When the two entities are

blurred or reversed, a poor outcome is more likely. Each tactical medical provider must be knowledgeable in the tactics of his or her team and trained to the satisfaction of the team leader in order not to jeopardize a team’s mission or increase the chances of an injury being mistreated. The medical providers must constantly reassess as much of the dynamic component of the operation as possible. Contingency planning and the ability to adapt to the fluid nature of these situations is required to be successful as a member of the SWAT team (Figure 25-18, D). The public safety agency developing a tactical medicine operational program should conduct a needs assessment to determine the level of emergency care required by the SWAT team to support its mission and operations. The operational program must consider the needs for medical oversight and coordination with the local EMS agency; medical direction; use of EMTs, paramedics, and other advanced life support personnel; and minimum training and equipment standards. The agency should develop policies and procedures for medical support during tactical operations. Approved tactical medicine training programs, which provide initial and refresher or update tactical medicine training to personnel, should adhere to the minimum training guidelines established by California POST and EMSA and the standards outlined in the guidelines. The goal of the guidelines manual is to describe minimum core competencies and to define the written and skills testing necessary to achieve the standards prescribed by California POST and EMSA. The guidelines that have been approved are available at the POST website at http://www.post.ca.gov/ Training/Tactical_Medicine/default.asp.

TACTICAL MEDICAL EQUIPMENT In general, tactical EMS medical equipment comes from other areas of emergency medicine and law enforcement and is combined into field-expedient, multifunction toolkits. Looking at the gear as a whole, a modular approach may be most helpful (Figure 25-19, A). The gear differs depending on the roles of the providers and the tactical unit.32 Basic equipment for the operator includes essential items. Typically an operator has a duty uniform consisting of a battle dress uniform.92 The uniform may undergo appropriate modifications depending on weather conditions. As with other areas of outdoor activity, it is wise to use a system of layers that can be easily adjusted to changing weather conditions. Waterproof and breathable outer layers may be a consideration, as are wicking underlayers. In addition to the standard duty uniform, a Nomex balaclava and gloves are worn on many entries to protect from exposure to pyrotechnic devices. Because this is an environment where gunfire may be encountered, ballistic protection in the form of body armor is needed. For the tactical medical provider, levels I and II-A are not advised. Level II is the bare minimum if the body armor is concealed under a shirt or uniform, but levels III-A to IV are better (Table 25-3 and Figure 25-19, B). These levels of protection have a good balance of bullet stopping power and ability to absorb blunt trauma. Many tactical operators combine body armor with ballistic plates made of metal or ceramic, which stop high-velocity rifle bullets. Body armor is chosen by the agency from a vast array of different types and styles. Some tactical medical providers also carry a Kevlar blanket or ballistic shield, which can be used to cover a patient in harm’s way or can be used as a mobile source of cover when providing care or extracting a downed victim. These blankets, although effective, are extremely heavy and bulky. Despite the best ballistic protection, limbs are very susceptible to ballistic trauma. As a result, uniforms with integrated tourniquets have become available. This simplifies the application of lifesaving tourniquets because they are already in place. The weight and bulk of all nonmedical tactical equipment hinders the ability to carry large amounts of additional material. The medic needs to decide how much can be carried and whether to wear a backpack or a load-bearing vest, or neither. In general, the tactical medical provider must be able to effectively carry equipment and operate in a tactical situation without hindering the rest of the team. Of the two general sets of medical equipment, one is carried for immediate care, typically worn in 497

CHAPTER 25  Tactical Medicine

TEAM HEALTH MANAGEMENT

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Radios with microphones and headsets are fairly standard for most tactical units. Radios should be set to secure channels. Some communications may even be encrypted. Simple communication during the operation between members may involve standard or specialized sign language (Figure 25-19, C ).

ENTRY AND BREACHING TOOLS

A

Specialized entry tools are used to gain access to barricaded subjects or closed doors. Typical items, familiar to firefighters and EMS personnel, include pry bars, battering rams, sledge hammers, hooks on chains or rope, stop blocks, and halligan tools (Figure 25-20). Ladders may be needed to gain access to an elevated or depressed point. In extreme cases, explosive devices are available to trained explosive experts in the tactical unit to gain entry to an area.

WEAPONS SYSTEMS

B

Whether a team medic should be a sworn law enforcement officer or an armed civilian has been a subject of much debate. Regardless, a provider must be familiar with the unit’s weapons systems. Weapons systems are constantly encountered in the tactical arena. A provider who is a sworn officer has a primary role as an operator on the unit and a secondary role as a medical provider.75,78 However, a provider who is first a medical officer would still have to protect himself or herself in a hostile situation and therefore would be armed defensively. In another scenario, the provider may be unarmed but may have to take charge of an officer’s weapon in a medical or tactical situation. An armed officer who is disoriented may become a danger to the team, so the provider would need to take charge of all of the officer’s weapons and render them safe. In the worst case, the provider may have to defend a downed officer using the officer’s weapon. Weapons system familiarity is paramount for the tactical medicine provider. A provider should be familiar with every handgun, shotgun, rifle, submachine gun, assault rifle, and smoke or chemical agent gun used by the team. All tactical team members, whether providers or not, should be able to use and render safe any weapon carried by a team member.88 The provider should not be exempt from this requirement (Figures 25-21 and 25-22). Weapons systems use a variety of ammunition (see Chapter 24) Typically there is a duty handgun, which shoots low-velocity handgun ammunition. This same ammunition may be used by a submachine gun, such as the Heckler and Koch (HK) MP5 UMP 40, or UMP 45. Calibers of the handgun and submachine gun should be matched to avoid the wrong caliber ammunition going into the wrong weapon, causing malfunction in a crisis situation. Law enforcement and military weapons such as the Colt M4, fire

C FIGURE 25-19  A, Blackhawk Products Group special operations medical backpack in use by tactical medics. B, Tactical heavy body armor ballistic vest, level III-A, showing trauma plate worn for law enforcement tactical operations. C, Communication with the entry team is critical for the tactical medic. This medic is equipped with headset, microphone, and encrypted radio. He is also staged behind the SWAT armored vehicle for hard cover. (B courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD; C courtesy International School of Tactical Medicine.)

a small backpack or load-bearing vest, and the second is carried in a larger backpack or duffel bag in the support vehicle. The latter is used for more extensive treatment, multiple casualties, and prolonged transports.57

COMMUNICATION Communication between team members and tactical medical providers outside the area of the operation is often essential. 498

FIGURE 25-20  Special tools and equipment are used to gain rapid entry by SWAT teams. (Courtesy International School of Tactical Medicine.)

Test Variables

Armor Type I

Test Round 1 2

II-A

1 2

II

1 2

III-A

1 2

III

—

IV

—

Special requirement

—

Test Ammunition 38 Special RN Lead 22 LRHV Lead 357 Magnum JSP 9 mm FMJ 357 Magnum JSP 9 mm FMJ 44 Magnum Lead SWC Gas Checked 9mm FMJ 7.62mm (308 Winchester) FMJ 30–06 AP *

Nominal Bullet Mass

Performance Requirements Minimum Required Bullet Velocity

Required Fair Hits per Armor Part at 0° Angle of Incidence

Maximum Depth of Deformation

Required Fair Hits per Armor Part at 30° Angle of Incidence

44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches)

2

44 mm (1.73 inches) 44 mm (1.73 inches)

2

44 mm (1.73 inches) 44mm (1.73 inches)

0

10.2 g 158 gr 2.6 g 40 gr 10.2 g 158 gr 8.0 g 124 gr 10.2 g 158 gr 8.0 g 124 gr 15.55 g 240 gr

259 m/sec (850 ft/sec) 320 m/sec (1050 ft/sec) 381 m/sec (1250 ft/sec) 332 m/sec (1090 ft/sec) 425 m/sec (1395 ft/sec) 358 m/sec (1175 ft/sec) 426 m/sec (1400 ft/sec)

4

8.0 g 124 gr 9.7 g 150 gr

426 m/sec (1400 ft/sec) 838 m/sec (2750 ft/sec)

4

10.8 g 166 gr *

868 m/sec (2850 ft/sec) *

1

4 4 4 4 4 4

6

*

2 2 2 2 2 2

0

*

From U.S. Department of Justice National Institute of Justice: Ballistic resistance of police body armor, NIJ Standard 0101.03; 5.2.1, April 1987. *See section 2.2.7 of reference. g, Grams; gr, grains.

.223-caliber high-velocity cartridges. The provider may be exposed to shotgun ammunition, typically 00 buckshot. The team sniper deploys with a .308 high-velocity rifle that is bolt action. The flight characteristics and ballistics of shotgun, rifle, and handgun ammunition vary depending on the weight, shape, and velocity of the ammunition. The provider should be familiar with

A

the characteristics of gunshot wounds in order to treat field wounds appropriately. In addition to traditional ammunition, the provider may be faced with distraction devices, chemical munitions, and less lethal munitions. Chemical munitions deliver a chemical agent to an intended target to disorient or incapacitate and facilitate capture or surrender without loss of life. Typical chemical agents used in tactical operations are tear gas or a derivative of pepper spray. Less lethal munitions are used to incapacitate and facilitate capture. Unfortunately, with this use of force, injury is common, so the provider should be familiar with the injuries and their treatments. These munitions are low-velocity projectiles of wood, hard rubber, foam rubber, plastic, or beanbags. They have enough force to cause pain and usually make an assailant stop aggressive action on contact. They usually cause minor blunt trauma, but they may achieve enough force and velocity to penetrate into body cavities (Figure 25-23). Tasers are another example of less lethal devices. A Taser delivers an electrical charge to incapacitate the attacker, but below the level that causes cardiac arrhythmias. The assailant experiences intense muscular contraction throughout his or her

B FIGURE 25-21  Law enforcement tactical medics receive training with the tactical pistol (A) and HK MP5 submachine gun (B). (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

FIGURE 25-22  Tactical medics receive training and familiarization with the 40-mm less-lethal munitions launcher. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

499

CHAPTER 25  Tactical Medicine

TABLE 25-3  U.S. Department of Justice Rating of Body Armor

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 25-23  Victim of a 40-mm round to the head with lethal consequences. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

body and loss of muscular control. The resultant injury patterns are typically a result of the subsequent fall to the ground. Clearance for booking should include an electrocardiogram, local wound care, removal of the electrodes from the skin, and an update of tetanus immunization if needed (Figure 25-24). Explosive breeching techniques and distraction devices are often deployed during tactical operations. The small explosives used to gain entry into an area can create injuries.66 For example, a distraction device that is hand thrown into an area to deliberately disorient a suspect and divert attention toward the device and away from the entry team. These devices usually have a nonexploding canister and a small explosive charge. The device is activated and thrown much like a military hand grenade. It creates a brilliant flash of light (6 to 8 million candlepower) and a thunderous noise of approximately 175 decibels. This is accomplished by venting explosive gases through multiple holes in the canister. Physical effects of distraction devices and explosive entries include major and minor burns, smoke-induced bronchospasm, vestibular dysfunction, transient visual disorientation, and emotional upset and anxiety. In general use, the distraction device has not been reported to cause ear drum rupture. Explosive breaching is the role of the team’s explosives expert, with whom

FIGURE 25-24  Tasered suspect. The darts are intact in the left lower back area. (Courtesy International School of Tactical Medicine.)

500

FIGURE 25-25  Tactical team training for explosive breeching. (Courtesy International School of Tactical Medicine.)

the medic should consult, as part of the medical threat assessment, about the types of explosives planned and the blast forces that may be encountered (Figure 25-25).

VISION Covert operations and low-light situations dictate the use of visual adjuncts. Binoculars, tactical mirrors, spotlights, periscopes, strobe lights, chemical lights, and headlamps are often deployed in a low-light tactical environment (Figure 25-26). Proper training and discipline are required for use of these devices in the tactical environment, because they may give away one’s position and alert a hostile opponent to the team’s position. Similarly, electronic night vision equipment, which operates outside of the range of visible light, is also extensively used.

MEDICAL THREAT ASSESSMENT Any mission planning must include a medical threat assessment (MTA). The SWAT commander uses information from many sources to create a tactical plan before execution of a mission, including available personnel, building layouts, street layouts, necessary support equipment, nature of the mission, available weaponry, and various sources of intelligence.63 An MTA is an important component of the intelligence the commander needs to properly execute the mission. It is the responsibility of the tactical medic to provide a concise and accurate medical briefing to the commander. MTA forms should be used on every mission to ensure systematic planning, because scenarios and problems may be unique. Only a systematic approach ensures complete assessment of the situation. The tactical medical team and its MTA are key factors in dealing with apocalyptic terrorist events, such as the Columbine

FIGURE 25-26  A SureFire headlamp setup can use white light or LED light in low-light tactical situations. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

Location Type of operation

Hostage #

Suspect #

Warrant #

Protection #

Open terrain search #

Terrorist #

Other teams

Tactical

EMS/medics

K9

Patrol

Detective

FBI/other

school shootings and the school hostage crisis in Beslan, Russia.84 Other venues, such as protection details and the war on drugs, rely heavily on a team’s internal capacity for medical care, as evidenced by the U.S. Marshals Service judicial protection training program.85 A complete threat assessment should include these elements: 1. Location of the operation, with a brief description of the goals of the mission and the other teams involved, with their needs and resources (Table 25-4). 2. Locations of all surrounding hospitals and medical care facilities, such as designated burn and trauma centers, with telephone numbers to facilitate communication. Local EMS numbers should be listed. 3. Helicopter flight plan. Before the mission, it should be ascertained that a helicopter is available and that there is an acceptable landing zone (LZ) for day or night conditions. This should include the exact Global Positioning System (GPS) coordinates of the LZ. Obstructions and debris should be cleared before the mission (Table 25-5 and Figure 25-27). 4. Weather. Factors to be evaluated include temperature, rain, wind, humidity, wet bulb temperature (TW), and windchill. Sunrise and sunset times should be recorded and logged. The TW is the lowest temperature to which air can be cooled by the evaporation of water into the air at a constant pressure, so it reflects the limit to which a person can shed heat through sweating in a hot environment. The TW is used to determine fluid requirements and the need for work–rest cycles. The weather-related components of the MTA are used to determine the appropriate uniform and shelter required to prevent overheating or hypothermia (Table 25-6). Water sources should be recorded before the mission as part of the MTA. 5. Plant and animal threats. Plant exposures, especially to poison ivy and poison oak, are common to snipers. Snakebites are common to team members working with police dogs. Anticipated animal threats should be recorded, along with telephone numbers for the police veterinarian, animal control, and poison control, including sources of antivenom (Table 25-7).

Without a medical record, there is no proof that appropriate medical care was given.

Medical Personal Protective Equipment Standard precautions against infectious diseases must be deployed; tactical medicine is no different from any other venue in this respect. Medical personal protective equipment includes masks, eye protection, gloves, and perhaps gowns. In remote locations, surgical treatment may be provided before transport to a tertiary care center. The basics for protection should be carried on the provider’s person in a readily accessible location. Some tactical medics don surgical gloves underneath their shooting gloves before an operation so they will be ready if the need arises. Although not sterile, they provide protection from blood and body fluid–borne pathogens.

PERSONAL SUPPLY MODULE To reduce the amount of equipment carried by the medic and to help team members help themselves, each member of the tactical unit should carry a personal supply module (PSM), or “self-help kit,” with medical supplies. A team member can thus provide self-help or aid another member, and the medic may not have to be summoned until the scene is more secure. A typical PSM should be vacuum sealed and contain supplies for basic trauma care and for IV access (Table 25-8). Vacuum sealing these contents provides protection from the elements and makes them last longer. It also cuts down greatly on bulk but adds some weight. Each medical provider should carry a casualty response kit. This kit should be small, lightweight, and contain the necessary components to specifically treat gunshot wounds, hemorrhage, tension pneumothorax, sucking chest wounds, eye injuries,

FORMS AND DOCUMENTATION Medical records should be kept for the team and for anyone treated or evaluated as a TEMS patient. Records should be stored for a minimum of 10 years and have proved to be indispensable as defense documents in several antipolice liability lawsuits. TABLE 25-5  Sample Form for Helicopter

Information

Helicopter

Obstructions?

LZ coordinates

LZ cleared before mission start? Landing zone (LZ)

Address:

Latitude

Longitude FIGURE 25-27  Air ambulance helicopter preparing for tactical casualty evacuation. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

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CHAPTER 25  Tactical Medicine

TABLE 25-4  Sample Form to Provide Operational Information

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 25-6  Sample Form for Weather-Related Information Temp high

Wet bulb temp °C (°F)

32.2(90)

Sunrise:

AM

Temp low

H2O qt/hr

0.5

0.5

0.5

0.5-1.0

1.0

1.0-1.5

2.0

Sunset:

PM

Rain %

Rest Min/Hr

0

0

0

10

15

30

40

Wind: mph

Cold casualties

Y/N

Work cycles

Heat casualties

Y/N

Yes/No

Uniform adjustments

Y/N

Shelter: Y/N

Humidity %

Night ops: Duration: Location:

TABLE 25-7  Animal and Plant Threats Animal Threats Yes/No

Animals present?

Yes/No

Police dog?

Types of animals

Number:

Do you anticipate wild animals?

Poisonous snake exposure:

Yes/No

# Yes/No

Veterinarian's address:

What type? Vet phone:

Yes/No Animal Control:

Poison Control:

973-470-2242

800-222-1222

Plant Threats Yes/No

Exposure to poisonous plants likely?

Yes

Type No

Tecnu or Ivy Block available?

Yes No

Uniform adjustments needed?

Yes

Recommendations:

No

burns, and lacerations. The drop leg configuration is often used by tactical medics because it is readily accessible (Figures 25-28 and 25-29).

BASIC MEDICAL MODULE In addition to a PSM, a basic medical module (BMM) should be carried by team medics. Because every team member in a tactical unit should have at least basic EMT certification, a BMM could be used by any team member to provide initial care to a victim. The BMM should have basic splinting material and dressing material (Table 25-9). Basic airway tools, such as nasal airways and pocket mask, should be included. A bag-valve-mask or a more compact alternative is advisable in the tactical environment. A simple bagvalve-mask alternative device (BVMAD) can be constructed out of respiratory supplies from a one-way valve, flexible tubing, and TABLE 25-8  Sample Contents of Personal Supply

Module

Trauma dressing IV start kit Minor dressings Saline bullets Medicines

Other wound items IV, Intravenous.

502

Bandages such as the Israeli bandage can be easily self-administered by the victim on most extremity wounds 100 mL IV fluid, an alcohol wipe, tourniquet, IV catheter (3), IV tubing, tape, flush and saline lock Adhesive bandages should be carried by all team members Foreign bodies in the eyes are very common on entries, and a bottle of eye drops (saline bullets) may allow an operator to continue on a mission Pain: acetaminophen, ibuprofen, narcotic analgesics Antibiotics: ciprofloxacin, metronidazole, cephalexin Surgical staples or liquid tissue adhesive

a mouthpiece (Figure 25-30).5 This is the preferred ventilatory device in the tactical environment, because it allows a rescuer to provide ventilation without unnecessary bulk. If the tubing is long enough, the person providing ventilation can work handsfree if the patient is intubated. The additional length leaves the rescuer’s hands free to carry the patient, perform other medical tasks, or to even defend the patient with a weapon. Oxygen is rarely useful in the immediate tactical environment, so oxygen cylinders are left in the support vehicle with a regular bag-valve-mask and retrieved when necessary. An automated external defibrillator (AED) should be carried in the support vehicle.3 A small collapsible litter for extrication of a downed person should be a part of every BMM.

INTERMEDIATE MEDICAL MODULE An intermediate medical module (IMM) is intended for use by paramedics and registered nurses. Unlike the BMM, it contains equipment and supplies suitable for advanced life support (ALS). Under standing orders from a team physician, ALS providers may provide advanced cardiac life support to a victim. An IMM is much more extensive than a BMM. It contains medications, IV

FIGURE 25-28  Saline bullets remove the most common injury: foreign bodies in the eyes. Personal medical kit typically carried by SWAT officers. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

FIGURE 25-29  Casualty response kit for tactical medics. It can be carried on the belt or MOLLE (modular lightweight load-carrying equipment) system or in the drop-leg configuration. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

tubing, IV fluids, endotracheal tube, Combitube, laryngoscope, light wand, and, if protocol allows, cricothyrotomy kit (Table 25-10 and Figure 25-31). These facilitate placement of a definitive airway before transport, which, when used with a BVMAD, permits hands-free ventilation of a patient, allowing extrication by one or two team members. Proficiency with the airway toolkit is of high priority.

ADVANCED MEDICAL MODULE The most complex module is the advanced medical module (AMM), intended for independent practitioners, such as nurse practitioners, physician assistants, and physicians. These practitioners can perform advanced surgical procedures and medical interventions that can make the difference between life and death on a long transport. Transport to definitive care should not be delayed unless medically necessary. However, if advanced care in the field is indicated, it can be provided by an independent practitioner with an AMM.

MAJOR TRAUMA MODULE Lengthy surgical interventions in the field are not advised and have extremely poor prognoses. Although rapid transport to a TABLE 25-9  Sample Contents of Basic Medical

Module

Splints Airway Litter Wound care Other

Two SAM splints Pocket mask, bag-valve-mask (BVM) or BVM alternative device (BVMAD), oral and nasal airways Fold-up stretcher Various trauma dressings Elastic (Ace) wraps and cravats

FIGURE 25-31  A well-stocked and functional tactical intermediate medical module (IMM) airway kit, containing a laryngoscope, a bagvalve-mask alternative device (BVMAD), oral airways, bougie, stylette, endotracheal tubes, tape, and surgical airway kit. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

trauma center should not be delayed, some surgical procedures may be of benefit when performed in the field: laceration repair to stop bleeding or facilitate evacuation, cricothyrotomy, and, in critical situations, chest tube insertion. These types of procedures can usually be performed using only the essential equipment found in a vacuum-sealed minor-surgery tray (Figure 25-32), which can be one component of the major trauma module (MTM) for advanced providers (Table 25-11). Many users include hemostatic dressings in trauma kits, but their use is not yet well studied.58,83 The efficacy versus the potential harm of hemostatic dressings is a subject of debate. Direct pressure with a sterile dressing is the initial approach to hemorrhage control. The traditional and time-tested approaches of pressure-point compression and tourniquets are useful adjuncts to any bleeding problem, so these materials should be included in the MTM. A set of combine dressings, gauze, petrolatum gauze, and Israeli dressings should also be carried.

SUPPORT VEHICLE MODULE Additional supplies and equipment are kept in the support vehicle module (SVM). Consumable items should be kept in the SVM so that other modules can be restocked from it (Table 25-12). The SVM contains equipment such as oxygen cylinders, an AED, airway adjunct devices, fiberoptic scopes, nebulizers, surgical trays, chest tubes, cervical collars, backboards, peroxide, TABLE 25-10  Sample Contents of Intermediate

Medical Module

Airway Medications

Endotracheal tubes, laryngoscope, stylette, bougie, bag-valve-mask alternative device (BVMAD) Intravenous setup and tubing, pain medication, rapid sequence intubation medications, antibiotics

503

CHAPTER 25  Tactical Medicine

FIGURE 25-30  The bag-valve-mask alternative device (BVMAD) as it is stored, with the mouthpiece (red arrow) over the exhaust port. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 25-32  A vacuum-sealed minor-surgery tray. Many procedures in the tactical environment can be accomplished with a minimum  of equipment. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

povidone-iodine, liter bags of crystalloid IV fluid, replacement filters for gas masks, and fiberglass splinting material. Field care is limited only by the equipment that can be transported and the training of the providers. Items carried by advanced providers include the following: • Central line • Cricothyrotomy/tracheotomy set • Retrograde intubation set • Laryngeal mask airway • Chest tube set • Fiberoptic intubation set • Blood products or blood substitutes

CHEMICAL, BIOLOGIC, RADIOLOGIC, OR NUCLEAR SPECIALTY MODULES Depending on the role of the tactical unit, chemical, biologic, radiologic, or nuclear (CBRN) threats may be encountered. These incidents require tactical emergency medical care because they involve large crime scenes with casualties. Individuals trained in tactical emergency medicine are much more familiar with evidence

collection and preservation, and they usually already have necessary security clearance to enter such an area. Until the scene is cleared, the tactical physician may be the only one who can provide medical care to victims. Chemical and biologic environments are specialized depending on the agent released. Various civilian and military protective gear and respirators or supplied air sources may need to be worn. Operating in CBRN protective gear requires extensive training in addition to regular tactical training. Antibiotic prophylaxis with ciprofloxacin, as well as agent detection equipment, may be carried by the medic. Several biologic and chemical diagnostic kits and meters are available but costly. Radiologic incidents potentially involve dispersal of a radiologic agent with conventional explosives, the combination often referred to as a dirty bomb. Nuclear detonations refer to splitting of a radioisotope and the resultant massive energy release from a nuclear bomb. Geiger counters are available for radiologic and nuclear situations. These situations require a great deal of additional training, but they are not beyond the realm of tactical emergency medicine. Hazardous material (hazmat) situations are frequently seen in civilian law enforcement raids on clandestine drug laboratories. Level A, B, or C protective suits with gas masks or supplied air may be required in these situations as well. Hazmat and CBRN situations are highly specialized in their nature and require extensive training, beyond the scope of this text.

The Tactical Mission Each mission has a number of phases:52,91 1. Warning order (issued when the tactical team is first requested and establishes the situation and chain of command) 2. Gathering of intelligence a. Building intelligence (includes location and surrounding areas, avenues of approach, escape routes, and rally points, as well as natural and man-made obstacles, fields of fire, opportunities for cover and concealment) b. Suspect or hostage intelligence (as detailed as possible) c. Medical threat assessment (complete) TABLE 25-12  Sample Contents of Support Vehicle

Module (SVM)

TABLE 25-11  Sample Contents of Major

Biohazard container Saline eye flush

Israeli dressing

Elastic wraps Splinting material

Trauma Module

Combine dressings Gauze pads Antibiotic packs Tourniquet Wound closures Minor-surgery tray Elastic wraps Splinting material IV fluids

Supplies Other IV, Intravenous.

504

May be self-administered by the patient with one hand; combines an elastic wrap, combine dressing, and tourniquet in one device To control heavy bleeding or cover eviscerated bowel and open fractures Multiple uses Pre-prepared medication packs for major trauma, containing pain medication and antibiotics Several excellent devices are available for tactical use Sutures, staples, and wound adhesives For performing surgical procedures that cannot wait for extrication or transport Strains, sprains, and fractures are common SAM splint or a short sealed roll of fiberglass casting material. Bullet wounds frequently fracture long bones For infusion of medication and management of shock as needed. Also used for wound irrigation and eye irrigation. Several IV start kits should also be on hand Gloves, tape, trauma shears, tweezers, adhesive bandages, roll gauze, cravats, nasal airways, 60-mL syringes, headlamp Duct tape, biohazard bags, medical record sheets, and trauma tags for multiple casualties

Intravenous (IV) fluids Ice packs

Wound dressings Advanced airway tools Spare uniforms Oxygen cylinders Bag-valve-mask (BVM) Automated external defibrillator (AED)

Disposal container for used sharps and medical waste Foreign bodies in the eyes are common on entries Strains, sprains, and fractures are common Fairly bulky and difficult to carry in the medical pack. Cervical collars are frequently kept here and may be retrieved when needed For prolonged transport or massive hemorrhage, more IV fluid should be kept in the SVM and not carried on entries. Multiple IV start packs for use when necessary Ice packs are commonly used, because ice is not always available in the field. If the location has a freezer, bags should be kept to use existing ice Additional adhesive bandages, Israeli dressings, combine dressings, ABD pads, and burn dressings Difficult-airway tools may be needed in the cold zone before transport to secure a definitive airway If decontamination is needed, the victim will need to be reclothed in a clean, dry uniform, particularly in cold or wet environments Best left in the support vehicle because of their weight Replaces the BVM alternative device when hooked up to oxygen in the cold zone The AED is proved to save lives but is too bulky to carry on entry

Reserve Programs The methods in which a tactical medical team is used by a law enforcement agency can differ widely, especially between the East Coast and the West Coast. For example, in the western United States, especially California, Arizona, Nevada, Washington, Utah, and Oregon, there are many reserve programs in the police and sheriff’s departments.61 In these programs, the tactical medical provider has additional, formal law enforcement training, such as found in the POST program in California. This program allows the provider to be a sworn peace officer (carry firearms and have powers of arrest), bringing about an enhanced comfort level for the department and potentially mitigating some issues of civil liability. On the East Coast, reserve opportunities are less common, and medical providers typically serve as auxiliary units borrowed from traditional fire and EMS agencies. The liability issues and expenses in this type of relationship are often resolved via a written “memorandum of understanding” between the participating agencies.79 Selecting appropriate providers must be accomplished through interviews, psychological testing, background investigations, and physical fitness testing. The tactical team leaders should use a careful approach in the selection process for each candidate, just as they do for other members of the team.56

Military Combat Field Units Field units vary significantly with the mission, service, and threat (Figure 25-33). Most often, medical care is provided in the open or in as secure a location as possible. It is done on the ground,

on a table, in the back of a Humvee, or on an aircraft or a watercraft. Specific types of shelter and equipment are available, most often in the far-forward care under fire and the tactical field care phases, but generally the equipment is as noted earlier. When CBRN threats or high explosives are added to the scenario, the forward elements are the same, with the exception of the appropriate protective clothing. Once evacuation occurs, the injured team member is taken to a standard unit with the capability for decontamination and treatment, much as is done in the civilian setting. Most larger military transport planes have the capability to accept a critical care air transport team, which has a physician trained in critical care (emergency medicine, anesthesiology, internal medicine), critical care nurse, and respiratory technician. Most larger Navy ships are equipped with fully functioning operating rooms and intensive care units, or they can expand to provide this service quickly. All the services have basic medical units, from the self-aid or buddy-aid, to an aid station (with a physician), to forward resuscitative systems (surgical and nonsurgical), to surgical companies, combat surgical hospitals, and their equivalents. All services also have teams that are available to move far forward to provide surgical capabilities quickly should the need arise. These units can operate on any semiflat surface, do resuscitative surgery, and package the patient for expeditious transport for further care.12

UNIFORMS AND PERSONAL PROTECTIVE GEAR The standard law enforcement tactical operator carries between 40 and 60 lb of equipment. For longer missions, gear is heavier. Clearly, the operator needs to be in excellent physical condition, and the mission commander must proactively manage nutrition, hydration, and exertion levels. From anecdotal reports, the military has seen a significant decrease in truncal injuries because body armor has improved. The medical personnel noted that the insurgent combatants in Operation Iraqi Freedom changed their IEDs to target the head, neck, and extremities more than the whole body. Continued development is under way to produce body armor that will protect against higher-energy weapons, protect extremities, and be sufficiently lightweight and flexible to allow fieldwork. Because protective clothing is not removed in the field, the medic must work under and around it. Vigilance is required to check all body areas for hidden wounds. This is clearly more difficult in the field, in the dark, with sound and light restrictions, and with clothing in place than when the patient is undressed on the trauma table. Because the medic carries all the usual combat equipment, medical equipment is additional. Stethoscopes are usually left behind, because the medic cannot use the earpieces under the helmet, the environment is not conducive to being able to hear anything, and the victim is usually wearing body armor. Advanced medical gear is usually found on the medevac vehicle, or farther to the rear where it is safe enough to remove protective equipment and further evaluate and treat the patient.

Education and Training Programs

FIGURE 25-33  Law enforcement tactical medical team during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

Tremendous advancement in tactical medicine education over the last decade has resulted in numerous training programs, many providing formal continuing medical education credits. These courses focus on the core issues of tactical medicine. A unique aspect of tactical medicine is application of ALS in an austere environment. The traditional approach to providing EMS is often not feasible in a tactical situation.86 Cost-effective tactical medicine training and education is available and should be afforded to all involved medical personnel, including prehospital care providers and physicians. All team medical personnel should be trained to the highest level possible. Such training provides emergency medical personnel with an understanding of tactical procedures and an appreciation for why some routine prehospital care techniques may not be appropriate in the tactical environment.51,55 Tactical medicine training should be as realistic as possible with live teaching scenarios in full tactical gear. This allows the medical 505

CHAPTER 25  Tactical Medicine

3. Operation order 4. Briefing phase a. Detailed planning b. Detailed briefing c. Equipment selection d. Move to staging 5. Execution phase a. Entry b. Secondary search c. Transfer to arrest team and investigation team d. End of mission 6. Debriefing phase a. All persons, weapons, equipment, injuries, shots fired, and ammunition must be accounted for. b. Any problems must be discussed. Medical personnel should have the opportunity to discuss the mission from their perspective. In general, a tactical mission follows this order, although it may differ somewhat between agencies and missions. Proper handling of each point is required for a mission to flow seamlessly. Without proper intelligence, a mission becomes hazardous.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 25-13  Sample Curriculum for Basic Tactical

TABLE 25-14  Sample Curriculum for Advanced

Day 1

Day 1

Medicine Training

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Introduction to Tactical Medicine Tactical Medical Equipment Tactical Equipment Team Concepts and Planning Slow and Deliberate Team Movement Introduction to Tactical Pistol Medical Aspects of Chemical Agents and Distraction Devices Forced Entry Techniques Dynamic Clearing Techniques Operational Casualty Care Wound Ballistics Hemostatic Techniques and Dressings Team Health Management Medical Aspects of Clandestine Drug Labs Tactical Medical Scenarios Introduction to MP5 Submachine Gun Special Operations Aeromedical Evacuation Medical Management of K-9 Emergencies Disguised Weapons and Street Survival Medical Threat Assessment Written Exam Safety Briefing Tactical Medical Scenarios

Tactical Medicine Training

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Pediatric Trauma Management Trauma Anesthesia Building Clearing Techniques Review Tactical Medical Scenarios Range Advanced Pistol–MP5 Advanced Airway Management Advanced Airway Management Skills Stations Environmental Injuries WMD Biological Weapons Part 1 WMD Biological Weapons Part 2 Medical Issues of Less-Lethal Weapons Low Light Tactics and Team Movement Tactical Medical Scenarios Pistol–MP5 Field Courses Explosive Entry Demonstrations Medical Management of Blast Injuries WMD Chemical Weapons WMD Nuclear and Radiation Injuries Written Exam Safety Briefing Tactical Medical Scenarios

From International School of Tactical Medicine, copyright 1996-2005. http://www.tacticalmedicine.com. WMD, Weapons of mass destruction.

From International School of Tactical Medicine, copyright 1996-2005. http://www.tacticalmedicine.com.

providers to more fully understand the unique aspects of law enforcement tactical operations and the roles and responsibilities of each team member, along with the integration and application of EMS. With an established body of knowledge and skills, graduates of such training programs are better prepared to effectively perform as safe tactical medical providers (Figure 25-34).62 The International School of Tactical Medicine (http://www. tacticalmedicine.com), a law enforcement agency program, is based at the Palm Springs Police Department Training Center in Palm Springs, California. This school offers a comprehensive 2-week, 80-hour program. The training and educational courses are designed for law enforcement agencies and military special operations teams to enhance their provision of medical care in the austere tactical environment. The program is approved by POST, EMSA, and the United States Department of Homeland Security. The curriculum for each course can be seen in Tables 25-13 and 25-14.

FIGURE 25-34  Tactical medics must be able to provide medical support under any and all operative conditions. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

506

The Tactical EMS School of Columbia, Missouri, offers a 70 hour Essentials of Tactical EMS course (http://www. tactical-specialties.com). The Counter Narcotics and Terrorism Operational Medical Support (CONTOMS) program offers a 56 hour TEMS program (http://www.casualtycareresearchcenter.org).

The Future of Tactical Medicine Tactical medicine will continue to grow as a medical discipline. Emergency medicine and wilderness medicine are the ideal specialties to collaborate on its development. Since the fall of 2002, under the leadership of the International Tactical EMS Association (ITEMS), a multidisciplinary group of subject matter experts has been working to achieve consensus on development of a standardized national curriculum for tactical medicine training.18 Emergency physicians and wilderness medicine physicians should have an understanding of tactical medicine, because they may well have the opportunity to treat an injured operator or victim of violence associated with a tactical law enforcement action.23,39 Tactical medicine is wilderness medicine taking place in both the urban environment and some of the most remote places on Earth. There is a need for research into the unique aspects of tactical medicine, such as injury prevention during operations, methods of ensuring optimal mental and physical preparedness for tactical operators, and evaluation of various standard EMS therapies for their feasibility and efficacy in tactical scenarios. In these times, when the threat of violence to civilians in our society is at an all-time high, we rely on law enforcement professionals and the military to do all they can to keep us safe and protected. It is the role of tactical medics, providing medical care under any and all operative conditions, to give back to these professionals by ensuring that someone is there to care for them if they are injured in the course of doing their duty. Because it is no longer a matter of “if” a law enforcement officer will be injured in the line of duty, it is a matter of “when,” it is no longer a matter of “if” the wilderness medicine physician will encounter medical care related to armed conflict, it is also a matter of “when.”

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 26 



Combat and Casualty Care MICHAEL E. FRANCO, EDWARD J. OTTEN, THOMAS F. DITZLER, SHON COMPTON, AND PATRICIA R. HASTINGS It is difficult to emphasize sufficiently the importance of initial treatment on the battlefield. What the wounded soldier does in his own behalf, or what his infantry colleagues do for him; and what the company aidman does for a traumatic amputation or gaping wound of the chest, in the thick of battle, in dust and heat or in blowing snow—on these simple procedures depend life and death. … A slight improvement in the skill and judgment of the company aidman will save … more human lives than will the attainment of 100 percent perfection in the surgical hospital. COLONEL (DR.) DOUGLAS LINDSEY, U.S. ARMY,

1951

It is not commonly recognized that many of the most significant advances in medical science have been made by medical officers in the armed services … working under the stimulus of wartime exigency. PROFESSOR JOHN FULTON, CIRCA

1953

Wilderness Medicine is Combat Medicine with the exception of heavy artillery and aerial bombardment. Both are charged with the delivery of medicine/lifesaving interventions in less than optimal environments, with minimal equipment, and varying evacuation times. MAJOR (PA-C) MICHAEL E. FRANCO,

The Beginnings of Military/ Operational Medicine Wilderness medicine practitioners and disaster, humanitarian, and nongovernmental organization workers venture into environments that are complex, often with unique geography, political/ governmental systems (or lack thereof), and unfamiliar cultures; economic and resource situations may be constrained or desperate. These areas may be involved in conflict, so it is beneficial to have an understanding of the nature of combat casualty care. The first “operational wilderness medicine” courses and training were created centuries ago by military forces. Operational and wilderness medicine requirements have shared a long and symbiotic relationship with exchange of information, lessons learned, and equipment between the military and those physicians and responders willing and able to work in austere environments. Much of the knowledge, both remotely and recently, has benefited emergency care in general and wilderness medicine in particular. Much of the equipment and expertise now used by the military have resulted from improvements and refinement of wilderness medicine professionals. One of the first wilderness medicine experts to document wilderness medicine knowledge was Ibn Al Jazzar (circa AD 895-979) a physician from the Medical School of Kairouan in what is now Tunisia, once known as Carthage, the home of Hannibal (circa 200 BC). He wrote the then landmark wilderness medicine manuscript, Zad El Mousa Fir-Wa Qaout El Hadhir (Provisions for a Voyager Traveling Afar and for the Day’s Subsistence).56 The word for healer in ancient Greek was iatros, meaning remover of arrows. Whether removing arrows in ancient Greece or shrapnel in the 21st century, the unfortunate reality of conflict as part of the human condition requires health care providers to be involved in operational and military medicine. Since the beginning of recorded history, advice for medical response to be applied during conflict has come from those often noted for medical progress unrelated to conflict. Hippocrates (460-370 BC) is known as the Father of Medicine and for the concept, “First, do no harm.” He also gave the advice that “He who would become a surgeon should join the army and follow it.”

2011

Early accounts of medicine in war came from the classic literature, such as Homer’s The Iliad and Virgil’s The Aeneid. The Romans learned from these wars and trained medics (medici vulnerarii); each soldier carried his own bandages, which is similar to the Improved First Aid Kit (IFAK) carried today by soldiers and wilderness trekkers. In these accounts, medicine was rudimentary. Medical intervention concentrated on basic issues of bleeding, infection, and injury. These were the leading early killers in war though the ages and remain so to this day.

Introduction In ancient times any significant injury was likely to result in death. In the Revolutionary War, lethality of combat injury was 42%. In the Civil War, the combat mortality rate was 33% for persons wounded; this decrease was due to improvements made in evacuation from the field with an ambulance corps and surgical care closer to the field. Even with the horrors of chemical munitions and trench warfare, World War I showed a decrease in war injury deaths to 21%. Great strides were made in World War II, including antibiotics and blood/plasma replacement; however, the combat mortality rate remained high at 30%. Korea moved Mobile Army Surgical Hospitals to the front and was the first conflict to routinely use air transport to get injured soldiers to the surgeons. The Korean conflict mortality fell to 25%. Vietnam further emphasized quick evacuation to combat hospitals, but the mortality rate remained steady at 24%.56 In Vietnam, fewer than 3% died after arrival at a combat hospital, attributed to meaningful medical interventions being made earlier.28,29,34 Most deaths were due to hemorrhage and airway/breathing compromise. Desert Storm in 1991, with a short but very intense combat phase, recorded 159 deaths from 626 total traumatic injuries, for a mortality rate of 25%. Military medical leadership studied previous lessons and created a better medical field response. The rates of mortality in the current conflicts of Operation Iraqi Freedom and Operation Enduring Freedom are the lowest seen in the history of conflict. Combat lifesavers (first responders) and then combat medics are at the scene immediately and buy time for injured soldiers. The likelihood of coming home is over 90%24,28,29,34,40 (Table 26-1).

For online-only figures, please go to www.expertconsult.com

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

who have advanced medicine on every front and in many cases have forged a path for others to follow.

TABLE 26-1  Lethality of War Wounds

War

Killed in Action (KIA)

Wounded or KIA

Lethality (%)

Revolutionary War (1775-1783) Civil War (1861-1865) World War I (1917-1918) World War II (1941-1945) Korean conflict (1950-1953) Vietnam War (1961-1973) Persian Gulf War (1990-1991) OIF/OEF (2001-2004) OIF/OEF (2001-present)

4,435 140,414 53,402 963,403 33,741 47,424 147 1,004 4,720

10,623 422,295 257,404 291,557 137,025 200,727 614 10,369 49,337

42 33 21 30 25 24 24 10 9.5

Data from Department of Defense: Operation Enduring Freedom (OEF) U.S. casualty status: Fatalities as of Nov 18, 2010, 10 am EST. http://www.defense. gov/news/casualty.pdf; and Department of Defense: Operation Iraqi Freedom (OIF) U.S. casualty status: Fatalities as of Nov 18, 2010, 10 am EST. http://www.defense.gov/news/casualty.pdf. OEF, Operation Enduring Freedom; OIF, Operation Iraqi Freedom.

In addition, disease, nonbattle injury (DNBI) has been a constant concern for the field surgeon and medic. The outcome of many conflicts has been determined by DNBI. Athens fell to Sparta in 430 BC as a result of an unknown communicable disease. DNBI affecting the outcome of conflict played out again in the trench warfare of World War I, and DNBI was deadly even in the same region of Gallipoli where the British and Australians lost many soldiers to dysentery and other nonbattle injuries.33 In the U.S. Civil War, for every death due to trauma, there were three deaths due to DNBI and starvation. In the Russian-Afghan war over the course of 10 years, the war’s outcome was influenced greatly by disease; some contend that Russia was “beaten by the bugs.”37 Combat by its very nature is a chaotic, dynamic, and unpredictable environment in which military medicine must function well to save lives. The methods and technologic advances used to kill and maim have increased the numbers of injured and the seriousness of the injuries. The nature of war has become less focused on armed conflict between sovereign nations fought by professional militaries and become an undertaking of insurgents, child soldiers, and terrorists. Battlefields often have “no front lines,” and conflict is more dangerous for soldiers, as well as deliberately targeted noncombatant civilians; military medical providers are using new skills to care for these patients. Forward military medicine, performed before reaching combat support hospitals (CSHs), shares attributes with wilderness medicine. These include minimal equipment, harsh climates, remote and austere settings, and sometimes primal conditions. In militaries of the past, operational and wilderness medicine were taught after initial training as “on-the-job training.” Today they are primary medical training and education. Austere conditions typically connote an image of uncivilized remoteness, but they are also found in large populated areas where medical conditions may be impacted by armed conflict, supply shortages, bad weather, and impassable evacuation routes. For persons who deliver prehospital care on the battlefield, in disaster or humanitarian situations, whether urban or rural, working in the “wilderness” is the norm, not the exception. Regardless of environment, combat units within a battle space require medical capability. This capability is also used for injured civilians and forces that have laid down their arms. As strong as military medicine is as a force multiplier, it is also often used as a national engagement tool to shorten conflict, because medicine’s center of gravity and power is science and humanity, not geography, religion, or politics. When used in this manner, medicine may enhance progress toward peace.60 This chapter reviews a few lessons learned from military medicine, with the battlefield as the construct. The intent is to provide operational civilian health care providers an understanding of unique military medical capabilities, the continuum of care, and unique battlefield injuries, as well as describe some of the medical treatments and evacuation issues from the point of wounding to definitive medical care. We thank the hard work and sacrifice of military medical providers throughout history 508

Combat Medicine Compared With Standard Civilian Prehospital Care In conflict environments, completion of the mission and preserving one’s own forces take precedence. Medicine has a place in the tactical environment but is relegated to a secondary role at certain points. Mission-focused combat care is divided into three distinct classifications designed to support the mission: decrease loss of life using principles of triage, take care of immediate life threats with simple interventions of proved benefit, and save as many lives as possible through rapid evacuation. These phases of care do not normally rely on a complete assessment, physical examination or evaluation of past medical history, as might be expected in a secure location in a routine field emergency situation.17,18 The first phase of care, also known as care under fire, can be thought of as any event in which one is called on to render aid in an uncovered, unsecure, or potentially life-threatening situation. One cannot and should not “treat in the street” in a hostile environment. The first action will be to return fire and take cover (or take cover and return fire if more appropriate). There are many reflexive and simultaneous actions that will take place in this phase if the soldiers have been trained and drilled to an adequate degree of fine muscle memory. If one is able to provide care in this phase, the clinical intervention is likely to be only the most basic, such as moving the patient to a covered area to avoid further injury or placing a tourniquet. The usual protocols for ABCs (airway, breathing, circulation) may be reordered to CAB in order to focus on the interventions most likely to have the greatest impact on outcome in the working time frame.63 Care under fire may simply determine whether or not a person is still alive. Mortal wounds or conditions such as an unresponsive patient without a carotid pulse are circumstances in which cardiopulmonary resuscitation would not be performed. After this phase is over, it is important to not forget security issues. These are easily overlooked because of euphoria that may result from the relief of surviving, or the need to begin to care for one’s comrades.18,63 Field medics have long noted that one of their most critical first actions is to provide a confident demeanor. If the casualty is alert and responsive, the medic asks, “Where are you hurt?” and uses words and body language to let the victim know, “I’ve got you, and we’re going to get you out of here.” This is important because the casualty will be trying to determine his or her survivability and prognosis from the medic’s reaction. Major Shon Compton (U.S. Army physician assistant) teaches, “If the mind quits or doubts its chances; the body soon follows …” Tactical field care is rendered after the situation is secure and allows care to proceed. Depending on how quickly the patient is extracted, tactical field care may be the first care provided. The next phase of care is casualty tactical evacuation, in which the patient is stabilized and transported to a more definitive level of care. Evacuation platforms most often are “nonstandard” and nonmedical vehicles that are quickly drafted into use for critical casualty evacuation (CASEVAC).

Scopes of Practice for Combat Lifesaver, Combat Medic Injured soldiers are unlikely to see a physician at the point of wounding. The Army has taken the civilian trauma system lessons of the “golden hour” to the next stage in what it calls the “platinum 10 minutes,” using combat lifesavers and combat medics to provide initial response on the battlefield. Many military emergency physicians note that in that first few minutes, there should be no qualitative difference in the response to traumatic injury between the medic and the physician. Given the same aid bag, the same set of circumstances, and the same patient, the expectation is that the same immediate lifesaving interventions will be made.63

airway skills include use of an adjunct such as a Combitube or King LT device and surgical cricothyrotomy (see Figure 26-1). The 68W is also taught the skills of needle chest decompression and chest tube placement. The 68W has the ability, with special training, to place an IV or intraosseous line and in certain cases administer blood products. The 68W has additional training in management of shock, including resuscitation from hypotension and prevention of hypothermia. Because closed head injury, burns, and stress reactions are prevalent wounds of the Iraq and Afghanistan conflicts, combat medics are entrusted with the initial evaluations of these problems. If the patient cannot be evacuated in a timely fashion, the combat medic may initiate protracted care, to include the placement of a nasogastric tube and urinary catheter. Combat medics also have the capacity to perform limited primary care, using protocols for minor sick call problems, and assist with monitoring for DNBI. They are given training in international humanitarian law (Geneva Law) focused on

Core skill requirements

CLS

68W

RN

PA/MD

Airway: cervical spine immobilization Airway: clear an upper airway obstruction Airway: insert an oral/nasopharyngeal airway Airway: insert Combitube Airway: insert laryngeal mask airway (LMA) Airway: perform endotracheal intubation Airway: perform rapid sequence intubation Airway: perform a needle cricothyroidotomy Airway: perform a surgical cricothyroidotomy Airway: perform endotracheal suctioning Breathing: perform needle chest decompression Breathing: place chest tube for hemo/pneumothorax Breathing: ventilate a patient with bag-valve-mask Breathing: ventilate patient using Impact 754 ventilator Circulation: control bleeding using pressure dressings Circulation: apply tourniquet to control bleeding Circulation: recognize signs/symptoms of shock Circulation: obtain vital signs and recognize changes Circulation: place peripheral intravenous line Circulation: place central line Circulation: perform venous cutdown Circulation: perform intraosseous line placement Circulation: initiate intravenous crystalloid infusion Circulation: administer blood/blood products Circulation: administer volume with Level 1 infuser Circulation: perform pericardiocentesis Circulation: apply a dressing to an open chest wound Circulation: apply a dressing to an open abd wound Circulation: apply a dressing to an open head wound Disability: recognize signs/symptoms of increased intracranial pressure Disability: splint a suspected fracture Exposure: prevent hypothermia Exposure: recognize and treat hypothermia FIGURE 26-1  Core skill requirements. ACLS, Advanced Cardiac Life Support; CLS, combat lifesaver; ECG, electrocardiogram; MD, physician; Continued PA, physician assistant; RN, registered nurse.

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CHAPTER 26  Combat and Casualty Care

Combat lifesavers are first responders that are sometimes called the “battle buddy” of the medic. They buy time for the patient after the initial trauma. Their primary military occupational specialty may be that of infantry, aviation, maintenance, or other military nonmedical specialty, but after the situation is secured, they offer an extra set of hands for the medic. In addition to basic first aid, they are able to provide such skills as to deploy nasopharyngeal airways, apply tourniquets, or perform needle chest decompression for breathing difficulty after a penetrating wound to the chest (Figure 26-1).5 They do not, however, initiate intravenous (IV) lines or perform certain other advanced skills. The combat medic is also known by the designation 68W (68 Whiskey). The scope of practice of the combat medic is most analogous to an EMT-Intermediate, with some special skills training in combat operational medicine based on the security, sick call, and unit issues with which the medic must deal. Additional

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Core skill requirements

CLS

68W

RN

PA/MD

Exposure: protect yourself from heat, cold, biting insects, and diarrhea and dysentery Adjuncts: place and monitor pulse oximeter Adjuncts: monitor ECG rhythm strip Adjuncts: perform hemodynamic monitoring Adjuncts: perform diagnostic peritoneal aspiration/lavage Adjuncts: insert naso/orogastric tube Adjuncts: perform arterial line placement Adjuncts: manage arterial line Adjuncts: insert urinary catheter Management: apply traction splint for extremity fracture Management: apply pelvic sheet/binder for pelvic fracture Management: ligate/clamp bleeding in traumatic amputation Management: provide initial treatment for burns Management: perform regional anesthetic techniques Management: administer first aid to a chemical agent casualty Management: manage combat stress reaction (battle fatigue) Disposition: request medical evacuation Disposition: perform initial triage of casualties ACLS: recognize cardiac arrest and dysrhythmias ACLS: use defibrillator to treat cardiac dysrhythmias ACLS: treat dysrhythmias pharmacologically ACLS: manage hemodynamic alterations pharmacologically FIGURE 26-1, cont’d.

the rights, duties, and responsibilities of combat medics in areas of armed conflict, as well as caring for detainees.

Levels of Care and Capabilities MILITARY HEALTH SYSTEM ECHELONS OF CARE The continuum of care in the military extends from the point of wounding to a battalion aid station (BAS), usually staffed by a physician assistant and/or physician, to the forward surgical team (FST) to the CSH (Figure 26-2).26 At each point of care, the level of surgical and holding capability increases. Military medical planning includes support at each of these levels.3,27,31,54 Level I The first medical care a soldier receives occurs at Level I, which may begin at the point of wounding. Initially, these first responder actions are provided by soldiers with combat lifesaver training, and later with assistance from the combat medic. If the service member is transported to a BAS, care is augmented by a senior medic or physician assistant. Level I initiates triage, patient collection, resuscitative care, and medical evacuation to higher levels of care. If the injuries or illness are minor, treatment is given and the disposition is “return to duty.” If the care required is more than minor, the patient is evacuated to a Level II or Level III facility. The decision is made based on the security situation, 510

distance, and nature of the injuries. The civilian equivalent is similar to a first responder ambulance squad with advanced skills. Level II Level II is broken down into Levels IIA and IIB. Level IIA is an expanded care hub for the BAS, called an area support medical battalion (ASMB); this is similar to an urgent care clinic. This level of care duplicates Level I and augments services, with limited dental, laboratory, optometry, preventive medicine, health service logistics, mental health services, and patient-holding capabilities. The ASMB can further evaluate a casualty to determine if evacuation to a CSH (Level III) is warranted. In remote locations, Level II facilities are often teamed with an FST, also designated as Level IIB, to provide initial damage control surgery. The FST has an orthopedic surgeon, two or three general surgeons, two anesthetists, and critical care nursing capability. It is configured to be able to complete 10 major surgeries per day. Level IIB is similar to an emergency department with emergency surgical services. Level III Level III may be a CSH, a hospital ship, or Air Force facility. These facilities are in the combat zone and are analogous to regional trauma centers, with a full complement of medical and surgical services. There are intensive care and patient wards. These facilities are modular and can expand from 44 to 248 beds. If the patient requiring rehabilitation or extended treatment can

En route care capability

CHAPTER 26  Combat and Casualty Care

Definitive capability

Full range of acute, convalescent, restorative, and rehabilitative care

Theater hospitalization capability Forward resuscitative capability First responder capability Prevention and protection capability Policy and resource acquisition capability

Full range of acute, convalescent, restorative, and rehabilitative care Forward advance emergency medical treatment performed Medical care rendered at the point of initial injury or illness Promotion and improvement of mental and physical well-being Policy formulation, planning, programming, budgeting, and disbursing resources

FIGURE 26-2  Taxonomy continuum of health care capabilities. (From Defense Medical Readiness Training Institute: Joint operations medical managers course guide, San Antonio, Tex, 2009.)

be evacuated in less than 48 hours, or will have a prolonged recovery time, he or she is evacuated out of the theater. Local national civilian patients are not evacuated out of the theater, and civilian care may require extended hospitalization and rehabilitation that was not initially planned. Level IV The backstop of theater military care is the regional trauma medical center. This facility is within the theater, but on the evacuation pathway out of the combat zone. Definitive care, rehabilitation, and medical specialty services are available. The average stay is short for patients not expected to return to duty. These patients are further stabilized and evacuated out of theater for continued care at a Level V facility. Level V Definitive care describes Level V (primarily continental United States/CONUS) care. The Department of Defense and U.S. Department of Veterans Affairs hospitals provide this care. There are mechanisms to increase bed space using civilian hospitals in the National Disaster Medical System if this is vital to the effort. Medical planning considerations loom large in the military because of the effects of practicing in an area of armed conflict often exacerbated by austerity of the environment itself. At one time an afterthought, military medical planning is now routinely considered at mission planning events. As for any wilderness medicine expedition, the specific characteristics of military health service support are determined by the mission, the threat, intelligence, anticipated number of patients, duration of the operation, the theater patient movement policy, available lift, and hospitalization and movement requirements. Military medical planners are expected to have an understanding of all the areas below: • Threats/medical intelligence considers opposing force actions; occupational, environmental, geographic, and meteorological; endemic diseases and psychological stressors; and weapons of mass destruction. • Patient movement and all this entails from planning, equipping, and patient care perspectives often have the greatest impact on the structure of the health service support design. Delays in transport will require holding capability and more assets for care . As for any expedition, weather, terrain and distance contribute greatly to decisions. • Preventive medicine and health surveillance

• Prevention of stress casualties—The medical system is responsible for care related to mental health issues; however, a great deal can be done to prevent problems through establishment of a collaborative relationship with unit leadership. • Veterinary service—The working dogs, civilian livestock in humanitarian situations, and any local animal issues such as rabies or disease reservoirs need to be considered in planning. Working dogs, in particular, are critical to many missions, such as security. These animals are considered soldiers in every sense of the word and may need full trauma resuscitation, including blood transfusions. • Dental readiness needs should be addressed before deployment. Dental pain is a frequent reason for movement to the rear in unprepared soldiers. • Medical care for prisoners of war and detained personnel— The care for this population may be more labor intensive than anticipated due to previous lack of medical care and significant traumatic injuries. • Mass casualty situations preparation

Theater Trauma System Much of the improvement in survival rates in the Afghanistan and Iraq conflicts is directly attributable to implementation of a trauma system. In both military and civilian populations, large numbers of patient requiring treatment for trauma or illness are best served through a “system approach.” The best systems have a designated trauma system director who is responsible for data acquisition, critical review of collected records, development of medical policy and practice guidelines, and ongoing evaluation of medical resources utilization, including staffing.37

JOINT THEATER TRAUMA REGISTRY The Joint Theater Trauma Registry (Figure 26-3) is a key component of the Joint Theater Trauma System and was implemented in November 2004. As would any civilian trauma system, it collects the usual demographic and mechanism of injury data points. In addition, it collects information on unique transportation solutions, protective gear, service affiliation of the injured, and some unique aspects of conflict injuries (e.g., chemical, nuclear). 511

Unique Aspects of Military Triage and Other Considerations As in civilian mass casualty situations, triage attempts to provide the greatest good for the greatest number of victims. In most cases, military triage categories mirror those for civilians: immediate, delayed, minimal, expectant. In military triage situations, the security situation is often grim, transportation may be delayed, and the triage category of wounded soldiers, who in a less dire situation might have a survivable injury, becomes “expectant.” In addition, the military trains for scenarios involving chemical, nuclear, and radiologic incidents to practice continued combat effectiveness. Triage and treatment may be delayed because of mission requirements. The apportionment of resources may be based on the need for mission success. An interesting illustration of the need for continued combat effectiveness was described in World War II, where penicillin was first used extensively for wound infections. Penicillin was very effective in the treatment of sexually transmitted diseases (STDs), also seen in the military population. Because of its limited availability, penicillin was rationed and at times used first for those soldiers with sexually transmitted diseases rather than for the badly wounded, to keep the fighting forces at the front.53 Military triage has a component related to international humanitarian law. Soldiers who have laid down their weapons are offered the same opportunity in triage for care and treatment of their combat-related injuries. Triage for persons experiencing an emotional stress reaction, with or without wounding, require disarming before care can proceed.

Trauma Record

Trauma Record

For use of this form, see DoD Memeo Subject: Trauma Record, dtd 1 APR 04; the proponent agency is OTSG AUTHORITY: PURPOSE: ROUTINE USES: DISCLOSURE:

DISCHARGE SUMMARY

AR 40-66 To provide a standard means of documenting all trauma care at echelons 1-3 The “Blanket Routine Uses” set forth at the beginning of the Army compilation of systems of records notice apply. This is protected health information. HIPAA laws apply.

MTF DESIGNATION: Number

CASUALTY NAME: FIRST

TYPE

Arrive Date-Time Group (DTG):

Rank

Non-MED GND ARRIVAL METHOD: SHIP EVAC WALKED GND AMB CARRIED AIR AMB Non-MED AIR OTHER ____________________________

Nation

Gender Male

Service

US Host Nation Enemy( Coalition(

MECHANISM OF INJURY: GSW/BULLET BLUNT TRAUMA SINGLE FRAGMENT MULTI FRAGMENT

Penetrate

Struck

UNK

HELMET

REGION

Female

SOF NGO( Other

Head & Neck (incl C-spine) Chest (incl T-spine)

3

8

12

15

CERAMIC PLATE UNC

EYE PROTECTION

STUPOR

LETHARGY

Abdomen (incl L-spine)

ALERT

TIME

OTHER: BURN (thermal, flash) CRUSH FALL SMOKE Inhalation

HEAT COLD BITE/STING OTHER _______ __________________

Pulse Temp

Pelvis

B/P Resp SpO2

UPPER/LOWER Extremities

TX & PROCEDURES: SEDATED

L

L

R

L

R

L

R

CHEM PARALYZED INTUBATED CRIC NEEDLE DECOMP Chest Tube IO line COLLOID CRYSTALLOID TOURNIQUET

Skin L

R

DISPOSITION

air/blood ml

LR/NS/HTS ml Time on Time off

OXYGEN

OR Start DTG: Stop DTG: PROVIDER:

BL Bleeding B Burn X Fracture

D F S

Deformity Foreign Body Stab Wnd

H Hematoma L Laceration G Gunsh Wnd

Units Units

CRYO

Units

Pits

Packs

ICU in DTG:

Fresh Whole Bld

Out DTG:

rFVlla

SPECIALTY:

Liters/min.

FFP

Off DTG:

EXT Fix/splint

EVAC to ___________________________ RTD DECEASED (see below)

Units mcg/kg

ANATOMIC: Airway Head Other PHYSIOLOGIC: Breathing CNS

Neck

Chest

Hemorrhage

COMMENTS:

Extremity

FIGURE 26-3  Joint theater trauma registry.

512

Hypothermic (10 units of red blood cells [RBCs] in under 24 hours) was instituted in March 2006. It endorsed a 1 : 1 fresh frozen plasma (FFP) to RBC transfusion ratio with less emphasis on crystalloid use.49,59,62 In most cases blood component therapy is used. However, in austere circumstances use of fresh whole blood (FWB) may be a way to augment the blood bank with “fresh” donors, especially if FFP and platelets are in limited supply or nonexistent. There is some indication that FWB may blunt the inflammatory response and organ failure seen in hemorrhagic shock states. In addition, oxygen-carrying capacity and decreased hemolysis (associated with hyperkalemia) are seen with FWB.

Factor VIIa Factor VII initiates the process of coagulation in conjunction with tissue factor, which is found on the outside of blood vessels and therefore is normally not exposed to the bloodstream. Upon vessel injury, tissue factor is exposed to the blood and circulating factor VII. Factor VII is activated to factor VIIa. Factor VIIa is a procoagulant that was first used in uncontrollable bleeding seen in hemophilia patients with factor VIII or IX deficiency and inhibitors against replacement coagulation factor. Factor VIIa was first reported used for trauma in 1999 for an Israeli soldier in extremis due to a high-velocity gunshot wound with disruption of the inferior vena cava.43 In the U.S. military, factor VIIa is used in uncontrollable hemorrhage with significant coagulopathy as an addition to FFP and packed red blood cells in a 1 : 1 ratio. Platelets are given if massive transfusion is necessary. Factor VIIA requires adequate platelets for optimal results. Acidosis must be corrected in order for it to work. There is a theoretic risk for deep vein thrombosis, pulmonary embolism, and myocardial infarction. However, prospective randomized trials and retrospective trials on combat wounded have not shown any increase in thromboembolic events. 516

Wounds Combat wounds range from minor to devastating. All require meticulous care and can initially be deceiving as to extent. For the initial combat wound, the soldier takes antibiotics that are supplied in the combat pill packs. The usual antibiotic is moxifloxacin 400 mg orally (PO) once a day. If the soldier is unable to take oral medications, then cefotetan 2 g IV or intramuscularly (IM) every 12 hours (or ertapenem 1 g IV or IM) once a day is administered. Even though most soldiers have current immunizations, one must consider tetanus immunization status in all wounds. This is especially true in nonmilitary personnel. Antibiotic prophylaxis is included for any penetrating wounds to the eyes/globe.* Wounds from blast injury include burns, tissue loss, and/or extensive maceration. These injuries should all be treated as though there is underlying structural injury until proved otherwise; these patients are often candidates for damage control resuscitation and surgery. Initially bleeding may be unimpressive, but it can increase with improvement in blood pressure, warming, and manipulation during exploration, debridement, and irrigation. Primary closure of wounds is rarely considered.10,50 After debridement, the wound should be packed with rolled gauze. If necessary, the skin is sutured over the packing for tamponade of bleeding. This is a temporary measure for life-threatening bleeding until damage control resuscitation is under control.3,10 Injuries to large arteries and veins need to be controlled and may require a tourniquet, pressure dressing, vascular shunt, or ligation. In initial damage control surgery, a nasogastric tube or IV tubing can be used as a temporary vascular shunt, and the aorta can be shunted with a small pediatric chest tube. If a shunt is performed and the patient is to be transferred, a tourniquet should be placed loosely (i.e., not tightened) proximal to the shunt for transport in case of shunt dislodgment. Similarly a nontightened tourniquet should be placed before evacuation after amputation to be prepared for bleeding.10 Unique aspects of blast injuries are the extensive damage and the path the blast may follow up the bone in an extremity. Although physicians are taught to spare as much tissue as possible during debridement, in blast/land-mine injuries a common problem is underestimation of the depth of the injury.

Wound Vacuum-Assisted Closure (VAC) Wound VACs are critical tools that have changed the face of wound care … seriously. No CSH should deploy without them. COLONEL (DR.) THOMAS G. CRABTREE, 2006 Wound care has been a defining characteristic of military medical care through the ages. The principles are cleansing, debridement, and elimination of effects harmful to the wound (such as wound cautery used in the Middle Ages and early Renaissance). In today’s battlefield, more soldiers survive blasts, high-velocity missile strikes, and other combat injuries because of better protective gear, highly trained combat medics, and faster evacuation to surgical care. These survivors have complex wounds with high probability of infection that are unable to be closed primarily. They require not only adherence to the basics, but new modalities and a team approach to care that involves physical and emotional care.3,10,50,54 Wound VAC devices are used extensively with good results for massive wounds with tissue loss seen in combat injuries. Other circumstances that benefit from this therapy are pressure ulcers, partial-thickness burns, orthopedic injuries with tissue loss, skin grafts, and abdominal wounds that are left open after damage control surgery. This therapy can decrease healing time and reduce risk for infection and other complications. Commercial devices consist of a dressing that is fitted with a tube and attached to the wound VAC device. *References 3, 10, 35, 41, 54, 63.

Burns Prehospital burn care is the same as that for civilians with a few additional considerations. The burn patient in a combat zone must be considered for additional injuries, wounds, hemorrhage, and possibly blast injury. If this is the situation, Hextend is used as per the shock protocols along with crystalloid (lactated Ringer’s) burn resuscitation. The amount of Hextend used should not exceed 1000 mL. The U.S. Army Institute of Surgical Research Burn Center, which serves as the U.S. Department of Defense burn center, developed a new fluid resuscitation “rule of 10” used for burns greater than 20%. It is based on current research regarding burn resuscitation.10,21

TO USE THE “RULE OF 10” 1. Calculate and round the affected body surface area (BSA) to the nearest 10%. Use a burn calculation sheet if possible. 2. Calculate the fluid resuscitation protocol: a. Initial IV/intraosseous (IO) fluid rate is calculated as percent BSA × 10 mL/hr for adults weighing 40 to 80 kg (88.2 to 176.4 lb). For every 10 kg (22 lb) over 80 kg (176.4 lb), increase the initial rate by 100 mL/hr. 3. Monitor urine output to achieve 30 to 50 mL/hr. Example: Casualty weighing 100 kg (220.5 lb) with 50% BSA affected:

The military is performing ongoing research into pain relief on the battlefield. The challenges are distance, security situations that may delay transport, provider inexperience, and severity of the injuries.9,38 Causalgia (reflex sympathetic dystrophy) was a common diagnosis seen after the Civil War, and chronic pain states are still seen today in patients without adequate pain management. Current studies indicate that the cause or exacerbation of post-traumatic stress disorder (PTSD) is related to poorly or untreated, unrelenting pain.38 The standard is that all casualties with pain are given analgesia. The determinants of type and route of medication are as follows: (1) is the casualty conscious? (2) is the casualty able to fight? and (3) is there IV access? At the point of wounding for severe pain, the combat medic (68W) is able to give morphine 5 mg in titrated doses IV (preferred), IO, or via IM injection. Oral transmucosal fentanyl citrate 400 to 800 mcg6,32 is an alternative to morphine for use before arrival at a combat support hospital. Naloxone is available for respiratory depression. Promethazine 25 mg (IV/IM/IO) every 6 hours as needed has been added to the prehospital pain medication regimen to treat the nausea that is common with injury and often seen with narcotic administration. If the patient is treated with these medications, his or her weapon is secured and the patient is no longer able to fight. Splinting, positioning, and emotional support are provided as the patient is prepared for evacuation. Military members in combat carry a combat pill pack, which is taken as soon as possible after injury or wounding. These are oral medications: meloxicam 15 mg (a cyclooxygenase-2inhibitor selective nonsteroidal antiinflammatory drug) once a day and acetaminophen 650 mg (bilayer caplet) two pills every 8 hours. These medications were chosen for the ability to relieve moderate pain without causing platelet dysfunction or decrease in mental alertness. The soldier is still able to carry a weapon and able to fight if necessary. An antibiotic is carried in the combat pill pack and used for all open combat wounds. Currently the antibiotic of choice is moxifloxacin 400 mg PO once a day.63 After arrival at a BAS, FST, or CSH, other medications and modalities are available. Low-dose ketamine is an excellent analgesic. In the future, intranasal ketamine may be an option10 Clonidine may be used in stable patients.9,38 Peripheral nerve blocks and regional blocks (if trained personnel are available) offer excellent relief. A fascia iliaca block is useful for pain relief of injuries involving the hip, anterior thigh, and knee. This block is useful for fractures of the hip and proximal femur, especially before prolonged transport. Intercostal blocks are beneficial for chest wall pain after trauma, especially in the presence of rib fractures.

50 × 10 mL = 500 mL/hr + 200 mL = total fluid rate of 700 mL/hr

Telemedicine

Abdominal compartment syndrome is a complication of massive crystalloid resuscitation and carries a high mortality. An intraperitoneal drain may allow for enough intraperitoneal fluid removal to avoid a decompressive laparotomy.

Telemedicine has been used successfully to diagnose dermatologic conditions, send radiologic studies for interpretation, and give reports on patients being evacuated to higher levels of care. Combat medics in remote sites have used e-mail contact with their unit physician assistant or physician to make determinations of evacuation or therapy for ill or injured soldiers. The U.S. Army Medical Research and Materiel Command and the Telemedicine and Advanced Technology Research Center have worked on surgical robots and mentoring programs to assist in surgery. Colonel Bruce Adams has successfully experimented with camera observation and advice to combat medics for assistance in performance of surgical cricothyrotomy on manikins. Although telemedicine currently has limitations because of bandwidth, privacy issues, and urgency of trauma patient consultations, it holds promise for the future.47

Pain Management Homer’s The Iliad has some of the first descriptions of war wounds and their treatment; pain relief was recognized as a principal tenet of combat medicine. The need remains the same today. There Patroclus made him [Eurypylus] lie at length, and with a knife cut from his thigh the sharp-piercing arrow, and from the wound washed the black blood with warm water, and upon it cast a bitter root, when he had rubbed it between his hands, a root that slayeth pain, which stayed all his pangs; and the wound waxed dry, and the blood ceased. (Figure 26-11, online) Pain is a common manifesting symptom in injuries directly related to combat. In the deployed environment, there are also other more ordinary causes of pain, such as motor vehicle accidents, long periods in confined spaces, heavy personal protective equipment, and lifting and training accidents.9,38

Casualty Evacuation (CASEVAC) Wilderness medicine providers operating in conjunction with the military should be aware that evacuation platforms, both ground and air, are tremendously different when compared with the civilian evacuation system. Civilian evacuation platforms (ground and air) are generally equipped to provide en route care (oxygen, diagnostics, medications, communication with medical control) 517

CHAPTER 26  Combat and Casualty Care

Before use of the device, the wound is meticulously debrided, irrigated, and cleansed. A sterile sponge (or reticulated open-cell foam) is cut to fit inside the wound, the wound is sealed with a film to prevent leaks, and a suction tube is placed in the sponge. The opening of the tube through the skin is also sealed and connected to a wound VAC device. The suction pressures are usually 50 mm Hg to 200 mm Hg (average 125 mm Hg). The device is turned off for dressing changes. For drainage, a wound VAC can be highly beneficial. The interval between dressing changes can be extended because the VAC drains fluids from the wound and leaves less media for bacteria. In cases that may compromise circulation because of edema, a wound VAC improves blood flow to the wound and surgical area. Vacuum wound closure systems and their benefits as an important adjunct to modern combat wound care are discussed in the U.S. Department of Defense’s Emergency War Surgery,3 First to Cut: Trauma Lessons Learned in the Combat Zone,10 and War Surgery in Iraq and Afghanistan: A Series of Case Studies, 2003-2007.54 These also describe field-expedient methods to produce a wound VAC system with available equipment.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

and are staffed with paramedics with advanced training. Military evacuation platforms are essentially patient transport platforms with very little en route patient care. The military places greater emphasis on casualty stabilization before evacuation because of this configuration. The military evacuation system is designed for speed of transport into and out of combat areas with active small arms fire. Hence, the ability of a lightweight, agile, fast, and rugged platform (ground and air) to enter and exit an active skirmish, while providing a modicum of safety to the patient and medical attendants, is vital. The speed and effectiveness of the military medical patient transport system are often overlooked; however, the success of the system is reflected in the less than 10% dead on arrival (DOA) rate seen in current conflicts. At the point of wounding, the evacuation platform is more often going to be a tactical vehicle than any sort of ambulance. Due to increased use of IEDs and RPGs, most vehicles are armored or hardened. The space is very limited, so to the greatest extent possible, any control of bleeding, placement of tourniquets, and other medical procedures are accomplished before transport. It is also important to work with equipment such as litters to make sure they will fit in the vehicles. During transport, it is critical to ensure medical interventions, such as control of bleeding, remain intact. For the badly injured casualty, evacuation from the time and point of wounding to the closest and most appropriate initial care at an FST or CSH averages about 1 hour. If the determination is that there is a lesser injury, the patient can be taken to a BAS for a determination of injury and evacuated to a higher level later if required.54 Casualty evacuation is a multifaceted transport system designed to enhance patient evacuation based on proximity of stage evacuation assets, not based on injuries. Regardless of the type of injury, a triage category and then an evacuation category will be assigned. During casualty evacuation planning, all platforms and locations are plotted to facilitate entry into the evacuation system. Helicopters are used extensively for casualty transport. In combat situations, a white light, such as that in a laryngoscope, in the helicopter compartment may be forbidden. Because the doors are often left open for security reasons, protection of the patient from the wind and hypothermia becomes more critical. If the patient is in a helicopter and the time to a CSH is not significantly greater than the FST, the decision may be made to go directly to the CSH. Although the FST has a great deal of surgical capability, its roles are lifesaving interventions and limited surgery to stabilize the patient to allow evacuation to the CSH. Transportation after initial advanced-level care often involves an intubated (and possibly ventilated) patient. Sedation and analgesia are essential for these transfers. In addition, no paralytic agent should ever be given without a potent sedative. Some evidence suggests that the administration of sedation and pain relief may decrease the probability of later PTSD. Absent hypovolemia, a sign of inadequate pain and sedation may be persistent tachycardia. The airway and patient should be adequately prepared because loss of the airway during combat evacuation is a major life threat. Reestablishment in a limited space with inability to hear breath sounds may necessitate a surgical airway. The attendant in transfer must have sufficient medications and doses to keep the patient comfortable and sedated and be able to provide an airway if the patient is extubated. For the most critical airways, the endotracheal tube may be wired onto the teeth.10 For any ground or air transport, including longer transports such as aeromedical (Air Force flying hospital; C-17) transfer out of the combat zone, a pretransport check to ensure necessary medical items (e.g., oxygen, tourniquets, sedation, analgesia, antibiotics, IV fluids, decompression needles, urinal) is important because the transferring facility is responsible for the patient’s medical equipment needs during movement. A patient with a minimal pneumothorax or on positive pressure ventilation is susceptible to a tension pneumothorax during transport, so the attendant must be able to address this. Other possible causes, such as a kinked tube or mucus or blood clot in the tube, need to be quickly ruled out. It is difficult to evaluate a patient in a helicopter; if there is any question as to which side is under tension treatment, a 3.25-inch 14-gauge needle is inserted into the second intercostal spaces bilaterally. If there is a question of 518

FIGURE 26-12  Example of the Fallen Soldier Battle Cross and the memorial service.

pneumothorax before transport, a chest tube should be placed before transport. Any patient who has had a tourniquet placed in the field, is a postoperative amputee, or has had a vascular repair is at risk for hemorrhage. As the patient becomes normotensive or coagulopathic, the area can rebleed when a tourniquet or suture is dislodged with movement. The same can happen with a vascular repair or vascular shunt. During transport, at least two tourniquets for each injured/operated extremity is judicious. The tourniquet can be preplaced on the injured extremity, to be tightened if there is the onset of exsanguinating hemorrhage.

Death In the midst of the savagery of war, it is critical to maintain the tether to humanity. Care of the deceased is an important service, not only for the soldier’s family, but for the unit’s morale and well-being. Although the care of remains is under the direction of the Quartermaster Corps, it is usual that no matter where the death occurs, the unit will bring the body to the medical personnel in the area. The body is cooled if at all possible. As in any medical examiner’s case in the United States, all medical procedure items are placed in the body bag with the deceased. Clothing and operational gear are transported with the remains. Any records of the incident are preserved and sent with the remains. A full autopsy is completed by the military to determine the cause of death and enter the data into the trauma registry. In response to the loss, the unit holds a memorial service, where the deceased soldier is represented by the Fallen Soldier Battle Cross. The cross consists of the soldier’s rifle with bayonet attached and stuck into the ground; the helmet is placed on top, accompanied by dog tags that hang from the rifle with the boots of the fallen soldier in front of it (Figure 26-12). Its purpose is to show honor and respect for the fallen at the battle site. The ceremony for the lost comrade is formal and used as a ritualized means to collectively acknowledge the commitment and sacrifice of the soldier and to mourn his or her loss. Commanders are cognizant of the distress brought by the death of a unit member, especially if the unit has suffered multiple losses. Commanders use this ceremony to reaffirm with unit members the sense of unity, cohesion, and commitment to each other as they pursue their shared sense of mission.

Veterinary Issues Dogs in conflict areas are ubiquitous. Despite education and warnings, soldiers often voluntarily interact with local dogs. U.S. military working dogs are vaccinated against rabies; the likelihood of rabies in local animals may be considerable. Dog bite treatment is similar to that in any emergency department, except

Unexploded Ordnance* Unexploded ordnance (UXO) may include aerial bombs, rockets, artillery and mortar shells, grenades, and mines. Any location where a war has been fought within the past century has potential for retaining these items. Crews excavating streets in urban areas of England, France, and Germany often uncover UXO from World War I or World War II. Many areas of the United States that have been used for bombing or artillery ranges are adjacent to wilderness regions. Although they are usually well marked as impact areas, they still may pose a risk for the unwary traveler. Many areas of the shallow ocean accessible to scuba divers contain sunken munitions transports and warships that contain massive amounts of unexploded bombs, shells, and torpedoes. Another problem that has arisen is the use of mines and booby traps to protect marijuana and opium fields and illegal drug laboratories. Currently, unexploded land mines represent a significant health problem in Southeast Asia, the Balkans, Central America, Egypt, Iran, and Afghanistan. The International Red Cross estimates that someone is killed or injured by a land mine every 22 minutes. The average number of mines deployed per square mile in Bosnia is 152; in Iran, 142; in Croatia, 92; and in Egypt, 59. There are a total of 23 million mines in Egypt alone.10 Land mines may be commercially manufactured or produced locally from available materials (Figure 26-13). Commercial land mines currently produced in the United States have a limited active life and self-destruct after their active life has expired. Unfortunately, this is not true of older types of mines or mines produced by other countries. Locally produced mines have no standard size, shape, or detonation pattern and may be very difficult to detect and defuse. These types of land mines are used extensively in El Salvador, Malaysia, and Guatemala. Land mines have two primary functions, the first of which is to cause casualties—the so-called antipersonnel mines. These may be blast or fragmentation type. Fragments may be accelerated at 4,500 ft/sec (3068 mph), or double the speed of a highvelocity rifle. The fragmentation type may be either directional or nondirectional (Figure 26-14). Antipersonnel mines may cause lethal or nonlethal injuries in several persons. Wounded soldiers require more care than do killed soldiers, and the tactical effect may be the same. The second primary function is to destroy vehicles, such as tanks, so mines intended for this purpose are usually much larger. All mines have three basic components: (1) triggering device, (2) detonator, and (3) main explosive charge. The triggering device differs depending on the type of mine. Blast mines usually involve a pressure type of trigger and occasionally are command detonated, especially for antitank purposes. Many antitank mines will not explode unless a pressure of 136 to 181 kg (300 to 400 lb) is applied. The M14 blast antipersonnel mine needs only 9 to 14 kg (20 to 30 lb) of pressure to trigger detonation. Fragmentation mines are usually triggered by trip wires or similar “touch” devices. The M18A1 fragmentation mine, or claymore mine, can also be command detonated by an electronic trigger. *Reference 63.

Main charge

Fire assembly adapter plug Soft metal plate

Wire

Striker Retaining wall Detonator Detonator adapter plug

Delay-arming mechanism

FIGURE 26-13  An example of an antipersonnel mine manufactured by the Soviet Union.

Booby traps other than land mines may be mechanical, chemical, or explosive. During the Vietnam War, venomous snakes were used, as well as the notorious sharpened bamboo spikes known as punji or tiger traps. The distribution of mines usually entails spreading them on the surface of the ground; by air along roads, railways, and defensive positions; or hiding them by burying or camouflage along trails or suspected routes of approach. The energy transmitted from blasts may cause extensive damage. When a detonation occurs, a solid or liquid is converted into a gas under pressure with extreme energy release. Detonation of a high-speed chemical reaction also causes high temperatures and pressures. Factors influencing the blast wave are the Mach stem, reflection, absorption, flow of the pressure wave, and the medium in which the blast occurs (e.g., air, water, soil). Injuries from land mines depend on several factors: type of mine (blast versus

A

B FIGURE 26-14  A, An improvised mine, or booby trap, manufactured from a hand grenade and materials at hand. B, A directional type of mine used against unarmored vehicles or personnel.

519

CHAPTER 26  Combat and Casualty Care

that the ability to catch and monitor the animal is decreased, so watchful waiting to determine vaccination status of an animal is not an acceptable approach. Therefore postexposure rabies immunization is started.10 The lessons learned have been consideration of preexposure rabies vaccination for personnel with high exposure to local dogs; this requires that adequate supplies of rabies vaccine are reasonably available. It is better to have the rabies vaccine on hand than have to transfer the service member to another location for treatment; this is especially true if the environment is not secure. Working dogs may be seen as patients in emergency treatment areas of the hospital, especially if a veterinarian is not immediately available. Care of working dogs is described in First to Cut: Trauma Lessons Learned in the Combat Zone.10 Basic damage control principles are used for resuscitation and surgery.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

fragmentation), position on the ground, method of detonation, whether it explodes above the ground, position of the victim, environment, and type of soil. Four general patterns of injuries occur with land mines. Pattern A injuries occur with small blast mines, such as the U.S. M14 and the Chinese Type 72. These injuries usually involve only the leg below the knee. Complete or partial foot amputations are most common, and trunk or head injuries are rare. Pattern B injuries are caused by larger blast mines, such as the Russian PMN. These mines contain four to six times as much highexplosive material, and the cone of explosion is much larger. The injuries seen with this type of land mine usually involve massive soft tissue injuries to both legs below and above the knee and also commonly the pelvis, abdomen, and chest. Pattern C injuries are generally caused by Russian PFM-1, or “butterfly,” mines. These mines are usually distributed by air, and the wings are designed to help spread the mines. They are triggered by pressure applied to the wings; handling the mine commonly does this. Most of the injuries involve amputation of the hand at the wrist; often the head, neck, and chest are also injured. Unfortunately, loss of one or both eyes is not uncommon with this mine. Pattern D injuries are caused by fragmentation mines. These may be bounding mines, such as the U.S. M16 or the Russian OZM, or directional mines, such as the U.S. M18A1 or the Russian MON. They are designed to spread metallic fragments over a wide area at the height of a person’s waist. The fragments lose their energy much faster than a bullet projectile but at close range can be devastating. The lethal range is usually 25 to 50 m (82 to 164 feet), with casualties occurring out to 200 m (656 feet). The injuries are quite similar to gunshot wounds and are often multiple. Large, unexploded artillery shells or bombs may cause a combination of blast and fragment injuries but on a larger scale, sometimes involving scores of victims. Many military and civilian casualties are caused by IEDs, which may be conventional explosives; improvised from fertilizer, propane, or other unconventional explosives; artillery, mortar, or other ordnance; or explosive charges removed from such ordnance. IEDs are commonly used by terrorist groups, which may detonate the devices either by timing mechanisms or by command, sometimes in suicidal attacks. These devices are usually detonated in crowded areas or near important political or military targets to create the greatest impact. Examples are attacks on Oklahoma City’s Alfred P. Murrah Federal Building, the Beirut Marine barracks, and multiple incidents in Iraq. Injuries from explosives can include any combination of blunt, penetrating, burn, or blast wave/pressure injury. Injury patterns are usually worse with closer proximity. These injuries can also involve cavitation, crush, embolism, fractures, lacerations, and perforations of organs. The primary blast injury is due to the pressure wave and the direct effects of the pressure pulses, both overpressure and negative pressures. Significant blast winds can be produced because of the detonation. Injury is most often associated with the gas-filled organs, middle ear, lungs, and intestines. Lung injuries cause the greatest morbidity and mortality. Rapid acceleration of shrapnel to 50 ft/sec (34.1 mph) lacerates tissue, and at 400 ft/sec (272.7 mph) shrapnel is able to penetrate body cavities. Because the wounds are deceptive, the need for amputation may first be recognized later. Tetanus prophylaxis must be rendered. The tertiary injuries involve the victim being accelerated by the blast and thereby impacting other objects when thrown any distance. The median lethal dose (LD50) of being thrown is about 26 ft/sec (17.7 mph), and the limit of human tolerance is about 10 ft/sec (6.8 mph). The other injuries that commonly may occur are burns, crush (from building collapse), and chemical exposures. A very important aspect of the care for any patient with an explosive munition mechanism of injury is the possible lack of any initial overt manifestation of injury. There must be a high index of suspicion because many victims will not manifest for several hours. The first sign of respiratory failure is usually increased respiratory rate. Acute respiratory distress syndrome may not manifest for 24 hours. Treatment of these injuries can be very complex and involves vascular, orthopedic, soft tissue, abdominal, and craniofacial procedures. In most of these injuries, massive debridement is necessary. Rarely, UXO may be 520

embedded in soft tissues and body cavities and must be removed in the operating room, possibly endangering the lives of medical personnel. Initial treatment involves airway control, treating tension pneumothorax, and controlling hemorrhage. Tourniquets are often necessary to control the bleeding from amputated limbs. Splinting the injured extremity and covering the wound to prevent further contamination is necessary. Initial debridement must be done carefully; removal of fragments may cause bleeding to recur. Penetrating injuries of the pelvis and abdomen usually require laparotomy, and soft tissue injuries may require multiple reconstructive procedures. The wounds are usually highly contaminated with soil, clothing, and fragments that may be driven deeply into tissue proximal to the obvious injuries.39 Broad-spectrum antibiotics and tetanus prophylaxis are appropriate in all cases, and fluid resuscitation is usually indicated with extremity injuries. Postsurgical infection of mine injuries is common and greatly increases morbidity and mor­tality. Most victims who survive never completely regain normal function, especially if the initial treatment was delayed or inadequate. Air-filled organs are most susceptible to damage. The tympanic membrane can rupture at a pressure of approximately 150 kPA (kilopascal) or 5 to 7 psi over atmospheric pressure. Blast injuries without fragmentation may cause tympanic membrane rupture, blast lung resulting from alveolar rupture, and intestinal rupture, although the latter is more common with underwater mine explosions. Pulmonary blast injury may manifest as contusions and hemoptysis. The victim may have subcutaneous emphysema, respiratory distress, and tachypnea. Arterial air embolism may occur with cardiac and neurologic manifestations. The mechanism is production of an overpressure wave that travels through tissue of various densities and causes tearing injuries at membrane interfaces. These injuries must be suspected in any victim involved in a blast, whether from a land mine or other explosive device. Solid organs, although more protected from overpressure, are very susceptible to missiles. Neurologic and head injuries are commonly associated with blast injury. Blast winds can cause extremity injury as severe as traumatic amputation. Scuba divers and swimmers who are involved in underwater explosions may have more serious injuries because of the increased speed of sound in a liquid medium. This can cause more severe tearing of membranes at the fluid–air interface and additional trauma secondary to a “water hammer” effect and spalling. The position of the victim and the number of shock waves caused by reflection of the blast wave off walls and ground may increase the amount of damage. Victims in contact with solid objects, such as the hull of a ship or vehicle, may have increased injuries because of increased velocity of the blast wave through solids. Burns and translational injuries, whereby the victim is thrown by the blast and has injuries similar to a fall or motor vehicle crash, also occur. Traumatic brain injury (TBI) is common in blast injuries and is referred to as the “hallmark injury” of the current Iraqi and Afghani conflicts. Symptoms can range from coma to mild cognitive dysfunction, depression, and behavioral changes. PTSD is often associated with TBI. Generally speaking, the closer the victim is to the blast, the greater the injury. The tympanic membrane will rupture at overpressures of 5 to 7 psi. This causes acute hearing loss, pain, and tinnitus. Blast lung is caused by the overpressure wave passing through the chest wall and may involve one or both lungs. Chest pain, dyspnea, and hemoptysis may manifest immediately or be delayed up to 48 hours. Chest radiograph may show patchy or diffuse infiltrates, pneumothorax, subcutaneous air, and hemothorax. Implosion of air into the vascular system may cause air embolism and sudden death. Abdominal injuries in air blast are uncommon, but in water blast may manifest as abdominal pain, nausea, vomiting, and tenesmus. Sigmoid and transverse colon injuries are most often seen, followed by small bowel and solid organ (such as liver and spleen) injuries from the water hammer effect. Abdominal injuries may have a delayed (up to several days) presentation. The key to therapy is to be suspicious of occult injuries in any victim of a blast, whatever the cause. Most injuries will manifest within the first hour; however, because injuries may be delayed in presentation, observation and close

succinctly—“The closer you are and the uglier it is, because the longer it lasts, the worse you’re going to feel.”

DEALING WITH RETAINED UNEXPLODED ORDNANCE

SOURCES OF PERSONAL TRAUMA

Any patient that has retained UXO requires extremely delicate handling. If it is possible to limit transportation and perform surgical removal, that is the best plan. There should be an explosive ordnance disposal specialist available to advise on UXO type and triggers. The surgical team should be limited to critical members only. Every member of the team wears complete protective gear, including protective eyewear and sandbags or other material to deflect any blast. This gear is also placed around the patient. Radiographs may be necessary to determine the extent of implantation and the best way to remove the ordnance. One should never use ultrasound or electrocautery on the patient, because these may set off the UXO. Similarly, avoid contact with the UXO with metal surgical instruments. Inhalational anesthesia is contraindicated due to explosive concerns, and patient monitoring will be limited. IV anesthesia is used; the patient should be well anesthetized and paralyzed to avoid movement.

Traumatic Emotional Stress in Austere Environments: The Continuum of Effects Traumatic emotional stress is a common and serious problem that is especially relevant to the field of austere medicine. The military has found that all military members, including enlisted soldiers and officers, can benefit from an overview of the causes and signs and symptoms that define the continuum of traumatic stress. This section reviews basic precepts, describes the general concept of traumatic stress, and cites some of the management strategies that have demonstrated their utility in the field. If the patient is armed, a safety issue that needs to be addressed is disarming the patient and ensuring safety of the team and the injured individual. Frederick M. Burkle, MD, stated, “Current studies support that no single pattern of psychological consequences to disasters exists. However, human generated disasters appear to result in more severe, intrusive, and long term psychological consequences than natural disasters.” 14 This certainly pertains to military personnel in areas of armed conflict and also holds true for other responders and aid workers.

CLINICAL ASPECTS OF PSYCHOLOGICAL TRAUMA It has been suggested that the two principal determinants of the severity of psychological trauma are the gradient of exposure and the magnitude of personal loss. The gradient of exposure describes how close one is to the event(s). Questions might include the following: Did you hear about it? Read about it in print media? See photographs? View it on television? Witness it personally? How much of it were/are you exposed to, and how many times? Did it happen to someone you know? To a loved one? To you? In general, the closer or more directly affected an individual is by the event, the greater the likelihood of significant psychological distress. The magnitude of personal loss describes the “comprehensiveness” of the event. Does the event produce meaningful physical or psychological pain or limit abilities because of injuries? Do losses affect areas such as physical mobility or capacity/ employment/future personal or professional opportunities? Were feelings of terror, horror, or helplessness involved? Informally the gradient of exposure and magnitude of personal loss might be reduced to the phrase “how close and how big?” Taken together, these are highly predictive of the degree of psychological distress—or, as it can be expressed *References 4, 15, 18, 24, 26, 30, 34, 53, 61, 63, 64.

We define our world with our senses. Armed conflict is, at its core, an assault on our senses. Our senses provide the sights, sounds, smells, and sometimes physical pain that create the psychological imagery of the indelible memories, intrusive thoughts, and disturbed feelings that are the cardinal features of psychological trauma.

HOW ARE MILITARY STRESS REACTIONS CHARACTERIZED? In general, the military recognizes three types of stress reactions. In ascending order of severity, these are combat and operational stress reaction (COSR), acute stress disorder (ASD), and PTSD. Although the military focuses principally on combat-related issues, the general template applies well to nonmilitary stress responses. Because the civilian sector does not use the term combat, one might substitute the word initial in its place for COSR. All three reactions may have a combination of common physical, emotional, and behavioral signs. The following is a list of the signs most commonly reported. Combat and Operational Stress Reaction It is not unusual for combat exposure or other circumstance of interpersonal violence or imminent danger to create physical and emotional problems. Such reactions may occur as the result of combat-like conditions that are present throughout the entire spectrum of military operations, which include training, traditional offensive and defensive operations, stability operations, and civil support activities. In the authors’ experience, civilian humanitarian workers involved in peace operations, disaster response, humanitarian support, and related missions may have experiences and responses that are similar to those of combat troops. Outward signs and symptoms of COSR often include a combination of physical, emotional, behavioral, and cognitive disturbances. Common physical complaints associated with COSR may include fatigue, exaggerated startle response, sweating, sleep disturbance, rapid heartbeat, dizziness, frequent urination, dry mouth, and persistent muscular tension. Emotional distress may include grief, distractibility, self-doubt, anger/agitation, loss of confidence in self or unit, and rumination about distressing events. Common behavioral representations of these emotions often include indecisiveness, irritability, distractibility, inattention, hypervigilance or withdrawal, decreased arousal/initiative, tearfulness, and inability to relax. The patient may also initiate or increase the use of mind-altering substances, from common substances (caffeine, nicotine, alcohol) to more powerful prescription or street drugs. Acute Stress Disorder ASD is a diagnostic category developed in 1994 to describe reactions to trauma that are time limited. ASD describes the behavioral disturbances that develop within a month of exposure to extreme psychological trauma. Such extreme events could include rape or other severe physical assault, near-death experiences during accidents, witnessing personal violence, and combat. In some cases, ASD can also result from actions taken or not taken by an individual that leave the person with meaningful feelings of guilt or shame. In addition to the COSR symptoms noted above, ASD may also include derealization, depersonalization, reduction in awareness of vicinity, psychological numbing, and dissociative amnesia. Derealization is a change in an individual’s experience of the environment, where the world around him or her feels unreal and unfamiliar. Depersonalization is a change in an individual’s self-awareness, such that they feel detached from their own experience, with the self, body, and mind seeming alien. Dissociation is also characterized by a sense of the world as a dreamlike or unreal place and may be accompanied by poor memory of the specific events, which in severe form is known as dissociative amnesia. The symptom of dissociation, which 521

CHAPTER 26  Combat and Casualty Care

follow-up are critical. Treatment is generally supportive for ear and lung injuries and operative for abdominal injuries.*

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 26-2  Difference Between ASD and PTSD ASD

PTSD

The diagnosis of ASD can be given only within the first month following a traumatic event.

If post-traumatic symptoms persist beyond a month, the clinician should assess for the presence of PTSD. The PTSD diagnosis does not include a dissociative symptom cluster.

It includes a greater emphasis on dissociative symptoms. An ASD diagnosis requires that a person experience three symptoms of dissociation (e.g., numbing, reduced awareness, depersonalization, derealization, or amnesia).

ASD, Acute stress disorder; PTSD, post-traumatic stress disorder.

reflects a perceived detachment of the mind from the emotional state or even the body, is a critical feature. Other features of ASD include symptoms of generalized anxiety and hyperarousal, avoidance of certain situations or stimuli that elicit memories of the trauma, and persistent, intrusive recollections of certain events via reexperiencing (“flashbacks”), dreams, or recurrent thoughts or visual images. Although ASD is not an “early” form of PTSD as such, it may proceed to PTSD if the individual does not receive appropriate care. Post-Traumatic Stress Disorder If the symptoms and behavioral disturbances of the ASD persist for more than a month, and if these features are associated with functional impairment or significant distress to the sufferer, the diagnosis is changed to PTSD. These terms describe the outward manifestations of trauma-induced anxiety. Essentially, the individual’s adaptive responses to an unstable environment have been internalized as a general mode of responding to all environments. In the words of one patient, “I know that I’m not in theatre (combat zone) now, but I still can’t stand being in a department store or any other crowd of people.” The symptoms of ASD and PTSD are very similar (Table 26-2). The proper diagnosis revolves around two issues that can be framed as questions: How long have the problems lasted, and are the problems getting better, worse, or remaining the same?

WHICH TREATMENTS WORK? In general, treatment focuses on helping people process their experiences in ways that decrease or eliminate their combat arousal state. Treatment strategies that have demonstrated usefulness include prolonged exposure therapy, eye movement desensitization and reprocessing, pharmacologic treatment, couple/ family counseling, and spiritual support. In addition, adjunct pharmacologic management for problems of mood or anxiety may also be indicated. There may be a role for medication in the prevention of PTSD. Recent research by Holbrook and colleagues suggests that administration of morphine during early resuscitation and trauma care at or near the point of injury is associated with a lower risk for PTSD following injury.38 One of the greatest historical barriers to care has been the stigma associated with the need for behavioral health support. U.S. Army Vice Chief of Staff, General Peter Chiarelli, is an outspoken advocate for the identification and treatment of PTSD and the often-related issue of TBI (http://www.neuroskills.com/ mtbi.shtml). He has been especially vocal in speaking about the terrible toll of stigma: The “signature wounds” of this war are post traumatic stress disorder and traumatic brain injury … I want to change the stigma linked to these wounds … They are in fact real … these are not phantom issues made up by weak Soldiers. They are as real as if you fell and broke your leg or lost an arm.” Leaders need to be careful on the tone they use with this issue. It affects how their subordinates view these conditions and if you believe anxiety and depression are signs of weakness, so will they. 522

To paraphrase General Chiarelli in a related comment, “Is your brain more important or less important than your leg … or hand?”

Mild Traumatic Brain Injury Mild traumatic brain injury (MTBI) is commonly known as concussion; it is rarely life threatening (Figure 26-15). Gioia and Collins stated the following: Concussion (MTBI) is a complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head. Disturbance of brain function is related to neurometabolic dysfunction, rather than structural injury, and is typically associated with normal structural neuroimaging findings (i.e., CT scan, MRI). Concussion may or may not involve a loss of consciousness (LOC). Concussion results in a constellation of physical, cognitive, emotional, and sleeprelated symptoms. Symptoms may last from several minutes to days, weeks, months or even longer in some cases.36 Further, the American Congress of Rehabilitation Medicine52 characterizes MTBI as “a traumatically induced physiologic disruption of brain function which involves at least one of the following: 1) any period of loss of consciousness; 2) any loss of memory for events immediately before or after the accident; 3) any alteration in mental state at the time of accident (e.g. feeling dazed, disoriented, or confused); 4) focal neurologic deficit(s) that may or may not be transient.” Specific causes of MTBI commonly include a blow to the head or violent shaking often caused by motor vehicle accidents, falls, and sports injury; among military personnel, the most common source is overpressure wave blast caused by explosion. Although not life threatening, the symptoms of MTBI can be serious and a meaningful threat to quality of life.

SIGNS AND SYMPTOMS In patients presenting with possible head injury, initial medical response focuses on identification and management of the most serious injuries, so the diagnosis of MTBI may be delayed. The signs and symptom of MTBI are highly variable in both type and time. Headaches, for example, often have rapid onset, whereas many of the cognitive and affective behavioral symptoms may begin subtly and not become problematic for days or weeks. Disturbances in executive function, including decision making, foresight, insight, judgment, and planning, are frequently present. Most people with MTBI recover completely, but the process can sometimes take considerable time. This is especially the case for sufferers who are older, have a history of previous head injury, or who are taking psychiatric medications. Although patients recover, different symptoms may resolve at different rates, making the course of recovery highly variable.19 In the immediate postconcussive phase, patients may experience brief unconsciousness. Even without unconsciousness, patients most commonly report feeling dazed or confused or

2000-2010 Penetrating 3304 Severe 1986 Moderate 31,974 Mild 144,453 Not classifiable 6553 Total – All severity 188,270

FIGURE 26-15  2000-2010: Traumatic brain injury categories. (From Defense and Veterans Brain Injury Center: Military Acute Concussion Evaluation. http://www.pdhealth.mil/downloads/MACE.pdf.)

“seeing stars.” In addition, patients may experience amnesia for the injury or event that caused the problem. Common motor and sensory symptoms include dizziness, fatigue, sleep disturbances, and sensory deficits involving vestibular and visual systems, muscle strength, and/or coordination. One of the most common pain symptoms of MTBI is headache that typically begins within the first 14 days. The patient may complain of a dull, aching pain that is typical of tension headache, but MTBI can also trigger migraine headaches in persons with a genetic disposition. Headaches often originate from structures external to the brain and skull, such as muscles and connective tissue of the skull, spine, and shoulder.52,58 Behavioral symptoms of MTBI can be especially problematic and may include a range of disturbances in affect, cognition, and behavior. The patient may become irritable, agitated, disruptive, or overtly aggressive and may demonstrate marked emotional lability, disinhibition, or impaired impulse control. Cognitive symptoms often include slowed thinking, impaired judgment, distractibility, and impaired cognitive focus. Patients may use terms such as feeling foggy or other terms representing a vague sense of being out of touch with their senses. Over time some persons may develop depression, substance abuse problems, or alterations in their baseline personality characteristics. These concerns must be referred to the appropriate health care provider for proper assessment and management.

IDENTIFICATION AND MANAGEMENT OF MILD TRAUMATIC BRAIN INJURY IN AN AUSTERE ENVIRONMENT (Table 26-3) The following comments describe techniques that have demonstrated their utility in caring for military personnel deployed to austere environments or those involving combat action. The response to mild-to-moderate TBI has four components: assess, inform, monitor, and evacuate. Assess.  Austere environments do not typically lend themselves to thorough assessment of TBI; this is especially true in complex emergencies or other situations where security limitations preclude administration of a more comprehensive evaluation.42 In response, the military and Department of Veterans Affairs have developed tools to screen, assess, and longitudinally track and treat MTBI as a subset of TBI. For first responders, the Military Acute Concussion Evaluation (MACE) screening tool has demonstrated its usefulness. The MACE tool includes the Standard Assessment of Concussion, a four-part cognitive screening in the domains of orientation, immediate recall, concentration, and

TABLE 26-3  Severity of Traumatic Brain Injury

Rating Scale

Severity

GCS*

LOC

Mild Moderate Severe

13-15 9-12 3-8

24 hr

AOC† (hr) 24 >24 >24

PTA >

10 1 4 7 9 11 12 14 15 16 17 18 19

5 5 10 13 15 17 19 21 22 23 24 25 26

30 min

0 11 16 19 22 24 26 27 29 30 31 32 33

5 16 22 26 29 31 33 34 36 37 38 39 40

10 min

10 22 28 32 35 37 39 41 43 44 45 46 48

15 28 35 39 42 44 46 48 50 51 52 54 55

20 34 41 45 48 51 53 55 57 58 60 61 62

25 40 47 51 55 58 60 62 64 65 67 68 69

30 46 53 58 61 64 67 69 71 72 74 75 76

35 52 59 64 68 71 73 76 78 79 81 82 84

40 57 66 71 74 78 80 82 84 86 88 89 91

45 63 72 77 81 84 87 89 91 93 95 97 98

5 min

FIGURE 41-1  Windchill chart. (From Bowman WD, Johe DH, American Academy of Orthopaedic Surgeons, National Ski Patrol System [United States]: Outdoor emergency care: Comprehensive prehospital care for nonurban settings, ed 4, Boston, 2003, Jones & Bartlett.)

779

CHAPTER 41  Essentials of Wilderness Survival

Basal body heat production is about 50 kcal/m2/hr. This can be increased by muscular activity (both involuntary [shivering] and voluntary), eating, inflammation and infection (fever), and in response to cold exposure. Shivering can increase heat production up to five times the basal rate, and vigorous exercise can increase it up to 10 times. Cold exposure increases hunger; secretion of epinephrine, norepinephrine, and thyroxin; and semiconscious activity, such as foot stamping and dancing in place. Eating provides both needed calories and the temporary increase in basal metabolic rate that occurs during digestion alone; this is specific dynamic action (SDA). The SDA of protein is five to seven times higher than that of fat and carbohydrates, and it lasts longer. However, onset of the SDA is much faster with carbohydrates than with protein or fat. Therefore, the person who is cold inside a sleeping bag at bedtime should eat carbohydrates for quicker warming and protein to stay warm all night. In hot weather, body heat production can be decreased by slowing muscular activity and avoiding foods with a high SDA. In cold weather, heat can be added to the body by exposure to a fire or another heat source (e.g., sunlight) and by ingesting hot food and drink. In hot weather, external heat addition can be decreased by staying in the shade, wearing clothing that blocks the sun’s rays, and avoiding hot objects and hot food and drink. The body loses heat to the environment by conduction, convection, evaporation, radiation, and respiration; it may gain heat from the environment by the same mechanisms (except for evaporation). The relative importance of these mechanisms depends on temperature, humidity, wind velocity, cloud cover, insulation, contact with hot or cold objects, sweating, and muscular exercise. With a resting body in still air at 21° C (70° F), radiation, conduction, and convection account for about 70% of total heat loss; evaporation accounts for about 27%; and urination, defecation, and respiration account for only 3%. During work, however, evaporation may account for up to 85% of heat loss. It is useful to think of the body as being composed of a core (i.e., the heart, lungs, liver, adrenal glands, central nervous system, and other vital organs) and a shell (i.e., the skin, muscles, and extremities). Most of the physiologic adjustments in response to cold or heat exposure occur in the shell. These adjustments are intended to maintain a relatively constant core temperature; in below-freezing weather, these adjustments may predispose parts of the shell to frostbite and other types of localized cold injury. The importance of avoiding travel and seeking shelter during storms and extreme cold cannot be overemphasized. The additive chilling effect of wind when added to cold is impressive. Wind-chill charts (Figure 41-1) show the relationship between actual temperature, wind velocity, and “effective” temperature at the body surface. The term wind chill refers to the rate of cooling; the actual temperature reached is no lower than it would be if wind were absent (unless evaporation of liquid is occurring at the body surface). The increase in heat loss as the wind rises is not linear; rather, it is more proportional to the square root of the wind speed.

shelter are more important than are involuntary mechanisms of adaptation to environmental stress.

PART 5  RESCUE AND SURVIVAL

At moderate ambient temperatures, the body’s core temperature is kept stable by constant small adjustments in metabolic rate, muscular activity, sweating, and skin circulation. When the body is chilled, automatic and semiautomatic mechanisms increase internal heat production by slightly increasing metabolic rate, shivering, and semiconscious activities (e.g., foot stamping), and they reduce heat loss by diminishing sweat production and shell circulation. The person has a strong urge to curl up into a ball, thereby reducing the body’s surface area. At the same time, the brain tells the body to decrease heat loss by adding insulation and wind protection, seeking shelter, and increasing heat gain by increasing muscular activity, building a fire, seeking sunlight, and eating. When the body overheats, these actions are reversed. The body increases heat loss by increasing circulation to the skin and extremities and by increasing sweating. These mechanisms require more water, which stimulates the thirst response. Heat production is decreased as a result of a feeling of sluggishness and languor, which leads to reduction in physical activity and in the amount of heat produced by the muscles. The brain tells the body to decrease heat gain and to increase heat loss by providing shelter from the sun, removing clothing, and fanning itself.

Cold Weather Survival Body temperature in a cold environment is maintained by decreasing body heat loss, increasing internal body heat production, or adding heat from the outside. The most efficient of these methods is the conservation of body heat by decreasing heat loss, generally with the use of clothing and shelter.

DECREASING BODY HEAT LOSS Heat loss from conduction and convection can be prevented by interposing substances of low thermal conductivity, such as clothing made of insulating materials, between the body and the outside air. Clothing creates a microclimate of warmed, still air next to the skin surface. Clothing’s value depends on how well it traps air, the thickness of the air layer, and whether these qualities are reduced by wetting (Table 41-1). Traditional insulating materials are wool, down, foam, and older synthetics such as Orlon, Dacron, and polyester. Wool retains warmth when wet because of a moderately low wicking action and its ability to suspend water vapor within its fibers without affecting its low thermal conductance. It can absorb a considerable amount of water without feeling wet, but is heavier than synthetics, “itchy,” and more difficult to dry. However, its toughness and durability make it a good choice for garments that are subject to hard wear, such as trousers, mittens, and socks. Cotton, particularly denim and corduroy, is a poor insulator. It dries slowly because of its low evaporative ability; high thermal conductance is further increased by wetting. Cotton has no place in the backcountry in cold weather. Orlon, Dacron, acrylic, and polyester were developed to duplicate wool’s properties without wool’s high cost and other perceived drawbacks. They traditionally have been used for hats,

shirts, sweaters, and long underwear. They are almost as warm and not as itchy as wool, and evaporate moisture better. A number of newer fabrics are woven from fibers that have lower thermal conductance, greater insulating ability, and better wicking action than do traditional fibers. Examples include polypropylene and treated polyesters such as Capilene, Thermax, and ThermaStat. Polyester is also made into pile and fleece; these are light, dry easily, trap air well, and stay warm when wet because the fibers do not absorb water. Examples include Polartec, Borglite, Polarplus, and Synchilla. Fibers used as fillers in quilted garments, such as parkas, include hollow synthetics, such as Hollofil II and Quallofil, which were designed on the basis of the principles of reindeer hair. Microfibers that provide good insulating ability with less bulk include Thinsulate, Thermoloft, and Thermolite. One of the newer fibers, Microloft, is supposed to be warmer than down of the same weight. New synthetics come on the market frequently, so one should consult trade journals and “gear” issues of outdoor magazines. The layering principle of clothing is effective for preventing both chilling and overheating. Multiple layers of clothing provide multiple layers of microclimate. Layers are added as necessary to prevent chilling or subtracted to prevent overheating that would cause perspiring. Because water conducts heat 25 to 32 times faster than air at the same temperature, clothing that is wet with perspiration or water may cause rapid heat loss from conduction and evaporation. The need to add or subtract layers should be anticipated before either chilling or heavy perspiring occurs. Clothing should be easily adjustable, sweaters should be closeable from the waist to the neck with a sturdy zipper, and outer layers should be cut full enough to allow for the expansion of inner layers to their full thicknesses. Zippers in the axillary, lateral chest, and lateral thigh areas are useful for ventilation. Loss of heat from convection can be prevented by wearing windproof outer garments. Typical examples include a parka with a hood and a pair of windproof pants (regular or bib style) or ski warm-up pants. Loss of heat from infrared radiation can also be prevented by insulation and emphasizing the proper covering of body parts with a large surface area–to–volume ratio. The uncovered head can dissipate up to 70% of body heat production at an ambient temperature of −16° C (5° F), partly because the body does not reduce blood supply to the head and neck in cold weather as it does to the extremities. High heat loss through radiation during cold nights can be decreased by sleeping in a tent or under a tarpaulin instead of out in the open. Coverage for the head, ears, hands, and feet should not restrict circulation. Developed initially for skiers, a tubular neck gaiter can be pulled up over the back of the head to form a hood or up over the lower face to form a mask. In addition to head and neck protection, this device also blocks some of the heat that would otherwise be lost by the bellows action of clothing that is caused by body motion. Heat loss from the respiratory tract can be diminished by avoiding overexertion and overheating that occur with excessively heavy breathing. When it is extremely cold, inspired air

TABLE 41-1  Fiber Characteristics of Natural and Synthetic Fibers Fabric Wool Cotton Nylon Polyester Acrylic Polypropylene

Specific Gravity* (Ratio to Water)

Thermal Conductance† (cal/m2)

Evaporative Ability‡

Wicking Ability

Moisture Regain§

1.32 1.54 1.14 1.38 1.15 0.91

2.1 6.1 2.4 2.4 2.4 1.2

Low Low High High High High

Moderate High Low Low High High

17 7.9 4 1 1 5

Modified from Davis AK: Nordic skiing: A scientific approach, Minneapolis, Minn, 1980, University of Minnesota. *The lower the specific gravity, the better the insulating ability. † The lower the thermal conductance, the slower the flow of heat from the body. ‡ The higher the evaporative ability, the shorter the amount of time that a fiber will be wet (i.e., in a reduced insulative state). § Moisture regain is the amount of moisture that a fiber can absorb before it feels wet.

780

DRESSING FOR COLD WEATHER Anyone who ventures outdoors in cold weather should have enough clothing of the proper kind, either on the body or in the backpack, for the most extreme environmental conditions that are likely to be experienced. Although building fires, carrying emergency shelters, and improvising survival shelters are discussed at length later in this chapter, the process of dressing for cold weather should be approached with the idea that clothing may become the only shelter and endogenous heat production the only heat available. Clothing and other types of insulating materials should be selected with the idea that they need to keep the body warm and dry even during periods of inactivity.

moderate conditions, sturdy leather climbing boots made of fullthickness leather and that are 15 to 20 cm (6 to 8 in) in height, that have rubber lug soles, and that are roomy enough to accommodate the desired numbers of socks are ideal. Boots made of leather and fabric (e.g., Gore-Tex) are lighter and suitable for trail hiking, but they may not be as durable for rough terrain. Boots must be long enough, their toes high enough, and their laces tight enough so that the wearer’s toes do not strike the inside of the front of the boot during downhill walking. Laces should also be tight enough to prevent the heel from moving up and down during walking but not so tight that circulation is restricted and the toes cannot wiggle easily. For colder temperatures, double boots are preferable. These can be all-leather boots, or they can have outer shells of plastic or nylon with inner boots of felt or foam. All-leather versions may be hard to find. The Canadian type of shoe pack with a removable inner felt liner is a good choice for light snowshoeing and other nontechnical outdoor activities in the cold. Special double ski boots are available for ski touring, Telemark skiing, and ski mountaineering, depending on the type of binding selected. Hat.  Hats should be of the stocking variety; made of wool, pile, Orlon, polypropylene, or wool/polypropylene; and large enough to cover the ears. A small bill feature is desirable to shade the eyes. “Bomber” caps with bills and pull-down earflaps and “Andean” caps with ear coverings are preferred by some. Some arrangement should be provided to protect the face from cold wind, as with a balaclava configuration or a separate face mask. A useful combination for very cold and windy weather is a ski hat together with a neck gaiter that can be pulled up to cover most of the lower face; the parka hood can then be pulled over the head from behind.

Pants.  Wool or pile pants are best and should have pockets that are easily accessible for hand warming. Pile pants should have reinforcements at the knees and buttocks and a zipper or Velcro fly for males. Full or partial lateral leg zippers are convenient, especially for removing pants without removing boots.

Third Layer Parka.  The parka can be a standard ski or mountain parka filled with down, Dacron, Quallofil, Thinsulate, or another lofting material. A more versatile combination is two separate garments: a pile jacket plus a water-resistant shell. For snow camping, a pile jacket with a thin outer cover of nylon (i.e., three-season, squall, or warm-up jacket) may be preferred, because, unlike an uncovered pile jacket, it does not collect snow when it is worn without the shell. The shell should have a hood with a drawstring, a two-way zipper with an overlying weather flap closed with full-length Velcro (in case of zipper failure, very cold hands, or upper extremity injury), a cloth flap to protect the chin from the metal zipper pull, armpit or lateral chest zippers for ventilation, and at least four outer pockets plus one or two inside pockets to contain frequently needed items (e.g., gloves, compass, map, sunglasses, neck gaiter). Outer pockets should be located where they can be reached while wearing a backpack with a fastened waist belt. The shell should be fingertip length unless bibs are worn. Zippers should have extra-long tabs added to facilitate closure with cold or mittened hands. Pockets with horizontal openings may close with Velcro, but those with vertical openings should close with zippers. Because the parka is anchored by the shoulders, when using one hand, it is generally easier to pull a vertical zipper down rather than up. In some brands of parkas, vertical zippers are pulled down to close the pockets; in other brands, they are pulled up. The authors prefer the former type: the danger of losing pocket contents as a result of difficulty with closing a zipper is worse than any perceived delay caused by difficulty with opening a zipper. For ventilation, there should be zippered openings at the armpits. These should be large enough so that the parka can be converted into a vest-like garment during warm conditions by inserting the wearer’s arms through the openings and tucking the sleeves inside the parka. Because these zippers usually perform more easily when they are pulled from the distal to the proximal direction, this direction should close them; increasing wind protection is usually more urgent than decreasing it (i.e., freezing is more dangerous than sweating).

Foot gear.  The type of boot chosen depends on the type of activity and the expected environmental temperatures. For

Wind pants.  Wind pants should be light and water repellent; a laminated garment such as Gore-Tex is a good choice. Long and

First Layer Long underwear.  Wool is an excellent choice for long underwear, but it is itchy and expensive, and it may be difficult to find. Merino wool is less itchy. Polypropylene, acrylic, and the newer polyesters may be preferable because of their lower cost, good insulating ability, and outstanding evaporative ability (see Table 41-1). Avoid cotton. Synthetics, more than wool, tend to retain body odor after washing. Socks.  One or two pairs of moderate to heavy wool or wool/ nylon blend socks are excellent, preferably with an additional pair of light polypropylene socks worn underneath next to the skin. Consider carrying at least one spare pair of wool socks. Thin gloves (glove liners).  Light propylene, wool, silk, or fingerless wool or pile gloves are useful for moderately cold conditions or when finger dexterity is required, such as when adjusting ski bindings. Polyester/Lycra gloves provide a tighter but more stretchable fit, which enhances fine finger movements. Second Layer Shirt.  Shirts should be made of light, soft wool or a durable synthetic such as acrylic, and they should have long sleeves. Large breast pockets with buttons or Velcro fasteners are handy to carry such items as sunglasses and a compass. For ventilation, the front of the shirt should open completely (i.e., it should have a button or zipper closure). A turtleneck feature protects the neck, as do neck warmers and mufflers that can be pulled up to protect the lower face.

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CHAPTER 41  Essentials of Wilderness Survival

can be warmed by pulling the parka hood out in front of the face to form a “frost tunnel.” Heat loss from conduction occurs as a result of direct contact with a colder object. Sitting on a pack, a foam pad, a log, or another object of lower heat conductivity is preferable to sitting in the snow or on a cold rock. At low temperatures, bare skin freezes to metal; avoid this by wearing light gloves when handling metal objects. Gasoline and other liquids with freezing points lower than that of water can cause frostbite if they are accidentally poured on the skin at low temperatures. During bivouacs in snow shelters, avoid contact with the snow by sitting on a foam pad or backpack or by improvising a mattress of evergreen boughs, grass, or dry leaves. In cold or windy weather, an injured person needs windproof insulating material under as well as over and around the body. Heat loss from conduction and evaporation can be lessened by avoiding wetting and by changing to dry clothes or drying out quickly when wet. Ideally, outer clothing should be windproof, and it should not collect snow. It should shed water but not be waterproof, because waterproof garments prevent the evaporation of sweat; laminated fabrics such as Gore-Tex and its relatives are designed for this purpose.

PART 5  RESCUE AND SURVIVAL

zippered side openings at the bottoms are useful to permit the donning of pants without removing boots as well as for ventilation and access to inner pants’ pockets. Hand gear.  Mittens and gloves provide hand protection from trauma and cold. Because survival depends to some extent on normal hand dexterity, gloves or mittens should be available to protect the hands from cuts, bruises, blisters, and possible resulting infections. In temperate weather, these can be light and unlined leather gloves. One of the more serious and still unsolved cold weather problems is how to keep fingers warm while leaving them sufficiently unhampered to do work. Mittens are warmer than gloves, because fingers that touch each other warm each other. However, even thin mittens do not allow for delicate finger movements. An important part of the cold-finger solution is to prevent core cooling and compensatory extremity vasoconstriction by addressing core temperature stabilization through exercise, eating, and wearing enough layers on the trunk. A common method is to wear a pair of thin gloves of polypropylene, silk, thin wool, or polyester/Lycra inside a wool or pile mitten covered with a windproof and water-resistant shell. For delicate finger work, the gloved hand is removed from the mitten, the work done as fast as possible, and then the hand returned to the mitten. However, because insulating materials insulate in both directions, when inside a warm mitten, cold fingers wearing gloves will not rewarm as fast as cold, bare fingers. Therefore, another solution is to use bare fingers, which will perform faster than gloved fingers, work as fast as possible, and then return them to warm mittens periodically until the task is done. However, this is not practical when working with metal in very cold weather. Another approach is to keep a pair of gloves warm in a pocket and put them on after removing the hands from mittens. Polyester/Lycra gloves are easier to don than are many other types of thin gloves. Excellent three-layer mitten sets include windproof shells with leather palms and two sets of removable pile mittens, at least one of which is fastened to the inner shell with Velcro. Another good system is a thin glove liner inside a heavy wool mitten (e.g., Dachstein, rag wool, wool/polypropylene) inside a GoreTex shell. An option that provides more finger dexterity in moderately cold conditions is a polypropylene glove liner inside a fingerless wool glove inside a shell. A newer combination is a fingerless wool glove inside a wool mitten that has a horizontal slit in the distal palm (i.e., Cordova’s rag wool convertible gloves). The distal tip of the mitten can be folded backward dorsally and secured with a Velcro patch, thereby allowing the hand that is covered with the fingerless wool glove to be exposed through the slit. However, more layers and increasing complexity mean more difficulty doing delicate hand tasks. Shells should have easily accessible nose warmers of pile or mouton on their backs, they should be long enough to cover the wrists, and they should have palms of soft leather or sticky fabric for securely holding ice axes and ski poles. Gaiters and overboots.  Gaiters, which are long nylon tubes that cover the lower leg and upper part of the boot, are designed to keep snow, sand, and gravel out of boots and socks. They extend upward to just below the knee, open at the side or in front with a zipper or Velcro, have a strap that fits under the boot sole to keep them snug on the boots, and a drawstring at the top to hold them up. Gaiters with a front opening that is closed by a wide Velcro strap are the easiest to put on and take off. Shorter versions that extend to just above the ankle are adequate for summer mountaineering and may be preferable for cross-country skiers who need access for tightening boot buckles before descents. High-altitude mountaineering requires special insulated overboots or lined gaiters. Fourth Layer The previous three layers are usually worn on the body. A fourth layer should be easily available in the pack; this layer should include quilted or pile pants and a jacket or vest. 782

Rain gear.  In moderate climates or in spring conditions, when rain and wet snow may be encountered, outer garments of GoreTex or similar material should be used. For maritime climates and during seasons of heavy rain, it may be better to have two separate sets of outer garments: a light, thin, windproof nylon jacket and pants and a waterproof (i.e., coated nylon) jacket and pants. Vapor barrier systems.  Waterproof garments and sleeping bag liners worn close to the skin are favored by many because they can prevent the wetting of outer clothing by sweat that might result in decreased insulating capacity. There also is claimed to be some reduction in water consumption requirements with such items. These types of vapor barriers seem to work better in very cold weather than at moderate temperatures. A light garment of polypropylene or similar material should be worn next to the skin, with the waterproof garment worn over this. Vapor barrier systems probably should be tried out in the field in nonsurvival conditions before being relied on in severe weather. Persons with hyperhidrosis and those who dislike clammy skin may not feel comfortable with such garments.

Shelter SUMMER EMERGENCY SHELTERS When faced with an unplanned night out, one’s first step should be to locate a place out of the wind. Getting behind a rock, moving to the lee side of a ridge, going down into the tree line, or even turning one’s back to the wind can make a difference. Eliminating windchill allows one to concentrate on dealing with ambient air temperature by using spare clothing and natural insulation and by starting a fire. Look for a space into which you can crawl, such as a rocky overhang or a space under dense evergreens or fallen logs. Experienced and prepared individuals will have some type of waterproof material (e.g., plastic bag, tube tent, tarp) into or under which they can crawl as well. Bright-colored (i.e., orange or red) materials are easier for searchers to spot. Getting out of the wind, rain, or snow quickly and being able to stay as warm and dry as possible are vital. When one is wet and cold, it may be very difficult—and sometimes impossible—to rewarm and dry out.

SPACE BLANKETS AND BAGS Space blankets and bags are lightweight, inexpensive, and compact, but they are of limited value in an emergency. Consider a typical scenario in which it is late in the day; it is cold, rainy, and windy; and the survivor is injured, hypothermic, or both. A space blanket is frequently difficult to get out of its package, to unfold, and to manage in windy conditions. Depending on the brand, space blankets are usually too small to fully encase an adult. When wrapped up, the survivor will find that a space blanket makes a shelter that is so noisy that even an approaching aircraft or ground search party may not be heard. Space blankets also tear easily when they are nicked or punctured. The space bag has the same flaws as does the space blanket except that it is easier to encase an individual and for that person to stay enclosed.

THERMAL BLANKETS Thermal blankets are similar to space blankets, but they are made from much heavier material that is reinforced with fiberglass threads and that has a grommet in each corner. They can be used as body wraps, but again, depending on the size of the person, they are often too small to encase an adult. Some survivors have attempted to use a thermal blanket as a shelter roof by tying lines to each corner and then stretching the blanket between various anchor points. In benign conditions, this may work; however, with any wind or snow loading, the grommets quickly tear or pull out.

Tube tents are usually about 2.4 m (8 feet) long and provide a tubular shelter that is 0.9 to 1.5 m (3 to 5 feet) high, depending on the brand. They can be pulled over the body to provide a quick shelter or pitched as a “pup tent.” To do this, find two anchors (e.g., rocks, trees) that are the proper distance apart, tie a line to one of them, spread the tent out along the length of the line, run the line through it, and then tie off the other end of the line. The height of the line should be such that the tent can be spread out to accommodate the occupant. To avoid ripping, the tent plastic should be 3 to 4 mils thick (1 mil = 0.0251 mm [0.001 inch]). Tube tents can be improvised from two plastic 55-gallon drum liners, which are 3 to 4 mil thick, or from large, heavy-grade, household trash bags by opening up the closed end of one bag, sliding it into the open end of the second bag, and then duct taping the bags together (Figure 41-2).

TARPAULINS Sheets of Visqueen plastic, painters’ drop cloths, large pieces of canvas, or other similar materials can be used to erect a wide variety of effective survival shelters. “Blue crinkly” plastic tarps made of a laminated polyethylene weave are readily available and inexpensive; they can be purchased from most hardware stores, they come in a variety of sizes, and have grommets inserted along the edges. A tarp, no smaller than 2.4 × 3 m (8 × 10 feet), is needed to protect an adult. Tarps of this size weigh about 0.7 kg (26 oz) and roll up into a tube that is 15 cm

FIGURE 41-2  Two large plastic bags can be taped together in tandem and used with a line to form a tube tent. (Courtesy Peter Kummerfeldt.)

(6 inches) in diameter by 30 cm (12 inches) long, which is convenient to carry tied to the outside of a daypack or a fanny pack. To save valuable time in a survival situation, tie 3 m (10 feet) of parachute cord to each corner grommet ahead of time. Tarps can be erected in a number of shelter styles, depending on weather conditions (Figure 41-3). To erect a lean-to shelter, first select a line that is long enough to stretch between two trees that are far enough apart for the tarp to be stretched tight. With the use of a timber hitch, tie off one end of the line to one of the trees at about chest height. Then, rather than passing the line itself through the grommet eyes, insert a small loop of the line

A

B

C

D

E

F

G

FIGURE 41-3  Four types of shelters that can be made from a tarp. A, A simple lean-to. B, An illustration of a method for attaching a line to a tarp. C, A pup-tent type of shelter. D, A lean-to shelter with an eave. E, A triangular tarp shelter. F, Creating a button for attaching a line to a tarp without grommets. G, Attaching a line to the neck of the button with the use of a girth or a clove hitch. (Courtesy Peter Kummerfeldt.)

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CHAPTER 41  Essentials of Wilderness Survival

TUBE TENTS

PART 5  RESCUE AND SURVIVAL

through the first grommet eye, and secure the loop with a short stick that is thrust through it on the opposite side (Figure 41-3, B). Repeat this process for each grommet, stretching the tarp tight each time. After the tarp is attached to the line, tie off the other end of the line to the second tree, with the line stretched as tightly as possible. The lower edge of the tarp is then pegged to the ground or anchored with large stones or a length of log. When making pegs, select a length of wood that is 3.8 to 5 cm (1.5 to 2 inches) in diameter and that is twice as long as needed. With a saw, make one 45-degree cut at the midpoint of the stick. In this way, one cut produces two pegs, both of which are sharp enough to be driven into the ground by pounding their blunt ends with the back of an ax head or a large rock. Fill in the sides of the lean-to with vegetation. If a fire will be built in front of the lean-to, the front opening should be parallel to the prevailing wind so that the smoke will be carried away from the shelter. If not, the back edge of the lean-to should point to the prevailing wind. To erect a pup-tent type of shelter (Figure 41-3, C), tie a line between two trees, drape the tarp over it, and peg down the sides. Block the ends with vegetation or personal equipment. A lean-to with an eave (Figure 41-3, D) gives more protection from rain and snow than does one without an eave. Instead of attaching the long edge of the tarp to the line between the two trees, drape the tarp over the line so that several feet are on the other side, and then tie the two corners to pegs for a downsloping eave. A triangular tarp shelter can be erected rapidly and provides good protection (Figure 41-3, E). It requires three pegs and an anchor point on a tree.

PLASTIC BAG SHELTERS Large, heavy-grade (3 to 4 mil), orange, plastic, 208-L (55-gal) drum liners make good short-term emergency shelters. Having one to crawl into quickly will speed warming and drying as well as shelter the survivor from further wetness and chilling. However, total enclosure in a plastic bag is both uncomfortable and dangerous as a result of increased wetting from the condensation of water vapor in exhaled air and perspiration plus poor ventilation, with a lack of oxygen and buildup of carbon dioxide. To minimize these problems, cut an opening in the bottom end of the bag that is just large enough for your head, and then pass the bag over your head so that your face is at the opening (Figure 41-4). If you get too warm, you can push your head through the hole. When creating the hole, cut the plastic at 90 degrees to the fold to reduce the likelihood of the bag tearing along the seam.

WINTER AND COLD WEATHER EMERGENCY SHELTERS Everyone who spends time in the winter wilderness should practice the construction of several types of emergency survival

TABLE 41-2  Thermal Conductivity of Various

Substances

Substance Air Down Polyester (hollow) Polyester (solid) Snow (old) Cork Sawdust Wool felt Cardboard Wood Dry sand Water Brick Concrete Ice

Conductivity*

Temperature Measured (° C)

0.006 0.01 0.016 0.019 0.115 0.128 0.14 0.149 0.5 0.8 0.93 1.4 1.5 2.2 5.7

0 20 — — 0 30 30 40 20 20 20 12 20 20 0

*Conductivity is the quantity of heat in gram calories transmitted per second through a plate of material that is 1 cm thick and 1 cm2 in area when the temperature difference between the sides of the plate is 1° C.

shelters before such shelters may be needed. The functions of a shelter are to provide an extension of the microclimate of still, warm air that is furnished by clothing; to contain the heat generated by the body, a fire, or other heat source; and to protect the individual from snow, rain, and wind. A properly designed shelter should allow easy and rapid construction with simple tools and should provide good protection from wind, rain, and snowfall. The type and size of shelter depend on the presence or absence of snow and its depth; on the natural features of the landscape, including the availability of natural building and insulating materials; and on whether firewood or a stove and fuel are available. If external heat cannot be provided, a shelter must be small and windproof to preserve body heat. If possible, a shelter should be constructed in the timber to provide protection from the wind and access to firewood. Generally shelters partway up the side of a ridge are warmer than those in a valley, because cold air tends to collect in valleys and basins during the night. Exposed windy ridges above the timberline are cold. Areas that are exposed to flooding (e.g., drainages, dry riverbeds), rockfalls, cornice falls, or avalanches or that are under dead trees or limbs should be avoided. If open water is available, the camp may be located nearby, although in nonsurvival conditions camps should be at least 61 m (200 feet) from bodies of water. To avoid drifting snow, tents and shelters should be located with the entrance parallel to the prevailing wind. Snow is a good insulator (Table 41-2). Its heat conductivity is 1/10,000 that of copper, and its insulating ability superior to wool felt, so snow shelters may be warmer than other types of constructed shelters as long as the inhabitants remain dry. Contact with the snow or cold ground is avoided by sitting on a foam pad, dry leaves, grass, a backpack, or (in survival conditions only) a bed of evergreen boughs.

NATURAL SHELTERS

FIGURE 41-4  Lean-to shelter. The sides should be closed with brush or snow and a fire built in front.

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Caves and alcoves under overhangs are good shelters and can be improved by building wind walls with rocks, snow blocks, or brush. A fire should be built in such a way that heat reflects onto the occupant. The fire should be 1.5 to 1.8 m (5 to 6 feet) from the back of the shelter, with a reflector wall of logs or stones on the opposite side of the fire; the occupant should sit between the fire and the back of the shelter (Figure 41-5). Adjustments may have to be made to prevent too much smoke from reaching the occupant. In deep snow, large fallen logs and bent-over evergreens frequently have hollows under them that can be used as small caves. Cone-shaped depressions around the trunks of evergreens (i.e., “tree wells”) can be improved by digging them out and roofing them over with evergreen branches or a tarp. A fire that is built to one side of such a shelter will reflect its heat off of

CHAPTER 41  Essentials of Wilderness Survival

A FIGURE 41-5  Example of two large plastic bags used to form a oneperson survival shelter. (Courtesy Peter Kummerfeldt.)

the snow toward the occupant. Ventilation must be adequate, and the fire should not be positioned under snow-laden branches than can extinguish the fire by dumping snow on it.

CONSTRUCTED SHELTERS When no snow is available, shelters can be built of small trees, branches, brush, and boughs. In cold weather with minimal or absent snow cover, the most satisfactory type is a lean-to covered by a tarp, with the two sides closed with brush or piled snow, a fire at the open front, and a wall of logs or stones on the far side of the fire to reflect heat into the interior of the lean-to (Figure 41-6). Walls or a roof of brush, branches, or broad leaves should be thatched (i.e., each layer should overlap the one below it).

SNOW SHELTERS A snow trench is the easiest and quickest survival snow shelter and the one that is least likely to make the diggers wet. It can be dug in most areas that are flat or on slight to moderate inclines as long as the snow is 0.9 m (3 feet) or deeper or can be piled to that depth. A 1.2 × 1.8-m (4 × 6-feet) trench can be dug in 20 minutes, with one end roofed over with a tarp or boughs and a fire built at the opposite end (Figure 41-7). Again, adjustments may need to be made to avoid excessive smoke exposure, which can be prevented to some extent by setting the long axis of the trench at a right angle to the apparent wind direction. If a large (2.4 × 3 m [8 × 10 feet]) tarp and a stove are available, a trench can be dug that is as comfortable as a snow cave;

Overhang

B FIGURE 41-7  Emergency snow trench. A, A pit is dug and overlaid with skis and poles. B, A tarp is placed over the skis and secured with snow and heavy objects.

this will hold two or three people. The object is to keep the maximal amount of snow around and over the trench. The trench is dug as narrow as possible at the surface while still providing sufficient room to shovel; a suitable size for the top is 1.2 m (4 feet) wide by 2.4 m (8 feet) long. It is undercut at the back and sides so that the bottom is 1.8 to 2.1 m (6 to 7 feet) wide by 2.7 to 3 m (9 to 10 feet) long (Figure 41-8). A narrow entrance helps to contain heat and can be closed with a small plastic sheet or a pack. Four or more skis or thick limbs are laid from side to side over the top of the trench, with ski poles or branches interwoven at right angles. A tarp is then laid on top of these and the snow piled around its edges to hold it down. In very cold weather, the entire tarp can be covered by a layer of snow; at least 20 cm (8 inches) is needed for proper insulation. When the entrance is closed, a small stove and the occupants’ body heat will raise the interior temperature to −4° to −1° C (25° to 30° F). Higher temperatures should be avoided so that clothing and bedding will not become wet from melting snow. Above the timberline in deep, wind-packed snow, a similar trench can be roofed with snow blocks that are laid horizontally, set as an A-frame, or laid on skis (Figure 41-9). Chinks between the blocks are caulked with snow.

SNOW CAVES

Reflector Fire

Backpack

FIGURE 41-6  Natural shelter.

Woodpile

Although a small snow cave that is large enough for one person can be dug with a ski or cooking pot, it is much better to have a shovel. Two shovels are best: a medium-sized general-purpose aluminum scoop shovel and a small, straight shovel (i.e., French type) to use while excavating the interior of the cave. The best site is a large snow drift, such as is found on the lee side of a small hill. Areas in avalanche zones or under cornices should be avoided. Because the diggers tend to become wet, water-resistant or waterproof jackets and pants should be worn. In the traditional snow cave, the entrance is dug so that it is just large enough to crawl through, and it is angled upward toward the sleeping chamber (Figure 41-10, A); this arrangement tends to trap warm air inside. It should be large enough for a stove and two occupants who are lying side-by-side. After the entrance is dug with the scoop shovel, the digger crawls inside, lies supine, and uses 785

PART 5  RESCUE AND SURVIVAL

Ski poles

Sides and ends undercut

A1

A2

Skis

Narrow entrance

B1

B2

Tarp

C1

Snow piled along edges

Ventilation hole for cookstove

C2

D FIGURE 41-8  A1 and A2, Three-person snow trench. A narrow entrance and a narrow top with undercut sides are advisable to trap as much warm air as possible. B1 and B2, Skis and ski poles or stout limbs form the roof support. C1 and C2, Finished trench with snow piled along the edges of the tarp to hold it down. Note the ventilation hole for the cook stove. D, Completed trench after a heavy snowfall.

A

B FIGURE 41-9  A, Above-timberline snow trench. B, Completed snow trench the morning after a heavy snowfall.

786

C

B

FIGURE 41-10  A, Snow cave entrance. B, Snow cave partly closed with snow blocks. C, Interior of snow cave.

the straight shovel to excavate the chamber until the space is large enough to allow room to use the larger scoop shovel. A long level bench about a foot higher than the floor of the cave is constructed and used for a sleeping area. A ventilation hole as large as a ski pole basket is cut in the roof over the cooking area. Because the traditional cave takes at least 2 hours to dig and gets the diggers quite wet, the alternate “T” method has found favor. This involves excavating a much larger entrance hole, which is shaped like a “T,” so that the digger can stand erect, have plenty of room to dig, and stay drier (see Figure 41-10, B). The crossbar of the “T” is at the level of the sleeping bench; the digger stands in the foot of the “T.” After the cave is finished, the top of the “T” is closed with snow blocks, leaving the foot of the “T” as a small access door hole. Pine branches or other natural materials are used to cover the floor if a sleeping pad is not available.

SNOW DOMES When the ground is flat or the snow cover is shallow, snow can be piled into a large dome that is 1.8 to 2.1 m (6 to 7 feet) high and left to harden for a few hours (Figure 41-11). A low entrance is dug on one side, and, from there, the interior is carved out to make a dome-shaped room that is large enough to sleep three people. A ventilation hole is cut in the roof over the stove. Another method is to make a “form” (i.e., a pile of vegetation or equipment), cover this form with snow, allow the snow to set, and then open one end and remove the form.

IGLOOS Igloos are the most comfortable arctic shelters, but they require experience and engineering skill. They are not recommended for the novice, but they may be worth the effort if the party will be stranded for any length of time. Igloos require one or, ideally, two snow saws and snow of the proper consistency. Wind-blown snow in a treeless area is best; otherwise, a large area of snow can be stamped well and left to harden over several hours. To mark the diameter of the igloo, an individual holds a ski pole by the handle, points it to the side, and then turns his or her body so that the pole basket makes a large circle in the snow that outlines the base of an igloo that is suitable for three people. Cutting some of the snow blocks from inside this circle will lower the floor so that fewer blocks are required for the dome. At least two persons are needed: one to cut and carry the blocks and the other inside the igloo to lay the blocks. The blocks should be about 18 inches wide, 30 inches long, and 8 inches thick. They are laid in a circle that leans in about 20 to 30 degrees toward the center of the igloo, with the sides trimmed for a snug fit. The tops of the first few blocks in the first circle are beveled so that a continuous line of blocks is laid, with the first few blocks of each succeeding circle cocked upward (Figure 41-12, A and B). A common error is to not lean the blocks sufficiently inward, which results in an open tower instead of a dome. Gaps are caulked with snow. The dome should be 1.5 to 1.8 m (5 to 6 ft) high inside and can be closed with a single capstone of snow. The entrance is dug as a tunnel under rather than through the edge of the igloo to prevent warm air from escaping (see Figure 41-12, C ).

TENTS Tents are generally comfortable and dry; however, in very cold weather, they are not as warm as snow shelters. They are preferable to snow shelters at mild temperatures, during damp snow conditions at temperatures above freezing, or when the snow cover is minimal. Because of their weight, they are not usually a component of emergency equipment.

A

B FIGURE 41-11  A, Preparing a snow dome. B, Completed snow dome.

BIVOUAC SACKS AND OTHER SMALL AND PORTABLE EMERGENCY SHELTERS These types of shelters are usually made of thin waterproof or water-resistant fabric or plastic; they do not include an insulating layer, and they hold one or occasionally two persons. Bivouac sacks are carried for emergencies or for sleeping purposes by climbers on long, alpine-style climbs. Their main value is to protect individuals from wind and rain. Many modern packs have extensions so that, when they are used with a cagoule or an anorak (i.e., roomy, knee-length, hooded pullover garments), they form an acceptable bivouac sack. Tube tents and plastic shelters were discussed in the previous section of this chapter. Caution: When spending the night in a snow shelter (e.g., trench, cave, igloo), always have a shovel and flashlight inside the shelter and within easy reach. 787

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A

PART 5  RESCUE AND SURVIVAL

Air vent

Cooking

Sleeping

Entrance

Entrance

C

B

A

E

D

FIGURE 41-12  A to C, Stages of igloo construction. D, Building an igloo on the southeast ridge of Mt Foraker. E, Double igloo for a party of five.

Increasing Body Heat Production Internal body heat production can be increased voluntarily by raising the level of muscular activity and by eating. To obtain maximal heat production from exercise, the body should be well fed and in peak physical condition. This is particularly important for persons with sedentary occupations who participate in vigorous outdoor sports and for rescue personnel who may be subject to severe, unplanned, and prolonged physical stress. A suitable physical conditioning program should develop both aerobic and motor fitness. The goal of aerobic exercise is the efficient extraction of oxygen from alveolar air. This is best developed by rhythmic endurance exercises such as running, cross-country skiing, cycling, swimming, and use of exercise bicycles, treadmills, or Nordic skiing simulators. The most effective activities

A

C

are those that exercise the lower and upper extremities simultaneously. Exercise should be vigorous enough to produce a heart rate of 75% of the age-related maximum (i.e., 0.75 × [220 − the participant’s age]) for at least 15 minutes 4 days a week. Motor fitness, which includes strength, power, balance, agility, and flexibility, is developed by vigorous competitive sports, select calisthenics, and weight-lifting exercises.

Adding Heat From the Outside The ability to build a fire under adverse conditions is an essential skill that should be practiced by all people who engage in outdoor activities (Figure 41-13). Not only does a fire provide warmth that may mean the difference between life and death, but it also cheers the spirit, improves morale, serves as a signal

B

D

E

FIGURE 41-13  Stages of building a fire. A, Select a spot that is out of the wind. Start by placing tinder (i.e., small, dry evergreen twigs) in a lean-to fashion against a larger branch. B, Add a layer of kindling (i.e., larger dry branches and split sticks) over the tinder, and be sure that air can reach each piece. C, Insert a lighted match, a candle, or a cigarette lighter into the base of the lean-to. D and E, Add larger pieces of kindling and fuel (i.e., large sticks and pieces of split wood) as the fire catches well. Keep the fire small so that you can get close to it.

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Heat Sources The devices that are carried to produce the initial source of heat that is needed to start a fire must be easy to use when the hands are cold and have lost their dexterity. These devices must function every time regardless of temperature, altitude, wind, or precipitation; the amount of heat supplied must be great and long lasting. Because survivors are often injured, the devices must function when only one hand can be used. The heat required to ignite tinder traditionally has been provided by matches or cigarette lighters. Metal matches (i.e., ferrocerium rods) are a third and less-commonly used source of fire-starting heat.

Pouring liquid paraffin over matches to waterproof them is a common procedure that sounds good but that in practice complicates a survivor’s ability to get a fire going. The paraffin must be scraped off of the match head before it can be struck. Other people recommend using nail polish and spar varnish to waterproof matches. For the reasons stated previously, this should not be done. In short, waterproof matches should not be included in a survival kit.

MATCHES

WINDPROOF MATCHES

Predecessors of the modern-day match date back to 577 AD and the Northern Qi court in China. Today, a match is a “consumable tool for lighting a fire in a controlled circumstance on demand.” (Wikipedia) Most matches that are currently for sale are not designed for field use but rather for lighting cigarettes or candles and other home uses. Two general categories of matches are safety matches, which can only be ignited by striking the match against a specially prepared surface found on one or two sides of a matchbox, and strike-anywhere matches, which, theoretically, can be struck on any abrasive surface.

Windproof matches have longer and fatter heads than do normal matches; as much as one-half of the matchstick is covered with pyrophoric material. These matches can be difficult to light under benign conditions and almost impossible in adverse weather. Most commonly, the matchstick breaks at the junction of the match head and the stick when pressure is applied. Some windproof matches, once lit, only smolder and have little if any flame (Figure 41-16).

SAFETY MATCHES For a safety match to light, the chemicals (i.e., the pyrophoric material) on the match head must be combined with the chemicals on the striking pad. The chemicals on the match head consist mainly of potassium chlorate (45% to 55%) and a filler material (20% to 40%) that are bound together with glue. The striking surfaces attached to the sides of the box are composed of powdered glass, red phosphorus, black carbon, and a binder. Safety matches can only be ignited by striking the match head on the striking pad on the box from which they were removed; a match taken from one box may not light by striking it on the pad of another matchbox, because the combinations of the chemicals may be different (Figure 41-14, online).

FIGURE 41-15  Waterproof safety match.

STRIKE-ANYWHERE MATCHES Strike-anywhere matches can be identified by their two-tone heads, which are usually blue and white, green and white, pink and white, or red and white. Both chemicals (phosphorus sesquisulfide and potassium chlorate) that are needed to initiate combustion are combined on the match head. The term “strike anywhere” would lead you to believe that they could literally be struck anywhere, but nothing could be further from the truth. These matches must be struck on the striking pad or on another material that is abrasive enough to produce combustion yet that is not so abrasive that the match head is ripped off; it should come as no surprise that such a surface can be difficult to find when the ground is covered in snow. Although some people have developed the ability to ignite strike-anywhere matches by

WATERPROOF MATCHES Commercial waterproof matches have been dipped in a lacquer that “waterproofs” the match head after it dries. To light a waterproof match, the match head must be struck against the striking pad repeatedly until the lacquer is worn away and the chemicals contained in the match head come in contact with the chemicals in the pad. For some matches, this may only take a strike or two, but with others many strikes are required to ignite the match. With every strike, the pad becomes more contaminated with the waterproofing material and eventually a point is reached where there are remaining matches but the pad is so contaminated that it no longer works. Some waterproof matchboxes only have a striking pad on one edge of the box, thus making a bad situation even worse (Figure 41-15).

FIGURE 41-16  Windproof and waterproof safety match.

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to rescuers, and reinforces hopes of rescue and survival. Necessary equipment (which is discussed later in this chapter) includes a knife, a fire starter, and dry matches at a minimum. Most commonly the need for a fire does not arise until a crisis is at hand: for example, the weather has become life threatening, a person has fallen into the river and needs to be rewarmed quickly, or a hunter needs a fire to stay warm when faced with spending a night out far from camp. The need for a fire becomes critical when the survivor’s clothing is inadequate and other shelter is not available. These are not the times to get one’s first practice at building a fire. It is advisable to obtain that practice ahead of time in the backyard when rain or snow is falling and the wind is howling; that is the time to determine the strengths and weakness of fire-starting equipment and the soundness of one’s fire-building skills.

PART 5  RESCUE AND SURVIVAL

FIGURE 41-20  Boy-Scout style match case. FIGURE 41-17  Strike-anywhere match.

rubbing them across the seat of their pants, by flicking the match head with a thumbnail, or even by using their teeth, these methods are not reliable in an emergency. When carrying strikeanywhere matches, always have a piece of the striking pad from the original matchbox in the kit (Figure 41-17).

STORM MATCHES Storm matches are often found in civilian and military survival kits. They differ from other matches by having a “strikeable” tip with as much as one-half of the matchstick coated with a pyrophoric material that continues to burn even in wet and windy conditions. Lifeboat matches, which are a common variety of storm match, should be avoided, because they are particularly difficult to light. The striking pad, which is located on the outside of the lid, is small and wears out very quickly (Figure 41-18, online). All of the matches that are currently available were tested under field conditions, and REI Stormproof Matches were found to be the best. They proved to be the most reliable for starting fires under adverse weather conditions, and they are particularly effective in windy and wet conditions. As long as any match head material remains, the REI matches cannot be blown out, and, if they are extinguished in water, they will relight when they are removed. These matches are propriety and are only sold under the REI brand. Two boxes of matches, each of which contains 25 3-inch long matches, are packaged together in a vinyl pouch. The pouch also contains additional pieces of the striker material that are sealed in a separate waterproof packet (Figure 41-19).

MATCH CONTAINERS The ability to light a match is tied directly to the condition of the matchbox, most of which are made from cardboard or thin wood with striking pads along each side. Neither of these materials is particularly durable, and both tend to disintegrate quickly when wet. For this reason, matches should be protected in a container that is waterproof, easy to open with one hand, and easy to find if dropped. Do not take it for granted that a match case is as waterproof as claimed; be sure to test it.

FIGURE 41-19  REI Stormproof Matches.

790

BOY-SCOUT STYLE A Boy-Scout style match container can be very difficult to open when the hands are cold or stiff or have lost both dexterity and strength. Grit or other debris that gets into the threads tends to jam the device in the closed position. Boy-Scout style match cases are almost impossible to open with one hand, especially with a nondominant hand. The “waterproofness” of these containers is questionable, and this style of match container is not recommended (Figure 41-20).

MILITARY STYLE Except for the olive drab green color, the military-style match case meets all of the criteria for a good match container. It is tough, waterproof, and easy to open with one hand. However, these cases can be difficult to find if they are dropped in the grass. Embedded in the base of the case is a small piece of metal match. Many people erroneously believe that a match can be struck on this material and ignited; rather, if this material is scraped with a sharp edge, sparks can be produced with which to ignite tinder (Figures 41-21 and 41-22).

ORANGE MILITARY-STYLE MATCH CASES Orange military-style match cases (Figure 41-23) are available in most sporting goods stores, where they are usually sold under the Coghlins brand name. These versions of the military-style match case are not quite as sturdy as the military versions, but they are much easier to find if dropped. This match case comes in two lengths, with the longer variety just long enough to accommodate the REI matches. If the shorter version is used, the REI matches must be shortened before they are placed in the case. When filling a match case with REI matches, place one-half of the match heads down and one-half with the match heads toward the top; this allows more matches to be carried in the case. Caution: A piece of the striking pad must also be inserted in the

FIGURE 41-21  Military-style match case.

OTHER METHODS OF IGNITING TINDER

FIGURE 41-22  Scrape the metal match material on the base of the match case to produce sparks.

case; be sure that, when you do so, the striking surface is placed toward the plastic wall and away from the match heads.

MULTIPURPOSE MATCH CASE The popular multipurpose match case should be avoided. The device, which includes a whistle, a mirror, a small piece of metal match, a compass, and a match case, combines all of these survival tools into one. On the surface, this sounds like a good idea. However, should the match case become lost or damaged, one loses the ability to build a fire, signal, and navigate successfully. It is better to buy individual pieces of equipment and not to put all of one’s eggs in one basket (Figure 41-24).

Cigarette lighters are frequently carried by inexperienced outdoorsmen, because these people are generally unaware of the shortcomings of lighters with regard to starting a fire. Consider the following: BIC-style lighters are pressure sensitive (i.e., the higher the altitude, the less the fuel will vaporize); they are temperature sensitive (i.e., the colder the temperature, the less the fuel will vaporize); they explode if they are accidentally dropped into a fire, thus sending shrapnel in all directions; and they require good hand dexterity to operate, which is not a problem when it is warm but quickly becomes a problem in cold conditions (Figure 41-25, online). Zippo lighters have a significant advantage over BIC-style lighters in that they will continue to burn until the cover is closed to extinguish the flame; BIC-style lighters continue to burn only as long as the fuel release remains depressed. This difference is put to good effect when, needing a fire, the survivor lights the Zippo, places it on the ground (stabilizing it with dirt), and then places twigs over the flame. One disadvantage of these lighters is that the fuel tends to evaporate rather quickly (Figure 41-26). Piezo ignition-style lighters use an electronic spark to ignite the fuel, which is similar to the spark produce by an outdoor gas grill lighter to ignite the fuel. This system is much easier to use than the BIC style, and it requires far less finger and hand dexterity. If you are going to carry a cigarette lighter, select one with a piezo ignition mechanism and a clear fuel reservoir to see how much fuel remains. When in cold conditions, carry the lighter in an inner pocket where it will stay warm (Figure 41-27, online). Colibri Quantum lighters are more expensive devices that are alleged to be waterproof, shockproof, and windproof, and it is claimed that they will ignite at higher altitudes. However, field testing of these lighters does not show this to always be the case (Figure 41-28). Metal matches are manufactured from a man-made metallic material that, when scraped with a sharp edge, produces a shower of very hot sparks that can be used to ignite tinder. Metal matches have been erroneously called “magnesium matches.” Although there is a small percentage of magnesium in the alloy (4%), the bulk of the mixture is made up of iron (19%), cerium

FIGURE 41-23  Orange military-style match case.

FIGURE 41-24  Multipurpose match container.

FIGURE 41-26  Zippo lighter.

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Regardless of the container used, the matches must be tightly packed in the match case. Loosely packed, the match heads quickly disintegrate. If space allows, a piece of household cotton ball placed in the cap also helps to prolong the life of the matches. It is also wise to replace the matches at least annually to ensure that the matches that are needed in an emergency are fresh and will ignite.

PART 5  RESCUE AND SURVIVAL

FIGURE 41-28  Colibri Quantum lighter.

(38%), and lanthanum (22%), with the remaining balance composed of other rare metals. The metal match material, which is also called ferrocerium or mischmetal, comes in rods of different lengths and thicknesses, and is usually mounted in a plastic, antler, or wooden handle (Figure 41-29). Select a metal match with a wooden handle. Should one find oneself without tinder to light, the wooden handle can be scraped to produce shavings that can be ignited by metal match sparks; the same cannot be said of plastic or antler. Choose a metal match that has a handle that is large enough to hold firmly when the hands are cold. Some metal matches are embedded in either a block or cylinder of magnesium (Figure 41-30). When a fire is needed, the magnesium block is scraped with a knife blade or another sharp edge to produce shavings that can be ignited by the sparks that are created from the metal match. However, several problems will be encountered. First, it takes both hands to produce the shavings. Second, it can be difficult to confine the shavings to one place when trying to start a fire in a windy location, so they may blow away. Third, magnesium shavings burn at a very high temperature (about 2760° C [5000° F]), but the burn time is very brief, which does not allow the survivor much time to capitalize on the heat. The shavings must be scraped into another flammable material that will ignite from the burning magnesium. Metal matches come in styles that require the use of both hands to operate (Figure 41-31) and those that can be operated with one hand (Figure 41-32). When the use of both hands is possible, the user holds the metal match in one hand and a sharp edge in the other. This “sharp edge” could be a knife blade or any other piece of metal that, when scraped down the length of the metal match, produces a shower of hot sparks. Usually the scraper is held between the thumb and index finger of the dominant hand. For a situation in which one only has a single

FIGURE 41-29  Metal match handles. From left to right: plastic, synthetic antler, and wood.

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FIGURE 41-30  Metal match embedded in magnesium.

FIGURE 41-31  Metal match with a hacksaw blade scraper.

functioning arm, it is possible to stabilize the metal match by stepping on it and then using the noninjured hand to produce the sparks. Metal matches that have been specifically designed for one-handed operation are easy to use. With these, the metal match is spring-loaded in a plastic housing that also contains the scraper. The tip of the metal match is placed on a hard surface, and, by pushing against the tip while simultaneously pressing on the scraper, a shower of sparks is created. When planning for a worst-case scenario, having a metal match that can be lit with one hand could mean the difference between a fire and no fire.

FIGURE 41-32  Ultimate Survival Blast Match and Sparkie Fire Starters.

BUILDING FIRES Throughout this description of fires and fire craft, the term build a fire has been used instead of the more commonly used phrase start a fire. This choice is deliberate. Building a fire implies that there is a process involved that, if followed, will result in success. Starting a fire involves only the first step in the fire building process: applying heat to the tinder and then hoping that it catches on fire and ignites other fuel. Many inexperienced people only think through the process as far as “starting the fire” step and forget that there is a lot more to the procedure than that. Consequently, their fire-building efforts are often unsuccessful. When the need for a fire is critical, the tinder must light easily, and the steps used to build the fire must quickly result in a selfsustaining fire, regardless of weather conditions. For a fire to burn, three elements are required. A heat source that is sufficient to ignite the tinder is necessary; oxygen must be available; and good-quality fuel must be on hand. Because it is the flammable gases contained within wood that ignite, the amount of heat provided by the initial heat source must be sufficient to drive off the gases that are contained within the tinder. The heat provided by the burning tinder must, in turn, drive off the flammable gases that are contained within the larger fuel. One of the most common mistakes made by inexperienced fire builders is trying to light fuel that is far too large for the amount of heat that is available to light it; the heat is then insufficient to produce the gases that are needed for combustion. Step number one in fire building is fuel collecting. Too often, people simply pick up sticks from the ground. Although this might work during the heat of summer, this fuel seldom burns well at other times of the year, when rain and snow saturate the wood that is lying on the ground. It is better to collect your fuel, especially that which will be used in the early stages of the fire, by breaking off dead branches that are found on standing trees. The moisture content of this wood is far lower than that in wood that would be collected from the ground. If the wood bends rather than snaps, it is probably green and should not be used. If there are green leaves or needles attached to the branch discard it, because it will not burn. The small, dry, dead branches found under the overhanging branches of evergreen trees, especially fir and spruce, are particularly good for the early stages of a fire (Figure 41-34, online). In some parts of the country (e.g., the Pacific Northwest), even this fuel can be wet, and it is often draped with moss. However, it is only wet and moss-covered on the outside (Figure 41-35); the interior is dry. Scrape off the moss and wet bark with a knife blade. If twigs and smaller sticks are not available, they must be fashioned by splitting large sticks into smaller pieces with the use of a knife and mallet (Figure 41-36). Splitting wood in this manner exposes the dry inner surfaces of the wood, which can be used as fuel when other dry fuel is not available. Gather far more fuel than you expect to need, and then go out and gather more; one can never have too much. Having accumulated a substantial pile of fuel, separate the wood into three piles by size. The first pile should be matchstick size or thinner; the second pile should be sticks up to the thickness of a thumb; and the rest of the pile is the remainder. When collecting fuel, gather it in long lengths. It is easier to carry or drag into the campsite, and the fire will burn the long lengths into shorter pieces, thereby saving the effort of needing to use a saw. It also saves energy if one can break the wood into pieces rather than having to saw it into pieces (Figure 41-37). When the ground is wet, it is advisable to assemble a platform of sticks that is approximately 0.3 m2 (1 foot2) to protect the

FIGURE 41-35  Wet moss and soggy bark can be scraped off to reveal the dry wood underneath.

FIGURE 41-36  A saw and a knife can take the place of an axe.

FIGURE 41-37  Wedge one end of a long branch between two trees to break off pieces.

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CHAPTER 41  Essentials of Wilderness Survival

When faced with choosing the best fire-starting device and comparing the fire-starting potential of a metal match versus a box of matches or a cigarette lighter, the metal match wins hands down. A typical box of matches contains 25 to 32 matches. For most people, who lack good fire-building skills, more than one match—sometimes many more—will be needed to start a fire. A single metal match has the capacity to start more than 500 fires (Figure 41-33, online). Each time a metal match is scraped, some of the material is removed, so eventually the match will have to be replaced.

PART 5  RESCUE AND SURVIVAL

As the twigs begin to burn and flames appear through the first layer of fuel, lay a second handful of twigs at a 90-degree angle over the first layer (Figure 41-41). As the flames appear above this layer, place another handful of slightly larger twigs on the fire, again at a 90-degree angle to the previous layer. (Figure 41-42, online). This process continues until the larger fuel has been added and until the fire will sustain itself without the immediate attention of the person building it. Your firebuilding success with the use of this method is contingent on the use of tinder that produces a lot of heat, that is well ventilated, and that graduates step by step from the smallest twigs to the largest sizes of fuel (Figure 41-43, online).

TOOLS THAT MAKE FIRECRAFTING EASIER FIGURE 41-39  Cotton ball saturated with petroleum jelly being lit with a metal match.

Hand and full-size axes have been the traditional tools carried by outdoorsmen to facilitate the cutting and splitting of large fuel wood (Figure 41-44, online). However, in the hands of an inexperienced person, an axe is an accident looking for a place to happen. Lacking the years of “chopping” practice that men and women a century ago accumulated during the course of their daily lives, men and women today put themselves at risk when using an axe. As compared with saws, axes are inefficient and dangerous tools that can cause wicked injuries. Do not carry an axe unless you are highly skilled in its use.

tinder (Figure 41-38, online). If tinder is placed directly on wet ground, it tends to absorb moisture from soil that may make it more difficult to light. There is no practical way for a survivor to build a fire on top of snow. Lacking a chainsaw with which to cut large logs to build a platform on the snow, the heat from the fire quickly melts the snow beneath a platform that is made from smaller sticks, so the fire is quickly extinguished. Try to locate an area where the snow is shallow enough to scrape it away down to ground level. Wind has a dramatic effect on fire-building efforts. To provide the best chance of having tinder ignite and continue to burn, place a log that is about 25 to 30 cm (10 to 12 inches) long and 10 cm (4 inches) in diameter along the windward side of the platform. Place the tinder in the lee of the log, where it is protected from the wind. When trying to build a fire in rainy conditions or when snow is falling, find a sheltered area that is protected from precipitation, or erect a temporary roof over the fire site to shelter the tinder until the larger fuel is burning. Before lighting the tinder, everything must be ready. The second most common mistake made by inexperienced outdoorsmen and women is igniting tinder and then having to scramble to find kindling to add to the rapidly burning tinder before it burns out. With everything ready to build out the fire, place the tinder on the platform in the lee of the windbreak, and ignite it (Figure 41-39). As soon as the tinder is burning, place a handful of the smallest fuel directly over the flames, with one end of the twig bundle resting on the log brace (Figure 41-40); this will only work well if you have resisted the urge to break the twigs into overly short pieces. The fuel should be broken into lengths that are 25 to 30 cm (10 to 12 inches) long. Resting one end of the twigs on the brace ensures that good airflow is maintained and that the tinder is not smothered when additional fuel is added. If it appears that more oxygen is needed, lift up on one end of the brace to allow more oxygen to flow to the core of the fire.

Linked-style survival saws.  The Ultimate Survival Technologies SaberCut Saw makes use of a flexible linked saw blade that resembles the blade that is found on real chainsaws. Unlike chainsaws, this blade cuts in both directions, and, as with all saws of this type, it requires the use of two hands for proper function. Although it is not designed to be used in this manner, two people could use it, with one pulling on each end. The SaberCut Saw works well but requires significantly more effort to use than does the pocket chainsaw, which is described next (Figure 41-46). Pocket chainsaws have a 56- to 69-cm (22- to 27-inch) flexible blade that looks very similar to the teeth on a conventional carpenter’s saw. This type of saw cuts in both directions. Depending on the model, there are nylon lanyards or metal rings through which a short length of stick can be inserted to serve as handles that are attached to each end of the saw. This is a useful tool that should be considered for a larger survival kit. Although two people could use it, the saw is best used by one person, assuming that the individual has the use of both hands.

FIGURE 41-40  Placing the first handful of twigs over a burning cotton ball.

FIGURE 41-41  Placing a second handful of twigs over a burning cotton ball.

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Saws Wire survival saws.  Wire survival saws can generally be considered a waste of time. However, because they are compact and lightweight, they are commonly found in commercial prepacked survival kits. They require two hands for cutting. With one exception (i.e., a wire saw that comes from Sweden), the cutting teeth are not very aggressive. Consequently, when pressure is applied, the saw binds up and eventually breaks (Figure 41-45).

must be collapsible and then assembled before they are used. However, assembly requires the use of both hands. Bow saws are made up of multiple parts; if any part is lost, the saw becomes nonfunctional. The size of wood that can be cut is in large part determined by the distance between the blade and the arch of the bow. This space is often quite shallow, which requires the user to have to continuously reposition the wood as it is cut. In addition, bow saw blades are notoriously brittle in cold weather (Figure 41-48). FIGURE 41-45  Commercial wire saw.

FIGURE 41-46  Ultimate Survival linked saw, bottom detail.

Folding saws are popular with outdoorsmen and can be effective cutting tools. They are usually lightweight and short enough to be carried in a fanny pack or daypack. To maximize energy expenditure, select a folding saw that cuts in both directions (i.e., some only cut when you pull). Select one that can be locked in the open position to preclude the blade folding back onto the user’s hand. When it comes to cutting wood, the diameter of the wood should be shorter than the length of the blade (Figure 41-47).

Pruning saw style.  The pruning saw style is the most advantageous for persons who need to quickly cut large quantities of wood. Because no assembly is required, this style of saw is particularly useful to a survivor who has an injured arm or hand. The blade length should not be shorter than 46 cm (18 in). This blade length allows for a full extension of one’s arm when sawing, which is efficient and conserves energy. In addition, a blade of this length is ideal for cutting snow blocks for snowblock shelters. Select a saw with a sturdy handle and one that cuts in both directions (Figure 41-49, online). Gardener’s shears are very useful when gathering smallerdiameter wood, such as that found above the tree line. At high altitudes or high latitudes, the only remaining fuel wood available can be obtained from low shrubby bushes. With shears, one can snip out the dead wood quickly and efficiently (Figure 41-50, online). Fire-Starting Aids Commercial fire-starting aids.  Many commercial products that are available in sporting goods stores and other retail outlets cater to persons who recreate or work in the outdoors. Select products carefully, and test them before they must be used in a survival situation (Figure 41-51).

Bow saw style.  There are many varieties of bow saws; some are ridged, and others are collapsible. To be practical, these saws

FIGURE 41-47  Pick a saw that cuts in both directions and that has aggressive teeth.

FIGURE 41-51  Commercial fire starter.

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FIGURE 41-48  Wyoming Saw.

PART 5  RESCUE AND SURVIVAL

Petroleum, oil, and lubricant (POL) products are often available from the fuel tanks of vehicles. These are frequently overlooked fire-building expedients. Many people are reluctant to use gasoline to assist with fire starting out of fear that they will be burned in the process. This fear is not without foundation, because many people are injured each year when gasoline is poured on a pile of sticks, a match is lit and thrown into the sticks, and an explosion results. Great care must be exercised when using POL products, because some—red and white gases in particular—vaporize quickly and explode when a spark or another open flame is applied. Red gas and white gas should never be poured over a pile of sticks and then ignited. Other POL products (e.g., aviation gasoline, depending on its octane) are difficult if not impossible to light with a flame or spark and may require the use of a wick to burn. Diesel fuel cannot be ignited with an open flame and requires the use of a wick (Figure 41-52, online). To use gasoline safely, pour about 2.5 to 5 cm (1 to 2 inches) of gasoline into a container (the bottom two inches of a pop can works well), and then place the container on the ground (Figure 41-53). The fuel vapor on the surface can be lit with a match, the sparks from a metal match, or another open flame source without an explosion, and the fuel vapors will burn in a controlled manner (Figure 41-54). When the fuel is burning, small sticks can be placed over the flames, and then gradually larger and larger fuel can be added (Figure 41-55, online). This process works particularly well when the available natural fuels are wet. Caution: Care must be taken not to upset the fuel container during the process of adding wood, because a violent explosion may occur. When larger containers are used with increased quantities of POL, place sand or other soil in the bottom of the container to add to its stability, and then light the fumes that seep to the surface. If you do not have a container, pour fuel directly into a small depression in the ground, and then light the vapor at the surface. In anticipation of having to siphon fuel from a vehicle, it is wise to carry a 1.2-m (4-foot) length of aquarium hose that can be snaked down into the fuel tank. Of all of the expedient heat sources available to a survivor, the best are household cotton balls that are saturated with petroleum jelly. This mixture is easy to make and ignite, it is windproof and waterproof, it burns for a long time, and it is inexpensive (Figure 41-56). Tease out a cotton ball (without tearing it into pieces) until you have a large, thin disc of cotton fibers (Figure 41-57). Use cotton balls that are actually made from cotton as opposed to “puffs,” which are made from synthetic fibers and which do not burn well. Smear large quantities of petroleum into the fibers,

FIGURE 41-54  Burning automobile gasoline.

working the cotton between the fingers until there is no dry cotton (Figure 41-58). Store the material in an airtight and watertight container until needed; a waterproof screw-top match case works well for this. When stored in this manner, the cotton ball and petroleum jelly mixture will last indefinitely. When needed, remove one or more cotton balls from the container. Take the cotton between the thumbs and forefingers of

FIGURE 41-56  A mixture of cotton balls and petroleum jelly makes very good tinder.

FIGURE 41-53  Pouring white gasoline into a container.

796

FIGURE 41-57  Creating a cotton ball disc.

FIGURE 41-61  Burning a cotton ball.

FIGURE 41-59  Tearing a cotton ball into two pieces and retaining the feathery edges.

each hand, and pull the cotton into two pieces (Figure 41-59). Being careful to retain the fluffy “fingers” that are produced, then stick the butts together and place the recombined cotton ball on a piece of aluminum foil, a bottle cap, the bottom half inch of a pop can, or another metallic surface (Figure 41-60). In a pinch, a small flat rock with a depression in it will work. If you do not have any of these materials, place the cotton ball on a bed of small sticks or, if necessary, directly on the ground. When the cotton ball is placed on a metallic surface, the oil that is created as the petroleum jelly liquefies from the heat is collected and contributes to burn time. Placing the cotton ball directly on the ground reduces burn time by one-third. A spark from a metal match or from any other heat source will easily ignite the cotton fibers, which in turn causes the petroleum jelly to burn (Figure 41-61). The value of the cotton ball and petroleum jelly mixture is in its windproofness, waterproofness, and burning duration: it will continue to burn in very windy conditions and in wet conditions, and it will burn for 12 to 15 minutes if it is sufficiently large. Before building any fire, careful consideration should be given to ensuring that the fire does not escape. Select a site that is free from materials that could inadvertently ignite and carry flames to other flammable materials. Scrape away any ground cover that might catch fire. Be careful when building a fire under overhanging vegetation that could ignite. During winter months, fires

FIGURE 41-60  Placing the cotton ball on a sheet of aluminum.

built under snow-covered branches will usually result in a cascade of snow into the fire; either shake the snow from the branches before building a fire, or select another site. Building a fire during windy conditions, when sparks could escape the immediate fire site, should be avoided if possible. If it is still necessary to build the fire, select a protected site that is out of the wind. Placing a log on either side of the fire helps to keep a fire from spreading. When it is no longer required, a fire should be completely extinguished. Dousing the fire with large quantities of water is usually the best way to do this, but, when water is not immediately at hand, mixing the coals with Earth until no hot embers remain is the next best method. Survival literature and other media sources are quick to recommend the use of aboriginal fire-making techniques (e.g., bow and drill, hand drill, fire plough) by a survivor who is in trouble (Figure 41-62). What is forgotten are the years of practice that have taken place to develop the proficiency to reliably use these techniques. To believe that a modern person could do the same—simply with the use of a diagram and some text in a survival manual—is ludicrous.

Food Although most persons who are faced with a survival emergency worry more about food than anything else, food is usually less important than shelter or water, because a person can survive for weeks without food, even in cold weather. However, enough water must be available, and energy expenditure must be kept to a minimum. Most wilderness parties carry adequate supplies of food; however, problems arise if food is exhausted, lost, or contaminated. Bare ridges, high mountains above the timberline, and dense evergreen forests are difficult places to find wild food, especially during winter. Success is more likely on river and stream banks, on lake shores, in the margins of forests, and in natural clearings. Because in most cases the amount of wild food

FIGURE 41-62  Bow and drill method of starting a fire.

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FIGURE 41-58  Smearing petroleum jelly into a cotton ball disc.

PART 5  RESCUE AND SURVIVAL

found by an untrained individual will not provide enough calories to replenish the energy expended by searching for it, it is important to always carry extra food for emergencies; this is true even for a short afternoon hike. Readers who are interested in the details of obtaining wild food should consult Chapter 71.

Water Water constitutes about 60% of the body weight of an average young adult male; the value for a female is slightly lower. The percentage of water tends to decrease with age. In a sedentary adult, normal daily water losses include about 1400 mL through the urine, 800 mL through the skin and lungs, and 100 mL through the stool, for a total of 2300 mL daily. Because about 800 mL of water per day is contained in food and 300 mL is produced by metabolism, a minimum additional daily intake of 1200 mL is necessary in a temperate climate at sea level to avoid dehydration. In a hot and dry climate, at high altitude, or with exertion, insensible losses and sweating increase considerably, so fluid intake should be increased proportionally. Monitoring urine output determines whether intake is adequate; 1 to 1.5 L of light-colored urine should be excreted per day. Adding fruit flavors and making hot drinks improve the palatability of water. Electrolyte drinks and salt tablets are generally unnecessary in cold or temperate weather, because the electrolytes lost in sweat are easily replaced by a normal diet. When water supplies are limited, avoid overexertion, and try to “ration” your sweat. Almost all surface water should be considered contaminated by animal or human waste, with the possible exception of small streams that descend from untracked snowfields or springs in high and uninhabited areas. At altitudes of less than 5488 m (18,000 feet), simply bringing water to a boil will kill Giardia cysts and most harmful bacteria and viruses. Water can also be disinfected by filtration or by the addition of chemicals (see Chapter 67). At subfreezing temperatures and in locations that are above the snow line, where liquid water is difficult to find, snow or ice must be melted to obtain water. This requires a metal pot (which should be included in every survival kit), fire-starting equipment, and wood for fuel. The time and effort required to obtain water and the decrease in the thirst response in cold weather favor the development of dehydration in cold-weather travelers. In the winter, whenever open water is encountered, individuals should drink their fill of disinfected water, and then top off all canteens. Each evening, enough snow should be melted to provide water for supper plus a full canteen, which is placed in the bottom of the sleeping bag to keep it from freezing and which is then ready for use during the night or for making breakfast in the morning. Before leaving camp in the morning, enough snow should be melted to provide everyone with at least a full canteen for the day. Melting ice or hard snow is more efficient than melting light and powdery snow. To avoid scorching the pot, the snow is melted slowly, or water is heated in the bottom of the pot before snow is added. On warmer, sunny days, snow can be spread on a dark plastic sheet for melting.

Emergency Snow Travel Travel in deep snow is almost impossible without skis or snowshoes. Snowmobilers, pilots, and other mechanized over-snow and above-snow travelers should carry snowshoes for emergencies. Although travel may be unwise for other reasons, wilderness foot travelers in both subarctic and temperate latitudes should know how to improvise snowshoes from natural materials in the event they are stranded by a late- or early-season snowstorm. Emergency snowshoes (Figure 41-63, A) can be made from poles that are 15 cm (6 feet) long, 1.9 to 2.5 cm (0.75 to 1 inch) thick at the base, and 0.6 cm (0.25 inch) thick at the tip and from sticks that are 1.9 cm (0.75 inch) thick and 25 cm (10 inches) long. Twelve long poles and 12 short sticks are needed. For each snowshoe, six long poles are placed side by side on the ground, and the middle point of the poles is marked. One short stick is lashed crosswise to the tail (base) of the poles, and three short sticks are lashed side by side just forward of the midpoint of the poles, where the toe of the boot will rest. Two sticks are lashed 798

A

B FIGURE 41-63  A, Emergency snowshoe. B, Detail of snowshoe binding.

where the heel of the boot will strike the snowshoes. The tips of the six poles are tied together. Each binding (Figure 41-63, B) is made of a continuous length of about 1.8 m (6 feet) of nylon cord (preferably braided, because it will eventually fray). The midpoint of the cord is positioned at the back of the boot and above the bulge of the heel. Each end of the cord is run under the three side-by-side short sticks at the side of the boot and then up and across the boot toe so that it crosses the other end on top of the toe, forming an “X.” At this point, each end is looped around the cord running along the opposite side of the boot, and the ends are brought around the back of the boot heel. The cord is pulled tight around the boot, and the ends are tied together at the lateral side of the heel (see Figure 41-63, B). When walking, the tip of the snowshoe should rise, the boot heel should rise, and the boot sole should remain on the snowshoe. Over-snow travelers should avoid stepping close to trees (because of funnel-shaped tree wells around tree trunks), large rocks (because of weak snow or moats around them), and overhanging stream banks. In snow country, a person who falls into a stream or lake should roll repeatedly in powdery snow to wick water from clothing, brushing off the snow after each roll. A fire completes the drying process.

Survival in Special Instances, Including Natural Catastrophes The general principles of survival in all catastrophes are the same, particularly the need for forethought, planning, and keeping emergency equipment, water, and food on hand. Nevertheless, different types of catastrophes require different approaches, particularly at first. Some common types are discussed in the following sections.

STALLED OR WRECKED AUTOMOBILES Anyone who drives faces the possibility of spending an unplanned night out in a vehicle. Causes include bad weather, breakdown, running out of fuel, and getting stuck. Winter driving is especially hazardous because of the dangers of driving on snow or ice and the threats of frostbite and hypothermia. Accepting the possibility of trouble, carrying communications equipment (e.g., cell phone, satellite phone or radio) and a vehicle survival kit, and giving some thought to survival strategies will help to prevent a night out in a car from deteriorating into a life-threatening experience. Most travelers dress to arrive at a destination and not to survive a night out. A vehicle survival kit (see Appendix C) should include extra clothing, blankets or sleeping bags, food, water, signaling equipment, a quart-sized plastic screw-top bottle to use as a urinal, and communication equipment (e.g., cell

AIRCRAFT ACCIDENTS Aircraft passengers routinely receive short lectures regarding the locations of exits and procedures for emergencies. The safest place to sit is as far back in the tail of the plane as possible. In a crash, this frequently breaks off, and most survivors of crashes were sitting in this area. When a crash is imminent, tighten your seatbelt, link arms with the people on either side of you, bend your head so that your chin is firmly on your chest, and lean forward over a folded coat or blanket. After the aircraft finally stops moving, leave it as instructed by the crew. Assist injured companions to leave, then get everyone away from the immediate area to avoid the hazard of fire. Do not stop to gather personal belongings or luggage. In a remote area crash, after the fire risk is over, revisit the wreckage to salvage food, clothing, water, and other useful items. Remember that aircraft fuselages are poorly insulated. Unless a stove is available, survivors are usually better off constructing a shelter that can be heated with a fire (as described previously) outside of but near the craft. Batteries can be used as fire starters. Oil and gasoline can be used as fuel if they are poured into a container that is full of dirt or sand. Despite the fact that air travel is quite safe (probably safer than ground travel per mile traveled), an argument can be made for wearing comfortable shoes and carrying a coat, cap, and cell phone. It is illegal to carry survival equipment such as matches and a Swiss Army knife.

Unless there is no chance that a search will be mounted to find the aircraft, you should remain close to it rather than trying to go for help; it is much easier for searchers to spot a crash site than to find survivors who are on foot in the wilderness.

FLOODS Flooding in wilderness areas may be caused by thunderstorms, unusual storms such as hurricanes, and the rapid melting of ice and snow during heat waves. Flash floods in canyons can occur both during and after rain, and they can be caused by rain many miles upstream. Submarine earthquakes can cause huge tidal waves (tsunamis) that may drown hundreds of thousands of shore dwellers. Whenever traveling or camping near bodies of water in the wilderness, one should keep in mind what might happen if overflow or rising water should occur. When traveling or camping in box canyons, below dams, close to banks of water channels, and on low ground such as valley bottoms, one should have a well-thought-out exit strategy in case flooding occurs. If you are along the shore and you receive a radio report of an impending tsunami or if you see that the sea has receded and exposed a large expanse of sea bed, flee immediately and seek high ground as far from the shore as possible. Persons who are caught in moving water have no recourse other than attempting to swim to the side or reach floating debris while trying to hang on to emergency supplies. Never attempt to cross an area of moving water unless you are sure that it is no more than knee deep.

THUNDERSTORMS Dangers from thunderstorms include flooding (as discussed previously), lightning strike (see Chapter 3), and exposure, including wetting and hypothermia. Severe thunderstorms may produce hailstones of varying sizes, including stones that are large enough to harm a struck individual. During a thunderstorm, it is wise to seek shelter; this requires getting into raingear and avoiding heavy rain and hailstones by getting into a metal vehicle or a dense grove of trees. If you are on the water, head for shore as soon as threatening weather approaches. If you are in an area in which you are the highest object around, leave immediately, or crouch down on your haunches. Avoid small buildings, electrical wires, metal objects, and rocky overhangs where you may be hit by side flashes from ground currents, solitary trees, and trees that are taller than surrounding trees.

TORNADOS Tornados are funnel-shaped clouds that typically form on a hot spring or summer afternoon in the midwestern United States. They are usually preceded by large cumulonimbus clouds from the bottoms of which a careful observer can occasionally see the formation of the tornado as a dimple that elongates into a typical conical funnel cloud. Persons who witness these phenomena should leave immediately by vehicle in a direction opposite to the tornado’s likely path or seek shelter on the spot. In houses, the best shelters are small interior rooms with non–weightbearing walls, preferably in the basement (but on the ground floor if no basement exists). Ditches and small buildings are not safe. Caves and outdoor root cellars are fairly safe, but vehicles are not.

HURRICANES Hurricanes are severe tropical storms that demonstrate extreme cases of the vortices of wind and rain that frequently form over tropical seas. By definition, they contain winds of 119 kph (74 mph) or stronger. They require ocean temperatures of 25.5° C (78° F) and a spawning area that is at least 10 degrees of latitude from the equator so that the earth’s rotation is strong enough to start them in motion. Deaths that are the result of hurricanes are usually caused by high winds, flooding from heavy rain, or coastal flooding as a result of storm surges. With modern technology, the formation of a tropical cyclone (i.e., tropical low) and its change into a 799

CHAPTER 41  Essentials of Wilderness Survival

phone, satellite phone, citizen’s band radio in remote areas without cell service). It is also generally better to stay with the vehicle, which provides significant protection and is more visible to rescuers than is a person on foot. In cold weather and especially for long-distance travel, drivers should keep their vehicles in the best possible mechanical condition by using winter-grade oil, the proper amount of radiator antifreeze, deicer fluid for the fuel tank, and antifreeze in the windshield-cleaning fluid. Windshield wiper blades that are becoming worn should be replaced. A snow brush and ice scraper should be carried. A can of de-icer is useful for frozen door locks and wiper blades. Snow tires (preferably studded, although these are illegal in some states) are desirable, but chains should be carried as well. All-wheel or four-wheel drive is optimal, and frontwheel drive is superior to rear-wheel drive. The battery should be kept charged, the exhaust system free of leaks, and the gas tank full (i.e., “drive on the upper half of your tank”). The marooned driver should tie a brightly colored piece of cloth (e.g., a length of surveyor’s tape) to the antenna and at night should leave the inside dome light on to be seen by snowplow drivers and rescuers; headlights use too much current. If it is necessary for heat, the standard recommendation is that the motor and heater be run for 2 minutes per hour (after checking to see if the exhaust pipe is free from snow). However, it has been stated that because it takes more gasoline to start a cold engine than a warm one, one should initially turn the heat up all the way and then run the engine until the inside is comfortable. At this point, shut off the engine and wait until it becomes uncomfortably cold, which could be 10 to 30 minutes, depending on the outside temperature. However, the engine will still be warm. Start the engine again, run the heater until the occupants feel warm, and then keep repeating this. Carbon monoxide poisoning is a real threat, so do not go to sleep with the engine running. Keep a downwind window cracked 2.5 to 5 cm (1 to 2 inches). A reusable carbon monoxide detector is a wise addition to the survival kit. One or two large candles (i.e., “fat Christmas candle” size) should be carried to provide heat and light if the gasoline supply runs out; two lit candles can raise the interior temperature well above freezing. However, resources should be used sparingly, because you are never sure how long you will be marooned. Anticipating a possible cold weather survival situation enough to include heavy clothing and blankets or sleeping bags in the cold-weather vehicle survival kit is better than relying excessively on external heat generation. Do not smoke or drink alcohol. If you have to get out of the vehicle, put on additional windproof clothing and snow goggles, and tie a lifeline to yourself and the door handle before moving away from the vehicle. In a blizzard, visibility can be as little as 30 cm (12 inches).

PART 5  RESCUE AND SURVIVAL

tropical storm and then a hurricane is predictable and reported in detail by the National Oceanic and Atmospheric Administration. Persons at risk should listen to the radio or watch television so that they will be aware when there is a need for evacuation. Most casualties involve persons who remain in the affected area against advice or who are caught by winds and flooding before they get far enough inland. Persons who live in hurricane-prone areas should have emergency caches of water and nonperishable food, clothing, bedding, a first-aid kit with supplies of any medications that are taken regularly; emergency lights (e.g., candles, matches, flashlights, spare batteries); and a cell phone with a battery or a crank-operated radio. They should also keep the gas tank full in their cars, and should be ready to head inland with these supplies as soon as they are advised to do so. Before they leave, they should board or shutter all of their windows, take inside any yard objects that might be blown away, and shut off electric power and gas.

Navigation (see Chapter 96) Even if they are in familiar territory, backcountry travelers should always carry a compass, map, and altimeter. Prior training and experience with map reading and compass use are necessary. An excellent type of compass for the layperson is the Swedish Silva compass, which was designed to be used during the sport of orienteering. The compass reading is always to be believed, even if it is at odds with one’s gut feelings about direction and location. Topographic maps are available at most outdoor stores in both the 7.5- and 15-minute series, and they can also be ordered from the U.S. Geographic Survey (1-888-ASK-USGS or http://www.USGS.gov). Travelers without a compass should still be able to find rough directions. At night, north can be found by identifying the Big Dipper (in the Northern Hemisphere only) and following the “pointers” (i.e., the farthest stars on the “bowl” of the dipper) to the North Star (Polaris); this is the most distal star in the handle of the Little Dipper, which is located about halfway between the Big Dipper and the W-shaped constellation Cassiopeia. On a sunny day, a nondigital watch set to standard time can be used to find direction. When the hour hand is pointed toward the sun, south will be one-half of the shorter of the two distances between the hour hand and 12 o’clock. The availability of small handheld GPS units has revolutionized wilderness navigation, but has not replaced the need for good map and compass skills.

Backcountry Weather Forecasting (see Chapter 42) Mountain weather is more unpredictable than weather in lower and flatter country. Winds frequently blow up and down mountain valleys, regardless of their orientation, because of the funnel effect of the valleys and the temperature differentials caused by solar radiation. The funnel effect may also cause heavy snowfalls at passes or at the higher ends of valleys. On a sunny day, the sun warms mountaintops and high slopes first, warm air rises, and winds blow up the slope. In the evening, the tops and high slopes cool first, cool air descends, and winds blow down the slope. Glaciers and large snowfields produce significant cool downslope winds. Except on the clearest days, mountaintops may have clouds over them or nearby because of the upslope winds that carry moist air high enough to reach its dew point. In the summer, mountains warm up during the morning and early afternoon, thereby creating cumulus congestus and cumulonimbus clouds that produce thunderstorms, lightning, and hail. Therefore, the standard caution for summer climbers is to arise early and reach the summit well before noon. Lightning usually precedes rain in a thunderstorm and can strike up to 8 km (5 miles) away from the storm. Distance is estimated by counting the seconds between the lightning flash and the first noise of thunder: 5 seconds suggests a distance of 1 mile (i.e., count “one and two and…” at a speaking pace that is slightly faster than normal). 800

Precipitation is frequently on the windward side of large mountain ranges; the leeward sides are usually much drier and, in low areas, may actually be desert. Stationary lens-shaped clouds (i.e., altocumulus lenticularis) are frequently seen near mountaintops in windy weather and signify high winds at the summits. High winds also produce long snow plumes from summits and ridges. The summit wind speed will be about twice the valley wind speed. Winds that are blowing at right angles to a mountain range tend to concentrate at any gaps or passes in the range, thereby creating high winds as a result of the Venturi effect. Warm downslope winds in the winter (i.e., Chinook or foehn winds) are produced when cool, dense air blowing over mountaintops loses its moisture as precipitation on the windward side; the drier air then warms rapidly as it descends on the lee side. These warm winds can melt snow rapidly. Weather is more stable at some times of the year than at others, but the times vary by geographic area. For example, in the northern Rocky Mountains, the best times to hike or climb in the summer traditionally have been the last week of July, all of August, and the first 2 weeks of September. The best time to ski tour or climb in the winter is February. In Alaska, the climbing weather in winter is during February and in spring and summer from April through June. In the Himalayas and the Karakorum, the best climbing weather is immediately before and after the summer monsoon (i.e., the seasonal northward flow of warm, moist air from the Indian Ocean). With global warming, these periods may widen; alternatively, they may narrow as a result of increasing storms. The principal value of understanding weather signs is for predicting severe, life-threatening storms and providing adequate time to seek shelter or the option to stay put rather than try for a summit. Travel in severe weather, especially above the timberline, should never be undertaken casually.

IMPORTANT TIPS FOR BACKCOUNTRY WEATHER FORECASTING 1. A blue sky, a few cirrus or cumulus humilis clouds, cool temperatures, low to medium winds, and a steady or dropping altimeter (i.e., a steady or rising barometer) are predictors of good weather. 2. A lowering cloud pattern (i.e., cirrus followed by cirrostratus, altostratus, and nimbostratus), rising temperatures, wind freshening and shifting to blow from the southeast or south, and an altimeter rise of 152 to 244 m (500 to 800 feet) or a barometer drop of 0.5 to 0.8 Hg (15 to 24 mb) indicate a possibly severe winter storm. 3. Building cumulus congestus clouds changing to cumulonimbus clouds indicate probable thunderstorms with lightning and possible hail. A thunderstorm is frequently preceded by a rush of cold air (i.e., a cold front). 4. Signs that a severe winter storm is abating include clouds thinning, cloud bases rising, temperature falling, altimeter dropping (i.e., barometer rising), and winds shifting to blowing from the north or northwest.

Sanitation Adherence to proper habits of cleanliness and sanitation is as important in the wilderness as at home. Hands should be washed with biodegradable soap after urinating or defecating, before cooking and eating, and before dressing open wounds. If soap is unavailable, snow or the cleanest available plain water is used. Dishes and pots are washed with hot water and biodegradable soap and rinsed well to remove all soap. Waste water is scattered over a wide area of ground and never dumped into a body of water. Bathing and washing clothes should be done at least 60 m (200 feet) from bodies of water with the use of water in a container. Gloves (preferably rubber or vinyl and impermeable) are worn when handling moist animal or human tissues, but be aware of a possible latex allergy. For defecation, dig a “cat hole” that is at least 46 cm (18 inches) deep, 15 cm (6 inches) wide, and downhill and at least 60 m (200 feet) from camp, water sources, or snow that is to be melted

Psychological and Organizational Aspects of Survival Dealing with the psychological aspects of survival is as important as confronting physical and environmental factors. As mentioned previously, the dangerous mindset that keeps a person continuing on a hazardous course—such as completing a climb or reaching a distant campsite despite conditions that would make a more prudent person bivouac or turn back—is a recurring scenario. In a survival emergency, a person with survival training, adequate oxygen, stable body temperature, shelter, water, and food may still die if he or she is unable to withstand the psychological stress. Conversely, persons have survived amazing hardships with little more than a strong determination to live. However, individual reactions cannot be predicted in advance. Groups that are faced with emergencies testify that courage and leadership appear in unexpected places. Still, if persons possess the necessary skills, have at least a minimum of survival equipment (see the appendices to this chapter), and have given some forethought to techniques of wilderness survival, the odds are strongly in their favor. Medical personnel have the advantage of being trained to suppress panic. Fear and surrender are normal reactions that must be opposed by whatever psychological tools are available. In some cases, religious faith or the desire to rejoin loved ones has been credited with survival. Anxieties that paralyze action include fear (of the unknown, being alone, wild animals, darkness, weakness, personal failure, discomfort, suffering, and death) and panic. Panic, which is the uncontrolled urge to run away, interferes with good judgment and results in inappropriate actions, such as abandoning weaker companions, dividing the party, and discarding vital survival equipment. Useless flight saps available energy, leads to exhaustion, and hastens death. Other psychological reactions include apathy and the normal desires to be comfortable and to avoid pain. Apathy involves “giving up”; it is a state of indifference, mental numbness, surrender, and unwillingness to perform necessary tasks. The victim shows resignation, quietness, lack of communication, loss of appetite, fatigue, drowsiness, and withdrawal. Apathy in one’s self is overcome by faith in one’s abilities and equipment and a belief in survival and the possibility of rescue. Apathy in others is combated by communicating plans and positive feelings about resources and outcomes to them and by including all group members in planning and survival activities. Comfort is not essential to survival. Marked discomfort as a result of injuries, illnesses, thirst, hunger, excessive heat or cold, sleep deprivation, and exhaustion is inevitable in a survival situation and must be tolerated so that one may continue to live. There are many accounts of adventurers who have survived many days with severe injuries (e.g., open fractures) because of the will to live, or who, despite multiple injuries, have dragged themselves for miles to find help. Providing an ill or injured party member with psychological support is important. This includes appearing calm, unhurried, and deliberate while trying to encourage optimism, patience, and cooperation. A person with a minor injury or illness should be encouraged to self-evacuate and be accompanied by at least one healthy party member. When a person with a severe injury or illness needs to be evacuated, the party must decide whether to use resources at hand or to send for help. The decision will depend on the weather, size of the party, training, available equipment, distance, type of terrain involved, type of injury or illness, victim’s condition, and availability of local search and rescue groups, helicopters, and other assistance. Unless the weather is excellent, the party strong and well equipped, the

route short and easy, and the victim comfortable and stable, the best course of action generally is to make a comfortable camp and send the strongest party members for help. A written note should include each victim’s name, gender, age, type of injury or illness, current condition, and emergency care given; the party’s resources and location (preferably map or GPS coordinates); and the names, addresses, and telephone numbers of relatives. The victim who must be left alone (e.g., because of a small party size) should have an adequate supply of food, fuel, and water. As soon as you realize that you are lost, stop, sit down in a sheltered place, calmly go over the situation, and make an inventory of survival equipment and other resources. If it is cold or becoming dark, start a fire, and eat if you have food. Take out your map or draw a sketch of your route and location that is based on natural features. Then, unless you know your location and can absolutely reach safety before dark, immediately begin to prepare a shelter for the night. Do not allow yourself to be influenced by a desire to keep others from worrying or the need to be at work or keep an appointment; one’s life is more important than someone else’s peace of mind. If you are alone and unquestionably lost and especially if you are injured, you must decide whether to wait for rescue or attempt to walk out under your own power. If rescue is possible, it is almost always better to use the time to prepare a snug shelter (before dark) and to conserve strength. If you decide to leave, mark the site with a cairn or with bright-colored material such as surveyor’s tape; leave a note at the site with information about your condition, equipment, and direction of travel; and then mark your trail. These actions will help rescuers and enable you to return to the site if necessary. Travel should never be attempted in severe weather, desert daytime heat, or deep snow without snowshoes or skis. If no chance of rescue exists, prepare as best possible, wait for good weather, and then travel in the most logical direction. The best way for a lost or stranded person to help potential rescuers is to do everything possible to draw attention to his or her location. Most modern rescues make use of ground parties, helicopters, and fixed-wing aircraft. When the latter locate victims from the air, they can drop supplies and vector helicopters or ground parties to the site. In addition to radios, cell phones, and other electronic equipment, signaling devices can be either auditory or visual. Three of anything is a universal distress signal (e.g., three whistle blasts, three gunshots, three fires). The most effective auditory device is a whistle. Blowing a whistle is less tiring than shouting, and the distinctive sound can be heard from farther away than a human voice. An effective visual ground-toair signal is a glass signal mirror with a sighting device, which can be seen up to 16 km (10 miles) away but requires sunlight. Special rescue beacons are available and can be carried as emergency equipment; these include strobe lights, laser signal lights, special beacons with both signaling and GPS capability, and personal locator beacons. Smoke is easily seen by day, and a fire or flashlight is seen well by night. On a cloudy day, black smoke is more visible than white; the reverse is true on a sunny day. White smoke stands out well against a green forest background but not against snow. Black smoke can be produced by burning parts of a vehicle, such as rubber or oil, and white smoke can be made by adding green vegetation to a fire. The lost person who anticipates an air search should keep a fire going with large supplies of dry, burnable material (e.g., wood, brush) and have a large pile of cut green vegetation close by. When an aircraft is heard, the dry materials are placed on the fire and allowed to flare, and then armloads of the green vegetation are piled on top; this produces lots of smoke and a hot thermal upward draft to carry it aloft. Ground signals (e.g., “SOS,” “HELP”) should be as large as possible (e.g., at least 0.9 m [3 feet] high and 5.5 m [18 feet] long) and should contain straight lines and square corners that are not found in nature. These types of signals can be tramped out in dirt or on grass, or they can be made from brush or logs. In snow, the depressions can be filled with vegetation to increase contrast. Many pilots do not know the eight traditional international ground-to-air emergency signals. However, these have 801

CHAPTER 41  Essentials of Wilderness Survival

for water. Cover feces completely with dirt or snow. No camp should be within 60 m (200 feet) of a lake or stream, which represents 70 to 80 steps for most adults. Travelers should urinate on rocks or dirt rather than on green plants. To avoid having to go outside, especially at night, when sleeping in a tent or snow shelter, males can use a 500-mL widemouth polyethylene bottle as a urinal. Funnels designed for use with the bottle are available for women.

PART 5  RESCUE AND SURVIVAL

been replaced by the following five simple signals adopted by the International Convention on Civil Aviation. Although in the age of helicopters these are not as important as they once were, they are worth remembering: V: I require assistance. X: I require medical assistance. N: No Y: Yes ↑: Proceeding in this direction Air-to-ground signals include the following: Message received and understood: rock plane from side to side Message received but not understood: make a complete righthand circle When using cell phones, radios, and other electronic devices, persons should move out of valleys and gullies to higher elevations if possible. Operational payphones in campgrounds that are closed for the season or other facilities can be used to call for help. Most will allow 9-1-1 or another emergency number to be dialed without payment, but carrying sufficient coins and memorizing your telephone credit card number are recommended.

Protection From Wild Animals Although persons in a survival situation often worry about wild animal attacks, these are rare. Many wild animals flee when they are confronted by shouting, moving humans. Exceptions include polar bears, grizzly bears, moose, bison, cougars, jaguars, wild pigs, elephants, lions, tigers, water buffalo, leopards, wolverines, females with young (particularly bears, moose, elk, and deer), rabid mammals, and feral dogs and cats (see Chapter 56). Polar bears, some grizzly and black bears, the great cats, and crocodiles may hunt humans as food. Venomous snakes, insects, arachnids (i.e., spiders, scorpions, and ticks) and marine animals are also of concerns (see Chapters 52, 53, 79, 80, and 81). The only effective weapon against large mammals and reptiles is a high-powered firearm, although pepper spray may discourage attacking bears and ungulates. Improvised weapons (e.g., a spear tipped with a hunting knife) are useless. Food should not be kept in a shelter or backpack during the night; all food should be placed in a nylon bag and hung between two trees on a high line. Above the timberline, small rodents such as mice may gnaw holes in expensive tents to reach food that is inside, so all food should be bagged and hung on a line between two high boulders. In warm weather, insect repellent should be carried and used liberally.

Summary of Preparations for a Possible Survival Situation 1. Keep in good physical condition by employing frequent exercise and healthful habits. Avoid tobacco and recreational drugs, and keep alcohol use to a minimum. Maintain current immunizations. 2. Develop the ability to swim well. 3. Learn how to use a map and compass, and know how to find directions without a compass. 4. Be able to build a fire under adverse conditions. 5. Have a working knowledge of local weather patterns, and be able to use an altimeter or a barometer, a thermometer, wind directions, and knowledge of cloud forms to predict storms. Avoid exposure to dangerous meteorologic conditions, such as blizzards and lightning strikes. 6. Be familiar with the special medical problems related to the type of wilderness that is involved. For example, in cold weather and at high altitude, be familiar with prevention, diagnosis, and treatment of hypothermia, frostbite, and altitude illnesses. Safe travel in the desert and tropics requires familiarity with poisonous and edible plants, tropical diseases, snakebite treatment, dangerous animals, tropical skin diseases, and heat illnesses. Understand, basic principles of prehospital emergency care and improvisation of splints, bandages, and stretchers. 802

7. Carry a survival kit that contains equipment appropriate for the topography, climate, and season (see the appendices to this chapter). At a minimum, the kit should include such things as fire-starting, shelter-building, and signaling and navigating equipment plus emergency food, water, spare clothing, and a first-aid kit. 8. Be able to construct appropriate types of survival shelters. 9. Acquire a working knowledge of the characteristics of natural hazards and how to avoid them. These include forest fires, lightning strikes, avalanches, rockfalls, cornice falls, flash floods, whitewater, deadfalls, storms of various kinds, and hazardous animals and plants of the area of travel. 10. Read and analyze accounts of survival experiences (see the Suggested Readings list online at www.expertconsult.com). Remember that more people are killed on simple day hikes than on long wilderness expeditions. 11. Be aware of the psychological aspects of a survival situation and of errors in judgment that can lead to a survival emergency. 12. Know the edible plants and animals of the area of projected travel as well as the poisonous or venomous species. Know how to obtain water. Basic hunting, trapping, and fishing skills are also valuable. 13. Be intimately familiar with the contents of your survival kit and how to use them. Practice and perfect survival activities (e.g., fire building, shelter building) before you need them. 14. Never travel alone. Hunters and other group members who may separate should have a means of communicating with each other, such as small radios with an 8-km (5-mi) range. Products are available that combine a GPS locator with a small radio. 15. Always let at least two responsible persons know your destination, the number of persons in the party, their names, the types of vehicles used and their license plate numbers, and the expected time of return. Add several hours to the latter for “normal” mishaps and miscalculations. To avoid unnecessary rescue attempts, do not fail to notify these persons of your return. Failure to follow these guidelines has led to many unsuccessful searches.

APPENDIX A 

SUGGESTED BASIC CONTENTS OF A TEMPERATE TO COLD-WEATHER SURVIVAL KIT The kit is divided loosely into fire-building, shelter-building, signaling and navigating, and miscellaneous items, all of which will fit into a small-frame backpack with a capacity of 52.4 to 65.5 L (3200 to 4000 inches3). The small items can be carried together in a small net bag for convenience and easy identification. Frequently used items (e.g., knife, map, dark glasses, compass) should be stored in a pocket or a belt pouch. Always remember to replace consumed items—especially first-aid items, repair-kit items, and emergency food—as soon as you return from a trip. Replace stored matches at least every year and first-aid kit medications before they expire.

APPENDIX B 

SUGGESTED ADDITIONS FOR WINTER SURVIVAL KIT (WHEN COLD WEATHER OR SNOW IS PRESENT OR EXPECTED) Basic survival items from Appendix A Spare clothing for severe weather to provide at least four layers total, including spare mittens

Fire-Building Equipment Two waterproof screw-top match containers filled with strike-anywhere matches (If the match container does not include a large, rough match-striking area, a strip of heavy sandpaper should be glued to the top or side of each container.) Candle Fire starter (e.g., cotton impregnated with petroleum jelly) in a waterproof container such as a film canister or an additional match container Metal match Knife: Swiss Army knife (consider a camping model with a saw, file, scissors, and so on; made by Victorinox)   Alternative: Leatherman tool with wire-cutting pliers, file, one serrated and two regular blades, saw, and scissors Shelter-Building Equipment 1 -inch braided nylon cord or parachute cord, 30.48 m (100 feet) 8 Rip-stop waterproof nylon tarp, approximately 2.4 × 3 m (8 × 10 feet) with grommets around the edges   Alternatives:   Tarp (blue and crinkly; laminated polyethylene weave)   or   One or two large, heavy-duty (3- to 4-mil), orange plastic bags, 0.9 × 1.7 m 3 × 5.5 feet Folding saw or small rigid saw (e.g., 18-in Dandy saw) Signaling and Navigating Equipment Headlamp or flashlight with spare bulb and batteries (A good choice is a headlamp with both light-emitting diode and bulb options. The light-emitting diode light uses up much less electricity but is more diffuse and does not cast a long beam. The bulb is brighter and casts a longer beam but uses much more electricity.) Plastic pea-less whistle on a lanyard Small notebook and pencil Small roll of orange surveyor’s tape Glass signaling mirror with sighting device Miscellaneous Metal pot with bale that contains emergency food of choice (e.g., tea, soup mix, power bars, small can of mixed nuts, trail mix) Metal cup with handle (for heating liquid by putting the cup at the edge of a fire) Plastic or Lexan spoon Toilet paper Sunscreen with a sun protection factor of 30 or more Lip balm with a sun protection factor of 30 or more Insect repellent (e.g., N,N-diethyl-meta-toluamide) First-aid kit, one per party (see Appendix D for contents) Canteen (1 to 1.5 L [34 to 50 fl oz] when full; metal or plastic) Sunglasses, preferably polarized, with side shields Light raingear (e.g., laminated [Gore-Tex] pants and jacket with hood) Repair kit that is adapted to the type of travel (e.g., ski, snowshoe, kayak) and that includes the following:   Small needle-nosed pliers with wire-cutting feature (if Leatherman tool not carried)   Small crescent wrench   Small screwdriver with multiple tips   Picture wire   Fiberglass tape, standard roll   Duct tape, small roll   Steel wool for shimming (e.g., ski binding repair)   Assorted nuts, bolts, and screws   Total weight of repair kit Total weight of basic survival equipment (not including shovel, snow saw, backpack, or cold weather fourth layer of clothing; see Appendix B) Other Useful Equipment for Consideration Nondigital watch Altimeter Magnifying glass Two sets of correct coins for pay phone; calling card Light pair of leather gloves (hand protection) Water disinfection equipment: chemicals (e.g., Potable Aqua) or filter Thermometer (plastic alcohol type clipped to the outside of the pack) Spare eyeglasses Electronic communication and navigation equipment:   Cell phone (if service is available in the area)   Global positioning system unit   Personal locator beacon (i.e., person emergency locator transmitter) Pepper spray (to repel bears, moose, and so on) Usual day-trip items to be added:   Small insulated drink cannister of hot or cold drink   Lunch   Binoculars   Camera

Approximate Weight in Grams (Ounces) 57 (2) 43 (1.5) 28 (1) 14 (0.5) 142 (5) 227 (8) 113 (4) 55.3 (19.5) 737 (26) 255-5100 (9-18) 340 (12) 212 (7.5) 14 43 57 57

(0.5) (1.5) (2) (2)

964 (334) 85 (3) 14 (0.5) 43 (1.5) 113 (4) 14 (0.5) 113 (4) 701 (25) 1091-1446 (38.5-51.0) 57 (2) 879 (31) 85 (3) 57 (2) 156 (5.5) 28 (1) 85 (3) 28 (1) 28 (1) 43 (1.5) 510 (18) Approximately 6520 to 7087 g (230 to 250 oz) or 6.5 to 7 kg (14 to 16 lb)

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CHAPTER 41  Essentials of Wilderness Survival

Item

PART 5  RESCUE AND SURVIVAL

Small snow shovel (e.g., a small, collapsible grain-scoop type with a Kevlar blade and detachable handle, with a 680-g [24-oz] capacity) Snow saw (consider this for above-timberline travel and potential igloo building; should have a 227-g [8-oz] capacity)

OPTIONAL ITEMS Three-quarter–length piece of open or closed cell-foam mattress or Therm-a-Rest mattress Sleeping bag Bivouac sac Small stove and fuel Light axe (e.g., Hudson’s Bay type) Small piece of closed-cell foam (0.6 × 0.6 m [2 × 2 feet]) for sitting on snow

MANDATORY FOR AVALANCHE COUNTRY Avalanche probe (folding) or ski poles that join together to form a probe for each party member Avalanche transceiver for each party member Shovels (preferably one for each party member) Inclinometer for measuring slope angles (this is included in some compasses)

APPENDIX C 

VEHICLE COLD-WEATHER SURVIVAL KIT Sleeping bag or two blankets for each occupant Emergency food Metal cup Waterproof matches Long-burning candles, at least two First-aid kit (see Appendix D) Extra doses of personal medications, if any Swiss Army knife or Leatherman Multi-Tool Three 1.4-kg (3-lb) empty coffee cans with lids for melting snow or collecting urine Toilet paper Citizen’s band radio, cell phone, or such other communication device, with charger Portable radio receiver, with extra batteries Battery booster cables Extra quart of oil (place some in a hubcap and burn it for an emergency smoke signal) Tire chains Jack and spare tire Road flares Snow shovel Windshield scraper and brush Tow strap or chain Small sack of sand or cat litter Two plastic gallon water jugs, full Tool kit Gas-line deicer Flagging (e.g., surveyors’ tape, which can be tied to the top of a radio antenna for use as a signal) Duct tape Notebook and pencil Reading material Long rope (e.g., clothesline) to act as a safety rope if you leave the car in a blizzard Carbon monoxide detector Axe Saw Full tank of gas Data from the Montana State Department of Transportation: Montana disaster & emergency survival guide. Available at http:// www.mdt.mt.gov/publications/docs/brochures/winter_maint/ winter_survival.pdf. Accessed May 1, 2011.

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APPENDIX D 

MINIMAL EQUIPMENT FOR SURVIVAL FIRST-AID KIT Because the most common significant medical problems in wilderness emergencies will be injuries, each item is selected on the basis of the likelihood of need, the possibility of multiple use, the urgency of need, the weight-to-usefulness ratio (i.e., the “biggest bang for the buck”), and whether it can be improvised from natural materials. As with the survival kit, the small items can be carried together in a mesh bag for more rapid retrieval.

BASIC ITEMS Small-Bag Items Cardiopulmonary resuscitation mouth shield Surgical gloves, preferably nonlatex 20-mL syringe with needle, catheter, or splash shield for wound irrigation Steel sewing needle (this can be part of a small sewing kit) Clinical thermometer (consider a low-reading thermometer for a cold environment) Small pill boxes that contain the following: Nonprescription analgesic of choice (e.g., acetaminophen, ibuprofen; consider ibuprofen if there is a frostbite risk) Prescription analgesic of choice (e.g., acetaminophen with codeine) Diphenhydramine, 25- or 50-mg caps Small tube of biodegradable soap Splinter forceps Seam ripper Small needle holder (this is useful for retrieving small things out of tight quarters) Small magnifying glass Four large safety pins Other Items One or two cravats Roll of 3-inch Ace or self-adhering roller bandage Roll of 2-inch adhesive tape (waterproof preferred) Small roll of 0.5-inch 3M Transpore tape Small prepackaged bandage strips, 1-inch wide (these can be cut in one-half lengthwise for smaller sizes) Nonadhering sterile gauze pads (Telfa or equivalent), 3 × l4 in Sterile compresses, 4 × 4 inch Alcohol pads for skin cleansing Duct tape or fiberglass strapping tape for improvising litters and splints (this can be carried in a repair kit)

ADDITIONAL ITEMS FOR CONSIDERATION Acetazolamide if there is a risk of acute mountain sickness (i.e., 125 to 250 mg twice daily to speed acclimatization) Plastic oral airways, three sizes Pocket mask instead of mouth shield (This device is easier to use, works better than a mouth shield, and protects the user from the victim’s saliva.) Povidone–iodine swabs for skin preparation 14-gauge intravenous catheter-over-needle for emergency chest decompression (A flutter valve can be improvised by using the finger cut from a rubber glove with its base tied around the base of the catheter and a hole cut in its tip.) Small bandage scissors or paramedic shears (scissors, a Swiss Army knife, or a Leatherman tool can be substituted.) SAM splint Persons who are taking regular medications should carry emergency supplies; anyone who has had an anaphylactic reaction should carry an emergency epinephrine kit (i.e., EpiPen).

SUGGESTED READINGS Suggested readings for this chapter can be found online at www.expertconsult.com.

CHAPTER 42 

Principles of Meteorology and Weather Prediction JOHN MIODUSZEWSKI, D. NELUN FERNANDO, AND DAVID A. ROBINSON

General Circulation and Atmospheric Profile CLIMATE CONTROLS AND RADIATION BALANCE Equatorial regions receive a net surplus and polar regions receive a net deficit of solar radiation because of differences in solar angle and beam dissipation at the poles and the equator. This heat imbalance between the equator and the poles drives the ocean–atmosphere circulation. Heat is transported in the atmosphere primarily through convection, conduction, and advection. Convection and conduction are important in vertical atmospheric heat transport. Latent and sensible heating is the key mechanism by which convective and conductive transport are enacted. Horizontal heat transport is achieved primarily through migration of air masses and through eddy circulation. The average global circulation on a simplified basis consists of three circulation cells. This structure is found in both hemispheres. The cell that straddles the tropics (0 degrees to approximately 30 degrees), known as the Hadley cell, is characterized by rising motion on its ascending limb along the equator and sinking motion on its descending limb at the subtropics (approximately 30 degrees). A second cell, known as the Ferrel cell, has an ascending limb at the midlatitudes and descending limb at the subtropics. The third cell, known as the polar cell, is characterized by rising motion at the midlatitudes and subsidence at the poles. Such a general circulation structure results in a climate with intense convective precipitation in the regions along the rising limb of the Hadley cell. This region is identified as the intertropical convergence zone (ITCZ) because it is a zone where intense heating leads to convective motion and low pressure. Low-level or surface convergence and upper-level divergence result in convective precipitation in this zone. Regions along the descending limb of the Hadley cell—approximately 30 degrees north and 30 degrees south—tend to be warm and dry as subsiding air warms and dries out the air column. It is no coincidence that deserts are found at this latitude. The midlatitudes (40 degrees to 50 degrees)—the rising limb of the Ferrel cell—have cells of low pressure and receive precipitation from storms and frontal systems. Polar regions along the subsiding limb of the polar cell are characterized by cold and dry climates. The three-division structure results in surface wind distribution characterized by winds blowing from the east (easterly) (trade winds) out of the subtropical high-pressure zone to the lowpressure zone at the equator; winds from the west (westerly) out of the subtropical highs to the midlatitude low-pressure zone; and polar easterlies flowing from the polar high-pressure zone to the midlatitude low (Figure 42-1). Such an east–west wind direction, as opposed to a north–south wind direction, prevails because of the Coriolis effect, which acts on the pressure gradient force and deflects winds to the right in the northern hemisphere and to the left in the southern hemisphere. The tricell structure is only a simplified representation of the general atmospheric circulation. In reality, the Ferrel cell does not persist throughout the year, as does the Hadley cell. The pressure gradient at the polar front is so intense that it results in eddies that are instrumental in poleward heat transport,

particularly during the winter, when the equator–pole pressure gradient is at a maximum. The midlatitudes are the regions most influenced by air masses. Eddy circulation is predominant at the boundary— known as the polar front—between the Ferrel cell and the polar cell.

ATMOSPHERIC PROFILE Lapse Rate The temperature generally decreases with altitude in the troposphere, as evidenced by decreasing temperature as one travels up a mountain. The rate at which air cools as it rises depends on the amount of moisture in the air, as well as the dynamics of the atmosphere itself. Moisture Humidity is a measure of the amount of moisture in the air, commonly measured by relative humidity and dew point temperature. Relative humidity is a ratio of the amount of moisture in the air to the amount the air can hold at that temperature. Atmospheric moisture is often given as relative humidity, but this must be accompanied by a temperature to be a valuable indication of the air’s moisture content. Dew point temperature is the temperature to which the air must be cooled to become completely saturated. If air is cooled

FIGURE 42-1  General circulation of the atmosphere. (Courtesy Deborah Mioduszewski.)

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PART 5  RESCUE AND SURVIVAL

to this temperature at the surface, fog will form. If air is forced to rise and cools to this temperature, clouds will form. Heat capacity is the amount of energy required to increase the temperature of a substance. The importance of this is due to the great difference in heat capacity of land and water. Water heats up and cools down much more slowly than does land, which has important implications for weather in interior continents, compared with coastal areas.

Climatic Regions Controlled by Latitude: Tropics, Midlatitudes, and Poles MIDLATITUDE AND POLAR CLIMATES Most weather systems, such as midlatitude cyclones and thunderstorms, form at the frontal boundaries between air masses of different densities and are steered by upper-level winds, typically to the east in the midlatitudes and west above about 60 degrees. This is in contrast to tropical cyclones, which are not influenced by air masses and only form over the ocean. Midlatitude cyclones are a powerful means by which air can be transported across latitudes. These differing air masses meet at boundaries called fronts. Cold and warm fronts are typically oriented around a cyclone as shown in Figure 42-2. The colder, typically polar air mass advances equatorward behind the cyclone at the cold front, while the warmer air mass advances poleward ahead of it behind the warm front. Typically, the faster-moving cold front catches up to the warm front as the cyclone matures and “occludes,” and the cyclone begins to lose its strength as the temperature differences from which it derives its energy dissipate. Occasionally neither air mass will be able to dislodge the other, and the front will become stationary. Stationary fronts can be conducive to prolonged periods of precipitation. These areas of low pressure have favored storm tracks that shift during the year and as larger-scale atmospheric conditions change. Often atmospheric patterns emerge where cyclones take the same track, moving through the same areas for up to several weeks. Conversely, locations removed from these storm tracks may experience persistent fair weather associated with an accompanying anticyclone. Cyclones often form and move along the polar front, where there is a sharp contrast in temperature and moisture. During winter, the precise track of a cyclone will determine whether rain, snow, or a mixture will fall in a given location, with snow more likely on the north side of the cyclone and rain on the south side. These cyclones bring the most noticeable changes to sensible weather in the mid- and high latitudes. In addition to the precipitation they bring, which ranges from drizzle and fog to severe

Highest probability of severe weather

Advancing cold air

Cold front

Warm, moist air

Warm front

FIGURE 42-2  Midlatitude cyclone model. L, Low pressure. (Courtesy Deborah Mioduszewski.)

806

thunderstorms, temperature and humidity levels vary greatly in different parts of the storm. Warm and moist air is advected in behind the warm front with a shift in the wind, causing extremely uncomfortable weather in the summer and thaws in the winter. Colder, dryer, and commonly breezy or blustery weather accompanies the passage of a cold front as air from higher latitudes is advected in behind a departing cyclone.

SUBTROPICAL AND TROPICAL CLIMATES The subtropics lie north and south of the Hadley cell, roughly at 35 degrees north and 35 degrees south. The subtropics are characterized by warm and dry climates. Tropical climates are found along the rising limb of the Hadley cell. Temperature is high throughout the year, with the average coldest temperature not dropping below 18° C (64.4° F). Convective processes and convective precipitation dominate the climate of the tropics but are not the sole climatic phenomena found there. Monsoons, tropical depressions, and cyclones account for much of the precipitation delivered over the tropics.

MONSOONS The term monsoon refers to the seasonal reversal in atmospheric circulation and associated precipitation in tropical and subtropical regions. Reversal of wind direction takes place with seasonal migration of the ITCZ, which induces a temperature difference between the land surface and ocean. The land–ocean temperature difference induces a land–ocean pressure gradient that drives the monsoonal winds. Regional components of the monsoon include the tropical and subtropical regions of Asia, Australia, Africa, South America, and southwestern North America. The onset of monsoonal rains varies among and within these regions.

TROPICAL CYCLONES Intense convective heating, particularly in the tropics, creates regions of low atmospheric pressure. Such regions of low pressure are characterized by rain-bearing clouds and windy conditions. If low-pressure systems form over warm oceans of the tropics and subtropics at least 5 degrees from the equator, they have the potential to develop into cyclones, which are intense, rotating low-pressure systems. Winds flow counterclockwise in the northern hemisphere and clockwise in the southern hemisphere around cyclones. Cyclones, hurricanes, and typhoons all refer to the same phenomenon. The norm is to use typhoons to identify severe cyclones in East Asia; hurricanes for severe cyclones in North America, and cyclones for severe cyclones that form over the Indian Ocean region. Cyclones form in areas of intense low pressure in the tropics and subtropics. Tropical cyclones are known for their destructive strength—often due to strong winds but also due to storm-surge flooding that occurs along coastal regions. Tropical cyclones form in all the major ocean basins, except in the South Atlantic and the Southeast Pacific. Minimum factors needed for tropical cyclones to develop are sea surface temperatures exceeding 28° C (82.4° F) and a minimal amount of vertical wind shear. Extratropical cyclones form at frontal boundaries. After formation, tropical cyclones tend to move westward and poleward. Some cyclones, particularly in the midlatitudes, recurve and enter the westerlies. Tropical cyclones tend to dissipate on making landfall. Cyclones are classified by their intensity as follows: • Tropical depression: winds up to 64 km/hr (39.8 mph) • Tropical storm: winds of 64 to 118 km/hr (39.8 to 73.3 mph) • Severe tropical cyclone, hurricane, or typhoon: winds greater than 118 km/hr (73.3 mph) These are further categorized using the Saffir-Simpson scale, ranging from category 1 to category 5 (most severe) (Table 42-1).

THUNDERSTORMS Thunderstorms result from atmospheric instability due to intense convective heating processes in the tropics and convergence of air masses of different temperatures in midlatitudes, particularly in continental climates. Cumulonimbus clouds are characteristic

Wind Speed

Storm Surge

Category

Pressure (mb)

km/hr

mph

m

ft

Damage

1 2 3 4 5

≥980 965-979 945-964 920-944 250

74-95 96-110 111-130 131-155 >155

1-2 2-3 3-4 4-6 >6

4-5 6-8 9-12 13-18 >18

Minimal Moderate Extensive Extreme Catastrophic

features of thunderstorms, as are electrical activity (lightning and thunder), wind gusts, and heavy rain. Hail may be encountered in some thunderstorms. Heavy thunderstorms in upstream regions of river catchments with sharp elevation gradients may induce flash flooding in downstream regions. One of the major dangers associated with thunderstorms is lightning. Lightning can strike more than 20 miles away from the parent thunderstorm, which may appear far enough away to present the illusion that there is no risk. When a thunderstorm is in the area, it is advisable to seek shelter away from high ground, water, and open spaces. Distance to a lightning strike can be calculated by counting the number of seconds between the flash of lightning and the thunder, keeping in mind that sound can travel a mile in 4.5 seconds. Types of Thunderstorms Severe thunderstorms are storms with wind speeds above 93 km/ hr (57.8 mph). Updrafts and downdrafts associated with severe thunderstorms often reinforce each other and intensify the storm. Mesoscale convective complexes (MCCs) are roughly circular organized storm systems composed of several thunderstorms. MCCs are common occurrences over North America and Canada, where mesoscale (10 to 1000 km in diameter) atmospheric processes provide conditions suitable for reinforcement of thunderstorm complexes. Severe weather in North America and Canada is often associated with MCCs. Frontal/squall-line thunderstorms tend to form parallel to and ahead of cold fronts in the presence of wind shear. They form a linear band of storm cells with a life span of about 0.5 day to 4 days. Supercell storms are violent storms that occur as isolated storms, each with a diameter ranging from 20 to 50 km (12.4 to 31 miles). Supercell storms may give rise to tornadoes. Tornadoes are extremely dangerous weather phenomena characterized by rapidly rotating air that reaches the ground beneath cumulonimbus clouds. They are preceded by a perceived lowering of one part of the cloud base, with rotation of this base (funnel cloud) often visible. All funnel clouds do not produce tornadoes, but all tornadoes are preceded by funnel clouds. Tornadoes most often occur in the interior of continents, particularly North America and Canada. Waterspouts, like tornadoes, are columns of rapidly rotating air that are visible due to condensation of water vapor in the funnel (not water being sucked up). Some are associated with supercells and therefore can be considered tornadoes over water. But most are termed “fair-weather waterspouts” because they generally are not associated with thunderstorms. Instead, they form under large cumulous clouds in light wind conditions. Their life span is typically less than 20 minutes, winds rarely exceed 112.6 km/hr (70 mph), and they are usually found in coastal regions. However, they can still cause considerable damage and injury, and it is advisable to avoid them.

ARID CLIMATES Arid climates are characterized by the presence of very little moisture. These are found most often along subtropical highpressure zones or in the interiors of large continents where the influence of moisture-laden oceanic frontal systems is limited. Deserts are characteristic ecosystems of arid climates. Extreme heat, high diurnal temperature ranges, wind, and often fire danger are important elements of desert climates.

MOUNTAIN CLIMATES The lifting of air because of the presence of mountains is known as orographic lift, which results in cooling of the air. If sufficient moisture is present, condensation takes place. Such convection can induce thunderstorm development on the windward side of the mountain (Figure 42-3). In the presence of steep topography, convective processes may be limited to the windward side because the mountain ridge can form a wet–dry divide. Air flowing over a mountain ridge and downward along the leeward side warms and dries through the process of adiabatic compression. Thus leeward winds are characteristically dry and warm. Such winds are known internationally as foehn winds, and as Chinooks in the United States. The Santa Ana winds that blow into Los Angeles are downslope winds. Wind direction typically reverses twice a day in mountain climates. During the day, wind flows upslope from the valley toward the mountain. At night, winds blow downslope from the mountain toward the valley. Horizontal temperature differences that develop in complex terrain produce diurnal mountain winds. Overnight and into the early morning, cold air accumulates in valleys and causes a temperature inversion. By morning, the valley bottoms are colder than are mountain slopes and a pressure gradient develops that drives upslope winds. Convective heating during the day dissipates the temperature inversion in the valleys. Varied topography in mountain ranges results in a myriad of microclimates. Factors such as exposure to sunshine, slope direction, elevation, and windward or leeward side of major weather systems determine the varied characteristics of microclimates found in mountainous regions.

MARINE/COASTAL CLIMATES The difference in heat capacity between land and ocean initiates a diurnal sea–land breeze circulation. During the day, land heats up much faster than does the ocean, establishing a land–ocean temperature difference that causes a pressure gradient. Wind blows toward the lower pressure over land to equalize the pressure difference. At night, land surfaces cool rapidly compared with adjacent oceans. The cycle is reversed at night, with winds blowing from the land toward the ocean to dispel the ocean–land temperature (and hence pressure) gradient (Figure 42-4). Ocean upwelling (cold) currents, particularly along the west coasts of continents, modify climate in adjacent land areas. Summers and winters in such locations are mild.

WEATHER PHENOMENA Precipitation refers to all liquid and solid forms of water that form in clouds and fall to the ground. Precipitation occurs when rising moist air condenses, which can occur for a variety of reasons. During the cold season in mid- and high latitudes, the type of precipitation that falls often depends on the profile of the atmosphere, which is influenced by factors such as storm track, wind direction, and topography. Snow occurs when the entire atmosphere is below freezing, whereas sleet (ice pellets) and freezing rain occur when there are intrusions of warmer air in the lower atmosphere. This often occurs either as snow is transitioning to rain (or vice versa) or during cold air damming events. These events are most common in the 807

CHAPTER 42  Principles of Meteorology and Weather Prediction

TABLE 42-1  Saffir-Simpson Scale of Tropical Cyclone Intensity

PART 5  RESCUE AND SURVIVAL

Rain ow shad

Prevailing winds

Evaporation

Warm ocean

FIGURE 42-3  Orographic precipitation. (Courtesy Deborah Mioduszewski.)

lee of mountain ranges such as the Appalachians. Hail is formed only in strong thunderstorm updrafts that are able to support ice chunks as the hail nuclei are accreted with more ice before becoming heavy enough to fall to the ground. Virga refers to precipitation that falls from clouds but evaporates or sublimates before reaching the ground. This can sometimes be seen as a rain shaft in the distance, with a veil of rain under the clouds becoming more streaky and disappearing before reaching the ground. Fog is formed when the temperature drops to near its dew point or when moisture is added to the air to saturate it. Radiation fog is typically a shallow layer of fog near the surface caused by rapid cooling of the land. The air just above the land cools to its dew point and condenses, although this type of fog typically dissipates quickly in the morning as the sun rises. Advection fog forms when moist air is transported horizontally (advected) over a cool surface. The surface cools the moist air to its dew point, causing condensation and fog. It is most common on land when warm air advects over a snow pack and the snow cools the air to saturation. It is most common over water when tropical air moves over a cool ocean current, with the same process ensuing. Upslope fog occurs as air is forced to rise. It cools to its dew point, and a cloud forms at the surface.

Human Comfort Wind chill refers to accelerated cooling of the human body that occurs because of atmospheric motion, particularly when temperatures are low—typically around 7° C (44.6° F). Weather forecasts report both absolute and relative (i.e., wind chill) temperatures. Heat index is a metric for describing “how hot it feels” when humidity is combined with actual air temperature. During summer months, particularly across eastern North America where humidity is higher, it is important to heed the forecast heat index values when planning outdoor activities. Table 42-2 provides an indication of the danger levels associated with various values of the heat index. Haze is reduced visibility caused by suspension of particulates in the air. Such particulates may either be aerosols (e.g., carbon particles, salt) or air pollutants (e.g., nitrogen oxides, ozone, and hydrocarbons). Haze generated by atmospheric pollutants is referred to as “photochemical smog.” Air Quality Index (AQI) is a measure of daily air quality in the context of human health. In the United States, the Environmental Protection Agency (EPA) calculates the AQI for five major air pollutants: ground-level ozone, particulate matter, carbon

TABLE 42-2  Categories of Heat Index Category

Heat Index

Extreme danger

130° F or higher (54° C or higher) 105-129° F (41-54° C)

Danger

FIGURE 42-4  Land–sea breeze circulation. H, High pressure; L, low pressure. (Courtesy Deborah Mioduszewski.)

808

Extreme caution

90-105° F (32-41° C)

Caution

80-90° F (27-32° C)

Possible Heat Disorders for People in High-Risk Groups Heatstroke or sunstroke likely Sunstroke, muscle cramps, and/or heat exhaustion likely. Heatstroke possible with prolonged exposure and/or physical activity. Sunstroke, muscle cramps, and/or heat exhaustion possible with prolonged exposure and/or physical activity. Fatigue possible with prolonged exposure and/or physical activity.

From http://www.srh.noaa.gov/ssd/html/heatwv.htm.

Weather Forecasting

Air Quality Index Levels of Health Concern

Numeric Value

OBTAINING DATA AND FORECASTS AND PREDICTING WEATHER IN THE NEAR TERM

Good

0 to 50

Air quality is considered satisfactory, and air pollution poses little or no risk.

Moderate

51 to 100

Air quality is acceptable; however, for some pollutants there may be a moderate health concern for a very small number of people who are unusually sensitive to air pollution.

Unhealthy for Sensitive Groups

101 to 150

Members of sensitive groups may experience health effects. The general public is not likely to be affected.

Unhealthy

151 to 200

Everyone may begin to experience health effects; members of sensitive groups may experience more serious health effects.

Very Unhealthy

201 to 300

Health alert: everyone may experience more serious health effects.

Hazardous

301 to 500

Health warnings of emergency conditions. The entire population is more likely to be affected.

Meaning

From http://www.airnow.gov/index.cfm?action=aqibasics.aqi.

monoxide, sulfur dioxide, and nitrous oxide. The AQI has a range from 0 to 500, with lower values (up to 50) associated with good air quality and higher values (300 and above) associated with levels of air pollution hazardous to health. The EPA uses color-coded categorizations of the AQI to indicate possible health effects associated with different values (Table 42-3). Vector-borne diseases, such as malaria, dengue, and Hantavirus, have been linked to climatic events. For example, in the tropics, dengue outbreaks occur at the onset of rainy seasons, such as the monsoons. Malaria and Hantavirus outbreaks in certain regions of the tropics have been associated with the warm phase of the El Niño Southern Oscillation (ENSO), when increased temperature is conducive to vector breeding. Stratospheric ozone prevents much of the sun’s ultraviolet (UV) radiation from reaching the earth’s surface. UV radiation that passes through the atmosphere is a health concern, primarily to the eyes and skin. The two primary factors in the risk for receiving unhealthy levels of UV radiation are angle of the sun and elevation. Higher levels of UV radiation are more likely at high elevations, where radiation has to pass through less of the atmosphere. The sun angle refers to both its varying angle throughout the day and its differing angles at different latitudes. At low latitudes, the sun angle remains high throughout the year, and therefore the risk for sunburn is always relatively high. At higher latitudes, the risk is especially high in late spring and early summer when the solar angle is highest. In either case, this risk is enhanced during the hours surrounding solar noon. In addition, clouds only scatter solar radiation; they do not block it. This allows UV radiation to reach the surface diffusely, where it is still harmful. Diffuse radiation is radiation that has been scattered, usually by clouds, but still reaches the ground. As a result, protection against the sun should be undertaken even when the sun is blocked by clouds. Stratospheric ozone is not evenly distributed around the world and tends to be thinner at higher latitudes, particularly during the spring. Therefore care should be taken to wear sunscreen and protective clothing and eyewear when engaged in outdoor activity, particularly in springtime in the mid- to high latitudes and at all times of the year in the tropics.

Weather forecasting in the wilderness requires data collection, whether from online sources (ideal) or with what is readily available and observable. Crude forecasts can be made by monitoring clouds and certain basic weather variables, such as temperature, humidity, and wind direction, if that is all that is available. If the Internet is available, reliable short-term forecasts can be obtained for most locations on Earth, typically provided by either private or public weather services. Therefore the primary use of online sources lies in the ability to monitor real-time weather information such as radar, satellite, and observations, in addition to obtaining forecasts. The primary purpose of data collection outdoors should be to make a rough forecast of ensuing weather conditions in the near term through 48 hours.

PORTABLE WEATHER INSTRUMENTS OF USE IN THE WILDERNESS Barometer Barometers are useful for assessing the evolution of weather systems, especially in the midlatitudes. Changes in atmospheric pressure at one location are small in comparison with changes as one moves up or down in elevation. Therefore barometers must be calibrated with changes in elevation if this is not already done automatically. In general the value of the atmospheric pressure is much less significant than its trend over time. A steady drop in pressure indicates the possibility of stormy conditions, whereas rising pressure generally portends fair weather. Thermometer Portable thermometers provide an indication of imminent changes in weather conditions such as those arising from the passage of a frontal system. They could also be consulted to ascertain the probability of freezing conditions and the risk for hypothermia. Because these applications do not require a high degree of precision, there is no need for a costly, high-precision instrument. Lightning Detector Portable lightning detectors are useful for detecting lightning within a 64.4- to 120.7-km (40- to 75-mile) radius, depending on the instrument. They detect the electromagnetic pulses of lightning, so they work best when used out of range of electronic equipment that may interfere with this signal. Lightning detectors operate with varying degrees of accuracy and can be limited in their ability to describe storm position and movement.

TYPES OF FORECASTS Forecasts vary by timescale, ranging from weather forecasts to seasonal climate forecasts. Weather forecasts assess the future state of the atmosphere and its constituent elements in reference to components such as temperature, wind, and precipitation. Weather forecasts are generated using numerical integrations of the equations of motion in the atmosphere. Such forecasts require accurate observations of initial atmospheric states. There are four types of weather forecasts: • Nowcasts: up to 0 to 3 hours, or 6 hours in some locations • Short-range forecasts: up to 48 hours • Medium-range forecasts: 3 to 7 days in advance • Long-range forecasts: greater than 7 days in advance Skill Accuracy of weather forecasts quickly declines with time because of the inherent chaos of the atmosphere. The details of midlatitude cyclones and smaller-scale events are impossible to forecast accurately beyond a few days, even if the pattern that produced them is relatively easy to identify. In the tropics, forecast skill is higher during years when either phase of the ENSO 809

CHAPTER 42  Principles of Meteorology and Weather Prediction

TABLE 42-3  Air Quality Index

PART 5  RESCUE AND SURVIVAL

phenomenon—La Niña or El Niño—is under way, because ENSO is the single most dominant mode of climate variability at the seasonal and interannual timescales.2 Seasonal climate forecasts seek to assess the mean weather of the upcoming season based on the conditions preceding the season by more than a month. They provide a prediction as to whether the coming season will on average be warm, cold, wet, or dry.3 At the seasonal timescale, the importance of initial conditions weakens,2 because detailed “memory” of initial atmospheric conditions is lost.3 Seasonal prediction thus depends on detailed changes in slowly varying boundary conditions.3 Shukla and Kinter4 provide the following list of surface boundary conditions: • Sea surface temperatures govern the convergence of moisture flux and sensible and latent heat fluxes between the ocean and atmosphere. • Soil moisture alters the heat capacity of the land surface and governs latent heat flux between continents and the atmosphere. • Vegetation regulates surface temperature and latent heat flux to the atmosphere from the land surface. • Snow influences the surface radiative balance through effect on surface albedo and latent heat flux by introducing a lag due to the storage of water in solid form in winter that gets melted or evaporated in spring and changes soil wetness. • Sea ice influences the energy balance and inhibits latent heat flux from the ocean. Anomalous boundary conditions can produce statistically significant anomalies in the seasonal mean atmospheric circulation. Such anomalous boundary conditions are more influential in the tropics than in the midlatitudes.4

How to Interpret Forecasts ACCESSING FORECASTS There are many online resources for weather forecasts for a particular location. In any country, the authoritative source for weather forecasts is the National Meteorological and Hydrological Services (NMHS) of that country. Links to the weather forecasts for cities issued by most NMHSs are available through http:// www.worldweather.wmo.int/ on the website of the World Meteorological Organization (WMO). North America In the United States, the National Weather Service (NWS) is responsible for all outlooks, forecasts, and advisories. Some of these responsibilities are handled by specialized centers within the organization. The National Hurricane Center (http:// www.nhc.noaa.gov/) issues all updates on tropical weather in the Atlantic and eastern Pacific Oceans, regardless of the impact on the United States. The Storm Prediction Center (http:// www.spc.noaa.gov/) handles all severe weather, including tornado and severe thunderstorm watches. Local NWS offices are responsible for issuing warnings on such events. Medium- to long-range discussions, outlooks, and forecasts are available from the Climate Prediction Center (http://www.cpc.noaa.gov/), and broader national forecasts and discussions for different regions of the country are available from the Hydrometeorological Prediction Center (http://www.hpc.ncep.noaa.gov/), which also provides guidance on quantitative precipitation forecasts (QPFs) and winter weather. In Canada, Environment Canada (http://www.weatheroffice. gc.ca) is responsible for all outlooks, forecasting, and advisories. These include data and forecasts regarding hurricanes, sea ice, aviation, and air quality. Environment Canada issues watches and warnings, and special weather statements for all of Canada, including its waters. International Forecasts The WMO has a dedicated website for severe weather warnings for various parts of the world. Such forecasts are categorized either by region (e.g., the European Union: http://www.meteoalarm. eu/) or by weather phenomena (e.g., tropical cyclones or thunderstorms: http://severe.worldweather.org/). Forecasts of severe 810

weather in maritime regions are available through the Global Maritime Distress and Safety System (http://weather.gmdss.org/).

FORECAST VARIABLES Seasonal Precipitation Forecasts Seasonal precipitation forecasts are presented as tercile probability forecasts in the United States. Tercile forecasts are based on the assumption that precipitation in a coming season has a 33% probability of falling within one of three possible categories: below-normal, near normal, or above normal. The forecast could be expressed either as the probability of seasonal rainfall being below normal, near normal, or above normal or in terms of expected rainfall anomalies. Temperature Forecasts Temperature forecasts are issued as expected daily minimum and maximum temperatures. In countries outside the United States, the convention is to express the two values in degrees Celsius. However, in most cases, Fahrenheit values will also be provided. Humidity Humidity forecasts are usually issued as expected relative humidity and range from 0% to 100%. Wind Direction and Speed Wind forecasts indicate direction (eight possible directions: N, NE, E, SE, S, SW, W, and NW) and speed (expressed either as kilometers per hour or miles per hour). In maritime environments, the convention is to use knots (1 knot is 1.852 km/hr [1.151 mph]). Precipitation Precipitation is forecast as probability of precipitation (POP) and, if applicable, QPF. POP should be interpreted as the percent of the area expected to receive measurable precipitation, although it is commonly misinterpreted as the chance that precipitation will fall at one specific point. QPF is the total amount of rain (or melted frozen precipitation) expected to fall in a specified period.

Forecast Products UNITED STATES According to the NWS, a warning is issued when a hazardous weather or hydrologic event is occurring, imminent, or likely. A warning means that conditions pose a threat to life or property. An advisory is also issued when such events are occurring, imminent, or likely, but the event is not expected to be as severe. The criteria for advisories and warnings varies among different NWS offices. Events such as heat index and winter weather, including snow, ice, and wind chill, may be perceived differently in different parts of the country. A watch is issued when the risk for a hazardous or hydrologic event is increasing, but its occurrence, location, or timing is still uncertain. As time advances, it could be replaced by an advisory or a warning. A watch is issued when warning-level conditions are anticipated. When a watch is issued, people should proceed with a plan of action for the predicted event and continue to be alert for further information and possible warnings.

INTERNATIONAL Regional Specialized Meteorological Centers (RSMCs) and Tropical Cyclone Warning Centers (TCWCs), established through the WMO, provide warnings on severe weather, particularly cyclones. Figure 42-5 shows the locations of the RSCMs and TCWCs. Tropical storm warnings use the Saffir-Simpson scale. Such warnings are often accompanied by a brief description of the damage likely to occur with the passage of each storm. Box 42-1 provides examples of the narrative used by the Indian Mete­ orological Department, responsible for RSMC-New Delhi, to

20°W

ESCAP/WMO Typhoon Committee

RA IV Hurricane Committee

20°E 40°E 60°E 80°E 100°E 120°E 140°E 160°E 180° 160°W 140°W 120°W 100°W 80°W 60°W 40°W 20°W

0°

60°N

60°N

40°N

RSMC New Delhi IV

20°N EQ

VIII RSMC La Réunion VI

20°S

40°N

RSMC Tokyo

VII

RSMC Nadi

IX Brisbane

Perth

II

III

X

XII

40°S

RSMC Miami

RSMC Honolulu

Port Darwin Moresby

V

60°S 20°W

CHAPTER 42  Principles of Meteorology and Weather Prediction

WMO/ESCAP Panel on Tropical Cyclones

I

20°N EQ

XI

Wellington

20°S 40°S

60°S 20°E 40°E 60°E 80°E 100°E 120°E 140°E 160°E 180° 160°W 140°W 120°W 100°W 80°W 60°W 40°W 20°W

0°

RA I Tropical Cyclone Committee for the Southwest Indian Ocean

RA V Tropical Cyclone Committee for the South Pacific and Southeast Indian Ocean

FIGURE 42-5  Location of the Regional Specialized Meteorological Centers and Tropical Warning Centers. (From http://www.nhc.noaa.gov/gifs/ wmo-tcp2.jpg.)

describe potential damage associated with a “deep depression” (28-33 knots) and a “severe cyclonic storm” (equivalent to a category 4 on the Saffir-Simpson scale).

• Gridded (2° × 2° resolution) monthly precipitation and temperature: http://iridl.ldeo.columbia.edu/SOURCES/. NOAA/.NCEP/.CPC/.CAMS/

How to Obtain Surface Observations

How to Access and Interpret Weather Satellite and Radar Data

UNITED STATES

In the United States, the NWS website has links to real-time radar and weather satellite imagery. The easiest method to track the passage (and associated precipitation) of a storm is to study radar imagery of a system available for different regions of the United States (Figure 42-6). Clicking on the region of interest takes one to a higher resolution image, where relevant warnings (such as thunderstorms) are marked on the imagery (Figure 42-7). The legend on the right enables the user to obtain an idea of the location of the highest intensity of precipitation. Table 42-4 provides an indication of the approximate rainfall intensity, which is associated with the units dBZ (known as “reflected intensities” or “decibels of Z”). Satellite images enable a user to obtain a quick estimation, on a large scale, of where overcast/stormy conditions are located and where clear weather prevails (Figure 42-8).

Surface observations for the United States are available online through the National Climatic Data Center (http://www. ncdc.noaa.gov/oa/climate/climatedata.html). Station-based data are available from hourly to monthly time resolution. The data are available free of charge to e-mail users with domains ending in .edu, .k12, .gov, and .mil; otherwise, fees apply to cover processing expenses. Data are also available from automated stations and volunteer observations through the NWS. Another source of data is the volunteer network of precipitation observers known as Community Collaborative Rain, Hail and Snow; data are available at http://www.cocorahs.org/.

GLOBAL DATA Surface observations from various part of the globe can be accessed through the Global Historical Climatology Network (GHCN). Such observations are available as station-based observations and as gridded products. Precipitation and temperature are the two variables commonly available through the GHCN. The following are links to GHCN data: • Monthly station-based precipitation: http://iridl.ldeo. columbia.edu/SOURCES/.NOAA/.NCDC/.GHCN/.v2beta/ • Daily station-based precipitation and minimum-maximum temperature: http://iridl.ldeo.columbia.edu/SOURCES/. NOAA/.NCDC/.GHCN_Daily/.version1/ • Monthly station-based temperature: http://iridl.ldeo. columbia.edu/SOURCES/.NOAA/.NCDC/.GHCN/.v2/

Weather Prediction in the Wilderness CLOUDS Clouds appear in various shapes and sizes and at different altitudes. Clouds are often classified according to their height and form (Figure 42-9): High clouds: cirrus, cirrostratus, and cirrocumulus Middle clouds: altostratus and altocumulus Low clouds: stratus, stratocumulus, and nimbostratus 811

PART 5  RESCUE AND SURVIVAL

BOX 42-1  Examples of Indian Meteorological

Department Narratives

What is the Damage Potential of a Deep Depression (28-33 knots) and What are the Suggested Actions? Structures: Minor damage to loose/unsecured structures Road/Rail: Some breaches in Kutcha road due to flooding Agriculture: Minor damage to banana trees and near coastal agriculture due to salt spray. Damage to rice paddy crops Marine Interests: Very rough seas. Sea waves about 4-6 m high. Coastal Zone: Minor damage to Kutcha embankments Overall Damage Category: Minor Suggested Actions: Fishermen advised not to venture into sea What is the Damage Potential of a Super Cyclonic Storm (120 knots [222 km/hr]) and Above? What are the Suggested Actions? Structures: Extensive damage to non-concrete residential and industrial buildings. Structural damage to concrete structures. Air full of large projectiles. Communication and power: Uprooting of power and communication poles. Total disruption of communication and power supply. Road/Rail: Extensive damage to Kutcha roads and some damage to poorly repaired pucca roads. Large scale submerging of coastal roads due to flooding and sea water inundation. Total disruption of railway and road traffic due to major damages to bridges, signals and railway tracks. Washing away of rail/road links at several places. Agriculture: Total destruction of standing crops/orchards, uprooting of large trees and blowing away of palm and coconut crowns, stripping of tree barks. Marine Interests: Phenomenal seas with wave heights more than 14 m. All shipping activity unsafe. Coastal Zone: Extensive damage to port installations. Storm surge more than 5 m, Inundation up to 40 km in specific areas and extensive beach erosion. All ships torn from their moorings. Flooding of escape routes. Overall Damage Category: Catastrophic Suggested Actions: Fishermen not to venture into sea. Large scale evacuations needed. Total stoppage of rail and road traffic needed in vulnerable areas. From http://www.imd.gov.in/section/nhac/dynamic/faq/FAQP.htm#q51.

Clouds with extensive vertical development: cumulus and cumulonimbus The frequency of occurrence of the different cloud types differs in the tropics and higher latitudes. Cumulus is the predominant cloud form in the tropics.1

CLOUDS AND WEATHER Clouds are among the best indicators of changing weather in the wilderness. Figure 42-10 shows the typical progression of clouds as a midlatitude cyclone moves through to the left of the observer, whereas a simplified version would apply when it moves to the right. Cirrus are often present 1 to 2 days before a storm and serve as the earliest indication that a cyclone is approaching. They should be noted as a sign that a storm may be on its way, bearing in mind that cirrus can be associated with storms that have no appreciable impact on a location, as well as with other innocuous disturbances. When cirrus begins to transition into a deck of altostratus, it can reasonably be assumed that the clouds are associated with a storm or front that is nearing. Stratus clouds are most commonly associated with warm fronts because they are a good indication that air is being forced to gradually rise over a wedge of cooler air, as is found in a warm front. In general, stratus occur as a warmer air mass is being lifted over a cooler one; the longer this occurs, the more likely the stratus are to be lower and begin precipitating. Therefore, as altostratus lower into a low, gray deck 812

of nimbostratus, it would be a good assumption that a light, steady rain or snow is on the way. Nimbostratus occurs in the vicinity of the warm front and near the center of low pressure where air is being lifted. The location of the low pressure can often be assessed using a simple rule called Buys Ballot’s law. When the observer stands with his or her back to the wind in the northern hemisphere, the low pressure will be to the left. This rule is reversed in the southern hemisphere and works best at higher latitudes. The weather conditions ahead of a warm front typically include winds from the east or southeast with cool conditions and a slowly dropping barometric pressure. After the front passes, the pressure continues to drop and the wind shifts clockwise to the south or southwest, in most regions bringing in warmer and moister air. This region of the cyclone between the cold and warm fronts is associated with the most instability, which allows for increased chances for convection and the highest probability of severe weather (see Figure 42-2). Because there is more instability, cumulous clouds dominate this sector. In the winter, warm air can rapidly be transported into this part of the storm, changing snow and ice to rain. The passage of the cold front is easy to observe because there are several sharp changes in weather conditions. Before passage, wind typically blows from the south or southwest, the dew point and temperature are relatively high, and air pressure is dropping. The strongest atmospheric lift is found near a cold front, so cumulonimbus with associated heavy rain and severe weather can be found at the frontal boundary. Typically, precipitation in the vicinity of a cold front does not fall for as long as it does ahead of a warm front because the slope, and therefore area of uplift, is much steeper and narrower with a cold front. After the front passes, wind typically shifts clockwise to the west or northwest, temperature and dew point slowly drop, and air pressure rises. Strong cold frontal passages can be observed as a deck of low or midlevel clouds sharply giving way to blue sky. Clearing skies are commonly observed relatively quickly after the front has passed, often with gusty winds remaining for a day or more. Dense cumulonimbus clouds in the tropics portend thunder showers and lightning. Altocumulus and altostratus clouds are associated with disturbed weather, such as tropical cyclones or in locations of large-scale orographic lifting.1 Cirrus clouds often form as leftover anvils from cumulonimbus clouds. However, they could also form independently and are usually associated with upper-atmospheric cyclones. Before a tropical cyclone, high cirrus clouds are often observed first, followed by midlevel and low-level stratus clouds. Eventually showery precipitation from cumulous and cumulonimbus arrives and increases in intensity as pressure steadily falls. Tropical cyclones have spiraling bands, often termed “rain bands,” of convective clouds. Intense upward motion and hence the heaviest rainfall occur within these rain bands and in the eye wall. Wind speeds increase toward the center of the cyclone. A dramatic decrease in pressure is observed within the eye of a storm.

BOUNDARY LAYER STABILITY Fronts and cyclones are not always needed for precipitation or severe weather. Strong daytime heating is all that is necessary to induce deep convection, which can occur frequently in more moist parts of the tropics and subtropics, as well as during the summer in midlatitudes. Stability of the boundary layer can be difficult to assess from observation, but it can be useful to determine how much potential there is for thunderstorms to grow. To achieve deep convection, air must be readily able to rise and overcome any resistance. Rising plumes of smoke or steam can give an indication of the stability of the lower atmosphere. If it rises to a certain level before spreading out horizontally, it is safe to assume that the lower atmosphere is at least somewhat stable. If nothing stops it from rising, the lower atmosphere may be quite unstable. In addition, a large amount of haze or pollution in the air is an indication of a stagnant environment where air moves very little, both horizontally and vertically. In arid regions, dust devils are also an indication of an unstable, albeit dry,

CHAPTER 42  Principles of Meteorology and Weather Prediction

FIGURE 42-6  Example of radar imagery over the United States.

FIGURE 42-7  Example of a Doppler radar image.

813

PART 5  RESCUE AND SURVIVAL

GOES WESTERN U.S. SECTOR IR IMAGE

Stormy weather

Fair weather

Western Conus Sector (IR Ch4) FIGURE 42-8  Example of the usefulness of satellite imagery in capturing stormy and clear conditions.

Cirrocumulus

Cirrus

30,000 ft HIGH CLOUDS Cirrostratus

25,000 ft

20,000 ft

Altostratus

15,000 ft

MIDDLE CLOUDS

Altocumulus

Cumolonimbus 10,000 ft

Stratocumulus Cumulus

Nimbostratus

LOW CLOUDS Stratus

FIGURE 42-9  Guide to different cloud types.

814

5000 ft

Cirrus Altostratus Cumulonimbus

Cumulus Nimbostratus

FIGURE 42-10  Progression of a midlatitude cyclone as seen from the ground.

TABLE 42-4  Doppler Radar Scale of Intensity dBZ

Rain Rate (inches/hr)

65 60 55 52 47 41 36 30 20 1 lasting > 48 hours) Headache Nausea or vomiting Myalgias Transient erythematous maculopapular rash 3. Acute neurological signs and symptoms (A, B, or C required) A. Altered mental status for >48 hours (>1 below are required) Marked lethargy that often incapacitates the individual Delirium or agitation Marked disorientation or confusion that often incapacitates the individual Profound sleepiness (sleeping all day for >2 days) Stupor or coma B. Brainstem or spinal cord signs that persist >48 hours (>1 below are required) Cranial nerve palsies Myelitis i. New focal weakness in one or more limbs that is not due to arthritis or limb pains lasting > 48 hours ii. Respiratory failure requiring intubation that is not solely due to pneumonia iii. Electromyographic evidence of recent denervation in more than one nerve root C. Cerebrospinal fluid (CSF) (all required if examined): Pleocytosis (rarely may be absent if lumbar puncture performed within first 2 days of central nervous system symptoms) Cerebrospinal fluid IgM antibody for West Nile virus Negative cultures for bacteria and negative Gram stain (if mycobacterial, fungal, or viral cultures were done, they should be negative) 4. Supportive criteria A. Focal neurological signs of acute onset (≥1 desired but not required) Hemiparesis Visual field loss or chorioretinitis Hyperactive deep-tendon reflexes or Babinski's sign Seizure Tremor or myoclonus Bradykinesia, spasticity, or rigidity Photophobia Severe generalized weakness and fatigue that keeps patient in bed B. Mosquitoes as vector (1 desired unless patient received transfusion or transplant organ): Positive West Nile virus (WNV) mosquito pools or infected horses in region within past 3 weeks or Recent cases of acute WNV infection in region or Travel within past 3 weeks to region with positive WNV mosquito pools or cases of WNV infection 5. Exclusion criteria (required) Underlying dementia, congestive heart failure, or chronic obstructive pulmonary disease that could cause altered mental status and no known other neurological disease that could cause the neurological signs Definite or Confirmed Diagnosis of West Nile Neuroinvasive Disease   Above criteria plus WNV serology/virology (A and B plus/or C or D) A. Demonstration of WNV IgM antibody in serum without vaccination with yellow fever or Japanese B viral vaccine in past 5 years or recent infection with other flavivirus, such as St Louis encephalitis virus. Note: If WNV has occurred in region in prior years, criterion B is needed because previously infected individuals may have prolonged persistence of IgM in serum. B. Fourfold or greater increase in serum WNV IgG or IgM antibody titer between acute and convalescent samples taken 10 to 28 days apart. C. Demonstration of WNV IgM antibody in CSF D. Identification of WNV in CSF by viral culture or of WNV nucleic acid by polymerase chain reaction From Davis LE, DeBiasi R, Goade DE, et al: West Nile virus neuroinvasive disease, Annals of Neurology 60:294, 2006.

possibly human breast milk.23 Because transmission from blood transfusions reached 2.7 cases per 10,000 units during the peak of the 1999 outbreak in New York, and because there were confirmed cases of WNV transmission to organ transplant recipients, routine screening of blood donors for WNV RNA began in the summer of 2003. In 2003 and 2004, 519 donors were identified by this method, resulting in removal of more than 1000 potentially infectious units of blood products from the Red Cross supply. All donated blood continues to be screened for WNV with nucleic acid amplification tests, either on individual samples or on “minipools” of up to 16 donations.169 A recent study of targeted nucleic acid amplification testing of individual donations in high-prevalence regions suggests that this approach may be cost-effective, because units with low levels of viremia may not be detected in minipools of blood donations.17 Despite reduction in transfusion-related transmission with universal screening of blood, this limitation has prevented eradication and cases are still reported.31 894

Clinical Presentation The virus has an incubation period of 3 to 14 days.143 Disease usually occurs in temperate zones either in late summer or early fall, or year-round in milder climates. Clinical syndromes caused by WNV include asymptomatic infection, WNF, and West Nile neuroinvasive disease (WNND). Most WNV infections in humans are asymptomatic. Of the 20% of symptomatic cases, the majority of patients develop WNF, which usually involves a mild influenzalike illness with malaise, headache, nausea, vomiting, anorexia, lymphadenopathy, and rash. In a case-series review of 98 community-dwelling patients with laboratory evidence of WNV infection but no evidence of neuroinvasive disease, fatigue was present in 96% of patients, fever in 81%, headache in 71%, and difficulty concentrating in 53%.181 Even in cases of WNF, the impact on quality of life can be severe. Of the 98 patients, 39% reported ongoing symptoms at 5 month follow-up, 82% reported limitations in household activities, and there was a median of

Diagnosis For public health and surveillance purposes, the CDC uses specific criteria for arboviral infections and includes disease caused by California serogroup viruses, eastern and western equine encephalitis viruses, Powassan virus, St Louis encephalitis virus, and WNV. This was most recently revised in 2004 (Box 48-1).35 Typical findings for severe disease usually include normal or slightly elevated leukocyte counts in peripheral blood, possible hyponatremia in individuals with WNV encephalitis, pleocytosis and increased protein in the CSF, and no findings on CT scans of the brain.37,143 Although MRI may yield abnormal results in 25% to 35% of cases, findings may be nonspecific.37,196 For definitive diagnosis, serum is ideally collected within 8 to 14 days of symptom onset, and CSF is collected within 8 days to give the highest diagnostic sensitivity. Serum or CSF should show IgM antibodies to WNV by IgM-capture ELISA (MAC-ELISA). There is, however, a chance that persistent IgM antibodies can be found in people years after living in places where WNV is epidemic. The diagnosis can be further confounded by the fact that these IgM ELISA tests have a cross-reactivity of up to 44% with other flaviviruses during acute infection.37,70 The most specific test for arthropod-borne flaviviruses is the plaque-reduction neutralization test (PRNT). It can be used both to negate the false-positive results sometimes seen in MAC-ELISA or other assays and to facilitate discrimination among the flaviviruses.37 Efforts have been made to develop more specific and rapid serologic assays. Promising candidates include a microsphere immunoassay that discriminates among different flavivirus infections, as well as an immunofluorescence assay that has less cross-reactivity among WNV IgM antibodies and closely related flaviviruses. PCR (as used for screening blood products in the United States) or viral culture can also isolate the virus, but sensitivity is not high because of the transient and low levels of viremia, because the virus quickly disappears from the periphery into the CNS in severe disease.37,143 However, one recent study showed that the combination of serologic assay and nucleic acid testing allowed for more accurate identification of WNV cases

BOX 48-1  2004 CDC Case Definition for Neuroinvasive

and Non-Neuroinvasive Domestic Arboviral Diseases

Clinical Criteria for Diagnosis Neuroinvasive disease requires the presence of fever and at least one of the following, as documented by a physician and in the absence of a more likely clinical explanation: • Acutely altered mental status (e.g., disorientation, obtundation, stupor, or coma), or • Other acute signs of central or peripheral neurologic dysfunction (e.g., paresis or paralysis, nerve palsies, sensory deficits, abnormal reflexes, generalized convulsions, or abnormal movements), or • Pleocytosis (increased white blood cell concentration in cerebrospinal fluid [CSF]) associated with illness clinically compatible with meningitis (e.g., headache or stiff neck). Non-neuroinvasive disease requires, at minimum, the presence of documented fever, as measured by the patient or clinician, the absence of neuroinvasive disease (above), and the absence of a more likely clinical explanation for the illness. Involvement of non-neurologic organs (e.g., heart, pancreas, liver) should be documented using standard clinical and laboratory criteria. Laboratory Criteria for Diagnosis Cases of arboviral disease are also classified as either confirmed or probable, according to the following laboratory criteria: Confirmed Case • Fourfold or greater change in virus-specific serum antibody titer, or • Isolation of virus from or demonstration of specific viral antigen or genomic sequences in tissue, blood, CSF, or other body fluid, or • Virus-specific immunoglobulin M (IgM) antibodies demonstrated in CSF by antibody-capture enzyme immunoassay (EIA), or • Virus-specific IgM antibodies demonstrated in serum by antibody-capture EIA and confirmed by demonstration of virus-specific serum immunoglobulin G (IgG) antibodies in the same or a later specimen by another serologic assay (e.g., neutralization or hemagglutination inhibition). Probable Case • Stable (less than or equal to a twofold change) but elevated titer of virus-specific serum antibodies, or • Virus-specific serum IgM antibodies detected by antibodycapture EIA but with no available results of a confirmatory test for virus-specific serum IgG antibodies in the same or a later specimen. Case Definition • A case must meet one or more of the above clinical criteria and one or more of the above laboratory criteria. From Centers for Disease Control and Prevention. http://www.cdc.gov/ncphi/ disss/nndss/casedef/arboviral_current.htm. CDC, Centers for Disease Control and Prevention.

compared with either approach alone.173 Such studies have recommended that these measures be used as an adjunct to serologic testing. Treatment and Prevention Currently there is no specific treatment for WNV, and supportive care remains the mainstay of therapy.66 Certain antivirals, antibodies, and drugs altering the inflammation process (e.g., interferon) are being tested. Nucleoside analogs have been studied in vitro,2,134 but the most advanced testing in vivo has been with ribavirin, with no reduction in disease88 or viremia116 shown. In a retrospective, uncontrolled, nonblinded study of 233 human WNV cases, ribavirin was associated with poorer outcome in bivariate analysis. Although this effect was not seen in multivariate analysis, ribavirin was ineffective.48 Similarly, there have been promising in vitro studies and human case reports evaluating the usefulness of interferon-α2,96,133 and intravenous immunoglobulin,1,10 but these treatment options remain controversial. Currently 895

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

10 days of missed school or work.181 In another follow-up study done in a population-based cohort of 656 nonfatal cases, 91% of patients reported limitations in routine daily activities secondary to WNV infection. Moreover, in cases of WNF alone, there was a median number of 16 school or work days missed, and 53% of this subset of patients reported symptoms of at least 30 days’ duration. The impact was even more significant in patients with WNND.139 West Nile neuroinvasive disease occurs in less than 1% of individuals infected with WNV and includes encephalitis, meningitis, meningoencephalitis, and acute flaccid paralysis/poliomyelitis.50 Older adult and immunocompromised patients are at increased risk for severe neurologic disease from WNV. In a retrospective medical chart review of 221 hospitalized WNV patients, 16% of those with meningitis and 32% of those with encephalitis had autoimmune disease, were immuno­suppressed, or were organ transplant recipients. Age over 50 years, alcohol abuse, and diabetes were also found to be associated with WNND.12 Clinical criteria for WNND are listed in Table 48-2. Although the clinical presentation of meningitis and encephalitis in WNV is nonspecific, one particular feature of WNV encephalitis is that it may manifest with parkinsonian features or other movement disorders, such as myoclonus or intention tremor. In a small prospective case-series, 94% of WNV-seropositive patients experienced dyskinesias compared with 13% in the control group.156 Another clinical syndrome associated with severe WNV disease is acute flaccid paralysis, which can rapidly progress to paralysis of one or up to all four limbs. It may also manifest as severe, asymmetric weakness, usually with sensation preserved. Affected limbs show decreased or completely absent deep tendon reflexes, most likely from anterior horn cell involvement similar to that seen in poliomyelitis.50,70,155,156 Other clinical findings may include ocular complications (e.g., optic neuritis, chorioretinitis, retinal hemorrhage, uveitis, conjunctivitis),44,102,191 bladder dysfunction,70 myocarditis, pancreatitis, and fulminant hepatitis.143

PART 6  ANIMALS, INSECTS, AND ZOONOSES

there are two randomized, double-blind, placebo-controlled studies being conducted to evaluate the potential therapeutic effect of interferon and a monoclonal antibody. Information regarding these trials can be found at http://www.nyhq. org/posting/rahal.html and http://clinicaltrials.gov/ct2/show/ NCT00927953, respectively. For prevention of disease, general control measures such as blood donor screening and precautions against mosquitoes can be taken, but so far there is no specific way to prevent WNV. Although vaccines have proved efficacious in multiple animal species, unfortunately no human vaccine exists. Theoretically there is potential for an inactivated virus to induce long-term immunity, because such a vaccine exists for JE and other flavivirus diseases. Multiple candidate vaccines against WNV are being evaluated, a couple of which have shown promise in small human studies. These include a chimeric virus (ChimeriVax-WN) based on the live, attenuated yellow fever 17D vaccine virus containing the premembrane and envelope proteins of WNV, and a single-plasmid recombinant DNA vaccine. ChimeriVax-WN was evaluated in a randomized, double-blind placebo-controlled study of 45 healthy adults. The vaccine was well tolerated, and within 21 days of receiving a single inoculation dose, all study subjects developed high titers of WN-specific neutralizing antibodies. In addition, 43 of 45 participants developed a WNVspecific T-cell response.130 The DNA vaccine was recently evaluated in an open-label phase 1 trial of 15 healthy adults. The vaccine was well tolerated, and in the 12 participants that completed the three-dose vaccination schedule, all developed WNVspecific neutralizing antibodies.120 Other WNV vaccines under development include a candidate live-attenuated chimeric WN vaccine that uses an infectious dengue virus type 4 cDNA clone as a backbone and a recombinant subunit WN vaccine.188 Surveillance and Reporting Reporting requirements for suspected WNV infections vary across local and state health departments, but WNV encephalitis is on the list of designated nationally notifiable conditions. The CDC may use results from commercial laboratories but may also request samples for diagnosis in its own laboratory. Information on how to send specimens can be found at http://www.cdc.gov/ ncidod/dvbid/misc/arboviral_shipping.htm. For ecologic surveillance, the CDC and other federal agencies have established specific guidelines and protocols to track avian, equine, and mosquito epizootics.

ST LOUIS ENCEPHALITIS The St Louis encephalitis (StLE) virus is a flavivirus related to Japanese encephalitis and West Nile virus that is also transmitted by mosquitoes.

occupations, and older age. Patients with symptomatic StLE present with high fever and headache, aseptic meningitis and encephalitis. Infants in particular may have occasional convulsions and spastic paralysis. Of recognized cases, 95% are hospitalized for CNS involvement. The case fatality rate is 3% overall and up to 30% in older adults.30 Diagnosis As with other arboviral diseases, clinical and epidemiologic features must be taken into account to make a presumptive diagnosis. However, StLE may be difficult to differentiate on clinical features alone. Thus definitive diagnosis is typically obtained by testing serum or CSF for serotype-specific monoclonal antibodies (IgM ELISA). Further confirmatory tests, such as demonstrating at least a fourfold increase in antivirus antibody titer between acute and convalescent period, may be done.30 Antigenic crossreactivity with other flaviviruses is a known problem, encour­ aging some facilities to use PRNT or develop discriminatory algorithms to differentiate infections.119 A potential additional option for diagnosis includes a newly developed rapid microsphere-based IgM assay that would shorten the test processing time to less than 5 hours.93,94 Treatment and Prevention As is the case for many viral illnesses, treatment is supportive care, because there are neither specific antiviral therapies nor vaccines. One interventional pilot study of 15 patients with meningoencephalitis due to StLE showed that treatment with interferon-α2b reduced severity and length of complications. Given the small number of participants and the nonrandomized nature of the study, further investigation must be conducted.148

EASTERN EQUINE ENCEPHALITIS First discovered in the brain of a horse with encephalitis in 1933 in New Jersey, eastern equine encephalitis (EEE) is a serious mosquito-borne disease that appears in the eastern half of the United States with a high case fatality rate. The virus is a member of the family Togaviridae, genus Alphavirus, and it is related to western and Venezuelan equine encephalitis viruses.118 Epidemiology and Transmission The transmission cycle involves birds and several species of mosquitoes, predominantly Culiseta melanura (Figure 48-16). Other possible mosquito vectors include species in the genera Aedes and Coquillettidia.118 Humans and horses are considered hosts with incidental infections that can progress to severe disease. EEE occurs mainly along the eastern and Gulf coasts of the United States, but cases have been documented in Canada as

Epidemiology and Transmission The Culex mosquito is the main species that transmits StLE virus, with birds as a reservoir and humans as another host. The viremia, however, does not cause illness in birds or mosquitoes. Around the Gulf Coast, Ohio and Mississippi River Valleys, the culprit mosquitoes are Culex pipiens and C. quinquefasciatus; in Florida, C. nigripalpus; and in the western states, C. tarsalis.30 StLE virus is found throughout much of the Americas. In temperate parts of the United States, disease usually occurs in late summer or early fall, but it can occur year-round in the southern United States. Outbreaks can occur almost anywhere in the United States, though epidemics have occurred mainly in the Midwest and Southeast. Between 1964 and 2008, less than 5000 human cases of StLE were reported in the United States.32,30 In some areas, it appears that WNV is displacing previously endemic StLE because of cross-protective avian herd immunity and differences in transmission efficiency.149 Historically few cases were reported from Central and South America, although there have been recent large outbreaks in both Argentina and Brazil.55,132,167 Clinical Presentation StLE has an incubation period of approximately 5 to 15 days, with a 300 : 1 ratio of asymptomatic to symptomatic cases. Risk factors for infection include low socioeconomic status, outdoor 896

FIGURE 48-16  Micrograph of eastern equine encephalitis virus.

Clinical Presentation Individuals who live (or visit) endemic areas and those who spend significant time outdoors are at risk for developing EEE, and individuals older than 50 years and younger than 15 years have a greater chance of developing severe disease. Clinical presentation can be within the spectrum from mild influenza-like illness to encephalitis, coma, and death. One study collecting the 36 cases from 1988 to 1994 in the United States showed that clinical signs included fever (83%), headache (75%), nausea and vomiting (61%), confusion (4%), myalgias and arthralgias (36%), chills (25%), seizures (25%), focal weakness (23%), abdominal pain (22%), respiratory symptoms (11%), and cranial nerve palsies (8%).53 The case fatality rate for EEE is 33%, making it the most severe of the arboviral encephalitides. Moreover, 50% of individuals who survive are left with mild to severe neurologic deficits.41,53 Diagnosis Peripheral blood may show leukocytosis, and analysis of CSF may reveal elevated protein with red and white cells in the range of 600 to 2000/mm3 (white cells being predominantly lymphocytes). Preliminary diagnosis may be completed by demonstration of IgM antibodies by capture ELISA. Definitive diagnosis lies in serologic evidence based on paired sera (acute and convalescent samples) in hemagglutinin-inhibition assays or in neutralization assays. Acute samples should be obtained within 10 days of symptom onset, and convalescent samples about 2 or 3 weeks after the symptom onset. It is possible to isolate the virus directly from the serum in acute infection, but this method is used less commonly.20,35,118 Other helpful diagnostic modalities include MRI, which may show focal changes, particularly in the basal ganglia, thalamus, and brainstem.53,68 Treatment and Prevention No specific treatment is available. There has been one case report of a child being treated with corticosteroids and intravenous immunoglobulin,68 but this has not been further studied. No human vaccine is available, but there are equine vaccines that should be employed in endemic areas. Surveillance and Reporting EEE is a nationally notifiable disease.

AUSTRALIAN ENCEPHALITIS (MURRAY VALLEY ENCEPHALITIS) Epidemiology and Transmission Occurring mainly in Australia and New Guinea, Murray Valley encephalitis (MVE) virus is from the family Flaviviridae, genus Flavivirus, and is transmitted via a bird-mosquito-bird cycle with Culex annulirostris. Because humans do not have high levels of viremia, they are seen as dead-end hosts. Clinical Presentation Most infections are asymptomatic, and only 1 in 1000 to 2000 infections actually develops into clinical illness.115 The clinical course is similar to that of JE, with headache, fever, myalgias, nausea and vomiting, and anorexia. The neurologic involvement can involve lethargy, irritability, confusion, or meningismus, as well as seizures, spastic paresis, and coma. Individuals who

succumb to progressive MVE infection have a poor prognosis; more than 30% die and 30% to 50% suffer neurologic sequelae, with a bimodal risk for children and older adults.57 Diagnosis As is true for many other viral illnesses, definitive diagnosis of MVE is by identifying IgM antibody via immunoassay of the CSF or a fourfold rise in serum antibody titers. Direct viral isolation or PCR can also prove the infection in tissue, blood, or CSF. However, these tests can be obscured by cross-reactive antibodies to Kunjin, JE, Edge Hill, Alfuy, Sepik, dengue, and other flaviviruses.177 Two-thirds of patients have normal CT scans. If the scans are abnormal, they may show nonspecific signs of encephalitis, including mild hydrocephalus and cerebral edema.103 Treatment and Prevention There is no specific treatment or vaccine for MVE. Prevention depends on adequate mosquito control and avoidance of mosquito bites.

CALIFORNIA (LA CROSSE) ENCEPHALITIS La Crosse (LAC) virus is a California serogroup bunyavirus that can cause encephalitis (usually in children) in the central and eastern United States. La Crosse encephalitis constitutes 8% to 30% of all cases of encephalitis in the United States, and is one of the major causes of arboviral illness.152 In fact, its incidence in endemic areas (20 to 30 cases per 100,000 population per year) exceeds that of bacterial meningitis.124 Epidemiology and Transmission Aedes triseriatus, the eastern tree hole mosquito, is the main vector, although A. albopictus, or Asian tiger mosquito, may be emerging as another significant species. Vertebrate hosts include chipmunks, tree squirrels, and foxes. The annual incidence in the United States is about 80 to 100 cases.27 Most infections are asymptomatic and occur from late summer to early fall in the central and eastern United States.21,27,59 Clinical Presentation The majority of cases are children less than 15 years of age.27,78,122 For 80% to 90% of infected persons, the clinical course is mild, with only headache, fever, and vomiting after an incubation period of 3 to 7 days. Approximately 10% to 20% of infected individuals develop a severe form of the disease within the first 8 to 24 hours of symptom onset.123 In one pediatric study of 127 hospitalized children, it was noted that 70% of patients presented with headache, fever, and vomiting. Of children, 46% had seizures (generally focal seizures, with some progression to status epilepticus), and 20% had focal neurologic findings. Encephalitis does not always occur, because aseptic meningitis was also found. Although all patients survived, over 10% had neurologic deficits at time of hospital discharge, and preliminary analysis suggested patients may suffer long-term cognitive and behavioral deficits as well.122 Only one case report has mentioned California encephalitis causing infarction of the basal ganglia, leaving a child with acute hemiparesis.112 The CDC recently described a case of possible congenital infection after identification of IgM antibodies in umbilical cord serum. The mother declined collection of infant serum to document seroconversion, but fortunately the infant remained asymptomatic and development was normal at 6-month follow-up. The CDC reports the case fatality rate to be less than 1%, although recent studies have found this to be an underestimate.36,77,78 Diagnosis Laboratory findings may reveal leukocytosis with polymorphonuclear leukocyte predominance and pleocytosis in the CSF (either neutrophilic or lymphocytic predominance), although studies of laboratory values for LAC and non-LAC cases show no statistically significant differences.82 More than one-half of patients have abnormal electroencephalographic findings. A CT scan may show nonspecific cerebral edema, if there are any findings at all, and MRI may reveal gadolinium enhancement in cortical areas.122 897

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

well as Central and South America. It occurs mainly in the summertime. Between 1964 and 2008, there were approximately 257 confirmed cases in the United States, with an average of 5 cases per year. Most of the cases have been in Florida, Georgia, Massachusetts, and New Jersey, near coastal areas and freshwater swamps. The real incidence is probably higher because of underreporting and underrecognition. In fact, in 2005, 21 cases were reported to the CDC, compared with an average of 8.2 cases per year from 2000 to 2004. This included an outbreak of 7 cases in New Hampshire, a state which was previously not known to have locally acquired EEE.32,29,41

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Definitive diagnosis is made with IgM antibody by capture immunoassay of CSF, a fourfold rise in serum antibody titers against LAC virus, or isolation of virus from or demonstration of viral antigen or genomic sequences in tissue, blood, or CSF.20 As in almost all other viral infections discussed in this chapter, IgM antibody capture with ELISA is the most common method, with the recommendation to confirm IgG antibody with another serologic assay such as a neutralization test. Treatment and Prevention No specific treatment is available beside general measures to control cerebral edema and seizures. Certain studies have looked at ribavirin,123 but there is no strong evidence to recommend its use. No vaccine is available against this virus.

EPIDEMIC POLYARTHRITIS (ROSS RIVER VIRUS) A mosquito-borne alphavirus in the family Togaviridae, Ross River virus (RRV) is a single-stranded, enveloped RNA virus in the same family as chikungunya, Sindbis, and eastern and western equine encephalitis. The virus is endemic and enzootic in Australia and Papua New Guinea and causes epidemic polyarthritis.84 It is the most common human arboviral disease in Australia, causing approximately 5000 reported cases a year.175 In the late 1970s, RRV spread to the South Pacific islands, but it disappeared after the end of an epidemic in which 500,000 people were infected; recent reports, however, show that there are new cases reappearing in Fiji.104 Epidemiology and Transmission The main vectors are Culex and Aedes (particularly Aedes vigilax) mosquitoes, and marsupials such as kangaroos and wallabies are important as vertebrate-amplifying hosts.151 Vertical transmission is possible from mosquito to offspring, and human-mosquitohuman transmission is also thought to occur. Tropical coastal regions with salt marsh habitats are the primary habitats for the mosquito vector species, and infections are most common in the spring, after summer rains, or after inundation of salt marshes by rain or tides.104 Clinical Presentation After inoculation, the virus is thought to replicate within macrophages. It causes local cell-mediated immune responses that appear to be the cause of arthritis. After an incubation of 3 to 9 days (or as long as 21 days), patients can present either with acute febrile illness with arthritis and rash; with acute fever, rash, or arthritis alone; with polyarthralgia; or with arthritis.63 The joints involved are usually symmetric and include the wrists, knees, ankles, and metacarpophalangeal and interphalangeal joints of the hands, with true arthritis present in 40% of infected individuals.170 About 50% have fever and a sparse maculopapular rash on the limbs and trunk that may occur before or after the arthritis. Whereas fever may resolve within several days, rash may persist for several months. Joint symptoms and fatigue, on the other hand, have been reported to last years, even after fever and rash have subsided.118 However, recent literature suggests that patients with chronic symptoms may have additional underlying comorbidities, such as rheumatic disease or depression.85,136,170 Diagnosis There are no laboratory findings specific for RRV infection. Patients often have normal leukocyte counts (although mild neutrophilia or atypical lymphocytes can be found) and possibly elevation in the nonspecific erythrocyte sedimentation rate. Joint aspiration may reveal viscous fluid with predominantly mononuclear cells and points to viral arthritis.63 Serum can be screened for IgM antibody against Ross River virus IgM, which can then be confirmed by PRNT. These tests are available at only a few reference laboratories, including the CDC.104 Viral culture and PCR are not commonly used for diagnosis of RRV infection. Treatment and Prevention There is no specific treatment. Management of arthralgias and myalgias is with standard analgesic and nonsteroidal 898

antiinflammatory drugs. There does not seem to be any direct association of mortality with RRV. As with other arboviral diseases, prevention depends on adequate mosquito control and avoidance of mosquito bites. One recent prospective case-control study showed that protective measures such as mosquito coils, repellants, and citronella candles decreased this risk for RRV infection twofold with a dose response for the number of protective measures used. In addition, light-colored clothing decreased risk threefold, whereas camping in the 3 weeks before symptom onset increased the risk eightfold.83 There has been additional research on understanding the environmental, anthropogenic, and social factors responsible for disease outbreaks. Some believe factors such as climate variability can affect virus replication, vector demographics, and even human behavior, each of which can be modeled to predict onset and severity of RRV epidemics. Early warning systems could potentially enable improved disease control measures.*

JAMESTOWN CANYON VIRUS Jamestown Canyon virus is a California serogroup bunyavirus widely distributed throughout the United States and Canada. White-tailed deer, Odocoileus virginianus, are the principal vertebrate host and boreal Aedes and Ochlerotatus mosquitoes are the primary vectors.3,4,64 Documented human infections are scant, but the virus usually causes a mild febrile illness, and rarely meningitis and encephalitis. There is a case report of Jamestown Canyon virus–induced encephalitis in an 8-year-old girl in rural southwestern Michigan, who presented with symptoms of headache and fever that quickly progressed to seizures and coma.71 The infection is difficult to distinguish from other California serogroup bunyaviruses, such as California encephalitis, snowshoe hare, Keystone, and trivittatus viruses, because of crossreactivity in the more common serologic tests and difficulty in isolating the actual virus.178 The virus has been posited as a possible emerging infectious disease,71,121 but there have been few identified cases and the literature on this subject is scant.

Mosquito Control GENERAL GUIDELINES FOR INDIVIDUAL PROTECTION For personal protection and prevention, individuals can take precautions such as avoiding mosquitoes at their most active time (from dusk to dawn) and wearing loose-fitting cotton clothing covering their arms and legs (see Chapter 47). Individuals may also apply repellents to exposed areas of skin. The most effective preparations contain N,N-diethyl-3-methylbenzamide (DEET),144 and generally concentrations need not exceed 20% to 35%.62 DEET is safe in children older than 2 months of age and pregnant women.37,106 However, it can rarely cause neurologic toxicity. Thus it should be kept away from mucous membranes and used sparingly to avoid systemic absorption. Studies have shown that a single application of a product containing 24% DEET confers an average of 5 hours (and up to 12) of protection against A. aegypti mosquitoes. Compared with DEET, newer formulations containing the compound IR3535 fared poorly.62 Picaridin (KBR 3023), a shorter-acting plant-derived repellent, is thought to be as effective as DEET and better tolerated.6,98 Agents such as p-menthane-3,8-diol (PMD) and BioUD have not been evaluated as well but are thought to be less effective compared with DEET. Permethrin-containing compounds and other residual insecticides that kill rather than simply repel mosquitoes may be applied to clothing and netting. Other strategies include using mosquito coils and sprays containing pyrethroids in sleeping areas. Citronella has been also shown to be mildly effective in reducing the number of bites, but it requires frequent applications if used topically (as opposed to the candle form).61 Current research in insect repellents involves sophisticated appreciation of the olfactory senses of mosquitoes and creating proteins to inactivate human-specific odorants.98,154 *References 90, 91, 100, 101, 175, 176, 186.

Aedes aegypti

17

In general, global eradication programs for all infectious diseases, including mosquito vector surveillance and control, have declined dramatically in the past few decades. Because of the success of control programs in the 1970s and the resultant decreased public health threat, less attention has been paid and fewer resources have been allocated to maintaining good control. One result is fewer trained personnel, because training programs are less well funded. The effect has been detrimental, with a reversal of previous gains. In Central and South America, for example, dengue fever was largely eliminated with eradication in the 1950s and 1960s of the A. aegypti mosquito, the main vector for the disease. However, because these programs were largely dismantled in the 1970s, the mosquito species has reinfested most of these tropical regions.73 Vector control has three arms: environmental management, biologic control, and chemical control.105 Environmental management consists of monitoring and intervening to reduce the vector population, as well as transmission factors that sustain the human-vector-pathogen contact. For example, simply removing old tires, covering water storage containers with tight lids, keeping floor drains cleaned and covered, and chlorinating ornamental pools and fountains (or populating them with larvivorous fish) can help prevent the breeding of mosquitoes. Biologic control includes using organisms that naturally prey on the vector. For example, larvivorous fish and Bacillus thuringi­ ensis H-14 (BTI) are commonly used against larvae. Biologic control, however, requires expense and time to raise these organisms, and the organisms may have limited success when the environment in which they are placed does not sustain their existence. Furthermore, even if they are effective in reducing the number of larvae, there is not conclusive evidence to show that this decreases transmission of disease, because a lower density of larvae in a certain area may mean healthier and stronger adult mosquitoes if food is limited. Chemical control is the most well-known vector control. It consists of using products such as pyrethrins (e.g., deltamethrin, resmethrin, permethrin) or organophosphate insecticides (e.g., fenthion, malathion, fenitrothion, temephos). These can be applied in several forms: larvicidal application, perifocal treatment, or space spraying. Larvicidal application is focal treatment to domestic water supplies that cannot be eliminated (e.g., for A. aegypti, either 1% temephos or methoprene can be used to regulate larvicidal growth, or BTI can be used to safely treat drinking water). Insecticides such as fenthion, malathion, and fenitrothion can be used as perifocal treatment for nonpotable sources of water to eliminate larvae and adult mosquitoes. Finally, space spraying can be used against adult mosquitoes, often in emergency situations. The chemicals mentioned here can be used as aerosols or mists applied by portable machines, vehicle-mounted generators, or aircraft. Parameters for use (e.g., grams of active ingredient per hectare, wind conditions that may limit effectiveness) depend on the type of chemical, equipment, and target vector. Table 48-3 shows selected insecticides and dosages for cold-spray control of A. aegypti. Precautions must be taken seriously when using these products, such as following instructions on labels, using physical protection such as gloves and masks, and correctly disposing of chemicals.187 Integrated vector control programs that incorporate all three methods, along with public education and campaigns, are the most effective ways to control disease.183 One recent study demonstrated success of a low-technology strategy for vector control involving community education and participation, as well as biologic control of mosquito larvae using Mesocyclops copepods. Although A. aegypti and dengue transmission were eliminated in 32 rural Vietnamese communities, it remains unclear and unlikely that such a strategy would be as effective in more urban or westernized areas.80,99 Nevertheless, such integrated initiatives should also encourage vaccination, not only of humans, but of the animal reservoirs for which vaccines are available. This includes, for example, equine vaccinations against West Nile virus. Recently, leading health organizations have been trying to reinstate vector and disease control, as can be seen by a short

Insecticide Organophosphates Malathion Fenitrothion Naled Pirimiphos-methyl Pyrethroids Deltamethrin Resmethrin Bioresmethrin Permethrin Cypermethrin Lambda-cyhalothrin

Dosage (Grams of Active Ingredient per Hectare) 112-693 250-300 56-280 230-330 0.5-1 2-4 5 5 1-3 1

From World Health Organization: Dengue haemorrhagic fever: Diagnosis, treatment, prevention and control, ed 2, Geneva, 1997, World Health Organization.

history of their efforts. In the 1950s, WHO embarked on a mission to eradicate malaria. Despite some early success, by the mid1970s, it was increasingly difficult to achieve the eradication goal for a number of reasons, including resistance to DDT and other insecticides. However, in 1998, WHO, the United Nations Development Programme, the World Bank, and UNICEF established the Roll Back Malaria initiative with a special focus on Africa. One arm of the campaign is to encourage widespread use of antimalarial drugs in clinics and health centers with a simple diagnosis. The other objectives are to plan and implement sustainable vector control. Experience has shown that pyrethroidimpregnated bed nets may be a better global strategy for eradicating disease, because this approach is less expensive than repeated spraying of household walls, reduces infections (and thus the human reservoir for infection in malaria), and is more effective in terms of horizontal implementation than top-down, or vertical, programming.14 Although source reduction through environmental management has been shown to be effective in some places,180 it is generally very difficult and may not be feasible everywhere.157 Resistance to insecticides is a very real problem. However, it is often a local phenomenon, so certain chemicals and insecticides should not be completely abandoned once reports of resistance are raised. For example, sampling sites only a few kilometers apart in Guatemala showed a large difference in resistance for Anopheles albimanus mosquitoes. Similarly, in the United States, resistance of Culex species to organophosphates is high in areas where vector control is well implemented, but is lower in rural areas.73 WHO has developed bioassays to determine resistance and keeps a database of resistance. This database, however, can be misleading because it is based on a single dataset from a single point in time that may be several years, or even decades, old and no longer relevant.73 There are newer diagnostic methods to test resistance, including genetic linkage and physical maps, that may elucidate factors in vector competence.15 A further step is to detect and contain epidemics through epidemiologic surveillance and then to train personnel and build local capacity to sustain these efforts. Vector surveillance is of primary importance, not only to learn the geographic distribution and density of mosquito vectors and to evaluate control programs but also to predict and intervene to stop the advance of preventable diseases. For mosquitoes, indices have been created to study immature and adult populations (e.g., the “house index” [percentage of houses infected with larvae or pupae], and an index of adult mosquitoes’ landing or biting rates per person-hour). Surveillance also includes verification of control measures, which includes periodically testing the vector’s susceptibility to certain insecticides. Ongoing inspection of areas free of disease and taking measures to prevent reinfestation by vectors (e.g., removing standing water sources and environmental habitats, such as tires and cemetery vases) should be instituted.189 A list of references the WHO currently uses toward the goal of integrated 899

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

TABLE 48-3  Insecticides and Cold-Spray Control of

GLOBAL PROGRAMS

vector management can be found at http://www.who.int/malaria/ publications/vector-management/en/index.html. Many countries are committed to the idea of vector and disease surveillance (particularly aided by the work of bodies such as the Pan American Health Organization, the CDC, and WHO), but hundreds still fall short of pursuing these initiatives and are thus ill prepared to effectively control disease. Concerted

international efforts to collect accurate information and relay it in a timely fashion is the next herculean, but worthwhile, task.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 49 

Malaria SHERAL S. PATEL

Malaria is a major international health problem. As global travel increases, malaria is found with increasing frequency in areas in which malaria is not endemic. Human malaria is typically caused by four species of parasitic protozoa—Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae—that are transmitted by mosquitoes. Prevention of malaria infection through counseling, chemoprophylaxis, and personal protective measures can significantly reduce the risk of malaria morbidity in travelers. Because malaria infection can be life threatening, awareness of rapid diagnosis and management of this disease by health care providers are essential.

TABLE 49-1  Risk of Malaria by Region Risk

Region

High

Sub-Saharan Africa, Papua New Guinea, the Solomon Islands, and Vanuatu Indian subcontinent and Haiti Southeast Asia, Central America, and South America

Intermediate Low (but significant)

From the American Academy of Pediatrics: Malaria. In Pickering LK, Baker CJ, Long SS, et al, editors: Red Book: 2006 report of the Committee on Infectious Diseases, ed 27, Elk Grove Village, Ill, 2006, American Academy of Pediatrics, pp 435-441.

Epidemiology Malaria is endemic throughout tropical areas of the world and is usually transmitted to humans through the bite of a female Anopheles mosquito (Figure 49-1, online). Nearly 48% of the world’s population live in malaria-endemic areas.25 According to the World Health Organization (WHO), there were an estimated 243 million cases (5th to 95th percentiles, 190 to 311 million cases) of malaria worldwide in 2008, which resulted in an estimated 863,000 deaths (5th to 95th percentiles, 708 to 1.3 million deaths).64 The majority of the cases occurred in the African region (89%).64 Most malaria-related deaths occur among infants and young children. In Africa, malaria accounts for 20% of all childhood deaths. P. falciparum and P. malariae are found throughout malaria-endemic areas of the world, including Latin America, sub-Saharan Africa, Asia, and the South Pacific. P. vivax is endemic in Latin America, Asia, and the South Pacific, but uncommon in areas of sub-Saharan Africa. Both P. falciparum and P. vivax were historically endemic in temperate areas such as North America and Europe, and transmission still occurs rarely in these areas.38 Specifically, in the United States, anopheline mosquitoes are present (at least seasonally) in all states except Hawaii. Low frequencies of P. ovale infection are prevalent in most malaria-endemic areas, especially in West Africa. The risk of acquiring malaria is highest for travelers to subSaharan Africa and Oceania (i.e., Papua New Guinea, Vanuatu, and the Solomon Islands), intermediate in the Indian subcontinent and Haiti, and lowest (but still significant) in Southeast Asia and the Americas (Table 49-1).7 There can be variability in transmission within endemic areas based on season, altitude, and type of travel. For example, the risk of acquiring malaria is lower for a business traveler to a Southeast Asian city staying in an air-conditioned hotel than for a backpacker hiking and sleeping in tents in East Africa. Rates of malaria among U.S. civilians have been rising as travel to malaria-endemic areas increases.32 In 2009, there were 1484 cases of malaria in the United States reported to the Centers for Disease Control and Prevention (CDC).32 The majority were imported from malariaendemic areas of Africa (73%) and Asia (14%) and caused by 900

P. falciparum (46%).32 In addition, cases of malaria have been acquired in the United States, which indicates that transmission is possible in temperate areas where Anopheles mosquitoes are present.16,32 Parasite resistance to antimalarials has been increasing (Table 49-2).56 In addition, P. falciparum is becoming resistant to other antimalarials, such as mefloquine, pyrimethamine–sulfadoxine, and halofantrine (Figure 49-2).7 Pyrimethamine–sulfadoxine resistance is common throughout Africa. Mefloquine resistance has been demonstrated in Burma (Myanmar), Thailand, Cambodia, Vietnam, and China.7 In Southeast Asia, partial resistance of P. falciparum to quinine or quinidine has also been reported. Areas with reports of chloroquine-resistant P. vivax include Indonesia, Papua New Guinea, the Solomon Islands, Vanuatu, Myanmar, India, Brazil, and Guyana.3 Chloroquine-resistant P. malariae has been described in Sumatra.31 Many genetic changes in human red blood cells occur in areas where malaria is or was historically endemic, which suggests that these polymorphisms have arisen to protect individuals from malaria. Sickle cell disease, thalassemia, glucose6-phosphate dehydrogenase (G6PD) deficiency, and Southeast TABLE 49-2  Antimalarial Drug Resistance in

Malarial Parasites

Plasmodium Species P. falciparum

P. vivax P. ovale P. malariae

Drugs for Which Resistance is Established Chloroquine, mefloquine, pyrimethamine– sulfadoxine, and halofantrine; partial resistance to quinine and quinidine; resistance to multiple drugs Chloroquine, pyrimethamine–sulfadoxine, and primaquine None established None established

For online-only figures, please go to www.expertconsult.com

CHAPTER 49  Malaria

FIGURE 49-2  Geographic distribution of mefloquineresistant malaria. (From the Centers for Disease Control and Prevention: CDC health information for international travel 2012: The yellow book, New York, 2010, Oxford University Press. From Map 3-11, http://wwwnc.cdc.gov/ travel/pdf/yellowbook-2012-map3-11-distribution-mefloquine-resistant-malaria.pdf.)

India China

Vietnam

Burma Laos

Gulf of Tonkin

Thailand

Cambodia

Andaman Sea

Gulf of Thailand

Mefloquine-Resistant Malaria

Indonesia

Asian ovalocytosis (including Gerbich negativity) have all been suggested to confer protection from falciparum malaria mortality.42,55 In sub-Saharan Africa, nearly 100% of the population is negative for the Duffy blood group and has absolute protection against P. vivax, which depends on the Duffy antigen as a receptor for invasion.35

Malaria Parasite ETIOLOGY The malaria parasite is an intra-erythrocytic protozoan that is part of the Plasmodium genus. Plasmodium species infect mammals, birds, and reptiles. The four species that typically infect humans include P. falciparum, P. vivax, P. ovale, and P. malariae. The simian parasite P. knowlesi has been documented as a cause of severe infections and fatalities in Southeast Asia.17

MOSQUITO VECTOR The female Anopheline mosquito is the arthropod vector for the malaria parasite (Figure 49-3). Of almost 430 Anopheles species, only 30 to 40 transmit malaria (Figure 49-4). These include Anopheles gambiae, Anopheles funestus, and Anopheles arabiensis in Africa; the Anopheles punctulatus group in Papua New Guinea; Anopheles culicifacies in India; Anopheles darlingi in

Malaysia

South America; and Anopheles quadrimaculatus in North America.29 The female mosquito’s proboscis pierces the skin of a person to obtain the blood meal necessary for her to produce eggs. Distinguishing features of Anopheles mosquitoes include sensory palps that are as long as the proboscis and discrete blocks of black and white scales on the wings.5 Both male and female Anopheles mosquitoes rest with their abdomens sticking up in the air as opposed to parallel to the surface on which they are resting.6

LIFE CYCLE The life cycle of the malaria parasite involves both vertebrate and arthropod hosts (Figure 49-5). The asexual haploid form of the malaria parasite in the mosquito is the sporozoite. Transmission of 8 to 12 sporozoites usually occurs through the bite of a nocturnal-feeding female Anopheles mosquito (see Figure 49-3). Sporozoites then rapidly migrate through the bloodstream to the liver, where they mature and produce 10,000 to 30,000 merozoites per sporozoite. The merozoites are released into the bloodstream 8 to 25 days later to invade circulating erythrocytes (see Figure 49-5).21 A subset of P. vivax and P. ovale parasites may remain dormant as hypnozoites in the liver and emerge as merozoites months to years after the initial inoculation to establish blood-stage infection. Merozoites enter red blood cells rapidly through specific erythrocyte receptors, many of which are 901

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 49-3  Female Anopheles gambiae mosquito feeding. Distinguishing features include sensory palps that are as long as the proboscis and discrete blocks of black and white scales on the wings. Both male and female Anopheles mosquitoes rest with their abdomens sticking up in the air. (From the Centers for Disease Control and Prevention: Public Health Image Library. http://phil.cdc.gov/phil/home.asp. Left, image no. 1665; right, image no. 1664. Courtesy Dr. Jim Gathany and the Centers for Disease Control and Prevention.)

yet undefined. P. falciparum has several invasion pathways, including glycophorins A and C, whereas P. vivax depends solely on the Duffy antigen for erythrocyte invasion.65 In the red blood cell, the asexual parasites consume hemoglobin and enlarge from the ring forms to become trophozoites and then schizonts. As the schizonts mature through multiple nuclear divisions, the red blood cell bursts and releases 6 to 24 merozoites to invade additional circulating erythrocytes.4 The blood-stage cycle takes place over 48 to 72 hours. Some parasites

develop into gametocytes (the sexual stage), which can infect mosquitoes when taken up during a feeding. After being ingested by an Anopheles mosquito, diploid zygotes are formed. Zygotes mature into ookinetes in the mosquito midgut.47 The resulting oocyst expands through meiotic reduction division within 7 to 10 days and releases sporozoites that localize through the hemolymph to the salivary gland of the mosquito.4 The sporozoites are subsequently transmitted to another human host during the next blood meal.

Messeae Atroparvus Superpictus Sinensis Pulcherrimus Sacharovi Quadrimaculatus Fluviatilis Anthropophagus Sergentii Multicolor Pharoahensis Funestus, arabiensis Minimus Funestus and Stephensi and gambiae s.s. Albimanus arabiensis Culicifacies Sundaicus Melas Nunez-tovari Arabiensis Funestus and Dirus gambiae s.s. Annularis Punctulatus group Aquasalis Maculatus Gambiae s.s. Flavirostris Gambiae s.s. and funestus Darlingi Pseudopunctipennis Barbirostris Farauti

Freeborni

Labranchiae

Arabiensis and funestus

No vector Albimanus Annularis Anthropophagus Aquasalis Arabiensis Arabiensis and funestus Atroparvus

Barbirostris Culicifacies Darlingi Dirus Farauti Flavirostris Fluviatilis Freeborni

Funestus and arabiensis Funestus, arabiensis, and gambiae s.s. Funestus and gambiae s.s. Gambiae s.s. Gambiae s.s. and funestus Labranchiae Maculatus Marajoara

Melas Messeae Minimus Multicolor Nunez-tovari Pharoahensis Pseudopunctipennis Pulcherrimus

Punctulatus group Quadrimaculatus Sacharovi Sergentii Sinensis Stephensi Sundaicus Superpictus

FIGURE 49-4  Global distribution of malaria vectors. (From Kiszewski A, Mellinger A, Spielman A, et al: A global index representing the stability of malaria transmission, Am J Trop Med Hyg 70:486, 2004.)

902

A

MAJOR CLINICAL FINDINGS B

C

E D

F

FIGURE 49-5  Malarial parasite life cycle. During the malarial parasite life cycle, sporozoites are transmitted through the bite of a nocturnalfeeding female Anopheles mosquito (A). Sporozoites then migrate to the liver (B) and mature to merozoites (C). A subset of P. vivax and P. ovale parasites remains dormant as hypnozoites emerging months to years after the initial infection to cause disease. Eight to 25 days after the initial infection, 10,000 to 30,000 merozoites are released to invade erythrocytes (D). Asexual parasites mature in 48 to 72 hours, each releasing 6 to 24 merozoites to invade more erythrocytes (E). Some parasites develop into gametocytes (sexual stages), which are taken up during a mosquito blood meal. Diploid zygotes form ookinetes and develop into haploid sporozoites (F). The sporozoites migrate to the mosquito salivary gland and continue the life cycle in humans with the next blood meal. (Courtesy Sheral S. Patel, with permission.)

RECURRENT AND PERSISTENT INFECTIONS Recurrent malaria infection can occur in several ways. First, relapses from P. vivax or P. ovale can occur when dormant hypnozoites mature and release merozoites, thus producing blood-stage infections. Second, incomplete treatment or a partially effective host immune response can lead to low-concentration parasitemia and may lead to recrudescence of blood-stage infections. Relapse and recrudescence are caused by the same parasite clone that was responsible for the initial infection. Although recrudescence can occur with any malarial species, it is most common with P. falciparum because of antimalarial resistance. Finally, in areas of intense transmission, simultaneous infection or reinfection with multiple parasite species or strains can occur. P. malariae is frequently associated with persistent infections that can remain in the bloodstream at undetectable levels for up to 20 or 30 years.

TRANSMISSION Natural transmission of malaria occurs through the bite of a female Anopheles mosquito. Blood-stage infection can also be established by transfusions of blood or blood products, by organ transplantation, or by sharing contaminated needles or syringes.32,45 Occasionally congenital malaria occurs when mothers of newborns are infected.32,54 It may be difficult to distinguish congenital malaria from natural mosquito-borne transmission when the diagnosis is made in neonates 2 to 3 weeks after birth.

Clinical symptoms of malaria can develop as soon as 7 days to as late as several months after exposure in an area with endemic malaria. The majority of individuals who are diagnosed in the United States experience the onset of signs of symptoms after they return to the United States. A febrile illness in a traveler who has returned from a malaria-endemic area within the previous 3 months should be evaluated urgently. Red blood cell lysis and the release of merozoites at the end of a period of intraerythrocytic asexual reproduction result in the classic presentation of a malarial paroxysm, which is characterized by high fevers, chills, rigors, sweats, and headache (Table 49-3). Without appropriate therapy, paroxysms can recur in a cyclic pattern (i.e., every 48 hours with P. vivax and P. ovale and every 72 hours with P. malariae). Although P. falciparum has a 48-hour asexual erythrocytic cycle, fever and chills typically occur without any periodicity, because erythrocyte lysis is not synchronized. Patients with malaria infection may also present with gen­ eralized weakness, backache, myalgias, vomiting, diarrhea, and pallor. If an appropriate travel history is not obtained, malaria infection can be mistaken for a viral syndrome or acute gas­ troenteritis. In addition, severe malaria can mimic other diseases (e.g., meningitis, typhoid fever, dengue, hepatitis) that are common in malaria-endemic countries. Partially immune individuals who have recently arrived from endemic areas (e.g., immigrants, refugees) may be asymptomatic or have jaundice or signs of hepatosplenomegaly. Laboratory studies may reveal anemia and thrombocytopenia. Perinatal transmission of malaria is usually caused by P. falciparum and P. vivax. Clinical manifestations of congenital malaria can mimic neonatal sepsis and include fever, poor appetite, irritability, and lethargy.

COMPLICATIONS OF P. FALCIPARUM Infection with P. falciparum has a greater risk for complications and death than infection with the other three human malarial species. First, P. falciparum can invade erythrocytes of all ages TABLE 49-3  Clinical Manifestations and

Complications of Human   Plasmodium Infection

Plasmodium Species All species

P. falciparum

Clinical Manifestations and Pathogenesis SUSCEPTIBLE POPULATIONS Patients with malaria present with variable and nonspecific signs and symptoms ranging from asymptomatic parasitemia to severe disease and death. Individuals living in malaria-endemic areas develop partial immunity through repeated infections with malaria parasites and rarely experience serious complications after childhood. Nonimmune individuals—such as travelers and immigrants from nonendemic areas, children from the age of 6

P. vivax and P. ovale P. malariae

Manifestations and Complications Fever, chills, rigors, sweats, and headaches Weakness Myalgias Vomiting Diarrhea Hepatomegaly Splenomegaly Jaundice Anemia Thrombocytopenia Hyperparasitemia Cerebral malaria: seizures, obtundation, and coma Severe anemia Hypoglycemia Acidosis Renal failure Pulmonary edema (noncardiogenic) Vascular collapse Splenic rupture Relapse months to years after primary infection because of latent hepatic stages Low-grade fever and fatigue Chronic asymptomatic parasitemia Immune complex glomerulonephritis

903

CHAPTER 49  Malaria

months to 5 years who are living in endemic areas, and pregnant women—are at risk for severe disease and complications, especially with P. falciparum infection.2

PART 6  ANIMALS, INSECTS, AND ZOONOSES

and thus produce overwhelming parasitemia. Second, red blood cells that are infected with P. falciparum adhere to endothelial cells, leading to microvascular pathology not observed with other malarial species.34 Third, P. falciparum is frequently resistant to antimalarials (see Figures 49-1 and 49-2; Figure 49-1, online). Travelers from nonendemic areas, children, and pregnant women are at greatest risk for developing complications from malaria infection. A person is considered to have complicated malaria when the manifesting signs include altered mental status, seizures, profound anemia, respiratory distress, gross hematuria, shock, or severe laboratory abnormalities, including hypoglycemia, acidosis, signs of disseminated intravascular coagulation, and hyperparasitemia (see Table 49-3). These are summarized as follows: • Cerebral malaria: Acute neurologic events, such as seizures, obtundation, and coma, are associated with cerebral malaria. Cerebrospinal fluid examination is typically unremarkable, thus differentiating cerebral malaria from bacterial meningitis. Pathogenesis is a result of microvascular obstruction by parasitized erythrocytes, but neurologic impairment can result from multiple factors, including hypoglycemia, acidosis, impaired cerebral oxygenation from anemia, and pulmonary edema.37,50 The mortality rate can be as high as 15% to 30% in endemic areas, and higher in nonimmune adults (e.g., travelers). Children surviving episodes of cerebral malaria often have subtle cognitive and motor deficits.28 • Severe anemia: Overwhelming parasitemia (i.e., >106 parasitized red blood cells/µL or >20% parasitized circulating red blood cells) can develop rapidly in nonimmune individuals, resulting in severe anemia (i.e., hemoglobin level of 3 times normal Serum total bilirubin >2.5 mg/dL >500,000 parasites/mL or >10,000 mature trophozoites and schizonts/mL Hemoglobin 10-20 kg: 1 pediatric tab¶ daily >20-30 kg: 2 pediatric tabs¶ daily >30-40 kg: 3 pediatric tabs¶ daily ≥40 kg: 1 adult tab‡ daily

5 mg/kg base (6.5 mg/kg salt) orally, once/wk, up to maximum adult dose of 310 mg base

310 mg base (400 mg salt) orally, once/wk

1 adult tab‡ orally, daily

5 mg/kg base (8.3 mg/kg salt) orally, once/wk, up to maximum adult dose of 300 mg base

Pediatric Dose†

300 mg base (500 mg salt) orally, once/wk

Adult Dose

TABLE 49-7  Medications Used for the Prevention of Malaria*

Gastrointestinal upset, vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis

Headache, nausea, vomiting, abdominal pain, diarrhea, increased transaminase levels, and seizures

Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia

Adverse Effects

Take with food or milk. Contraindicated in persons with severe renal impairment (i.e., creatine clearance of 10 minutes) from the fang puncture wounds and from new injuries such as veni­ puncture sites and old partially healed wounds is the first clinical evidence of consumption coagulopathy. Spontaneous systemic hemorrhage is most often detected in the gingival sulci (see Figure 55-52, A). Bloodstained saliva and sputum usually reflect bleeding gums or epistaxis. True hemoptysis is rare. Hematuria may be detected a few hours after the bite. Other types of spon­ taneous bleeding are ecchymoses; intracranial and subconjuncti­ val hemorrhages; bleeding into the floor of the mouth, tympanic membrane, and gastrointestinal and genitourinary tracts; pete­ chiae; and larger discoid and follicular hemorrhages. Bleeding into the iliacus muscle may result in weakness of hip flexion. Hemorrhagic infarction of the anterior pituitary (resembling post­ partum Sheehan’s syndrome) may complicate envenoming by Russell’s vipers in Burma and India,234 and single cases have been 1074

reported from Brazil (alleged to have been caused by Bothrops jararacussu) and Sri Lanka.6 Menorrhagia and antepartum and postpartum hemorrhage have been described after envenoming by vipers.20 Severe headache and meningism suggest subarach­ noid hemorrhage. Evidence of a developing central nervous system lesion (e.g., hemiplegia), irritability, loss of consciousness, and convulsions suggest intracranial hemorrhage (see Figure 55-52, D) or cerebral thrombosis. Abdominal distention, tender­ ness, and peritonitis with signs of hemorrhagic shock but no external blood loss (hematemesis or melena) suggest retroperi­ toneal or intraperitoneal hemorrhage. Incoagulable blood result­ ing from defibrination or disseminated intravascular coagulation is a common and important finding in patients systemically envenomed by members of the following genera: Atheris, Daboia, Vipera, Echis, Gloydius, Calloselasma, Deinagkistrodon, and Trimeresurus (sensu lato). Intravascular hemolysis, causing hemoglobinemia (pink plasma) and black or grayish urine (hemoglobinuria or methe­ moglobinuria), has been convincingly described in patients bitten by Sri Lankan Russell’s viper (Daboia russelii),159 the Saharan horned viper (Cerastes cerastes)186 (see Figure 55-56), and Aus­ tralian western brown snakes (Pseudonaja spp.).98 Features of microangiopathic hemolysis that have suggested hemolytic uremic syndrome may progress to severe anemia and renal failure.186 Circulatory Shock (Hypotensive) Syndromes A decrease in blood pressure is a common and serious event in patients bitten by vipers, especially in the case of some of the Old World Viperinae (e.g., D. russelii, D. siamensis, D. palaestinae, V. berus, Bitis arietans, B. gabonica, and B. rhinoceros) (see Figure 55-51).138,148,275 Sinus tachycardia suggests hypovolemia resulting from external hemorrhage, blood loss into the tissues, or local or generalized increase in capillary permeability. Patients envenomed by Burmese Russell’s viper (D. siamensis) may develop conjunctival edema, serous effusions, pulmonary edema, hemoconcentration, and decrease in serum albumin concentra­ tion, all evidence of increased vascular permeability (see later discussion).148,219 Pulse rate may be slow or irregular if the venom affects the heart directly or reflexly (e.g., V. berus, B. arietans, Calloselasma rhodostoma). Vasovagal syncope may be precipi­ tated by fear and pain. Early, repeated, and usually transient syncopal attacks with features of anaphylaxis develop in patients bitten by some Viperidae (e.g., D. palaestinae, V. berus, V. aspis, D. siamensis, and D. russelii). Vomiting, sweating, colic, diarrhea (with incontinence), shock, bronchospasm, urticaria, and angio­ edema of the face, lips, gums, tongue, and throat may appear as early as 5 minutes or as late as many hours after the bite. Hypo­ tension is an important feature of anaphylactic reactions to anti­ venom (see later text). Renal failure can complicate severe envenoming by any species of snake, but it is common and the most frequent cause of death in victims of Russell’s viper. People bitten by Russell’s viper may become oliguric within a few hours of the bite. Loin pain and tenderness may be experienced within the first 24 hours and, in 3 or 4 days, the victim may become irritable, comatose, or convulsing, with hypertension and evi­ dence of metabolic acidosis. Neurotoxicity Neurotoxicity attributable to venom PA2s is a feature of enven­ oming by a few species of Old World Viperidae (e.g., Gloydius blomhoffii, G. brevicaudus, Bitis atropos, other small South African Bitis species, and Sri Lankan and south Indian Russell’s viper), some populations of Vipera aspis and V. berus,133,134 and New World tropical rattlesnakes (Crotalus durissus sub spp.). The clinical features are the same as with elapid envenoming (Figure 55-84; see Figures 55-53, E, and 55-54, A). Progression to respiratory or generalized paralysis is unusual but has been described. Associated generalized myalgia suggests the possibil­ ity of rhabdomyolysis. Pupillary dilation, causing visual distur­ bance from loss of accommodation, is a feature of severe envenoming by small Bitis species (e.g., B. peringueyi) and may be a permanent neurologic sequela that can be corrected tran­ siently by instillation of pilocarpine, as in some cases of krait bite envenoming.

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FIGURE 55-81  Asian cobras. A, Chinese cobra (Naja atra) (Hong Kong). B, Monocellate cobra (N. kaouthia) (Thailand). C, Indian spectacled cobra (N. naja) (Sri Lanka). Black and white (D) and brown (E) phases of Indo-Chinese spitting cobra (N. siamensis) (Thailand). F, Equatorial spitting cobra (N. sumatrana) (Singapore). (Copyright D.A. Warrell.)

ENVENOMING BY VIPERINAE Europe Envenoming by European Vipers (Figure 55-85).*  The common viper, or adder (V. berus) (Figure 55-85, C), the only venomous snake found in Britain, occurs in England, Wales, Scotland, and northern Europe (Figure 55-85, D and E), extending into the Arctic Circle and through Asia as far east as Sakhalin Island and south to northern Korea (see Figure 55-42, online). Four other vipers are widely distributed in mainland Europe: the nose-horned or sand viper (V. ammodytes) (Figure 55-85, A and B) in the Balkans, Italy, Austria, and Romania; the asp viper (V. aspis) in France (south of Paris), Spain, Germany, Switzerland, and Italy; Lataste’s viper (V. latastei) in Spain and Portugal; and Orsini’s viper (V. ursinii) in southeastern France, central Italy, and Eastern Europe. The Ottoman viper (Montivipera xanthina) (Figure 55-85, G) occurs around Istanbul and in some eastern Aegean islands, northern Greece, and Asia Minor. The Milos viper (Macrovipera schweizeri) (Figure 55-85, F) inhabits some of the Cyclades Islands, southeast of Greece, whereas the Levantine viper (Macrovipera lebetina) occurs on Cyprus. Clinical Features of the European Adder (Vipera berus) Bite.  Pain usually develops quickly at the site of the bite, and local *References 104, 140, 171, 251, 254, 257.

swelling is evident within a few minutes but is sometimes delayed for 30 minutes or longer. Local blisters containing blood are uncommon (Figure 55-86, A). Swelling and bruising with lymphan­ gitis may advance to involve the whole limb within 24 hours, extend to the trunk, and, in children, become generalized (Figure 55-86, B to D). A few cases of compartment syndromes and necro­ sis have been described. Pain, tenderness, and enlargement of local lymph nodes are sometimes noticeable within hours. Dra­ matic early systemic symptoms may appear within 5 minutes of the bite or be delayed for many hours. These include retching; vomiting; abdominal colic; diarrhea; incontinence of urine and feces; sweating; vasoconstriction; tachycardia; shock; angioedema of the face, lips, gums, tongue, throat, and epiglottis; urticaria; and bronchospasm. These symptoms may persist for as long as 48 hours. Hypotension is the most important sign. It usually develops within 2 hours. It may be transient, resolving spontaneously within 2 hours, persistent and recurrent, or progressive and fatal. ECG changes (see Figure 55-51, B) include flattening or inversion of T waves, ST-segment elevation, second-degree heart block, bradyar­ rhythmias or tachyarrhythmias, atrial fibrillation, and myocardial infarction. Defibrination (incoagulable blood) or milder degrees of coagulopathy and spontaneous bleeding into the gastrointesti­ nal tract, lungs, (see Figure 55-86, E) or urinary tract are uncom­ mon. Other clinical features include fever, drowsiness, and, rarely, coma and seizures secondary to hypotension or cerebral edema, respiratory distress/pulmonary edema (in children), acute kidney injury, cardiac arrest, intrauterine death, acute gastric dilation, 1075

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FIGURE 55-82  Envenoming by monocellate Asian cobra (Naja kaouthia). A, Local swelling and early darkening. B, Blistering and demarcated necrotic area. C, After debridement of necrotic tissue. D, Severe hypoxic brain damage in a boy bitten on his left ankle in Vietnam. There was a delay in resuscitating him after development of respiratory paralysis. (Copyright D.A. Warrell.)

paralytic ileus and acute pancreatitis. Laboratory findings include neutrophil leukocytosis (more than 20 × 109/L in severe cases), thrombocytopenia, initial hemoconcentration and later anemia, resulting from leakage of plasma and blood cells out of blood vessels into the bitten limb, and, rarely, hemolysis, elevation of serum creatine kinase, and metabolic acidosis. Deaths usually

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occur from 6 to 60 (average 34) hours after the bite. Most adder bites cause only trivial symptoms; patients must be assessed indi­ vidually. Children may be severely envenomed; in a French series, there were three deaths in a group of seven children between 2.5 and 10 years of age. The dangers of adder bite should not be underestimated.

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FIGURE 55-83  Venom ophthalmia after venom “spitting” by black-necked spitting cobra (Naja nigricollis) in Nigeria. A to C, Acute effects— blepharospasm, inflammation, leukorrhea, epiphora. D, Hypopyon. E, Panophthalmitis following neglected corneal abrasion. F, Corneal opacity causing blindness. (Copyright D.A. Warrell.)

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FIGURE 55-84  Neurotoxic envenoming by Viperidae. Ptosis (A) and mydriasis (B) after berg adder (Bitis atropos) bite in Drakensberg, South Africa. C, B. atropos specimen from South Africa. (A and B courtesy Craig Smith; C copyright D.A. Warrell.)

Envenoming by other European and Mediterranean vipera produces similar features, most severe in the case of M. lebetina (Cyprus), V. ammodytes, and V. aspis bites, and least severe in V. ursinii and V. latastei bites. It is surprising that bites by M. schweizeri (Cyclades Islands, Greece) do not appear to result in severe envenoming. Some populations of V. aspis zinnikeri and V. aspis in southeastern France and of V. berus in Hungary can cause mild neurotoxic envenoming.133,134

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Africa Envenoming by Saw-Scaled or Carpet Vipers (Genus Echis) (Figure 55-87; See Figures 55-14, A and 55-18, C).*  This genus of vipers is of great medical importance. It is widely distributed in *References 249, 265, 267.

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FIGURE 55-85  European Viperidae. A, Vipera ammodytes. B, V. ammodytes (Montenegro). C, Vipera berus (England). D, Melanistic V. berus (Russia). E, V. berus bosniensis (Hungary). F, Macrovipera schweizeri (Milos). G, Montivipera xanthina (Turkey). ( A to D, F, and G copyright D.A. Warrell; E courtesy Tamás Malina.)

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FIGURE 55-86  Envenoming by Vipera berus. A, Hemorrhagic blister at site of bite. B, Swelling of bitten limb. C, Bruising of the bitten limb. D, Generalized swelling and bruising in a 4-year-old child in Sweden. E, Chest radiograph showing extensive intrapulmonary bleeding. (A copyright D.A. Warrell; B courtesy Mark Brueton; C and E courtesy H. Bowker; D courtesy Hans Persson.)

the northern third of Africa from Senegal in the west to the Tana River in Kenya in the south and through the Middle East. Through­ out this range, it is usually the most important cause of human snakebite morbidity and mortality. Bites are most common in West Africa, where E. ocellatus (see Figure 55-18, C) is the most important species.55,242,267,268 In Nigeria, only 4% of patients admit­ ted to the hospital lacked signs of envenoming, the lowest rate of “dry bites” reported in any large case series. The remainder had both local and systemic envenoming. Twelve percent devel­ oped local blistering, and 9% developed necrosis (Figure 55-88, A and B). Coagulopathy (attributable to venom prothrombin activators and factor X activators) was universal; 55% of victims showed spontaneous systemic bleeding (see Figures 55-52, A, B, E, and F and 55-88, C to G), usually from the gingival sulci (Figure 55-88, C), but thrombocytopenia (platelet count less than 103 × 109/L or 103,000/mm3) was detected in only 7%. Soluble fibrin complexes and fibrin/fibrinogen breakdown products were detected, but heparin does not inhibit Echis thrombin in vitro or in patients.55,97,267 The case fatality rate of 3.6% was attributable to hemorrhagic shock (three cases) (Figure 55-88, E to G; see Figure 55-52, F) and intracerebral hemorrhage (two cases) (Figure 55-88, D). Envenoming by eastern and North African E. pyramidum is generally less severe, but fatalities are reported in Turkana and Wajir in northern Kenya and in Somalia. One patient bitten by a Tunisian E. leucogaster developed transient ptosis.74,262 Echis species cause most fatal snakebites in the Middle East.247,249,253 Envenoming by African Puff Adders (Bitis arietans) (Figure 55-89; See Figure 55-11).*  This species (or species complex) is thought to be responsible for many of the bites throughout the African savanna region. Local swelling is often very extensive, commonly extending to involve the entire bitten limb and spread­ ing to the trunk (Figure 55-90, A).275 This extravasation of plasma causes hypovolemic shock, a common manifesting feature. Local blistering and necrosis may be extensive, requiring amputation of the bitten digit or even part or all of the bitten limb (Figure 55-90, B). Major arteries may become thombosed or entrapped by swollen tissue22 in the bitten limb, increasing local tissue damage. Compartment syndromes may develop, especially involving the anterior tibial compartment after bites on the feet *References 249, 284.

1078

and ankles. These may lead to ischemic muscle necrosis, as in Volkmann’s ischemic contracture of the forearm. Direct myocar­ dial effects and arrhythmias, commonly sinus bradycardia, may contribute to hypotension. In West Africa, envenoming by B. arietans causes spontaneous bleeding, bruising and petechial hemorrhages on serosal surfaces, attributable to thrombocytope­ nia but not coagulopathy. However, in East and South Africa, coagulopathy, and rarely even cerebral thrombosis, have been reported. This regional variation in the pattern of envenoming suggests that there may be different species of puff adder. Envenoming by Giant Rain Forest Vipers or Adders (Bitis gabonica, Bitis rhinoceros and Bitis nasicornis) (Figure 55-91; See Figure 55-34, B).*  These giant rain forest species are the commonest cause of snakebite in some areas of Africa, for example in southern Nigeria and the eastern Democratic Repub­ lic of Congo. In light of their wide distribution, prodigious size, enormous fangs, and massive yield of highly potent venom, it is surprising that so few cases of envenoming have been reported. Local effects of envenoming may be less severe than those pro­ duced by puff adder bites, but swelling, bruising, blistering, and necrosis are common (Figure 55-92). Systemic symptoms may be early and dramatic, including dizziness, chest tightness, nausea, and vomiting. In one case, there was early paralysis of visual accommodation and deafness, suggesting neurotoxicity. Cardio­ vascular abnormalities, including hypotension and hypovolemic and cardiogenic shock, arrhythmias, and ECG changes, are reported. Spontaneous systemic bleeding is a common feature, whereas hemostatic abnormalities include thrombo­cytopenia, inhibition of platelet aggregation, and evidence of thrombin-like and fibrinolytic activities.138 Envenoming by the Berg Adder (B. atropos) (See Figure 55-84).  This mountain species has been responsible for enven­ oming rock climbers and mountain travelers in Zimbabwe and South Africa. It is the most neurotoxic of African vipers and can cause other unusual symptoms. After initial severe pain and rapidly spreading local swelling (with rare development of necro­ sis), there are paresthesias of the tongue and lips, blurring of vision, loss of the senses of taste and smell, nausea, vomiting, *References 249, 262.

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FIGURE 55-87  Saw-scaled or carpet vipers. A, Echis carinatus carinatus (Tamil Nadu, India). B, Echis carinatus multisquamatus (Russia). C, Echis carinatus sochureki. D, Echis coloratus (Saudi Arabia). E, Echis jogeri (Senegal). F, Echis pyramidum leakeyi (Baringo, Kenya). (A to D, F and G copyright D.A. Warrell; E courtesy Wolfgang Wüster.)

and dizziness. In one series of cases, ptosis, external/internal ophthalmoplegia, dilated pupils, loss of visual accommodation, and anosmia were reported in 93% of cases (see Figure 55-84). There was respiratory paralysis in 72%, hyponatremia (attributed to a natriuretic hormone–like toxin) and dysphagia in 64%, and convulsions in 29%.146Only one fatal case has been reported. Envenoming by Bush Vipers (Genera Atheris, Proatheris, and Others) (Figure 55-93).*  These mainly arboreal species seem more likely to bite Western snake enthusiasts than indig­ enous Africans. Envenoming by them has been underestimated. Bites by Atheris ceratophora, A. desaixi, and A. nitschei caused only local effects: transient pain, swelling, bruising, and residual arthrodesis. However, a prominent feature of severe envenoming by A. squamigera and A. chlorechis was hypotension, perhaps attributable to a new class of peptides containing small poly-His and poly-Gly segments identified in venoms of A. squamigera, A. chlorechis, and A. nitschei. A man bitten by a large green bush viper (A. squamigera) developed massive swelling of the bitten limb and incoagulable blood. He died 6 days later in hemorrhagic shock following hematemesis. In other cases of bites by this species, there were immediate severe pain, swelling, local bruis­ ing, dizziness, shivering, nausea, and local lymphadenopathy. A man bitten by a Western bush viper (A. chlorechis) developed a severe bleeding diathesis, hypotension, acute kidney injury, and

*References 259, 262.

C

hemolysis but survived. Three men were bitten by captive speci­ mens of lowland or swamp adders (P. superciliaris). All experi­ enced severe and persistent pain, initially in the bitten limb but later spreading to the trunk and back; local swelling (local necro­ sis in one); intravascular hemolysis (schistocytes in one) with hyperbilirubinemia; thrombocytopenia; fibrinolysis (elevated Ddimer); elevated aspartate aminotransferase and other serum enzymes; oliguric acute kidney injury requiring dialysis in two cases; and slow recovery over several weeks. One presented with severe persistent nausea, vomiting, and diarrhea. Two had con­ sumptive coagulopathy, two hematuria or hemoglobinuria, and two became hypertensive and developed pulmonary congestion with arterial desaturation. In one case, imaging suggested bilat­ eral intrarenal vascular occlusion that progressed to renal cortical necrosis, and later myocardial ischemia, leaving him with intrac­ table renal failure.259 Envenoming by Desert Vipers (Genus Cerastes) (Figure 55-94).*  C. cerastes, C. gasperettii, C. vipera, and Pseudocerastes persicus inhabit the vast arid deserts of North Africa and the Middle East, where they are the most common cause of snake­ bite. A few fatal cases were reported in the 19th-century French colonial military literature, but there have been no recent reports. Envenoming usually results in local pain and swelling, compli­ cated by necrosis in some cases. Nausea, vomiting, spontaneous

*Reference 186.

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FIGURE 55-88  Envenoming by West African carpet viper (Echis ocellatus) in northern Nigeria. A and B, Local necrosis. C, Bleeding from gums and into floor of mouth. D, Subarachnoid hemorrhage causing meningism. E to G, Autopsy finding of bleeding into the lungs, kidneys, and bladder. (Copyright D.A. Warrell.)

Asia Envenoming by Saw-Scaled or Carpet Vipers (Genus Echis) (See Figure 55-88, A to C ).*  E. carinatus occurs in western Asia, as far north as the Aral Sea, and throughout the Indian subcon­ tinent, including Sri Lanka, as far as the border of West Bengal. It is prodigiously common in some areas of India and Pakistan (e.g., in Sind and Jammu), where it is the major cause of snake­ bite morbidity and mortality.20,111,265 In northern India ( Jammu) and in western India (Rajasthan), envenoming by E. carinatus sochureki caused symptoms similar to those observed in Nigeria (see Figures 55-50, F, 55-52, B and F, and 55-88, D to G).20,111

Envenoming by Western and Eastern Russell’s Vipers (Daboia russelii and D. siamensis) (See Figure 55-13).*  These medically important species occur from Pakistan in the west through India and Sri Lanka, north into Nepal21 and Bhutan (D. russelii), and as far east as West Bengal; and in Southeast Asia, southern China, Taiwan, and in parts of Indonesia19 (D. siamensis) (Figure 55-95, online). Throughout this range, there are intriguing geographic variations in the clinical mani­ festations of envenoming that reflect differences in venom composition.56,162,231,243,244 Sri Lanka.  D. russelii (see Figure 55-13, A) is a major cause of venomous snakebites. Of patients bitten by this species, 28% showed no clinical evidence of envenoming.8,11,159 Apart from typical features of viperine envenoming (local envenoming, coag­ ulopathy, bleeding, and sometimes shock [see Figures 55-50, B to F, and 55-51]), there were distinctive features of neuromyo­ toxicity attributable to venom PLA2: ptosis (77%), external

*References 250, 262.

*References 244, 262.

bleeding, and coagulopathy have been observed in some cases. Recently, disseminated intravascular coagulation, microangio­ pathic hemolysis, and acute tubular necrosis were described in two proven cases of envenoming by C. cerastes (see Figure 55-56).186

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FIGURE 55-89  African puff adder (Bitis arietans). A, Specimen from Saudi Arabia. B, Dorsal view of head showing large nostrils. C, Showing fangs. (Copyright D.A. Warrell.)

ophthalmoplegia (82%) (Figure 55-96, A), inability to open the mouth (23%) or to swallow and protrude the tongue, generalized muscle tenderness (32%), and myoglobinuria (27%) (Figure 55-96, B). Most patients showed evidence of intravascular hemo­ lysis. Acute renal failure was a common feature of severe enven­ oming. Single or multiple medium-to-large cerebral arterial thromboses have been described,71 as well as the more familiar hemorrhagic strokes. Similar findings have been reported from envenoming by D. siamensis in Tawain.95 A single case of hypo­ pituitarism has been detected.6 India.  In most parts of the country, D. russelii is an important cause of snakebite, but in Jammu in the northeast, only 4 of 310 identified viperine bites were caused by this species.20 In Kerala, South India, neurotoxic signs, such as ptosis and ophthalmople­ gia, associated with hemostatic disorders, are familiar signs of envenoming by this species, and bilateral parotid enlargement is also described.54 Features of panhypopituitarism, manifesting between 1 month and 1 year after the bite, were observed in 7 of 1000 cases of snakebite, and there was 1 case of diabetes insipidus. Especially in the south, Russell’s viper bite is the most common cause of acute kidney injury in both adults and children. Burma.  Russell’s viper (D. siamensis) is the most important cause of snakebite morbidity and mortality. However, about onethird of all patients hospitalized after proved Russell’s viper bites

A

B FIGURE 55-90  Envenoming by puff adder (Bitis arietans). A, Swelling and blistering of bitten limb. B, Necrosis in neglected case (KwaZulu Natal, South Africa). (A copyright D.A. Warrell; B courtesy Paul Rollinson.)

develop no clinical evidence of envenoming at any stage. In Tharrawaddy, north of Rangoon, two distinct populations of Rus­ sell’s vipers were found to be responsible for bites during the November to January rice harvest. Smaller snakes (125 to 375 mm [4.9 to 14.8 inches] in total length) had probably been born that year, whereas the larger snakes (500 to 1125 mm [19.7 to 44.3 inches] in total length) had been born in previous years.233 Bites by larger snakes were associated with more intense local swelling (Figure 55-96, C) and a higher risk for systemic envenoming.233 Severe systemic envenoming can result, despite there being little or no local evidence of envenoming. Spontaneous bleeding (gums, epistaxis, hemoptysis, hematemesis, hematuria) develops within a few hours and may result in fatal cerebral hemorrhage (see Figure 55-52, D). A sign, apparently unique to Russell’s viper bite in Burma, is orbital and conjunctival edema with conjunctival hemorrhages (Figure 55-96, D and E), which develops in severe cases and is evidence of generalized increase in capillary perme­ ability. Other manifestations of this permeability syndrome are facial edema, pleural effusions, ascites, pulmonary edema (Figure 55-96, F), and transient proteinuria with hypoalbuminemia.219 Other clinical features include hypotension and shock (see Figure 55-51, A and C), epigastric and chest pain, and development of acute renal failure within 3 to 4 days of the bite (see Figure 55-55, A and B). This is associated with bilateral loin tenderness and hypertension. In some cases, spontaneous diuresis began within 7 to 10 days, followed by complete recovery without residual renal abnormalities. Some patients developed a late hemorrhagic syndrome with recurrent shock and at autopsy were found to have hemorrhagic infarction of the anterior pituitary (Figure 55-96, G), and in some cases adrenal glands, intracranial hemor­ rhage, and swollen hemorrhagic kidneys.6,234 Renal angle tender­ ness predicted the development of oliguria (sensitivity 0.7, specificity 0.9).219,224 Russell’s viper venom contains a number of different components that affect hemostasis, including procoagu­ lants (activating factors X, IX, and V, and protein C), fibrinolytic agents, platelet aggregating and inhibiting factors, an anticoagu­ lant, and a hemorrhagin.97 In human patients, the most striking laboratory features are depletion of fibrinogen, factors V, X, and XIIIa, antithrombin III, plasminogen, antiplasmin, protein C, and platelets. There are high levels of fibrin/fibrinogen-related antigen, mostly cross-linked in the form of D-dimer.210,211 At autopsy, there is widespread evidence of bleeding but also fibrin deposition, occluding small blood vessels in the pituitary, lungs (Figure 55-96, H), and kidneys.209 Some patients who survived the acute pituitary adrenal crisis described presented later with more insidious symptoms of panhypopituitarism, including loss of libido, impotence, loss of secondary sexual hair, hypotension, amenorrhea, and features of hypothyroidism (Figure 55-96, I).234 Thailand.  Russell’s viper bites are common in the central rice-growing area of Thailand, but although the snake is appar­ ently the same species (D. siamensis) as in adjacent Burma, clinical features are generally less severe, although there have been deaths attributed to shock, cerebral hemorrhage, and acute kidney injury.125 1081

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FIGURE 55-91  Giant rain forest vipers or adders. A, Eastern Gaboon/Gabon viper (Bitis gabonica) (South Africa). B and C, Western rhinoceros viper (Bitis rhinoceros) (Ghana). D to F, Rhinoceros-horned viper or river jack showing nasal horns (B. nasicornis) (Cameroon). (Copyright D.A. Warrell.)

pain, shock, acute renal failure, bleeding gums, and ecchymoses. Neurotoxic features are confined to ptosis and external ophthal­ moplegia, which can develop between 1 and 48 hours after the bite. In the oriental region of China, north of latitude 25 degrees north, the Chinese mamushi (G. brevicaudus) is the most common cause of snakebite. There is local swelling, together with neuro­ toxic symptoms, such as blurring of vision, ptosis, and diplopia within 24 hours of the bite. Breathlessness, dysphagia, and dif­ ficulty opening the mouth are associated with symptoms suggest­ ing generalized rhabdomyolysis. Some patients require assisted ventilation.

ENVENOMING BY PIT VIPERS (CROTALINAE)* Envenoming by Japanese and Chinese Mamushis (Gloydius [Agkistrodon] blomhoffii, G. brevicaudus, and others) (Figure 55-97) In Japan, bites by the Japanese mamushi (G. blomhoffii) are mainly inflicted on the hands. There is local swelling with blister­ ing, nausea, vomiting, fever, headache, abdominal and lumbar *References 249, 256.

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FIGURE 55-92  A and B, Envenoming by Gaboon viper (Bitis gabonica) showing pulmonary edema, swelling, and bruising after a bite on the wrist. (From McNally T, Conway GS, Jackson L, et al: Accidental envenoming by a Gaboon viper (Bitis gabonica): The haemostatic disturbances observed and investigation of in vitro haemostatic properties of whole venom, Trans Roy Soc Trop Med Hyg 87:66, 1993; copyright D.A. Warrell).

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FIGURE 55-93  African bush vipers. A, Usambara bush viper (Atheris ceratophora) (Tanzania). B, Mt Kenya bush viper (A. desaixi) (Kenya). C, Rough-scaled bush viper (A. hispida) (Kakamega, Kenya). D, A. squamigera. E, Swamp adder (Proatheris superciliaris) (Malawi). (Copyright D.A. Warrell.)

Envenoming by the Malayan Pit Viper (Calloselasma rhodostoma) (Figure 55-98)*

55-52, B and D). Most patients have profound thrombocytopenia, probably resulting from sequestration. Fatal cases in Thailand were attributed to cerebral hemorrhage, shock, tetanus, septice­ mia, and anaphylaxis.125

This species is an important cause of snakebite in northwestern Malaysia, Thailand, Laos, Cambodia, Vietnam, and Java (see Figure 55-98, A). It inhabits coffee and rubber plantations and rice fields in areas of cleared jungle. Bites are a major occupa­ tional hazard of plantation workers (see Figure 55-47, C). About one-half the patients develop minimal or no envenoming, but in the remainder, local swelling starts within minutes and reaches its maximum after 24 to 72 hours (see Figure 55-50, B to D). Local necrosis develops in 11% of victims and is always preceded by blistering (Figure 55-99, A to C). Secondary infection by bac­ teria peculiar to the venom and oral cavity of the snakes is common, and fatal tetanus may ensue (Figure 55-99, E).215 The blood becomes incoagulable as early as 30 minutes after the bite and, in untreated patients, may persist for 1 to 26 days.173 There is associated bleeding from sites of trauma (see Figure 55-49), gums, ecchymoses, and elsewhere (see Figures 55-50, D and

Envenoming by Asian Arboreal Pit Vipers (Genera Trimeresurus, Cryptelytrops [Trimeresurus], Viridovipera, Protobothrops [Trimeresurus], and others) (See Figures 55-39 and 55-40)* In Thailand, the white-lipped green pit viper (C. albolabris) is the most widely distributed venomous snake and the second most common cause of snakebite (27% of cases).239 Pain and swelling develop early after the bite, spreading to involve more than one-half the bitten limb in 46% of cases. Local bruising and tender enlargement of local lymph nodes are common, whereas local blistering and necrosis are rare (Figure 55-100, A to C ). Coagulopathy, thrombocytopenia, and leukocytosis may develop. In Burma, C. erythrurus bites resulted in no evidence of envenoming in 65% of cases. In the rest, there

*References 173, 175, 272.

*References 96, 250, 271.

A

B

FIGURE 55-94  A and B, Sahara horned viper (Cerastes cerastes) (Algeria) showing supraocular horns. (Copyright D.A. Warrell.)

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A

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

B

C

D

G

E

H

F

I

FIGURE 55-96  Envenoming by Russell’s vipers in Sri Lanka (Daboia russelii)—A, Neurotoxicity. B, Myotoxicity. In Burma (Daboia siamensis). C, Local swelling, blistering, and necrosis. D and E, Chemosis and subconjunctival hemorrhage. F, Pulmonary edema. G, Hemorrhagic infarction of anterior pituitary. H, Fibrin deposition in pulmonary blood vessels. I, Chronic pan-hypopituitarism showing loss of secondary sexual hair and testicular atrophy. (A to G and I copyright D.A. Warrell; H courtesy Nicholas Francis.)

FIGURE 55-97  Chinese (short-tailed) mamushi (Gloydius brevicaudus) (Beijing). (Copyright D.A. Warrell.)

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was local swelling without necrosis, incoagulable blood, and thrombocytopenia. In Bangladesh, most victims of bites by this species show no coagulopathy and recover without antivenom treatment. Although the Indian bamboo viper (T. gramineus) is the most abundant pit viper in the southern half of India, there is little reliable information about the effects of envenom­ ing. In south India, the Malabar pit viper (T. malabaricus) is said to commonly cause local necrosis.96 In Thailand, the dark green pit viper (Cryptelytrops [Trimeresurus] macrops) is a common cause of mild envenoming in some areas, notably in gardens in central Bangkok, whereas the Kanchanaburi pit viper (Cryptelytrops [Trimeresurus] kanburiensis) is capable of causing severe envenoming (Figure 55-100, D).271 The Chinese habu (P. mucrosquamatus) causes about one-third of venom­ ous snakebites in Taiwan and results in an 8% case fatality rate, whereas the Chinese green pit viper (V. stejnegeri), although responsible for 53% of bites in Taiwan, carries a case fatality rate of only 1%. Bites by P. mucrosquamatus are more likely to cause local necrosis and rhabdomyolysis.36

Probable distribution range Localities from which specimens have been collected

Burma (Myanmar)

Laos

Thailand Vietnam

?

Cambodia

Brunei Sabah

West Malaysia

B

Sarawak Kalimantan Sumatra

A

Karimunjawa Archipelago Kangean Islands Java

D

C

FIGURE 55-98  Malayan pit viper (Calloselasma rhodostoma). A, Distribution. B to D, specimens from Thailand showing dorsal pattern and fangs (A courtesy Jenny Daltry; B to D copyright D.A. Warrell.)

Envenoming by Latin American Pit Vipers (Genera Bothrops, Bothriopsis, Crotalus, Lachesis)* Agkistrodon, Bothrops (Bothriopsis), and Others (Figure 55-101; See Figures 55-7, 55-22, E, and 55-34, A).  Local envenom­ ing may appear within 15 minutes but rarely may be delayed for *Reference 256.

A

D

B

E

several hours. Swelling spreads rapidly, sometimes to involve the entire bitten limb and adjacent areas of the trunk (Figure 55-50, E). There are associated pain, tenderness, and enlargement of regional lymph nodes. Bruising may extend up the bitten limb, especially in lines along the path of superficial lymphatics and over regional lymph nodes. There may be persistent bleeding from the fang marks if the blood is incoagulable. Blistering may appear at the site of the bite within the first 12 hours, and necro­ sis of skin, subcutaneous tissue, and muscle develops in up to

C

FIGURE 55-99  Envenoming by Malayan pit viper (Calloselasma rhodostoma). A, Severe blistering and bruising. B, Diffuse ecchymoses, shock, and gangrene of the bitten arm 4 days after the bite, when the patient was finally brought to the hospital. C, Gangrene. D, Bleeding gums. E, Tetanus complicating snakebite wound infection. (Copyright D.A. Warrell.)

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China

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

B

C

D

FIGURE 55-100  Envenoming by arboreal green pit vipers (genus Cryptelytrops [Trimeresurus]): bites by white-lipped green pit viper (C. albolabris). A and B, Swelling of bitten arm and the snake responsible (Thailand). C, Local necrosis (Vietnam). D, Local swelling after a bite by a Kanchanaburi pit viper (C. kanburiensis) (Thailand). (Copyright D.A. Warrell.)

A

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G

B

C

E

F

H

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FIGURE 55-101  Latin American pit vipers. A, Cantil (Agkistrodon bilineatus) (Mexico). B, Central American jumping viper (Atropoides mexicanus) (Guatemala). C, Small-eyed toad-headed pit viper (Bothrocophias microphthalmus) (Garagoa, Boyaca, Colombia). D, Terciopelo (Bothrops asper) (Caucasia, Colombia). E, Common lancehead (Bothrops atrox) (Para, Brazil). F, Papagaio (Bothrops bilineatus smaragdinus/Bothriopsis bilineata smaragdina) (Napo, Ecuador).G, Jararaca (Bothrops jararaca). H, Jararacuçu (Bothrops jararacussu) (Brazil). I, Serpent of St. Lucia (B. caribbaeus). (Copyright D.A. Warrell.)

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A

B

D

F

I

epistaxis, hematemesis, hematuria, intracranial (Figure 55-102, J) and subconjunctival hemorrhages and bleeding into the gastro­ intestinal and genitourinary tracts. Women may develop menor­ rhagia and pregnant women antepartum or postpartum may develop hemorrhages with hemorrhagic abortion of the fetus. Severe headache and meningism suggest subarachnoid hemor­ rhage, whereas hemiplegia and other lateralizing neurologic signs, irritability, loss of consciousness, and convulsions suggest intracranial hemorrhage or cerebral thrombosis. Abdominal

C

E

G

H

J

FIGURE 55-102  Envenoming by South American lanceheads (genus Bothrops). A, Swelling and bruising after bite on hand by papagaio (B. bilineatus smaragdinus) (Largo Agrio, Ecuador). B, Local blistering after bite by jararaca (B. jararaca) (São Paulo, Brazil). C, Severe blistering after bite by common lancehead (B. atrox) (Pucallpa, Peru). D, Blistering and necrosis after bite by B. atrox (Pucallpa, Peru). E, Liquefaction-necrosis of anterior tibial compartment after bite by B. marajoensis (Marajo, Brazil). F, Gangrene after bite by terciopelo (B. asper) (Pedro Vicente Maldonado, Ecuador). G, Abscess developing 5 days after bite by B. atrox (Pastaza, Ecuador). H, Bleeding gums after bite by B. jararaca (São Paulo, Brazil). I, Spitting out blood in sputum after B. atrox bite (Pastaza, Ecuador). J, Cerebral hemorrhage after bite by B. atrox (Pastaza, Ecuador). (A to E and G to J copyright D.A. Warrell; F courtesy David Gaus.)

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10% of hospitalized cases (Figure 55-102, A to F). Bites on the digits (fingers and toes) and in areas draining into the tight fascial compartments, such as the anterior tibial compartment, are par­ ticularly likely to cause necrosis. Absence of detectable local swelling 2 hours after a viper bite usually means that no venom has been injected. Secondary bacterial infections may manifest as subcutaneous abscesses or more diffuse cellulitis (Figure 55-102, G). Spontaneous systemic hemorrhage occurs from the gingival sulci (see Figures 55-52, A and 55-102, H and I) as

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

C

B

D

FIGURE 55-103  Latin American rattlesnakes (genus Crotalus). Tropical rattlesnakes (Brazil). A, C. durissus cascavella. B, C. durissus collilineatus. C, C. durissus ruruima. D, Central American rattlesnake (C. simus) (Guerrero, Mexico). (Copyright D.A. Warrell.)

distention, tenderness, and peritonism with signs of hemorrhagic shock but no external blood loss suggest retroperitoneal or intra­ peritoneal hemorrhage. Hypotension and circulatory shock causing loss of vision and then consciousness may occur a short time after the bite. Acute kidney injury can complicate cases of severe envenoming (see Figure 55-55, C). Thromboses of smallto medium-sized cerebral, pulmonary, coronary, or mesenteric arteries are features of envenoming by the fer de lance of Marti­ nique (B. lanceolatus) and the serpent of St Lucia (B. caribbaeus) (see Figure 55-101, I).80,131,220 Cerebral thrombosis has also been described in patients envenomed by Daboia russelii in Sri Lanka, D. siamensis in Taiwan, Bitis arietans in South Africa, and some species of North American rattlesnakes (e.g., Crotalus oreganus helleri). The terciopelo (B. asper) and common lancehead (B. atrox) are responsible for many cases of severe envenoming in Central and South America, resulting in death or permanent disability.155 The larger, B. asper (exceptionally up to 2.5 m (8.2 feet) in total length), seems even more inclined than B. atrox to strike if cor­ nered, molested, or inadvertently trodden upon or touched. Its habit of raising its head high off the ground can result in bites above knee level. The jararaca (B. jararaca) is an important cause of envenoming in southeastern Brazil and in adjacent northeastern Paraguay and northern Argentina. Clinical effects are generally less severe than with B. asper and B. atrox enven­ oming, but coagulopathy, bleeding, and local necrosis are common.31,181,256 The jararacuçu (B. jararacussu) is a bulky snake with a high yield of unusually potent venom. It has a formidable reputation for causing severe bleeding, fibrin deposition, local necrosis, shock, and acute kidney injury that often prove fatal.143 Crotalus (Figure 55-103; See Figure 55-16).  The two species of Latin American (tropical) rattlesnake, Crotalus simus in Central America and C. durissus in South America, pose a serious medical problem in many parts of their ranges. Severe systemic envenom­ ing by the tropical rattlesnake (C. durissus terrificus) may occur in the absence of local signs. Neurotoxic envenoming develops only in victims of populations of some subspecies of C. durissus, such as C. d. terrificus, C. d. collilineatus, and C.d. cascavella. 1088

Typical elapid-type descending paralysis (Figure 55-104, A; see Figure 55-53, E) may result in life-threatening respiratory paraly­ sis. Venom myotoxins cause myoglobinemia and myoglobinuria (see Figure 55-54, A), which may result in acute kidney injury.15,16 Other life-threatening clinical effects include coagulopathy and spontaneous systemic hemorrhage,180,256 hypotension, and shock. Local envenoming, however, is usually trivial, restricted to pain, mild swelling, and erythema (Figure 55-104, B and C). In contrast, envenoming by C. simus in Central America produces clinical effects more reminiscent of rattlesnake bites in North America: severe local envenoming with massive swelling, blistering, and necrosis. Systemic envenoming involves some hemostatic disor­ ders such as hypofibrinogenemia, but spontaneous systemic bleeding is unusual, acute kidney injury has rarely been reported, and neurotoxicity is controversial. Lachesis (See Figure 55-36).  Bushmasters may reach a length of nearly 4 m (13.1 feet) and are the longest venomous snakes in the western hemisphere. Envenoming by all four species may cause local swelling, blistering, bruising, and necrosis with coag­ ulopathy, spontaneous systemic bleeding, shock, and acute kidney injury reminiscent of other pit vipers. However, a distinc­ tive syndrome has been described in a proportion of cases. Within 10 to 15 minutes of the bite, there are nausea, abdominal colic, repeated bilious vomiting, watery diarrhea with profuse sweating, hypersalivation and other features of autonomic hyper­ activity, bradycardia, visual disturbances, profound shock, and syncope. Local effects of envenoming may leave permanent impairment.100

RISK FOR ENVENOMING Even when the fangs of a venomous snake have pierced the skin, envenoming is not inevitable. About 20% of patients bitten by Calloselasma rhodostoma and Daboia russelii show absolutely no evidence of envenoming, and as many as 80% of those bitten by sea snakes and Australasian eastern brown snakes (Pseudonaja textilis) and 50% by C. rhodostoma or Russell’s vipers, have trivial or no envenoming. These are the so-called dry bites.

A

C

FIGURE 55-104  Envenoming by tropical rattlesnakes (Crotalus durissus) in Brazil. A, Neurotoxicity (C. durissus marajoensis) (Marajo, Brazil). B and C, Evolution of local swelling and demarcated erythema after bite by C. durissus terrificus (São Paulo, Brazil). (A courtesy Pedro Pardal; B and C copyright D.A. Warrell.)

RISK FOR DEATH Untreated snakebite mortality is hard to assess, because hospital admissions include a disproportionate number of severe cases, and data for untreated snakebites are available only from the preantivenom era or from occasions when antivenom supply is limited, an antivenom of low potency is used,265 or when anti­ venom is withheld by doctors who doubt its efficacy. The mortal­ ity rate of E. ocellatus bites has been reduced from about 20% to 3% with antivenom.265,267 In Brazil, untreated and treated case fatalities for Bothrops and Crotalus durissus terrificus envenom­ ing were estimated as 8% and 0.7% and 72% and 12%, respec­ tively.176 In Australia, case fatality before development of antivenom was 50% for Acanthophis, 45% for Notechis, and 19% for Pseudonaja.221 Prognosis appears to be the worst in infants and in older adults, but there is no convincing evidence that older children have a worse prognosis than do young adults, despite the larger dose of venom they may receive relative to their body weight.

INTERVAL BETWEEN BITE AND DEATH Death after snakebite may occur as rapidly as within a few minutes (reputedly after a bite by the king cobra, O. hannah) or as long as 41 days after a bite by the saw-scaled or carpet viper (E. carinatus). However, the speed of killing has been exaggerated. Most elapid deaths occur within hours of the bite, most sea-snake bite deaths between 12 and 24 hours, and viper bite deaths within days.

RATE OF EVOLUTION AND RECOVERY OF ENVENOMING Local swelling is usually evident within 2 to 4 hours of bites by vipers and cytotoxic cobras. Swelling is maximal and most exten­ sive on the second or third day after the bite. Resolution of swelling and restoration of normal function in the bitten limb may be delayed for months, especially in older people (e.g., after bites by the European adder V. berus). The earliest systemic symptoms, such as vomiting and syncope, may develop within minutes of the bite, but even in the case of rapidly absorbed elapid venoms, patients rarely die less than an hour after the bite. Defibrination may be complete within 1 to 2 hours of the

bite (e.g., saw-scaled or carpet viper E. ocellatus).242,267 Neuro­ toxic signs may progress to generalized flaccid paralysis and respiratory arrest within a few hours. If the venom is not neutral­ ized by antivenom, these effects may be prolonged. Defibrination can persist for weeks (Echis spp. and C. rhodostoma).173,242,267 Patients with neurotoxic envenoming have recovered after being artificially ventilated for up to 10 weeks. Tissue necrosis usually declares itself within a week of the bite. Sloughing of necrotic tissue and secondary infections including osteomyelitis may occur during subsequent weeks or months. Deaths occurring from neurotoxic envenoming are caused by airway obstruction or respiratory paralysis, whereas later deaths may result from technical complications of mechanical ventilation or intractable hypotension. Late deaths, more than 5 days after the bite, are usually the result of acute kidney injury. Delayed shock with recurrent spontaneous hemorrhage has been described in victims of Burmese Russell’s viper; pituitary and other intracranial hemor­ rhages have been found at autopsy.

CHRONIC SEQUELAE OF SNAKEBITE Tissue loss, amputations, contractures, arthrodeses, hypertrophic and keloid scars, tendon damage, and complications of surgery are the most common causes of persistent morbidity in survivors of snakebites (Figure 55-105, A). Chronic ulcers, pyogenic arthri­ tis, and osteomyelitis are described. Malignant transformation (Marjolin’s ulcer) has been seen in patients with chronic ulcer­ ation after bites by N. nigricollis269 and C. rhodostoma (Figure 55-105, B).90,272 Chronic renal failure (bilateral cortical necrosis) and panhypopituitarism (from Sheehan’s-like syndrome) are reported complications of Russell’s viper bites.6,234,244 An unknown number of patients who develop acute bilateral renal cortical necrosis after viper bite envenoming, even by small species such as Hypnale hypnale, may be left with chronic renal failure.12 Cerebral hemorrhage complicating viperid, colubrid, and Austral­ asian elapid bites may result in chronic neurologic deficits, and it is possible that survivors of severe presynaptic neurotoxicity (e.g., from krait and Australasian elapid envenoming) may be susceptible to a late poliomyelitis-like syndrome. Apart from these purely objective abnormalities, snakebite victims may com­ plain of chronic or recurrent symptoms in the bitten limb and attribute a wide variety of physical and mental problems to that unforgettable, dramatic, and traumatic event of their snakebite. 1089

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

muscle-derived enzymes, myoglobin, and potassium concentra­ tions. Plasma is stained brownish by myoglobin and pink by hemoglobin. Heparinized blood should be allowed to sediment spontaneously (without centrifugation) to reveal these pigments. Evidence of Intravascular Hemolysis Patients with intravascular hemolysis have black urine (as in malarial “blackwater fever”). It is brownish, pinkish, or reddish in patients with hematuria or myoglobinuria.

A

B FIGURE 55-105  Permanent sequelae of snakebite. A, Hypertrophic scar with contractures and arthrodeses at site of spitting cobra bite (Naja nigricollis, Nigeria). B, Marjolin’s ulcer—malignant transformation to squamous cell carcinoma at site of chronic osteomyelitis following bite by Calloselasma rhodostoma in Thailand. (Copyright D.A. Warrell.)

Laboratory Investigations HEMATOLOGY Systemic envenoming is usually associated with a neutrophil leukocytosis: counts above 20 × 109/L indicate severe envenom­ ing. Initially, hematocrit may be high from hemoconcentration when there is generalized increase in capillary permeability (e.g., Burmese D. siamensis). Later, hematocrit falls because of bleeding into the bitten limb and elsewhere, and from intravas­ cular hemolysis or microangiopathic hemolysis in patients with disseminated intravascular coagulation. Thrombocytopenia is common (e.g., D. russelii, C. rhodostoma, B. arietans).

EVIDENCE OF RENAL DYSFUNCTION AND ACID-BASE IMBALANCE Blood urea or serum creatinine and potassium concentrations should be measured in patients who become oliguric, especially in cases with a high risk for renal failure (e.g., D. russelii, ter­ restrial Australasian snakes, sea snakes, and Colubridae). All snake-bitten patients should be encouraged to empty their bladder on admission. Urine should be examined for blood/ hemoglobin and protein (by dipstick test) and for microscopic hematuria and red cell casts. Severely sick, hypotensive, and shocked patients will develop lactic acidosis (suggested by an increased anion gap). Those with renal failure will also develop metabolic acidosis (decreased plasma pH and bicarbonate con­ centration, reduced arterial PCO2), and patients with respiratory paralysis will develop respiratory acidosis (low pH, high arterial PCO2, decreased PO2), or respiratory alkalosis if they are mechani­ cally overventilated.

ELECTROCARDIOGRAPHIC ABNORMALITIES (See Figures 55-51, B and C and 55-66, D)* ECG abnormalities include sinus bradycardia, ST-T wave changes, varying degrees of atrioventricular block, and evidence of hyper­ kalemia. Shock may induce myocardial ischemia or infarction in patients with diseased coronary arteries.

CHEST RADIOGRAPHY (See Figures 55-86, E and 55-96, F ) Chest radiography is useful for detecting pulmonary edema (e.g., European Vipera and D. russelii/D. siamensis), pulmonary hemorrhages and infarcts, pleural effusions, and secondary bronchopneumonia. *References 119, 120, 171, 242, 254, 257, 267.

Twenty-Minute Whole Blood Clotting Test* Incoagulable blood is a cardinal sign of systemic envenoming by most of the Viperidae, many of the Australasian elapids, and the medically important Colubridae. For clinical purposes, a simple, bedside, all-or-nothing test of blood coagulability is adequate. A few milliliters of blood taken by venipuncture are placed in a new, clean, dry, glass vessel; left undisturbed at room tempera­ ture for 20 minutes; then tipped once to see if there is clotting (Figure 55-106).

OTHER TESTS OF HEMOSTASIS More sensitive laboratory tests that are rapid and relatively simple to perform are whole blood or plasma prothrombin times and detection of elevated concentrations of FDP by agglutination of sensitized latex particles or of D-dimer. Serum concentrations of creatine kinase, aspartate transferase, and blood urea are com­ monly elevated in patients with severe envenoming, because of local muscle damage at the site of the bite. Evidence of Muscle Damage Generalized rhabdomyolysis caused by sea snake, Australasian elapid, tropical rattlesnake, and Sri Lankan Russell’s viper bites causes a steep rise in serum creatine kinase and other *References 179, 267.

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FIGURE 55-106  Twenty-minute whole blood clotting test. Blood taken by venipuncture from a patient bitten by Papuan taipan (Oxyuranus scutellatus), placed in a new, clean, dry glass tube and left for 20 minutes undisturbed has failed to clot, indicating consumption coagulopathy or presence of venom anticoagulants. (Copyright D.A. Warrell.)

Detection of venom antigens in body fluids of snakebite victims using enzyme immunoassays has proved a valuable research tool for confirming the species responsible for envenoming (immu­ nodiagnosis), as a prognostic index of the severity of envenom­ ing, and to assess efficacy of antivenom treatment*. Venom gland mRNA has been detected in stored venom samples using reverse transcription–polymerase chain reaction (RT-PCR).35 Of the various techniques used, enzyme immunoassay has proved the most rapid, sensitive, and specific. However, commercial venom detection kits for clinical diagnosis are available only in Australia (Venom Detection Kit).206 They are highly sensitive, but specific­ ity may be inadequate to distinguish between envenoming by different species in the same genus or in closely related genera.206,229 Envenomed patients develop persisting levels of antibodies to venom antigens, including individual toxins190 detectable by enzyme immunoassay, but they have proved insuf­ ficiently specific to allow reliable retrospective diagnosis.90,240

Management of Snakebite† FIRST-AID TREATMENT‡ Principles of First Aid • Reassure the victim, who is often terrified. • Do not tamper with the bite wound in any way, but immo­ bilize the bitten limb using a splint or sling. If the patient is thought to have been bitten by a dangerously neurotoxic elapid snake (including sea snakes), consider pressureimmobilization (see later text). • Take the patient as quickly as possible to the nearest medical care facility. The entire patient should be immobi­ lized, especially the bitten limb, because any muscle con­ tractions will promote spread of venom. Ideally the patient should be transported by motor vehicle, bicycle (as a pas­ senger), boat, or on a stretcher. • Avoid harmful and time-wasting treatments (see later text). • Because species diagnosis is critically important, the snake should be taken along to the hospital if it has already been killed. However, if the snake is still at large, do not risk further bites and waste time by searching for it. Even snakes that appear to be dead should not be touched with bare hands, but carried in a bag or dangling across a stick. Some species (e.g., Hemachatus haemachatus) sham death, and even a severed head can inject venom!

PRESSURE IMMOBILIZATION AND PRESSURE-PAD The splinting and pressure bandaging method (illustrated in Chapter 54) developed and advocated by Struan Sutherland in Australia proved effective in limiting the absorption of Australian elapid toxins in restrained monkeys.205 Although never subjected to formal clinical trials, the method has proved successful and safe, as judged by some anecdotal reports of delayed systemic enven­ oming and rapid deterioration after release of the bandage, in some cases supported by measurements of venom antigenemia. However, there have been practical difficulties in implementing this discovery, and, even in Australia, only 18% to 53% of the bandages in place when patients arrived in the hospital had been correctly and effectively applied. The method is still regarded by some experienced physicians as of unproved benefit.37 Bandaging aims to exert a pressure of about 55 mm Hg (1.06 psi), that of a venous tourniquet. In practice, it is difficult to judge how tightly the bandage should be applied and difficult for the patient to put it on unaided,258 explaining why so many are incorrectly applied.37 A recent study found that the technique was difficult to teach and that elasticized bandages were superior to traditional crepe ban­ dages.264 External compression increases intracompartmental pres­ sure and may accentuate the effects of some necrotic snake *References 76, 90, 91, 152, 195, 213, 214, 235. † References 29, 123, 140, 206, 226, 255, 263, 264, 285. ‡ References 37, 245, 246, 258, 264.

venoms, but animal studies found little evidence that this was deleterious and reinforced the lifesaving effects of lymphatic/ venous compression.25,139 However, if a patient is bitten by a dan­ gerously neurotoxic elapid (such as a mamba, king cobra, or taipan) or by a sea snake, there is a risk that respiratory paralysis might develop en route to the hospital. In these cases, it is recom­ mended that an elastic bandage and splint be applied firmly, but not so tightly as to obliterate the peripheral arterial pulse. Lym­ phoscintigraphy studies in simulated envenoming showed that excessive pressure (>70 mm Hg [1.35 psi]) and movement of the other limbs increased lymphatic flow.93 The patient should lie down and remain as immobile as possible during the journey to hospital. A recent study of lymaphatic flow in human volunteers and in rats showed that nitric oxide (NO) donating drugs, such as glyceryl trinitrate, applied topically to the bitten limb, slowed lymphatic flow substantially, presumably by inhibiting the intrinsic lymphatic pump, despite movement of the limb. In rats challenged with Eastern brown snake venom, death was delayed. It is sug­ gested that topical application of NO donating drugs might prove to be a useful adjunct to pressure-immobilisation and pressure-pad (see below) first-aid methods.182 Monash Pressure-Pad Method An alternative, simpler method of local compression was devel­ oped by Anker and colleagues5 and tested in Burmese Russell’s viper bite cases by Tun-Pe and colleagues in Burma.232 Applica­ tion of a foam rubber pad directly over the bite wound, at a pressure of about 70 mm Hg, delayed systemic envenoming, as assessed by measurements of venom antigenemia, and the method appeared safe and effective in a preliminary field trial.232

REJECTED OR CONTROVERSIAL FIRST-AID METHODS* Traditional treatments are widely preferred by inhabitants of rural parts of the developing world.150 However, even in the West, tourniquets, constriction bands, wound cauterization, incision or excision, amputation of the bitten digit, suction by mouth, vacuum pumps26 or “venom-ex” apparatus, instillation of chemi­ cal compounds such as potassium permanganate, application of ice packs (cryotherapy), “snake stones,” electric shocks, and many other outlandish first-aid treatments have been advocated. These are absolutely contraindicated in that they are harmful and have no proved benefit.83,246 Incisions can provoke uncontrolled bleeding when the blood is incoagulable; may damage nerves, blood vessels, or tendons; and introduce infection.20 Suction, chemicals, and cryotherapy can cause tissue necrosis. Snake stones do not remove venom from the wound and usually require an incision to make them adhere. This can result in persistent bleeding and infection.

DANGERS OF TIGHT TOURNIQUETS Tight (arterial) tourniquets have been responsible for terrible morbidity and even mortality in snakebite victims and should never be used. Dangers of tourniquets include ischemia and gangrene if they are applied for more than about 2 hours, damage to peripheral nerves (especially the lateral popliteal [common peroneal] nerve when a tourniquet presses against the neck of the fibula), increased fibrinolytic activity, congestion, swelling, increased bleeding, increased local effects of venom, and shock, rapid development of life-threatening systemic envenoming, or even pulmonary embolism after their release (see later text).245,246

TREATMENT OF EARLY SYMPTOMS BEFORE THE PATIENT REACHES THE HOSPITAL Distressing and dangerous manifestations of envenoming may appear before the patient reaches the hospital: • Local pain: This may be intense. Oral acetaminophen is preferable to aspirin or nonsteroidal antiinflammatory *References 246, 257.

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IMMUNODIAGNOSIS

PART 6  ANIMALS, INSECTS, AND ZOONOSES

agents, which carry the risk for gastric bleeding in patients with incoagulable blood. Severe pain should be treated with opiates. • Vomiting: This is a common early symptom of systemic envenoming. Patients should be laid in the recovery posi­ tion (on their left side) with the head down to avoid aspira­ tion. Persistent vomiting can be treated with intravenous promethazine (12.5 to 25 mg in adults, 0.1 to 0.25 mg/kg in children older than 2 years of age). • Syncopal attacks and anaphylactic shock: Patients who collapse within minutes of the bite may show features of either a vasovagal attack with profound bradycardia or of anaphylaxis with angioedema, urticaria, asthma, abdominal colic, and diarrhea. Anaphylaxis should be treated with aqueous epinephrine 0.1% (1 : 1000) (0.3 to 0.5 mL in adults, 0.01 mL/kg in children) by intramuscular injection, followed by a histamine H1-blocker such as chlorphenira­ mine maleate (10 mg in adults, 0.2 mg/kg in children) given by intravenous or intramuscular injection. In patients with incoagulable blood, injections can cause hematomas. Pressure dressings should be applied to all injection sites to prevent oozing. • Respiratory distress: This may result from upper airway obstruction if the jaw, tongue, and bulbar muscles are para­ lyzed or from paralysis of the respiratory muscles. Patients should be placed in the recovery position, the airway cleared if possible using a suction pump, an oral airway inserted, and the jaw elevated. If the patient is cyanotic or respiratory movements are weak, oxygen should be given by any available means. If clearing the airway does not produce immediate relief, artificial ventilation must be initi­ ated. In the absence of any equipment, mouth-to-mouth or mouth-to-nose ventilation can be lifesaving. Manual ventila­ tion by bag-valve-mask device is rarely effective for a prolonged period of time. Ideally, a cuffed endotracheal tube should be introduced using a laryngoscope, or a cuffed tracheostomy tube inserted. The patient can then be ventilated by bag. If no femoral or carotid pulse can be felt, external cardiac massage should be instituted. Examination of Pregnant Women Potential complications of envenoming in pregnancy include antepartum and postpartum hemorrhage indicated by vaginal bleeding, premature labor, abortion/stillbirth, and fetal dis­ tress.81,82 If possible, uterine contractions and fetal heart rate should be monitored continuously. Fetal distress may be signaled by fetal bradycardia, tachycardia, or late deceleration after each uterine contraction. If there is vaginal bleeding or the likelihood of imminent surgery, correction of antihemostatic abnormalities after antivenom treatment should be accelerated using blood products. Lactating women should be encouraged to continue breastfeeding.

MEDICAL TREATMENT IN THE HOSPITAL Snakebite is a medical emergency. The history, symptoms, and signs must be assessed rapidly to direct urgent appropriate treat­ ment. Patients may arrive at the hospital soon, or in some cases many days, after being bitten. They may therefore show early or late signs of envenoming or its complications. It is essential that all patients with a history of snakebite be assessed rapidly; they may be moribund but still salvageable by appropriate resuscita­ tion. Cardiopulmonary resuscitation may be needed, including clearance of the airway, oxygen administration by face mask or nasal catheter, and establishment of intravenous access to allow treatment with drugs and intravenous fluids. Airway, respiratory movements (breathing), and arterial pulse (circulation) must be checked immediately. Vital signs must be recorded: blood pres­ sure, pulse rate, and respiratory rate.

NEEDS FOR RAPID ASSESSMENT AND RESUSCITATION Patients with severe envenoming may present with the following problems requiring urgent intervention: 1092

• Profound hypotension and shock, resulting from: • Direct cardiovascular effects of the venom (e.g., V. berus, D. russelii, D. siamensis, B. arietans, O. scutellatus). • Hypovolemia secondary to blood loss, persistent vomit­ ing, or other causes of dehydration. • Autopharmacologic effects of the venom (activation/ inhibition of physiologic vasomotor systems, such as the angiotensin-renin-bradykinin systems, by venom toxins). • Rarely, anaphylaxis provoked by antivenom given outside the hospital and, even more rarely, provoked by venom in habitual snake handlers who have been sen­ sitized by previous exposure. • Sudden deterioration after release of a tourniquet or com­ pression bandage, resulting in shock, bleeding, or respira­ tory paralysis.281,290 These bands, bandages, or ligatures are often removed too hastily by hospital staff before antive­ nom treatment has been initiated and appropriate staff and equipment are on hand in the event that resuscitation is needed. • Airway obstruction, resulting from aspirated vomitus, a foreign body, or the tongue blocking the upper airway, especially in patients with evolving bulbar paralysis who have not been transported to hospital in the left lateral (recovery) position. Vomiting can be the result of systemic envenoming or ingestion of emetic herbal remedies. • Terminal respiratory failure from progressive neurotoxic envenoming that has led to paralysis of respiratory muscles. • (Hours after the bite) Cardiac arrest resulting from hyper­ kalemia in patients with massive generalized skeletal muscle breakdown (rhabdomyolysis) after sea-snake bites. • (Days after the bite) Acute renal failure. • (Days after the bite) Septicemia complicating aspiration pneumonia (see earlier text) or infection of incisions made at the site of the bite.

CLINICAL ASSESSMENT Four important preliminary questions are as follows: 1. In which part of your body have you been bitten? 2. When and under what circumstances were you bitten? 3. Where is the snake that bit you? Did you bring it and, if not, what did it look like? 4. How are you feeling now? If the snake has been killed but not brought, someone should be dispatched to collect it. Alternatively, a high-quality digital photograph(s) may be obtained. Only if the snake can be identi­ fied confidently as nonvenomous can the bitten patient be dis­ charged after a booster dose of tetanus toxoid. Patients should be asked whether they have taken any drugs or alcohol, whether they have vomited, fainted, or have noticed any bleeding or other ill effects of the bite, and whether they have passed urine since being bitten. Physical signs should be assessed before any com­ pression bandage or tourniquet is removed. Fang marks are sometimes invisible and rarely help the diagnosis, although the discovery of only two or three discrete puncture marks suggests a bite by a venomous snake. Local swelling, tenderness, and lymph node involvement are early signs of envenoming. The gingival sulci are usually the earliest site of detectable spontane­ ous bleeding (see Figures 55-52, A, 55-75, C and D, 55-88, C, 55-99, D, and 55-102, H). Bleeding from venipuncture sites, recent wounds, and skin lesions suggests incoagulable blood. If the patient is in shock (collapsed, sweating, cool, cyanotic extremities, low blood pressure, tachycardia), the foot of the bed should be raised, and an intravenous infusion of a plasma expander, such as fresh frozen plasma, dextran, Haemaccel (3.5% colloidal solution), Gelofusine (succinated gelatin), or fresh blood started immediately. The central venous pressure should be observed. The earliest symptoms of neurotoxicity after elapid bites are often blurred vision, feeling of heaviness in the eyelids, and drowsiness. The earliest sign is contraction of the frontalis muscle (raised eyebrows and puckered forehead) even before true ptosis can be demonstrated. Signs of respiratory muscle paralysis (dyspnea, “paradoxical” abdominal respiration, and cya­ nosis) are ominous. Patients with generalized rhabdomyolysis may have trismus and muscles that are stiff, tender, and resistant

Early Clues That a Patient May Be Severely Envenomed • The snake is identified as a dangerously venomous species and was perhaps a large specimen. • Rapid early spread of local swelling from the site of the bite. • Enlarged, painful, and tender lymph nodes draining the site of the bite indicate early spread of large-molecular-weight venom components into the lymphatic system. • Early symptoms of systemic envenoming include collapse (hypotension, shock); nausea, vomiting, and diarrhea; severe headache; “heaviness” of the eyelids; pathologic drowsiness or early ptosis/ophthalmoplegia. • Early spontaneous systemic bleeding occurs, for example, from the gums or nose, or in vomitus, feces, or urine. • Urine is dark brown or black.

ANTIVENOM (ANTIVENOM, ANTIVENENE, ANTISNAKEBITE SERUM)* Antivenom is the concentrated whole gamma immunoglobulin (IgG) or enzyme-refined gamma IgG fragments (F[ab′]2 or Fab) of horses or sheep, which have been immunized with venom.77,154,218,289,292 It is the only specific treatment available and has proved effective against many of the lethal and damaging effects of venoms. In the management of snakebite, the most important clinical decision is whether or not to give antivenom, because only a minority of snake-bitten patients need it, it may produce severe reactions, and it is expensive and often in short supply. Clinical testing of the effectiveness and safety of antivenoms in human patients has been generally neglected in favor of inad­ equate testing in animals, usually mice. Recently, attempts have been made to encourage routine preclinical and phase I (equiva­ lent) and phase II/III clinical trials.†

neutrophil leukocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, hemoconcen­ tration, uremia, raised serum creatinine, oliguria, hypox­ emia, acidosis, and vomiting in the absence of a history of ingesting emetic agents • Severe local envenoming: local swelling that is spreading rapidly or that extends more than halfway up the bitten limb; extensive blistering or bruising, especially in patients bitten by species known to cause local necrosis (e.g., Viperidae, Asian cobras, African spitting cobras). Bites by these species inflicted on the digits carry a high risk for necrosis and warrant antivenom treatment. In Europe, to improve the rate of recovery after bites by V. berus, anti­ venom has been recommended in adults with swelling extending beyond the wrist or ankle within 2 hours of a bite.171,251,254,257 Special Indications for Antivenom in Specific Areas Europe (Adder—Vipera berus—and Other European Vipera).*  Zagreb antivenom, or Protherics ViperaTAb (Table 55-4), is indicated to prevent morbidity and reduce the length of convalescence in patients with moderately severe envenoming, as well as to save the lives of severely envenomed patients. Indications are as follows: • Fall in blood pressure with or without signs of shock • Other signs of systemic envenoming (see earlier text), including spontaneous bleeding, coagulopathy, pulmonary edema or hemorrhage (shown by chest radiograph), ECG abnormalities, peripheral leukocytosis, profound anemia, or elevated serum creatine kinase • Severe local envenoming—swelling of more than one-half the bitten limb developing within 48 hours of the bite— even in the absence of systemic envenoming • In adults, early swelling extending within 4 hours of the bite beyond the wrist after bites on the hand or beyond the ankle after bites on the foot Patients bitten by European Vipera who show any evidence of envenoming should be admitted to a hospital for observation for at least 24 hours. Antivenom should be given whenever there is evidence of systemic envenoming (see earlier text) even if its appearance is delayed for several days after the bite. Contraindications to Antivenom Treatment There are no absolute contraindications to antivenom in cases of life-threatening envenoming. However, patients with atopic asthma and those who have reacted to equine antiserum on previous occasions have an increased risk for developing severe antivenom reactions. In such cases, antivenom should not be given unless there is evidence of systemic envenoming. If anti­ venom is given, pretreatment with adrenaline (epinephrine), an antihistamine, and a corticosteroid is recommended. Rapid desensitization is not recommended.

CHOICE OF ANTIVENOM IN A PARTICULAR CASE: MONOVALENT AND POLYVALENT ANTIVENOMS

Indications for Antivenom • Systemic envenoming • Hemostatic abnormalities: spontaneous systemic bleed­ ing, incoagulable blood or prolonged clotting time, severe thrombocytopenia • Cardiovascular abnormalities: hypotension, shock, abnormal ECG, cardiac arrhythmia • Neurotoxicity • Generalized rhabdomyolysis • In patients with definite signs of local envenoming, the following indicate significant systemic envenoming:

The range of venoms neutralized by an antivenom is usually stated on the package insert and is to be found in compendia of antivenoms.† If the biting species is known or strongly sus­ pected, the appropriate monovalent (monospecific) antivenom should be used. Monovalent antivenom is raised against the venom of a single species and is effective for treating envenom­ ing by that species of snake alone, or, in some cases, for enven­ oming by a few closely related species. They are generally less expensive than polyvalent antivenoms,226,229 but this is no longer true for CSL taipan and polyvalent antivenoms. In cases of known taipan envenoming, CSL polyvalent antivenom is preferred. In parts of the world where several species produce identical signs, patients who fail to bring the dead snake (or, in Australia, who cannot be diagnosed by venom detection kits) must be treated with polyvalent (polyspecific) antivenom. Polyvalent antivenom

*References 289, 292. † References 1, 2, 40, 197, 218, 292.

*References 104, 251, 254, 257. † References 140, 217, 285, 290-292.

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

to passive stretch. Urine output may dwindle very early in the course of Russell’s viper bite. Dark urine suggests myoglobinuria or hemoglobinuria. If there is initially no evidence of envenoming, the patient should be admitted for observation, ideally for 24 hours.84 Every hour, symptoms, level of consciousness, degree of ptosis, pulse rate and rhythm, blood pressure, respiratory rate, extent of local swelling, and other new signs should be recorded. If there is any evidence of neurotoxicity, ventilatory capacity should be recorded every hour. Useful investigations include the 20-minute whole blood clotting test (or other tests of coagulation), peripheral leukocyte count, hematocrit, urine microscopy and dipstick testing, and electrocardiography. If a tourniquet or tight compression bandage is in place, it may create distal edema through venous congestion even in the absence of envenoming and, if applied tightly enough to prevent arterial perfusion, might cause a cold, pulseless, and cyanotic extremity. Blockage of venous drainage from a limb into a pow­ erfully procoagulant venom that has been injected by the snake may promote deep vein thrombosis and subsequent pulmonary embolism when the tourniquet is released. Such occlusive devices must not be released until intravenous access has been estab­ lished and antivenom, plasma expanders, and adequate medical staff are available to cope with the dramatic deterioration that may follow.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

is raised against the venoms of a selection of the most important species of snakes in a particular geographic region. Polyvalent antivenoms do not necessarily contain lower concentrations of species-specific antibody per unit volume (or total protein content) than do monovalent antivenoms, because immunizing animals with the venoms of two or more related species may produce an augmented antibody response to conserved epit­ opes.170 Polyvalent antivenoms do not necessarily carry a higher risk for reactions than do monovalent antivenoms. The chosen antivenom must have demonstrated ability to protect against the venom of the species thought to have been responsible. Non­ specific antivenom is generally of no benefit to the patient and

may cause reactions (see later text). Some antivenom manufactur­ ers claim a wide range of “para-specific” neutralization for their products, but mere immunologic cross-reactivity in the laboratory is inadequate grounds for relying on an antivenom to be effective clinically.158 Table 55-4 lists some important antivenoms for this region. In some cases, clinical trials have established an average initial dose. Conservation of Antivenom and Expiration Dates Liquid antivenoms stored at temperatures below 8° C (46.4° F) usually retain most of their activity for 5 years or more.289 Freezedried (lyophilized) antivenoms are even more stable. Under

TABLE 55-4  Guide to Initial Dosage of Some Antivenoms for Treating Bites by Medically Important Snakes

Outside the Americas

Species Latin Name

English Name

Manufacturer, Antivenom

Acanthophis species Bitis arietans Africa

Death adder Puff adder

Bitis arietans Middle East

Puff adder

Bothrops asper Bothrops atrox Bothrops bilineatus Bothrops jararaca Bothrops lanceolatus B. caribbaeus Bungarus caeruleus Bungarus candidus

Terciopelo Common lancehead Papagaio Jararaca Lesser Antillean fer de lance Common krait Malayan krait

CSL* Death Adder or Polyvalent Antivenom Sanofi-Pasteur (“Fav Afrique” or “FaviRept” polyvalent; SAVP† polyvalent NAVPC‡ Polyvalent Snake Antivenom Vacsera Polyvalent or Anti-Viper Venom Antiserum ICP§ polyvalent, LBS|| Antivipmyn Tri Butantan, FED¶ Antibotropico polyvalent Butantan polyvalent Butantan polyvalent Sanofi-Pasteur BothroFav

Bungarus fasciatus

Banded krait

Bungarus multicinctus

Chinese krait

Calloselasma (Agkistrodon) rhodostoma Cerastes species

Malayan pit viper

Crotalus durissus

Tropical rattlesnakes

Crotalus simus Cryptelytrops albolabris, C macrops Daboia (Vipera) palaestinae

Central American Green pit vipers

Daboia (Vipera) russelii, D siamensis

Russell’s vipers

Dendroaspis species Dispholidus typus Echis species Africa

East/South African mambas African boomslang Saw-scaled or carpet Vipers

Echis species Middle East

–––––––––

Echis carinatus India Gloydius (Agkistrodon) blomhoffii Hydrophiinae Lachesis sp

––––––––– Chinese Mamushi

Micropechis ikaheka

New Guinean small-eyed snake

1094

Desert (horned) vipers

Palestine viper

Sea snakes Bushmasters

Indian manufacturers** polyvalent TRC†† Malayan Krait Antivenin monovalent or neuro-polyvalent TRC†† Banded Krait Antivenin Monovalent or neuro-polyvalent Shanghai Vaccine & Serum Institute Antivenom of Bungarus multicinctus Blyth Taiwan NIPM Taipei Naja-Bungarus antivenin TRC†† Malayan Pit Viper Antivenin monovalent or haemato-polyvalent NAVPC‡ Polyvalent Vacsera AntiViper or Polyvalent Butantan or FED¶ Anticrotalico or Antibotropico-crotalico ICP§ LBS|| polyvalent TRC†† Green Pit Viper Antivenin or haematopolyvalent Rogoff Medical Research Institute, Tel Aviv, Palestine viper monovalent Myanmar Pharmaceutical Factory, monovalent Indian manufacturers** polyvalent TRC†† Russell’s Viper Antivenin monovalent or haemato-polyvalent SAVP† Dendroaspis or Polyvalent Antivenoms SAVP† Boomslang Antivenom SAVP†, Echis, monovalent Sanofi-Pasteur (“Fav Afrique”) MicroPharm EchiTAb-G ICP§ EchiTAb-plus-ICP NAVPC‡ Polyvalent Snake Antivenom Vacsera Polyvalent and Anti-Viper Venom Antiserum Indian manufacturers|| polyvalent Shanghai Vaccine & Serum Institute Mamushi antivenom CSL* Sea Snake Antivenom ICP§ polyspecific, FED¶Antibotropico laquetico, Butantan Antiophidico CSL* Polyvalent Antivenom

Approximate Average Initial Dose (reference) 1-3 vials (285) 80 mL (275) 80 mL (247,253) 80 mL 5-20 vials (154) 2-12 vials (197) 2-4 vials (197) 2-12 vials†† 2-6 vials (220) 100 mL 50 mL 50 mL 5 vials 5 vials 100 mL (272) 30-50 mL 30-50 mL 5-20 vials 5-15 vials 100 mL (96) 50-80 mL 80 mL (148) 100 mL (8,11) 50 mL 50-100 mL 1-2 vials 20 mL (267) 100 mL 1 vial (1,2) 3 vials (1,2) 50 mL 50 mL 50 mL 5 vials 1-10 vials 10-20 vials ?2 vials

Outside the Americas—cont'd

Species Latin Name

English Name

Manufacturer, Antivenom

Approximate Average Initial Dose (reference)

Micrurus corallinus, M. frontalis M. nigrocinctus,   M. mipartitus,   M. multifasciatus Naja kaouthia

Brazilian coral snakes

Butantan “Antielapidico”

1-5 vials

Central American coral snakes

ICP monovalent

1-5 vials

Monocellate Thai cobra

TRC†† Cobra Antivenin monovalent or neuro-polyvalent Indian manufacturers** polyvalent SAVP2 and Sanofi-Pasteur Polyvalent

100 mL

Vacsera Polyvalent Venom Antiserum NAVPC‡ Bivalent Naja/Walterinnesia or Polyvalent Snake Antivenom SAVP† and Sanofi-Pasteur Polyvalent

100 mL 100 mL

Vacsera Polyvalent Venom Antiserum TRC†† neuro-polyvalent antivenom

100 mL 100 mL

CSL* Tiger Snake or Polyvalent Antivenom TRC†† King Cobra Antivenin or neuro-polyvalent CSL* Polvalent (or Taipan) Antivenom CSL* Brown Snake or Polyvalent Antivenom CSL* Black Snake Antivenom Japanese Snake Institute, Nitta-gun   Yamakagashi antivenom

1-3+ vials (285)

Naja naja, N oxiana Naja haje, N anchietae,   N annulifera, N melanoleuca, cobras   N nivea, N senegalensis Naja haje (Middle East) Naja haje arabica

Indian cobras African neurotoxic

Naja nigricollis, N mossambica etc Naja (nigricollis) nubiae Naja siamensis, N. sumatrana Notechis scutatus

African spitting cobras

Ophiophagus hannah

King cobra

Oxyuranus scutellatus Pseudonaja species Pseudechis species Rhabdophis tigrinus,   R subminiatus

Australian/Papuan taipans Australian brown snakes Australian black snakes Japanese yamakagashi,   SE Asian red-necked keelback Green pit vipers

Trimeresurus albolabris,   T macrops Vipera berus and other European Vipera

Walterinnesia aegyptia

§

Egyptian cobra Arabian cobra

Egyptian spitting cobra Indo-Chinese and other SE Asian spitting cobras Tiger snake

European adder

Black desert cobra

100 mL 100 mL

100 mL (269)

100-200 mL 1-6+ vials (285) 1-6+ vials (285) 1-3 vials (285) 1-2 vials

see Cryptelytrops above Immunoloski Zavod-Zagreb Vipera polyvalent Protherics Fab monovalent “ViperaTAb” NAVPC‡ Bivalent Naja/Walterinnesia or Polyvalent Snake Antivenom

10-20 mL (257) 100-200 mg 50 mL

*Commonwealth Serum Laboratories, Parkville, Australia † South African Vaccine Producers, formerly SAIMR, Johannesburg ‡ National Antivenom and Vaccine Production Center, National Guard Health Affairs, Riyadh, KSA § Instituto Clodomiro Picado, San Jose, Costa Rica || Laboratorios Bioclon, Silanes, Mexico ¶ Fundação Ezequiel Dias, Belo Horizonte, Brazil **Indian Manufacturers: Bharat Serums and Vaccines, Mumbai, Biological E (Evans), Vins Bioproducts, Hyderabad †† Thai Red Cross Society, Bangkok

expedition conditions, liquid antivenoms can be expected to retain their activity even if exposed to environmental tempera­ tures above 30° C (86° F).289 Antivenoms retain much of their activity well beyond stated expiration dates. Although the use of such out-of-date material could never be recommended, situa­ tions may arise in the developing world when there is no alterna­ tive.153 Opaque solutions should not be administered, because precipitation of protein indicates denaturing with loss of activity and increased risk for adverse reactions.

SUPPLY OF ANTIVENOMS Antivenom manufacturers and suppliers change often, so avail­ ability of antivenom is uncertain. For this reason, a timely Internet search (see Useful Websites) followed by confirmation of clinical efficacy and safety, as well as immediate availability, are essential, well in advance of the time when antivenom is needed. In urgent cases, some national poison centers (e.g., London, UK) and zoo

networks hold stocks of antivenoms covering most exotic and local species. Europe, Asia, and Australia are reasonably well supplied with antivenoms, but there is currently a crisis in anti­ venom supply to the sub-Saharan countries of Africa and to New Guinea.77,115,116,287 This problem may be relieved by the production of new “pan-African” polyvalent antivenoms, raised against appropriate African venoms, by manufacturers outside of Africa.27,77,115,116,188 Purchasers of antivenom should be aware that some clinically ineffective, nonspecific but highly reactogenic antivenoms raised against Indian venoms (e.g., Naja, Echis) are sold in African and Asian countries and in Papua New Guinea, where they are pur­ ported to be effective against venoms of the local snakes.260

ANTIVENOM REACTIONS Antivenom treatment may be complicated by early anaphylactictype, pyrogenic, or late (serum sickness–type) reactions. 1095

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

TABLE 55-4  Guide to Initial Dosage of Some Antivenoms for Treating Bites by Medically Important Snakes

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Early Anaphylactic–Type of Reactions These reactions usually develop within 10 to 180 minutes of starting antivenom. There are itching, urticaria, fever, tachycardia, palpitations, cough, nausea, and vomiting. Up to 40% of patients with early reactions show features of severe systemic anaphy­ laxis: bronchospasm, hypotension, or angioedema—but deaths are rare. The reported incidence, which varies between antiven­ oms and according to dose, ranges from 3% to 84%. Safety can be improved by attention to the manufacturing processes.218,292 These reactions are not usually type I IgE-mediated hypersensitiv­ ity reactions to equine serum proteins and are therefore not predicted by hypersensitivity tests.44,130 For this reason, it is inap­ propriate and misleading to apply the adjectives immediate, allergic, or hypersensitivity to early antivenom reactions in general. Antivenoms activate complement in vitro,204 whereas the clinically similar reactions to homologous serum are associated with complement activation and immune complex formation in vivo. The complement system is probably activated by aggregates of IgG or its fragments, but there is little evidence that pepsin digestion, which removes complement-activating Fc fragments, reduces the incidence of reactions.154 Unless patients are watched carefully for 3 hours after treatment, mild reactions may be missed and deaths misattributed to the envenoming itself. Early reactions should be treated as for anaphylaxis of any cause.97,199 They respond readily to aqueous epinephrine/adrenaline given by intramuscular injection of between 0.5 and 1.0 mL of 0.1% (1 : 1000, 1 mg/mL) in adults (children, 0.01 mL/kg) at the first sign of trouble. Antihistamines, such as chlorphenamine maleate (adult dose 10 mg, children 0.2 mg/kg), should be given by intravenous injection to combat the effects of histamine released during the reaction. Pyrogenic Reactions Pyrogenic reactions result from contamination of the antivenom by endotoxin-like compounds. High body temperature develops 1 to 2 hours after treatment and is associated with rigors, followed by vasodilation and decreased blood pressure. Febrile convul­ sions may be precipitated in children. Patients should be physi­ cally cooled and given antipyretic drugs such as acetaminophen by mouth, via nasogastric tube, or by suppository. Aspirin and nonsteroidal antiinflammatory agents are not safe in patients with hemostatic problems. Late (Serum Sickness–Type) Reactions Late reactions develop 5 to 24 (mean 7) days after treatment. Their incidence and speed of development increase with the dose of antivenom. Symptoms include fever, itching, urticaria, arthralgias (which may involve the temporomandibular joint), lymphadenopathy, periarticular swellings, mononeuritis multi­ plex, albuminuria, and (rarely) encephalopathy. This immune complex disorder responds to an antihistamine such as chlorphe­ niramine (adults, 2 mg 4 times a day; children, 0.25 mg/kg per day in divided doses), or, in more severe cases, to corticosteroids (prednisolone 5 mg 4 times a day for 5 days in adults; 0.7 mg/ kg per day in divided doses for 5 days for children).

PREDICTION OF ANTIVENOM REACTIONS Hypersensitivity testing by intradermal or subcutaneous injection or intraconjunctival instillation of diluted antivenom has been widely practiced in the past. However, these tests delay the start of antivenom treatment, are not without risk, and have no predic­ tive value for early (anaphylactic) or late (serum sickness type) antivenom reactions, which are not usually manifestations of IgE-mediated type I hypersensitivity.44,130

PREVENTION OF EARLY ANTIVENOM REACTIONS Prophylactic antihistamines (anti-H1 and anti-H2), corticosteroids, and epinephrine have been very widely used, singly or in combination, on empirical grounds, but not without risk. A few randomized controlled trials have now been completed, and several more are in progress. Intramuscular promethazine proved 1096

ineffective,58 but in two published studies, subcutaneous epi­ nephrine (adrenaline) (0.1%, adult dose 0.25 mg) reduced the incidence of early antivenom reactions.163,288 A study purporting to demonstrate the efficacy of combined hydrocortisone and antihistamine infusion was underpowered.72 A review of 10 years of experience with various premedication regimens in Papua New Guinea288 illustrated the heterogeneity and lack of standard­ ization of snakebite victim care in developing countries while suggesting efficacy of some prophylactic regimens, as did the study of Caron and colleagues32 in Ecuador. Recently, data were published comparing the premedication of 1007 Sri Lankan snakebite victims with promethazine, hydrocortisone, and adren­ aline in a dose of 0.25 mL of 1:1000 subcataneously, each alone and in various combinations. Compared with placebo, adrenaline significantly reduced severe reactions to antivenom by 43% (95%, CI 25 to 67) at 1 hour and by 38% (95%, CI 26 to 49) up to and including 48 hours after antivenom administration. Hydrocorti­ sone and promethazine were ineffective and addition of hydro­ cortisone negated the benefit of adrenaline.47

ADMINISTRATION OF ANTIVENOM Antivenom should be given as soon as it is indicated, but it remains potentially effective as long as signs of systemic enven­ oming persist (e.g., up to 2 days after a sea-snake bite and many days or even weeks for prolonged defibrination following bites by Viperidae).172,173,267,268 In contrast, local effects of venoms are probably not reversible by antivenom delayed for more than 1 to 2 hours after the bite.222,242,269,275 Route of Administration The intravenous route is most effective. Although intramuscular injection is associated with a lower rate of early anaphylactoid reactions, absorption is very slow, especially when the gluteal site is used (but see later text). An infusion over 30 to 60 minutes of antivenom diluted in isotonic fluid may be easier to control than an intravenous “push” injection of reconstituted but undi­ luted antivenom given over 10 to 20 minutes. There is no differ­ ence in the incidence of severity of antivenom reactions in patients treated by these two methods,130 but greater dilution and slower infusion should be tested.29 Further trials are in progress.7 Snakebite in Remote (Wilderness) Locations If someone is bitten by a snake in a remote location and signs of envenoming develop, but there is no one in the group capable of giving an intravenous injection, antivenom may be given by deep intramuscular injection at multiple sites into the anterolat­ eral aspect of the thighs (not into the gluteal region, from which absorption is exceptionally slow), followed by massage to promote absorption. An algorithm has been developed to guide the use of antivenom in these circumstances (Figure 55-107). However, the volumes of antivenom normally required would make this route not practical, as would the risk for hematoma formation in patients with incoagulable blood. Dose of Antivenom Ideally, the initial dose of a particular antivenom should be based on results of clinical studies when available, depending upon species of snake responsible and severity of envenoming. However, most manufacturers’ recommendations are based on mouse assays, which may not correlate with clinical findings.278 Clinical trials of antivenom have been carried out since 1973,268 but are inappropriately neglected, even though they are the only reliable means of obtaining efficacy and safety data. Initial doses of some important antivenoms are given in Table 55-4. The apparent serum half-lives of antivenoms in envenomed patients range from 26 to 95 hours, depending on which IgG fragment they contain.89,213 Children must be given the same doses of antivenom as adults. Recurrent Envenoming Recurrence of clinical and laboratory features of systemic enven­ oming, including recurrent venom antigenemia, several days after an initially good response to antivenom, was clearly documented

No or ?

Signs of envenoming appear (in less than 30 minutes)

Yes Reassure, clean wound (tetanus toxoid)

No Observe and reassess every 30 minutes: signs of envenoming appear

No

Yes

Hospital less than two hours away

Available: someone capable of giving intravenous injection  antivenom.1 Epinephrine (adrenaline) 2 and other drugs for treating anaphylactic antivenom reaction 3

No Available: someone capable of giving intramuscular injection  antivenom.1 Epinephrine (adrenaline) 2 and other drugs for treating anaphylactic antivenom reaction 3 No Conservative management. Then evacuate on stretcher.

Yes

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

Snake definitely nonvenomous

Yes

No

Yes

Immobilize bitten limb (pressure).4 Then evacuate on stretcher to hospital.

Yes

Give antivenom1 by slow intravenous injection with full precautions. Observe carefully for signs of antivenom reaction. Then evacuate on stretcher.

Give antivenom1 by intramuscular injection with full precautions. Observe carefully for signs of antivenom reaction. Then evacuate on stretcher. Notes: “Antivenom” means appropriate specific antivenom for the species of snake involved. “Epinephrine (adrenaline)” means 0.1% (1:1000) adrenaline for intramuscular injection (adult dose 0.3-0.5 mL). “Other drugs for treating anaphylactic antivenom reaction” means antihistamine and hydrocortisone for intravenous injection. 4 “Immobilize bitten limb (pressure)” means immobilization of the bitten limb with a splint or sling. “Pressure” means use of the pressure immobilization method employing several long elasticized bandages on the pressure-pad method (see previous text). This should only be used when a bite by a neurotoxic elapid snake cannot be excluded. 1 2 3

FIGURE 55-107  Algorithm indicating appropriate management for snakebite in a patient while in a remote wilderness location. (From Warrell D, Anderson S, Dallimore J, et al: Oxford handbook of expedition and wilderness medicine, New York, 2008, Oxford University Press, pp 517-520.)

in patients envenomed by Malayan pit vipers (C. rhodostoma) in Thailand in the 1980s, although this work was overlooked when the phenomenon was rediscovered after the introduction of CroFAb in the United States.90,246,272 Recurrent envenoming is probably the result of continuing absorption of venom from the injection site after antivenom has been largely cleared from the circulation or perhaps by redistribution of venom from tissue in response to antivenom.13,90 Paradoxically, venom absorption may increase after a hypotensive, shocked patient has been resusci­ tated. It is more likely to occur when a rapidly eliminated small IgG fragment antivenom, such as Fab, is used.8,142 This suggests that an initial dose of antivenom, however large, may not prevent late or recurrent envenoming. Repeated Dosing The response to antivenom will determine whether further doses should be given. Neurotoxic signs may improve within 30 minutes of antivenom treatment, but this usually takes several hours. Hypotension, sinus bradycardia, and spontaneous sys­ temic bleeding may respond within 10 to 20 minutes. Blood coagulability is usually restored between 1 and 6 hours, pro­ vided sufficient antivenom has been given. A second dose of antivenom should be given if severe cardiorespiratory symptoms persist for more than about 30 minutes and when incoagulable

blood persists for more than 6 hours after the start of the first dose. The “6-Hour Rule” Studies of envenoming by several species of snakes whose venoms cause coagulopathy have demonstrated that once an adequate neutralizing dose of antivenom has been given, blood coagulabil­ ity (assessed by the 20-minute whole blood clotting test) will be restored within a median of 6 hours.264 This reflects the ability of the liver, highly activated by circulating fibrin/fibrinogen break­ down products, to restore coagulable levels of clotting factors in patients with consumption coagulopathy. This important observa­ tion is the basis for a simple method of titrating antivenom dosage in individual patients whose blood is initially incoagulable. The 20-minute whole blood clotting test is performed at 6-hour inter­ vals, and the initial dose of antivenom is repeated every 6 hours until blood coagulability is restored. After that, the 20-minute whole blood clotting test is checked at 12-hour intervals for at least 48 hours to detect recurrent envenoming. Very large doses of antivenom may be required to treat patients bitten by species capable of injecting enormous amounts of venom or extremely potent venom. A patient bitten by the king cobra (O. hannah) was given 1150 mL of specific anti­ venom and prolonged artificial ventilation and survived.223 1097

PART 6  ANIMALS, INSECTS, AND ZOONOSES

SUPPORTIVE TREATMENT (ASSUMING THAT AN ADEQUATE INITIAL DOSE OF ANTIVENOM HAS BEEN GIVEN) Neurotoxic Envenoming Artificial Ventilation.  This was first suggested for neurotoxic envenoming more than 130 years ago, but patients continue to die due to lack of vital respiratory support. Bulbar and Respiratory Muscle Paralysis.  Inability to swallow is indicated by accumulation of secretions in the pharynx. Stridor indicates paralysis of the vocal cords; it can be accentuated by extending the neck. Early paralysis of intercostal respiratory muscles is suggested by “abdominal breathing” (or “paradoxical respiration”) in which exaggerated compensatory contraction of the diaphragm causes the paralyzed abdomen (rather than the chest) to expand on inspiration. Objective measurement of ven­ tilatory capacity is very useful to monitor respiratory paralysis. This can be achieved with a peak flow meter, spirometer, or respirometer (if the patient is using a face mask or is intubated) or by asking the patient to blow into the tube of a sphygmoma­ nometer to record the maximum expiratory pressure. If patients are adequately oxygenated, even those with profound general­ ized flaccid paralysis from neurotoxic envenoming are fully con­ scious. However, because their eyes are closed (ptosis) and they do not move or speak, they are commonly assumed to be uncon­ scious, and their level of consciousness cannot be properly assessed by the conventional Glasgow Coma Scale. Tactless remarks made by medical staff can be heard by the apparently comatose patient! Opening his or her eyes so that he or she can see the surroundings is very reassuring for a ptotic and com­ pletely paralyzed patient. They may still be able to flex a finger or toe, allowing simple “yes or no” communication. It is very important not to assume that patients with snakebite neurotoxic­ ity have irreversible brain damage, although they may be are­ flexic, unresponsive to painful stimuli, and have fixed, dilated pupils. Neurotoxic effects are fully reversible with time. A patient bitten by B. multicinctus in Canton recovered completely after being ventilated manually for 30 days, and a patient probably envenomed by T. carinatus recovered after 10 weeks of mechan­ ical ventilation in Queensland, Australia. Endotracheal intubation or tracheostomy using a cuffed tube is needed. The patient can be ventilated manually with an anesthesia bag or, preferably, with a mechanical ventilator. For technical details of airway management and assisted ventilation, see http://www.searo. who.int/EN/Section10/Section17.htm. Anticholinesterase Drugs Anticholinesterase drugs have limited usefulness in neurotoxic envenoming but may produce rapid improvement in neuromus­ cular transmission in patients suffering the effects of postsynaptic neurotoxins, for example, from envenoming by some species of Asian and African cobras, mambas, death adders (Acanthophis species), and kraits.118,273,278,282 It is worth trying the “Tensilon test” in all cases of severe neurotoxic envenoming, as for a patient with suspected myasthenia gravis. Baseline observations or mea­ surements are made against which to assess the effectiveness of the anticholinesterase. Atropine sulphate (0.6 mg for adults; 50 mcg/kg for children) or glycopyrronium is given by intrave­ nous injection followed by neostigmine bromide or methylsul­ phate (Prostigmin) (or distigmine, pyridostigmine, ambenomium, and others in appropriate doses) by intramuscular injection 0.02 mg/kg for adults, 0.04 mg/kg for children. Short-acting edrophonium chloride (Tensilon) is ideal for this test but is rarely available in the region. It is given by slow intravenous injection in an adult dose of 10 mg or 0.25 mg/kg for children. The patient is observed over the next 30 to 60 minutes (neostigmine) or 10 to 20 minutes (edrophonium) for signs of improved neuromus­ cular transmission. Ptosis may disappear and ventilatory capacity (peak flow, forced expiratory volume in 1 second [FEV1], or maximum expiratory pressure) may improve. Patients who respond convincingly can be maintained on neostigmine meth­ ylsulphate, 0.5 to 2.5 mg every 1 to 3 hours up to 10 mg/24 1098

hours maximum for adults or 0.01 to 0.04 mg/kg every 2 to 4 hours for children by intramuscular, intravenous, or subcutane­ ous injection together with atropine to block muscarinic side effects. Patients able to swallow tablets may be maintained on atropine 0.6 mg twice each day, neostigmine 15 mg 4 times each day, or pyridostigmine 60 mg 4 times each day. Patients must be observed closely for symptoms of cholinergic crisis. The “ice test” is a possible alternative to the Tensilon test.75 In patients with myasthenia gravis who have bilateral ptosis, application of an ice-filled plastic glove to one eye for 2 minutes resulted in improvement in ptosis on that side, possibly due to inhibition of anticholinesterase. This quick and simple test might obviate the need for the Tensilon test. However, it has not yet been evalu­ ated in patients with neurotoxic snake envenoming.

HYPOTENSION AND SHOCK Hypovolemia is a common cause of hypotension and shock and should be treated by infusing a plasma expander. Central venous pressure is the safest way to control volume replacement. Hypo­ tensive patients envenomed by the Burmese Russell’s viper responded to dopamine, 2.5 mcg/kg per minute by intravenous infusion; however, methylprednisolone, 30 mg/kg, and naloxone were not effective.148 Anaphylaxis, whether it is a primary response to envenoming, the result of hypersensitization, or a reaction to antivenom, should be treated promptly with epinephrine/adrenaline.199,200

ACUTE KIDNEY INJURY* If urine output drops below 400 mL/24 hours, urethral and central venous catheters should be inserted. If urine flow fails to increase after cautious rehydration, diuretics should be tried (e.g., furosemide by slow intravenous injection, 100 mg followed by 200 mg if urine output fails to increase). If these measures fail to restore urine flow, the patient should be placed on strict fluid balance. Peritoneal dialysis or hemodialysis will be required in most patients with established renal failure. For technical details of assessment and treatment of acute kidney injury, see http:// www.searo.who.int/EN/Section10/Section17.htm.

LOCAL INFECTION A booster dose of tetanus toxoid should be given. Following bites by Latin American pit vipers99 and some other species such as Malayan pit vipers (C. rhodostoma),215 local bacterial infections with formation of wound abscesses occur in about 10% of cases. A wide range of bacteria has been implicated, some peculiar to snakes’ oral cavities and venom.194 Even a case of Buruli ulcer (Mycobacterium ulcerans) has been attributed to snakebite. Pro­ phylactic antibiotics are not justified unless the wound has been incised or there is evidence of necrosis.99 Penicillin, erythromycin, or chloramphenicol is appropriate, as would be an antibiotic effective against the bacterial flora of the buccal cavity and venoms of local snakes.215 An aminoglycoside such as gentamicin should be added for 48 hours. Bullae are best left intact.

NURSING SNAKE-BITTEN LIMBS Excessive elevation of snake-bitten limbs should be avoided, in that this has been shown to increase the risk for compartment syndromes.136

SURGICAL MANAGEMENT OF SNAKE-BITTEN LIMBS† Debridement of Necrotic Tissue Necrotic tissue should be debrided as soon as possible and the denuded area covered with split-thickness skin grafts. Muscle should not be excised just because it looks dark or even black, *References 196, 290. † Reference 277.

COMPARTMENT SYNDROMES* In a snake-bitten limb, swelling of muscles within tight fascial compartments, such as the anterior tibial compartment, may raise tissue pressure to such an extent that perfusion is impaired and ischemic damage (as in Volkmann’s contracture of the forearm) is added to the effects of the venom. Risk factors include pressure bandaging and excessive elevation of the limb that reduce arterial perfusion pressure in the compartment but cannot reduce local venous pressure below tissue pressure. Reduction of the arteriovenous pressure gradient was associated with decreased muscle PO2 and nerve conduction velocity.136 The classic signs of compartment syndrome include excessive pain, weakness of the compartment muscles and pain when they are passively stretched, hypoesthesia of areas of skin sup­ plied by nerves running through the compartment, and obvious tenseness of the compartment.136 These features have been char­ acterized as “the seven P’s:” pain at rest, pain on possible movement, paralysis, pallor, paresthesia, poikilothermia, and pulselessness. Unfortunately, local effects of envenoming often result in a painful, immobile, pale, cyanotic, cold, tensely swollen, and apparently pulseless limb with poor capillary refill in the absence of any demonstrable compartment syndrome. These appearances may mislead inexperienced surgeons into diagnosing compartment syndrome without objective evidence and encourage them to proceed to fasciotomy. The discovery of dark or even black-looking muscle tissue may reassure the surgeon that the operation was necessary, but envenomed yet viable muscle often looks black because of hemorrhage. Dangers of fasciotomy include neglect of early adequate antivenom treat­ ment, severe persistent bleeding if the venom-induced hemo­ static abnormalities have not been corrected by adequate doses of antivenom, delayed recovery of function, prolonged hospital admission, persistent morbidity from damage to sensory nerves, and contractures from keloid formation or hypertrophic scarring in some ethnic groups. Palpation of peripheral pulses or their detection by Doppler ultrasound does not exclude compartmen­ tal ischemia. However, direct measurement of intracompartmen­ tal pressure is reasonably simple, using a perfusion pump and saline manometer system or a commercial transducer such as the Stryker apparatus. An intracompartmental pressure of more than 45  mm Hg in an adult or 30  mm Hg in a child indicates a high risk for ischemic necrosis. In these circumstances, fasci­ otomy may be justified to relieve the pressure in the compart­ ment, but this treatment did not prove effective in saving envenomed muscle in animal experiments.70 Necrosis occurs most frequently after digital bites. Fasciotomy must never be undertaken until blood coagulability has been restored by ade­ quate doses of specific antivenom, followed by transfusion of fresh whole blood, clotting factors, or platelets as required.

2. Analgesia by vasoconstrictors with weak mydriatic activity (e.g., 0.5% adrenaline/epinephrine) or a single topical administration of local anesthetic (e.g., 0.4% oxybupro­ caine hydrochloride (Novesin), 4% lidocaine hydrochlo­ ride, or tetracaine hydrochloride (Dicaine). 3. Exclusion of corneal abrasions by fluorescein staining and/or slit lamp examination and application of a pro­phylactic topical antibiotic such as tetracycline, chloram­ phenicol, soframycin, ciprofloxacin, gatifloxacin, penicillinstreptomycin or polymixin B sulphate. 4. Prevention of posterior synechiae, ciliary spasm and dis­ comfort with a topical cycloplegic such as 2% atropine, scopolamine, or homatropine. 5. Antihistamines in case of allergic keratoconjunctivitis. Topical or intravenous antivenom and topical corticosteroids are contraindicated. Topical heparin proved promising experi­ mentally but has been untested clinically.

Prevention of Snakebite The risk for snakebite can be reduced by simple precautions. Snakes should never be disturbed, attacked, or handled unneces­ sarily, even if they are thought to be harmless species or appear to be dead. Some venomous species, such as the ringhals (Hemachatus haemachatus), a South African spitting elapid, sham death (Figure 55-108). Venomous species should never be kept as pets or as performing animals. Protective clothing—boots (not open sandals), socks, long pants (trousers)—should be worn when walking in undergrowth or deep sand, and a flashlight should always be carried at night. Particular care should be taken while collecting firewood; moving logs, boulders, boxes, or debris likely to conceal a snake; climbing rocks and trees covered with dense foliage; or swimming in overgrown lakes and rivers. Where there are sea snakes, wading in the sea, especially in sand or near coral reefs, is a dangerous pastime and should be avoided if possible. Shuffling is safer than a high-stepping gait. Divers should keep clear of sea snakes. Fishermen who catch sea snakes in nets or on lines should return them to their element without touching them; their heads and tails may be difficult to differentiate. In the camp, sleep off the ground in a hammock, on a camp bed or in a tent with a sewn-in ground sheet, especially in krait country. A study in Nepal proved that a well tucked-in mosquito net afforded good protection against snakebites.34 Remove unnecessary junk and litter that might attract rodents, because rodents attract snakes. Various toxic chemicals, such as naphtha­ lene, sulfur, insecticides (e.g., DDT, dieldrin, and pyrethrins), and fumigants (e.g., methyl bromide, formaldehyde, or tetrachloro­ ethane), are lethal to snakes, but no true repellent has been identified that is acceptably safe for peridomestic use where there are children, domestic animals, and valuable wildlife. Prophylactic immunization against snakebite using venom toxoids has been attempted, for example, against habu

INAPPROPRIATE TREATMENTS Corticosteroids, heparin, antifibrinolytic agents such as aprotinin (Trasylol) and ε-aminocaproic acid, antihistamines, trypsin, and a variety of traditional herbal remedies have been used and advocated for snakebite. Most are potentially harmful and none has been proved to be effective.

TREATMENT OF SNAKE VENOM OPHTHALMIA† Management of venom ophthalmia consists of the following: 1. Urgent decontamination by copious irrigation: The “spat” venom should be washed from the eye or mucous mem­ brane as soon as possible using large volumes of water or any other available bland fluid. Even urine is better than nothing! *References 136, 290. † References 41, 255, 274.

FIGURE 55-108  South African ringhals, a spitting elapid (Hemachatus haemachatus: family Elapidae), shamming death. (Copyright D.A. Warrell.)

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

because intense hemorrhage may produce this appearance in viable muscle.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

(Protobothrops flavoviridis) among farmers in the Amami and Ryuku Islands of southern Japan, where it proved ineffective.183 The analogy with immunization against infectious diseases is misleading, because the immunized person would not have time to develop an enhanced secondary (anamnestic) response to the venom after being bitten. Protection would depend solely on levels of neutralizing antibody circulating at the time of the bite.

Venomous Lizards The overtly venomous helodermatid lizards (Gila monster and Mexican beaded lizard) are discussed in Chapter 54. Recently, evidence has been published that the saliva of other groups of lizards contains toxins: Iguania (e.g., iguanas and agamids) (see Figure 55-1, Pogona) and Anguimorpha (e.g., varanid or monitor lizards) (Figure 55-109, A, Varanus salvator).65 These lizards have mandibular glands, but only those of Varanidae/Lanthanotidae and Helodermatidae are segregated into specialized serous protein-secreting glands with thick capsules. Glands of members of four Anguimorph families (Anguidae, Lanthanotidae, Shinisau­ ridae [Figure 55-109, B], and Varanidae) were shown to secrete a variety of toxins, including cysteine-rich secretory proteins (CRiSP), kallikrein, helokinestatin, hyaluronidase, lectin, natri­ uretic peptides, PLA2s, and new cardiopetides.67 The clinical significance of these findings is doubtful, because lizard bites rarely cause more than mild trauma, transient pain, and swelling. However, it has been claimed that envenoming might contribute to the massively traumatic predatory attacks launched by Komodo dragons against large mammals and occasionally humans (see later text).

Dangerous Large Reptiles GIANT PYTHONS (FAMILY BOIDAE) Bites by most species of python can be locally traumatic and sometimes complicated by infection (Figure 55-110, B). Several species have been responsible for rare fatal attacks reported from South America (anaconda, Eunectes murinus) (Figure 55-111, A); Africa (rock python, Python sebae) (Figure 55-111, B to D); south and Southeast Asia, especially Indonesia (reticulated python, Python reticulatus [Figure 55-111, E], and the Indian python, Python molurus); and Australia, where a 5.2-m (17-foot) long scrub python, Morelia amethistina, killed its keeper.144 The victims were asphyxiated and crushed by constriction and in some cases swallowed after the clavicles had been broken147,263 (Figure 55-110, A). In 1974, a man attacked by P. sebae near Harrar, Ethiopia, died 48 hours later as a result of perinephric

A

A

B FIGURE 55-109  Lizards whose saliva contains toxins.67 A, Asian water monitor (Varanus salvator: family Varanidae) (Muda Ganga, Balapitiya, Sri Lanka). B, Chinese crocodile lizard (Shinisaurus crododilurus: family Shinisauridae) (Yao Shan E Xi, China). (Copyright D.A. Warrell.)

hematomas resulting from crush injuries. Recently, a 34-year-old man in the United States was strangled to death by his 2.7-m (9-foot) long, 11.3-kg [25-lb] boa constrictor, reemphasizing the danger posed by even modest-sized pythons.

KOMODO DRAGON (VARANUS KOMODOENSIS) This giant lizard, which can reach 3.1 m (10.2 feet) in length and 166 kg (366 lb) in weight, is restricted to Komodo, Rinca, Flores, and Gili Motang Islands in Indonesia. Until recently it was believed that it killed its prey (deer, cattle, pig, and occasionally humans) by brute force or through debilitation through contami­ nation of bite wounds with pathogenic bacteria, such as Pasteurella multocida.14 Recently, Fry and associates68 found that these

B

FIGURE 55-110  Attacks by pythons. A, Man killed and swallowed by a large reticulated python (Python reticulatus). B, Tooth marks made by a brown water python (Liasis fuscus) that seized a 7-year-old child while she was asleep near the Adelaide River in Australia. (A courtesy Exel Sawuwu; B courtesy Bart Currie.)

1100

B

D

C

E

FIGURE 55-111  Giant pythons. A, Anaconda (Eunectes murinus) (Brazil). B to D, African rock python (Python sebae) showing head (note supralabial heat-sensitive pit organs) and multiple teeth. E, Reticulated python (Python reticulatus). (Copyright D.A. Warrell.)

monitors possessed compound mandibular venom glands whose six compartments ducted to openings between the serrated pleur­ odont teeth. The venom contains toxins capable of causing hypotension (CRiSP, kallikrein, and natriuretic toxins), bleeding (PLA2 toxins), and hyperalgesia (cramping AVIT toxins), which, they argue, contribute to the predation strategy. In support of envenoming, they note that prey animals are reported to be unusually quiet after being bitten and that they rapidly go into shock. There are anecdotal reports of persistent bleeding in human victims after bites by V. komodoensis.

Internet Resources SNAKEBITE MANAGEMENT AND ANTIVENOMS Africa http://www.afro.who.int/en/clusters-a-programmes/ hss/essential-medicines/highlights/2358-whoafro-issuesguidelines-for-the-prevention-and-clinical-management-ofsnakebite-in-africa.html South and Southeast Asia: http://www.searo.who.int/EN/ Section10/Section17.htm (see under Technical Guidelines) Global (“Antivenoms website” [Venomous Snakes Distribution and Species Risk Categories] and “WHO Guidelines” [for the Production, Control and Regulation of Snake Antivenom

Immunoglobulins]): http://www.who.int/bloodproducts/ snake_antivenoms/en/ Global (especially Australasia): http://www.toxinology.com/ Global VAPA Guide: http://vapa.junidas.de/cgi-bin/WebOb jects/vapaGuide.woa/wa/getContent?type=page&id=1

ANTIVENOMS ONLY Munich AntiVenomINdex (MAVIN): http://toxinfo.org/anti venoms/ CSL Australian antivenoms: http://www.toxinology.com/gene ric_static_files/cslb_index.html Global crisis solutions center: http://globalcrisis.info/late stantivenom.htm For poison centers’ prescribers only: https://www.pharmacy. arizona.edu/avi/verify.pl#top

VENOMOUS SNAKE TAXONOMY UPDATES http://pages.bangor.ac.uk/~bss166/update.htm

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

A

CHAPTER 56 

Bites and Injuries Inflicted by Wild and Domestic Animals JOHN E. BRADFORD AND LUANNE FREER

Wild and domestic animal bites are distinct from other injuries suffered by humans. Tearing, cutting, and crushing injuries may be combined with blunt trauma caused by falls. Animal bites may cause local infection, and offending bacteria reside in numerous environmental sources. However, few traumatic lacerations are as regularly contaminated with as broad a variety of pathogens as are animal bites. Domestic animal bites are common, and their incidence is rising.43,201,297 Wild animal attacks are often more spectacular; however, in the developed world, injuries from domestic animals have a much greater health and economic impact. Humans are not a preferred natural prey of any animal, and, although some attacks are predatory, most attacks are caused by fear of humans (real or perceived), territoriality, protective instinct, or accident. Unfortunately, wild animal attacks may be sensationalized by the lay press, and animals given anthropomorphic characteristics that do not accurately reflect their instinctive responses; this may lead to public misunderstanding of animal behavior. Press reports may ignore the fact that wild animal attacks are rare and that wild animals are far less likely to cause injury than are their domestic counterparts. As human settlements and populations continue to grow and encroach on the natural world, the incidence of human–animal encounters will increase. Adventure-seeking humans may also seek out animal encounters that historically would have been avoided. A wolf sighting 100 years ago would have been cause for alarm, yet today people travel to Yellowstone National Park to see wolves in the wild and hope to get close enough to take pictures. The increased pressure of human proximity to animals increases the likelihood of an encounter resulting in a negative outcome (Figure 56-1).40 Other special features of human–animal encounters include attacking animals that may terrorize the victim and transmission of systemic diseases, many of which might cause substantial morbidity and mortality (for a discussion of zoonoses, see Chapter 59). In addition, treatment decisions are often made without a strong scientific basis, and management of wild animal attack victims is often based on a much more robust experience with domestic animal attacks (i.e., dog and cat bites). It is important to note that animal-caused injuries are usually preventable. When experience allows humans to understand the typical behavior of a species, people can take proper precautions

FIGURE 56-1  Yellowstone visitors approach bull elk. (Courtesy Luanne Freer, MD.)

1102

near potentially dangerous animals. For instance, when an animal attacks to defend itself or its territory, it is likely to cease this behavior when the person leaves and the perceived threat is diminished. However, during a predatory attack, the intent of the animal is to kill and not allow its prey to escape. Understanding how to react in these situations decreases the potential for a disastrous outcome. This chapter interprets the present state of knowledge and makes logical and specific recommendations for all of these conditions.

General Epidemiology According to the 2008 National Pet Owner Survey, 39% of all households in the United States own a total of 74.8 million dogs, and 34% own 88.3 million cats.10 During 1 year in Pennsylvania, county health officials reported 16,000 animal bites, 75% of which were dog related; the highest incidence of dog bite was among children less than 5 years old. Three-quarters of persons injured received wound treatment, and one-half received antimicrobials. Postexposure rabies prophylaxis administration was prescribed for attacks by species as follows: 44% for cats, 30% for dogs, 7% for raccoons, 4% for bats, 2.5% for squirrels, 2.1% for groundhogs, 2% for foxes, and 8% for all other species.230 Each year, dogs bite 1.8% of all Americans, resulting in 4.7 million wounds. More than 750,000 of these victims seek medical attention.75 Bites to children are common, especially among boys between the ages of 5 to 9 years.75 Over the course of 1 year in Pittsburgh, Pennsylvania, 790 dog bites were reported, but an estimated 1388 went unreported; the annual incidence was 58.9 bites per 10,000 individuals.81 Of 279 reported injuries caused by animals to travelers, 51% were caused by dogs, 21% by monkeys, 8% by cats, and 1% by bats.144 In India, where stray dogs cause 96% of rabies cases, the annual dog bite rate is 25.7 per 1000 individuals, and the most common victims are males.3,86 The annual incidence of cat bites in the United States is approximately 400,000.303 A cat bites one in every 170 people each year, and 80% of these bites become infected.156 Biting cats are typically stray females, and most human victims are female. Of the approximately 30 million Americans who ride horses, 50,000 a year are treated for horse-related injuries in an emergency department, principally because the rider is unrestrained and can fall off while traveling at speeds of up to 64.4 km/hr (40 mph). Horses can kick with a force of up to 907 kg (1 ton), and frequently bite. A 2-year review of animal bites in Oslo, Norway, revealed that horses caused 2% of 1051 recorded bites; 53% of these horse bite victims were children.104 The American Ferret Association estimates that 6 to 8 million domesticated ferrets reside in the United States. The Centers for Disease Control and Prevention (CDC) reports that the number of bites inflicted by ferrets—65 reported bites in 10 years—is substantially lower than that caused by dogs and cats (i.e., between 1 and 3 million)23 (Table 56-1). In Arizona, 11 ferret bites were reported over 11 months; with the ferret population estimated at 4000, the reported bite-to-ferret population ratio is approximately 0.3%.316 The risk of attack by a ferret is greatest among infants and small children. In Sweden, 3 in 1000 citizens are injured by animals each year.46 Domestic animals accounted for more than 90% of injuries, moose accounted for 6% (almost all were involved in auto accidents), and all other animals accounted for 4%. However, bites were not examined separately, and many injuries occurred during

For online-only figures, please go to www.expertconsult.com

Study Species Dog Cat Rodent Monkey Skunk Lagomorph Large mammal Reptile Bat Raccoon Human Other animal

A

B

C

89 4.6 2.2 0.1*

91.6 4.5 3 0.2 0.02 0.5 0.01‡

78 16 viruses.

1334

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.75 Many filters constructed with various designs and materials are marketed for field use. Surface, membrane, hollow-fiber, 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, because 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 removes a tiny layer of the filter medium. Hollow-fiber and pleated filters rely on large surface area to avoid clogging by particles. The size of a microorganism is the primary determinant of its susceptibility to filtration (Table 67-6 and Figure 67-1). 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. Waterborne pathogens often adhere to larger particles or clump together, making them easier to remove by physical processes.178 Therefore observed reductions are often greater than expected based on their individual sizes.257 In general, portable filters for water treatment can be divided into microfiltration with pores down to 0.1 µm, ultrafiltration that can remove particles as small as 0.01 µm, and nanofiltration with pores sizes as small as 0.001 or less. Microfilters are effective for removing protozoa and bacteria, algae, most particles, and sediment but allow dissolved material, small colloids, and some viruses to pass through. Ultrafiltration membranes are required for complete removal of viruses, colloids, and some dissolved solids. Nanofilters can remove other dissolved substances, including sodium chloride, from water. All filters require pressure to drive the water through the filter element. The smaller the pore size, the more pressure required.

Ultrafiltration Nanofiltration Reverse osmosis Size (µm) 0.001 0.01

0.1

1.0

10

100

1000

Visible to naked eye Beach sand Protozoan cysts Bacteria Viruses Colloidal clays and particles Organic compounds that add “tea” color to water Pesticides, taste and odor compounds Dissolved salts, metal ions

FIGURE 67-1  Relative size of microorganisms determines susceptibility to mechanical filtration. Mechanical filters span a wide range of pore sizes.

Filters are a reliable means to removing protozoan cysts.18 A membrane with a pore size of 0.2 µm can remove enteric bacteria. Giardia and E. histolytica cysts are easily 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.238 Helminth eggs and larvae, which are much larger, can be removed by a 20-µm filter. Cyclops (the water dwelling copepod that ingests the larva and transmits dracunculosis) can be removed by passage through a fine cloth.251 Adsorption and aggregation during passage through microfilters reduce viruses. Virus particles may adhere to the walls of diatomite (ceramic) or charcoal filters by electrostatic chemical attraction, which can be enhanced by a coating on the filter or a positive charge.93,108,111,223 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.219,286 Thus turbidity (cloudiness from contaminants) may help remove pathogens with filtration, while it inhibits chemical disinfection. 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.198 Furthermore, adsorbed viral particles can be subsequently dislodged and eluted from a filter because of competitive binding and competing electrostatic forces.108,215,276 Some ceramic filters now remove 99% to 99.9% of viruses, but the fourth log required by water treatment units remains a challenge. First Need filter has been able to meet the EPA standards for water purifiers, including 4-log removal of viruses, apparently through use of a charged media111 (Appendix A). Ultra filters like Sawyer 0.02 µm hollow fiber filter (or reverse osmosis nanofiltration) can mechanically filter viruses. In general, however, microfilters should not be considered adequate for complete removal of viruses, except with special equipment.293 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.286 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.73 Small hand-pump reverse-osmosis units have been developed. Their high price and slow output currently prohibit use by landbased wilderness travelers, but they are important survival items

for ocean travelers. Battery- or power-operated units are standard equipment on large boats. The U.S. Department of Defense uses large-scale mobile reverse-osmosis units for water treatment. These are considered the most fuel-efficient mobile units, producing the highest quality water from the greatest variety of raw water qualities, capable of producing potable water from fresh, brackish, or salt water, as well as from water contaminated by nuclear, biologic, or chemical agents. The units use pretreatment, filtration, and desalination, then disinfection for storage.5 Forward Osmosis Osmotic pressure also can be used to draw water through a membrane to create highly purified drinking water from lowquality source water, including brackish water. These products use a double chamber bag or container with the membrane in between. A high-osmotic substance is added to the clean side that draws water from the dirty side. Because some form of sugar and/or salt is often used to create osmotic pressure, this may result in a sweetened solution similar to a sports-electrolyte drink (see Appendix A). Choice of Filter (See Preferred Technique and Appendix A) There are extensive data on the effectiveness of filtration in other settings, but few data are available to compare different filters for field use. Most data are from testing organized by the filter manufacturer, so nearly all filters perform well. The ceramic filters have been tested most extensively and generally perform well for their claims.93,201,276 Gravity ceramic filters for household use have been extensively field tested in developing countries and are generally effective.59,262 As with all types of filters, results depend on the characteristics of the materials (e.g., ceramic), water quality, product engineering, and prior extent of filter use. Schlosser and colleagues248 tested three hand-pump filters (Katadyn Mini Ceramic, First Need Deluxe, and Sweetwater Walkabout), all of which removed 3 log (99.9%) or more of viable bacteria, leaving none in the effluent. Filters and granular charcoal media are sometimes coated with silver to prevent bacterial growth on the surface, but this does not maintain sterility. (See discussion of silver in Miscellaneous Disinfectants, later.) The military preventive medicine group has enumerated the requirements for individual filters for field use.279 Choice should be based on anticipated water quality, number of persons to be served, mode of travel and need for portability, and availability of power source. Hollow microfiber filters, adapted from medicine and industry, are the newest addition to point-of-use field filtration. For domestic use and in pristine protected watersheds where pollution is minimal and the main concerns are bacteria and cysts, microfiltration can be used as the only means of disinfection. For foreign travel and for surface water with high levels of human use or sewage contamination, however, higher levels of filtration or supplemental methods should be used.93 Ultrafilters, now available with hollow-fiber technology or nanofilters (see Reverse Osmosis, earlier) are an alternative. Otherwise, additional treatment with heat or halogens before or after filtration guarantees effective virus removal.223 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.191 Filters are also useful as a first step to remove parasites and Cryptosporidium organisms that have high resistance to halogens. Improvised Filters Filtration using simple, available products is of interest for use in developing countries and in emergency situations.257 Rice hull ash filters, crushed charcoal, sponges, and various fabrics have all been used. Typically, bacteria and viruses can be reduced by as much as 50% to 85% and larger parasites by 99%, depending on the media. Fine woven cotton fabric is effective at removing larger parasites, such as schistosome cercariae, Fasciola species, and guinea worm larvae. Kozlicic and associates151 tested five commonly available household materials (newspaper, filter paper, cotton, four-layer gauze, and white cotton cloth) for filtration efficiency. Newspaper performed poorly, being too slow. Cotton cloth performed best for both physical and microbiologic 1335

CHAPTER 67  Field Water Disinfection

Microfiltration

PART 8  FOOD AND WATER

parameters of water (although the latter was poorly studied). He incidentally noted that melted snow with the top 4 to 5 cm (1.6 to 2 inches) removed was a better quality water source than rainwater from roof runoff. Biosand Filters Sand filters employ a technology that has been proved over centuries of time and is still used widely in municipal plants. When constructed properly they are very reliable, but with slow flow rates. Sand filters are constructed by forming layers of aggregate increasing in size from the top to the bottom. The top layer is very fine sand and the bottom layer consists of large gravel. The container needs an exit port on the bottom. Water on the top layer forms a biolayer where micro-organisms “eat” the pathogens that pass through them. Over time, the biolayer grows to the point where it will not allow any water to pass through. At this point, the layer needs to be removed by either drying out the layer and then removing it, or stirring it up and removing dirty water from the top. The optimum depth of a sand filter is 2 m (6.6 feet). A column of fine sand 60 to 75 cm (23.6 to 29.5 inches) deep that permits no more than 200 L/m2/hr of water is capable of removing turbidity and greater than 99% of organisms.221 Diameter is determined by the volume of water needed. A family of four adults needs 16 L (4.2 gal) per day, which would require a 0.5-m (1.6-foot)-diameter tank. A sand filter can be improvised with stacked buckets or barrels. An emergency sand filter can be made in a 20-L (5.3-gal) bucket, composed of a 10-cm (3.9-inch) layer of gravel beneath a 23-cm (9.1-inch) layer of sand; a layer of cotton cloth, sandwiched between two layers of wire mesh, separates the sand and gravel layers.150

Chemical Disinfectants HALOGENS (CHLORINE AND IODINE) Worldwide, chemical disinfection is the most widely used method for improving and maintaining microbiologic quality of drinking water. Chemical disinfectants used for water disinfection are strong oxidants. Halogens, chiefly chlorine and iodine, are the most common chemical disinfectants used in the field; however, chlorine dioxide is now available in small-use applications and gaining acceptance. Germicidal activity results from oxidation of essential cellular structures and enzymes.50,156,191,196 Halogenated amines may be synthesized by white blood cells as part of the body’s natural defenses to destroy microorganisms.294 The disinfection process is determined by characteristics of the disinfectant, the microorganism, and environmental factors.52,130,190 Dilute solutions do not sterilize water. The relative potency of common disinfectants to inactivate waterborne microbes is as follows:

ozone > chlorine dioxide > electrochemically generated mixed species oxidant > free chlorine or iodine > chloramine Ozone and chlorine dioxide are discussed under Miscellaneous Disinfectants. Variables With Chemical Agents Understanding the principal factors of chemical disinfection allows intelligent and flexible use (Table 67-7). Concentration and Contact Time.  The major variables in the disinfection reaction are the amount of disinfectant (concentration) and the exposure time of the microorganism to the disinfectant (contact time). Concentration of disinfectant 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, halogen (iodine or chlorine) 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.130,295 This means that 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 67-2).295 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.13 In field disinfection, this can be used to minimize halogen dose and improve taste or, conversely, 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 (Cnt = 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 shielded by aggregation or other particles (Figure 67-3).117,123,130 Contaminants.  Organic and inorganic nitrogen compounds from decomposition of organisms and their wastes, fecal matter, and urea complicate chemical disinfection and must be considered in field water treatment. Vegetable matter, ferrous ions, nitrites, sulfides, and humic substances also affect oxidizing disinfectants.90,191,295 These contaminants react, especially with chlorine, to form compounds with little or no disinfecting ability, effectively decreasing the concentration of available halogen.

TABLE 67-7  Factors Affecting Halogen Disinfection

Primary Factors Concentration Contact time Secondary Factors Temperature

Water contaminants, cloudy water (turbidity) pH

1336

Effect

Compensation

Measured in milligrams per liter (mg/L) or the equivalent, parts per million (ppm); higher concentration increases rate and proportion of microorganisms killed. Usually measured in minutes; longer contact time ensures higher proportion of organisms killed.

Higher concentration allows shorter contact time for equivalent results. Lower concentration requires increased contact time for equivalent levels of kill. Contact time is inversely related to concentration; longer time allows lower concentration.

Cold slows reaction time.

Some treatment protocols recommend doubling the dose (concentration) of halogen in cold water, but if time allows, exposure time can be increased instead, or the temperature of the water can be increased. Doubling the dose of halogen for cloudy water is a crude means of compensation that often results in a strong disinfectant taste on top of the taste of the contaminants. A more rational approach is to first clarify water to reduce halogen demand. Compensating for pH is not necessary for most surface water.

Halogens reacts with organic nitrogen compounds from decomposition of organisms and their wastes to form compounds with little or no disinfecting ability, effectively decreasing the concentration of available halogen. In general, turbidity increases halogen demand. The optimal pH for disinfection is 6.5-7.5. As water becomes more alkaline, approaching pH 8.0, much higher doses of halogens are required.

E. histolytica cyst

Iodine (mg/L)

10

E. coli 1.0 Poliovirus

0.1 1.0

10

100

Contact time (min) FIGURE 67-2  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 Chang SL: The use of active iodine as a water disinfectant, 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, 1980, Arlington, Va.)

Temperature.  Temperature influences the rate of the disinfection reaction.90,156,191 Cold water affects germicidal power and must be offset by longer contact time or higher concentration to achieve comparable disinfection.114 The common rule is a twofold to threefold increase in inactivation rate per 10° C (18° F) increase in temperature. Temperature can be estimated in the field. Some treatment protocols recommend doubling the dose of halogen in cold water, but if there is no urgency, time can be increased instead of dose. Data for killing Giardia in very cold water (5° C [41° F])

2 ppm iodine 100 30° C

80 60 40 20 0

0 15 30 45 60 75 90 105 120 135 150 165 180 195 210 225 240

4 ppm iodine 100 Cyst inactivation (%)

Halogen Demand and Residual Concentration.  Halogen demand is the amount of halogen reacting with impurities. The concept applies to all chemical disinfectant agents. Residual concentration is the amount of active disinfectant remaining after 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.266 Halogen demand and residual concentration in 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 in otherwise clean water.52,115,266 Scant data are available on halogen demand of surface water (Table 67-8). 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 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, but in general, chlorine demand rises with increased turbidity.155,158 In addition, particulate turbidity can shield microorganisms and interfere with disinfection.75,143,158 (See earlier discussion of turbidity.) The initial dose of halogen must consider halogen demand. For clear alpine waters, 1 mg/L demand can 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; however, in cloudy water, 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 tastes 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

15° C 5° C

30° C 15° C

80

5° C

60 40 20 0 0

15

30

45

60

75

90

105

120

75

90

105

120

8 ppm iodine 15° C 30° C

100 80

5° C

60 40 20 0 0

15

30

45

60

Time (min) FIGURE 67-3  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, Gentile D, Krivoy D, et al: Giardia cyst inactivation by iodine, J Wilderness Med 3:351, 1992.)

1337

CHAPTER 67  Field Water Disinfection

coagulation–flocculation or filtration, significantly reduce halogen demand. (See clarification techniques.) Several simple color strip tests are available for field use, similar to those used for swimming pools and spas to 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.295

PART 8  FOOD AND WATER

TABLE 67-8  Halogen Demand of Surface Water Halogen Demand (mg/L)

Source Cloudy river water, Portland, Oregon Cloudy water from clay particles Clear water with 10% sewage added Lily pond and turbid river water Colorado River; cloudy from inorganic sand, clay Unspecified surface waters Municipal wastewater High-elevation spring Western river Six watersheds in western Oregon Small stream, Australia Bolivian village (well and collected rain) Spring and well water, Haiti Cloudy surface water (ponds, rivers)— household water sources in western Kenya

Reference

3-4

Jarroll, 1980138

None

Chang, 195352

2

Chang, 195352

5-6

Chang, 195352

0.3

Tunnicliff, 1984277

2-3

Culp, 197474 Culp, 197474 Ongerth, 1989200 Ongerth, 1989200 LeChevallier,1981158

20-30 0.3 0.7 0.4-1.6 1.3 2

Thomson, 1985272 Quick, 1999218

≤1

Colindres, 200765 Crump, 200572

100-150

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.102,124If feasible, raising the temperature by 10° to 20° C (18° to 36° F) allows a lower dose of halogen and more reliable disinfection at a given dose. pH.  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 7.5.52,189As 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 any chemical agent used. 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.130 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. 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.50,191 Organisms, in order of increasing resistance to halogen disinfection, are enteric (vegetative) bacteria, viruses, protozoan cysts, bacterial spores, and parasitic ova47 (Tables 67-9 and 67-10); 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.50,191 Relative resistance between organisms is similar for iodine and chlorine. The physical state of the microbes also determines their susceptibility. Microbes that are aggregated in clumps or embedded in other matter or organisms may be shielded from disinfectants. Bacteria.  All vegetative bacteria are extremely sensitive to halogens. Inactivation involves oxidation of enzymes on the cell membrane and does not require penetration.295 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.130 Although halogens were first used to disinfect water during cholera epidemics in 1850, recent cholera epidemics prompted review of data that reaffirmed the susceptibility of V. cholerae to low levels of chlorine and iodine.70 Campylobacter has susceptibility similar to that of other enteric pathogens.25

TABLE 67-9  Disinfection Data for Chlorine* Halogen†

Organism

HOCl FAC FRC Free Cl FRC Free Cl HOCl FRC Free Cl Free Cl

Free Cl

Escherichia coli Campylobacter 20 enteric virus 6 enteric viruses Hepatitis A virus Hepatitis A virus Amebic cysts Amebic cysts Giardia cysts Giardia lamblia cysts Giardia muris cysts G. muris cysts Giardia Giardia Cryptosporidium Schistosome cercariae Nematodes

Free Cl

Nematodes

FRC

Ascaris eggs

Free Free Free Free Free FRC

Cl Cl Cl Cl Cl

Concentration(mg/L)

Time (min)

pH

Temp

0.1 0.3 0.5 0.5 0.5 0.5 3.5 3.0 2.5 0.85

0.16 0.5 60 4.5 1 5 10 10 60 90

6.0 6.0-8.0 7.8 6.0-8.0 6.0 6.0

3.05 5.87

50 25

7.0 7.0 6.0 6.0

5° C (41° F) 25° C (77° F) 2° C (35.6° F) 5° C (41° F) 25° C (77° F) 5° C (41° F) 25° C (77° F) 30° C (86° F) 5° C (41° F) 2°-3° C (35.6°-37.4° F) 5° C (41° F) 5° C (41° F) 0.5° C (32.9° F) 5° C (41° F)

7.0

28° C (82.4° F)

7.0 6.0-8.0 8.0

Disinfection Constant (Ct) .016 0.15 30 2.5 0.5 2.5‡ 35 30 150 77 153 139 170 120 7200 30

80 1.0

90 30

2-3

120

(Not lethal)

95-100

30

(95% lethal)

200

20

5.0

37° C (98.6° F)

2000

FAC, Free active chlorine; FRC, free residual chlorine; Free Cl, free chlorine; HOCl, hypochlorous acid. *Also see reference 47. † 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.

1338

Reference White, 1992295 Blaser,198624 Briton,198030 Engelbrecht, 198091 Grabow, 1983115 Sobsey, 1975256 Chang, 197050 Stringer, 1970266 Rice, 1982229 Wallis, 1988291 Rubin, 1989244 Rubin, 1989244 Hibler, 1987124 Hibler, 1987124 Korich,1990149 World Health Organization, 1981301 National Academy of Sciences, 1980191 National Academy of Sciences, 1980191 Krishnaswami, 1968152

Concentration (mg/L)

Halogen*

Organism

FRI

Escherichia coli

1.3

I2 I2 I2 FRI FRI I2 I2 I2 I2 FRI FRI FRI

Amebic cysts Amebic cysts Amebic cysts Poliovirus 1 Poliovirus 1 Poliovirus 1 Coxsackie virus Amebic cysts Bacteria, viruses Giardia cysts Giardia cysts Giardia cysts

3.5 6.0 12.5 1.25 12.7 1 0.5 8 8 4 4 4

Time (min) 1 10 5 2 39 5 6 30 10 20 15 45 120

pH

Temp

6.0-7.0

2°-5° C (35.6°-41° F)

6.0 6.0 7.0 7.0 4.0-8.0 5.0 5.0 5.0

25° C (77° F) 25° C (77° F) 25° C (77° F) 25° C (77° F) 25° C (77° F) 18° C (64.4° F) 5° C (41° F) 23° C (73.4° F) 0°-5° C (32°-41° F) 30° C (86° F) 15° C (59° F) 5° C (41° F)

Disinfection Constant (Ct) 1.3 35 30 25 49 63 6 15 80 160 60† 170† 480†

Reference National Academy of Sciences, 1980191 Chang, 197050 Chang, 197050 Chang, 197050 Berg, 196416 Berg, 196416 Berg, 196416 Berg, 196416 Chang, 195352 Chang, 195352 Fraker, 1992102 Fraker, 1992102 Fraker, 1992102

*FRI (free residual iodine) and I2 (elemental iodine) are nearly equivalent measurements of the residual concentration of active iodine disinfectant compounds. † 100% kill; viability tested only at 15, 30, 45, 60, and 120 minutes.

Bacterial spores, such as Bacillus anthracis, are relatively resistant to halogens, but with chlorine, spores are not much more resistant than are Giardia cysts.13,295 Quantitative data are not available for iodine solutions, but iodine kills spores. Fortunately, sporulating bacteria do not normally cause waterborne enteric disease.128 Viruses.  Enteroviruses are more resistant than are enteric bacteria,191 but they constitute such a large and diverse group of organisms that generalization is especially difficult.51,156,286 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,31 or penetrates the protein capsid by chemical transformation and then attacks the nucleic acid core, as in cyst inactivation.295 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.91,282Current data suggest that HAV is not significantly more resistant than are other enteric viruses.115,207,259,273 In one test using iodine tablets, HAV was inactivated under difficult conditions more readily than was poliovirus or echovirus.258 Norovirus may be more resistant to chlorine than are several other viruses, which may account for its importance in waterborne outbreaks.146 Clumping and association of viruses with cells and particulate matter are thought to be significant factors affecting viral dis­ infection, causing departure from first-order kinetics.91,258,282 Cell-associated HAV was 10 times more resistant than was dispersed HAV. Cysts and Parasites.  Protozoal cysts are considerably more resistant than are enteric bacteria and enteric viruses, probably because of cysts’ physiologically inactive outer shell, which the disinfectant must penetrate to be effective.50,295 Halogens can be used in the field to inactivate Giardia cysts (see Figure 67-3). Testing on G. lamblia indicates similar sensitivity to both iodine and chlorine.139 Lower temperature decreases the effectiveness of halogens on Giardia: longer contact time is required in cold and dirty water.109,123,136,258 Review literature frequently attributes exaggerated resistance of Giardia to halogens.129 Jarrol and colleagues137,138tested 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. Cryptosporidium oocysts differ greatly from other protozoan cysts and are highly resistant to halogens. The Ct constant for Cryptosporidium in warm water with chlorine has been estimated to be 9600.40 Other data demonstrated 90% inactivation with 80 ppm of chlorine after 90 minutes, 14 times more resistant than Giardia cysts.149 The current recommendation for

decontaminating chlorinated swimming pools is 20 mg for 9 hours (Ct 10,800).34 From 65% to 80% of Cryptosporidium oocysts were inactivated after 4 hours by two iodine tablets in “general case” water.109 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.76,238,249,295 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. Both Cryptosporidium and Giardia are susceptible to chlorine dioxide.57,149 Schistosome cercariae are susceptible to low concentrations of chlorine.296 Limited data on parasitic helminth larvae and ova indicate the presence of such high levels of resistance that chemical disinfection is not useful.152,191,251However, 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.130,191 The latter is especially a problem for cysts and viruses, which cannot be cultured easily.246 The end point for disinfection effectiveness is now standardized by the EPA guidelines; 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 of different disinfectants for inactivation of specific microorganisms.130 To use halogens for disinfection, a consensus organism (the most resistant target) determines the Ct.130,156,295For 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 and the preference of CDC and WHO for individual household disinfection of drinking water where there is no community-level treatment, so extensive data support its use (see Table 67-9).47,155,295 1339

CHAPTER 67  Field Water Disinfection

TABLE 67-10  Disinfection Data for Iodine

PART 8  FOOD AND WATER

Toxicity

Chemistry 90,295

Chlorine reacts in water to form the following compounds: Cl 2 + H2O → HOCl + H + Cl +

−

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, the HOCl/OCl− ratio is 1 : 1; and above pH 7.5, OCl− predominates.295 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.156,295 Chloride ion (Cl−, NaCl, or CaCl2) is germicidally inactive. In addition, chlorine readily reacts with ammonia to form monochloramines (NH2Cl), dichloramines, or trichloramines, referred to as combined chlorine. Chloramines have weak disinfecting power and are calculated as a disinfectant in municipal sewage plants130,189,191,295; however, in field disinfection these compounds are not considered, and only free residual chlorine should be measured. However, at doses of a few milligrams per liter and contact times of about 30 minutes, free chlorine generally inactivates greater than 99.99% of enteric bacteria and viruses.260 The CDC-WHO Safe Water System for household disinfection in developing countries provides a dosage of 1.875 or 3.75 mg/L of sodium hypochlorite with a contact time of 30 minutes, sufficient to inactivate most bacteria, viruses, and some protozoa that cause waterborne diseases.150,155 Chlorine bleaches organic matter, making water sparkling blue, as in swimming pools.295

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.295 Animal studies using long-term chlorination of drinking water at 100 to 200 ppm have not shown toxic effects.191 Sodium hypochlorite is not carcinogenic; however, reactions of chlorine with certain organic contaminants yield chlorinated hydrocarbons, chloroform, and other trihalomethanes, which are considered carcinogenic.191,286 Public health regulations limit residual chlorine in public systems to decrease ingestion of trihalomethane. The concern is now fueled more by public fears than by scientific conclusion.295 The risk for death from infectious diseases if disinfection is not used is far greater than any risk from chlorine disinfection by-products.231,286 These compounds are not likely to form in clean wilderness surface water, since the organic precursors are not present. Products and Techniques for Chlorination Free chlorine is the most widely available and affordable of chemical water disinfectants.260 For household or field water treatment, free chlorine can be obtained in liquid, granular, and tablet forms or generated from electrolysis of salt (Appendix B; for dosage information, see Tables 67-11 to 67-13). 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, activity is rapidly lost after a few days of continuous exposure to air with high heat and

TABLE 67-11  Water Disinfection Techniques and Halogen Doses Add to 1 Liter or Quart of Water Iodination Techniques Iodine tabs   Tetraglycine hydroperiodide   EDWGT   Potable Aqua   Globaline 2% iodine solution (tincture) 10% povidone–iodine solution† Saturated solution: iodine crystals in water Saturated solution: iodine crystals in alcohol Chlorination Techniques§|| Sodium hypochlorite (household bleach 5%) 1% bleach (CDC-WHO Safe Water System)¶ Calcium hypochlorite** (Redi Chlor [0.1-g tab]) Sodium dichloroisocyanurate (NaDCC)†† (Aquatab, Kintab) Chlorine plus flocculating agent (Chlor-Floc)

Amount for 4 ppm

Amount for 8 ppm

0.5 tab

1 tab

0.2 mL 5 gtt* 0.35 mL 8 gtt 13 mL 0.1 mL‡

0.4 mL 10 gtt 0.70 mL 16 gtt 26 mL 0.2 mL

Amount for 5 ppm

Amount for 10 ppm

0.1 mL 2 gtt 8-10 gtt 0.25 tab

0.2 mL 4 gtt 0.5 tab 1 tab (8.5 mg NaDCC) 1 tab‡‡

EDWGT, Emergency drinking water germicidal tablet. *Measure of a drop varies from 16-24 gtt/mL, median 20 gtt/mL is used here. † Povidone–iodine solutions release free iodine in levels adequate for disinfection, but scant data are available. ‡ Measure with dropper or tuberculin syringe. § Recommended concentration of chlorine for emergency point-of-use water treatment varies across health agencies, but generally does not exceed 5 mg/L. For long-term household use in developing areas, CDC Safe Water System establishes a maximum of 2 mg/L, which is the limit of taste tolerance for many people (see reference 155). || For treatment of large volumes, see reference 280 for TB MED 577. ¶ Safe Water System for long-term routine household point-of-use water disinfection recommends a hypochlorite dose of about 2 mg/L in clear water and 4 mg/L in slightly turbid water. This results in a low yet effective target residual concentration with acceptable taste, but requires testing in a particular water source to ensure sufficient residual. **Concentrated source of hypochlorite available as granules or tablets. Useful for treating larger volumes of water. Commonly used to treat swimming pool water. †† Available in different strengths to treat different volumes of water. Check packaging to determine proper dose. ‡‡ Yields 8 ppm.

1340

With Halogenations in the Field

Concentration of Halogen 2 ppm 4 ppm 8 ppm

Contact Time in Minutes at Various Water Temperatures 5° C (41° F)

15° C (59° F)

30° C (86° F)

240 180 60

180 60 30

60 45 15

Note: 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.

humidity. To extend shelf-life, many tablets are individually wrapped in foil. Superchlorination–Dechlorination.  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. This method of chlorination can readily be adapted to field use. High doses of chlorine are added to the water in the form of calcium hypochlorite crystals to achieve concentrations of 30 to 200 ppm of free chlorine. These extremely high levels are above the margin of safety for field conditions and rapidly kill all bacteria, viruses, and protozoa and could kill Cryptosporidium with overnight contact times. 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 + 2H2O → 2HOCl + Ca ++ ( OH − )2 Ca( OCl )2 + 2H2O2 → CaCl 2 + 2H2O + 2O2 Excess hydrogen peroxide reacts with water to form oxygen and water. Chloride has no taste or smell. Hydrogen peroxide is also a weak disinfectant,307 although not in common use.

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 (70% available chlorine) loses only 3% to 5% of available chlorine per year. Thirty-percent hydrogen peroxide is corrosive and burns skin, so it should be used cautiously. There is currently no commercial formulation; however, the ingredients can be easily obtained and packaged in small Nalgene bottles.

IODINE Iodine has been used as a topical and water disinfectant since the beginning of the 20th century.156 Iodine is effective in low concentrations for killing bacteria, viruses, and cysts, and in higher concentrations against fungi and even bacterial spores, but it is a poor algicide52,114,191 (see Table 67-10 and Figure 67-3). Iodine has been used successfully in low concentrations for continuous water disinfection of small communities.148 Despite several advantages over chlorine disinfection, it has not gained general acceptance because of concern for its physiologic activity. Recently the European Union has stopped the sale of iodine products used for water disinfection. 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:52,114 I2 + H2O → HOI + I− + H +

TABLE 67-13  Chlorine Dose for Large-Volume Water Disinfection Gallons to be Chlorinated

1 mg/L*

2 mg/L

5% Liquid Bleach 5 6 gtt 0.75 mL 10 0.75 mL 1.5 mL 25 2 mL 3.8 mL 36 3 mL 5.5 mL 50 4 mL 1.5 tsp 100 7.7 mL 3 tsp 400 2 tbsp 4.25 tsp 500 3 tbsp 0.33 C 1000 0.33 C 0.67 C 70% Available Chlorine (Calcium Hypochlorite or Solution Concentrate†) 5 0.9 mL 1.7 mL 10 1.7 mL 3.3 mL 25 4.1 mL 8.3 mL 36 6 mL 11.9 mL 50 8.3 mL 16.6 mL 100 16.6 mL 33 mL 400 0.92 mL 1.9 mL 500 1.3 mL 0.5 tsp 1000 0.5 tsp 1 tsp

5 mg/L

10 mg/L

1.9 mL 3.8 mL 2 tsp 2.75 tsp 4 tsp 3 tbsp 0.75 C 1C 1.75 C

3.8 mL 1.5 tsp 4 tsp 2 tbsp 3 tbsp 5 tbsp 1.5 C 1.75 C 3.25 C

4.1 mL 8.3 mL 20.7 mL 29.8 mL 0.6 mL 0.25 tsp 1 tsp 1.25 tsp 2.5 tsp

8.3 mL 16.6 mL 41.4 mL 0.9 mL 0.25 tsp 0.5 tsp 2 tsp 2.5 tsp 5 tsp

100 mg/L 8 tsp 16 tsp 1C 1.25 C 1.75 C 3.25 C 3 qt 1 gal 2 gal 0.25 tsp 0.5 tsp 1.25 tsp 1.75 tsp 2.5 tsp 5 tsp 19 tsp 0.5 C 1C

Data from U.S. Army: Sanitary control and surveillance of field water supplies, Dept. of Army technical bulletin (TB Med 577), Washington, DC, December 15, 2005, Departments of the Army, Navy, and Air Force. *For all chlorine residual concentrations in water, values in parts per million (ppm) are equivalent to values in milligrams per liter (mg/L). † The shaded area of the table indicates the volume of a concentrated solution made from dissolving 1 tsp of 70% calcium hypochlorite (most commonly used for swimming pool chlorination) in water.

1341

CHAPTER 67  Field Water Disinfection

TABLE 67-12  Recommendations for Contact Time

PART 8  FOOD AND WATER

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, because inactivation of organisms depends directly on oxidation potential, without involving cell wall diffusion.50 Their relative concentrations are determined by pH and concentration of iodine in solution.52 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.52 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 disadvantage of iodine is its physiologic activity, with effects on thyroid function, potential toxicity, and allergenicity.204 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 (0.07 to 0.14 oz) of free iodine or 29.6 to 59.1 mL (1 to 2 oz) of strong tincture.100 Iodide is absorbed into the bloodstream but has minimal toxicity (thus its use for radiographic imaging). Sensitivity reactions, including rashes and acne, may occur with usual supplementation levels of iodine. Given the physiologic 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.204 Chronic iodide poisoning, or iodism, occurs after prolonged ingestion of sufficiently high doses, but marked individual variation is seen. Symptoms simulate upper respiratory illness, with irritation of mucous membranes, mucus production, and cough. Thyroid Effects of Iodine Ingestion.  Iodine is an essential element for normal thyroid function and health in small amounts of 100 to 300 mcg/day. 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. Most persons can tolerate high doses of iodine without development of thyroid abnormalities,29 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.29,243 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 older adults, 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 iodinesufficient areas and had antithyroid antibodies, suggesting underlying thyroiditis; one had a mother and sister with Hashimoto’s thyroiditis.162 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. Goiters were discovered among a group of Peace Corps volunteers in Africa and were linked epidemiologically to the use of iodine resin 1342

water filters.102,146a 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:29,243,297 (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 older adults, 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.  The reported incidences of goiter, hypothyroid effects, and hyperthyroid response vary so widely that they provide no clear dose limits.204 These data and other controlled trials of high doses have been reviewed.9 The use of iodine for decades as a field water disinfectant by military and civilian populations without reports of associated clinical thyroid problems suggests that the risks are minimal and would be outweighed by the risk for enteric disease. Biochemical assays show that changes in thyroid function tests are common with excess iodine intake; however, changes in thyroid function usually remain subclinical. All changes reverted to normal within weeks to months without persistent thyroid disease. Studying longer duration of ingestion, Freund104 found minimal changes and no clinical problems when water with 1 mg/L of iodine was used to disinfect water at a prison for up to 3 years. Referring to the same project, Thomas and colleagues271 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. The military studied long-term toxic effects of iodine, adding sodium iodide to drinking water at a naval base for 6 months.188 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 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 were evident. Recommendations.  The 2001 U.S. Department of Agriculture (USDA) Recommended Dietary Intake suggested an upper limit of 1.1 mg/day for adults, weight adjusted for children. WHO did not set a guideline value for iodine in drinking water, because of a paucity of data and because it is not recommended for longterm disinfection. The EPA and 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. However, this period of short use appears arbitrary. The European Union revoked approval of iodine for water purification on October 25, 2009, and it can no longer be sold for this purpose. Available data suggest the following: • High levels of iodine, such as those produced by recommended doses of iodine tablets, should be limited to periods of 1 month or less. • Iodine treatment that produces a low residual (1 mg/L or less) appears safe, even for long periods in people with normal thyroid function. This would require very low doses of iodine added to the water or an activated charcoal stage to remove residual iodine. • Persons planning to use iodine for a prolonged period should have the thyroid gland examined and thyroid

Preparation

Iodine (%)

Iodide (%)

Type of Solution

2.0

2.4 (sodium)

Aqueous

5.0 2.0 7.0

10.0 (potassium) 2.4 (sodium) 9.0 (potassium)

Aqueous Aqueous-ethanol Ethanol (85%)

Iodine topical solution Lugols solution Iodine tincture Strong iodine solution

function measured to ensure that a state of euthyroidism exists. • 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

Products and Techniques for Iodination Several formulations of iodine are available for field use. (See Tables 67-10 and 67-15 for efficacy, Tables 67-11 to 67-14 for product dosing, and Appendix B for details on commercial products, including tablets and crystalline iodine.) Resins.  Iodine can be bound to an inert resin to create a disinfectant with unique properties. These are considered demand disinfectants because iodine transfers from the resin to the microorganism on contact, aided by electrostatic forces, but limited amounts of iodine dissolve in the water. Iodine binds to the wall or capsule, penetrates, and kills the organism. This effectively exposes the organisms to high iodine concentrations and allows reduced contact time compared with dilute iodine solutions. Residual iodine concentration in the water depends on the properties of the resin, the temperature of the water, and presence of an activated charcoal stage.

Resins have proved effective against bacteria, viruses, and cysts but not against C. parvum oocysts or bacterial spores.170 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.278 Data suggest that both contact time and iodine residual are important for optimal results.99,171,170 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.171 A simple resin filter 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 desired results.110 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.92 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).170 Iodine Resin Filters.  Iodine resins have been used for water disinfection in individual or small systems and incorporated into filter designs for field use. Iodine filters are generally designed with two stages in addition to the iodine resin. A microfilter, generally 1 µm, effectively removes Cryptosporidium, Giardia, and other halogen-resistant parasitic eggs or larva. Because iodine resins kill bacteria and viruses rapidly, limited contact time is required for most water.110 Addition of a third stage of activated charcoal removes dissolved residual, which may decrease efficacy.171,275 In the United States, inconsistent results of product testing under variable conditions led to withdrawal of most filter models from the market. It was not clear whether failure to achieve desired results was related to inadequate contact with the resin or insufficient contact time with iodine residual. Resins are now being used in point-of-use household devices in other countries with generally good but variable microbial removal or inactivation. Significant levels of residual iodine are noted without a charcoal stage.58

TABLE 67-15  Data on Efficacy of Iodine Tablets Halogen

Dose

Chlor-Floc

1 tab or 2 tabs

Globaline

1 tab 2 tabs

FRC (mg/L)

Time min

4-7 4-14

5 20 5 20 12 20 45 20 60 40 30-40

AquaPure

2 tabs 1 tab

7-11

Globaline

2 tabs 1 2 1 or 2

10

Iodine tabs

8-16 8 16

20 60 180 120 60 60 60

Temperature 10°-20° C (50°-68° 10°-20° C (50°-68° 10°-20° C (50°-68° 10°-20° C (50°-68° 25° C (77° F) Various 5° C (41° F) 5° C (41° F) 5° C (41° F) 5° C (41° F) 15°-25° C (59°-77° 15°-25° C (59°-77° 15°-25° C (59°-77° 15°-25° C (59°-77° 15° C (59° F) 5° C (41° F) 5° C (41° F) 5°-25° C 5° C (41° F) 5° C (41° F)

Organism

Log reduction

Reference

F) F) F) F)

Bacteria Giardia muris Rotavirus Poliovirus Poliovirus Bacteria G. muris Rotavirus Poliovirus

6 3 4 Inadequate Inadequate 6 3 4 60

Powers, 1994212

F) F) F) F)

Bacteria Rotavirus Poliovirus G. muris Giardia Giardia Giardia Hepatitis A Poliovirus, echovirus Poliovirus, echovirus

6 4 2 2 3 3 3 4 Insufficient 4

Powers, 1992214

Powers, 1991213 Sobsey, 1991261

1343

CHAPTER 67  Field Water Disinfection

TABLE 67-14  Iodine Solutions

PART 8  FOOD AND WATER

Given some of the variability in results and uncertainty of mechanism of action, the U.S. outdoor gear companies have abandoned iodine resin–containing portable hand-pump filters, and only drink-through bottles remain on the U.S. market. Other products may still be available outside the United States or via Internet retailers.

CHLORINE VERSUS IODINE A large body of data proves that both iodine and chlorine are effective disinfectants with adequate concentrations and contact times, except for dealing with Cryptosporidium.128 Under identical water test conditions and using recommended dose and contact time, chlorine and iodine tablets are similar in their biocidal activity211 (see Tables 67-11, 67-12, and 67-15). A few investi­ gators have reported data suggesting ineffectiveness of common halogen preparations. Jarroll and associates138,139tested 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.163 Ongerth and colleagues201 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. Schlosser and co-workers248 found that sodium hypochlorite tablets, sodium dichloroisocyanurate tablets, and iodine in ethanol used according to package instructions removed 2 to 3 log of bacteria in clear water, but less in turbid river water. This suggests the need for clarifying dirty water before halogen use and, if possible, providing extra contact time in any situation. Iodine has some 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.75,114,148,191 The major disadvantage is its physiologic activity. Taste Objectionable taste and smell are the major problems with acceptance of halogens. Most objectionable taste in treated water is derived from dissolved minerals, such as sulfur, and from chlorine compounds, chloramines, and organic nitrogen compounds, even at extremely low levels. People are familiar with the taste of chlorine compounds; 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 used to the faint taste of chlorine in water note a distinct taste at 5 ppm and a strong, unpleasant taste at 10 to 15 ppm.236 With the promotion of chlorination for household use, focus groups on taste testing have found that the majority of CDC-WHO Safe Water System users are comfortable drinking water with a free chlorine residual of up to 2 mg/L; however, there is significant regional variation in the acceptable maximum residual, and many found the taste objectionable and unsuitable at 3 to 4 mg/L.155 The higher sodium hypochlorite dosages necessary to ensure maintenance of chlorine residual in turbid waters exacerbate the taste and odor concerns.150 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.23,75,107 Distinct taste and odor are produced by 8 ppm of iodine; however, tablets yielding these concentrations were preferred by military personnel over tincture of iodine in equivalent doses.52,190 Taste tolerance or preference for iodine over chlorine is individual. Opposite preferences have been documented when direct comparisons are done.199,214Informal taste tests suggest that most 1344

BOX 67-10  Improving the Taste of Halogens • Decrease dose and increase contact time. • Clarify cloudy water, allowing decreased halogen. • Remove halogen. • Use granular activated charcoal. • Chemical reduction techniques • Ascorbic acid • Sodium thiosulfate • Chlorination-dechlorination • Zinc-copper (KDF) media • Alternative techniques: • Heat • Filtration • Chlorine dioxide or mixed species (Miox)

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. Taste can be improved by several means (Box 67-10). Minimizing Dose.  The relationship between halogen concentration and time allows use of the minimum necessary dose, with a longer contact time (see Tables 67-11 and 67-12). 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 67-3). 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 one-half but can be added to 2 qt instead of 1 qt of water to yield concentrations consistent with the other preparations. The recommended doses of the liquid iodine preparations yield 4 mg/L. Because even clear surface water has some halogen demand, this dose of 4 mg/L should generally not be reduced for surface water, but for backing up tap water in developing countries or prefiltered water, the dose may routinely be cut in one-half for an added dose of 2 ppm with a few hours of contact time.102,124,156 A similar approach can be used for chlorination methods. None of these concentrations will destroy Cryptosporidium oocysts. Temperature and organic matter in the water may be manipulated. Increasing the temperature of the water, especially when initially near 5° C (41° F), decreases the Ct constant (see Tables 67-11 and 67-12 and Figure 67-3). Filtering water before adding halogen improves the reliability of a given halogen dose by decreasing halogen demand, allowing a lower dose of halogen.191 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. UV light also depletes free chlorine.295 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. In superchlorination– dechlorination, hydrogen peroxide “dechlorinates” water treated with calcium hypochlorite by forming calcium chloride.

Miscellaneous Disinfectants CHLORINE DIOXIDE Chlorine dioxide (ClO2), a potent biocide, has been used for many years to disinfect municipal water and in numerous other large-scale applications. Until recently, the benefits of chlorine dioxide have been limited to large-scale applications, because it is formulated as a volatile gas that must be produced on-site with sophisticated chemical-generation equipment. Newer methods enable cost-effective and portable chlorine dioxide generation and distribution for use in an ever widening array of small-scale applications (Box 67-11). For point-of-use treatment of water, chlorine dioxide is produced on site from the reaction of sodium chlorite with acid.21,257 For example: 5NaClO2 + 4 HCl → 4ClO2 + 5NaCl + 2H2O It is capable of inactivating most waterborne pathogens, including C. parvum oocysts, at practical doses and contact times. It is as least as effective a bactericide as chlorine, and far superior as a virucide.295 Chlorine dioxide is not as unstable as ozone but does not produce a lasting residual. It does not form chlorinated compounds in the presence of organics and is efficacious over a wide pH range. By-products of chlorine dioxide are chlorite (ClO2−) and chlorate (ClO3−). There are several new commercial point-of-use applications using chlorine dioxide in liquid or tablet form (see Appendixes).

MIXED SPECIES DISINFECTION (ELECTROLYSIS) Passing a current through a simple brine salt solution generates free available chlorine, as well as other “mixed species” disinfectants that have been demonstrated effective against bacteria,

BOX 67-11  Chlorine Dioxide Advantages Effective against all microorganisms, including Cryptosporidium Low doses have no taste or   color Portable device now available   for individual and small group field use and simple to use More potent than equivalent doses of chlorine Less affected by nitrogenous wastes

Disadvantages Volatile, so do not expose tablets to air and use generated solutions rapidly No persistent residual, so does not prevent recontamination during storage Sensitive to sunlight, so keep bottle shaded or in pack during treatment

Relative susceptibility of microorganisms to chlorine dioxide: bacteria > viruses > protozoa.

viruses, and bacterial spores.245 The process is well described and can be used on both large and small scales. It is practical and economic enough to be useful in developing areas of the world. The exact composition of the resulting solution is not well delineated because many of the compounds are evanescent and unstable. However, the resulting solution has greater disinfectant ability than a simple solution of sodium hypochlorite. It has even been demonstrated to inactivate Cryptosporidium, suggesting that chlorine dioxide is among the chemicals generated.289 A pointof-use commercial product is now available (Miox, see product appendixes for more information).

SOLAR PHOTOCATALYTIC DISINFECTION Advanced oxidation processes uses sunlight to catalyze production of hydroxyl radicals (OH−) and free electrons, which are potent oxidizers. Various semi-conductor materials can be used, but the most efficacious is titanium dioxide (TiO2). High energy short-wavelength photons from sunlight promote the photochemical reactions. In addition to being an excellent disinfectant for various micro-organisms, this process is unique in its ability to break down complex organic contaminants and most heavy metals into carbon dioxide, water, and inorganics, which is driving considerable research for industrial processes and largescale water treatment. For field water disinfection, nanoparticles coated with TiO2 can be integrated into a plastic bag and remain active for hundreds of uses (see Appendix A).23a

OZONE Ozone is an unstable form of oxygen, with the chemical formula O3. In solution, it decays to O2, producing free hydroxyl radicals. Both ozone and the hydroxyl radicals are two of the most powerful oxidants used in water treatment.21 It is a highly effective disinfectant widely used in municipal water treatment plants.295 Ozone and chlorine dioxide are the only chemical disinfectants that have been demonstrated effective against Cryptosporidium in typical concentrations.18,57,149,203 Advantages of ozone disinfection are that it has high efficacy against all groups of microorganisms and that it produces very few disinfection by-products.18 The main disadvantage is its chemical instability: there is no stable product that can be used in the field. Ozone is a colorless gas manufactured by passing air or oxygen through a high-voltage current discharge. The resulting ozone-rich gas is then dissolved in water. Clearly this is not conducive to small, point-of-use generation, so consumers should be skeptical of techniques claiming to rely on ozone.

SILVER Silver ion has bactericidal effects in low doses. The literature on antimicrobial effects of silver is confusing and contradictory.132,168,191,295,299 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 with an upper limit of 10 g per lifetime—NOAEL (no observed adverse effect level). This would be reached only after drinking 3 L/day containing 0.1 mg/L over 70 years. WHO acknowledges that the daily intake of silver when used to maintain the bacteriologic quality of drinking water can constitute the major route of oral exposure but states that “It is unnecessary to recommend a healthbased guideline value because [silver] is not hazardous to human health at concentrations normally found in drinking water.” At the recommended concentration of 50 ppb for water treatment, disinfection requires several hours. Experimental results indicate 18% survival of E. coli at 3 hours at 40 mcg/L. S. typhi 1345

CHAPTER 67  Field Water Disinfection

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.199,236 Sodium thiosulfate similarly “neutralizes” iodine and chlorine. A few granules in 1 qt 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. This is the active ingredient in Katadyn Antichlorine drops. Copper-zinc alloys act as catalysts to reduce free iodine and chlorine through an electrochemical reaction (see Copper and Zinc, later).

PART 8  FOOD AND WATER

was reduced more than 5 log at 50 mcg/L with a 1-hour exposure; poliovirus was not reduced at 50 mcg/L with a 1-hour exposure.14 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.50,191 Nevertheless, water disinfection systems using silver have been devised for spacecraft, swimming pools, and other settings.295 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.170 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.53 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. Micropur Forte tablets release free chlorine for disinfection and silver for prolonged persistence of antimicrobial activity. Silver impregnation of filters may inactivate pathogens that pass through the filter pores or limit bacterial growth in the filter itself (bacteriostatic). Ceramic filters coated with silver have higher removal rates of bacteria, and filters that had been just recoated with silver initially yielded much higher disinfection efficiencies but were not able to sustain them.14,19,107 Filter cartridges impregnated with silver typically become colonized with heterotrophic bacteria, and effluent bacterial populations are about as large as units without silver. These bacteria have not been linked to increased illness.14,93,107,223 Colonization of filters with pathogenic coliforms has not been demonstrated, but protective effect cannot be attributed to silver impregnation.93,223

POTASSIUM PERMANGANATE Potassium permanganate is a strong oxidizing agent with some disinfectant properties. It is used in municipal disinfection to control taste and odor. It has been used in a 1% to 5% solution as a drinking water disinfectant190 and is still used for this purpose in some countries, as well as for washing fruits and vegetables. 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 30 minutes at room temperature; 30 mg/L was effective in inactivating HAV within 15 minutes.273 Although potassium permanganate clearly has disinfectant action and is frequently used in some parts of the world, it cannot be recommended for point-of-use water disinfection unless no other means are available, because quantitative data are not available for viruses and no data are available for protozoan cysts. 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.”54 The solutions are deep pink to purple and stain surfaces. The 1346

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.26,191,307 Small doses (1 mL of 3% H2O2 in 1 L water) are effective for inactivating bacteria within minutes to hours, depending on the level of contamination. Tested against seven bacterial strains, hydrogen peroxide killed 1 × 106 colony-forming units per milliliter overnight, with 80% kill in 1 hour. Viruses require extremely high doses and longer contact times. It is a promising sporicidal agent in high (10% to 25%) concentrations. Hydrogen peroxide is 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, yielding the innocuous end products oxygen and water. It is considered nature’s disinfectant, because it is naturally present in milk and honey, helping to prevent spoilage. Solutions lose potency in time, but stabilizers can be added to prevent decomposition.26 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.

PERACETIC ACID Peracetic acid (CH3COOOH) consists of a quaternary mix of acetic acid, hydrogen peroxide, peracetic acid, and water with a pH value close to 2. It has been used with success in water disinfection because of its strong oxidizing properties.

CITRUS Citrus juice has biocidal properties. Lemon or lime juice has been shown to destroy V. cholerae at a concentration of 2% (equivalent of 2 tbsp/L of water) with a contact time of 30 minutes. A pH of less than 3.9 is essential, which depends on the concentration of lemon juice and the initial pH of the water.78 Lime juice also killed 99.9% of V. cholerae on cabbage and lettuce and inhibited growth of V. cholerae in rice foods, suggesting that adding lime juice to water, beverages, and other foods can reduce disease risks.257 More research is needed before this can be recommended as more than an ancillary or emergency measure. Commercial products using citrus cannot be recommended as primary means of water disinfection.

ULTRAVIOLET LIGHT UV lamp disinfection systems are widely used to disinfect drinking water at the community and household levels (Box 67-12). In sufficient doses, all waterborne enteric pathogens are inactivated by UV radiation (UVR). The germicidal effect of UV light is the result of action on the nucleic acids of bacteria and depends on light intensity and exposure time.49 Bacteria and protozoan parasites require lower doses than do enteric viruses

BOX 67-12  Ultraviolet Irradiation Advantages Effective against all microorganisms Imparts no taste Portable device now available for individual and small group field use and simple to use Available from sunlight

Disadvantages Requires clear water Does not improve water esthetics No residual effect—does not prevent recontamination during storage Expensive Require power source Requires direct sunlight, prolonged exposure; dose low and uncontrolled

Relative susceptibility of microorganisms to ultraviolet: protozoa > bacteria > viruses.

Advantages Improves the microbiologic   quality of drinking water; including protozoan cysts Does not change the taste of water Simple in application; can be   used at household level Utilizes sunlight Requires no special equipment   or power; relies on local resources and renewable   energy Can be used in austere environments

Disadvantages Requires clear water No residual effect—does not prevent recontamination during storage Does not improve water esthetics Not useful to treat large volumes of water; use maximum 2-L bottle. Requires strong, direct, abundant sunlight, prolonged exposure; dose low and uncontrolled

Relative susceptibility of microorganisms to SODIS: protozoa > bacteria > viruses.

and bacterial spores. However, all viruses, including hepatitis A and norovirus, are susceptible with relatively minor differences, and follow similar kinetics.126 Bacteria (vegetative cells) are significantly more susceptible to UVR than are viruses. Giardia and Cryptosporidium are susceptible to practical doses of UVR and may be more sensitive because of their relatively large size.18,126,164 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 irradiation with lamps requires a power source and is costly. UV light has no residual disinfection power; water may become recontaminated, or regrowth of bacteria may occur.93 Particulate matter can shield microorganisms from UV rays. A portable field unit, Steri-PEN, is now available (see Appendix A). Solar Irradiation There is now strong evidence that UV irradiation by sunlight in UV-A range can substantially improve microbiologic quality of water and reduce diarrheal illness in developing countries. Recent work has confirmed efficacy and optimal procedures of the solar disinfection (SODIS) technique49,66,197,257(Box 67-13). Transparent bottles (e.g., clear plastic beverage bottles) are exposed to sunlight for a minimum of 4 to 6 hours, but some investigations demonstrate improved benefit from several sequential days. Multiple studies demonstrate reduction of enteric bacteria, viruses, and protozoan cysts, and some data exist for reduction of bacterial spores.147,176,177,262 With a water temperature of 30° C (86° F), 6 hours of mid-latitude midday summer sunshine are required to achieve a 3-log reduction of fecal coliforms.179 UV and thermal inactivation were strongly synergistic for 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.175 Whereas thermal inactivation is effective in turbid water, UV effects are inhibited.142 If cloudiness is greater than 50%, the plastic bottles need to be exposed for 2 consecutive days in order to produce water safe for consumption. However, if water temperatures exceed 50° C (122° F), 1 hour of exposure is sufficient to obtain safe drinking water. The treatment efficiency can be improved if the plastic bottles are exposed on sunlight-reflecting surfaces such as aluminum or corrugated iron sheets. Use of a simple reflector or solar cooker can achieve pasteurization temperatures of 65° C (149° F). Oxygenation induces greater reductions of bacteria, so agitation is recommended before solar treatment in bottles. Various types of transparent plastic materials are good transmitters of light in the UV-A and visible range of the solar spectrum. Plastic bottles are made of either polyethylene terephtalate (PET) or polyvinylchloride (PVC). The use of bottles made from PET instead of PVC is recommended because PET contains fewer

additives than do bottles made from PVC. Glass bottles are not used for SODIS because the transmission of UVR through glass is determined by its content of iron oxide; ordinary window glass of 2-mm thickness transmits almost no UVA light. Because UVR is reduced at increasing water depth, the containers used for SODIS should not exceed a water depth of 10 cm (3.9 inches). Aged or heavily scratched plastic bottles show reduced UV transmittance, which in turn can result in less efficient inactivation of microorganisms.179 In summary, where strong sunshine and clear water are 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.179

COPPER AND ZINC Kinetic degradation fluxion (KDF) is a high-purity copper-zinc formulation that uses a basic chemical process known as redox (oxidation-reduction) to remove chlorine, heavy metals such as lead and mercury, iron, and hydrogen sulfide from water supplies. Its main actions are through its strong redox potential of 500 mV due to the propensity to exchange electrons with other substances. The redox reactions change contaminants into harmless components: chlorine into chloride (removing the taste of chlorine or iodine from treated water), 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 and is used for this purpose in GAC beds and carbon block filters, extending the life of carbon and improving its effectiveness. KDF or copper alone has bacteriostatic with some bactericidal activity; microorganisms may be killed by the electrolytic field, and by formation of hydroxyl radicals and peroxide water molecules.168 Although KDF has been ruled a “pesticidal device” by the EPA, it should not be used as the sole means of water treatment and is best combined with filtration or chlorination. KDF media can be manufactured as granules, fine steel wool– like media, or brushes with wire bristles. Currently, this technique is mostly applied in industrial settings and household in-line filters. No portable products are currently targeting the outdoor market.

Comparative Studies and Preferred Techniques Presumably, standard protocols for product testing in experienced laboratories would provide comparable and reproducible results. However, studies that directly compare techniques or products often yield results that vary widely from the individual product testing. Data for the effectiveness of water disinfection techniques for wilderness travelers are essentially all done in the laboratory and not in field settings during actual use. On the other hand, many studies have recently been done on point-of-use devices in households and refugee settings in developing countries, where contamination and the risk for illness are many times higher, so techniques can be evaluated for both microbiologic reduction under real use and reduction of illness attributable to water treatment (Table 67-16). Moreover, these techniques are necessarily low cost, simple to use, and include some improvised methods, which make them particularly valuable for survival, disaster, or other austere situations characterized by suboptional conditions and supplies. Furthermore, the need for household point-of-use water treatment in developing countries is stimulating innovative approaches to disinfection that combine multiple treatment steps in series, as is done in municipal plants. For those tasked with engineering water solutions for communities or populations in austere environments, point-of-use methods were found to be more effective than were source solutions.60,155 Several studies comparing halogens are noted in the Iodine Versus Chlorine section.128,137,139,211,248 Lee and Lee160 compared iodine, chlorine dioxide, mixed oxidants, and UV radiation (UVR) 1347

CHAPTER 67  Field Water Disinfection

BOX 67-13  Solar Disinfection (SODIS)

PART 8  FOOD AND WATER

TABLE 67-16  Efficacy and Effectiveness of Point-of-Use Technologies for Developing World Households Treatment Process

Pathogen

Ceramic filters

Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa

Free chlorine Coagulation/chlorination Biosand filtration SODIS

Optimal Log Reduction*

Expected Log Reduction†

Diarrheal Disease Reduction‡

2 0.5 4 3 3 3 7 2-4.5 3 1 0.5 2 3 2 1

63% (51%-72%) for candle filters 46% (29%-59%) for bowl filters 37% (25%-48%)

6 4 6 6 6 5 9 6 5 3 3 4 5.5 4 3

31% (18%-42%) 47% (21%-64%) 31% (26%-37%)

Data from multiple studies, analyzed and summarized by Sobsey and colleagues.262 SODIS, Solar disinfection. *Skilled operators using optimal conditions and practices (efficacy); log reduction: pretreatment minus post-treatment concentration of organisms (e.g., 6 log = 99.999% removal). † Actual field practice by unskilled persons (effectiveness). Depends on water quality, quality and age of filter or materials, following proper procedure, and other factors. ‡ Summary estimates from published data. Vary with consistency and correct use of technique, integrity of techniques (e.g., cracked filter), and other household sanitation measures.

contamination, methods of disinfection available, and tolerance of risk.

for disinfection of coccidian oocysts to represent Cryptosporidium and found that only UVR consistently inhibited sporulation. Iodine in recommended contact times was little better than controls, and chlorine dioxide left nearly one-quarter of oocysts viable in moderately contaminated water and was similar to controls in highly contaminated water. One important factor may have been the large number of organisms added to the water, which greatly exceeded likely levels encountered in surface water. Betancourt and Rose reviewed methods for removal of Cryptosporidium and found UVR and filtration effective.18 Sobsey and colleagues262 reviewed data for point-of-use methods for household disinfection in developing countries. All methods had high levels of optimal effectiveness, but their actual efficacy was much less over time, likely impacted by inconsistent use. Verma and Arankalle290 evaluated eight different higher-technology household disinfection units sold in India that each used some combination of filtration, iodine resin, chlorination, and UVR. Average removal of hepatitis E virus was 1 to 3 log, except for a hollow-fiber membrane unit that achieved 6.5-log removal. This study highlights the incorporation of common disinfection techniques into household appliances for point-of-use water treatment and the discrepancy between optimal and actual efficacy for these devices, which would certainly apply to field units as well. Similarly, another study compared ceramic filters and iodine resin household devices and found high levels of bacterial removal, but that reduction of viruses and microspheres did not meet standards of EPA protocols.59 One recently developed household device that does not require power and combines the complementary methods of filtration and disinfection did meet EPA criteria for microbiologic reduction.59 Although the gap between optimal and actual efficacy is disturbing, it is reassuring that in actual field conditions, all point-of-use techniques will markedly decrease the number of microorganisms and risk for illness.60,262 As in any wilderness medical situation, some basic assessment must be done of the likely level and type of

PREFERRED TECHNIQUE Field disinfection techniques and their effects on microorganisms are summarized in Table 67-17. The optimal technique for an individual or group in the wilderness or traveling in developing countries depends on the number of persons to be served, space and weight available, quality of source water (Table 67-18), personal taste preferences, and availability of fuel. The most effective technique may not always be available, but all methods will greatly reduce the load of microorganisms and reduce the risk for illness. A multibarrier approach for drinking water treatment in which a combination of various disinfectants and filtration technologies are applied for removal and inactivation of different microbial pathogens will provide a lower risk for microbial contamination.18 A combination of clarification using coagulation–flocculation and filtration followed by chlorination remains the standard for water treatment worldwide. The CDC and WHO also promote chlorine for household level point-of-use disinfection in the developing world.155 In austere situations such as disasters or refugee camps, hypochlorite (household bleach) or chlorination– flocculation packets may be available. If not, the SODIS technique or sand filters can be used with improvised materials. For environments with a high-quality, low-risk source water, any of the primary techniques is adequate, understanding that the limitation for halogens is Cryptosporidium oocysts, and that microfilters may not remove all viruses. 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 heat, ultrafiltration, UVR, or a two-stage process of filtration and halogens. Chlorine dioxide or mixed species techniques are currently the only one-step

TABLE 67-17  Summary of Field Water Disinfection Techniques

Heat Filtration Halogens Chlorine dioxide

Bacteria

Viruses

Giardia/Amebae

Cryptosporidium

Nematodes/Cercaria

+ + + +

+ +/−* + +

+ + + +

+ + − +

+ + +/−† +/− †

Most filters make no claims for viruses. Reverse osmosis and Sawyer 0.02 µm hollow-fiber filter technology can be effective. General Ecology claims virus removal. Eggs are not very susceptible to halogens but are very low risk for waterborne transmission.

*

†

1348

“Pristine” Wilderness Water With Little Human or Domestic Animal Activity Primary concern

Giardia, enteric bacteria

Effective methods

Any single-step method† Low-risk water; many would choose to drink untreated

Developed or Developing Country Tap Water in Developing Country

Clear Surface Water Near Human and Animal Activity*

Bacteria, Giardia, small numbers of viruses Any single-step method†

All enteric pathogens, including Cryptosporidium 1. Heat 2. Filtration plus halogen (can be done in either order) 3. Hollow-fiber ultrafiltration 4. Chlorine dioxide 5. Ultraviolet (commercial product, not sunlight)

Risk varies depending on country; judgment required for decision to treat

Cloudy Water All enteric pathogens plus microorganisms CF followed by second step (heat, filtration, or chemical)

CF, Coagulation–flocculation. *Includes agricultural run-off with cattle grazing or sewage treatment effluent from upstream villages or towns. † Includes heat, filtration, halogens, chlorine dioxide, ultraviolet irradiation.

chemical processes available. 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 for removing most chemicals. Water from cloudy low-elevation rivers, ponds, and lakes in developed or developing countries that does not clear with sedimentation should be pretreated with coagulation–flocculation and then disinfected with heat or halogens. Tablets combining coagulation–flocculation and chlorination are readily available and have extensive testing to demonstrate effectiveness.72,87,211,225 Filters can be used but will clog rapidly with silted or cloudy water. A sand filtration unit can be improvised.150 Coagulation– flocculation will also remove some chemical contamination. The preferred method of treatment for the military, when large-scale equipment can be brought to the site, is a reverse osmosis water purification unit, because it can produce highquality water from a low-quality source. For smaller groups, the military relies mainly on monitored chlorine. Individual means include iodine tablets, Chlor-Floc tablets, and chlorine liquid bleach.280 Chemical agents 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 for stored water, including cost, ease of handling, and minimal volatilization in tightly covered containers.185 A minimum residual of 3 to 5 mg/L should be maintained in the water. Superchlorination–dechlorination 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, because it is a poor algicide. Silver has been approved by the EPA for preservation of stored water. Chlorine dioxide does not maintain a residual concentration. On ocean-going 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.

Prevention and Sanitation Studies in developing countries have demonstrated a clear benefit in the reduction of diarrheal illness and other infections from safe drinking water, hygiene, and adequate sanitation.* Although

*References 60, 134, 166, 182, 217-218, 226, 260.

a benefit can be demonstrated for these interventions independently, the benefit is greater when all are applied together, especially with appropriate education.53 Wilderness travelers essentially live in conditions similar to the developing world, without running water or sanitation. Unfortunately, many wilderness travelers confuse the continuing need for hygiene with the need to relax their standard of cleanliness.

HAND WASHING Personal hygiene, mainly hand washing, prevents spread of infection from food contamination during preparation of meals.181 A widely publicized study in the United States demonstrated that only 67% of Americans wash hands after using a public toilet. No one with a diarrheal illness should prepare food. A study of Appalachian Trail hikers showed that water disinfection, routine hand washing, and proper cookware cleaning were all associated with decreased diarrhea.27 A Shigella outbreak among river rafters on the Colorado River was investigated and assumed to be waterborne from adjacent Native American communities, but was finally traced to infected guides who were shedding organisms in the stool and contaminating food through poor hygiene.181 Simple hand washing with soap and water purified with hypochlorite (bleach) significantly reduced fecal contamination of market-vended beverages in Guatemala.255 Extensive research in the developing world has demonstrated that water is often recontaminated before use, and proper storage techniques can decrease this risk for contamination.260,304 In a refugee camp, using only a simple improved bucket that did not allow dirty hands or a ladle to touch the water, there was a 69% reduction in mean fecal coliform levels in the household water and 31% less diarrheal disease in children under 5 years of age among the group.235 For water access, narrow-mouth jars or containers with water spigots prevent contamination from repeated contact with hands or utensils.225,235,255

KITCHEN AND FOOD SANITATION Sanitation should extend to the kitchen or food preparation area.166 In addition to hand washing, dishes and utensils should be disinfected by rinsing in chlorinated water, prepared by adding enough household bleach to achieve a distinct chlorine odor. Hargreaves tested various combinations of wash and rinse water in three-bowl systems to determine what worked best for cleanliness, bacterial disinfection, and residual smell or taste of disinfectant. The optimal combination was water plus detergent in bowl 1 to remove the majority of food residue and grease; water with 10 mL added bleach in bowl 2 to remove the remaining food residue and provide disinfection; and plain water in bowl 3 to remove residue of disinfectant. This is a variation of the most commonly used method that adds the disinfectant to bowl 3 instead of bowl 2. If there is insufficient water or containers to provide a three-bowl system, omit bowl 3.119 1349

CHAPTER 67  Field Water Disinfection

TABLE 67-18  Choice of Method for Various Source Water

PART 8  FOOD AND WATER

Washing fruits and vegetables in purified water is a common practice. 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 biofilms or other particulate matter, which is why it is safer to peel most fruits and vegetables with rough skins.145 When lettuce was seeded with oocysts, then washed and the supernatant examined for cysts, only 25% to 36% of C. 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.202 A review of washing lettuce with various disinfectant solutions shows that high concentrations usually reduce level of viruses by 1 to 3 log.10 Chlorine, iodine, or potassium permanganate are often used for this purpose in higher concentrations than would normally be palatable for drinking water. In the United States, chlorine wash at 20 to 200 ppm is the most commonly used sanitizing treatment by the fresh produce industry. The ultimate responsibility for wilderness travelers is proper sanitation to prevent contamination of water supplies from human waste. Some suggest that campers smear feces on rocks. Desiccation occurs, and UV rays in sunlight eventually inactivate most microorganisms, but rain may first wash pathogens into a water source.56 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.220 Despite more rapid decomposition in sunlight rather than underground, burying feces is still preferable in areas that receive regular use. In the soil, microorganisms can survive for months.283 A Sierra Club study found more prolonged survival in alpine environments.220 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 50.8 cm (20 inches) of the surface, but in sandy soil this increases to 22.9 to 30.5 m (75 to 100 feet)5; viruses can move laterally 22. 9 to 92 m (75 to 302 feet).246 When organisms reach groundwater, their survival is prolonged, and they often reappear in surface water or wells.283 The U.S. military and U.S. Forest Service recommend burial of human waste 20.3 to 30.5 cm (8 to 12 inches) deep and a

minimum of 30.5 m (100 feet) from any water.5,287Decomposition is hastened by mixing in some dirt before burial. Shallow burying is 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.

APPENDIX A 

WATER DISINFECTION DEVICES AND PRODUCTS FOR FIELD USE Product lines are continuously evolving, and prices change frequently and vary widely. For most of these products, claims are substantiated only by company sponsored and designed testing. Some results have been extrapolated to similar products. Products are tested using a standardized Environmental Protection Agency (EPA) protocol: depending on claims, filters must demonstrate removal or inactivation of 103 cysts (99.9%), 104 viruses (99.99%), and 106 bacteria under varying water conditions of temperature and turbidity. Objective, comparable test results for these products are not available. Filter capacity is highly variable, depending on clarity of water. Numbers cited for capacity are usually based on clear water; testing using slightly turbid river water and following manufacturer instructions for cleaning reveals markedly different values. For all filters, it is recommended to pump dilute bleach solution through the unit after each trip and dry thoroughly before storage to decrease bacterial growth in the filter.

APPENDIX A Katadyn Endurance Series Product

http://www.katadyn.com Price

Pocket Filter (Figure 67-4, online)

$250-290

Combi (Figure 67-5, online) Accessories: prefilter bottle adaptor, carrying bag

$130

Expedition (Figure 67-6, online)

$1200

Ceradyn (Figure 67-7, online) and Gravidyn

$200-250

Siphon filter (Figure 67-8, online)

$65

1350

Structure/Function Endurance filters contain a 0.2-µm ceramic candle filter, silver impregnated to decrease bacterial growth. Large units also contain silver quartz in center of filter. Hand pump; 40-inch intake hose and strainer, zipper case; in-line carbon cartridge available; size: 10 × 2.4 inches; weight: 20 oz; flow: 0.75-1 L /min; capacity: 50,000 L. Small hand pump with ceramic filter and activated charcoal granule stage; with the optional “PLUS” package, the Combi can be connected to a water faucet for use in campers, cottages, or boats. Size: 2.4 × 10.4 inches; weight: 21 oz; flow: 1.0 L/min; capacity: up to 50,000 L; charcoal capacity: 200 L. Large hand pump with steel stand for medium to large groups; size (packed in case): 23 × 6 × 8 inches; weight: 12 lb; flow: 4 L/min; capacity (per filter element): up to 100,000 L. Gravity drip from one plastic bucket to another with three ceramic candle filter elements. Ceradyn uses ceramic candle filters, whereas Gravidyn filter candles combine ceramic and activated carbon elements; size: 18 inches × 11 inches diameter (26 inches high when assembled), 10 L water container; weight: 7 lb; flow: 4 L/hr; capacity: up to 150,000 L. Gravity 0.2-µm ceramic siphon filter element without reservoir bag that can be used to make a gravity system out of any water container. Place one or more Siphon filter elements into a container, and let the water run through the hose into a lowerpositioned vessel. Size: 6.3 × 2.6 inches; weight: 16 oz; flow: 5 L/hr; capacity: about 20,000 L.

Katadyn Backcountry Series Product

Price

Vario (Figure 67-9, online)

$90

Hiker and Hiker Pro (Figure 67-10, online)

$60-80

Base Camp (Figure 67-11, online)

$70

Structure/Function Hand pump; 0.3-µm pleated glass fiber filter with 143 inches2 surface area, ceramic prefilter, and activated charcoal stage; attaches directly to water bottle; size: 7.5 × 4.0 inches; weight: 15 oz; max flow: 2 L/min (36 stokes/L); capacity: 2000 L. Hand pump; 0.3-µm pleated glass fiber with 107-square-inch surface and activated carbon core; size: 6.5 × 2.4 × 3 inches; weight: 11 oz; flow: 1 L/min (48 strokes/L); capacity: 750 L. Gravity filter with a 0.3-µm glass fiber filter (Hiker filter cartridge) plus granular charcoal; includes dirty water reservoir bag and tubing; size: 3 × 6.5 × 2.4 inches; weight: 11 oz; flow: 1 L/hr; capacity: 750 L.

Katadyn Ultralight Series Product Mini (Figure 67-12, online)

Price $90

Water bottles Exstream MyBottle (Figure 67-13, online)

$50

Microfilter

$40

Structure/Function Smaller, lighter hand pump; 0.2-µm ceramic filter with activated carbon; 31-inch intake hose and strainer, hard plastic enclosure and pump; size: 3.2 × 7 × 2 inches; weight: 8 oz; flow: 0.5 L/min; capacity: approx 7000 L. Drink-through bottle with three-stage water filter: 1-µm plastic membrane cyst filter for protozoa, pentaiodide iodine resin(ViruStat), and activated carbon; weight: 7 oz, size: Exstream 21 oz (bike bottle size), XR 28 oz; cartridge capacity: 26 gal. Drink-through bottle with 0.3-µm glass fiber filter and activated charcoal (optional iodine resin); weight: 8 oz; size: 10 inches high, 24 oz; capacity: up to 26 gal.

Katadyn Claims Endurance series and mini with ceramic and carbon filter elements remove bacterial pathogens, protozoan cysts, parasites, nuclear debris. Clarifies cloudy water. If filter clogs, brushing the filter element (which can be done hundreds of times before needing to replace the filter element) can restore flow, or filter elements can be replaced. Claims for removal of viruses by ceramic filters not made in the United States. Pocket Filter has a lifetime warranty. Vario and Hiker are microfilters designed for high-quality surface water. They will eliminate Giardia, Cryptosporidium, and most bacteria; activated carbon core “reduces chemicals and pesticides, plus improves taste of water.” Filters with large surface area are “guaranteed not to clog for 1 year.” Exstream with iodine resin filter passed EPA tests to remove 3-log cysts, 4-log viruses, and 6-log bacteria. Patented ion-release technology and carbon scrubber dramatically reduce residual iodine. I5 is 1000 times more effective than I3 resin. Comments Well-designed, durable products that are effective for claims. However, high filter volume capacity is optimistic and not likely to be achieved filtering average surface water. Backpacker magazine field tests found the flow comparatively slow, requiring more energy to pump and frequent cleaning. Abrading the outer surface can effectively clean ceramic filters; after multiple cleanings, it is necessary to use the gauge to indicate when filter thickness becomes too thin. Pocket Filter is the original individual or small group filter design. Metal parts make it durable, but the heaviest for its size. 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. Vario and Hiker were designed for the domestic backpacking market with higher water quality, where cysts and bacteria are threats, but viruses are less of a problem. The Hiker received top ratings by Backpacker magazine for field tests evaluating user-friendliness. These filters may be used with a halogen disinfectant for international travel or conditions, where high levels of contamination are possible. Bottle filter with iodine resin is currently the only water bottle or filter product available with iodine resin (see text). Drink-through design limits to single-person day use. The filter design with charcoal removing residual iodine and ingestion directly from the filter allows no contact time and may not provide complete viral protection in all situations. Katadyn Desalinators Reverse Osmosis Filters Desalinator Survivor 06 (Figure 67-14, online) Survivor 35 (Figure 67-15, online)

$1425

Powersurvivor 40E

$2499

$550

Hand-operated 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 0.9 L /hr. Hand-operated pump, reverse osmosis membrane filter with prefilter on intake line; size: 3.5 × 5.5 × 22 inches; weight: 7 lb; flow: 30 strokes/min yields 4.5 L/hr. Smallest power-operated model in this line of reverse osmosis filters; uses only 4 amps, so can run for extended periods on 12-volt power source; converts to manual operation in emergencies; contains 40% fewer parts than its predecessor; pump size: 6.75 × 16.5 × 15.5 inches; prefilter 12 × 6 inches; Weight: 11.33 kg (25 lb); flow: 5.7 L/hr.

Reverse Osmosis Filters Claims Reverse osmosis units desalinate, removing 98% of salt from seawater by forcing water through a semipermeable membrane at 800 psi. In the process, microorganisms are filtered out. The manual operation of these units makes them unique and useful for survival at sea or for use in small craft without power source. Comments Reverse osmosis units are nanofilters capable of removing sodium molecules, as well as all microorganisms, including viruses. They are included here for sea kayaking and small boat journeys in open water. These units can obviate the need for relying solely on stored water or can be carried for emergency survival. Reverse osmosis filters currently are not practical for land travel because of cost, weight, and flow rates; however, the U.S. military uses truck-mounted reverse osmosis filters on land for their ability to handle brackish water and remove all types of microorganisms. Note that 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. Higher-flow power models are available from the company (Model 80E, 160E). Continued

CHAPTER 67  Field Water Disinfection

APPENDIX A—cont’d

PART 8  FOOD AND WATER

APPENDIX A—cont’d British Berkfeld

U.S. distributor: James Filter http://www.jamesfilter.com/

Product

Price

Berkey Filters Models include: Travel, Big Berkey, Royal, Imperial, Berkey Light (Lexan, not stainless steel) SS-4

Structure/Function A line of stainless steel stacked bucket filters that operate by gravity drip and can accommodate variable numbers of candle filter elements. There are two types of filter elements: (1) ceramic with carbon core and silver impregnation, and (2) compressed carbon impregnated with silver (Black Berkey). The size of the lower reservoir varies from 1.5-6 gal. Price varies by size and number of filter elements. Flow depends on number of filters elements. Stacked stainless steel containers with four 7-inch ceramic filters with activated carbon core; gravity flow; size: 20 × 8.5 inches (15 inches when nested); weight: 6.0 lb; flow: 24 gal/day; 2 gal capacity of lower container, capacity: 6,000 gal.

$220

British Berkfeld Claims and Comments Ceramic filter is 0.9 µm absolute, but filters >99.99% of particles larger than 0.5 µm. Removes 100% cysts and 4-5 log bacteria. Complete protection requires chlorine treatment as the first step. Black (compressed carbon) filters remove 4- to 5-log cysts and bacteria. The bucket filters are excellent for stationary base camps or expatriate homes. Ceramic candle filters will perform better than the carbon ones. AquaRain Filter Systems AquaRain 200 (Figure 67-16, online) AquaRain 400 (Figure 67-17, online)

$160-200 $240-320

http://www.aquarain.com Stainless steel containers (3 gal each) with one to four silver impregnated ceramic filters with carbon core; gravity flow; size: 22 × 10.25 inches; weight: 10 lb; flow: 1 gal/hr with four elements, 16 gal/day with two; capacity: 30,000-60,000 gal. Price depends on size and number of filter elements.

AquaRain Claims and Comments Filter has 0.2-µm absolute pore size, removes 100% cysts and 4-log reduction of bacteria. Ceramic elements can be cleaned 200 times before replacement. Similar design as Berkfeld and Katadyn bucket drip filters, although ceramic elements differ slightly. No claims for viruses. General Ecology, Inc Product

http://www.generalecology.com Price

Structure/Function

All filters contain 0.1-µm (0.4-µm absolute) Structured Matrix filter in removable canister. Hand pump with intake strainer; outflow end connects directly to common water bottle and adaptors available for Platypus bottles; self-cleaning prefilter float; size: 6 × 6 inches; weight: 15 oz; flow: 2 L/min; capacity: 600 L. Trav-L-Pure (Figure 67-19, $198 Filter and hand pump in rectangular housing (1.5-pt capacity); pour water into housing, then online) pump through prefilter and microfilter; size: 4.5 × 3.5 × 6.75 inches; weight: 22 oz; flow: 1-2 pt/ (Carrying case included.) min; capacity: 100-400 L. Trav-L-Pure Camper (Figure $88 Trav-L-Pur canister with attachment to hose bib for recreational vehicles and trailers requires 67-20, online) water pressure of 20 psi; flow: 0.5 gal/min (1.9 L/min); capacity: 570 L Base Camp (see Figure 67-11, $650 Stainless steel casing and hand pump connected by tubing; size: canister 4.1 × 8.8 inches, pump online) 1.5 × 10.5 inches; weight: 3 lb; flow: 2 L/min; capacity: 500 gal. Also available with electric pump and can be hooked up in series to provide higher capacity and flow. General Ecology has an extensive product line of larger-capacity filters for use on cars, boats, aircraft, and other situations requiring high-volume output where power is available. These use the Seagull IV purifier cartridge with a pump that pushes water through the system and a prefilter that can be cleaned. They can be operated off regular current or vehicle battery. General Ecology Filters Claims First Need Filter is a proprietary blend of materials including activated charcoal. “Microfiltration” with 0.1 µm retention (0.4 µm absolute) “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. Does not remove all dissolved minerals or desalinate. Proprietary process also creates ionic surface charge that removes colloids and ultra-small particles through “electrokinetic attraction.” Has passed laboratory tests as a purifier under single-pass conditions without added chemicals or hold time, reducing test virus by 104 as well as bacteria by 106 and Cryptosporidium by 103. Comments Reasonable design, cost, and effectiveness. All units use the same basic filter design. Most testing with Escherichia coli and Giardia cysts show excellent removal. Although they have not tested with hepatitis virus, testing with rotavirus and poliovirus indicate effectiveness against viruses. Charcoal matrix will remove chemical pollutants. Despite viral claims, recommend caution in highly polluted water; prior disinfection with halogen or clarification with coagulation–flocculation would provide additional security, and coagulation–flocculation would extend filter life, whereas filter carbon would subsequently remove halogen. The filter cannot be removed to clean, although it can potentially be back-flushed; so it must be replaced when clogged. First Need XL Portable Water Filter (Figure 67-18, online)

$109

Cascade Designs and MSR Product

http://www.cascadedesigns.com/MSR Price

Miniworks EX (Figure 67-21, online)

$90

SweetWater Microfilter (Figure 67-22, online) Purifier Kit with Microfilter, purifier solution and Platypus water bag Purifier solution

$90 $90

$10

Structure/Function Hand pump with cylindric ceramic filter with block carbon core, porous foam intake filter, and 10-µm stainless steel wire mesh screen; pressure-relief valve releases at 90-95 psi; storage bag (2 or 4 L) attaches directly to outlet of pump; size: 2.75 × 7.5 inches; weight: 16 oz; flow rate: 1 L/min (85 strokes/L); capacity: 400-2000 L (400 L under average conditions). Lexan body and pump handle; 80-µm metal prefilter; in-line 4-µm secondary filter; labyrinth filter cylinder of borosilicate fibers removes pathogens to 0.2 µm; granular activated carbon; safety pressure-relief valve; end-of-life indicator; outflow tubing has universal adapter that fits all water bottles; optional input adapter that attaches to sink faucet while traveling; size: 7.75 × 2 inches; weight: 11 oz; flow: 1.25 L/min (new filter); capacity: 750 L. A chlorine-based purifier solution containing 3.5% sodium hypochlorite; add 5 drops to each liter of filtered water, mix for at least 10 seconds, and wait 5 minutes

Product

Price

Structure/Function

HyperFlow (Figure 67-23, online)

$100

Hand pump using 0.2-µm hollow-fiber filter; attaches directly to top of water bottle for pumping; maintenance kit and replacement cartridges available; size: 7 × 3.5 inches; weight: 7.4 oz; flow: 3 L/min (1 L/20 strokes); capacity: about 1000 L.

AutoFlow (Figure 67-24, online) Platypus CleanStream Gravity Filter (Figure 67-25, online) Miox Purifier (Figure 67-26, online)

$100

Gravity drip filter using hollow-fiber filter cartridge; size: 4 × 6 inches; reservoir capacity: 4 L; weight: 10.5oz; flow: 1.75 L/min; capacity: about 1500 L/cartridge. 0.2-µm hollow-fiber filter cartridge gravity drip in-line system or can be used in personal hydration pack system; size: 1.8 × 5.7 inches; weight: 13.7 oz; flow: 4 L in under 2.5 min; capacity: about 1500 L. New technology created by military, uses salt, water, and electrical current generated from camera batteries to produce mixed-species disinfectant solution that is added to water; kit comes with pen, batteries, salt packet, indicator strips, instructions, storage sack; refills of salt cartridge are available; size: 7 × 1 inches; weight: pen 3.5 oz, kit 8 oz; battery life: about 200 L.

$90 $140

Cascade Designs and MSR Claims Miniworks EX Fully field-maintainable, meaning that all elements can be removed, cleaned, and replaced. Removes protozoa (including Giardia and Cryptosporidium), bacteria, pesticides, herbicides, chlorine, and discoloration. Meets EPA standards for removal of cysts and bacteria. Ceramic filters reduced turbidity from 68.8 NTU to 0.01 NTU. Carbon has been shown to reduce levels of iodine from 16 mg/L to 2 yr. High volume unit that uses UV LEDs; size: 28 × 8 × 19 inches; weight: 89 lb; flow: 200-500 gal/day; power: 640 watts; pressure 15-60 psi; life span: 10 yr.

Claims Works through multiple photo-chemical processes. Selected wavelengths of UV light generate hydroxyl radicals (OH−) without any chemical additives. Disassociates and eliminates organic compounds from the water. Reduces heavy metal to less toxic, more elemental state and irreversibly adsorbs heavy metals, including mercury, lead, chromium, and arsenic. Disinfects pathogens more effectively than standard UV irradiation. After 2 hours in the sun on an 80° F sunny day, process will reduce 7-log bacteria, 5-log viruses, 90% heavy metals, and 90% organics. Comments This is a new and promising technology for field water disinfection and purification. Significant testing and literature is available because it has multiple applications in industry and community level water treatment. Testing according to the EPA protocol is currently being done, and the field product is expected to be commercially available soon. Blue food dye can also be used to assure continued function of bag.

Hydration Technology Innovations (HTI)

http://www.htiwater.com/hti.html

Product

Price

Structure/Function

X-Pack Ten 2-oz sports drink syrup charges and dye tabs

$64 $16.50

SeaPack Includes eight 4-oz. syrup charges Expedition Includes ten 120-mL syrup pouches, cleaning kit

$75

A plastic pouch with two compartments separated by a semipermeable membrane that provides ultrafiltration to 0.0005 µm (5 angstroms); fill one side with dirty or contaminated suspect water; add to the other side a specially formulated syrup supplied with the kit that contains salts and sugars. Volume: 1.8 L; weight: 3 lb, includes syrup charges; flow: 1 L/4 hr, can produce a total of over 5 L of hydration drink per day; capacity: good for a total of 10 days of use after first use. Dual-chamber pouch, 1.8 L capacity each, separated by semipermeable membrane with nominal pore size of 3-5 angstroms; flow: 0.5 L/ 5 hr at 20° C (68° F); capacity: 4 L from seawater, or up to 24 L from freshwater; filter life: 10 days. Dual-reservoir water bladder for use with clean or contaminated water; uses osmotic filter cartridge that works by forward osmosis from osmotic syrup; one 4-oz. (0.12 L) syrup pouch will filter about 2.5 L of water; capable of filtering fresh to brackish water; clean reservoir volume: 3.0 L, dirty reservoir volume: 2.5 L; flow: about 1 L/hr; filter life: 30-90 days (clean weekly). Dual 20-L cans with osmotic filter built into a standard water can cap; forward osmosis driven by one sports syrup pouch that fits into the cap; one syrup pouch will filter one 20-L can of fresh to brackish water; flow: about 1.7 L/hr; filter life: 30-90 days (clean weekly)

$299

HydroWell $389 Includes twenty 410-mL syrup pouches, cleaning kit Claims Forward osmosis—water is driven across the membrane, not by hydraulic pressure, but by osmotic pressure created by a standard sport drink powder on the clean side of the membrane. This syrup is formulated much like the concentrate for a typical sports drink containing about 4% sugar (this compares with some other sports drinks at 6% and soda at 12%). Capable of filtering highly turbid water (tested to 800 NTU). Minimum 3 yr shelf life when stored below 90° F. Comments Forward osmosis is based on sound technology, and these products provide a good solution for disaster supplies or survival cache with long shelf life. Less optimal when on the move, although the bags could be primed and carried throughout the day while filtering. For those who prefer fresh water, the resulting sweetened solution is a major disadvantage. Simple filters or chemical solutions are lighter and faster for fresh water but cannot handle brackish water like some of the HTI products can. Household and Large-Scale Field Products The following are included as examples of multistage products that are available for household or large-volume field water treatment. This is not a comprehensive list of products, and many others are available, including trailer-mounted reverse osmosis systems. These products require a power source and may require truck or trailer for transportation. Most chemical systems can be scaled up through using large containers or water bladders and multistation distribution systems. Hindustan Lever Limited

http://www.pureitwater.com/IN

Product

Structure/Function

Pureit

Microfiber mesh, carbon block prefilter, chlorination, granular activated carbon (GAC) final stage; designed to operate without fixed power source (but does require batteries) and without a piped-in water supply; weight: 4.1 kg; chamber capacity: 9 L; flow: 9 L/2-3 hr; disinfection capacity: 1500 L.

Claims By combining filtration with disinfection, the treatment unit has overcome some of the shortcomings of other household-based water treatment systems intended for low-income populations. Provides the protection-meeting criteria established by the U.S. EPA for water purifiers (6-log reduction of bacteria, 4-log reduction of viruses, and 3-log reduction of protozoan cysts) while being affordable ($0.01/L) and capable of achieving scaled-up and sustained adoption by vulnerable populations. Comments Rational combination of filtration, chlorination, and charcoal and an example of technology being developed for developing countries with poor water quality that is available to expatriates or base camps. Published test results. Global Hydration Water Treatment Systems Inc Can Pure Water Purification System Various models available

http://www.globalhydration.com/canpure-water-purification-system.htm

First Water Systems, Inc Responder, Outpost, Villager

http://firstwaterinc.com/Suwanee, Ga All units use high-strength UV bulb for disinfection with in-line prefilter for large particulates, a sediment filter to reduce turbidity, a carbon block for improving taste and smell; all units can be supplemented with residual chlorination system; run off variety of power sources, including solar, battery, or generator. Water bladder and distribution system available; filling station enables either four or six lines of people to obtain water at any given time. Aqua Bags for transport of clean water are 3-gal heavy-gauge food-grade plastic bags that weigh about 20 lb when full. Portable model with canister configuration that runs on solar, on-board 12-volt battery, AC or DC power; size: briefcase size, 20 × 17 × 9 inches; 45 lb, including wheeled case; flow: 4 gal (16 L)/min, or about 600 gal (2500 L)/day per battery. Semiportable model water purification system runs exclusively off integrated solar system and an on-board battery; size: fits in the back of a pickup truck, SUV, minivan, mounted on wheeled frame; weight: 160 lb; flow: 4 gal (16 L)/min, or about 600 gal (2500 L)/day per battery (enough water for a thousand persons per day with multiple batteries)

Dual-process purification system incorporating six-stage microfiltration system and UV disinfection; optional residual chlorination using NaDCC tablets; size: 58 × 58 × 74 cm; weight: 41 kg; output: 19,000 L/day, 13 L/min, up to 50,000 L/day; power requirements: small generator (130 watts), can also be run on 12-volt DC. Complete stand-alone water treatment system designed to produce potable water in remote field conditions, emergency and disaster situations. Compact, portable, capable of running off gas or diesel generator without electricity or gravity.

Responder Outpost-4

Comments The UV system forces the water to circulate around the UV bulb twice, providing significantly greater “contact time” and greater ability to neutralize biologic contamination. Cigarette lighter plug adapters for additional battery power and AC power. Using multiple batteries 1355 extends the usable time and the amount of water produced. All filters easily detach for rapid cleaning or replacement.

CHAPTER 67  Field Water Disinfection

APPENDIX A—cont’d

PART 8  FOOD AND WATER

APPENDIX B 

CHEMICAL DISINFECTION PRODUCTS See text for further discussion of halogens, chlorine dioxide, and silver.

IODINATION Iodine Solutions Iodine solutions commercially sold as topical disinfectants contain iodine, potassium or sodium iodide in water, and ethyl alcohol or glycerol (see Table 67-14). Iodide improves stability and solubility but has no germicidal activity and adds to the total amount of iodine ingested and absorbed into the body. “Decolorized” iodine solution contains iodide and should not be used for water disinfection.

IODOPHORS (POVIDONE–IODINE) These solutions bind diatomic iodine to a neutral polymer of high molecular weight, giving the iodine greater solubility and stability with less toxicity and corrosive effect.52,114 Povidone– iodine is a 1-vinyl-2-pyrrolidinone polymer with 9% to 12% available iodine. The iodophors are routinely used for topical disinfection, because they have less tissue toxicity than iodine solutions. Povidone is nontoxic. In aqueous solution, povidone–iodine provides a sustainedrelease reservoir of halogen; free iodine is released in water solution depending on the concentration (normally, 2 to 10 ppm is present in solution). Data indicate persistence of about 2 ppm of free iodine at a 1 : 10,000 dilution,114 equivalent to 0.1 mL (2 drops) added to 1 L of water. One report found these compounds similar in germicidal efficiency to other iodine-iodide solutions.52 Conflicting values for available iodine and free iodine in dilute solutions result from the complex chemistry of povidone–iodine.17,131

CRYSTALS (SATURATED SOLUTION) Because of limited solubility in water, iodine crystals may be used to generate an iodine solution for disinfection. 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. To formulate this solution at home, put 4 to 8 g (exact amount does not matter) of crystalline iodine in a 1- or 2-oz bottle, and fill with water. Because iodine crystals evaporate in air, always keep covered with water. An alternative technique is to add 8 g of iodine crystals to 100 mL of 95% ethanol. 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). Residual iodine can be removed with granular activated carbon. Product Polar Pure http://www.polarequipment.com/ Price: $16.00 Widely available through suppliers of outdoor products Formulation Eight grams of iodine crystals in a 3-oz glass bottle filled with water; 30 to 50 µm fabric prefilter provided; "trap" in bottle to catch crystals when pouring off water; capacity: 2000 qt; weight: 5 oz Instructions The bottle cap is used to measure iodine solution: one capful is approximately 6.5 mL. Directions and color-dot thermometer are printed on the bottle. Recommended dose: 2 capfuls if iodine solution is 20° C (68° F) yields 4 ppm iodine when added to 1 qt of clean water. To shorten contact time, warm water to 20° C (68° F) before adding iodine. Comments Saturated aqueous solution of crystalline iodine is an excellent and stable source of iodine. Recommendations are adequate for clear, warm water; but, because it is not feasible to warm all 1356

water, extend contact time to 1 to 2 hours for very cold water. Temperature of the iodine bottle also affects the concentration of iodine in the saturated solution (200 ppm at 10° C [50° F), 300 ppm at 20° C [68° F], 400 ppm at 30° C [86° F]),52,114 which is the reason for the color-dot thermometer on the bottle. 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 crystals309; 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. The absence of iodide decreases total amount of iodine ingested. The glass bottle can break, and there are anecdotal reports of freezing in very cold temperatures. Iodine in alcohol is a viable option that allows for much smaller doses because of higher solubility of iodine in alcohol. Currently there is no commercial product, but it can easily be formulated at home.

IODINE TABLETS The tablets contain tetraglycine hydroperiodide, which is 40% I2 and 20% iodide.52,190 They were originally developed by the military for individual field use because of their broad-spectrum disinfection effect, ease of handling, rapid dissolution, stability, and acceptable taste.199,210,236 One tablet contains 20  mg tetraglycine hydroperiodide that releases 8  mg/L of elemental iodine into water; both diatomic iodine (I2) and hypoiodous acid (HIO) are released. An acidic buffer provides a pH of 5.5 to 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 iodine if bottles are left open for 4 days in high heat or humidity. Products Potable Aqua (Wisconsin Pharmacal Co, Jackson, Wis) http://potableaqua.com/ Price: 50 tablets, $5.00; with PA Plus Neutralizing tablets, $8.00 Widely available through suppliers of outdoor products Also sold as Globaline and EDWGT (emergency drinking water germicidal tablets) Instructions One tablet is added to 1 qt of water. In cloudy or cold water, add two tablets. Contact time is only 10 to 15 minutes in clear, warm water; much more in cold, cloudy water (see Tables 67-10 to 67-12). To remove taste and color of iodine, add one tablet of Potable Aqua PA Plus, mix, and wait 3 minutes. PA Plus should be used after the 30-minute waiting period for Potable Aqua. If the tablets are gray or dark brown in color, they are still likely to be effective. If they are light green or yellow, it means they are probably no longer effective. An opened bottle should not be kept for more than 1 year. Comments This method was developed by the military for troops in the field. Advantages are unit dose and short contact time, but these concentrations create strong taste that is not acceptable to many wilderness users. The military requirements dictated a short contact time (10 minutes in clear, warm water), thus the relatively high concentration of iodine (8 to 16 ppm). With adequate contact time and moderate temperatures, one tablet can be added to 2 qt of water to yield 4 ppm of free iodine (see Table 67-15). Rather than use two tablets in cloudy water, clarify the water first. PA Plus “neutralizing” tablet contains approximately 45 mg of ascorbic acid (vitamin C), which converts iodine to iodide and removes the taste and color of iodine but has no disinfecting action. However, iodide is physiologically active, so concerns about toxicity or physiologic activity remain. For short-term use, iodine is safe and removing the taste is a major benefit. Ascorbic acid powder can be purchased at many health food stores and used to neutralize any iodine disinfecting solution.

Free chlorine is available from several compounds and widely available in liquid and tablet formulations. (See text discussion and Tables 67-11 and 67-12.) Chlorine test strips or meters are widely available for large groups or disaster/community situations where testing for adequate chlorine residual is desired. Simple field test kits or swimming pool test kits with color strips are widely available to ensure adequate residual chlorine, for example: SenSafe Free Chlorine Water Check http://sensafe-test-kits.com/ Detection Ranges for 0, 0.05, 0.1, 0.2, 0.4, 0.6, 0.8, 1.2, 1.5, 2, 2.6, 4, 6 ppm (mg/L) http://www.serim.com Serim Residual Chlorine Test Strips measure free chlorine concentrations of 0 to 10 ppm with color block increments at 0, 0.5, 1, 2, 5, and 10 ppm. Price: $30.00 for 100 strips

SODIUM HYPOCHLORITE Household Bleach Liquid household bleach is a sodium hypochlorite solution, most often 5.25%. It has the convenience of wide availability, low cost, and high stability. 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 21.1° C (70° F) and freezes at 4.4° C (40° F). The liquid is corrosive and stains clothing if the bleach container breaks or leaks in a pack. Sodium hypochlorite solution in a squeeze dropper bottle is paired with several portable microfilter products to ensure viral disinfection, for example, SweetWater Viral Stop 2-oz squeeze dropper bottle. The Centers for Disease Control and Prevention (CDC)–World Health Organization (WHO) Safe Water System promotes products worldwide with 1% sodium hypochlorite for water disinfection.155

CALCIUM HYPOCHLORITE (DRY CHLORINE) Calcium hypochlorite is a stable, concentrated, dry source of hypochlorite that is commonly used for chlorination of swimming pools. The usual formulation contains 70% concentration of chlorine. Calcium hypochlorite is available in tablets or tubs of granules through chemical supply or swimming pool supply stores; one common brand is HTH, but there are many commercial products. Redi-Chlor (Gripo Laboratories, New Delhi, India) http://www.gripolabs.com 50 tablets in blister packs Price: $9.95 Multiple strengths, including: 0.5 g, 1.0 g, 2.0 g, 2.5 g, for treating 20, 80, 200, 240 L, respectively Available from multiple suppliers Formulation Redi-Chlor tablets come in different sizes and can be broken in half or fourths to treat different quantities of water. Recommended dose results in 2 to 5 mg/L residual chlorine. Add more for very cold water or if faint chlorine smell is not detected after contact time. Available in blister packs of 50 0.1-g tablets that treat 1 gal per tablet or 0.25-g tablets that treat 5 gal per tablet. Instructions For situations where many water containers are to be disinfected, it is easier to use a concentrated disinfecting solution. U.S. Environmental Protection Agency (EPA) instructions: Add and dissolve one heaping teaspoon of high-test granular calcium hypochlorite (approximately 0.25 oz) for each 2 gal of water. The mixture will produce a stock chlorine solution of approximately 500 mg/L (100 to 200 times desired strength for drinking). To disinfect water, add the chlorine solution in the ratio of one part of chlorine solution to each 100 parts of water to be treated. This is roughly equal to adding 1 pt (16 oz) of the stock chlorine solution to each 12.5 gal of water or (approximately 0.5 L to 50 L of water) to be disinfected. U.S. military instructions: See Table 67-13 for more details for dosing calcium hypochlorite for various strengths of chlorine and volume of water.

Comments This is a convenient source of concentrated hypochlorite, which can also be used for superchlorination (see text).

HALAZONE TABLETS Aquazone (Gripo Laboratories, New Delhi, India) www.gripolabs.com 100/250/500/1000 tablets in plastic container or 50/60 tablets in blister packs Tablets contain a mixture of monochloraminobenzoic and dichloraminobenzoic acids.90 Each tablet releases 2.3 to 2.5 ppm of titratable chlorine.199 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 yield 15 mg/L with recommended contact time of 60 minutes) for reliable disinfection under all conditions.236 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 has mainly been replaced by newer tablet formulations of chlorine.

SODIUM DICHLOROISOCYANURATE Sodium dichloroisocyanurate (NaDCC) is a stable, nontoxic chlorine compound that releases free active chlorine and forms a mildly acidic solution, which is optimal for hypochlorous acid, the most active disinfectant of the free chlorine compounds. Free chlorine is in equilibrium with available chlorine that remains in compound, providing greater biocidal capacity. NaDCC is more stable and provides more free, active chlorine than other available chlorine products for water disinfection. Manufacturers and Product Formulations Gripo Laboratories (New Delhi, India) http://www.gripolabs.com/nadcc_tablets.html Tablets available in sizes to treat 1 L to 100,000 L Kintab (Bioman Products) (Mottram, Hyde, Cheshire, UK) http://www.bioman.co.uk Aquatabs (Medentech, Wexford, Ireland) Six tablet strengths: 3.5 mg; 8.5 mg; 17 mg; 33 mg; 67 mg; 167 mg, depending on the volume to be treated, in individual foil-wrapped packets or strips. Larger quantities are available in tubs. Also available through Global Hydration Water Treatment Systems (Kakabeka Falls, Ontario, Canada) http://www.globalhydration.com/aquatabs-water-purificationtablets.htm Packs of 24 or 50 tablets to treat 1 L/tab or 30 tablets to treat 20 L (5 gal)/tab Formulation/Instructions When dissolved in 1 L of water, each effervescent tablet releases 10 mg of free chlorine; 50% of the available chlorine remains in compound and released as free chlorine is used up by halogen demand. Aquatab also makes slow-dissolving tablets for larger quantities of water that contain trichloroisocynuric acid (TCCA), which acts similarly to NaDCC. Disinfection of clear surface water is accomplished at 10 mg/L in 10 minutes, 1 mg/L for tap water and 2 to 5 mg/L for well water. NaDCC is also used to wash fruits and vegetables in concentrations of at least 20 mg/L. The tablets have a 3- to 5-year shelf life. Comments This is a good source of chlorine available in multiple doses and formulations, including individually wrapped tablet form; higherconcentration tablets allow for disinfection of large volumes of water or for shock chlorination of tanks and other storage systems.

CHLORINATION–FLOCCULATION Tablets contain alum and 1.4% available chlorine in the form of 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. 1357

CHAPTER 67  Field Water Disinfection

CHLORINATION

PART 8  FOOD AND WATER

Testing by the U.S. military demonstrated biocidal effectiveness similar to iodine tablets under most conditions.211,212,214 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 method is optimal for humanitarian disasters where available surface water is often highly turbid.87 Testing in households in developing countries demonstrates reduction of diarrhea episodes with proper use.55,72,225 Chlor-Floc (Deatrick & Associates, Alexandria, Va) 30 tablets individually sealed in foil packets; weight 1.6 oz.; capacity: 30 L (8 gal); Price: $8.00 Widely available through camping, military surplus, and survival websites Formulation/Instructions One tablet for the clarification and disinfection of 1 L of water from polluted sources at temperatures of 25° C (77° F). At 5° C (41° F) use two 600-mg tablets to provide 2.8% available chlorine. To strain the sediment, pour the water through the cloth provided. The tablets are stable for 3 years if stored out of the heat in their packaging. At 25° C (77° F), add 1 tablet; wait 7 minutes. At 15° C (59° F), add 1 tablet; wait 15 minutes. At 10° C (50° F), add 1 tablet; wait 15 minutes. At 5° C (41° F), add 2 tablets; wait 15 minutes. (1) Add 1 or 2 tablets (600 mg) to 1 L (1.1 qt) of water. (2) Shake for 1 minute to make sure that the tablets dissolve completely. (3) Wait for 7 to 10 minutes (or the necessary time), then strain through a piece of broadly woven cloth (e.g., T-shirt material) into clean container. (4) The clarified water is now ready for drinking. (5) If water is still murky, add an additional 0.5 tablet and repeat steps 2 and 3. After decanting, the water looks markedly clearer and is left with a free chlorine residual that produces microbiologically safer water without pronounced chlorine taste or odor.55 PUR Purifier of Water (Proctor and Gamble) www.pghsi.com Sachet of powder containing ferric sulfate as a coagulant and calcium hypochlorite as a disinfectant. Add one sachet to 10 L of water, and agitate vigorously. After the floc has settled to the bottom, filter through a clean cotton cloth and wait 20 minutes to drink. This product is available to large relief organizations for use outside the United States in disaster and conflict situations. They will also begin distribution for individual users in the developing countries. Comments This is one of the individual field methods for U.S. military troops and suggested for potential use in developing countries by the World Health Organization. It is an excellent one-step technique for cloudy and highly polluted water (see Table 67-15.). PUR has been used at the household level in many developing world communities and disasters.55,65,71,72,225 Alum and ferric sulfate are widely used flocculants that cause suspended sediment, colloids, and many microorganisms to clump, settle to the bottom, and readily be filtered or strained. Most Cryptosporidium oocysts would be removed by the flocculation. Some chlorine reacts with contaminants and is inactivated. It is important to confirm some chlorine taste and smell at the end of the contact time. For added safety, prolong the contact times up to 1 hour contact time in cold polluted and dirty water. In clear water without enough impurities to flocculate, the alum causes some cloudiness and leaves a strong chlorine residual. After treatment, water should be poured through a special cloth to remove floc and decrease turbidity. Both products have undergone extensive testing in field situations.

CHLORINE DIOXIDE Until recently, chlorine dioxide could be used only in large-scale water treatment applications, as a volatile gas that must be generated on site. Chemical methods for generating chlorine dioxide 1358

using either tablet or liquid formulations are now available for point of use in the field. Advantages of chlorine dioxide are greater effectiveness than chlorine at equivalent doses and the ability to inactivate Cryptosporidium oocysts with reasonable doses and contact times.

TABLETS Katadyn Micropur MP-1 http://www.katadyn.com/usen/katadyn-products/ Price: 20 tablets, $9.95; 30 tablets, $13.95 Available through many suppliers of outdoor products Potable Aqua Chlorine Dioxide Water Purification Tablets (Wisconsin Pharmacal Co, Jackson, Wis) Price: 20 tablets, $9.00; 30 tablets, $13.00 Available from many outdoor suppliers Aquamira (McNett Corp) http://www.aquamira.com/ Pristine (Advanced Chemicals Ltd, Port Coquitlam, BC, Canada) http://www.pristine.ca/ Tablets in blister packs Price: 12 tablets, $8.00; 24 tablets, $14.00; 50 tablets, $24.00 Formulation/Instructions The primary chemistry reaction that produces chlorine dioxide (ClO2) in Katadyn MP-1 tablets is the acid–chlorite reaction using sodium acid sulfate as the acid, a well-known reaction for ClO2. 5NaClO2 + 4 NaHSO4 → 4ClO2 + NaCl + 2H2O + 4 Na 2SO4 A small amount of chlorine in the tablet also catalyzes the otherwise sluggish reaction. These tablets generate chlorine dioxide only when coming into contact with water. Shortly after a tablet is immersed into water, a saturated solution of the soluble solid constituents forms within the matrix of the tablet. ClO2 is rapidly formed within the pores and then carried into the bulk solution by CO2 effervescence, which ensures that the resultant solution is well mixed without the user having to agitate the container. After the chlorine dioxide gas is released, the material reduces into common salts. Katadyn company product testing shows killing of bacteria and viruses within 15 minutes in any water conditions, and inactivation of Giardia and Cryptosporidium within 30 minutes in clear warm water and 4 hours in cold and dirty water. One tablet is used for treating 1 qt of water. Instructions are to insert rapidly into water after removing from package and avoid exposure to sunlight during disinfection contact time. Wisconsin Pharmacal would not provide information or testing data for their chlorine dioxide product. Comments This is an important addition to chemical methods for field disinfection. Several products have met the criteria for EPA registration as an antimicrobial water purifier. The extended contact time in cold, dirty water ensures that sufficient chlorine dioxide is generated and adequate residual remains for sufficient time to treat water in all conditions. Where possible, clarify the water to improve taste and esthetics and warm the water to reduce contact time. Available tests appear well designed with multiple controls. There is also documentation that residual concentrations of chlorine dioxide were well maintained during the recommended contact times. Chlorine dioxide does not have extended persistence in water, so it should not be used to maintain microbiologic purity of stored water. Sunlight breaks down chlorine dioxide, so for optimal effect, keep the water bottle in a dark location, such as inside a pack or bag, during disinfection time.

LIQUID CHLORINE DIOXIDE PRODUCTS Aquamira (McNett Corp) http://www.aquamira.com/ Pristine (Advanced Chemicals Ltd, Port Coquitlam, BC, Canada) http://www.pristine.ca/ Personal size: Two 1- oz plastic bottles; Capacity: up to 120 L (30 gal) of water; $15.00

Aquarius Bulk Water Treatment http://www.advancechemicals.ca/Aquarius-Bulk-WaterTreatment-System Includes 10 kits of Pristine solution to treat 50,000 L Available as a system with Terra Tank water bladders (5,000to 10,000-L capacity), Honda pump to fill the bladders, mixing and injection units, and six- to eight-spigot water-dispensing system. The system is packed in metal chests and weighs 200 lb. Formulation/Instructions A stabilized solution of chlorine dioxide is mixed with phosphoric acid, which activates the chemical and is then mixed with water for disinfection. Contact times for inactivation of Cryptosporidium by Pristine range from 15 minutes in warm water using a triple dose to 7 hours using a single dose in very cold water. The two solutions are mixed together in a mixing cap and added to the water for treatment. Comments The chemistry of generating chlorine dioxide through a similar method is well described. Aquamira solution was not able to meet EPA purifier standards in cold, dirty water. Currently claims for the solution include “kills odor causing bacteria and enhances taste of stored water.” The Canadian liquid product makes full claims, including Cryptosporidium. Given the volatility of chlorine dioxide and slow reaction times, concentrations may be variable due to mixing process and time delay. Cold and dirty “worst-case” test water may be an issue in disaster situations but is not often encountered by wilderness users. Aquamira tablets are registered as an EPA purifier, suggesting that tablets are the more stable and reliable form of chlorine dioxide.

MIXED SPECIES DISINFECTION (WITH CHLORINE DIOXIDE) Miox Purifier, Cascade Designs/MSR (Seattle, Wash) http://www.cascadedesigns.com/MSR/Water-Treatment-AndHydration/Expedition-Water-Treatment-And-Hydration/MIOXPurifier/product See Appendix A for more information on this product, which uses salt and an electrical current from camera batteries to generate chlorine dioxide, free chlorine species, and perhaps other disinfectants such as ozone. Electrolysis of salt to produce chlorine has been used for more than a century. Passing a current through a simple brine salt solution generates free available chlorine, as well as other “mixed species” disinfectants that have been demonstrated effective against bacteria, viruses, and bacterial spores.245 The process is well described and can be used on both large and small scale (http://www.miox.com/). Mixed oxidants behave like chlorine dioxide and ozone, although these disinfectants have not been detected in finished water treated with the Miox mixedoxidant solutions using classical analytical methods. The only residual, measurable species is hypochlorite; however, the resulting solution has greater disinfectant ability than a simple solution of sodium hypochlorite, including inactivation of Cryptosporidium.289 Additional testing is available on the Miox website.

SILVER Micropur Forte Tablets from Katadyn http://www.katadyn.com/chen/katadyn-products/ Widely available in Europe, but not marketed in the United States, these tablets contain silver chloride 0.1% and NaDCC 2.5%. The chlorine kills viruses, bacteria, and Giardia. The silver adds to the disinfection capacity, as well as preventing recontamination if water is stored for up to 6 months. Contact time is 20 to 120 minutes, depending on the temperature of the water. Shelf life is 5 years, stored in cool, dry conditions. Available as tablets, liquid, or powder and in various quantities for individual or large-scale use. One tablet treats 1 L of clear water. Claims Eliminates bacteria and viruses in 30 minutes and Giardia in 120 minutes. Conserves drinking water for up to 6 months. Can

be used in plastic or glass but not all metal containers. Shelf life: 5 years in original packaging and if stored under 25° C (77° F). Cloudy water can weaken the effect of chlorine and silver ions. Use filter for cloudy water. Micropur Classic from Katadyn This product releases silver ions. Available in two sizes of tablets (for 1 qt or 5 qt), liquid (10 drops/gal), or crystals for treating larger quantities of water. Claims Conserves clear water for up to 6 months. Deactivates bacteria after 2 hours of contact. The silver ions cling to the cell walls of microorganisms, thus hindering their growth. Affected by some metal containers. Shelf life: tablets, powder: 10 years from manufacture date, liquid: 5 years. Comments Although having proved antibacterial effects, silver tablets are not licensed as a water purifier in the United States; however, they are widely used in Europe for this purpose. In addition to poorly documented effects on many different types of microorganisms, there is some difficulty controlling the residual concentration and concern over chronic effects. This product makes no claims for viruses and protozoa, because concentrations may not be adequate to kill these organisms. Silver has the advantage of having no taste, color, or odor. It has been approved by the EPA to be marketed in the United States as a “water preservative” to maintain bacteria-free water for up to 6 months.

MISCELLANEOUS PRODUCTS The following products cannot be recommended because of insufficient effectiveness data. Traveler’s Friend (NutriBiotic) Description Extract from citrus seeds in 10-mL plastic dropper bottle. Price: $6.00 Claims “All natural treatment for drinking water.” Nontoxic, noncorrosive, proved effective as disinfectant for bacteria, viruses, protozoa. Recommended dose (drops/qt): 5 to 10 for filtered water, 10 to 15 for ice water, 10 to 20 for tap water, 15 to 25 for untreated water. Allow 30 minutes contact time. Comments Citrus extract is known to have some bacteriostatic effect (see text). This product was introduced into the health food market and is now looking for a broader market. Company data from independent laboratories support bacteriocidal and virucidal effects. However, protozoal tests were done with trophozoites, not cysts. The data have gaps, and too much of the marketing is testimonial to allow a recommendation at this time. Aerobic Oxygen and Aquagen These products claim to contain other forms of oxygen electrolytes that kill harmful bacteria in stored water and to have multiple health benefits when ingested in water or used topically. Aerobic Oxygen was initially introduced into the health food market but is now being offered to the general travel market. It is advertised not only as a water disinfectant, but for qualities from strengthening the immune system and energizing to curing headaches and tropical fish diseases. Company literature implies that the active disinfectants are chlorine dioxide, ozone, and free-oxygen radicals, but this is not credible because these are not chemically stable. Company-sponsored testing demonstrates activity against bacteria and viruses, but not against cysts. No dose-time response has been developed to compare the product with other disinfectants.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 67  Field Water Disinfection

Pristine also makes 2-oz bottles ($17.00) and larger packages for relief agencies to disinfect large quantities.

CHAPTER 68 

Infectious Diarrhea From Wilderness and Foreign Travel JAVIER A. ADACHI, HOWARD D. BACKER, AND HERBERT L. DUPONT

Acute infectious diarrhea is one of the most common and significant medical problems in any population, second only to acute upper respiratory diseases. Worldwide, diarrheal diseases were reported to cause nearly 1 billion episodes of illness in 1996.182 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 spp.), persistent diarrhea (defined as illness lasting 14 days or longer), malnutrition, and increased susceptibility to other infections still cause significant morbidity and mortality.182 Specific groups of U.S. populations, including international travelers to developing regions, gay males practicing unsafe sex, non-toilet-trained toddlers in some day care centers, and mentally impaired residents of custodial institutions, can have rates of diarrhea approximating those seen in the developing world. This chapter provides information to help to decrease exposure to risk factors and enteric pathogens, reducing the chance of acquiring diarrheal 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 specific treatment. 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, “travelers” includes business or pleasure travelers as well as wilderness venturers.

General Principles of Enteric Disease EPIDEMIOLOGY

Fecal–oral contamination through ingestion of contaminated water and food (waterborne or foodborne) is the usual route of transmission of the enteric pathogens causing acute infectious diarrhea. The relative importance of food and water depends mainly on location and precautions taken. The majority of pathogens that cause traveler’s diarrhea (TD) or wilderness-acquired diarrhea can be either foodborne or waterborne; however, waterborne pathogens from drinking untreated surface water or from an inadvertent ingestion during water recreational activity probably account for most infectious diarrhea acquired in the U.S. wilderness. Prevention of infection from all these pathogens includes proper sanitation and water disinfection. Person-toperson transmission is seen with pathogens that have small infectious doses, such as Shigella species, hepatitis A virus, Giardia, and noroviruses. These infections are most common in select 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 hand washing and personal hygiene. Other, less common routes of fecal–oral transmission are through aerosols (some viruses), contaminated hands or surfaces, and sexual activity. In 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 1360

lower incidence of infectious diarrhea in industrialized areas of the world. Travelers to foreign countries and wilderness areas often leave behind sanitation in the forms of flush toilets and safe tap water and do not have proximity to advanced medical care. Similar hygiene conditions are created in many other settings. Outbreaks of infectious diarrhea in day care centers among non-toilet-trained toddlers are associated with low inoculum organisms, including Shigella, Cryptosporidium, Giardia and the viral pathogens. Hospitals, especially intensive care units and pediatric wards, institutions for mentally handicapped patients, and nursing homes are also locations with a high incidence of diarrheal diseases. Clostridium difficile is the most important definable pathogen in those settings.160 Salmonella species, rotavirus, and enteropathogenic Escherichia coli (EPEC) may on occasion cause nosocomial outbreaks. Antimicrobial therapy is indicated for moderate to severe TD. When a specific bacterial or parasitic pathogen is identified (see later details), C. difficile infection (CDI) is frequently related to recent use of an antimicrobial agent (or cytotoxic agent) in debilitated hospitalized patients with a high rate of CDI recurrence.75 In developing areas of the world, children under 5 years of age have the highest morbidity of diarrhea, and infants under 1 year of age experience the highest mortality rates.40 The enteropathogens more common in infectious diarrhea during childhood are rotavirus, enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroaggregative E. coli (EAEC), Campylobacter spp., and Giardia. 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.122 Organisms are shed in the stools during asymptomatic and symptomatic infection and for a period after illness. Long-term fecal shedding or chronic carrier states are reported to be important only for typhoid fever, whereas in other intestinal protozoal infections, the parasite may be persistently shed, as is seen in amebiasis, giardiasis and cryptosporidiosis. These cases may act as reservoirs for spreading infection, even in areas with low risk for infection. A few enteric pathogens have animal reservoirs and are spread to exposed persons. These zoonotic organisms include Salmonella spp., Yersinia, Campylobacter, Giardia, Balantidium coli, Sarcocystis, and Cryptosporidium. Food intoxication, caused by ingestion of preformed toxins from Staphylococcus aureus or Bacillus cereus, typically has a short incubation period (2 to 7 hours) and causes common source outbreaks involving multiple persons.41 Infection and diarrhea caused by a living enteropathogen must first traverse the stomach and infect the small bowel or colon, explaining a longer incubation period of 14 or more hours, usually more than 1 day. Immunocompromised patients, including those with advanced infection by the human immunodeficiency virus (HIV), and persons with metastatic cancer are prone to acquire infection by a wide variety of enteropathogens, to develop infectious diarrhea, and to experience recurrent infections. Advanced AIDS is associated with chronic diarrhea secondary to ultrastructural changes in gut morphology and malabsorption, or because of reduced immunity and coinfection with enteropathogens. The agents responsible for diarrheal diseases in advanced AIDS include Mycobacterium avium-intracellulare complex, Cryptosporidium, Giardia, Isospora, Cyclospora, Microsporidium,

PATHOPHYSIOLOGY Three intestinal mechanisms lead to acute 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 is associated with release of proinflammatory cytokines. The second mechanism is malabsorption or presence of nonabsorbable substances in the lumen of the bowel, including lactase deficiency and AIDS-associated malabsorption. The third mechanism of diarrhea is altered intestinal motility. Secretory mechanisms best explain acute infectious diarrhea, while malabsorption and altered motility are more important in chronic

TABLE 68-1  Enteropathogens Found in Tropical

and Wilderness Travel

Agents Bacteria Enterotoxigenic Escherichia coli Enteroinvasive E. coli Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter spp. Vibrio cholerae Yersinia enterocolitica Aeromonas spp. Plesiomonas shigelloides Viruses Norovirus Rotavirus Hepatitis A Protozoa Giardia lamblia Entamoeba histolytica Cryptosporidium parvum Isospora belli Cyclospora cayetanensis Microsporidia Balantidium coli Sarcocystis Blastocystis hominis

Travel to Developing Tropical Regions

Wilderness Travel in Industrialized Regions

Yes

Rarely

Rarely Yes

Rarely Rarely

Yes Yes Yes Limited Rare Yes Yes

Yes Yes Yes Not currently Limited Yes Rarely

Yes Yes Yes

Yes Rarely Yes

Yes Yes Yes

Yes Rarely Yes

Limited Limited

Rarely Rarely

Limited Limited Limited Limited

Rarely Rarely Rarely Rarely

TABLE 68-2  Bacterial Enteropathogens: Virulence

Properties

Pathogen

Virulence Properties

Vibrio cholerae Vibrio parahemolyticus

Heat-labile enterotoxin Invasiveness (?), enterotoxin, hemolytic toxin Heat-stable and heat-labile enterotoxins, colonization factor antigens Shigella-like invasiveness Enteroadherence Cholera-like toxin, invasiveness Shiga-like toxin, invasiveness Cholera-like toxin, invasiveness Hemolysin, cytotoxin, enterotoxin Heat-stable enterotoxiin, invasiveness Toxins A and B Preformed toxin Preformed toxin Preformed toxin

Enterotoxigenic Escherichia coli Enteroinvasive E. coli Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter jejuni Aeromonas spp. Yersinia enterocolitica Clostridium difficile Clostridium perfringens Bacillus cereus Staphylococcus aureus

forms of diarrhea, such as tropical and nontropical sprue, Whipple’s disease, intestinal scleroderma, irritable bowel syndrome and inflammatory bowel disease. Table 68-2 shows the virulence factors of the most important enteric pathogens related to infectious diarrhea. In secretory diarrhea, the unformed stools are usually of large volume and small in number (characteristically less than six bowel movements per day). Stools do not contain blood and fever is unusual. Examples of pathogens in this group are Vibrio cholerae, ETEC, preformed enterotoxins, noroviruses, rotavirus, Giardia, and Cryptosporidium. Dehydration is the major complication, especially in the extremes of age. Without adequate therapy, secretory diarrhea can be followed by renal insufficiency. Invasive pathogens involving the distal ileum and colon damage the mucosa and elicit an inflammatory response that is associated with secretory diarrhea and colitis. In this form of colitis, stools are typically liquid, small-volume, and may contain blood and many leukocytes. The common microorganisms in this group are Shigella, Salmonella, EIEC, Shiga-toxin producing E. coli (STEC), Yersinia enterocolitica, Campylobacter spp., Aeromonas, Vibrio parahaemolyticus, and E. histolytica. Complications include dehydration and systemic involvement, especially in children with malnutrition.151

Traveler’s Diarrhea Traveler’s diarrhea 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.42 Inter­ national 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, 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 subtropical regions of Latin America, Southeast Asia, or Africa). More than 100 million persons travel each year from industrialized countries to high-risk areas, resulting in more than 30 million travelers with diarrhea.42 Multiple episodes of diarrhea may occur on the same trip. Attack rates remain high for the first 4 weeks in a country of risk,54 then decrease, but not to the levels of local inhabitants. Immunity to ETEC infection, 1361

CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

cytomegalovirus, herpes simplex virus, and HIV itself (so called “AIDS enteropathy”). Treatment of HIV with highly active antiretroviral therapy and treatment of the enteric infection(s) are associated with improved symptomatology and decreased rates of infection. Most cases of acute diarrhea are caused by infectious microorganisms, including bacteria, viruses, and protozoa. Fungal agents have been reported rarely. Table 68-1 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. A rare cause of food poisoning that results in paralysis is botulism, caused when the neurotoxin of Clostridium botulinum is ingested. Other foodborne pathogens are viruses, including rotavirus and small round viruses (noroviruses, astrovirus, etc.), and intestinal protozoal agents, including Giardia, Entamoeba histolytica, and Cryptosporidium.

PART 8 FOOD AND WATER

either asymptomatic or symptomatic, occurs after repeated or chronic exposure, which supports the feasibility of developing a vaccine.72 Although any waterborne or foodborne enteropathogen can 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.155

TABLE 68-4  Clinical Syndromes in Enteric Disease

DEFINITION

Vomiting (predominant symptom) Persistent diarrhea (>14 days) Chronic diarrhea (>30 days)

TD refers to an illness contracted while traveling, although in 15% of sufferers symptoms first become ill after returning home. Most clinical studies define TD as 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, bloody–mucoid stools, nausea, and vomiting.45

Syndrome

Agent

Acute watery diarrhea

Any agent, especially with toxin-mediated diseases (e.g., enterotoxogenic Escherichia coli, Vibrio cholerae) Shigella, Campylobacter jejuni, Salmonella, Enteroinvasive E. coli, Aeromonas spp., Vibrio spp., Yersinia enterocolitica, Entamoeba histolytica, inflammatory bowel disease Viral agents, particularly noroviruses, preformed toxins of S. aureus or B. cereus

Febrile dysentery

Protozoa, small bowel bacterial overgrowth, inflammatory or invasive enteropathogens (Shigella, enteroaggregative E. coli) Small bowel injury, inflammatory bowel disease, irritable bowel syndrome (postinfectious), Brainerd diarrhea

ETIOLOGY Because the incidence of TD reflects in part the extent of environmental contamination with feces, the etiologic agents are pathogens causing illness in local children. A list of etiologic agents important in TD is provided in Table 68-3). Twenty years ago, specific pathogens were found in only 20% of cases. Currently, etiologic agents can be identified in up to 80% of TD episodes.103 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.53 Overall,

TABLE 68-3  Major Pathogens in Traveler’s Diarrhea

(Travel to Developing Tropical Regions)

Agent Bacteria Enterotoxigenic Escherichia coli

Frequency (%) 50-80 5-50

Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter jejuni Aeromonas spp.

5-30

Plesiomonas shigelloides Other Viruses Rotavirus

0-5 0-5 0-20 0-20

Norovirus

1-20

Protozoa Giardia lamblia

1-5 0-5

Entamoeba hystolitica

0-5

Cryptosporidium parvum

0-5

Unknown

1-15 1-15 1-30 0-10

10-40

For details on published studies see reference 177.

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Distribution Developing countries, tropical areas, infants, travelers Infants, worldwide Worldwide Worldwide Worldwide Worldwide, especially Thailand, Australia, Canada Worldwide

Worldwide, children 6-24 mo Worldwide, cruise ships Worldwide, zoonosis, alpine areas Developing and tropical countries, especially Mexico, India, western and South Africa, parts of South America Worldwide, including cooler developed countries

the major etiologic agents and their frequency of isolation are remarkably similar worldwide. ETEC is the most common cause of TD worldwide,177 accounting for about one-third to one-half of cases. Since the last edition of this book, EAEC has been identified as the second most common bacterial cause of TD, causing up to 30% of TD cases in some areas of the world.3 One study has shown that the source of both types of E. coli is food. Viable ETEC and EAEC were found in hot sauces served on the table in popular restaurants in Guadalajara, Mexico.4 Shigella and Campylobacter species cause around 20% of illness. Other causes of TD include Salmonella (4% to 5% of cases), Vibrio, Aeromonas, Plesiomonas, viruses (10%), and parasites.177 Specific pathogens may predominate at a particular time or location.

CLINICAL SYNDROMES Table 68-4 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 abdominal cramping and watery diarrhea. 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 affected persons experience moderately severe illness, with three to five unformed stools per day and distressing symptoms that force a change in activities or itinerary. Only 1% to 3% of persons with TD occurring in Latin America or Africa experience febrile dysenteric illness,64,129 whereas approximately 9% of travelers with diarrhea acquired in Asia (Indian subcontinent) develop this more serious form of illness.187 TD may lead to a chronic illness43 and postinfectious irritable bowel syndrome (PI-IBS).147,190 TD should be considered a self-limited nonfatal condition. An illness associated with vomiting without important diarrhea is commonly seen in travelers and is characteristically due to noroviruses.6,113 Symptoms lasting more than 1 to 2 weeks suggest a protozoan etiology such as Giardia, E. histolytica, Cryptosporidium or other parasite.43 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 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 spp. Fever can also be produced by strains of EIEC, V. parahaemolyticus, Aeromonas, C. difficile, and viral pathogens. Vomiting as the predominant symptom in a traveler usually suggests norovirus infection. Vomiting is also seen in “food poisoning” secondary to consumption of pre-formed enterotoxin produced by S. aureus or B. cereus.

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.43 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. The etiology of persistent or chronic diarrhea often differs from that of acute diarrhea. Important causes of persistent diarrhea include (1) protozoal parasitic agents (Giardia, Cryptosporidium, Cyclospora, and E. histolytica), (2) bacterial infection (Salmonella, Shigella, Campylobacter, and Y. enterocolitica), (3) lactase deficiency induced by a small bowel pathogen (Giardia, rotavirus, or norovirus), 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. When chronic diarrhea follows a bout of TD, a pathogen is not identified and the patient fails to respond to empiric antimicrobial therapy, PI-IBS, or activation of an underlying condition such as inflammatory bowel disease or celiac or tropical sprue should be considered. Even with eradication of microbial pathogens with antimicrobial therapy, bowel habits may not return to normal for several weeks. This represents slow repair of the damage to the intestinal mucosa. Small bowel bacterial overgrowth has been identified in patients with persistent diarrhea after a bout of TD. Finally, there first occurred in the 1980s an idiopathic form of chronic diarrhea called Brainerd diarrhea after the name of the city in Minnesota where the first outbreak was identified.150 The known vehicles of transmission of Brainerd diarrhea are raw (unpasteurized) milk150 and untreated water, such as well water.152 There is no diagnostic test or therapy, and the diagnosis is suspected based on the epidemiologic history (exposure to

FIGURE 68-1  Methylene blue stain of a fecal smear from a patient with bacillary dysentery (×400). Numerous polymorphonuclear leukocytes are present. This indicates the presence of diffuse colonic inflammation.

unpasteurized milk or untreated water just before onset of illness). Although the average duration of Brainerd diarrhea is 2 years, persons with this condition invariably become totally well. 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 of freshly passed stools. Dietary modification in all cases should initially include avoidance of milk and dairy products because of the possibility of lactase deficiency. Treatment should be specific, following the results of the microbiologic tests. Because most of these chronic forms of diarrhea are selflimited, it is unwise to employ empiric antibiotics in these patients. A single, limited empiric trial with metronidazole for possible Giardia infection is considered an option by some experts if all tests are negative.

LABORATORY TESTS AND PROCEDURES Several laboratory tests are useful in evaluating patients with diarrheal disease (Table 68-5). In clinical practice, laboratory testing is reserved for illness continuing after the patient returns home or when empiric treatment is unsuccessful. Persons with milder forms of diarrhea usually need only clinical evaluation; etiologic assessment is unnecessary. Laboratory tests are reserved for persons with moderate to severe diarrhea and those with persistent illness. The presence of fecal leukocytes is a reliable indicator of diffuse colonic inflammation. For moderate to severe illness, this is the most rapid, useful test and the ideal screening procedure. A large number of polymorphonuclear leukocytes (PMNs) per high-power field using dilute methylene blue stain or trichrome stain (which also helps with identification of parasites) can be helpful in making an etiologic diagnosis (Figure 68-1) of Shigella, Salmonella, or Campylobacter spp.88 Other

TABLE 68-5  Indications for Laboratory Test in Diarrheal Diseases and Possible Diagnoses Laboratory Test

Indication

Diagnosis/Agent

Fecal leukocytes or fecal lactoferrin Stool culture

Moderate to severe cases

Diffuse colonic inflammation, invasive bacterial enteropathogen Any bacterial enteric pathogen

Blood culture Parasite examination Parasite enzyme immunoassay Amebic serology Rotavirus antigen Clostridium difficile toxin by EIA or PCR

Moderate to severe diarrhea, fever, persistent diarrhea, fecal leukocytes or lactoferrin (+), male homosexual Enteric fever, sepsis Persistent diarrhea, travel to specific areas, day-care centers, male homosexuals Persistent diarrhea, travel to specific areas, day-care centers, male homosexuals Persistent diarrhea, liver abscess Hospitalized infants (14 days) Vomiting, minimal diarrhea Diarrhea in pregnant women

Oral fluids and symptomatic therapy (can give antibiotics† or loperamide) Symptomatic treatment with loperamide and antibiotics† after passage of first unformed stool Antibiotic† after passage of first unformed stool Azithromycin, 1000 mg in single dose; loperamide is not recommended Parasite examination and stool culture; consider gastrointestinal evaluation Oral fluids and consider using bismuth subsalicylate Fluids and electrolytes; if severely ill, treat with azithromycin 500 mg once a day for 3 days.

*Treatment should be self initiated during travel without evaluation. † Antibiotic options include: norfloxacin 400 mg twice a day for 1-3 days, ciprofloxacin 500 mg twice a day for 1-3 days, ofloxacin 300 mg twice a day for 1-3 days, or levofloxacin 500 mg once a day for 1-3 days; or rifaximin 200 mg three times a day for 3 days; or azithromycin 1000 mg in a single dose.

TABLE 68-8  Antimicrobial Therapy for Organism-Specific Diarrhea in Adults Diagnosis

Recommendation

Enterotoxigenic and enteroaggregative Escherichia coli diarrhea

Rifaximin 200 mg three times a day for 3 days; or ciprofloxacin 500 mg twice a day for 1-3 days; or norfloxacin 400 mg twice a day for 1 to 3 days; or levofloxacin 500 mg once a day for 1-3 days; or azithromycin 1000-mg single dose Ciprofloxacin 1000-mg single dose; norfloxacin 400 mg twice a day or levofloxacin 500 mg once a day for 3 days; or doxycycline 300-mg single dose Norfloxacin 400 mg twice a day for 5 days, or ciprofloxacin 500 mg twice a day for 5-7 days, or levofloxacin 500 mg once a day for 7-10 days Antimicrobial therapy controversial if systemically ill (high fever and toxicity) or in a high risk group: sickle cell anemia, age 64 yr, on corticosteroids, undergoing dialysis, those with inflammatory bowel disease (if decision to treat, use regimen like systemic salmonellosis above) Norfloxacin 400 mg twice a day for 3 days, or ciprofloxacin 500 mg twice a day for 3 days, or levofloxacin 500 mg twice a day for 3 days Erythromycin 500 mg four times a day for 5 days; azithromycin 500 mg once a day for 3 days or 1000 mg in single dose

Cholera Systemic salmonellosis (typhoid fever or bacteremic infection) Salmonellosis (intestinal nontyphoid salmonellosis without systemic infection) Shigellosis Campylobacteriosis

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

TABLE 68-6  Nonspecific Drugs for Therapy in

PART 8 FOOD AND WATER

PREVENTION AND PROPHYLAXIS Care in Food and Beverages Consumed During Travel Food and water transmit the pathogens that cause infectious diarrhea and TD.4,195,206 When diarrhea occurs, however, the exact source cannot be determined. Being careful about what is eaten is recommended and may be helpful in reducing the occurrence of illness,115 but dietary habits usually cannot be rigidly controlled.179 Food in developing countries is often contaminated with fecal coliforms and enteropathogens.206 V. cholerae remains viable for 1 to 3 weeks in food,68 and Salmonella can survive 2 to 14 days in water or in the environment in a desiccated state. Risk of illness is lowest when most of the meals are selfprepared and eaten in a private home, intermediate when food is consumed at public restaurants, and highest when food is obtained from street vendors.16 The following standard dietary recommendations for prevention are based more on known potential vehicles for transmission of illness than on strong evidence. 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. 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.11 Bottled carbonated beverages are considered safe because of the antibacterial effects of the low acidity. Alcohol in mixed drinks does not disinfect contaminated ice cubes unless the alcohol content is at very high and potentially unsafe concentrations.38 2. Avoid unpasteurized dairy products. These may be the source of infection with Salmonella, Campylobacter, Brucella, Listeria monocytogenes, Mycobacterium spp., and others.158 3. Avoid raw meat and vegetables. Raw vegetables in salads may be contaminated by fertilization with human waste or by washing in contaminated water. 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 traditional dishes such as ceviche and sashimi, has been associated with increased risk of TD. Shellfish concentrate enteric organisms from contaminated water and can carry hepatitis A, noroviruses, 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 Taenia 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 transmit Salmonella, Shigella, ETEC, or EAEC. Food served on an airplane, train, boat, or bus probably has been catered in the country of origin. Problems of food hygiene pertaining to these forms of public transportation may be related to employee handling of food, even in the United States.

Generally safe foods are those served steaming hot, dry items such as bread, freshly cooked food, foods that have high sugar content (e.g., syrups, jellies, jam and honey), and fruits that have been peeled. Chemoprophylaxis Chemoprophylaxis with antibiotics was shown in the 1950s and 1960s to effectively prevent TD among international travelers.111 This was the first evidence that bacterial pathogens were the most important causes of TD. Preventive antibiotics are generally recommended to be used for trips of 2 weeks or less and will require a prescription from a physician (Table 68-9). Because of safety and efficacy, rifaximin is the optimal drug when prophylaxis is employed: the dose is one 200 mg tablet twice a day with major daily meals for trips up to 2 weeks in length. Another effective dosage formulation of rifaximin is a 550 mg tablet taken once for breakfast each day of the trip to high-risk regions. The medication should be started the day of arrival to a high-risk region and can be stopped once leaving the area. Most wilderness travelers taking their own food or preparing their own food are not at high enough risk for TD to justify chemoprophylaxis with antibiotics. Several non-antimicrobial 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%.90 Of the non-antibiotic drugs, only bismuth subsalicylate (BSS), the active ingredient of Pepto-Bismol, has been shown by controlled studies to offer reasonable protection and safety.49,61 The currently recommended dose of BSS is two tablets with each meal and two tablets at bedtime or two tablets four times a day (2.1 g/day) while in a high-risk region for trips of 2 weeks or less. Mild side effects include constipation, tinnitus, and temporarily blackened tongue or stools. BSS should not be used by someone with a history of aspirin allergy or in young children. 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.83 Indications for recommending antimicrobial chemoprophylaxis in TD prevention are as follows:45,59,67,81 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 with 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. An evidence-based analysis of the available data on chemoprophylaxis in the prevention of TD was published by the International Society of Travel Medicine.48 Immunoprophylaxis Spurred by the emergence of in vitro resistance among enteropathogens to antimicrobial agents, including the fluoroquinolones, and with the knowledge that persons develop natural

TABLE 68-9  Prophylactic Medications for Prevention of Traveler’s Diarrhea* Agent Bismuth subsalicylate Fluoroquinolones Rifaximin

Protective Efficacy 65% 90% 70-80%

Prophylactic Dose

Comment

30 mL or two 262-mg tablets before meals and at bedtime Norfloxacin 400 mg, ciprofloxacin 500 mg, or levofloxacin 500 mg once a day Rifaximin 200 mg twice a day with meals

Safe, temporary darkening of stools and tongue Side effects and toxicity unacceptable, concern with development of antibiotic resistance Safe, nonabsorbable, no increased resistance, should be considered the standard agent for prophylaxis during high-risk travel

*Not generally recommended for healthy travelers able to carry out preventive measures, to be used in special situations (see text) and for no longer than 2 weeks.

1366

Bacterial Enteropathogens ESCHERICHIA COLI The diarrheagenic E. coli represent a heterogenous group of organisms that belong to one taxonomic species, but have different virulence properties, epidemiologic characteristics, and clinical features. At least six groups have been characterized, based on genotypic or phenotypic markers.140 We will discuss207 here the pathotypes of diarrheagenic E. coli important in TD. Enterotoxigenic E. coli.  ETEC strains were first identified in the 1970s and shown to produce one or two enterotoxins that act on the small intestine through different cyclic nucleotide pathways showing different time responses in the gut.140 One of these toxins is a heat-labile cholera-like toxin (LT), a highmolecular-weight protein immunologically and physiologically similar to cholera toxin. Human ETEC strains also have a lowmolecular-weight, poorly antigenic toxin that is heat stable (ST).165 One common method for the diagnosis of ETEC is identification of specific DNA plasmid sequences, using a hybridization technique.140 More recently, polymerase chain reaction (PCR) has been used to improve the level of detection.* ETEC has worldwide distribution and is the major cause of TD, accounting for 30% to 40% of cases in series from Latin America, Africa and south Asia (Indian subcontinent).177 It also accounts for a large percentage and is frequently the majority of enteritis in local pediatric populations of developing countries, where contaminated food and water are the primary sources of infection. Person-to-person spread is infrequent because of the large infectious dose (106 to 1010 organisms).52 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,118,166 EIEC must be considered in the differential diagnosis of febrile dysenteric diarrhea. EIEC strains cause a small fraction of TD cases.203 Enteroaggregative E. coli.  EAEC strains are an important cause of TD in all regions of the world.3 These strains adhere to HEp-2 cells in a typical aggregative, “stacked brick” pattern. Several bacterial markers have been studied as possible diagnostic aids, but no single marker is present in all strains. 94,96,102 Some studies

*References 8, 14, 73, 197, 199, 207.

suggest that EAEC should be considered a phenotypically and genotypically heterogeneous group.* Although the pathophysiology of EAEC is not completely understood, presence of multiple virulence factors and stimulation of inflammatory cytokines/ chemokines have been described.† EAEC has been associated with acute and persistent diarrhea in children living in developing countries.30,94,143,174,209 Diffusely Adherent E. coli.  These strains show a diffuse, nonaggregative, adherence pattern to HEp-2 cells. There is limited evidence that these strains are causes of TD134,198 and diarrhea in children in developing countries.77 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.139 New serologic and molecular diagnostic techniques under investigation may become available in the future to differentiate these organisms.‡ Most cases of E. coli diarrhea are brief and self-limited and treatment is with rifaximin, ciprofloxacin, or azithromycin. EIEC should be treated as for shigellosis with 3 days of therapy with a fluoroquinolone or 1000 mg azithromycin in a single dose.

SALMONELLA Salmonella infections may result in four different clinical syndromes: gastroenterocolitis, enteric (typhoid) fever, bacteremia with focal extraintestinal infection, and asymptomatic carriage.19,173 Gastroenterocolitis and typhoid fever are the two most important forms for travelers. Although the incubation period for typhoid fever is usually 1 to 2 weeks, it is only 8 to 48 hours for intestinal infections with nontyphoid Salmonella.156 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 younger than age 3 months 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 a week after resolution of diarrhea suggest a complication or another diagnosis.107,156 In healthy adults, Salmonella bacteremia occurs in 5% to 8% of infections and is not distinguishable from other causes of sepsis. Diagnosis is made by isolation of Salmonella from stool or blood cultured onto selective media (MacConkey or SalmonellaShigella agar). Supportive treatment with fluids is sufficient therapy for most cases of uncomplicated Salmonella enterocolitis. Antimicrobial therapy is indicated for persons who have symptomatic Salmonella infection with fever, systemic toxicity, or bloody stools. Fluoroquinolones are the treatment of choice for most forms of systemic salmonellosis because they shorten the duration of illness. Doses are the same as those recommended to treat shigellosis, although treatment is continued for 7 days (14 days if the patient is immunosuppressed). For known intestinal salmonellosis, antibiotics are used only in the more severely ill or when bacteremia is suspected. 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 available with two licensed, protective vaccines. The first is a live attenuated strain Ty21a that is given as one oral dose every other day for four doses.9,76 The second is an inactivated Vi polysaccharide

*References 22, 34, 96, 119, 139, 140. † References 21, 84, 95-97, 102, 104, 138, 209. ‡ References 8, 11, 15, 73, 124, 141, 162, 184, 199.

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protection against TD as they remain in a high-risk area, vaccines are being developed to prevent TD. Several vaccines are being or have been developed for protection against rotavirus, Shigella, V. cholerae, and ETEC. The vaccine most relevant to TD is ETEC. ETEC is the most important cause of TD and typically occurs during the first 2 weeks in a country of risk.2 An orally administered ETEC vaccine is marketed as Dukoral in many European countries. The vaccine uses a recombinant form of the binding subunit of cholera toxin that resembles the heat-labile toxin of ETEC (LT). The vaccine was successfully employed in a study of Finish travelers to Morocco.153 The vaccine fails to immunize against the nonantigenic heat stable toxin of ETEC (ST). Adding whole cells containing gut attachment fimbriae of ETEC has been one approach to increase the spectrum of activity of this oral vaccine. Making sure the correct fimbrial adhesin is included in the vaccine is a challenge of this approach.170 An exciting new vaccine in development is a LT skin patch vaccine. When LT is applied to the skin after minimal abrasion of the stratum corneum, a brisk antibody develops.78 The vaccine has prevented moresevere forms of ETEC diarrhea in volunteers131 and in a phase II trial among international travelers to Mexico and Guatemala, the patch vaccine had a protection rate against moderate and severe diarrhea of 75%.72 At the time of this writing, this vaccine is in a phase III trial in Mexico, Guatemala, and India.

PART 8 FOOD AND WATER

preparation given as a single parenteral immunization.1 Both preparations are of approximately equal cost and effectiveness.

SHIGELLA Shigellae are nonmotile, nonsporulating, and gram-negative rods in the Enterobacteriaceae family. There are four species or groups: A (Shigella dysenteriae), B (Shigella flexneri), C (Shigella boydii), and D (Shigella sonnei); the first three contain numerous serotypes. Fecal–oral contamination is the mode of spread, most commonly from contaminated food in the case of TD. With an infectious dose as low as 10 to 200 organisms, person-to-person spread also occurs.60 The essential virulence factor of Shigella is invasiveness associated with a large (120- to 140-megadalton) plasmid. As with most enteric pathogens, infection with Shigella may be asymptomatic, mild, or severe. In the classic form of shigellosis, after 1 to 3 days of small bowel disease, colonic involvement causes progression to clinical dysentery. In the 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. 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 blood cells. Diagnosis is made by stool culture on selective media (MacConkey or Salmonella-Shigella agar), which is positive in most infected patients.56 Patients with fever and dysentery should be treated with absorbed antimicrobial agents, including fluoroquinolones or azithromycin. The current dosage recommendations for fluoroquinolones are norfloxacin 400 mg twice a day, ciprofloxacin 500 mg twice a day, or levofloxacin 500 mg once daily, for a total of 3 days. Single-dose therapy is probably effective in milder forms of illness. For children, azithromycin (10 mg/kg/day for 3 days) or a 3-day course of a fluoroquinolone can safely be used, even though this class of drugs is not approved for use in children.

CAMPYLOBACTER The organism is a small, curved, and gram-negative rod, formerly classified as Vibrio. Campylobacter jejuni/coli strains are widespread in the environment, most often spread from contaminated food. The most important source for human illness is poultry, but epidemics have also been associated with ingestion of raw milk.17,18 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 geographic area and time of year. TD secondary to C. jejuni is more prevalent in Southeast Asia and accounts for about 3% of cases in rainy summertime and in up to 15% of cases during drier wintertime.17,130,172 All segments of the small and large intestine may be affected in intestinal campylobacteriosis.  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. C. jejuni infection has been associated with occurrence of Guillain-Barré syndrome.17,98,136,164 The mechanism of development of this postinfectious complication relates to molecular mimicry with development of antiganglioside antibodies stimulated by infection by specific strains of Campylobacter.79 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. C. fetus may be grown from the blood in patients with systemic illness. Treatment is primarily supportive with oral fluids; dehydration is usually mild. Early antibiotic therapy appears to be effective in intestinal campylobacteriosis.17 The antibiotic of choice is erythromycin or azithromycin.82,116 1368

VIBRIOS Cholera is a severe form of watery diarrhea often associated with dehydration. The disease is caused by V. cholerae O group 1 (O1), 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.169 Non-O1 V. cholerae strains also produce diarrheal illness, but they show less potential for epidemic disease.108,117 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 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 intestinal wall. Some cholera infections are asymptomatic, and 60% to 80% of clinical cases are presented as mild diarrhea that never raise suspicion for cholera.93 After an incubation period of 2 days (range 1-5 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.108,169 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. A dysentery-like syndrome with mucoid bloody diarrhea is often seen in disease outbreaks.20 Infections are usually brief, lasting an average of 3 days, with spontaneous resolution. Diagnosis for any of the Vibrio strains 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.108 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 in motion. 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. 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. 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. The current parenteral cholera 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 not recommended for travelers to endemic areas.108 Outside the United States, two additional vaccines are available: an oral killed whole cellcholera toxin recombinant B subunit (WC-rBS) and an oral live attenuated V. cholerae vaccine (CVD 103-HgR), both with 60% to 100% rate of protection against V. cholerae O1 for at least 6 months. They are not active against V. cholerae O139.168 Finally, a bivalent (CVD103-HgR plus CVD 111) oral vaccine has been shown to be more effective than is the monovalent one.10,12,87,194

Intestinal Protozoa

GIARDIA LAMBLIA

Protozoal infections may be pathogenic or commensal (having little or no effect) for the human host. Although acute self-limited diarrheal illness may occur, only a small proportion of cases of acute TD are caused by parasites. Symptoms are nonspecific, and diagnosis is often made on stool examination. Most protozoal infections are suspected on the basis of subacute or chronic GI symptoms, which may fluctuate over time. Several factors have increased the prevalence of intestinal parasites in the United States and worldwide: an increase in

G. lamblia (also known as Giardia intestinalis or Giardia duodenalis) is a flagellate protozoan. Classification of Giardia species remains controversial, but there are at least six species and other genotypes, primarily distinguished by host. G. duodenalis is the species of major concern for human infection.5 Giardia is the most common protozoal intestinal parasite isolated worldwide, including the United States. Prevalence ranges from 3% to 7% in the United States to 30% or more in developing areas with poor sanitation. All age groups are affected.

Aeromonas species and P. shigelloides are gram-negative, facultative 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.91,92,101,202 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.101,175,200 Aeromonas strains are susceptible to antibiotics used to treat TD. P. shigelloides 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.92 Plesiomonas is susceptible to anti-TD antibiotics.

VIRAL ENTERIC PATHOGENS

TABLE 68-10  Antiparasitic Therapy for Giardiasis* Adult Treatment

Pediatric Treatment and Other Drugs

Tinidazole 2000 mg single dose, or Nitazoxanide 500 mg twice a day for 3 days, or Metronidazole 250 mg three times a day for 5-7 days or 2 g/day in a single dose for 3 days (high dose has more side effects), or Albendazole 400 mg single dose or once a day for 5-7 days (single dose less effective), or Diloxanide (Furamide), adults and children aged 12 yr and older: 500 mg three times a day for 5-10 days

Tinidazole 50 mg/kg single dose Children aged 1-4 yr: nitazoxanide 100 mg twice a day for 3 days; Children aged 4-11 yr: nitazoxanide 200 mg twice a day for 3 days Metronidazole 15 mg/kg/day divided three times a day for 5-7 days Albendazole 10 to 15 mg/kg once a day for 5-7 days Children up to age 12 yr: diloxanide 20 mg/kg/day in three divided doses for 5-10 days

*References 23, 24, 31, 66, 70, 74, 85, 125, 137, 145, 148, 154, 157, 167, 176, 181, 183, and 204.

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Noroviruses have been shown to be important causes of approximately 10% of TD cases.6,28,99,113 These viruses are highly infective (10 to 100 organisms per inoculum), and infection is spread by common-source vehicles with a propensity for secondary personto-person spread (high secondary attack rate).89 Humans are the only known carriers of these viruses. Norovirus is known as the “cruise ship virus” based on its importance in that setting. Between 20% and 67% of outbreaks of noroviruses have been associated with food.26,144 After a cruise ship has experienced a norovirus outbreak, this viral infection can continue to be a problem in future trips with the involved ship, despite extensive sanitization.99 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 without 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. Currently, there are immunoassays and molecular techniques (reverse-transcription PCR) available for detection of these small round RNA viruses in stool.6,27 Vaccine development is being explored for the noroviruses, but the studies are in a very early stage.114

immunocompromised patients, who frequently become infected by these organisms; improvement in diagnostic techniques; increase in group settings (day care centers and nursing homes); more frequent international travel; and in the United States, increased immigration of people from developing countries.110,128 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.208 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. 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 (see Cryptosporidium, later), cause a wide spectrum of GI complaints, including malabsorption (resulting in foul stools and flatulence) and weight loss in persistent infections. Although many protozoa are capable of superficial mucosal invasion, only E. histolytica and B. coli, which colonize the colon, can ulcerate the bowel wall, cause dysentery, and spread to other tissues.86 Most infections are asymptomatic and self-limited in immunocompetent persons but can be persistent and severe in immunocompromised hosts. Treatment of intestinal protozoal infections is summarized in Table 68-10. Prevention of infection is focused on interruption of fecal–oral transmission and is similar to other bacterial and viral causes of traveler’s diarrhea, including personal hygiene, water disinfection, basic food precautions, and care in food preparation. Currently, no vaccines are available for enteric protozoan infections, although there are efforts to develop a vaccine for E. histolytica.

AEROMONAS SPECIES AND PLESIOMONAS SHIGELLOIDES

PART 8 FOOD AND WATER

In the United States, a seasonal peak in case reports coincides with the summer recreational water season and likely reflects increased outdoor activities and exposures, such as camping and use of communal swimming venues (e.g., lakes, rivers, swimming pools, and water parks).208 Persons at increased risk for infection reflect the fecal–oral transmission through food, water, and person to person and a low infectious dose, including (1) travelers to disease-endemic areas; (2) children in child care settings; (3) close contacts of infected persons (family or household contacts); (4) persons who ingest contaminated drinking water, contaminated recreational water (lakes, rivers, and pools), or untreated surface water (backpacking or camping); (5) persons who have contact with infected animals; and (6) men who have sex with men. Giardia accounts for a small percentage of TD. 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 travel to a developing region. Epidemiologic studies suggest 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 occurs. Reservoir Giardiasis usually represents a zoonosis and has been detected in nearly all classes of vertebrates, including domestic animals and wildlife, including beavers, cattle, dogs, cats, rodents, and sheep. Although G. intestinalis infects both humans and animals with cross-infectivity, molecular epidemiology suggests that the role of zoonotic transmission to humans and the importance of animal contamination of food and water may be less than previously thought.208 Transmission and Infectious Dose Giardia infection is transmitted by the fecal–oral route and results from the ingestion of Giardia cysts through consumption of fecally contaminated food or water or through person-to-person (or, to a lesser extent, animal-to-person) transmission. The cysts are infectious immediately on being excreted in feces. Infected persons have been reported to shed 108 to 109 cysts in the stool per day and to excrete cysts for months. 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%. Infectivity apparently depends on both host and parasite factors.148 Person-to-person spread may be the most common means of transmission for humans. Areas and populations with poor hygiene and close physical contact have higher rates of infection, and infection of other household members is common. Venereal transmission occurs between homosexuals through direct fecal– oral contamination. Water is a major vehicle of infection in community outbreaks, from small water systems that use untreated or inadequately treated surface water, and may play a significant role in U.S. wilderness travelers who develop intestinal illness.109,208 Cysts retain viability in cold water for as long as 2 to 3 months. Giardiasis has been called backpacker’s diarrhea, because of the common association with alpine mountain waters. Pathophysiology and Clinical Presentation The pathophysiologic mechanisms of diarrhea and malabsorption in giardiasis are poorly understood, and more than one mechanism, including altered gut motility and hypersecretion of fluids, is probably involved. Most small bowel biopsies in human patients demonstrate minimal or no changes. Enterotoxins have not been found.148,157 Most infections are asymptomatic, but carriers can excrete high numbers of cysts in stools. Giardia is found in healthy people. The attack rate for symptomatic infection in the natural setting varies from 5% to 70%. Correlation between inoculum size and infection rates has been noted, but not with numbers of cysts passed or severity of symptoms. The incubation period averages 1 to 2 weeks, with a mean of 9 days. A few people experience abrupt onset of explosive watery diarrhea accompanied by abdominal cramps, foul flatus, vomiting, 1370

low-grade fever, and malaise. This typically lasts 3 to 4 days before transition into the more common subacute syndrome. In most patients, 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 tract symptoms, typically exacerbated postprandially, accompany stool changes, but they may be present in the absence of soft stool. These include midabdominal 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. Unusual presentations include allergic manifestations, such as urticaria, erythema multiforme, and bronchospasm. Some Giardia infections are associated with chronic illness. Adults may have a longstanding malabsorption syndrome and marked weight loss, and children may have failure-to-thrive syndrome.65,86 Immunologic responses are effective in the majority of infections because spontaneous clinical recovery is common with or without the disappearance of organisms. The average duration of symptoms in all ages ranges from 3 to 10 weeks. Both cellular and humoral responses to Giardia have been demonstrated. Diagnosis Direct stool examination may be used when newer immunologic tests are not available. Cyst passage is extremely variable and not related to clinical symptoms, so multiple stool collections (i.e., three stool specimens collected every other day) increase test sensitivity. One stool sample will allow detection of 60% to 80% of infections, two stool samples will allow detection of 80% to 90%, and three stool samples will allow detection of more than 90%. Trophozoites may be found in fresh, watery stools (Figure 68-2) but disintegrate rapidly. Stools should be preserved in a fixative, such as polyvinyl alcohol, or a formalin preparation if not immediately examined. 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 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. Another noninvasive office test is duodenal mucus sampling, using a string test (Enterotest), which has a reported sensitivity of 10% to 80%. Duodenal biopsy is a sensitive test, but should rarely be necessary.128 Direct fluorescent antibody (DFA) testing is an extremely sensitive and specific detection method and is considered the “gold standard” by many laboratorians. Immunoassays using ELISA or enzyme immunoassay (EIA) on stool approach 100% sensitivity and specificity. Moreover, EIA is much easier and requires less experience than does microscopy. Other molecular techniques are available but not commonly used in clinical settings.

FIGURE 68-2  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.

Pathophysiology and Clinical Course

Because of the difficulty and expense of confirming the diagnosis in some patients, a therapeutic trial of drugs may be attempted when suspicion is high. In the field, it is reasonable to initiate presumptive treatment for Giardia for secretory diarrhea (nondysentery) lasting more than 1 week that does not respond to a trial of antibiotic therapy. Symptomatic patients should be treated for comfort and to prevent 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, a longer course of two drugs taken concurrently has 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 from treatment failure. The three groups of drugs currently being used are nitroimidazoles (metronidazole, tinidazole, albendazole, ornidazole, nimorazole), nitrofuran derivatives (furazolidone), and acridine compounds (mepacrine, quinacrine).24,74 Tinidazole and nitazo­ xanide (Alinia) have similar or better effectiveness (average 85 to 90%) than does metronidazole and have been approved by the FDA for this use in the United States. Tinidazole is licensed for children older than age 3 years, and nitazoxanide is available in suspension for children as young as age 1 year. Albendazole has comparable effectiveness with metronidazole and is used commonly outside the United States because of its broad activity against other parasitic worms.183 Other alternatives include furazolidone, which results in cure rates between 80% and 96% and is also available as a pediatric suspension. Paromomycin (Humatin) is a nonabsorbable drug that is recommended for pregnant women or for use in severely symptomatic individuals. Quinacrine (Atabrine) achieves high cure rates, but it is no longer available in the United States because it produces more frequent side effects, especially in children. Mebendazole and ornidazole are two other nitroimidazoles that have been used successfully, but less data are available for these drugs. Treatment of giardiasis has been extensively reviewed by Gardner and Hill.74

The pathogenicity of E. histolytica is still not well understood. Invasion may be a function of motility, soluble toxins, cysteine protease, or lytic enzymes.171,185 The cecum and ascending colon are most frequently involved, followed by the rectum and sigmoid colon, with lesions of increasing severity and depth of inflammation and ulceration. Extraintestinal spread is hematogenous. Abscesses containing acellular debris develop primarily in the liver but may involve the brain and lung. The incubation period ranges from 1 to 4 months. Although 80% to 99% of infections result in asymptomatic carriers, a spectrum of GI diseases may result, with considerable variation in severity. Most often, colonic inflammation without dysentery causes lower abdominal cramping and altered stools, sometimes containing mucus and blood.100 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 after a period of mild symptoms. Affected persons may have frequent passage of bloody stools, tenesmus, moderate to severe abdominal pain and tenderness, and fever.163,185 Amebic liver abscess is the most common and serious complication from hematogenous spread. Individuals can present with liver abscess months to years after travel or residency in an area of endemicity. The disease should be suspected in anyone with an appropriate exposure history (residency or travel in an area of endemicity) presenting with fever, right upper quadrant pain, and substantial hepatic tenderness. 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 annular inflammatory lesion of the ascending colon containing live trophozoites. A postdysenteric syndrome can occur in patients with acute amebic dysentery and can be confused with ulcerative colitis. Asymptomatic carriers of E. histolytica can develop invasive disease, but more often the infection resolves spontaneously. Humoral antibodies increase with invasive disease and persist for long periods. Although they do not protect against reinfection or bowel invasion, they may prevent recurrent liver infection. Mucosal immunity may provide some protection against recurrent intestinal infection with E. histolytica; 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. Oral vaccines and DNA-based vaccines have been successfully tested in animal models, but human testing has not been done and no vaccine is currently available.185,186

ENTAMOEBA The genus Entamoeba contains many species. Six that can reside in the human intestinal lumen are E. histolytica, Entamoeba dispar, Entamoeba moshkovskii, E. polecki, Entamoeba coli, and Entamoeba hartmanni. E. histolytica is the only species definitely associated with clinical pathology in humans. The others are considered commensal; however, E. polecki and E. moshkovskii have been suspected of causing lower intestinal symptoms in cases involving heavy infection.69 In addition, isoenzyme analysis has recognized 22 different zymodemes of E. histolytica, which may explain geographic differences in rates of invasive disease.161 Epidemiology and Risk E. histolytica is found worldwide. Similar to Giardia, transmission is fecal–oral through person-to-person contact or contaminated food or water. Cysts remain viable outside the body for weeks to months, as opposed to the fragile trophozoites. Unlike Giardia, there is no zoonosis, and the reservoir of infection is human. Approximately 12% of the world’s population is infected. The higher prevalence (30% to 50%) in tropical countries is related to increased risk of fecal–oral contamination, which depends on sanitation, cultural habits, crowding, and socioeconomic status.185 E. histolytica is a leading cause of death by parasitic infection worldwide. The WHO estimates that E. histolytica infects 500 million people per year, causes disease in 50 million, and kills 100,000 individuals annually. Importation of infections by travelers and immigrants accounts for most cases in the United States and other temperate countries. Amebiasis accounts for less than 1% of TD.

Diagnosis Routine screening of asymptomatic persons of high-risk groups is not cost-effective, except perhaps for food handlers and persons returning from extended stay in endemic countries. The diagnosis of invasive amebiasis is most commonly attempted by a combination of microscopy of a fecal specimen, serological testing, and, where indicated, colonoscopy and biopsy of intestinal amebic lesions or drainage of a liver abscess. Where available, detection of E. histolytica–specific antigen and DNA in stool and other clinical samples (enzyme-linked immunosorbent assay [ELISA]) may replace microscopic stool exam, which is complicated by morphologically similar nonpathogenic species. Antigen detection using ELISA is both rapid and technically simple to perform and can be used in laboratories that do not have molecular facilities, making it appropriate for use in the developing world where amebiasis is most prevalent.192 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. In combination with ultrasound or other abdominal imaging, serology is helpful for diagnosis where PCR is not routinely available. Because they also do not distinguish between current and prior infections, serologic tests are more useful in developed countries with low 1371

CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Treatment

PART 8 FOOD AND WATER

incidence of infection. The combination of serological tests with detection of the parasite (by antigen detection or PCR) offers the best approach to diagnosis.69 New antigen detection techniques can differentiate between E. histolytica and E. dispar. PCR techniques have been developed and show greater than 95% sensitivity and specificity. Diagnosis of intestinal amebiasis by microscopic identification of cysts or trophozoites in stool still plays a significant role where other techniques are not available. 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 be examined later with trichrome stain. Fecal shedding of cysts is irregular, but three stools on alternate days identify most infections. 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. Finding cysts does not confirm the diagnosis of symptomatic intestinal amebiasis. The key to establishing the diagnosis is finding motile trophozoites with ingested red blood cells. It is rare to identify E. histolytica in stool samples from patients with liver abscesses. Culture techniques are available, but not generally used in clinical laboratories because they are expensive and time consuming. Treatment There are multiple benefits to treatment, including reducing the infectious period, length of illness, risks of transmission to others, rates of severe illness, and preventing complications of invasive disease.35 U.S. guidelines suggest that asymptomatic carriers should be treated, because a cyst passer represents a potential health hazard to others, and reinfection in the United States is uncommon. Moreover, asymptomatic colonization with E. histolytica, if left untreated, can lead to invasive disease. Treatment of amebiasis is based on the location of infection and the degree of symptoms. Medications are divided into tissue amebicides (e.g., metronidazole, tinidazole, emetine, dehydroemetine, chloroquine), which are well-absorbed drugs that combat invasive amebiasis in the bowel and liver, and poorly absorbed drugs (e.g., iodoquinol, paromomycin, diloxanide furoate) for luminal infections. In general, treatment is effective for invasive infections but disappointing for intestinal colonization. The current drug of choice for asymptomatic carriers is iodoquinol. Side effects are mild and consist of abdominal pain, diarrhea, and rash. Diloxanide furoate (Furamide) is another drug of choice, but in the United States it is classified as an investigational drug, available only through the Centers for Disease Control and Prevention. Paromomycin is also effective. Although metronidazole has been used in asymptomatic carriers with 90% success, most reserve this drug for invasive and symptomatic infections.13,161 Invasive disease is treated with a tissue-active drug, followed by a luminal agent (in the same dosages as for asymptomatic infection). Tinidazole or metronidazole are the drugs of choice for oral therapy of amebic dysentery or liver abscess. Tinidazole has slightly better effectiveness and fewer side effects than does metronidazole. Other nitroimidazoles that have been tested include ornidazole, nitazoxanide, and secnidazole. Emetine and dehydroemetine 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 development of cardiac arrhythmias requiring hospitalization for cardiac monitoring. Because this class of drugs is related to ipecac, the drugs also cause vomiting. Successful resolution of symptoms from E. polecki has been reported with metronidazole followed by diloxanide furoate in the same dosages as for amebiasis.

CRYPTOSPORIDIUM* Cryptosporidium is a coccidian parasite related to Toxoplasma and Plasmodium. Other coccidia capable of causing human intestinal infection include Microsporidia, Cyclosporidia, and Isospora. In *References 25, 29, 32, 33, 36, 85, 112, 133, 146, 167, 181.

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the environment, Cryptosporidium exists as a hearty, 5-mm-­ diameter oocyst containing four sporozoites. As with Giardia, the cysts are infectious when excreted. Humans and animals are infected by ingesting these oocysts, which travel through the gut lumen to the small intestine, where they release the sporozoites. Epidemiology and Risk for Wilderness and International Travelers The epidemiology and transmission of Giardia and Cryptosporidium parvum are similar. C. parvum causes a ubiquitous zoonosis with worldwide distribution. Cryptosporidium infects a wide variety of domestic and wild animals. Molecular analysis has revealed at least 14 species of Cryptosporidium that are distinguished primarily, but not solely, by host and cannot be distinguished by morphology. It is a reemergent enteric pathogen in humans. The prevalence of infection in human populations varies from 0.1% to 3% in cooler, developed countries (in Europe, North America) to 0.5% to 10% in warmer countries (Africa, Asia). The infection has been described in persons who have contact with animals, such as veterinarians and farmers; infants in day care centers; travelers to endemic areas; and patients who have AIDS or who are otherwise immunocompromised. It has infected large numbers of individuals in community-wide waterborne outbreaks.208 Cryptosporidium poses a risk to wilderness users because oocysts are found widely in surface water and have high degree of resistance to chlorine.120,121 (see Chapter 67) The infective dose of Cryptosporidium for humans is low (mean 132 cysts in a human challenge trial), similar to that seen with Giardia species.44 Fecal–oral contamination is the mode of transmission. 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; sexual, with no association with specific behavior; and zoonotic. Pathophysiology and Clinical Course The pathophysiologic mechanisms of diarrhea and malabsorption are not completely understood. The parasites may activate cellular and humoral immune and inflammatory responses, leading to cell damage and ultimately producing malabsorption and osmotic diarrhea. Clinical manifestations depend on the patient’s immune status, but asymptomatic infection occurs in both normal and immunocompromised hosts. 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, lasting 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 resolution of symptoms, but may persist for up to two months after recovery. Reinfection of an immunocompetent person has been documented. Rarely, Cryptosporidium can infect other organ systems, include the respiratory system, liver and biliary system, and stomach, particularly in immunocompromised persons. Diagnosis Oocysts can be found in the stools routinely in intestinal infections, even though shedding may be intermittent. Concentration techniques and staining with modified acid-fast, Giemsa, or Ziehl–Neelsen techniques facilitate identification of Cryptosporidium oocysts. The Enterotest (string test to sample duodenal mucus) is also useful in the diagnosis of cryptosporidiosis. Newer immunologic techniques (immunofluorescence and enzyme immunoassay) to detect antigen in stools are faster and have adequate sensitivity and excellent specificity. Several other molecular diagnostic methods have been developed, but their efficacy in the clinical setting is not yet known.

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. Treatment is indicated for immunocompetent persons with persistent infection and in immunocompromised patients. Some effectiveness with paromomycin, azithromycin, and nitazoxanide has been found against Cryptosporidium. Paromomycin, roxithromycin, ionophores, sulfonamides, and mefloquine have also been tested against cryptosporidiosis, especially in patients with AIDS and chronic diarrheal disease, with variable but generally positive effects. The most effective prevention in HIV patients is antiretroviral therapy (HAART) that supports the immune system.

ISOSPORA BELLI* Isospora belli is a coccidian protozoal parasite. It is an uncommon cause of diarrhea in humans, but its prevalence, like that of Cryptosporidium, has been increasing in immunocompromised patients. Ingested oocysts release sporocytes in the small intestine that develop into trophozoites. Epidemiology and the Risk for Wilderness and International Travelers Humans are the only host (although there are a few reports in dogs), and infections are transmitted by fecal–oral contamination through direct contact of food and water, so rates are typically higher in settings with high density of people, close contact, or poor hygiene. I. belli is endemic in areas of South America, Africa, and Asia. The prevalence is not precisely known, but ranges from 0.2% to 3% in U.S. patients with AIDS and from 8% to 20% in Haitian and African patients with AIDS. 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. Pathophysiology and Clinical Course The life cycle and pathogenesis of I. belli are similar to those of Cryptosporidium. The organism invades mucosal cells of the small intestine, causing an inflammatory response in the submucosa and variable destruction of the brush border. In immunocompetent persons, 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. Generally, infection is self-limited, ending in 2 to 3 weeks, but some persons have symptoms lasting months to years. Infections in immunocompromised patients tend to be more severe and follow a more protracted course. Rarely, acalculous cholecystitis or reactive arthritis has been reported. Recurrences are common. Diagnosis 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 can also be 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. Treatment Successful treatment has been reported with trimethoprim– sulfamethoxazole (TMP-SMX). Other options are pyrimethamine with folinic acid, metronidazole, and nitazoxanide (for patients *References 33, 80, 125, 128, 157, 204.

allergic to sulfonamides). In patients with HIV infection, chronic lifetime suppression therapy is indicated with either TMP-SMX or pyrimethamine plus folinic acid daily.

CYCLOSPORA CAYETANENSIS* Cyclospora species were initially thought to be blue-green algae (cyanobacteria-like organisms). The life cycle and pathogenesis of Cyclospora cayetanensis are not completely understood. Oocysts need about 7 to 15 days to sporulate and become infectious, so they are not immediately infectious on passage. Epidemiology and the Risk for Wilderness and International Travelers C. cayetanensis has been shown to be an important cause of acute and protracted diarrhea. Fecal–oral transmission occurs through food, water, and soil. The organism is endemic in many developing countries in all continents. There are numerous reports of Cyclospora infection with diarrhea in travelers to Nepal, Haiti, Peru, and Guatemala. In the United States, most of the outbreaks have been food-borne, associated with ingestion of contaminated imported raspberries. Humans are the only known reservoir; there is conflicting evidence for a zoonosis. Pathophysiology and Clinical Course The onset of diarrhea is usually abrupt, with symptoms lasting 7 weeks or even longer. Other symptoms include anorexia, nausea, flatulence, fatigue, abdominal cramping, and weight loss. In patients with AIDS, the duration may be longer and severity greater. This is a familiar clinical picture from intestinal protozoa. Diagnosis Small spheric organisms can be detected in fresh or concentrated stool. They show variable staining with acid-fast methods, but stain best with carbolfuchsin. Phase-contrast microscopy and autofluorescence are also useful in the diagnosis. A PCR method is used primarily for research. Treatment The treatment of choice is TMP-SMX. This treatment provides rapid clinical and parasitologic cure, with few recurrences. In patients with AIDS, chronic suppression with TMP-SMX may be required. Ciprofloxacin has been used successfully in persons with sulfa allergy.

MISCELLANEOUS PARASITIC AGENTS Microsporidia† More than 100 genera and 1000 species of microsporidia exist in the phylum Microspora. Most species infect insects, birds, and fish. Only 12 species have been reported to infect humans, and of these, only two, Enterocytozoon bieneusi and Encephalitozoon intestinalis, have been found to cause diarrhea in humans. Microsporidia are obligate intracellular protozoa. Transmission is thought to be fecal–oral or urinary–oral and the infection zoonotic. Spores are environmentally resistant, so waterborne transmission also occurs. Prevalence of microsporidiosis in patients who have AIDS and chronic diarrhea is 7% to 50%. Diarrhea from microsporidia has been reported in travelers to the tropics. Clinical manifestations of intestinal microsporidiosis are chronic diarrhea, loss of appetite, weight loss, malabsorption, and fever. 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. Electron microscopy is considered the gold standard. Immunologic and molecular biologic techniques are still under evaluation.

*References 7, 33, 80, 126, 149, 157, 178, 189. † References 31, 33, 39, 71, 80, 123, 128, 135, 180, 204, 205.

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Treatment

The most effective drug against most species is albendazole (400 mg twice a day for 2 to 4 weeks). Other drugs that show different efficacies include atovaquone, metronidazole, furazolidone, azithromycin, itraconazole, and sulfonamides. 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. Balantidium  B. coli is a rare pathogen in humans.176,204 It is the largest and only ciliated protozoa that infects humans. The life cycle involves only trophozoite and cyst stages. Many aspects of the epidemiology are unclear. Pigs appear to be the primary reservoir, although other animals have been implicated. There is no intermediate host. Transmission is fecal–oral, and water is the most common vehicle. Infection is most common in tropical and subtropical regions with poor hygiene. Clinical features resemble those of 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 a stool wet mount. Trophozoites are seen much more often than are cysts. Recommended treatment is tetracycline or metronidazole. Nitazoxanide is an alternative. *References 33, 80, 176, 204.

Blastocystis* The role of Blastocystis hominis in diarrheal disease is still controversial. The life cycle of B. hominis continues to be debated. The organism is frequently identified in stool samples by its characteristic appearance, but has not been directly correlated with symptoms, which might be caused by other undetected pathogens. Treatment is not warranted in asymptomatic infections. When found in large numbers as the sole pathogen, B. hominis is suspected as the potential etiologic agent of diarrheal illness. The few treatment trials yield mixed reports and are supported by in vitro studies. 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. Identification can be done from stool samples, a fixative, and nearly any type of stain. Treatment of D. fragilis is effective with iodoquinol and tetracyclines. There are also reports of successful treatment with metronidazole, paramomycin, and secnidazole.176,204

*References 127, 188, 191, 204. † References 105, 176, 204.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 69 

Nutrition, Malnutrition, and Starvation  E. WAYNE ASKEW

How does it feel to starve? 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. OBSERVATIONS BY A TEST SUBJECT, MINNESOTA STARVATION STUDY, AFTER 24 WEEKS OF SEMI-STARVATION (1570  KCAL/DAY, 24% WEIGHT 58 LOSS) (IN THE BIOLOGY OF HUMAN STARVATION, VOL. II ) 1374

Importance of Nutrition in Stressful Environments Nutrition has a profound underlying importance to human physiologic homeostasis and functioning on a day-to-day basis in everyday life; it becomes even more important when humans work or recreate in particularly challenging or “extreme” environments.10 The central role of nutrition is often underappreciated in wilderness expedition planning and may even be thought by some to be of minor importance. 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 re-supply is feasible, the importance of nutrition may seem to diminish compared with other aspects of wilderness medicine. However, when a stressful physical environment is superimposed on the physically demanding tasks associated with wilderness activities, the role of nutrition rapidly becomes of prime importance for maintenance of performance and for prevention of disease and injury, as evidenced from the description of Napoleon’s disastrous 1812 winter retreat from Moscow: The ice and deep snow with which the plains of Russia were covered, impeded … calorification in the capillaries and

For online-only figures, please go to www.expertconsult.com

Fortunately, situations encountered in wilderness activities are usually less grim than those faced by Napoleon’s army. There is usually some food available, and few enter these environments unprepared. However, misfortune, combined with suboptimal or haphazard nutritional planning, can spell disaster for even the best-prepared adventurer. A wrong turn on the trail, an injury, unanticipated terrain, an unexpected storm, or a downed airplane can deplete or isolate a victim from anticipated food sources. Food becomes an overriding consideration in a survival situation, particularly as the supply is exhausted. Although a shortage of food is certainly of concern, it does not necessarily imply impending disaster. Humans are remarkably adaptable and can subsist on nonideal dietary patterns for prolonged periods without dis­ astrous effects on health and performance. As long as some baseline level of energy intake is present, at least a minimal intake of vitamins and minerals will be ensured, forestalling the eventual onset of malnutrition and clinical nutrient deficiency states. Hunger is not comfortable; optimism wanes, weight loss results, and performance may suffer, but a food-deprived individual can still function for an extended period of time. One purpose of this chapter is to review some of the physical and mental consequences of suboptimal nutrition that might be anticipated under varying degrees of food restriction. The medical planner can use this information to anticipate limitations in expedition progress or capabilities and to recognize the state of health of rescued victims of starvation or food restriction. Equally important is the proper way to re-aliment a victim after a prolonged period of unintentional starvation. This can be critically important in a rescue situation, where transport of a victim to a medical facility requires several days of refeeding en route. Although the goal of expedition food planning is to meet daily energy and micronutrient requirements, it is not always possible to provide optimal nutrition because of logistic or situational constraints. Three nutritional states or situations may be anticipated or encountered in the wilderness: (1) optimal nutrition for effective functioning in environmental extremes, (2) suboptimal nutrition or malnutrition, and (3) lack of nutrition or starvation. Dietary planning for both wilderness expeditions and emergencies will be discussed, along with some specific food or nutrient items that may be particularly useful in wilderness expeditions.

ENVIRONMENTAL STRESS AND NUTRIENT REQUIREMENTS The physical and physiologic conditions of an individual (e.g., body weight, strength, coordination, fluid and electrolyte balance, and core temperature) play a significant role in determining nutritional requirements to maintain homeostasis. These conditions also directly influence survival time, especially when humans are deprived of food or water. In the short run, the most important nutrient is water.9 If an adequate supply of water is not available, all discourse on the physiology of starvation and malnutrition is pointless, because death from dehydration will occur prior to depletion of energy stores. Humans can survive food deprivation for extended periods of time—weeks or even months—depending on their level of body fat. A nonobese adult may live as long as 60 to 70 days while fasting in clinical setting.52 At the end of this time, almost all body fat and one-third of the lean body mass would be lost.51 James Scott, a victim of unintentional situational starvation, was marooned in a snow cave in the Himalayas with water but no food. He survived 43 days without food while losing one-third of his body weight, although he was near death at the time of rescue.104 Death from starvation in nonobese individuals is imminent if approximately 50% of body weight has been lost.

This usually corresponds to a body mass index (BMI) of 12 kg/ m2, although under some circumstances, a BMI of as low as 11 may be encountered prior to death.31 Time to death after complete water deprivation is measured in days—estimates run from 6 to 14 days, depending on the rate of body water loss, which is influenced by the temperature, humidity, and activity level.51 Water is critical because it, more so than any other nutrient, is responsible for maintaining homeostasis of the internal environment.9 It provides an aqueous medium to transport heat from cells to blood, to solvate and pass nutrients between blood and cells, to serve as a medium for intracellular reactions, and to transfer metabolic products for redistribution or excretion via urine. Both the quantity of reactants and the volume of fluid in which they are dissolved influence cellular chemical reaction rates; hence, imbalances in hydration status can alter cellular and tissue function, such as the body’s ability to regulate temperature. Muscle contraction depends on transformation of chemical energy (ATP) to mechanical energy. Nearly three-fourths of the energy used for muscle contraction is released as heat. Unless localized heat production from metabolism and muscle contraction is dissipated, the heat burden can be structurally damaging to enzymes or other proteins. Water absorbs heat produced at the cellular level and transfers it to the surface of the skin, where it can be dissipated to the external environment. The importance of water is discussed in greater detail in Chapter 70. The focus of this discussion is on energy restriction and assumes an adequate supply of water. For planning purposes, most wilderness expeditions require 3 to 5  L (about 3 to 5  qt) of potable water per person per day. Advances in food processing, preservation, and nutrient fortification have resulted in modern camping foods and the military equivalent, field rations, that can support health and performance in a variety of temperate environments, even if they are not consumed to complete caloric adequacy.73 However, nutrition that was marginally adequate in a temperate environment may rapidly become inadequate in wilderness environments characterized by extreme temperatures, terrain, and physical demands.72,74 Rodahl and Issekutz100 observed, “While short-term nutritional deficiencies in men at room temperature appear to have little or no detrimental effect on the capacity to do short-term, heavy work, there is a marked reduction in physical work capacity when a nutritional deficiency or nutritional stress is superimposed on a cold stress.” Superimposed stressors, such as extreme heat, cold, altitude, sleep deprivation, physical exertion, and food restriction, influence nutrient requirements7 and can jeopardize performance.* The complex interrelationship between environment and nutrition, and its effect on human physiology and performance, is depicted in Figure 69-1. Stressors in the form of environmental extremes can have serious consequences on health and performance. Proper nutrition can help counter detrimental environmental influences on physical and mental performance.2-7 Energy and fluid deficits arising from the interaction of environment and nutrition can negatively impact both physical39 and mental77 performance. Volitional physical activity as well as mood can suffer under caloric deprivation, depending on the magnitude and duration of the restriction. Motivation may be more acutely influenced by undernutrition than is actual physical performance.77 Nutritional deficits may have a greater effect on what individuals are willing to do (i.e., on their perceived mood, symptoms, and self-motivation) than on what they can do (psychomotor performance).108 Nutritional Considerations in Planning for Wilderness Activities Current national nutritional recommendations are revised periodically and can be found in the most recent dietary reference intakes published by the Institute of Medicine, National Academies.54 The dietary reference intakes (DRIs)88 are reference values for nutrient intakes that can be used to assess and plan diets for healthy people. Publications that list DRIs can be

*References 10, 39, 68, 72, 74, 77.

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CHAPTER 69  Nutrition, Malnutrition, and Starvation

pulmonary organs. The snow and cold water, which the soldiers 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. BARON D. J. LARREY, INSPECTOR GENERAL, NAPOLEON’s MILITARY MEDICAL STAFF (IN HYPOTHERMIA AND WARFARE, 90 NAPOLEON’s RETREAT FROM MOSCOW, 1812 )

PART 8  FOOD AND WATER

Increased energy requirements

Increased water requirements

Inappropriate appetite response Decreased availability of food

Inappropriate thirst response Extreme environments (heat, cold, altitude)

Negative energy balance

Decreased availability of water Dehydration

Impaired thermoregulation Depleted muscle glycogen Deterioration of fine motor coordination Impaired effectiveness Diminished work capacity

FIGURE 69-1  The influence of extreme wilderness environments on food and fluid intake and on physical and mental performance. (Redrawn from Askew EW: In Hickson JF Jr, Wolinski I, editors: Nutrition in exercise and sport, Boca Raton, Fla, 1989, CRC Press, pp 367-384.)

clothing ensemble, and level of physical exertion.74 Work in cold environments can be adequately supported by various combinations of fat, carbohydrate, and protein, although certain combinations of macronutrients may be more beneficial than others in helping a person withstand cold exposure.4 As an example, Mitchell and colleagues81 demonstrated that cold tolerance (the length of time body core temperature could be defended during a controlled cold challenge) was favored by previous diets high in fat as opposed to diets higher in carbohydrate or protein. Subsequent research has indicated that the macronutrient source is less important in the cold than consuming enough total calories to support activity and thermogenesis.4,45

obtained through the National Academies website (http:// www.nap.edu/catalog.php?record_id=11767) and the National Institutes of Health website (http://ods.od.nih.gov/Health_ Information/Dietary_Reference_Intakes.aspx). The DRIs include four categories: estimated average requirement (EAR), recommended dietary allowance (RDA), adequate intake (AI), and tolerable upper limit (UL). EAR is the nutrient intake level estimated to meet the needs of 50% of the individuals in a population group. RDA is the nutrient intake level sufficient to meet the needs of 97% to 98% of individuals in a population group. AI is an estimate of adequate intake when an EAR cannot be established. AI and RDA are similar but not identical. The UL is the highest daily consumption level of a nutrient; when UL is exceeded, the nutrient poses a risk of adverse health effects. In general, for nutritional planning for wilderness expeditions, the basic daily diet should meet or exceed the DRI recommendations, especially if the traveler plans to subsist on them for prolonged periods of time (greater than 10 days). In the short run (less than 10 days), adequate energy provision is likely to be the predominant dietary concern. In the short run, certain nutrients may assume more critical or primary roles in environmental extremes than they might normally fulfill in everyday life. Cold, heat, and altitude stressors and their influences on macronutrient vitamin and mineral requirements have been a focus of considerable military and civilian research.8 Research conducted primarily in the era since World War II (WWII) and the Korean conflict has established that vitamin and mineral requirements are not significantly increased by cold exposure, although caloric requirements for thermogenesis and work may be elevated to varying degrees, depending on the cold challenge,

Oxidation of energy substrates from the diet or body stores

ATP

Utilization

UCP1

HEAT ~35%

Synthesis

Food and Adaptive Thermogenesis.  Mild cold exposure, even without increased physical activity, elevates energy expenditure in mammals, including humans.59,70,127 This process is called adaptive thermogenesis. Adaptive thermogenesis, or regulated production of heat by the body, is influenced by environmental temperature and diet.70 Figure 69-2 depicts the major sources of metabolic heat production in mammals. Heat can be generated from synthetic, oxidative, and/or uncoupling processes. Mitochondria, the organelles that convert food to carbon dioxide, water, and ATP, are fundamental in mediating effects on energy dissipation in response to an energy demand stimulus.48 Adaptive thermogenesis is a complex cascade of cell signaling events and primarily regulated by two major hormonal effectors: β-adrenergic agents and thyroid hormone. Thyroid hormones are major endocrine controllers of energy expenditure.48 Thyroid hormones are critical in providing a vigorous response to cold exposure and to sustaining that response by providing glucose and fatty acids

Biologic work. Muscular contraction, metabolic processes

HEAT ~60%

Brown adipose tissue. Up-coupling oxidation from phosphorylation

HEAT ~100%

FIGURE 69-2  Energy transforming pathways and heat production.

1376

Coffee

Green tea

Caffeine

Catechins (−)

(+)

(−) COMT

NFκ-β

(+) Phosphodiesterase

Norepinephrine (+)

(−)

Adenyl cyclase (+)

(+) Cold

cAMP

ATP

(+)

(+)

PGC1-α

Lipolysis

AMP (+) UCPs

(+) PPARs (+)

Fatty acid oxidation

(+)

(+) Energy expenditure/thermogenesis

FIGURE 69-3  Cell signaling , activation of thermogenesis and mecha­ nism of green tea and coffee stimulation of thermogenesis. Abbre­ viations: NFκB, nuclear factor kappa B; COMT, catechol O-methyl transferase; PC1-α, peroxisome proliferator-activated receptor gamma coactivator-1α; PPAR, peroxisome proliferator activated receptors; UCP, uncoupling protein; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; AMP, adenosine monophosphate. (Modified from Hursel R, Westerterp-Plantenga MS: Thermogenic ingredients and body weight regulation. Int J Obes 34:659, 2010.)

little attention in recent years, possibly because of the current focus of thermogenic research on obesity and perhaps because of the perception that advances in clothing and equipment make internal heat generation somewhat less critical as a mechanism to prevent hypothermia. Based mostly on older research, we know that dietary approaches incorporating frequent small meals, fat, caffeine/ephedra, or capsaicin seem to be the most practical and proven approaches to augmenting diet-induced thermogenesis. Other Potential Thermogenic Nutrients.  Recent research on the thermogenic properties of green tea seem to provide support for tea as a historically favored hot beverage for cold weather and high-altitude expeditions. In research directed at the possible role of green tea in stimulating thermogenesis in conjunction with weight loss diets to combat obesity, it has been found that green tea stimulates thermogenesis in a manner that cannot be completely attributed to its relatively low caffeine content.35,36 Green tea contains catechins that inhibit the enzyme catechol O-methyltransferase (COMT), which degrades catecholic compounds such as norepinephrine. Diminishing COMT’s net effect would be to permit higher and more sustained levels of norepinephrine, which in turn would permit a more sustained lipolytic response to support increased energy expenditure. Besides the catechin inhibition of COMT, green tea, as well as coffee, contains caffeine, which enhances thermogenesis by inhibiting the enzyme phosphodiesterase. Inhibition of phosphodiesterase prevents degradation of cyclic AMP, permitting lipolysis to continue and provide additional fatty acids for eventual oxidation.53 1377

CHAPTER 69  Nutrition, Malnutrition, and Starvation

to fuel energy production and thermogenesis.109 Thyroid hormone acts synergistically with catecholamines of the sympathoadrenal system during cold adaptation, times of high energy output and, conversely, when energy demands should be reduced, such as during starvation.109 Physiologic stimuli, such as cold exposure, elicit these thermogenic hormones, which in turn interact with specific cellular tissue ligand-activated nuclear receptors called peroxisome proliferator activated receptors (PPARs) in brown and white adipose tissue, liver, heart, and skeletal muscle. PPARs act as fatty acid sensors to control many metabolic pathways essential for energy homeostasis.125 PPARs are mainly expressed in white and brown adipose tissue, where they control expression of several proteins involved in upregulation of lipid metabolism, subsequent energy generation and thermogenesis. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a tissue-specific transcriptional coactivator protein that interacts with the nuclear receptor PPAR-γ. This permits interaction of this protein with multiple transcription factors, thus serving as a coactivator that enhances the activity of many nuclear receptors and coordinates cellular transcriptional programs important for energy metabolism and energy homeostasis. PGC-1α can interact with, and regulate the activities of, cAMP response element binding protein and nuclear respiratory factors that are involved in energy metabolism and thermogenesis. Uncoupling protein-1 (UCP1) is an uncoupling protein found in the mitochondria of brown adipose tissue (BAT). It is used to generate heat by non-shivering thermogenesis. Adrenergic and thyroid hormones have an impact on energy dissipation and subsequent heat production by the mitochondria in brown fat and skeletal muscle via a complex signaling mechanism involving PGC-1α, PPARγ, and UCP1.96 PPARγ is a nuclear receptor, subject to transcriptional coactivation by PGC-1α. PGC-1α is a transcription coactivator that plays a central role in regulation of cellular energy metabolism. It is induced by cold exposure, linking this environmental stimulus to adaptive thermogenesis.66 Induction of increased mitochondrial activity through activation of PGC-1α results in an increase in oxidative-type muscle fibers that in turn leads to enhanced resistance to muscle fatigue and increased tolerance to cold.63 PGC-1α is expressed at high levels in tissues where mitochondria are abundant and oxidative metabolism is active, such as BAT, heart, and skeletal muscle.96 The schematic relationship of these cell signaling and response elements and their potential interaction with cold, caffeine, and catechins is depicted in Figure 69-3. Although considerable research has been accomplished recently on basic cell signaling mechanisms influencing gene activity in response to thermogenic stimuli, less applied research has been conducted on nutrients and whole-body cold tolerance. Older studies of food and cold tolerance have largely used core temperature responses to actual cold exposure along with a dietary intervention; more recent cold tolerance research has incorporated aspects of basic cell signaling research described above in response to other food-derived components. Most notably, resveratrol, a plant polyphenol found in abundance in sources such as grapes and Japanese knotweed, has been shown to induce mitochondrial activity via activation of PGC-1α, which in turn increases oxidative-type muscle fibers, enhanced resistance to fatigue, and increased tolerance to the cold in a rat model.63 Assuming the rat model research has applicability to human cold tolerance, these effects are all potentially beneficial attributes for facilitating strenuous cold weather activities. Human resveratrol cold tolerance studies are lacking. It is unlikely that the food products containing resveratrol could be consumed in quantities adequate to exert a similar effect to that seen in the supplemented rat model. However, numerous concentrated resveratrol supplements and even food bars containing as much resveratrol as 50 glasses of wine are commercially available, making a comparable dose level of resveratrol perhaps feasible for human ingestion. Predicting significant effects of nutrients on cold tolerance based on the thermic effect of food (specific dynamic action of dietary component carbohydrate, fat, and protein) has not proved to be a reliable indicator of the ability of the body to resist cold exposure. Human cold tolerance thermogenic research, quite active in the World War II/Korean conflict, has received relatively

PART 8  FOOD AND WATER

In addition to inhibition of key enzyme responders in the body’s “braking system” of the stimulatory effect of norepinephrineactivated lipolysis, catechins also inhibit nuclear factor kappa B (NFκB), a transcription factor that normally regulates PPARs. Upregulation of key enzymes involved in fatty acid oxidation by PPARs increases energy expenditure along with enhanced stimulation of fatty acid release afforded by elevated cAMP. Finally, catechins have a direct effect on expression of several uncoupling proteins that also can influence thermogenesis via uncoupling or decreasing the efficiency of oxidative phosphorlyation.61,70 The role of green tea and coffee in enhancing energy expenditure (thermogenesis) is shown schematically in Figure 69-3. Other thermogenic “nutrients” may also have application in cold tolerance. Capsaicin is the major pungent compound found in certain pepper species and a common spice in many food products. It has been studied with mixed results for its thermogenic properties and influence on increasing fat oxidation.111 Capsaicin is believed to increase thermogenesis by enhancing catecholamine secretion from the adrenal medulla through activation of the central nervous system, resulting in β-adrenergic stimulation.53 It possibly upregulates certain uncoupling proteins in response to the catecholamine release.76 Polymorphisms in the receptor and promoter regions of genes of individuals may explain the variability in efficacy of capsaicin stimulation between individuals53 and some of the differences in capsaicin study results reported in the literature.46,50,111 Brown adipose tissue has been extensively studied in infants and animals under a variety of conditions. It helps maintain body temperature. It was formerly thought that this energy-rich and heat-generating tissue regresses with age.64,65 The recent discovery that humans contain more BAT than previously thought33,124 and that cold exposure activates BAT thermogenic activity in humans123 has stimulated BAT research in adult humans. In human cold exposure studies, BAT activity was inversely correlated with changes in distal skin temperature, suggesting a role for BAT in maintaining core body temperature.123 The unique uncoupling properties of BAT that make it such an efficient heatproducing organ may also be shared by other tissues, such as skeletal muscle. Wijers and colleagues127 have found that mitochondrial uncoupling in skeletal muscle during cold exposure may be one mechanism facilitating cold adaptive thermogenesis in humans. Dietary or pharmacologic approaches to stimulating BAT activity may be a promising way to turn on heat production during cold exposure. Future research on the metabolic and dietary control of adaptive thermogenesis may have particular relevance to diverse metabolic outcomes, such as obesity and weight loss research, as well as human cold tolerance. Fat, Carbohydrate, and Protein Content of the Diet May Be Tailored to Different Environments.  Although the most important nutritional concern in challenging environments, aside from water, is total energy intake, when wilderness activities shift from a sea-level, cold-weather environment to a moderateor high-altitude, cold-weather environment, the macronutrient balance in the diet should be reconsidered. Although fat is an efficient and well-tolerated energy source during relatively lowpower-output, cold-weather activities at sea level, it is not as well tolerated at high altitude.5 Substituting carbohydrate for fat and, to a certain degree, for protein can theoretically provide metabolic advantages to the individual’s critical oxygen economy when working at altitude.3 This is because carbohydrate is a more efficiently metabolized fuel at altitude than is fat, because it is already partially oxidized (i.e., it contains a higher ratio of oxygen atoms to carbon atoms) and therefore requires less oxygen to combust its carbon skeleton to CO2, H2O, and energy. Metabolizing carbohydrate for energy requires approximately 8% to 10% less inspired oxygen than is required to obtain a similar amount of calories from fat. A high-carbohydrate diet can reduce the symptoms of acute mountain sickness, enhance short-term highintensity work as well as long-term submaximal efforts, and lower the effective “felt” elevation by as much as 300 to 600 m (984 to 1969 feet) by requiring less oxygen for metabolism. Initial altitude exposure frequently results in anorexia and subsequently reduces energy and carbohydrate intake.25 Anorexia 1378

(and thus food intake) usually improves with time and acclimatization (3 to 7 days at altitude), but, depending on the altitude, may never match that at sea level. Weight loss and performance decrements are quite common under these conditions. Carbohydrate supplementation of the diet at elevations exceeding 2200 m (7218 feet), particularly with carbohydrate-containing beverages, is usually an effective method to increase carbohydrate and total energy intakes.3,25,37 Some,32 but not all,117 studies of carbohydrate supplementation at altitude have demonstrated a decrease in the adverse symptoms resulting from acute altitude exposure. Enhancement of short-term, high-intensity performance,26 as well as long-term, submaximal performance,3,14 by carbohydrate supplementation has also been noted in some studies involving altitude exposure. The beneficial effects of carbohydrate at altitude most likely depend on the type of exercise performed (intensity and duration) and the degree of prior muscle glycogen depletion experienced by the test subject, because of varying degrees of anorexia. Muscle glycogen is related to the caloric adequacy of an individual’s prior diet; carbohydrate intake usually parallels the overall dietary intake of the antecedent diet.3 It is a good plan to consume a mixed diet with snacks high in carbohydrate. The most effective form of carbohydrate supplementation in environmental extremes is usually liquid beverages; people will drink even when they are reluctant to eat.3,14,25,37 Increasing fluid intake along with carbohydrate intake is also beneficial at altitude, where increased fluid losses occur as the result of diuresis and of respiration in the dry (low-relative-humidity) atmosphere.9 The “Right” Macronutrient Mix for Work at Altitude.  There are two schools of thought regarding the most advantageous mixture of dietary macronutrients for work at altitude. Some believe that food preferences change markedly as elevation increases during the climb, and that carbohydrate becomes more palatable to the anorexic appetite. Others believe that once appetite recovers from the initial period of altitude acclimatization, the relative proportions of carbohydrate and fat in the diet are not as important as eating to energy demands to prevent loss of lean body mass. Early work published by Teasdale119 and later advocated by Pugh97 and Consolazio32 favored carbohydrate for work at altitude largely because of its structural oxygen content; carbohydrate is more highly oxidized than is fat or protein and therefore theoretically should require less atmospheric oxygen (which is, in effect, reduced at the reduced barometric pressure at altitude) for its metabolism to CO2 and ATP. This line of reasoning also agrees with what we know about the need for glycogen replenishment. Glycogen stores would be important energy providers for intense physical climbing work at altitude if one was working at a high percentage of V˙ O2max. However, as Teasdale119 aptly pointed out in his writings on “The Diet Problem for Mountaineers in the Himalayas,” the actual amount of work in foot-pounds done at altitude is usually self-limited and may be relatively low compared with that at sea level; the real problem is not the amount of energy that is expended but rather oxygen availability. Teasdale119 recommended that climbers should seek a diet “demanding as little oxygen as possible” and his recommendation for accomplishing this was the ingestion of carbohydrate at frequent intervals. He also was one of the first to point out the oft-encountered “vicious” cycle of human physical deterioration at altitude: loss of appetite– partial starvation–metabolism of climbers’ fat stores for energy– ketoacidosis–further anorexia and loss of appetite–loss of weight–deteriorated physical performance. This cycle of events, along with dehydration, is depicted schematically in Figure 69-1. Many of these situational/physiologic turning points leading to physical performance decrements can happen in other extreme environments, but the climber at high altitude seems to experience these adverse factors sooner and to a more significant degree than do workers in other environments. Washburn126 emphasizes that dietary carbohydrate becomes particularly more critical as altitude increases above 10,000 feet, and Consolazio32 identified carbohydrate as an important factor in lessening the initial severity of altitude illness. Although early observations by Pugh97 and subsequent research by other investigators seem to indicate that carbohydrate is better “tolerated” or preferred at

ENERGY: HOW CRITICAL IS IT? When planning for a prolonged wilderness outing, the following question should be asked: “If we run short on food, will we suffer severe consequences in our progress along our route and experience difficulty carrying our heavy packs?” For optimal performance, it is total energy intake, especially carbohydrate intake, that is the key for sustaining high-level work capacity for extended periods. However, performance across a broad spectrum of backcountry tasks, including load-bearing work, is not always severely degraded by short periods of suboptimal energy and carbohydrate intake. A review of the effect of energy restriction on military work performance indicated that soldiers can maintain relatively normal work capacities for short time periods (24 hours to fully rehydrate via water and electrolyte replacement.4,129,138 While daily strenuous activity in a hot environment can result in mild water balance deficits even with unlimited access to food and fluids,9,183 adherence to recognized water intake 1394

guidance9,30,165 minimizes water deficits, as determined by daily body mass stability.35 An adequate intake (AI) for daily total water is 3.7 L and 2.7 L for adult males and females, respectively.84 Of these prescribed volumes, 20% of the AI for water is found in food eaten during meals and snacks and the remaining 80% (approximately 3 L for males and 2.2 L for females) can come from beverages of all types. Daily water intake, however, varies greatly for individuals and between groups. For example, the daily water needs of sedentary men are approximately 1.2 L to 2.5 L1,137 and increase to approximately 3.2 L if performing modest physical activity.76,79 Compared with sedentary adults, active adults who live in a warm environment are reported to have daily water needs of approximately 6 L,201 and highly active populations have been reported to have markedly higher values.162 Data are limited regarding fluid needs for women, but typically they exhibit lower daily water turnover rates than do their male counterparts. In general, fluid requirements vary based on an individual’s body size, activity level, and the environment in which he or she works, lives, or performs activity.

HYDRATION ASSESSMENT Human hydration assessment is a key component for prevention and proper treatment of fluid and electrolyte imbalances.41,109,146 When fluids are limited, illness strikes, or there is exposure to extreme environments, cumulative fluid deficits can threaten homeostasis, health, and performance.109,165 Health is also threatened by fluid deficits, which can increase the risk of serious heat illness, and by fluid surfeits, which increase the risk of hyponatremia.28,123 In many clinical and most sports and wilderness medicine situations, hypertonic-hypovolemia occurs when there is net loss of hypotonic body fluids.41,109,165 However, substantial solute (electrolyte) can also be lost in situations where there is heavy work, and heat stress induces profuse sweating, during cold or high-altitude exposure, and in numerous illnesses and disorders (e.g., gastroenteritis, hyperemesis, diuretic treatment, dialysis) producing an isotonic or hypotonic-hypovolemia.41,109,165 An appreciation for the different types of body fluid losses that occur in response to illness, fluid restriction, or exposure to extreme environments is fundamental to proper hydration assessment41,109 (Table 70-1). Most circumstances involving strenuous work in austere environments require formation and vaporization of sweat as a principal means of heat removal. Thus, when sweat losses result in a body water deficit, there is a predictable rise in extracellular tonicity, which modulates renal function and urine composition in accordance with the body water deficit.156 The basic principles of body fluid regulation thus provide the framework for using blood (osmolality, sodium, fluid regulatory hormones) and urine (osmolality, specific gravity, color) as principal body fluid hydration assessment measures. Similarly, because humans maintain a relatively stable total body water pool despite diverse factors that affect water requirements (e.g., climate, activity, dietary solute load),84 acute changes in body mass may be used to accurately

Technique Complex Markers Total body water (dilution) Plasma osmolality Simple Markers Urine concentration

Advantages

Disadvantages

Accurate, reliable (gold standard) Accurate, reliable (gold standard)

Analytically complex, expensive, requires baseline Analytically complex, expensive, invasive

Easy, rapid, screening tool

Body mass Other Markers Blood: Plasma volume Plasma sodium Fluid balance hormones Bioimpedance Saliva Physical signs Tilt test (orthostatic challenge)

Easy, rapid, screening tool

Easily confounded, timing critical, frequency and color subjective Confounded by changes in body composition

No advantages over osmolality (except hyponatremia detection for plasma sodium)

Analytically complex, expensive, invasive, multiple confounders

Easy, rapid Easy, rapid Easy, rapid Rapid

Thirst

Positive symptomatology

Requires baseline, multiple confounders Highly variable, immature marker, multiple confounders Too generalized, subjective Highly variable, insensitive, requires tilt table or ability to stand Develops too late and is quenched too soon

measure dehydration across medical disciplines.14,35,195 Physical signs and symptoms (dizziness, headache, tachycardia, capillary refill time, sunken eyes, skin turgor) only manifest when fluid losses are severe and become debilitating.64,191 These findings are too nonspecific to be useful in athletic settings116 since they share symptoms indicative of other ailments (e.g., acute mountain sickness) and their use in assessment could lead to an incorrect diagnosis. All hydration assessment methods vary greatly in applicability because of limitations such as the necessary circumstances for reliable measurement, principles of operation, cost and complexity.84,146 Table 70-2 provides the advantages and disadvantages of numerous approaches and should be consulted when deciding on the choice of hydration marker. Definitive hydration assessment requires monitoring of changes in hydration state.38,117 Although change can provide good diagnostic accuracy, it requires a valid baseline, control over confounding variables, and serial measures.38,117 Large population heterogeneity explains, in part, why there are presently few hydration status markers that display potential for high nosologic sensitivity from a more practical, single measure.38,103 Although Table 70-3 provides euhydration thresholds for the most useful of hydration assessment measures, they too require considerable methodologic control,

TABLE 70-3  Biomarkers of Hydration Status

expense, and analytical expertise to be of practical use for dayto-day hydration monitoring of athletic sojourners. There is presently no scientific consensus for how to best assess hydration status in a field setting. However, in most field settings, the additive use of first morning body mass measurements in combination with some measure of first morning urine concentration and gross thirst perception provides a simple and inexpensive way to dichotomize euhydration from gross dehydration resulting from sweat loss and poor fluid intakes. This approach is represented using a Venn Diagram decision tool (Figure 70-1).41 It combines three of the simplest markers of hydration, including body mass (weight), urine, and thirst (WUT). No marker by itself provides enough evidence of dehydration, but the combination of any two simple self-assessment markers means dehydration is likely. The presence of all three makes dehydration very likely. The balance between science and simplicity in the choice of these measures for field hydration assessment is outlined below.

W

Measure

Practicality

Validity (Acute vs. Chronic Changes)

Euhydration Cut-Off

TBW Plasma osmolality Urine specific gravity Urine osmolality Urine color *Body weight

Low Medium

Acute and chronic Acute and chronic

1% dehydration). The measure of productivity was the amount of time to stack and debark 2.4 cubic meters of pulpwood. When subjects were dehydrated, productivity of stacking and debarking pulpwood was reduced by 12%.

DEHYDRATION AND COGNITIVE FUNCTION Cognitive/mental performance, which is important when concentration, skilled tasks, and tactical issues are involved, is degraded by dehydration and hyperthermia.80,158 The evidence is stronger for a negative effect of hyperthermia than for mild dehydration on degrading cognitive/mental performance,42 but the two are closely linked when performing exercise in warm/hot weather. The relative hyperthermia associated with dehydration could diminish psychological drive24 or perhaps alter central nervous system function independent of temperature. Adolph4 reported that dehydrated subjects fainted more quickly when faced with a change in body posture (orthostatic challenge test). Likewise, Carter and associates27 reported that subjects who were dehydrated by >2% of body mass from heat exposure exhibited significant reduction in cerebral blood flow velocity and possibly cerebral oxygen availability, when going from a seated to a standing posture. Intracranial volume is altered in response to dehydration,54 although the exact functional consequence of this is unknown. Dehydration has been shown to adversely influence decision making and cognitive performance, which may contribute to decline in work capacity and could possibly be associated with increased risk of accidents. Dehydration has been reported to impair visual motor tracking, short-term memory, attention, and arithmetic efficiency74 and to bring about greater tiredness, reduced alertness, and higher levels of perceived effort and concentration,192 with as little as 2% dehydration. The negative impact of dehydration on short-term memory and fatigue may persist for up to 2 hours following rehydration.42 It is possible that factors associated with dehydration such as greater tiredness, reduced alertness, difficulty in concentrating/ decision making, or orthostatic intolerance could contribute to accidents. Although there are no reported links, it is also possible that dehydration-mediated reductions in cognitive function and reaction time may be indirectly connected. In a classic study by Vernon,198 accident rates were shown to be at their lowest at temperatures of approximately 20° C (68° F) and increased by 30% in environments of approximately 24° C (75° F). It is in warm/hot environments that fluid turnover is highest and individuals most likely to become dehydrated. Changes in reaction time have been reported to accompany dehydration. Figure 70-7 depicts a 23% change in reaction time74

DEHYDRATION AND WORK PRODUCTIVITY As previously discussed, during physical work in the heat, sweat output often exceeds water intake, which leads to body water losses. Bishop and colleagues19 observed that in simulated industrial work conditions, encapsulated protective clothing produced sweating rates up to 2.25 L/hr. Likewise, wearing protective equipment such as full- or half-face masks can make fluid consumption more difficult and further contribute to dehydration in the workplace. Firefighters wear heavy protective clothing and are exposed to intense heat. Rossi160 reported that firefighters wearing protective clothing and equipment while performing simulated work tasks in the heat can have sweat rates up to 2.1 L/hr. It is also the case that workers often not only become dehydrated on the job but also may start the work day with a fluid deficit. Brake and co-workers21 observed fluid losses and hydration status of mine workers under thermal stress working extended shifts (12 hours). By measuring USG at the start of a work shift, they observed that 60% of the miners reported to work dehydrated and that their hydration status did not improve during the 10- to 12-hour shift. While many studies have observed the effect of dehydration on physical work capacity, few studies have observed dehydration’s impact on manual labor productivity. Wasterlund and Chaseling200 studied forest workers in a 15° C (59° F) environment 1400

25 Percent change in Rxn time

PART 8  FOOD AND WATER

environments, dehydration further degrades aerobic exercise performance and that with longer duration exercise (>60 minutes), greater degradations in performance can be expected. However, by maintaining a well-hydrated state, the contribution of dehy­ dration to the degradation in exercise performance can be alleviated. One explanation for the impact of dehydration on exercise performance is that during exercise in the heat, sweat output can often exceed water intake and lead to overall loss of body water and reductions in plasma and blood volume. The amount of body fluid lost through thermoregulatory sweating can vary widely, but commonly is in the range of 0.5 to 1.5 L/h. The upper limits for fluid replacement during exercise heat stress are set by the maximal gastric emptying rates, which have been reported to be 1.0 to 1.5 L/hr for the average adult,121,132 but are reduced by exercise heat stress and dehydration.33 Although gastric emptying may or may not be sufficient to maintain hydration (depending on sweating rate), people tend to drink only after thirst develops. As presented earlier in the chapter, the sensation of thirst appears at approximately 295 mmol/kg156 or approximately 2% of body mass loss. Thus, a significant amount of fluid loss occurs before the sensation of thirst drives fluid intake. During activity, if fluid intake occurs after being signaled by thirst sensation and is less than fluid loss through thermoregulatory sweating, the outcome is progressive dehydration. As a result of blood pooling in the skin and reduction in plasma volume secondary to sweating, cardiac filling is reduced and larger fractional utilization of oxygen is required at any given workload.11 Ultimately, these responses have a negative impact on exercise/work performance, especially in warm/hot environments. The negative impact of dehydration on work performance can increase risk in a field or wilderness setting. Dehydration, in combination with heat stress, reduces maximal oxygen uptake, increases relative effort, and reduces work output. When dehydrated, an individual will either not be able to trek as far or as fast compared to when euhydrated. For example, when on a hike, dehydration can increase the duration of time required to complete the hike beyond what is to be expected for a given distance and terrain, especially when in warm/hot environments. In the scenario of a day hike, or a hike to a destination, this increases the time to complete the hike and could result in a hiker being caught unprepared. If the expected plan for the day’s trek is to complete the hike during daylight hours, or to arrive at a destination that has supplies, adequate food and water, proper clothing, maps, then GPS, headlamps or a compass may not be brought. Without the supplies and equipment mentioned, hikers may run the risk of getting lost or injuring themselves in the dark (trip or fall), becoming more dehydrated without sufficient food and water, or becoming hypothermic as temperatures fall.

20 15 10 5 0 BAC .08 4% DEH

FIGURE 70-7  Percent change (slowing) in reaction (Rxn) time relative to percentage loss in body mass and blood alcohol content. (From Gopinathan PM, Pichan G, Sharma VM: Role of dehydration in heat stress-induced variations in mental performance, Arch Environ Health 43:15, 1988; and Moskowitz H, Burns MM, Williams AF: Skills performance at low blood alcohol levels, J Stud Alcohol 46:482, 1985.)

DEHYDRATION- AND REHYDRATIONRELATED ILLNESS

hyponatremia include seizures, coma, pulmonary edema, and cardiorespiratory arrest. Hyponatremia tends to be more common in long-duration activities and is precipitated by consumption of hypotonic fluid (water) alone. The interaction between drinking rate (water only) and plasma sodium concentration is illustrated in Figure 70-8 for a 70-kg individual, in 28° C (82° F) hiking at a moderate pace (6 km/hr), drinking at three different rates (200, 400, and 600 mL/ hr). Figure 70-8, A predicts the percentage change in body mass over time for the three drinking rates, whereas Figure 70-8, B predicts the expected plasma sodium concentration. The slowest drinking rate (200 mL/hr) over the duration of the hike (12 hours) predicts an elevated plasma sodium level well above that of asymptomatic hyponatremia (135 mEq/L). However, this drinking rate also results in a >4% level of dehydration, a level of fluid loss that would substantially degrade performance (see Figure 70-8, A yellow zone). Because the drinking rate is well in excess of sweating rate, the fastest drinking rate (600 mL/hr) actually results in a body mass gain and is predicted to result in asymptomatic hyponatremia within 5 to 6 hours of activity and symptomatic hyponatremia (sodium 350 mmol/kg produce neurologic symptoms in animals, such as seizures and coma; death in humans has been consistently observed in patients with Posm >370 mmol/kg.8 Postmortem analysis of human vitreous humor samples in cases of death from dehydration show marked sodium elevations (>170 mmol/L).108 By using the formula 2.1 × Na+ to estimate osmolality,82 a value of 357 mmol/kg is obtained. It therefore appears that a plasma osmolality value of 350 mmol/ kg can be considered as an approximate limit for human survival. The level of lethal dehydration (Posm >350 mmol/kg) and the time required to reach it can be estimated. If we assume that a 70-kg person possesses 42 L of body water and has a resting Posm of 285 mmol/kg, then the degree of pure water loss required to concentrate Posm to the lethal limit is (285/350) × 42 = 34.2 L, or 7.8 L water loss. However, because electrolytes are also lost in urine and sweat, a reasonable correction can be applied (7.8/0.94), which gives 8.3 L. This gives a level of dehydration of almost 12% body mass and 20% of total body water. Although higher estimates have been made (approximately 20% body mass), it is cautioned that as much as one-half of fasting weight losses derive from nonwater sources.23 Under fasting conditions, Brown and colleagues23 estimate that urine losses will stabilize at 0.5 L/day after the first day. The remaining losses from sweat depend on environmental temperature and body heat production. Under hospitable indoor conditions, obligatory urine23,84 and insensible sweat losses84,98 add up to about 1.2 L/day, which makes survival without water possible for almost 7 days. This is longer than the 100-hour rule of thumb (about 4 days),149 but highly dependent on environmental and behavioral factors. For example, in a worst-case desert scenario where there are 10 hours of daytime temperature exposure (>40° C [104° F]) and 14 hours of nighttime temperature exposure (90°

NL NL NL NL 50/10 min

0.5 0.5 0.75 0.75 1

NL 50/10 min 40/20 min 30/30 min 20/40 min

0.75 0.75 0.75 0.75 1

40/20 min 30/30 min 30/30 min 20/40 min 10/50

0.75 1 1 1 1

NL, No limit to work time per hour. Notes: Fluid Intake should not exceed 1.42 L (1.5 qt) per hour or 11.36 L (12 qt) per day. The work/rest times and fluid replacement volumes will sustain performance and hydration for at least 4 hours of work in the specified heat category. Individual water needs will vary ±0.24 L (0.25 qt) per hour. Rest defined as minimal physical activity (sitting or standing), accomplished in shade if possible. Wearing body armor: add 5° F to WBGT index. Wearing mission-oriented protective posture (MOPP, chemical protection) over-garment, add 10° F to WBGT index. *Weapon maintenance; walking hard surface at 4 km/hr (2.5 mph), ≤13.6-kg (30-lb) load; manual handling of arms; marksmanship training; drill and ceremony. † Walking on loose sand at 4 km/hr (2.5 mph), no load; walking on hard surface at 5.6 km/hr (3.5 mph), ≤18.14-kg (40-lb) load; calisthenics; patrolling; individual movement techniques (e.g., low crawl, high crawl); defensive position construction; field assaults. ‡ Walking on hard surface at 4 km/hr (3.5 mph), ≥18.14-kg (40-lb) load; walking on loose sand at 4 km/hr (2.5 mph) with load.

determining individual sweat rates would be impractical. These recommendations specify an upper limit for hourly and daily water intake, which safeguards against overdrinking and water intoxication. However, it is recommended that individuals performing endurance activities validate their sweat rates, because the guidelines do not account for individual variability.

ACSM FLUID REPLACEMENT RECOMMENDATIONS The most current knowledge regarding exercise with respect to fluid replacement is presented in the 2007 American College of Sports Medicine Position Statement on Exercise and Fluid Replacement.165 The position statement summarizes current knowledge regarding exercise with respect to fluid and electrolyte needs and the impact of their imbalances on exercise performance and health. The recent statement stresses the fact that individuals have varying sweat rates and as such, fluid needs for individuals performing similar tasks under identical conditions can be very different. Specifically the ACSM Position Statement provides recommendations in relation to hydration prior to, during, and following exercise/activity. Before Exercise.  The objective is to begin the physical activity euhydrated and with normal plasma electrolyte levels. If sufficient beverages are consumed with meals and a protracted recovery period (8 to 12 hours) has elapsed since the last exercise session, then the person should already be close to being euhydrated.84 However, if the person has suffered substantial fluid deficits and has not had adequate time or fluids/electrolytes in quantities sufficient to reestablish euhydration, then an aggressive pre-hydration program may be merited. When hydrating prior to exercise the individual should slowly drink beverage (for example, approximately 5 to 7 mL/kg body mass, 350 to 490 mL for a 70-kg individual) at least 4 hours before the exercise task. If the individual does not produce urine, or the urine is dark or highly concentrated, the individual should slowly drink more beverage (e.g., another approximately 3 to 5 mL/kg body mass, 210 to 350 mL for a 70-kg individual) about 2 hours before activity. By hydrating several hours prior to exercise, there is sufficient time for urine output to return toward normal before activity. Consuming beverages with sodium (20 to 50 mEq/L) and/or small amounts of salted snacks or sodium-containing foods at meals will help to stimulate thirst and retain the consumed fluids.113,153,183 Hyper-hydration can be achieved either by overdrinking or ingesting fluids (e.g., water) that expand the extra- and intracellular spaces. Simple overdrinking usually stimulates urine production,84 and body water rapidly returns to euhydration within

several hours.61,142,183 This means of hyperhydrating greatly increases the risk of having to void during activity/exercise61,142 and provides no clear physiologic or performance advantage over euhydration.91,99,100 In addition, hyperhydration can substantially dilute and lower plasma sodium61,142 before starting exercise and therefore increase the risk of dilutional hyponatremia if fluids are aggressively replaced during exercise.123 Enhancing palatability of ingested fluids is one way to help promote fluid consumption, before, during, or after exercise. Fluid palatability is influenced by several factors, including temperature (preferred between 15° and 20° C [59° and 68° F]), sodium content, and flavoring. During Exercise.  The objective is to drink enough fluid to prevent excessive dehydration (>2% body mass loss from water deficit) during exercise by replacing sweat losses to help sustain performance. The amount and rate of fluid replacement depend on the individual sweating rate, exercise duration, and opportunities to drink. Individuals should periodically drink (as opportunities allow) during activity; if it is expected, they will become excessively dehydrated from not drinking. Care should be taken in determining fluid replacement rates, particularly in prolonged exercise lasting greater than 3 hours. The longer the exercise duration, the greater the cumulative effects of slight mismatches between fluid needs and replacement, which can exacerbate dehydration or dilutional hyponatremia.123 It is recommended that individuals should monitor body mass changes during training/activity to estimate their sweat loss during a particular exercise task with respect to the weather conditions. This allows customized fluid replacement programs to be developed for each person’s particular needs; however, this may not always be practical. The Institute of Medicine also provides general guidance for composition of “sports beverages” for persons performing prolonged physical activity in hot weather.83 They recommended that fluid replacement beverages should contain approximately 20 to 30 mEq/L sodium (chloride as the anion), approximately 2 to 5 mEq/L potassium, and approximately 5% to 10% carbohydrate.83 The need for these different components (carbohydrate and electrolytes) depends on the specific exercise task (e.g., intensity and duration) and weather conditions. The sodium and potassium are used to help replace sweat electrolyte losses, while sodium also helps to stimulate thirst, and carbohydrate provides energy. These components also can be consumed using non-fluid sources such as gels, energy bars and other foods. Carbohydrate consumption can be beneficial to sustaining exercise intensity during high-intensity exercise events of approximately 1 hour or longer, as well as less intense exercise/activity sustained for longer periods.18,49,50,88,202 Carbohydrate-based sports 1403

CHAPTER 70  DEHYDRATION, REHYDRATION, AND HYPERHYDRATION

TABLE 70-5  Fluid Replacement Guidelines for Warm-Weather Training (Applies to Average Heat Acclimated

PART 8  FOOD AND WATER

beverages are sometimes used to meet carbohydrate needs, while attempting to replace sweat water and electrolyte losses. Carbohydrate consumption at a rate of 1 g/min has been demonstrated to maintain blood glucose levels and exercise performance.49,50 Most typical sport beverages contain carbohydrate sufficient to achieve this goal if drinking a liter per hour or less. It should be noted that this rate of carbohydrate consumption was observed in highly fit, elite athletes. Most individuals would not work or perform exercise at a high enough intensity or for long enough duration to utilize 1g/min. The greatest rates of carbohydrate delivery are achieved with a mixture of simple sugars (e.g., glucose, sucrose, fructose, maltodextrin). If fluid replacement and carbohydrate delivery are going to be met with a single beverage, the carbohydrate concentration should not exceed 8%, or even be slightly less, as highly concentrated carbohydrate beverages reduce gastric emptying.87,199 Finally, caffeine consumption might help to sustain exercise performance48 and likely will not alter hydration status during exercise.50,203 After Exercise.  If recovery time and opportunities permit, consumption of normal meals and snacks with a sufficient volume of plain water will restore euhydration, provided the food contains sufficient sodium to replace sweat losses.84 If dehydration is substantial (>2% body mass) with a relatively short recovery period (