Medicine For Mountaineering and Other Wilderness Activities (6th Edition) (2010) (James A. Wilkerson)

MEDICINE
FOR MOUNTAINEERING
& Other Wilderness Activities
SIXTH EDITION
MEDICINE
FOR MOUNTAINEERING
& Other Wilderness Activities
Edited by James A.Wilkerson, M.D.

Ernest E. Moore, M.D.
Ken Zafren, M.D.
THE MOUNTAINEERS
BOOKS
is the nonprofit publishing arm
of The Mountaineers Club, an
organization founded in 1906
and dedicated to the
exploration, preservation, and
enjoyment of outdoor and
wilderness areas.
1001 SW Klickitat Way, Suite 201,

Seattle, WA 98134
© 1967, 1975, 1985, 1992, 2001, 2010

by James A. Wilkerson, M.D.
All rights reserved
First edition 1967. Second edition

1975. Third edition 1985. Fourth
edition 1992. Fifth edition 2001. Sixth
edition 2010.
No part of this book may be

reproduced in any form, or by any
electronic, mechanical, or other means,
without permission in writing from the
publisher.
Distributed in the United Kingdom by

Cordee, www.cordee.co.uk
Manufactured in the United States of

America
Copy Editor: Heath Lynn Silberfeld /

enough said
Cover Design: Peggy Egerdahl
Layout: Marge Mueller, Gray Mouse
Graphics
Illustrators: Marjorie Domenowske,
Dana Peick, Marge Mueller, Jill Rhead
Front cover photograph: Panoramic

view of the Karwendel Range by full
moon. ©Josef Beck/age fotostock
Library of Congress Cataloging-in-

Publication Data
Medicine for mountaineering & other

wilderness activities / edited by James
A. Wilkerson, Ernest E. Moore, Ken
Zafren. -- 6th ed.
p. ; cm.
Includes bibliographical references and
index.
ISBN 978-1-59485-076-9 (ppb : alk.
paper)
ISBN 978-1-59485-393-7 (e-book)
1. Mountaineering injuries. 2. Outdoor
medical emergencies. 3. First aid in
illness and injury. I. Wilkerson, James
A., 1934-II. Moore, Ernest Eugene.
III. Zafren, Ken. IV. Title: Medicine for
mountaineering and other wilderness
activities.
[DNLM: 1. Mountaineering. 2.
Wilderness Medicine. 3. First Aid. 4.
Sports Medicine. WB 107 M489
2009]
RC1220.M6M4 2009
617.1’027--dc22
2009038107
Printed on recycled paper

CONTENTS
Contributors
Foreword
Preface
Introduction
SECTION I: GENERAL PRINCIPLES

Chapter 1: Diagnosis
Medical History
Physical
Examination
Examining Trauma
Victims
Medical Record
Chapter 2: Basic Medical
Care
Nursing Care
Fluid Balance
Care for Trauma
Victims
Fever and Chills
Chapter 3: Life-Threatening
Problems
Safety and
Leadership
The ABC’s: Airway,
Breathing, and
Circulation
Food Aspiration
Shock
Chapter 4: Psychological
Responses to Wilderness
Accidents
Psychological
Responses of
Rescuers
Posttraumatic Stress
Disorder
Psychological
Responses of
Accident Victims
Selection of
Rescuers
Chapter 5: Immunizations
Sources of Up-to-
Date Information
Scheduling
Immunizations
Traveling with
Children
Specific Vaccines
Chapter 6: Sanitation,
Arthropod Avoidance, and
Water Disinfection
Sanitation
Arthropod
Avoidance
Water Disinfection
Desirable
Characteristics of
Water Disinfection
Systems
Goals of Water
Disinfection
Techniques for
Wilderness Water
Disinfection
Chapter 7: Rescue and
Evacuation
Decisions That
Prevent Problems
Carrying an Ill or
Injured Person
Rescues by Airplane
and Helicopter
Improvised
Transportation
Other Improvised
Techniques
SECTION II: TRAUMATIC

DISORDERS
Chapter 8: Head and Neck
Injuries
Brain Injuries
Facial Injuries
Dental Injuries
Ear Injuries
Neck Injuries
Vertebral Fractures
Chapter 9: Chest Injuries
The Mechanics of
Respiration
Closed Chest
Injuries
Penetrating Chest
Injuries
Chapter 10: Abdominal
Injuries
Assessment
Treatment
Nonpenetrating
Injuries
Penetrating
Abdominal Injuries
Chapter 11: Fractures and
Related Injuries
Diagnosis
Treatment
Specific Fractures
of the Upper
Extremity
Specific Fractures
of the Lower
Extremity
Specific Fractures
of the Trunk
Dislocations
Other Injuries of
Bone and Related
Structures
Back Injuries
Snowboarding
Injuries
Chapter 12: Soft-Tissue
Injuries
Controlling
Bleeding
Controlling Infection
Bandaging
Specific Injuries
Chapter 13: Burns
Evaluating Burn
Severity
Burn Shock
Evacuation
Treating the Burn
Fluid Replacement
Control of Pain
Facial Burns
Oxygen
Additional
Measures
SECTION III: NONTRAUMATIC

DISORDERS
Chapter 14: Neural
Disorders
Signs and Symptoms
Common Nervous
System Disorders
Chapter 15: Eye Disorders
Red Eyes
Ocular Surface
Disorders
Trauma
Retina and Optic
Nerve Disorders
Refractive
Correction
Chapter 16: Ear, Nose,
Throat, and Dental
Disorders
Disorders of the
Nose
Sore Throat
(Pharyngitis)
Disorders of the
Mouth
Dental Emergencies
Ear Infections
Chapter 17: Heart and
Blood Vessel Disorders
Physical
Examination of the
Cardiovascular
System
Heart Disease in the
Wilderness
Major Heart
Diseases
Disorders of
Cardiac Rhythm
Minor Disturbances
of Cardiac Rhythm
Devices for Heart
Rhythm Management
High Blood Pressure
(Hypertension)
Vascular Disease
Heart Health and
Physical Activity in
the Wilderness
Chapter 18: Respiratory
Disorders
Symptoms
Physical
Examination
Chronic Lung
Disease
Disorders of
Breathing Rhythm
Infectious Disorders
Other Pulmonary
Disorders
Venous Thrombosis
and Pulmonary
Embolism
Chapter 19: Gastrointestinal
Disorders
Nausea and Vomiting
Diarrhea
Specific Causes of
Diarrhea
Severe Diarrheas
Constipation and
Rectal Problems
Peptic Ulcer and
Related Problems
Diseases of the
Liver
Chapter 20: Acute
Abdominal Pain
Diagnosis
Conditions That Do
Not Require
Evacuation
Conditions That
May Require
Evacuation
Conditions
Requiring
Evacuation
Nasogastric
Intubation
Chapter 21: Genitourinary
Disorders
Acute Urinary Tract
Disorders
Urethral
Catheterization
Other Urinary Tract
Disorders
Female Genital
Problems
Male Genital
Problems
Sexually
Transmitted
Infections
Chapter 22: Infections
Antibiotics
Bacterial Infections
Viral Infections
Parasitic Disorders
Acquired
Immunodeficiency
Syndrome (AIDS)
Chapter 23: Allergies
Hay Fever
Hives
Contact Dermatitis
Poison Ivy, Poison
Oak, and Poison
Sumac
Anaphylactic Shock
SECTION IV: ENVIRONMENTAL

INJURIES
Chapter 24: Disorders
Caused by Altitude
Mountain Altitudes
Responses to
Increasing Altitude
Altitude Illness
Other High-Altitude
Conditions
Preexisting Medical
Problems and
Altitude
Chapter 25: Altitude and
Common Medical
Conditions
Altitude Stress
The Effect of
Altitude on
Respiratory
Disorders
The Effect of
Altitude on
Cardiovascular
Problems
The Effect of
Altitude on
Pulmonary Vascular
Disorders
The Effect of
Altitude on
Hematologic
Problems
The Effect of
Altitude on
Neurologic
Conditions
Stroke, TIA,
Cerebrovascular
Disorders, and
Altitude
The Effect of
Altitude on Diabetes
Mellitus
The Effect of
Altitude on
Pregnancy
Children at Altitude
Alcohol at Altitude
Future Directions
Chapter 26: Cold Injuries
Mechanisms of Heat
Exchange
Physiologic
Limitation of Heat
Loss
Preventing
Hypothermia
Recognizing
Hypothermia
Treating Mild
Hypothermia
Treating Moderate
and Severe
Hypothermia
Cold Water
Immersion
Frostbite
Trenchfoot
Chapter 27: Heat and Solar
Injuries
Heat Illness
Injury by Solar
Radiation
Chapter 28: Drowning
Definitions Related
to Drowning
Epidemiology of
Drowning
Mechanisms of
Drowning
Pathophysiology of
Drowning
Cold Water
Drowning
Presentation of
Survivors
Management of
Survivors
Preventing
Drowning
Effects on Families
Chapter 29: Lightning
Injuries
Lightning Fatalities
Physics of Lightning
Areas with Greatest
Lightning Risk
Mechanisms of
Lightning Injury
Effects of Lightning
Strikes
Care for Individuals
Struck by Lightning
Preventing Lightning
Injuries
Chapter 30: Avalanche
Injuries
Avalanche Mortality
Avalanche Survival
Probability
Avalanche Trauma
Prevention of
Avalanche Asphyxia
Prevention of
Avalanche Burial
Treatment of
Individuals Buried
by Avalanches
Hypothermia
Chapter 31: Large Animal
Attacks
Large Animal
Attacks: North
America
Large Animal
Attacks: Africa,
Asia, and Elsewhere
Care for Individuals
Attacked by Animals
Chapter 32: Rabies
Rabies Within the
United States
Transmission of
Rabies
Treating the Bite of
a Rabid Animal
Bat Exposures
Rabies in
Developing
Countries
Preexposure Rabies
Vaccination
Reliability of
Rabies Postexposure
Therapy
Chapter 33: Envenomations
Venomous
Snakebites
Spider, Scorpion,
Ant, and Other Bites
and Stings
APPENDIXES
Appendix A: Medications
Medications for the
Relief of Pain
Medications for
Sleep or Sedation
Antipsychotic
Agents
Antimicrobial
Agents
Antifungal Agents
Antimalarial Agents
Antiseptics
Medications
Affecting the Heart,
Blood Vessels, and
Respiratory System
Decongestants
Antihistamines
Medications for
Gastrointestinal
Disorders
Appendix B: Therapeutic
Procedures
Administering
Medications
Instrument
Sterilization
Appendix C: Medical
Supplies
Personal Medical
Supplies
Outing Medical Kit
Expedition Medical
Kit
Appendix D: Legal and
Ethical Considerations
Legal
Considerations
Ethical and Legal
Responsibility
Appendix E: Glossary
Index
CONTRIBUTORS
C. KIRK AVENT, M.D., Professor
of Medicine (retired),
Infectious Disease Division,
The School of Medicine, The
University of Alabama in
Birmingham; Birmingham,
Alabama
BEN EISEMAN, M.D., Emeritus
Professor of Surgery,
University of Colorado School
of Medicine and Veterans
Administration Hospital,
Denver, Colorado
BLAIR D. ERB, SR., M.D., Internal
Medicine and Cardiology; Past
President Wilderness Medical
Society, Townsend, Tennessee
BLAIR D. ERB, JR., M.D., FACC,
President, Montana Chapter of
the American College of
Cardiology; Cardiology
Consultants of Bozeman, PC,
Bozeman, Montana
MICHAEL A. FLIERL, M.D.,
Orthopedist, Department of
Orthopaedic Surgery, Denver
Health Medical Center,
University of Colorado
Denver School of Medicine,
Denver, Colorado
GORDON G. GIESBRECHT,
PH.D., Professor of
Thermophysiology, University
of Manitoba; former board
member, Wilderness Medical
Society; Winnipeg, MB,
Canada
ANDREA R. GRAVATT, M.D.,
FAAP, FAWM, Pediatric
Emergency Physician, Mary
Bridge Children’s Hospital,
Tacoma, WA; Clinical
Assistant Professor,
Department of Pediatric
Medicine, University of
Washington School of
Medicine, Seattle, Washington
COLIN K. GRISSOM, M.D.,
Critical Care Medicine,
Intermountain Medical Center,
Murray, Utah; Associate
Professor, University of Utah
Health Sciences Center;
President, Wilderness Medical
Society; Park City, Utah
PETER H. HACKETT, M.D.,
Clinical Professor of
Emergency Medicine, and
Clinical Director, Altitude
Research Center, University of
Colorado Denver School of
Medicine; Director, Institute
for Altitude Medicine,
Telluride, Colorado
CHRISTOPH E. HEYDE, M.D.,
Orthopaedic Surgery,
University of Leipzig, Leipzig,
Germany
CHARLES S. HOUSTON, M.D.,
Internist and Cardiologist,
Burlington, Vermont; formerly
Professor of Medicine, The
University of Vermont College
of Medicine, Burlington,
Vermont
ERIC L. JOHNSON, M.D.,
Emergency Physician,
Director, Emergency Services,
Teton Valley Hospital;
Associate Clinical Faculty,
University of Washington
School of Medicine; Past
Society; Driggs, Idaho
ERNEST E. MOORE, M.D.,
Director, Rocky Mountain
Regional Trauma Center,
Denver Health Medical
Center; Vice Chairman,
Department of Surgery,
Denver, Colorado
HUNTER B. MOORE, BA, MS IV,
Denver, Colorado
BRUCE B. PATON, M.D., Emeritus
Professor of Clinical Surgery,
University of Colorado Health
Sciences Center; Past
Society; Denver, Colorado
MARTIN I. RADWIN, M.D.,
Gastroenterologist;
Professional Member,
American Avalanche
Association; Medical
Committee, Mountain Rescue
Association; Chief of
Gastrointestinal Endoscopy,
Pioneer Valley Hospital, Salt
Lake City, Utah
LAWRENCE C. SALVESEN, M.D.,
Psychiatrist; former Staff
Psychiatrist, Outpatient Stress
Unit, Veterans Administration
Hospital, Togus, Maine;
Mental Health Member,
Southern Maine and Tri-
County Stress Debriefing
Teams, Pownal, Maine
JOSEPH B. SERRA, M.D.,
Orthopedist, Assistant Clinical
Professor of Orthopedics,
University of California Davis
School of Medicine, Stockton,
California
PHILIP F. STAHEL, M.D.,
Orthopaedic Surgery, Denver
Health Medical Center,
University of Colorado School
of Medicine, Denver,
Colorado
GEOFFREY C. TABIN, M.D.,
Professor of Ophthalmology
and Visual Sciences; Director,
Division of International
Ophthalmology, John A.
Moran Eye Center, University
of Utah Health Sciences
Center; Co-Director
Himalayan Cataract Project,
Park City, Utah
BUCK TILTON, MS, WEMT;
author or coauthor of twenty-
six books, more than 1000
magazine articles, and a
column for Backpacker;
cofounder of the National
Outdoor Leadership School
(NOLS) Wilderness Medicine
Institute, Lander, Wyoming
URS WIGET, M.D., Expedition
Physician; Medical Director,
Reavita AG; past president,
Commission for Mountain
Emergency Medicine (ICAR
MedCom), Zürich,
Switzerland
FORREST C. WILKERSON,
Attorney-at-Law; Rock Hill,
South Carolina
JAMES A. WILKERSON, M.D.,
Pathologist (retired); former
Associate Professor of
Pathology, The School of
Medicine, The University of
Alabama in Birmingham; Park
City, Utah
GILBERT C. WONG, M.D.,
Resident, Ophthalmology, John
A. Moran Eye Center,
University of Utah Health
Sciences Center, Salt Lake
City, Utah
KEN ZAFREN, M.D., Emergency
Physician, Alaska Native
Medical Center; Clinical
Assistant Professor, Division
of Emergency Medicine,
Stanford University Medical
Center; Medical Director of
the Alaska Mountain Rescue
Group, Anchorage, Alaska
FOREWORD
Buck Tilton, M.S., WEMT
At a convention in Salt Lake City,

Utah, James A. Wilkerson, M.D.,
introduced himself and asked if I
would be willing to write this
foreword. I believe I responded
with “Are you kidding?” but it
could have been something equally
inappropriate. I was flabbergasted.
No one can appreciate what that
moment meant to me, but here is my
attempt at an explanation.
Back in 1967, in the middle of
uncertainty and greatly expanding
protests against the war in Vietnam,
I registered for my sophomore year
of college and purchased, hot off
the press, the first edition of
Medicine for Mountaineering
because I wanted to know all there
was to know about climbing
mountains and being an outdoor
leader. (“Outdoor leadership,” by
the way, wasn’t a career field in
1967; it was something you did
until you found a real job.) I
devoured the book in the manner of
a reader who can’t put down a great
novel.
Jim Wilkerson and his fellow
contributors had filled a huge void.
The incomparable
Mountaineering: The Freedom of
the Hills (The Mountaineers
Books) was already available in its
second edition, but first aid was,
let’s say, thinly dealt with. No
firstaid courses, in fact, existed to
prepare the climber adequately for
medical emergencies. Now the
mountaineer had at hand, if he or
she was willing to pack the weight,
a compendium of information on
caring for the injured and sick far
from definitive medical attention.
And those who chose to leave the
book behind had something truly
relevant to study at home. We who
went way out there were mightily
blessed, and even more so those
that got clobbered.
Almost as an aside, Jim
Wilkerson wrote, way back when,
that Medicine for Mountaineering
was a “handbook of medicine—not
first aid” and gave birth, in my
opinion, to the field of wilderness
medicine, the field that did become
my career. Medicine for
Mountaineering, in other words,
was the catalyst that generated what
has been my life’s work.
But the role of Medicine for
Mountaineering was far from over.
The material was updated and
expanded with the second edition in
1975, and then again with the third
in 1985. Despite the title, the value
of Medicine for Mountaineering
had been known, and the book used,
for years by people who left
hospitals far behind but whose
outdoor activities were
nonclimbing. Medicine for
Mountaineering was the source,
and it was pulled from the packs of
backpackers, the dry bags of
canoeists, and the saddlebags of
horse packers. Wide appeal was
recognized with a change on the
cover of the fourth edition in 1992
to Medicine for Mountaineering &
Other Wilderness Activities, a title
that continued with the fifth edition
in 2001.
For those who haven’t done the
math yet, this sixth edition takes Jim
Wilkerson’s pioneering and pivotal
effort well into its fifth decade. But
all the preceding is merely history.
With the proliferation of books
on wilderness medicine, why has
endured? Within these pages you
will continue to learn—or be
introduced to—the most up-to-date
and very best response, both acute
and long term, for those in need of
medical assistance. You will read
the information in a style that is not
only engaging but also clear and
concise. There is no beating around
the medical bush, a favored
response of physicians when you try
to pin one down for specific advice
with a question such as “Hey, what
should I do if … ?” Probably more
important than anything else,
Medicine for Mountaineering tells
you how to avoid problems,
whenever that sort of advice
applies.
Yes, there are other great
wilderness medicine books out
there, but Medicine for
Mountaineering was and remains
the “gold standard” by which newer
publications are judged. So, thank
you very much, Dr. Wilkerson, on
behalf of the many thousands you
have helped and will help,
including me.
PREFACE
The sixth edition has provided an
opportunity to make major changes
in Medicine for Mountaineering.
One of the biggest changes has been
the addition of two new editors.
Ernest E. Moore is a trauma
surgeon, Director of the Rocky
Mountain Regional Trauma Center
at the Denver Health Medical
Center, and Medical Advisor for
the Steamboat Springs Ski Patrol.
Ken Zafren is an emergency
physician in Anchorage, Alaska,
with many years of experience in
mountaineering and mountain
rescue; he is Medical Director of
the Alaska Mountain Rescue Group,
represents the United States on the
International Commission for
Mountain Emergency Medicine, and
is Associate Medical Director for
the Himalayan Rescue Association
of Nepal.
Their knowledge of clinical
medicine, their experience from
participating in a variety of
challenging wilderness activities,
including wilderness rescues, and a
considerable amount of dedicated
effort have greatly enriched the
information that is presented.
The book has been expanded
from twenty-five to thirty-three
chapters. A new chapter, “Rescue
and Evacuation,” has been
contributed by Ken Zafren and Urs
Wiget. Geoff Tabin, who has
recovered the eyesight of untold
thousands with clinics for cataract
surgery he has established in Nepal,
Pakistan, and Africa—and was the
fourth person to climb the seven
summits—has contributed a chapter
on eye disorders. A new chapter on
drowning has been added with the
help of Gordon Giesbrecht and
Andrea Gravatt. Eric Johnson has
contributed a new chapter on
lightning injuries. Colin Grissom
and Marty Radwin, developers of
the AvaLung®, have written a new
chapter on avalanche injuries. So
much new material was added to
the chapter on bites and stings that it
was expanded into three chapters:
Large Animal Attacks, Rabies, and
Envenomations. Buck Tilton has
written a very flattering Foreword.
Blair Erb, Jr., a cardiologist
from Montana, has joined with his
father, Blair Erb, Sr., to update the
chapter on diseases of the heart and
blood vessels. Philip Stahel,
Michael A. Flierl, and Christoph
Heyde from the Departments of
Orthopedic Surgery at Denver
Health Medical Center and the
University of Leipzig have worked
together to rewrite the material on
brain and vertebral injuries in the
chapter on head and neck injuries.
Hunter Moore, a medical student at
the University of Colorado School
of Medicine, has joined with his
father, Ernest E. Moore, and Ben
Eiseman on the chapter on
abdominal injuries.
Unfortunately, Charlie Houston,
one of America’s premier
mountaineers and early
investigators of high-altitude
disorders, who enthusiastically
supported this publication since its
development first began and made
major contributions to the
discussion of altitude disorders,
was forced by health problems to
drop out. His many friends were
deeply saddened by the news of his
demise just as this volume was
going to press. Fred Darvill has
succumbed to health problems after
having written and updated the
chapter on gastrointestinal
disorders for the first five editions.
In early editions, contributors’
names were not listed with their
chapters because all chapters were
edited, some extensively, to
conform to a uniform format, which
is considered essential for a text of
this type. In this edition, as in the
fifth edition, contributors’ names
are listed with the chapters as
Principal Contributors, not as
authors, because the text is still
edited for uniformity.
Since the first edition of
appeared, interest in wilderness
medicine has grown exponentially.
The Wilderness Medical Society
has been founded and continues to
grow. It annually provides a number
of leadingedge educational
programs for physicians, other
medical professionals, and others
interested in wilderness activities.
It supports the publication of
Wilderness and Environmental
Medicine, a peer-reviewed journal
that is included in the Index
Medicus, and the magazine
Wilderness Medicine. Individuals
wanting to learn more about
wilderness medicine and to keep
abreast of new developments are
urged to join that society. Its
website is www.wms.org.
Alternatively, inquiries can be
addressed to Wilderness Medical
Society, 2150 South 1300 East,
Suite 500, Salt Lake City, UT
84106; phone 801-990-2988.
Jim Wilkerson
Park City, Utah
INTRODUCTION
Anyone who partakes in the range
of wilderness activities that demand
skill, knowledge, strength, and
stamina—mountaineering, hiking
and backpacking, skiing and
snowboarding, cross-country
skiing, white-water kayaking and
rafting, scuba diving, and others—
must expect sooner or later to be
involved in misfortune, if not his
own, then someone else’s. The
outcome of such misfortune often
depends on the medical care the
individuals receive. For accidents
or illnesses that occur at a
considerable distance from a
physician or hospital, ordinary first
aid often does not suffice. If the
individuals are to recover with
minimal permanent disability, the
admonition “Don’t do any harm
until the doctor comes!” is not
adequate because in many
wilderness situations the doctor is
not coming.
In addition to injuries resulting
from falls or similar accidents,
members of wilderness outings
must cope with the problems
presented by high terrestrial
altitudes and extremes of heat and
cold. They must be prepared to
provide immediate, appropriate
treatment for anaphylactic reactions
to insect stings, or to institute
cardiopulmonary resuscitation for
individuals who have drowned or
been struck by lightning. They must
avoid the infectious and parasitic
disorders that are a threat in the
wilderness and often a greater
threat in developing countries. And
they must be prepared to deal with
a variety of medical problems
usually cared for by physicians.
Infectious diseases such as hepatitis
and poliomyelitis, noninfectious
disorders such as thrombophlebitis
and strokes, and surgical problems
such as appendicitis have all
occurred on wilderness outings.
The ability to rationally analyze
a problem or situation and select
and pursue a direct, logical course
to a solution is a rare talent known
as “common sense.” No ability is
more important in caring for
individuals with medical disorders
in wilderness situations. However,
the body’s functions and the
intricacies of its varied disorders
are highly complex, and only those
knowledgeable about the principles
of diagnosis and therapy can
provide optimal medical care for
injured or ill individuals,
particularly in remote situations.
has been compiled by physicians
who actively pursue a variety of
wilderness interests, and it is
intended to be a source for the
information needed to care for
medical problems that may be
encountered in such circumstances.
It is a handbook of medicine—not
first aid. The treatments described
for some conditions include potent
medications or sophisticated
therapeutic procedures. Such
remedies are necessary to care for
many disorders but could lead to
disaster if used incorrectly. In the
forty years since the publication of
the first edition, wilderness
enthusiasts who are not medical
professionals have demonstrated an
ability to assimilate such
information and use it
appropriately.
To reduce potential
complications from the use of
medications, dosages for most
drugs, which were provided in
previous editions, have been
eliminated. Most of those
medications can only be obtained
by prescription from a physician
who should make certain the person
obtaining the drugs knows their
proper use, including the dosage
and frequency of administration.
Descriptions of the drugs and
warnings about precautions that
must be observed whenever a drug
is administered are provided only
in Appendix A (not in the text) to
avoid undue repetition.
Because no alternate methods for
treating some disorders are
available, a few procedures are
included that would be impractical
or impossible in many wilderness
circumstances. Intravenous fluid
therapy is an example. A small
wilderness party would almost
never carry intravenous fluids and
the equipment for administering
them. Even a large expedition might
have difficulty keeping such
materials in locations where they
could be obtained quickly.
However, intravenous fluids are the
only means for keeping alive
individuals with some disorders,
and instructions for their use are
included. (In recent years large
expeditions have left behind a
considerable quantity of medical
supplies, and on some popular
routes a significant supply of items
such as intravenous fluids is
available.)
The members of wilderness
outings should know how to
provide basic medical care; should
have the ability and the equipment
to communicate by cellular
telephone, radio, or satellite
telephone and obtain guidance; and
should be prepared to administer
any treatment that may be needed.
The knowledge and medical
equipment required depend upon
the location and duration of the
outing. Traumatic disorders—the
injuries produced by physical
forces such as falls or falling
objects—are most common in
wilderness situations, particularly
on outings of only a few days. Signs
and symptoms of nontraumatic
disorders, such as infections or
diseases of the heart or lungs,
usually develop gradually over a
period of several days and often do
not become apparent during short
trips. On longer trips, the slower
onset may permit individuals to be
evacuated under their own power
before becoming incapacitated. In
addition, wilderness enthusiasts
tend to be young and healthy and are
less susceptible to nontraumatic
disorders.
Members of any wilderness
outing, regardless of its location or
duration, should be capable of the
following:
Caring for soft-tissue injuries,
including anticipating and
treating hemorrhagic shock
Anticipating and treating
anaphylactic shock, particularly
after insect stings
Recognizing and caring for
fractures
Diagnosing and treating head
injuries, including maintaining
an airway while evacuating an
unconscious individual
Diagnosing and treating thoracic
and abdominal injuries
Recognizing a need for, and
performing, cardiopulmonary
resuscitation
Threatening environments may
call for the following capabilities:
Recognizing and treating heat or
cold injuries
Recognizing and treating altitude
disorders
Members of extended
expeditions should, in addition,
develop these skills:
The ability to take a simple
medical history and perform a
physical examination
Familiarity with the techniques
of patient care, particularly
administration of medications
Knowledge of the medical
disorders, particularly
infectious disorders, likely to be
encountered on that specific
expedition
All participants in wilderness
activities should undergo regular
examinations by a physician
knowledgeable about and
sympathetic with their interests.
Wilderness organizations probably
should require such examinations
before anyone participates in an
outing. (Medical disorders that a
physician would recognize during
an examination and treat are too
complex for inclusion in a manual
such as this.) For prolonged
expeditions into isolated areas, a
prior medical examination is
essential. Individuals with a peptic
ulcer, gallstones, hernia, pregnancy
(particularly in the first and third
trimesters), a history of intestinal
obstruction following an abdominal
operation, or chronic malaria with a
large spleen must be aware of the
risk in prolonged isolation where
surgical help is not available.
Additional information can be
found at the Centers for Disease
Control and Prevention (CDC)
website, Travelers’ Health,
www.cdc.gov/travel/default.aspx,
and at the World Health
Organization website, International
Travel and Health,
www.who.int/ith/en/index.html.
SECTION I
GENERAL
PRINCIPLES
CHAPTER 1
DIAGNOSIS
James A. Wilkerson, M.D.
Principal Contributor
“Disease manifests itself by

abnormal sensations and events
(symptoms), and by changes in
structure or function (signs).
Symptoms, being subjective, must
be described by the patient. Signs
are objective and these the
physician discovers by means of
physical examination, laboratory
studies, and special methods of
investigation.”1
This statement succinctly
describes the way medical
disorders are diagnosed. Injuries
resulting from physical forces
(trauma) are identified primarily by
physical examination. Symptoms
play a greater role in the
recognition of nontraumatic
disorders. The absence of
laboratories, diagnostic imaging, or
other facilities should not prevent
attempts at identification of
common disorders in the
wilderness. Most disorders have to
be at least suspected before
appropriate investigative studies
can be ordered.
Diagnosis is usually the most
difficult aspect of care for a person
with a nontraumatic disorder.
Physicians commonly expend more
effort identifying problems than
treating them. In this chapter,
outlines help caregivers recognize
the organs related to a disorder.
Later chapters contain diagnostic
features of the common disorders of
specific organs. Caregivers should
consult these sources repeatedly.
“Mistakes are just as often caused
by lack of thoroughness as by lack
of knowledge.”2
Effectively examining someone
with a medical disorder is not an
easy, straightforward procedure. A
calm, understanding, and
sympathetic manner is essential.
The ability to appraise the
individual’s personality and to
adopt an approach that instills
confidence is vital. A seriously ill
or injured person cannot be
expected to be cheerful and
understanding or, on some
occasions, even cooperative.
If an individual has traumatic
injuries, an initial cursory
examination should identify
problems that require immediate
attention, such as bleeding, an
obstructed airway, or fractures.
However, a complete, unhurried,
and uninterrupted examination
should be carried out as soon as
possible, although evacuation from
a position of imminent danger, such
as falling rock, may be necessary
first.
MEDICAL HISTORY
Each individual should be
encouraged to describe symptoms
in their own words. Leading
questions should be avoided,
although some prompting or direct
inquiries are almost always
necessary. Failure to describe a
symptom must not be considered a
reliable indication that the symptom
is not present.
The time and circumstances in
which symptoms appear and their
chronological sequence are
significant. The precise location of
pain, the time it began, whether the
onset was gradual or sudden, the
severity of the pain, and the quality
of the pain—cramping, stabbing,
burning—should be ascertained.
Symptoms must be evaluated to
determine if they are continuous or
intermittent; how they are
aggravated or relieved; how they
are related to each other; and how
they are affected by position, eating,
defecation, exertion, sleep, or other
activities. Nonpainful symptoms
such as tiredness, weakness,
dizziness, nausea—or their absence
—may be highly significant,
particularly at high altitude.
An account of any past illnesses
must always be obtained, even
though in the wilderness the current
illness is usually the most
significant part of the history. If the
person’s illness is a recurrence of a
previous disease, awareness of that
disorder can provide the key to its
recognition. In addition, preexisting
diseases, such as diabetes or
epilepsy, must be identified so that
necessary treatment can be
continued; individuals with
traumatic injuries can have such
disorders and should be carefully
questioned about them.
MEDICAL HISTORY
Past History
Previous Illnesses: Bronchitis,
asthma, pneumonia, pleurisy,
tuberculosis, rheumatic fever;
any other heart or lung disease
Malaria, diabetes, epilepsy,
anemia; any other severe or
chronic illnesses
Operations: Date, nature of
operation, complications
Injuries: Date, nature of injury,
residual disability;
wilderness-related injuries,
particularly cold injury or
altitude illness
Medications: Any medications
taken regularly, whether
currently or in the past
Exposure: Recent exposure to
infection or an epidemic
Immunizations: When
administered; boosters
Allergies: Allergy to food, insect
stings, or drugs, particularly
penicillin and sulfa drugs
Review of Systems (Including
Both Present and Past Illnesses)
Head: Headache, dizziness,
hallucinations, confusion, or
fainting
Eyes: Inflammation, pain, double
vision, loss of vision
Nose: Colds, sinus trouble,
postnasal drip, bleeding,
obstruction
Teeth: General condition,
abscesses, dentures
Mouth: Pain, bleeding, sores,
dryness
Throat: Sore throat, tonsillitis,
hoarseness, difficulty
swallowing or talking
Ears: Pain, discharge, ringing or
buzzing, hearing loss
Neck: Stiffness, pain, swelling, or
masses
Heart and Lungs: Chest pain,
palpitations, shortness of
breath (greater than that
experienced by others during
similar exercise at the same
altitude), cough, amount and
character of material that is
coughed up, coughing up blood
Gastrointestinal: Loss of appetite,
nausea, vomiting, vomiting
blood or material that looks
like coffee grounds,
indigestion, gas, pain,
constipation, laxative use,
diarrhea, bloody or tarry or
black stools, pale or clay-
colored stools, hemorrhoids,
jaundice
Genitourinary: Increase or
decrease in frequency of
voiding; color of urine (light
yellow, orange); back pain,
pain with voiding; passage of
blood, gravel, or stones; sores,
purulent discharge, venereal
disease, or sexual contact;
menstrual abnormalities such
as irregular periods, increased
bleeding with periods,
bleeding between periods,
cramps
Neuromuscular: Fainting whether
total or incomplete (Chapter
17: Heart and Blood Vessel
Disorders), unconsciousness
from other causes, dizziness or
vertigo, twitching,
convulsions; muscle cramps,
shooting pains, muscular or
joint pain; total or partial loss
of sensation, tingling
sensations, weakness,
incoordination, or paralysis
Skin: Rashes, abscesses or boils
General: Fever, chills, weakness,
easy fatigability, dizziness,
weight loss
PHYSICAL EXAMINATION
If a physical examination is to
provide useful information, the
examiner must have some prior
experience, particularly for
examining the chest and abdomen.
For the inexperienced, comparison
with a normal individual may be
helpful, but nothing can substitute
for tutelage by a physician.
A thorough physical examination
is essential in the evaluation of
anyone with a medical disorder.
Even a person with traumatic
injuries must be completely
examined to ensure no wounds are
overlooked, particularly in the
presence of an obvious injury. For
the examination the individual
should be made comfortable and
protected from wind and cold. The
examiner’s hands should be warm,
and touch must be gentle. Any
roughness makes obtaining
diagnostic information more
difficult and could aggravate the
individual’s disorder.
To ensure that all areas of the
body are examined, a definite
routine should always be followed.
The following outline is relatively
complete and is adequate for both
traumatic and nontraumatic
disorders. The examination of some
anatomical areas, particularly the
chest and abdomen, is described in
more detail in the chapters dealing
with those areas.
General (Vital Signs): Pulse rate,
respiratory rate, temperature,
blood pressure, general
appearance
Skin: Color, texture, rashes,
abscesses or boils
Eyes: Eyebrows and eyelids, eye
movements, vision, pupil size
and equality, reaction of pupils
to light, inflammation
Nose: Appearance, discharge,
bleeding
Mouth: Sores, bleeding, dryness
Throat: Inflammation, purulent
exudates
Ears: Appearance, discharge,
bleeding
Neck: Limitation of movement,
enlarged lymph nodes
Lungs: Respiratory movements,
breath sounds, voice sounds,
bubbling
Heart: Pulse rate, regularity, blood
pressure
Abdomen: General appearance,
tenderness, rebound and
referred pain, spasm of
muscles, masses
Genitalia: Tenderness, masses
Rectum: Hemorrhoids, impacted
feces, abscesses
Back: Tenderness, muscle spasm,
limitation of movement
Extremities: Pain or tenderness,
limitation of movement,
deformities, unequal length,
swelling, ulcers, soft-tissue
injuries, lymph node
enlargement, numbness,
sensitivity to pin prick and/or
light touch (a wisp of cotton),
muscle spasm
EXAMINING TRAUMA
VICTIMS
Individuals with traumatic injuries
may have respiratory impairment or
severe bleeding that must be cared
for immediately (Chapter 3: Life-
Threatening Problems). After these
emergencies have received
attention, however, the care
provider must pause and,
essentially, start from the beginning.
An account of the accident and the
time and circumstances in which it
occurred should be obtained.
Frequently the nature of the accident
provides clues to injuries that
should be anticipated. If the person
is unconscious, witnesses must be
asked whether unconsciousness
caused the accident or resulted from
the accident. Witnesses and
companions also should be asked
whether the individual had any
preexisting medical conditions that
may have contributed to the
accident or that may require
treatment.
The individual’s pulse,
respiratory rate, and blood pressure
should be measured and recorded
immediately and every ten to fifteen
minutes until they are clearly stable.
If a blood pressure cuff is not
available, blood pressure should be
estimated as described under
Hemorrhagic Shock in Chapter 3:
Life-Threatening Problems. If the
individual is moved, the vital signs
should be rechecked immediately;
an increase in pulse rate or fall in
blood pressure at such times is
often an early sign of shock. For
individuals who have an extremity
fracture, the pulses in both
extremities must be compared; a
weak or absent pulse on one side
indicates that the fracture has
interfered with the arterial blood
supply.
Although a few injuries, such as
fractures, may have to be cared for
first, any individual must be
completely and thoroughly
examined. Concealed injuries must
be carefully sought. Injuries of the
back are most frequently
overlooked, even in hospital
emergency rooms. If the individual
is lying on his or her stomach, the
back should be examined before
turning the person over so as to
ensure the absence of bleeding or
other evidence of injury—unless
suspected fractures of the vertebral
column dictate that such an
examination be postponed.
A systematic routine must be
followed so that no areas of the
body are overlooked. Chest injuries
are unquestionably more threatening
than hand injuries and deserve
attention first, but failure to
recognize and care for a hand injury
can result in a permanent deformity.
“Many errors in care are due to
incomplete diagnosis or to
overlooking some serious injury
while concentrating on the obvious.
Systematic examination decreases
the likelihood of making such
errors.”3
If evacuation requires more than
one day, examinations must be
repeated to monitor the individual’s
condition and to ensure that all
injuries have been found. Any
individual who is unconscious at
the time of the initial examination
must be reexamined immediately
upon regaining consciousness.
MEDICAL RECORD
For disabling diseases or injuries, a
written account of the history and
examination findings is an essential
element in the person’s medical
care, particularly when a
physician’s help is more than a few
hours away. In the confusion
associated with an accident and
subsequent evacuation, a medical
attendant may be unable to
remember whether a symptom was
present or physical changes were
detectable, even a few hours after
the examination. Memory is not a
dependable record of numerical
data, such as pulse and respiratory
rates, temperature, and blood
pressure. If any medications have
been administered, a written
account of the doses and times they
were given is essential. All
treatment must be recorded.
For individuals with
nontraumatic illnesses, a written
record allows the examiner to
systematically review his findings
while trying to arrive at a
diagnosis. Written records help
ensure no details are forgotten when
trying to obtain help by such means
as radio or cellular telephone.
Written records of vital signs
(pulse, respiratory rate, blood
pressure, and temperature) and
other features of the person’s illness
make detecting small changes in
these signs easier. Such changes
usually precede more obvious
indications that the individual’s
condition is worsening and allow
treatment to be instituted earlier,
when it often is more effective.
These changes may also indicate a
response to treatment and presage
more obvious improvement in the
person’s overall condition, perhaps
allowing a difficult evacuation to
be delayed until circumstances are
more favorable.
When evacuation is prolonged,
written records allow more than
one person to share in the
individual’s care. Because all can
determine what the signs or
symptoms were at any time, all can
recognize changes and initiate any
therapy that is needed. Written
records are also essential for
preventing omission or duplication
of doses when administering
medications.
If the person is evacuated,
written records are essential for the
physician who provides care,
particularly when attendants are
unable to accompany the individual.
If evacuation takes place several
days after onset of an illness or
injury and more than one person has
been involved in the person’s care,
a written record is the physician’s
only source of accurate information
about the individual’s original
condition, how that has changed,
and what treatment has been given
—particularly medications that
have been administered.
Medical records play such a
vital role in medical care that their
compilation is begun immediately
when someone enters a hospital
emergency room or physician’s
office. Such records are
subpoenaed at the beginning of any
medically related litigation, and
omissions are often damaging to the
physician’s defense, which might be
a significant consideration for
nonphysicians in an increasingly
litigious society.
The outlines provided in this
chapter for the medical history and
physical examination are entirely
appropriate for the medical record.
Obviously, all abnormalities should
be recorded, but the absence of
abnormalities is frequently of equal
importance, particularly for
nontraumatic disorders. Without a
specific statement that a sign or
symptom was not present, a
physician subsequently caring for
the individual may be unable to
determine whether that indicator
was really absent or simply was not
noticed.
For traumatic injuries, an
account of the accident should be
recorded at the earliest opportunity.
All injuries should be carefully
described. The absence of injuries,
or signs such as swelling or
discoloration that are suggestive of
injury over major areas of the body
—chest, abdomen, head, arms, or
legs—should also be noted. The
vital signs should be recorded
every thirty to sixty minutes for at
least four hours, but for longer if
these signs are not stable. After
stabilization, vital signs need to be
recorded only about every four
hours until the person is well on the
way to recovery. Any preexisting
medical conditions should be
described. The dosage, route, and
time of administration of all
medications must be accurately
logged. Notes about any other
treatment or changes in the person’s
condition must include the time.
The written record must be
accessible—not buried away in a
pack. Notations of changes in the
individual’s condition or the
administration of medications must
be made immediately and not
recorded from memory later.
____________
REFERENCES
1. Adams, F. D. Cabot and
Adams Physical Diagnosis, 14th
ed. Baltimore: The Williams &
Wilkins Co., 1958. Quoted by
permission of the author and
publishers.
2. Ibid.
3. Kennedy, R. H. in Committee
on Trauma, American College of
Surgeons: Early Care of Acute Soft
Tissue Injuries. Chicago, 1957.
(Quoted by permission of the
publishers.)
CHAPTER 2
BASIC MEDICAL CARE
Most individuals injured in

accidents or contracting an illness
in the wilderness are evacuated
within hours or, at the most, one to
two days. Occasionally, however,
bad weather, difficult terrain,
distance from a hospital or
transportation—particularly on an
expedition—insufficient personnel
for evacuation, or other problems
may force an individual to remain
in a remote situation. Some persons
may not need evacuation if they are
expected to recover enough to walk
out or resume activity within a
relatively short time.
NURSING CARE
Anyone confined to bed (or
sleeping bag) by illness or injury
has certain needs that require
attention. Ministering to those needs
is most readily identifiable as
“nursing care.” The objective of
this care is simple: to allow the
body to heal itself.
Comfort and Understanding

Comfort and understanding—the
essence of nursing—are needed by
all, regardless of the nature or
severity of the medical problem.
Some have a greater need than
others; some, particularly young
men, try to deny their need.
Regardless of the situation, the
medical supplies on hand, or the
sophistication of available medical
knowledge, interest and concern,
sympathy and understanding can
always be shown; comfort and
reassurance can always be
provided. All are essential.
Rest
Rest promotes healing in several
ways. Exertional and emotional
stress are reduced. Additional
injury to damaged tissues is
avoided. Rest can allow
opportunity for improved nutrition,
and the nutrients can be used for
healing instead of muscular effort.
Individuals with heart or lung
disease, and individuals with
severe injuries, particularly
fractures, may need to be
immobilized, but most do not need
such confinement. Often, remaining
in camp rather than hiking or
climbing is all that is required to
hasten recovery.
Sedation
In the absence of brain injury or
disease, medications that promote
sleep may be given at altitudes
below 10,000 feet (3000 m). At
higher elevations, sleeping
medications should not be
administered because they reduce
blood oxygenation during sleep,
which often aggravates symptoms of
altitude sickness. The sleeplessness
and irregular breathing associated
with high altitude can be relieved
safely with acetazolamide (Chapter
24: Disorders Caused by Altitude).
Analgesia
Analgesics should be supplied
liberally, but judiciously, in
wilderness situations. The risk of
narcotic addiction for individuals
with painful injuries or illnesses is
essentially nonexistent, particularly
when the agents are administered
for a week or less.
The hazard of strong analgesics
consists largely of further
depressing cerebral activity in a
person whose central nervous
system function is already impaired
as the result of a head injury or an
illness. Depressed cerebral function
is typically manifested by impaired
respiration—breathing is slower
and shallower. Further depression
of respiration by narcotics can lead
to significant hypoxia, particularly
at high elevations. A person with a
severe head injury might stop
breathing altogether, which usually
is catastrophic.
For individuals who do not have
a head injury, analgesics can
relieve severe discomfort and the
associated emotional distress. For
many individuals with traumatic
injuries, control of pain reduces the
severity of shock. Analgesia
promotes healing by allowing
people with painful injuries or
illnesses to sleep restfully. Many
individuals are more aware of pain
at night when nothing is diverting
their attention. For three or four
days after a major injury—
sometimes even longer—strong
analgesia may be needed.
Major analgesics have so much
sedative effect that a sleeping
medication is not needed. Indeed,
administering a sleeping medication
with a major analgesic would be
hazardous.
Warmth
Individuals who are ill or
injured must be kept warm. At low
environmental temperatures,
persons with severe illnesses or
injuries may not be able to generate
enough heat to maintain body
temperature, even in a sleeping bag,
and like individuals with
hypothermia, may require external
sources of heat (Chapter 26: Cold
Injuries).
Lower Altitude
Evacuation from altitudes above
15,000 feet (4600 m) promotes
recovery. Individuals with diseases
of the lungs or heart should be taken
as low as possible, preferably
below 8000 feet (2400 m), and
provided with supplemental oxygen
if it is available.
Coughing
People who are immobilized
with a severe injury or illness
usually do not breathe deeply,
particularly if breathing is painful.
As a result of diminished
respiratory excursions, their lungs
are not fully expanded and fluid
accumulates in the immobile
segments. These collections are an
ideal medium for bacterial growth,
which leads to pneumonia. (Such
infections are the most common
cause of death for elderly persons
confined to bed with fractured hips
or similar injuries.)
To eliminate the fluid, expand
the lungs, and reduce the danger of
infection, individuals must be
encouraged—or forced—to breathe
deeply and to cough at frequent
intervals. Coughing may be difficult
for someone who is very ill or very
painful for someone with a chest or
abdominal injury, but such
individuals are the most prone to
pulmonary infections and most in
need of clearing their lungs. The
practice in most hospitals is to have
individuals sit up, hold their sides,
and cough deeply—not just clear
the throat—at least every two
hours. A similar routine should be
adopted in wilderness
circumstances, particularly at
higher altitudes where any
compromise in pulmonary function
could be disastrous.
Elimination of fluid from the
lungs can also be increased by
postural drainage. If the head and
chest are slightly lower than the rest
of the body, gravity helps get rid of
the fluid. In a tent, such positioning
can best be achieved by elevating
the abdomen, pelvis, and legs. After
the person has recovered enough to
be able to walk around, forced
coughing or postural drainage are
usually no longer necessary.
Ambulation
Anyone confined to bed as a
result of illness or injury should be
encouraged to walk several times a
day. Such exercise increases the
circulation in the legs and helps
prevent thrombophlebitis (Chapter
18: Respiratory Disorders). The
only major exceptions to this rule
are individuals with injuries that
prevent walking, as well as
individuals who have already
developed thrombophlebitis and
should remain as immobile as
possible until the disorder has
resolved.
Diet
Food is not as important during
the acute stages of an illness as an
adequate fluid intake. Unless a
specific disorder dictates a
particular diet, the person should
eat whatever is desired, although
bland diets are usually more
acceptable. During convalescence
more attention can be given to a
nutritionally adequate diet, perhaps
with extra protein.
Bowel Care
Difficulties with bowel
evacuation are common for persons
confined to bed who repress the
urge to defecate, have a low food
intake, and become dehydrated. If
not corrected, fecal impaction often
results (Chapter 19:
Gastrointestinal Disorders). Even
though stool volume is reduced in
the absence of solid food in the
diet, bowel movements should
occur every three to four days. The
best way to ensure normal
elimination is to make certain fluid
intake is adequate; roughage or
fiber in the diet increases stool bulk
and is helpful. Laxatives or enemas
should rarely be needed to prevent
impaction in a bedridden
individual.
Convalescence
Although physical activity
should be encouraged during
convalescence, strenuous exercise
undertaken too early may delay
recovery, particularly at high
altitudes. In addition, individuals
are more susceptible to other
injuries during convalescence. To
be certain that recovery is
complete, delaying a return to full
activity for two or three extra days
may be desirable.
FLUID BALANCE
An adequate fluid intake is
essential. A person can live for
weeks without food but only for a
few days without water. Fluid
balance implies equilibrium
between losses (through the
kidneys, skin, and lungs—or other
routes) and gains (from fluids and
foods that have been ingested).
During an illness that increases
fluid losses and makes fluid intake
difficult or impossible, fluid
balance can become critical. As an
example, dehydration from massive
diarrheal fluid loss kills two to
three million children annually in
developing countries.
An adult of average size
normally loses 1500 ml to 2000 ml
of water from the body each day.
The “sensible loss” excreted by the
kidneys ranges from 1 to 2 liters per
day. The “insensible loss” through
perspiration (even in cold climates)
and evaporation from the lungs (to
moisten air that is inhaled) is 0.5 to
1 liter per day in temperate climates
and at low altitudes. In hot climates
or during high fever, several liters
of water may be lost daily through
perspiration (which is no longer
insensible). At high altitudes up to 4
liters of water can be lost through
the lungs each day.
Salt (sodium chloride),
potassium, and bicarbonate, known
collectively as electrolytes, are
vital constituents of body fluids. As
with water, a balance between
intake and loss must be maintained.
The daily salt requirement for an
average adult is 3 grams. When
large amounts of salt are lost
through perspiration, needs may be
considerably higher.
Normally functioning kidneys
are very sensitive to changes in the
body’s fluid balance and react
immediately to conserve or
eliminate water. The urine volume
and color are highly reliable
indicators of fluid status. A twenty-
four hour volume of less than 500
ml, or urine that has a deep yellow
or orange color, is indicative of
fluid depletion; a volume of 2000
ml of very lightly colored urine is
typical of a high fluid intake.
These water and electrolyte
requirements represent the needs of
a healthy adult. Individuals with
heart or kidney disease may be
unable to get rid of excess salt and
water and can have quite different
requirements. The administration of
normal quantities of electrolytes
and water (particularly salt) to
persons with one of these disorders
may have serious consequences.
When an illness, such as
dysentery or cholera, causes high
fluid losses through vomiting and
watery stools, the volume of fluid
lost should be estimated to keep
current on the person’s fluid status.
Insensible losses must be estimated
also, taking into consideration
fever, environmental temperature,
and altitude. The volume of fluid
ingested must be recorded to ensure
enough is consumed. These
measurements and estimates must
be written down so the individual’s
fluid needs can be calculated.
Urine volume and color are good
indicators of a person’s fluid
balance but tend to reflect what has
already happened. Measuring
losses and gains as they occur
provides more immediate insight
into the condition of someone with
a fluid-losing disorder.
Dehydration at Altitude
Higher altitudes tend to cause
dehydration, and this tendency
becomes progressively greater as
the elevation increases and the
environment becomes colder.
Almost all trekkers or climbers are
dehydrated above 18,000 feet
(5500 m) Some investigators have
suggested that the depression,
impaired judgment, and other
psychological and intellectual
changes that commonly occur at
high altitudes—and have been
blamed on hypoxia—may actually
be the result of dehydration.
The principal cause of
dehydration at high altitude is the
increased fluid loss associated with
more rapid and deeper breathing of
cold air. Air is warmed to body
temperature and is saturated with
water as it passes through the upper
air passages; it has a relative
humidity of 100 percent when it
reaches the lungs. Since cold air
contains essentially no moisture (at
5°F or −15°C the vapor pressure of
water is 1.24 mm Hg), it requires
more water for humidification.
Most of this moisture, and the heat
expended to warm the air to body
temperature, is lost when the air is
exhaled. (Some of the water may be
regained during expiration by
condensation in cool upper air
passages, but mouth breathing
bypasses the air passages where
most condensation occurs.) In
addition, loss of heat through
evaporation of water and through
warming inhaled cold air is a
significant contributor to
hypothermia at high altitudes.
If individuals are not careful
about managing clothing to
minimize sweating, particularly
with the bulky clothing required to
keep warm during periods of
immobility at high altitude, fluid
loss from this source may not be
held to the lowest levels possible.
Decreased fluid consumption
often contributes to dehydration at
high elevations. The need to carry
fuel and melt snow to obtain water
for drinking or cooking, as well as
the dulling of the sensation of thirst
that accompanies the loss of
appetite, nausea, or even vomiting
of acute mountain sickness, both
tend to reduce fluid intake.
Individuals who are active at
high altitudes must consciously
force themselves to drink large
volumes of fluid. Thirst alone is not
a reliable indicator of the need for
water. Above 15,000 to 16,000 feet
(4600 to 4900 m) fluid
requirements often exceed 4 liters
per day. Urine color and volume
indicate the adequacy of fluid
intake. Darkly colored urine—
orange instead of light yellow—and
the absence of a need to void upon
awakening from a night’s sleep are
indicators of significant
dehydration.
Fluid Replacement
The easiest and most reliable
method for replacing fluids is to
drink more. Almost any
nonalcoholic liquid is suitable, but
fruit juices, soft drinks, soups, and
similar liquids should be
encouraged since water contains no
electrolytes. (Coffee, tea, and hot
chocolate are not as satisfactory
because they contain caffeine, a
diuretic that increases renal fluid
loss.)
Seriously ill individuals with
very little appetite often refuse
liquids and solid foods. However,
they can usually be persuaded to
drink small quantities, just two or
three sips, at intervals of fifteen to
twenty minutes. With tenacity,
patience, and gentle encouragement,
such persons can be coaxed to drink
several liters of fluid over a
twenty-four hour period.
Some individuals, particularly
those with intractable vomiting or
in coma, are unable to take fluids
orally. If medical attention can be
obtained within one or two days
and fluid losses are not increased,
the intervening fluid depletion is
usually not too severe. However,
longer periods without fluid, and
disorders that increase fluid loss,
can produce severe dehydration. If
drugs that control vomiting—
odansetron disintegrating tablets
(Zofran ODT®), or Compazine®,
or Phenergan® suppositories—are
not available, fluids must be
administered intravenously.
Only knowledgeable persons
experienced with such therapy
should attempt administering fluids
intravenously. Fluids suitable for
intravenous administration cannot
be improvised and would only be
carried by a well-equipped
expedition, although such fluids
might be obtained by airdrop. Such
fluids are often left behind by
expeditions, and in some popular
areas a significant supply has
accumulated. These fluids come
from many nations with labels
printed in many languages, but the
contents are usually stated in
standard chemical symbols or
English.
The volume of fluids to be given
intravenously must be determined
each day. Fluids are required to
replace both normal and abnormal
losses. Two liters of 5 percent
glucose and 0.5 liter of an
electrolyte solution (preferably a
balanced salt solution, but normal
saline if only that is available)
usually fulfill the body’s daily
needs when no abnormal losses are
occurring. Fluids lost through
vomiting, diarrhea, or excessive
perspiration should be replaced
with an electrolyte solution.
Excessive fluid loss through the
lungs due to high altitude should be
replaced by a glucose solution
since no electrolytes are lost with
the moisture in expired air.
Most electrolyte solutions
contain little potassium. Individuals
with poor kidney function cannot
rid themselves of excessive
potassium, which may rapidly
accumulate to lethal levels.
However, persons with normal
renal function excrete potassium in
the urine. As a result, blood
potassium concentrations can fall to
dangerously low levels during
prolonged intravenous fluid therapy
if the potassium is not replaced.
Therefore, individuals receiving
intravenous fluids for more than
two to three days, or losing large
volumes of fluid with diarrhea, who
have a normal urine volume, should
receive an extra 15 to 20 mEq of
potassium per liter of electrolyte.
(The occasions when such
potassium supplements are
available in wilderness
circumstances must be rare. When
available, the supplements are
usually supplied in a solution that
can be added directly to the
electrolyte solution.)
If a person with a healthy heart
and normally functioning kidneys is
provided with an adequate intake of
water (as glucose) and electrolytes
(balanced salt solution), the kidneys
compensate for any imbalance. The
inevitable inaccuracies inherent in
measuring fluid intake and output
are fully corrected. However, an
individual with preexisting heart
disease, particularly congestive
heart failure, a person with kidney
disease, or someone with acute
renal failure as a result of his
disease or injury requires much
more precise therapy, which can
only be provided with hospital
facilities. For such individuals, any
error in administering fluids must
be made on the side of not giving
enough.
CARE FOR TRAUMA VICTIMS

Traumatic injuries are by far the
most common medical problems
encountered in the wilderness.
Emergencies
True medical emergencies in
which a delay of a few minutes in
providing care can significantly
affect the outcome are rare. In
wilderness accidents the
opportunity to provide such
treatment may pass before anyone is
able to get to the individual.
Nonetheless, wilderness travelers
must be familiar with the
procedures for treating traumatic
medical emergencies if they are to
deal with them successfully when
the rare opportunities do occur.
True emergencies do not allow time
for referral to a textbook.
If immediate action is necessary
to prevent loss of life following an
accident, the order in which
problems should receive attention
is as follows:
Cardiopulmonary
Resuscitation (CPR). An open
airway must be established first;
interference with breathing by
chest wounds must be
immediately corrected. If
needed, CPR should be started.
Emergency rescue personnel
approaching an unconscious
person follow the acronym
ABC, which stands for airway,
breathing, and circulation.
Control of Bleeding. After the
person is breathing or being
resuscitated, bleeding should be
controlled by direct pressure at
bleeding sites, not by
tourniquets or pressure points.
Treatment for Shock. After
cardiac and respiratory function
have been established and
bleeding has been controlled,
attention should be directed to
treating or preventing shock.
Treatment given in anticipation
of shock is more effective than
treatment instituted after shock
has developed.
Although the order of the first
two actions may appear reversed
because control of severe bleeding
should take only seconds but CPR
can be prolonged, in reality they are
not. Anyone whose heart has
stopped does not bleed. Therefore,
CPR must take first priority.
Furthermore, anyone who has bled
so severely the heart has stopped
cannot be resuscitated. The
combination of cardiac arrest and
severe hemorrhage is essentially
always lethal. (These problems are
discussed in greater detail in
Chapter 3: Life-Threatening
Problems.)
Other Injuries
All injuries should be treated as
completely as possible before any
person is moved. Open wounds are
always contaminated to some
extent; further contamination should
be avoided. Soft-tissue wounds
should be covered with voluminous
dressings that apply pressure to
control bleeding, provide
immobilization, minimize swelling,
and control infection. Even when no
fractures are present, severely
injured extremities should be
immobilized and elevated slightly
to aid blood circulation. If the
lower extremities are injured and
evacuation requires walking or
climbing, the person should stop
periodically to lie down and
elevate the feet. Splinting fractures
before the person is moved is
particularly important. “Splint ’em
where they lie” is a timeproven
adage.
The equipment necessary for the
treatment of some injuries, such as
injuries of the chest, is not
available on most short outings.
However, this equipment should
always be available in popular
wilderness recreation areas and
should be part of the emergency
gear of all wilderness rescue
organizations.
FEVER AND CHILLS

Fever and chills are signs of
infections but can be signs of other
disorders.
Fever
Normal body temperature
averages 98.6°F (37°C) when
measured orally, ranges from
96.5°F (35.8°C) to 100°F (37.8°C),
and usually varies 1.25° to 3.75°F
(0.7° to 2.1°C) daily. The lowest
temperature occurs between 3:00
and 5:00 A.M. and the highest in the
late afternoon or early evening in
individuals who are active during
the day and sleep at night. The
temperatures of women of
childbearing age rise about 1.0°F
(0.5°C) at the time of ovulation and
remain elevated until menstruation
begins. During vigorous exercise, a
healthy, well-conditioned athlete’s
temperature can climb to 104°F
(40°C) or higher if he is generating
heat faster than it can be lost.
In a moderate or hot wilderness
environment, a person should not be
considered to have a fever until the
temperature at rest exceeds 100°F
(38°C) orally or 101°F (38.5°C)
rectally. In a cold environment,
hypothermia can mask a fever—
sometimes a very high fever—by
reducing the body’s temperature to
normal or subnormal levels.
Oral temperatures are easier to
measure but are affected by recently
consumed food or beverages,
smoking, or mouth breathing and
talking. Oral temperatures should
not be taken for at least ten minutes
after eating or smoking, and the
person should preferably have been
sitting or lying quietly. Rectal
temperatures are more reliable and
usually are about 1°F (0.5°C)
higher than the oral temperature. If
rectal measurements are necessary,
a rectal thermometer is preferable.
It should be lubricated, gently
inserted about 1.5 inches into the
rectum, and left for three minutes.
Any person who is delirious or
thrashing about must be watched
carefully and perhaps restrained to
prevent breaking the thermometer
regardless of where the temperature
is measured. Taking the temperature
may have to be postponed until the
person is calmer.
As long as an illness persists,
the temperature and pulse rate
should be recorded every four
hours. Fevers sometimes follow
specific patterns that are
diagnostically helpful. The
temperature may go up and stay up,
gradually coming down at the
termination of the illness, or it may
spike to high levels and then fall to
normal or below normal every day
or every second or third day. A
record is essential for such patterns
to be recognized. (A soundly
sleeping individual rarely needs to
be awakened just to have the
temperature taken.)
A moderate fever, although it
may make the person
uncomfortable, does not produce
lasting harmful effects. In contrast,
temperatures above 106°F (41°C),
which in adults usually occur only
with heat stroke, can cause
irreversible damage to a number of
organs if not promptly lowered.
Covering the individual’s body and
extremities with wet cloths (or
wetting the clothes being worn) and
fanning the individual to increase
evaporation and cooling is the
technique used in many emergency
rooms.
Cooling should be continued
until the temperature is below
103°F (39.5°C) (Chapter 27: Heat
and Solar Injuries). If the fever is
not the result of heat stroke,
antipyretic drugs may be given
orally to fully conscious individuals
or rectally to stuporous or comatose
individuals. Ibuprofen (Advil®),
acetaminophen (Tylenol®), and
aspirin are all effective for
reducing fever. Because high fevers
frequently recur quite rapidly, the
temperature must be watched very
carefully until the individual is
clearly recovering.
Although the individual’s
temperature may need to be
lowered, protection from
environmental extremes of heat or
cold must be provided, including
redressing in clothing similar to that
being worn by everyone else. The
individual should not be closed up
in a sleeping bag that traps the heat
and can cause the temperature to go
up again, unless sleeping bags are
necessary for everyone else to keep
warm.
Chills
An individual with a chill
shivers uncontrollably and feels
cold and miserable. These
symptoms are produced by the entry
of showers of microorganisms into
the bloodstream. In comparison
with the usual chills resulting from
exposure to cold, chills caused by
infection are much more severe and
produce violent, uncontrollable
shaking of the entire body. Teeth
chatter, the lips and nails turn
purple, and the skin becomes pale
and cold. (In years past, when many
hospital beds rattled distinctly, a
chill could be diagnosed when the
occupant was shaking hard enough
to make a bed rattle.) The cold
feeling persists despite blankets and
heating pads until the chill has run
its course, usually five to fifteen
minutes. Typically, a chill is
followed by a fever that may reach
high levels.
A chill is almost always the first
sign of an infection, and treatment
consists of caring for the underlying
disorder. Pneumonia, meningitis,
and “strep throat” are frequently
introduced with a single shaking
chill. Recurrent chills characterize
malaria, infections of the kidneys or
the liver and bile ducts, and
generalized bacterial infections.
Occasionally individuals
develop chills fifteen to thirty
minutes following prolonged severe
exertion, particularly when they are
not in good physical condition and
food intake has been limited. Such
chills appear related to a reduction
in blood sugar (hypoglycemia) and
are not a sign of infection.
CHAPTER 3
LIFE-THREATENING
PROBLEMS
Ken Zafren, M.D.
Principal Contributors
Some medical conditions are

immediately life threatening.
Prompt recognition and appropriate
action are required for safe
evacuation of the individual to a
medical facility for definitive care.
SAFETY AND LEADERSHIP

The safety of the rescuers is always
the first priority, particularly when
injuries have been caused by
hazards such as rockfall or
avalanches. No uninjured person
should attempt a rescue until scene
safety has been ensured.
Rescuers who may have contact
with blood or other body fluids
should use universal precautions,
primarily gloves. Many people are
now allergic to latex gloves, and
vinyl gloves are unreliable. The
best current choice for glove
material is nitrile. Latex-free
dishwashing gloves are more
durable than medical gloves and
serve as an effective barrier.
Most rescuers prefer to perform
mouth-tomouth rescue breathing
with a barrier device, such as a
mask, that separates them physically
from the person while allowing
mouth-to-mouth ventilation.
Gloves and mouth-to-mouth
barriers should be available in
medical kits but can be improvised.
A plastic bag of any type can be
used as a glove when tied with
string or taped at or above the
wrist.
A nitrile glove with a slit cut in
the middle finger can be used as an
improvised mask. The middle
finger is placed in the mouth of the
individual being resuscitated so that
blowing into the glove inflates that
finger and forces air through the slit
into the person’s mouth. The
person’s nose must be held closed
when blowing into the glove so that
air is forced into the lungs instead
of out through the nose. Releasing
or uncovering the nose between
breaths allows the individual to
exhale. The slit acts as a one-way
valve to prevent saliva from
entering the glove.
If more than one rescuer is
present, one should be designated
the leader. Ideally, the leader
should direct resuscitation and
medical care, plan for evacuation,
and coordinate calls for help but
should not lose sight of everything
that is happening by performing
resuscitation or administering care.
THE ABC’S: AIRWAY,

BREATHING, AND
CIRCULATION
Evaluation and treatment of
every ill or injured person begins
with the ABC’s: airway, breathing,
and circulation. The leading
preventable cause of death from
trauma is obstruction of the airway.
Death resulting from failure of
oxygen to reach the brain occurs if a
person does not have an open
airway or does not breathe for
approximately four minutes—
except for individuals who are
moderately to severely
hypothermic. In an unconscious
person, the tongue may obstruct the
airway (Figs. 3-1 and 3-2).
Opening the airway may be as
simple as repositioning the jaw
(Fig. 3-3).
Once the airway is open,
breathing should be evaluated. If the
person is not breathing, rescue
breathing is necessary.
After an open airway and
breathing are ensured, the next step
is to evaluate the circulation. If the
person does not have a pulse, no
effective circulation is present, and
providing cardiopulmonary life
support (CPR) may be necessary
for the person to survive.
Learning rescue breathing or
CPR from a book is not advisable.
Management of the ABC’s,
including CPR, is taught in basic
life-support classes available to the
public. Participants in wilderness
activities should take one of these
courses and a refresher every two
years.
Figure 3-1. Structures of the mouth,
throat, and airway in a normal,
conscious person
Figure 3-2. Position of the tongue and
epiglottis in an unconscious person
Figure 3-3. Position of the tongue and
epiglottis in an unconscious person
with the head and neck extended to
relieve airway obstruction
Airway
If an ill or injured person can talk
normally, the airway is open and
breathing is normal. If the person is
not breathing, the cause may be
obstruction of the airway.
If a person is unresponsive,
breathing should be checked first.
An individual who is face down
should be turned face up. If a back
or neck injury may be present, the
person should be logrolled while
protecting the back (Chapter 8:
Head and Neck Injuries). In the
field, breathing can be detected by
looking, listening, and feeling:
looking for respiratory efforts,
listening for air movement, and
feeling whether air is moving in and
out. If the chest rises and falls and
air is moving, then the person is
breathing. If the person is not
breathing, the airway should be
opened.
The most common cause of
airway obstruction in an
unconscious person is the tongue.
When an individual is unconscious,
the muscles of the tongue relax and
the tongue falls back in the throat,
blocking the airway. If the person
has not sustained trauma and no
neck injury is suspected, the airway
can be opened by tilting the head
back slightly and performing a jaw
thrust by placing the fingers at the
angles of the person’s jaws and
pulling forward (Fig. 3-3).
Alternatively, a finger or thumb can
be hooked behind the teeth of the
lower jaw and the jaw pulled
forward. If the possibility of a neck
injury exists, the airway should be
opened using a jaw thrust while the
neck is stabilized in a neutral
position (Fig. 3-4).
If these maneuvers do not open
the airway, the rescuer should look
in the mouth for foreign material,
usually vomit, and remove it by
sweeping two gloved fingers
through the mouth or by using a
device that provides suction, if
available. If the tongue is the cause
of the obstruction in an unconscious
person and not enough rescuers are
available to keep holding the
airway open, an oral or nasal
airway can be inserted (Fig. 3-5). If
no other equipment is available, a
large safety pin can be placed
through the tip of the tongue and
secured to the lower lip, chest, or
clothing to keep the tongue from
falling back and obstructing the
airway.
Advanced airway management is
beyond the scope of this chapter,
but members of wilderness
expeditions with appropriate
training may use other devices, such
as a Combitube® or endotracheal
intubation to manage the airway. In
extreme circumstances with
appropriate expertise available, an
emergency tracheostomy or
cricothyrotomy may be warranted.
Figure 3-4. Jaw thrust technique
Cricothyrotomy
A cricothyrotomy, a surgical
airway similar to a tracheostomy, is
rarely needed in the wilderness but
may be lifesaving for an
unconscious injured person who
needs to be safely transported or for
an individual with an extensive
facial or jaw injury that results in
uncontrollable bleeding into the
mouth and throat or obstruction of
the airway. However, the neck
contains major blood vessels close
to the trachea. Cricothyrotomy
should only be attempted by an
individual experienced with the
procedure or, under extreme
conditions, instructed by a
physician through
telecommunication. Optimally, a
skin antiseptic and local anesthesia
should be available.
Figure 3-5. Oropharyngeal airway in
place in an unconscious person
The steps in an emergency

cricothyrotomy in the wilderness
are:
1. The injured person should be in a
supine position with a roll of
clothing behind the neck, unless a
cervical vertebral fracture is
suspected.
2. If time permits, attendants should
scrub their hands and forearms
and the injured individual’s neck
from the chin to the clavicle with
soap. An antiseptic, such as
Betadine® or alcohol, should be
painted on the cleansed neck.
Attendants should put on sterile
gloves if they are available.
3. A cricothyrotomy is so named
because the opening in the
trachea is made between the
cricoid cartilage and the thyroid
cartilage (Fig. 3-6). This site is
usually four or five fingertips
above the sternal notch. A
potential error is choosing the
space between the hyoid bone
and thyroid cartilage, which is
much higher in the neck.
4. A vertical incision
approximately 1.5 inches long
should be made over the
cricothyroid space. Minor
bleeding from the skin and
underlying fat is often
encountered and should be
ignored. A horizontal incision
approximately 0.5 inch in
sternocleidomastoid muscles
carotid arteries thyroid gland
thyroid cartilage length should be
made through the cricothyroid
membrane.
Figure 3-6. Location of crycothyroid
membrane
5. Ideally, a cuffed endotracheal

tube should be inserted through
the opening, but a variety of
commercial tubes can be used for
the cricothyrotomy. If none are
available, any firm tube the size
of the injured person’s little
finger, such as the casing of a
pen, can be inserted through the
opening. The tube should only be
advanced 3 inches so that it does
not block one of the bronchi
(usually the right). With each
breath, the tube should become
fogged. Looking for movement
and listening for breath sounds
on both sides of the chest can
ensure the tube is in a good
position.
6. The tube should be taped
securely to the neck to prevent
dislodging it or forcing it too
deeply into the trachea.
7. If available, supplemental
oxygen should be administered
through the tubing.
Breathing and Circulation
If the person is not breathing and
the airway is open, two rescue
breaths, each lasting more than one
second, should be given. The chest
should rise with each breath. After
the rescue breaths, the circulation
should be assessed by checking the
carotid pulse for five to ten
seconds. (In hypothermic
individuals, assessing the pulse
usually takes much longer.) If no
pulse is present, CPR with rescue
breathing and high-quality
compressions should be
considered.
Ideally, all teenagers and adults
venturing into the wilderness should
be prepared to provide
cardiopulmonary resuscitation
(CPR). Such preparation must be
obtained through certified courses
provided by organizations such as
the American Red Cross, the
American Heart Association, and a
wide variety of medical facilities.
A review course should be taken at
least every two years. Such courses
employ manikins for training, a
facility that cannot be duplicated.
Simply reading about this technique
is not adequate. Therefore, no
instruction about the technique of
CPR is provided in this book.
If an automated external
defibrillator (AED) is available,
shocks as indicated by the AED can
be provided.
At the same time the airway is
being opened, rescuers should
quickly examine the rest of the
person, looking particularly for
external bleeding. Any major
source of bleeding should be
controlled immediately, by direct
pressure if possible. If bleeding
from an extremity cannot be
controlled by direct pressure, a
tourniquet should be used (Chapter
12: Soft-Tissue Injuries).
If the airway is open and the
individual still is not breathing but
a pulse is present, the rescuer must
perform rescue breathing until the
person starts breathing again or
resuscitation efforts are terminated.
Lightning strikes can disrupt
breathing and heart activity, but the
heart usually restarts promptly.
Breathing, on the other hand, may
not restart for many minutes—even
hours. If rescue breathing is not
performed, the heart and brain are
deprived of oxygen, and eventually
the heart begins to fibrillate and
stops. If effective rescue breathing
is done, the respiratory centers in
the brain eventually start working
again and the person resumes
breathing. Full recovery usually
follows as long as breathing has
been adequately supported.
Therefore, if possible, rescue
breathing should not be stopped as
long as effective heart action is
present (Chapter 29: Lightning
Injuries).
Starting and Stopping

Resuscitation
If cardiac arrest is the result of
trauma, CPR in a wilderness
situation is futile. If a traumatized
individual has no pulse, CPR
should not be started.
Other reasons for not starting
resuscitation include signs that the
person has been dead for some time
or has injuries not compatible with
life, such as a massive brain injury
or other mutilating injuries. The
earliest sign that an individual is
dead and cannot be resuscitated is
dependent lividity, a red or purple
color that results from settling of
blood that is not circulating in the
dependent portions of the body.
This discoloration typically covers
the back if the person is lying face
up (supine) but is not present over
the shoulders, buttocks, or other
pressure points where pressure
from the body keeps the blood from
entering the tissues. The
discoloration is in other areas if the
person is lying face down (prone)
or on one side. Rigor mortis
(stiffening of the muscles) develops
well after dependent lividity.
Decomposition is a very late
change. The major exception to this
rule is that a severely hypothermic
person can have dependent lividity
and may be stiff but can
occasionally still be resuscitated
under ideal circumstances.
In nontraumatic cardiac arrest,
the most common cause is a heart
rhythm disturbance. In general, if
CPR can be started in less than four
minutes and a shock administered to
restart the heart within ten minutes,
the person has a chance of survival
with good neurologic outcome. If
the individual does not respond to
CPR after fifteen minutes (when an
AED is not available) or to CPR
and attempts to defibrillate after
thirty minutes, resuscitation efforts
should be terminated.
Prolonged CPR may be justified
in hypothermic individuals and, as
mentioned, people struck by
lightning may require prolonged
ventilatory support. Following
drowning, particularly drowning in
cold water, CPR should be started
immediately after the person has
been recovered from the water
unless submersion is known to have
lasted for more than an hour. Chest
compressions may be applied while
the individual is being recovered,
although cardiac compressions
would be futile without a firm
surface on which to place the
person (Chapter 28: Drowning).
Individuals trapped in avalanches
can sometimes be resuscitated if
they can be recovered promptly
(Chapter 30: Avalanche Injuries).
FOOD ASPIRATION
A common cause of respiratory
obstruction is the aspiration of
food. Prior to the development of
the Heimlich maneuver, a procedure
that usually dislodges impacted
food and was named for its
originator, an estimated 4000
people died each year from this
type of accident just in the United
States. (Approximately 450,000 die
each year from sudden cardiac
arrest.) Alcohol consumption is
commonly associated with such
events. Surprisingly large food
fragments can be impacted in the
larynx and obstruct the passage of
air, usually completely. Since no air
can move through the larynx, the
individual cannot speak, cough, or
breathe, a critical sign of such
obstruction.
While eating, the person
suddenly indicates choking, usually
rises from a sitting position, and—
after a brief struggle—collapses.
Because the food is jammed in the
larynx, the individual cannot speak.
A signal has been devised for the
individual to indicate choking and
consists of thrusting the V between
the thumb and first finger against the
throat (Fig. 3-7).
Figure 3-7. Signal that a person has
choked on aspirated food, cannot
speak, and needs assistance, usually
the Heimlich maneuver
Attempts to dislodge the food by

inserting a finger or a special
device developed for that purpose
through the mouth are rarely
successful and may only force the
food farther down. Pounding on the
back may help and should be tried,
but no more than a few seconds
should be spent this way. Airway
obstruction by aspirated food is a
true emergency, and only three or
four minutes are available to
correct the problem.
The Heimlich maneuver, which
should be learned in a life-support
class, consists of thrusting a hand or
fist into the upper abdomen in such
a way that the diaphragm is
suddenly forced upward. The
abrupt pressure on the diaphragm
forces air out of the lungs and
usually pops the obstructing food
out of the larynx. The food is
commonly ejected completely out of
the person’s mouth. The maneuver
is so effective it can be used to
evacuate aspirated objects that do
not completely obstruct the airway.
A conscious individual can be
stood up. Without delay, the
rescuer’s arms should be extended
around the individual and one fist
placed in the top of the V formed by
the ribs just below the sternum. The
second hand should be placed on
top of the first, and both should be
pulled inward and upward as
sharply as possible (Fig. 3-8).
Several attempts may be required to
expel the food.
When performing the maneuver
in this manner, little pressure should
be placed on the person’s ribs.
(Some is unavoidable.) Squeezing
the ribs does not expel the food;
thrusting against the diaphragm
does. Squeezing the ribs has led to
fractures, in a few cases multiple
fractures, but that is less harmful
than asphyxia by the aspirated food.
If the individual is unconscious
or obese, he should be placed on
his back on the flattest surface that
can be found. The rescuer should
straddle the person (not kneel
beside him) and place both hands,
one on top of the other, on the upper
abdomen just below the sternum.
Pressing downward and toward the
head briskly forces the diaphragm
upward and dislodges the food
(Fig. 3-9).
If the Heimlich maneuver does
not dislodge the food after several
tries, a tracheostomy or
cricothyrotomy must be performed
as quickly as possible. Artificial
respiration through the opening may
be necessary for a short time if the
person has stopped breathing.
However, most poor outcomes have
not resulted from lack of success
with the Heimlich maneuver but
from failure to use it in time to
prevent permanent brain damage.
Figure 3-8. Position for Heimlich
maneuver with the individual standing
Figure 3-9. Position for Heimlich
maneuver with the individual lying
down
SHOCK
Shock is an abnormal physiologic
state caused by inadequate
oxygenation of vital organs.
Adequate oxygen delivery
fundamentally requires the
following:
An effectively pumping heart
Table
Causes of Shock
3-1
Hemorrhagic Shock:
inadequate circulating
blood volume due to
acute blood loss
Neurogenic Shock:
inadequate circulating
blood volume due to
spinal cord paralysis
Cardiogenic Shock:
ineffective heart
pumping due to
mechanical reasons
Septic Shock: due to
overwhelming
infection
Anaphylactic Shock: due
to an overwhelming
allergic reaction
Sufficient circulating blood
volume to transport oxygen
Although shock may be produced
by a number of mechanisms, the
causes likely to be encountered in
the wilderness are summarized in
Table 3-1.
Hemorrhagic Shock
Hemorrhage or acute blood loss
is the most common cause of shock
after injury. The acute blood loss
may be from obvious open wounds
but is more typically the result of
bleeding from internal organs
(Chapter 10: Abdominal Injuries).
The signs of shock depend on the
magnitude of blood loss and the rate
of bleeding. The amount of external
blood loss is usually overestimated,
particularly on snow, whereas rapid
internal bleeding may not be
evident when it occurs in the chest,
abdomen, or pelvis. With
significant reduction of circulating
blood volume, compensatory
mechanisms occur that attempt to
preserve blood flow to vital
organs: Arteries in the skin and
muscle constrict to divert blood to
critical organs, and the heart pumps
at an increased rate to circulate the
blood faster and allow a smaller
volume of blood to carry more
oxygen. At the same time, the rate of
breathing is increased to enhance
the loading of oxygen as blood
transverses the lungs.
The American College of
Surgeons provides a classification
of hemorrhagic shock into
progressive levels I to IV based on
the magnitude of acute blood loss
(Table 3-2). Circulating blood
volume is best estimated by body
weight:
7% x ideal body weight in kg =
approximate blood volume in ml
Thus, a person 6 feet (180 cm)
tall and weighing 175 pounds (80
kg) has a circulating blood volume
of roughly 6000 ml, whereas an
individual 5 feet 2 inches (155 cm)
tall and weighing 110 pounds (50
kg) has a blood volume of about
4000 ml.
Although this classification is
designed to assist in the
management of shock in the
hospital, the relative class of shock
may be helpful to a rescue team to
determine the urgency of
evacuation, such as calling for
helicopter transport or recognizing
the likelihood of death when prompt
evacuation is impossible.
The vital organ affected early by
inadequate oxygen delivery is the
brain. The earliest manifestation of
shock is anxiety, and the most
objective measure of significant
blood loss is a rapid heart rate. An
injured person who is restless with
a sustained heart rate greater than
120 per minute and cool extremities
should be assumed to have life-
threatening acute blood loss. As
compensatory mechanisms fail with
continued blood loss, the injured
person deteriorates from confusion
to lethargy.
Measuring blood pressure with a
blood pressure cuff and a
stethoscope would be one way to
evaluate the severity of shock, but if
this equipment is not available a
rough estimate of blood pressure
can be made by palpating for pulses
at different areas. (Normal blood
pressure is approximately 120
mmHg systolic and 80 mmHg
diastolic.) If a pulse can be felt at
the wrist (radial pulse), the systolic
blood pressure is usually at least 80
mmHg. If the radial pulse cannot be
detected but a pulse can be felt in
the groin (femoral pulse), the
systolic blood pressure is
approximately 70 mmHg. If the
femoral pulse cannot be detected
but a pulse can be felt in a carotid
artery, the systolic blood pressure
is approximately 60 mmHg.
Table Classification of
3-2 Hemorrhagic Shock
Several initial management

principles deserve emphasis.
Treatment of hemorrhagic shock
begins with a complete examination
of the injured person and quick
assessment of the circumstances of
the inciting event. Optimally, the
injured individual should be kept on
the ground where found until a
spine injury can be excluded.
Injured persons, however, may have
to be moved expeditiously from the
potential path of falling rock or an
avalanche for their safety as well as
that of the rescue team. The first
maneuver is to apply direct
pressure to external active bleeding
sites. Extremity tourniquets,
however, are rarely indicated
(Chapter 12: Soft-Tissue Injuries).
The injured individual should be
supine and, if unconscious, the
airway should be assessed. If the
individual manifests signs of
hemorrhagic shock, the feet should
be elevated approximately 12 to 18
inches to empty venous blood from
the legs and maximize the
circulating blood available to vital
organs.
Ultimately, the successful
management of severe hemorrhagic
shock requires evacuation for
treatment at a medical facility.
However, several additional
measures may enhance the chance
for survival. Hypothermia should
be avoided, and body temperature
must be maintained. Wet clothing
should be removed, and extra dry
clothing from the rescue party,
sleeping bags, and blankets should
be used to cover the injured person
completely. An external heat source
should be added in cold conditions
because an individual in shock is
unable to generate heat. Extremity
fractures and dislocations should be
immobilized to minimize additional
blood loss. Pain, particularly from
fractured large bones, may
compromise the individual’s
physiologic compensation to shock
and should be alleviated with
narcotics unless a severe head
injury exists.
Intravenous administration of
opiates is ideal because the onset is
rapid and the dosage can be titrated,
but intramuscular injection is a
reasonable alternative with the
cautions that the effects may be
delayed and dosing must be more
constrained. Supplemental oxygen
by mask should be added when it is
available. Intravenous
administration of saline is key to
restoring circulating blood volume
outside the hospital and should be
instituted when it is available.
Antibiotics should also be given if
either an abdominal injury is
suspected or open soft-tissue
wounds are present.
The timing of evacuation of an
individual with overt hemorrhagic
shock due to chest, abdominal, and
pelvic injuries is not
straightforward. Clearly, immediate
evacuation is rational if the distance
to prompt air transport is relatively
short. Conversely, a long overland
trek of a person with ongoing
bleeding from a liver or spleen
injury or a major pelvic fracture
may prove fatal, whereas
maintaining the individual at the
injury site to permit spontaneous
clot formation may allow safe
delayed evacuation. One of the
authors witnessed this dilemma on
the Western Breech of Mount
Kilimanjaro in 2005. A young
climber was struck by a rock that
fractured his pelvis. He was
reportedly initially conversant but
unable to ambulate. The local
guides fashioned a sling from a tarp
and transported the climber down
the Breech. Unfortunately, over the
ensuing hours, he became
progressively lethargic and then
somnolent from continued bleeding
into his pelvis. Shortly before we
arrived on scene, he suffered a
refractory cardiopulmonary arrest.
We speculate that wrapping the
climber’s pelvis and awaiting
transport on a firm stretcher could
have been life saving.
The decision of when to
evacuate any seriously injured
person should be determined
ideally by radio communication
with a physician.
Cardiogenic Shock/Tension
Pneumothorax
In the wilderness, the most likely
cause of cardiogenic shock—which
is shock resulting from the inability
of the heart to pump blood—is a
punctured lung (pneumothorax)
from a fractured rib. (In urban
surroundings, heart disease of
various types is the most common
cause.) A wound on the surface of
the injured lung can act as a one-
way valve that allows air to enter
the space surrounding the lung
(pleural space) but does not allow
it to escape. If air accumulates
progressively within the pleural
space, the lung of the injured side
collapses and pressure eventually
rises to a point that interferes with
blood traveling through the heart.
This process is termed tension
pneumothorax and requires release
of the abnormal collection of air in
the pleural space. Typically, tension
pneumothorax requires
considerable time to develop.
The injured person initially
complains of shortness of breath,
the breathing rate increases
progressively, and then the heart
rate increases. Ultimately, the
person becomes confused and then
unconscious. Optimally, release of
the air under pressure surrounding
the lung should be done by a health
care provider familiar with the
process but, under desperate
conditions, this could be
accomplished with instruction by
radio. A tube is introduced between
the ribs—tube thoracostomy
(Chapter 9: Chest Injuries)—and
ideally connected to a one-way
valve, which could be fashioned
from the finger of a rubber glove.
Another cause of cardiogenic
shock following trauma is direct
injury of the heart, but such injuries
are nearly always fatal in the
wilderness and no temporizing
interventions other than the general
supportive care for shock are
available.
Neurogenic Shock
Neurogenic shock refers to signs
of shock similar to those observed
with acute blood loss that occurs in
individuals with spinal cord injury
(Table 3-1) manifested by
paraplegia or quadriplegia. The
symptoms are due to a reduction in
oxygen delivery to vital organs
resulting from a greatly expanded
capacity for the individual’s
circulating blood volume, which
occurs because the nerves that
normally constrict the blood vessels
are interrupted and the vessels
dilate.
The initial care for such an
individual parallels that for
hemorrhagic shock, but it is
particularly critical to minimize
motion of the spine because
occasionally paralysis is reversible
(Chapter 8: Head and Neck
Injuries). Elevation of the legs
should be done carefully to avoid
further injury to the spinal cord, but
this maneuver to enhance blood
return to the heart may be
particularly effective for
individuals with neurogenic shock.
If the signs of progressive shock
develop, associated acute blood
loss may be present, which is
critical in considering the timing of
evacuation.
Septic Shock/Infection
Septic shock occurs with
overwhelming infection. The signs
of shock are similar to hemorrhagic
shock, with the notable exception
that the individual invariably has a
high fever and warm extremities.
Septic shock requires considerable
time to develop, but its occurrence
is an ominous sign mandating
immediate evacuation. Antibiotics
should be given according to the
likely site of infection.
Anaphylactic Shock
Anaphylactic shock is caused by
exposure to a substance to which an
individual is allergic, and typically
the offending allergen is contained
in food (Chapter 23: Allergies).
Virtually always, the affected
individual is aware of significant
allergies and has had similar
previous symptoms.
CHAPTER 4
PSYCHOLOGICAL
RESPONSES TO WILDERNESS
ACCIDENTS
Lawrence C. Salvesen, M.D.
Emotional reactions to traumatic

accidents by the people involved
and by their rescuers should be
expected. Most responses are
normal and tend to be consistent.
Many are beneficial; only a few are
harmful. Everyone involved in an
accident can benefit from attention
to their psychological responses.
For some individuals, care for
emotional needs is as essential as
care for physical needs if they are
to return to a functioning role in
society.
PSYCHOLOGICAL
RESPONSES OF RESCUERS
Psychological reactions by first
responders have been well
recognized by police, fire, and
emergency medical services. Many
have professional counselors on
their staffs or on call to help with
such reactions. In most situations,
such aid is provided for
humanitarian reasons. However,
financial considerations alone
would justify counseling because
individuals leave their jobs when
the cumulative response to
psychological trauma becomes
overwhelming and training
replacements is expensive.
The potential magnitude of
personnel losses was dramatically
illustrated by the response to the
crash of American Airlines Flight
191 in 1979. This wide-bodied jet,
a DC-10, lost the hydraulic system
in one wing when the engine on that
side pulled loose from its mounting
during takeoff. The flap on that side
retracted, and the aircraft rolled,
inverted, and crashed. None of the
271 passengers and crew survived,
and two people on the ground were
killed. The city of Chicago had
staged a rescue drill only two
weeks before this accident, and 351
rescuers were at the scene within
twenty minutes. Experiencing
hundreds of mutilated bodies was
devastating for these responders,
but no program to alleviate the
emotional impact had been
established. One year later, 275 of
those individuals had left their
positions for jobs that did not
involve rescue!
Wilderness rescuers also
respond psychologically to
accidents, and their reactions
require attention, but this need has
not been as well recognized as the
needs of police, fire, and
ambulance service members. Such
problems, labeled “rescue trauma,”
are well known to many rescuers,
but few discuss them with their
colleagues, possibly from fear of
appearing unmanly or even
unbalanced.
Case Study: Rescuer’s Responses

A professional rescuer was on a
Himalayan trek with a close friend
who became seriously ill and
clearly needed to be evacuated. The
leader decided to split the party,
most continuing to their objective,
while the rescuer and two
physicians stayed behind with the
person who was ill. After the main
party had moved on, the ill person’s
condition deteriorated
catastrophically, and over a period
of days the three rescuers worked
virtually to the point of exhaustion
to save him.
During this ordeal, the rescuer
became aware of several strong
feelings. He found that attending to
a close friend aggravated normal
feelings of inadequacy and guilt,
particularly guilt for not having
more forcefully cautioned the
person before he became so ill. He
also felt guilt for not having resisted
more vigorously the decision to
split the party, which left the person
who was ill with a support team
barely able to provide for his care.
In retrospect, the rescuer
realized that he had deferred to the
leader, despite his own
considerable judgment and
experience, because the leader was
a physician. During and after the
subsequent vigil, the rescuer began
to question his confidence in the
leader, in his associates, in himself,
and even in the categories of people
(doctors) who were members of the
rescue group. His confidence was
further eroded following reuniting
of the party when people he
considered significant acted like
nothing had happened.
The rescuer kept these feelings
hidden for some time, not realizing
that others were experiencing the
same emotions. Only months later,
when he made an offhand comment
that he was considering dropping
out of the group, did he have an
opportunity to share his pain and
begin to reconstruct relationships.
Since then he has made a variety of
recommendations, particularly that
the emotional residue of stressful
situations be discharged through
debriefings.
He also observed that even
though support from associates is
helpful, in the long run the benefits
fade unless rescuers recognize the
value of their efforts and learn from
their mistakes, rather than
wallowing in destructive self-
criticism. To grow, everyone must
accept responsibility for their
actions, both good and bad.
Dissociation
Performing well in rescue
situations requires a high level of
objectivity. The rescuer’s emotional
response to those involved in an
accident and to their injuries must
not interfere with caring for them.
To maintain objectivity, most
rescuers dissociate, or split, their
intellect from their feelings, and
deny, or block out, the emotional
shock of the events surrounding
them. Such defensive dissociation
or splitting is effective but cannot
be kept up indefinitely. Eventually
rescuers develop symptoms of
decompensation—the inability to
maintain defense mechanisms in
response to stress—which results in
personality disturbances or
psychological imbalance.
Symptoms of decompensation
are highly variable. Some rescuers
become withdrawn and appear
dazed, apathetic, forgetful, or tired.
Others are open and expressive but
become irritable, irrational,
destructive, or violent. Some shut
off their feelings and become less
able to experience intimacy with
their families and friends. Some
become increasingly reliant on
alcohol or other drugs.
Overload may come on
suddenly, particularly after a major
disaster that produces many
casualties with mutilating injuries,
or it may come on insidiously from
the accumulated stress of a series of
less distressing accidents. A
rescuer’s susceptibility to overload,
termed rescue trauma threshold,
may change from day to day as the
result of events or circumstances
entirely unrelated to the rescue,
such as poor health, family
problems, or insufficient sleep.
Sources of Rescue Stress

The many causes of rescue stress
are interrelated, but they can be
categorized as overt and covert.
Overt sources of stress are
immediately related to the accident.
Sights or smells at the scene may
assail the senses. The person to be
rescued may be dead or may die
during the rescue. Rescue
equipment may be inadequate. The
available personnel may be
insufficient in number or lacking in
knowledge and ability, resulting in
great demands being placed on a
few people. Wilderness accident
casualties frequently must be
evacuated over miles of difficult
and dangerous terrain, often at
night, which requires hours of
exhausting labor. (For example,
rescues require an average of
twelve hours in the White
Mountains of New England; they
can require days in more remote
areas when helicopters are not
available.)
Covert sources of stress include
fatigue or illness that may weaken
rescuers. They may be preoccupied
with financial, legal, or family
problems. The attitude of other
participants can be stressful.
Rescuers with high expectations of
success at the start of an operation
may be frustrated by the death of
one or more of the people involved
in the accident, by their or their
coworkers’ fallibility, or by lack of
appreciation for their work,
including inaccurate, critical, or
even censorious reports in the
media.
Another source of stress is the
enforced inactivity a portion of the
rescue team experiences after
arriving at an accident scene. Many
stretcher bearers are required to
carry a loaded litter through
difficult terrain, but only a few can
administer medical treatment.
While the rest wait, their energy
and enthusiasm ebb. Some sink so
low they need to have their morale
boosted by others if they are to
participate enthusiastically in
evacuating the individual. The
stress of this middle period in a
rescue is often overlooked and
appears to result from feeling
unneeded, from fatigue, and
sometimes from newness of the
rescue experience.
Normal Reactions to Stress

Totally normal reactions to
stress may be immediate or
delayed. Immediate reactions that
occur among rescuers at the
accident site include anxiety and
apprehension, doubts about their
abilities, or hopelessness and
despair, which are often mixed with
denial or splitting. Some rescuers
experience cognitive difficulties,
forgetting where they put things and
finding decisions hard to make. All
these reactions are normal.
Rescuers in all types of incidents
report nausea, a pounding sensation
in their hearts, muscle tremors,
cramps, profuse sweating, chills,
headaches, and muffled hearing.
These symptoms tend to dissipate
within one to three days, but if the
underlying emotions are not
recognized and allowed to surface
within a reasonably short period of
time, they eventually work their
way into rescuers’ daily lives and
can cripple them emotionally,
cognitively, and physically.
Delayed stress reactions appear
hours to weeks—sometimes months
to years—after an accident and may
be directed inward or outward.
Inward reactions include
depression, apathy, or feelings of
guilt for not helping or for further
injuring the individual. Nightmares,
insomnia, or occasional visual
flashbacks or physical symptoms
such as headache, loss of appetite,
or nausea may be experienced.
Outward reactions typically include
irritability, explosiveness, and in
some cases anger with others who
contributed to the stress of the
incident, particularly with the press
for inaccurate or distorted
reporting. Like immediate stress
reactions, these delayed reactions
are entirely normal.
Preventing Adverse Stress

Reactions
Rescuers, whether amateurs or
professionals, must be emotionally
prepared for the worst casualties—
the mutilated, dying, or dead—and
for the worst situations. Watching
helplessly while individuals
involved in accidents die because
they are inaccessible, equipment is
inadequate, or they just do not
respond to the best possible
medical care is a devastating
experience. In preparing for the
worst, participants must be aware
of their limitations and must
balance their expectations with
reality.
Rescuers must be prepared to
serve under leaders who do not
have time for explanations or who
are not aware of the needs of their
crew members. They must expect
sparse recognition and abundant
criticism, and they should not be
surprised when rescue work turns
out to be 90 percent drudgery and
10 percent terror.
Despite training and experience,
rescuers must withdraw from
situations they find particularly
stressful, such as accidents that
involve family or friends, injuries
to children who are similar to their
own children, and some specific
injuries. The leader and associates,
as well as rescuers, must respect
such sensitivity.
Rescuers must realize that stress
overload is virtually inevitable,
regardless of training and
experience, if sharing it with others
does not relieve accumulated
emotional stress. To ensure the
emotional health of rescuers,
established preventive or
therapeutic measures are essential.
The following is one example:
Within twenty-four hours after a
rescue, team members should
engage in vigorous exercise to
relieve tension and achieve greater
muscular relaxation.
Within twenty-four to seventy-
two hours after a stressful rescue, a
mandatory emotional debriefing
should be held for the entire team.
(Making such sessions routine
instead of mandatory reduces the
obligatory aspect of participation.)
Effective sessions require an hour
or more and promote expression
and sharing of emotional reactions
to the rescue—specifically the pain,
sadness, terror, guilt, or feelings of
helplessness experienced by each in
different ways. These emotions
must be expressed and accepted
without shame or embarrassment.
The participants must share their
humanity and support each other.
After debriefing, rescuers must
eat and rest well, rounding out the
recovery of the entire organism.
Only after physical and
emotional recovery has been
ensured should the rescue team
critique the rescue objectively,
learning from successes as well as
mistakes, and plan for the future.
The debriefing session must be
entirely nonjudgmental. There can
be no right or wrong, correct or
incorrect, as long as emotions did
not interfere with the rescue. To
ensure absolute confidentiality, no
records should be kept.
Although some groups can
manage this process quite well by
themselves, particularly if they have
gone through it a number of times,
such exercises frequently are more
effective when guided by someone
experienced in stress management
and not directly involved in the
rescue. Completely resolving the
stress may require more than one
meeting, but all meetings should be
conducted as close to the event as
possible, preferably within three
days. Delays of a week or more
increase the risk of converting
early, tenuous emotional reactions
into entrenched, chronic disorders.
The debriefing must be conducted
without alcohol or other drugs; to
maximize the benefits, the minds of
all must be fully functional.
POSTTRAUMATIC STRESS
DISORDER
If rescuers do not work through
their normal reactions, they risk
developing a more severe
abnormality, posttraumatic stress
disorder (PTSD). This condition
has been repeatedly described and,
depending on its origin, has been
given widely varying names that
include shell shock and combat
fatigue. The term posttraumatic
stress disorder unites these
conditions under one label. This
condition has been recognized with
surprising frequency in veterans of
the Iraq War.
The following are the features of
PTSD:
1. The individual has undergone a
recognizable stressful experience
that would evoke significant
symptoms of distress in almost
everyone.
2. The individual reexperiences the
event in one or more ways:
Recurrent and intrusive
recollections
Recurrent dreams of the event
Sudden acting or feeling as if
the traumatic event were
recurring due to the stimulus
of an environment or thought
associated with the event
3. The individual has numbed
responsiveness to or reduced
involvement with the external
world that began some time after
the event and is manifested by
one or more of the following:
Markedly diminished interest
in one or more significant
activities
Feeling of detachment or
estrangement from others
Constricted affect
4. The individual usually has two
or more of the following
symptoms that were not present
before the event:
Hyperalertness or exaggerated
“startle” response
Sleep disturbances
Guilt about surviving when
others have not, or about the
behavior required for survival
Memory impairment or
difficulty concentrating
Avoidance of activities that
arouse recollections of the
traumatic event
Intensification of symptoms by
exposure to events that
symbolize or resemble the
traumatic event
Diagnostic studies suggest that
with sufficient unrelieved stress,
anyone would develop PTSD.
Vietnam veterans who developed
this disorder shared five
characteristics that correlate with
experiences of wilderness rescuers
(Table 4-1).
Treating PTSD is the province of
professional therapists. However,
the earlier the disorder is
recognized, the faster and more
successful is the outcome.
Recognizing stressful events, taking
measures to relieve the emotional
pressures they engender, and
recognizing the symptoms of
emotional disorders are certainly
within the abilities of rescuers and
their friends and should be the
responsibility of their leaders.
Stress Sources for Vietnam

Table Veterans and Wilderness
4-1 Rescuers
VIETNAM WILDERNESS
VETERANS RESCUERS
A positive
attitude toward
Unrealistic
the war before
expectations
engaging in
combat
A high level of
exposure to
A high level of hazardous terrain
combat exposure or weather, and
to massive
trauma
Immediate Infrequent
separation from opportunities to
the military share emotional
service upon experiences;
returning to the “suffering in
United States silence”
A negative
perception of
Lack of support
family
or appreciation
helpfulness upon
returning home
Feeling that
uncontrollable
factors such as
weather, timing,
inadequate
A feeling that personnel or
forces beyond equipment,
their control were communication
directing the failures, or
course of their accidents
life involving
members of the
rescue group
have determined
the outcome of
the rescue
PSYCHOLOGICAL
RESPONSES OF ACCIDENT
VICTIMS
The emotional responses of people
involved in accidents are similar to
the bereavement or grief that
follows loss of a loved one.
Because many more individuals
have experienced grief than have
been involved in wilderness
accidents, the emotional reactions
to such events may be more
understandable when compared
with grief reactions. This
comparison also demonstrates that
most psychological reactions to
accidents are normal, even though
they may seem abnormal to
individuals who have not
experienced such phenomena.
Grief Reactions
The period of mourning that
follows loss of a loved one can be
lengthy and painful, but if grief is
worked through appropriately,
survivors reconcile themselves to
the loss and resume their lives. Like
other emotional states, bereavement
is more easily resolved when
shared with others.
Grief evolves through several
stages, and the boundary between
normal and abnormal is often
blurred (Fig. 4-1). Bereaved
persons commonly display
attitudes, beliefs, and behavior that
smack of irrationality. Stunned
shock and denial characterize the
first stage of this emotional
response, which has been labeled
the protest phase: “He can’t be
dead!” Anger commonly follows
and may be directed illogically at
the person or circumstance that
caused the loss, at the deceased, or
at oneself for not having prevented
the loss, or even for surviving. The
bereaved frequently manifest
emotional pain by crying,
weakness, loss of appetite, nausea,
or sleep disturbances. Survivors
may search for their loved ones or
mementos of their loved ones.
After days or weeks, bereaved
individuals move into a stage
dominated by despair. They
experience anguish, grief, and
depression; think slowly; display
emotional pain; and continue to
search for loved ones and
remembrances of them. After weeks
or months, they move slowly into
the detachment stage, during which
they lose interest in life and want to
withdraw and give up. They appear
bland, lack spontaneity and social
energy and exhibit robotic or
zombielike behaviors.
Figure 4-1. Diagram of reaction cycle
associated with grief 1
Normally the cycle of protest,

despair, and detachment takes six to
eighteen months. The bereaved
finally work through their loss, say
their final good-byes, and
restructure their lives and
personalities, reconciled with their
loss.
Stress Imposed by an Accident

The normal emotional state of an
individual involved in any sudden,
unpredictable, and overwhelming
crisis is similar to an acute grief
state. If the incident is traumatic, the
overwhelming emotion results from
experiencing the possibility of
death and fearing for one’s life. An
accompanying sense of
helplessness, of having lost control
over survival, adds to the impact.
Individuals often are aware of
seeking to escape and of being
weak, vulnerable, and helpless.
Their self-esteem and sense of
competence have been assaulted,
and they see themselves as unable
to keep out of harm’s way or as
having acted with poor judgment.
Hours to weeks after the incident
—depending upon the individual
and the nature of the incident—the
people involved are subjected to
secondary stresses such as the
prospect of being immobilized and
isolated without food or shelter, the
prospect of being totally dependent
upon strangers for rescue, or the
more distant prospect of not being
able to go back to work or to other
valued activities.
Responses of Accident Victims

During accidents, one-eighth to
one-fourth of the people involved
react effectively. They are often too
busy to worry. About three-fourths
are stunned and bewildered. They
show no emotion, are inactive or
indecisive, and are usually docile.
They may be totally unresponsive
or behave in an automatic, robotlike
manner. Manifestations of fear such
as sweating, palpitations, tunnel
vision, or a dry mouth may be
present. This type of reaction is
known as psychological shock but
should not be considered an
abnormal reaction. A final one-
eighth to one-fourth of people
involved in accidents react
inappropriately with incapacitating
anxiety or hysteria.
Immediately after an accident,
responses that are similar to the
stages of the grief reaction occur.
During the stage of protest or
denial, the person may not be able
to deny that a problem exists but
refuses to admit the magnitude of
the problem. The problem is
understood intellectually but not
emotionally, and the individual is
blasé and unconcerned.
Some individuals are stunned
and confused; others are vigilant
and cool. Some are emotionally
expressive, displaying anxiety,
anger, sobbing, a sense of relief, or
a tendency to blame others. Others
are controlled, exhibit little
distress, and appear composed.
Both behaviors reflect denial and
emotional exhaustion or shock. Both
reactions are normal, but
individuals need acceptance of their
responses and assurance that they
are normal. People may be
vulnerable to damaged self-esteem
if they perceive their behavior as
inadequate or abnormal.
Some people may say “This will
hit me later.” They should be
reassured (or informed) that indeed
it will hit them later and that
emotional responses may require
time and talking out.
During the stage corresponding
to the despair phase of the grief
reaction, 90 percent of the
individuals involved in accidents
become aware of problems but
regard them as overwhelming and
unbearable. Tightening of muscles,
sweating, restlessness, difficulty in
speaking, sadness and weeping,
irritability and anger, or passive
dependency and childlike behavior
are manifestations of strong
emotions. Some persons develop a
zombielike gaze, staring ahead
blankly. Many need to tell and retell
the experience.
During the stage corresponding
to the detachment phase of the grief
reaction, individuals begin to return
to normal, accept their problems,
and make efforts to solve them.
They are more hopeful and
confident, and emotions from the
second stage are less intense.
The final phase of a disaster
takes place six to twelve months
after the incident and may consist of
a lifetime of personal and social
aftereffects of the incident.
The normal reaction after
recovery from an accident is to
return to normal activities. A sense
of well-being returns, and
individuals are able to make
decisions and act on them. Grief
that was encountered is successfully
worked through. Many survivors
develop altered attitudes toward
life and death and display a definite
philosophical mellowing and
growth.
Abnormal reactions occur
occasionally and have been labeled
the “delayed stress syndrome.” The
characteristics of this disorder are
PTSD, psychosomatic or physical
illness, depression, proneness to
accidents, accidental death, or
suicide. People often need
professional counseling to work out
the problems of this syndrome.
However, proper emotional support
during rescue can significantly
reduce the severity of such
disorders or prevent them
altogether.
Abnormal Responses to Accidents

Abnormal psychological
reactions to accidents may affect
four functional areas:
Orientation to time, place, and
person
Observable motor and physical
acts
Verbal behavior
Emotional or affective
expression
Since typical abnormal behavior
patterns are rather easily
recognized, they are outlined
without further discussion.
ORIENTATION
Mild Derangement (adequately
aware of time, place, events, and
person)
Dazed, confused
Minor difficulty understanding
what is being said
Minor difficulty thinking clearly
or concentrating
Slow or delayed reactions
Severe Derangement (confused

about time, place, events, and
person, but may gradually
respond to information and
reassurance, unlike individuals
with brain trauma, which must be
considered)
Forgetful of own name and
names of associates
Unclear about date—year or
month
Unable to clearly describe the
location
Unable to recall clearly events
of the previous twenty-four
hours
Regresses to an earlier period of
life
Complains about memory gaps
of thirty minutes or more
Confused about identity or
occupation
Appears unaware of what is
happening
MOTOR BEHAVIOR
Mild Derangement
Wringing hands or clinching
fists; stiff and rigid appearance;
continuously sad expression
Some restlessness; mild
agitation and excitement
Difficulty falling asleep or
keeping down food
Rushing about trying to do many
things at once but accomplishing
little
Feelings of fatigue inconsistent
with previous and current
activity
Halting or rapid speech that is
out of character; difficulty
getting words out
Severe Derangement
Agitated movements; inability to
sleep or rest quietly
Grimacing or posturing of recent
onset
Markedly reduced activity; sits
and stares; remains immobile
for hours
Incontinence
Mutilation of self or objects for
no reason
Repeated ritualistic acts of no
functional significance; attempts
to prevent the acts create
resistance and excessive
emotion
Excessive use of drugs or
alcohol
Inability to carry out simple
functions such as eating,
dressing, organizing equipment
VERBAL BEHAVIOR
Mild Derangement
Verbalizes hopelessness: “It’s no
use,” “I can’t go on”
Incapable of making a decision
Doubts ability to recover
Overly concerned with small
things and neglectful of more
pressing, major problems
Denies any problems;
overconfident; rejects offers of
assistance
Blames the problems on others
Has difficulty making plans or
discussing future actions
Severe Derangement
Hallucinations, auditory or
visual, unverifiable by others
Verbalizes fear of losing mind;
claims the world seems
unrecognizable and unreal;
claims body feels unreal and
completely different
Preoccupied with an event or
idea to the exclusion of anything
else
Unrealistic claims that an
agency, object, group, or spirit
intends to cause harm to self and
to others, such as family or
friends
Expresses inability to make a
decision to carry out familiar
activities
Expresses a real fear of killing
or harming self or others; far
exceeds simple statement of
anger or hopelessness
EMOTIONAL EXPRESSION
Mild Derangement (significantly
different from most individuals
but largely appropriate to
situation)
Frequent uncontrolled tearing
and weeping; rehashing of
traumatic events
Blunted expression of feelings;
apathetic; seemingly withdrawn
emotionally and unable to react
with feeling to what is
happening
Unusual laughter and gaiety
Overly irritable; quick to get
angry over trivia
Severe Derangement (markedly
unusual affect or emotion)
Excessively flat emotionally;
virtually no expression of
feeling
Excessive emotional expression;
inappropriate joy, anger, fear, or
sadness for situation
Trauma or Disease Simulating

Psychological Abnormalities
A number of disorders,
particularly those that cause
hypoxia or metabolic derangements,
produce abnormal behavior that
simulates abnormal psychological
reactions. Hypoxia is common and
results from altitude, but it is also
produced by pneumonia, chest
injuries, shock, and other disorders.
Hypothermia typically produces
changes ranging from forgetfulness
and slow thought processes, through
loss of coordination and greater
mental dullness, to irrationality, and
finally coma. Hyperthermia can
cause headache, irritability,
agitation, and mental dullness
before progressing to stupor and
coma. Hypoglycemia produces
restlessness, irritability, lethargy,
poor judgment, agitation,
disorientation, and finally coma.
Severe hypoglycemia is almost
always a complication of diabetes,
but milder glucose depletion occurs
in normal individuals who are
exhausted and have not maintained
an adequate food intake.
Dehydration can produce similar
abnormalities.
Head injuries may result in
immediate or delayed changes that
include drowsiness, apathy, and
irritability; disorientation;
forgetfulness and wandering off;
bizarre behavior, including
homicidal or suicidal mania; or
convulsions and finally
unconsciousness. Signs such as
unequal pupils or abnormal reflexes
may be present. Severe infections
of the nervous system can produce
such signs, as can pneumonia or
severe generalized infections.
Intoxication by drugs (including
alcohol) or drug withdrawal
(particularly from alcohol and
sedatives) can have similar effects.
Generally, personality changes
such as silliness, irritability,
agitation, belligerence, and lethargy
occur first. Loss of cognitive
functions, which progresses from
mild mental dullness through
disorientation to time, place, and
person (despite frequent
reminders), loss of calculating
ability and specialized knowledge,
to loss of judgment and memory
appear next. Eventually, obvious
confusion supervenes with anxiety
or hallucinations and may be
associated with staggering and
slurred speech, tremors,
convulsions, and unconsciousness
progressing to deep coma and
eventual death.
If sedation is essential for
evacuating a person whose
behavior is uncontrollable, an
antipsychotic with sedating
properties such as haloperidol
(Haldol®) is preferable. These
drugs do not depress respiration.
Small doses of benzodiazepines
such as diazepam (Valium®) can
also be used, but these medications
suppress breathing in higher doses.
Opiates complicate the neurologic
abnormalities, depress respiration,
and should be avoided.
Psychological Aid for Accident

Victims
Persons injured in an accident,
uninjured members of the party, and
rescuers must cope with the
reactions at the scene of the
accident or during evacuation.
Assistance provided at that time can
greatly diminish emotional
aftereffects. Rescue leaders and
their crew members must be
prepared to provide as much
psychological help as possible with
constructive, understanding
listening.
The essence of psychological
care is listening effectively and
creatively. Individuals must be
allowed to express their feelings
openly and freely; counselors must
understand that such expression is
the major purpose of the
conversation. Counselors cannot
judge what the persons should feel,
and they certainly must not express
or otherwise convey an opinion.
Counselors must look directly at the
person who is speaking, giving their
complete attention, and asking
questions or paraphrasing
statements only to emphasize their
attentiveness or to make certain they
fully understand what is being said.
Preferably, counselors should be
the same gender as the injured
persons. They should remain in
constant contact and should be the
person who remains by the
individual’s head throughout the
evacuation to listen and offer
encouragement and counseling.
The following are some goals
for rescue leaders and counselors:
To create acceptance of an
injured person’s feelings as
normal reactions to stress
To reduce feelings of guilt by not
assessing blame for the accident
To reduce panic and rage
To allow ventilation of feelings
and to accept them
To give realistic, honest answers
balanced with judicious
omissions
To be aware of the special needs
due to the person’s sex when
immobilized and dependent (as
on a litter)
To restore a feeling of well-
being with food and water,
warmth, attention to injuries,
physical restraint when
necessary, analgesia when
indicated, and comfort and
support through listening and
touching
To restore a sense of hope and of
belonging through quiet, firm,
and knowledgeable leadership
with clearly understood goals
and sensitivity to the needs of
injured or ill individuals and
their rescuers
To maintain awareness that
supposedly unconscious
individuals often hear some of
what is said around them
People’s self-esteem and sense
of mastery are also based on
their judgment of how well they
respond to problem situations.
Success heightens self-esteem;
failure lowers it. The rescuer
must constantly seek ways to
help persons involved in an
accident preserve their dignity,
particularly by helping in the
rescue operation. Participation
is essential for restoring and
preserving self-esteem and a
sense of mastery and control and
for minimizing psychic trauma,
guilt reactions, and delayed
stress reactions. Rescue leaders
must be aware of this need and
do all they can to ensure it is
met.
Some attitudes or actions rescue
leaders and counselors must try to
avoid are these:
Callousness or flippancy (the
“M*A*S*H syndrome”)
Lying to provide unrealistic
optimism and reassurance
Talking around a person without
talking to the person
Telling the person how to feel or
imposing ideas; not really
listening (authoritarian style)
Expecting a person to function at
top level too quickly
Expecting too little of a person,
damaging chances to salvage
self-esteem
Oversolicitousness that
interferes with a person’s
recovery of self-esteem
(“chicken soup” style)
“Democratic” leader(less)ship;
floundering by committee, with
no definitive leader, goals, plans
for achieving them, or
communication within the party
Case Study:
Injured Person’s Responses
Some insights into the
psychology of individuals involved
in accidents and helpful
recommendations for rescuers were
made by Ray Smutek, editor of Off
Belay, in his account of his own
mountaineering accident and rescue.
When describing his fall he recalls
“accelerated mental activity, the
detached over-view of the situation,
the recollection of past events.
Most amazing was the absence of
pain, coupled with a very acute
awareness of the damage being
done.”2
He observes that potentially the
most dangerous stage of an accident
is immediately afterward, “not
necessarily to the victim …. I think
the natural tendency in a situation
like this is to rush to the victim,
perhaps unbelayed. Action! Do
something! Don’t just stand there!”
But Smutek continues, “this is not
the time to rush; few situations
require that immediate an action.
There is only one thing that you
should do immediately and that is to
think.”
He describes directing his
immediate rescue and first aid to
the extent that he was conscious and
able to state what his injuries were
and what he was capable of doing.
Further into the article he writes
that the long wait for rescue
“psychologically was the worst part
of the entire episode. There was
nothing to do but worry.” He was
very happy to have the company of
a fellow climber and thinks
everyone in a similar situation
should have an “official comforter.”
When rescue did come, some of
the rescuers were “over their
heads,” and Smutek states, “nothing
is more devastating to a person’s
morale than an obviously
incompetent rescuer.” Finally, he
reports that administration of a
painkiller muddled his mind and
increased his anxiety because he
could not understand the procedures
to which he was being subjected.
He feels that rescuers should use
pain medication on a highly
selective basis, particularly if that
medication may interfere with a
person’s need to feel in control and
be aware of what is happening.
These feelings clearly reflect
Smutek’s need to maintain a sense
of self-efficacy. On the other hand,
some people are not used to being
in control and may be more
comfortable being medicated or
being told that everything is being
cared for.
Case Study:
Injured Person’s Responses
In The Breach, Rob Taylor
traces the various phases of his
devastating accident on
Kilimanjaro, his almost miraculous
rescue, his prolonged recovery, and
his reactions to them. Following a
fall in which he suffered a severe
compound fracture of his lower leg,
he subsequently descended a
perilously steep snow slope on his
own and survived a solitary,
exposed, life-threatening bivouac
that lasted several days. During this
ordeal his thoughts and behavior
were strikingly organized. His self-
control becomes more
understandable with these words:
“Unrestrained emotions and
unbridled feelings in the end, after
the fact, are fine, but during the
crisis they are illusory defenses.” 3
Nonetheless, while on the
mountain Taylor experienced grief
over the loss symbolized by the
injury to his leg. He also felt
anguish over the days of waiting for
the unknown but was preparing for
and accepting the worst. He writes
of “the need to re-live the event”
during his recovery and of
becoming “daily more aware of the
positive aspects of the pilgrimage
… and (of a) renewal of a
reverence and deep appreciation of
the gift of life.” Finally, he tells of a
heightened sense of self-definition,
of altering his concept of death, and
of coming to realize that he “must
make the most of each encounter,
each meeting” as a result of his
experience.
Taylor recommends to rescuers
the therapeutic use of concern,
small talk, encouragement, and
infectious optimism.
SELECTION OF RESCUERS
Physical condition, interest, and
enthusiasm alone are not adequate
qualifications for wilderness
rescuers. In addition to technical
expertise and support persons who
are the same gender as the
individuals involved in the
accident, members of rescue teams
should have the following
characteristics:
A reasonable personality that is
not excitable, impulsive, or
prone to harbor anger
The ability to initiate actions
The ability to cooperatively
follow others
Attentiveness to details of
procedure and equipment
A sense of humor
Empathy; ability to feel for
another’s plight without being
overwhelmed
Optimism, although prepared for
the worst
The ability to minimize or
shelve worry or fear and yet be
able to accept those feelings as
normal several days. During this
ordeal his thoughts and
____________
REFERENCES
1. Lamers, W. Death, Dying
and Bereavement. Symposium,
Stockholm, Sweden. 20 June 1982.
(Reproduced by permission.)
2. Smutek, R. Good morning,
I’m your guest victim for today. Off
Belay, February 1978. (Quoted by
publisher.)
3. Taylor, R. The Breach:
Kilimanjaro and the Conquest of
Self. New York, Coward, McCann,
and Geoghegan, 1981. (Quoted by
publisher.)
CHAPTER 5
IMMUNIZATIONS
In developing countries, infections

are a constant threat. Preventing
illnesses in wilderness areas,
where disease is coupled with
inaccessibility, has obvious
advantages. Immunization is the
easiest and most reliable method
for preventing infections. Only a
limited number of effective
vaccines are available, but those
that are only partially effective can
significantly reduce the likelihood
of infection and lessen the impact
should infection occur. (The
immunologic principles upon which
immunizations are based are
discussed in Chapter 23: Allergies.
The prevention of malaria and some
other infections for which
immunization is not possible is
considered in Chapter 22:
Infections.)
SOURCES OF UP-TO-DATE
INFORMATION
Recommendations for immunization
change frequently. The U.S.
Department of Health and Human
Services’ Centers for Disease
Control and Prevention (CDC)
maintains very complete
information about all aspects of
immunization at www.cdc.gov.
The International Association for
Medical Assistance to Travelers
(IAMAT; www.iamat.org) is a
volunteer organization of health
care centers and physicians that
provides travelers with access to
physicians who speak English or
French and who meet IAMAT’s
standards, which are similar to U.S.
medical licensing standards.
Membership in IAMAT and a
directory of its affiliated institutions
in more than 115 countries are free.
The organization offers a number of
free publications, including
informational pamphlets on malaria,
schistosomiasis, and Chagas’
disease, and its World Immunization
Chart lists the potential risk for
over a dozen infections, country by
country, in a quick reference format.
The address of the U.S. affiliate is
IAMAT, 736 Center Street,
Lewiston, NY 14092.
Travel medicine clinics not only
provide up-todate recommendations
about immunizations for travelers
but also usually have the vaccines
available along with a staff to
administer them. The International
Society of Travel Medicine
maintains a list of travel medicine
clinics and their addresses at
www.istm.org.
The yellow International
Certificate of Vaccination or
Prophylaxis is the best way to
record immunizations and is
required for entrance into a number
of countries. The current form has
been in use since December 15,
2007, and must be used to document
yellow fever vaccinations.
However, the old form is
acceptable as documentation of
yellow fever until it expires ten
years after the date of vaccination.
SCHEDULING
IMMUNIZATIONS
Months of planning and preparation
usually precede foreign travel.
Immunizations are a critical part of
such preparations and must not be
put off until the last minute. Starting
immunizations six months in
advance is not only entirely
appropriate but is necessary for
immunizations such as hepatitis A
that require two injections six
months apart.
Vaccinations for diptheria,
tetanus, pertussis (whooping
cough), measles, mumps, rubella
(German measles), varicella
(chicken pox), poliomyelitis,
hepatitis B, Haemophilus
influenzae type b, and pneumococal
disease are routinely administered
in the United States, mostly in
childhood. If travelers do not have
a history of adequate protection
against these diseases,
immunizations appropriate to their
age and previous immunization
status should be obtained, whether
or not international travel is
planned.
The CDC advises that “All
commonly used vaccines can safely
and effectively be given
simultaneously … without
impairing antibody responses or
increasing rates of adverse
reactions”
(www.cdc.gov/travel/yellowBookCh
GenRecVaccination.aspx). In
general, inactivated (killed-virus)
vaccines may be administered
simultaneously at separate sites.
However, when vaccines commonly
associated with local or systemic
reactions are given simultaneously,
reactions can be accentuated.
Simultaneous administration of
acellular pertussis (DTaP—
diphtheria, tetanus, and whooping
cough); inactivated poliovirus;
Haemophilus influenzae type b;
measles, mumps, and rubella
(MMR); varicella; pneumococcal
conjugate; and hepatitis B vaccines
is encouraged for persons who are
the recommended age to receive
these vaccines and for whom no
contraindications exist.
Yellow fever vaccine may be
administered simultaneously with
all other currently available
vaccines. Limited data suggest that
the immunogenicity and safety of
Japanese encephalitis (JE) vaccine
are not compromised by
simultaneous administration with
pertussis vaccine. No data are
available on the effect of concurrent
administration of other vaccines,
drugs such as chloroquine or
mefloquine, or biologicals on the
safety and immunogenicity of JE
vaccine.
Inactivated vaccines generally
do not interfere with the immune
response to other inactivated or
attenuated live-virus vaccines. An
inactivated vaccine may be given
either simultaneously or at any time
before or after a different
inactivated vaccine or a live-virus
vaccine.
However, the immune response
to a live-virus vaccine such as
MMR, varicella, or yellow fever
might be impaired if administered
within twentyeight days of another
live-virus vaccine. Whenever
possible, injected live-virus
vaccines administered on different
days should be given at least
twentyeight days apart. If two
injected live-virus vaccines are not
administered on the same day but
less than twenty-eight days apart,
the second vaccine should be
readministered at least four weeks
later.
Viral vaccines, including
hepatitis A and B, and toxoid for
tetanus and diphtheria can be given
six months or more before
departure because such
immunizations persist for years.
Bacterial immunizations such as
typhoid fever are not as enduring
and should be given closer to the
date of departure.
Immune globulin is not routinely
administered because effective
vaccines for hepatitis A are now
available.
TRAVELING WITH CHILDREN
For travel to developing countries,

children should be up-to-date with
all routine childhood vaccinations,
particularly when they can be
expected to have contact with local
children and local caretakers.
Travel-related time constraints may
require infants and young children
to have vaccinations at earlier than
optimum ages. The intervals
between doses may have to be
shortened, and receiving only one
or two doses of a three-part
immunization schedule may be
possible before departure. Such
modifications usually decrease the
immune response and additional
vaccinations must be given later,
usually six to twelve months later
(which causes no known untoward
effects). Generally, immunizations
given at an age earlier than
recommended should not be
counted toward long-term immunity.
Children probably should
receive preexposure rabies vaccine
if they are to visit developing
countries where rabies is endemic.
One-half of all rabies deaths are in
children fifteen years old or
younger. Children are attracted to
animals, are more likely to suffer
bites, and may not report minor
bites and scratches. (Preexposure
rabies vaccination does not
eliminate the need for proper
wound care and additional
vaccination after an animal bite. It
does eliminate the need for
administration of immune globulin,
which is in severely short supply
worldwide.)
Hepatitis A is not routinely given
to children less than one year old
(two years old in the United States).
Younger infants who will be
exposed to hepatitis A should be
protected with immune globulin.
Meningococcal meningitis
vaccine for serogroup A is not
effective for children younger than
three months. Vaccine for serogroup
C is not effective for children
younger than two years. Serogroup
B is present in some countries, but
no effective vaccine exists for those
organisms.
Vaccines for typhoid fever have
not been well studied in children
younger than five to six years.
Younger children may not be able to
swallow the capsules by which the
live, attenuated vaccine is
administered.
Yellow fever vaccinations in
children less than nine months old
have been associated with
encephalitis and usually should not
be administered. Infants from six to
nine months may be vaccinated, but
only when traveling to an area in
which ongoing yellow fever is
epidemic and they cannot be
protected from mosquitoes.
Although no vaccine for malaria
is currently available, it is
appropriate to point out that most of
the three million malaria deaths
worldwide each year occur in
children five years old and younger.
Parents of such young children must
be vigilant in their administration of
antimalarial medications and
protection from mosquitoes.
SPECIFIC VACCINES
Recommended immunizations for
healthy adult travelers are listed in
the following sections.
Immunizations for children may be
different and are constantly being
changed. Parents should consult
their physician or a travel medicine
specialist about immunizations for
children. Individuals who are
immunocompromised as the result
of infection such as HIV, therapy for
a wide variety of diseases including
malignancies, or from other
conditions that require
immunosuppressive therapy also
need unique measures and should
consult an experienced travel
medicine physician.
Cholera
Cholera immunization is not
recommended for travelers by the
CDC or the World Health
Organization and is not available in
the United States. Cholera
immunization is no longer required
for entry into any country.
Older cholera vaccines had
limited effectiveness. Vaccines
produced from organisms
genetically modified to eliminate
virulence and administered orally
to stimulate gastrointestinal
mucosal immunity are being
investigated. Dukoral®, a vaccine
produced by the Swedish drug
company Crucell SBL Vaccines, is
not licensed in the United States.
Information is available at
www.sblvaccines.se.
Hepatitis A
A simple RNA virus that is most
commonly transmitted by fecal
contamination of water produces
hepatitis A, the most common
vaccinepreventable infection
encountered by travelers. Diligent
water disinfection effectively
prevents this infection. Although the
mortality rate averages only 0.3
percent, it is 1.8 percent in
individuals older than fifty years of
age. Hepatitis A causes about a
hundred deaths a year in the United
States. It is far more common in
developing countries, and
vaccination for travelers is highly
recommended.
The safety of hepatitis A
vaccination during pregnancy has
not been determined. Because
hepatitis A vaccine is produced
from inactivated virus, the
theoretical risk to the developing
fetus is low. The risk associated
with vaccination in pregnant women
should be weighed against the risk
for hepatitis A, which may be high.
Two inactivated vaccines,
Havrix®, manufactured by
GlaxoSmithKline, and Vaqta®,
manufactured by Merck, are
available. Both vaccines are made
with inactivated hepatitis A virus
and were licensed in the United
States in 1995. Two injections six
months apart provide excellent
protection. The first injection
provides a high level of protection
for travelers who are planning to
depart in less than six months. The
second injection prolongs immunity.
Another vaccine, Twinrix®,
combines hepatitis A and hepatitis
B vaccines. It can be received by
travelers needing immunization for
both infections.
The CDC provides no
recommendations for boosters.
High levels of immunity after six to
eight years have been documented,
and vaccination appears to be
effective for twenty years or more.
Hepatitis B
Hepatitis B is caused by a large,
complex DNA virus that is quite
different from the hepatitis A virus
and is primarily transmitted by
body fluids, particularly blood and
semen. However, contaminated
water or food also can transmit the
infection. Two safe, effective
vaccines are available:
Recombivax HB®, manufactured by
Merck, and Engerix-B®,
manufactured by GlaxoSmithKline.
The usual schedule of primary
vaccination for adults consists of
three intramuscular doses of
vaccine, the second and third at
intervals of one and six months after
the first. A third vaccine, Twinrix®,
manufactured by GlaxoSmithKline,
is a preparation that contains both
hepatitis A and hepatitis B vaccine
and can be administered on the
same schedule.
Everyone should obtain hepatitis
B vaccination except individuals
who have previously come into
contact with this virus, developed
natural immunity, and do not need to
be vaccinated. Such subclinical
infections are common in health
professionals, individuals living
with persons infected with hepatitis
B, injecting drug users, and
homosexual men. Testing for
preexisting immunity is not cost
effective for others.
Pregnancy is not a
contraindication to hepatitis B
vaccination.
Hepatitis C, D, and E
Hepatitis D or delta agent is
associated with hepatitis B
infection and can be prevented by
vaccination against hepatitis B.
Although hepatitis C and hepatitis E
are common infections, no vaccines
are available.
Influenza
The risk for exposure to
influenza during travel depends on
the time of year and destination. In
the tropics, influenza can occur
throughout the year. In the temperate
regions of the Southern
Hemisphere, most influenza occurs
from April to September (the winter
season). In temperate climate zones
of the Northern and Southern
Hemispheres, travelers also can be
exposed to influenza during the
summer, especially when traveling
as part of large organized tourist
groups or on cruise ships that
include persons from areas of the
world where influenza viruses are
circulating.
Persons at high risk for
complications of influenza and
those who were not vaccinated with
influenza vaccine during the
preceding fall or winter should
consider receiving influenza
vaccine before travel if they plan
any of the following:
Travel to the tropics
Travel with organized tourist
groups at any time of year
Travel to the Southern
Hemisphere during April
through September
Two influenza vaccines are
available: an inactivated (killed-
virus) vaccine that must be injected
and an attenuated live-virus vaccine
that is administered as an intranasal
spray. The inactivated vaccine is
cheaper and is recommended for all
routine immunizations.
The nasal-spray flu vaccine
(FluMist®) is approved for use in
people two to forty-nine years of
age who are not pregnant and who
do not have an underlying medical
condition that predisposes them to
influenza complications. Persons at
high risk for influenza-related
complications and severe disease
include children aged six months to
five years, pregnant women,
persons older than fifty years,
persons of any age with chronic
medical conditions such as
diabetes, heart disease, or lung
disease, and health care workers.
More information about the
nasal-spray flu vaccine is available
at the CDC site
(www.cdc.gov/flu/about/qa/nasalspra
Detailed information about the
prevention and control of influenza
is available at
www.cdc.gov/mmwr/preview/mmwr
Japanese Encephalitis
Japanese encephalitis is a major
problem in much of Asia but is an
uncommon infection among
travelers, among whom CDC
investigators estimate the incidence
to be less than one per million (Fig.
5-1). Vaccination is recommended
only for travelers who plan to
spend a month or longer in endemic
areas during the transmission
season—which is different for each
country. (Detailed information
about different countries is
available at
www.cdc.gov/travel/diseases.htm#he
However, CDC warns that travelers
with extensive unprotected outdoor,
evening, and nighttime exposure in
rural areas, such as might be
experienced while bicycling,
camping, or engaging in certain
occupational activities, may be at
high risk even if their trip is brief.
To avoid being bitten by the
mosquitoes that transmit the
infection, repellents, appropriate
clothing, and mosquito nets must be
used.
Ixiaro®, a new vaccine for
Japanese encephalitis, was licensed
by the FDA on March 30, 2009.
(The old vaccine is no longer being
produced.) The new vaccine is
considered safer and freer from the
side effects (which included
anaphylactic reactions) associated
with the old vaccine. It is indicated
for active immunization against JE
virus for persons seventeen years of
age and older.
Ixiaro® is an inactivated
vaccine based on cell culture
technology. It provides a good
immune response and is well
tolerated. The vaccine is provided
as a ready-to-use liquid formulation
in prefilled syringes. It should be
administered in two doses twenty-
eight days apart.
Lyme Disease
A successful Lyme disease
vaccine for humans has been
developed. However, the vaccine
was expensive and
recommendations for its use by the
Advisory Committee for
Immunization Practices (ACIP) of
CDC would have limited it to
approximately 1 percent of the
population. Some concern about its
safety apparently existed also,
although the available data on
outcomes did not support these
concerns. Sales of the Lyme vaccine
for humans were so small that the
product was withdrawn from the
market in February 2002.
Figure 5-1. Distribution of Japanese
encephalitis 1
Efforts to develop a more

effective, less expensive vaccine
are being actively pursued by some
vaccine manufacturers.
Measles
Measles can be a severe
disease, particularly in adults.
Many of the cases occurring in the
United States are contracted in
other countries. Whether or not
individuals plan to travel, those
born after 1956 who have not had a
documented vaccination or
physician-diagnosed infection, or
who do not have laboratory
evidence of immunity, should
receive the vaccine. It produces
lasting, probably lifelong, immunity
and since its introduction has
essentially eradicated subacute
sclerosing panencephalitis, a
postmeasles complication.
Meningococcus
Outbreaks of meningococcal
infection occur sporadically in both
industrialized and developing
areas. Major epidemics occur in the
meningitis belt of sub-Saharan
Africa (Fig. 5-2). Individuals
traveling to countries in which such
outbreaks are occurring should
receive meningococcal vaccine
before departure. Vaccination is
required for entrance to Saudi
Arabia, and unvaccinated
individuals will receive
vaccinations before being admitted.
Vaccination is recommended for
India and Nepal.
Figure 5-2. The sub-Saharan
meningitis belt 2
The older vaccine licensed in

the United States, Menomune® A,
C, Y, W-135, is composed of
capsular polysaccharide antigens
from those four serogroups. A new
quadrivalent A/C/Y/W-135®
meningococcal conjugate vaccine,
Menactra®, was licensed in the
United States in January 2005 for
use among persons eleven to fifty-
five years old. In 2007 it was
approved for persons two through
ten years old. This vaccine is safe
and immunogenic, is considered
somewhat superior to the older
vaccine, and is expected to offer a
longer duration of protection.
Vaccination consists of a single
subcutaneous injection of vaccine
and is effective for three years.
Vaccination can be administered at
the same time as other vaccines but
in a different deltoid or gluteal
subcutaneous site.
Poliomyelitis
Poliomyelitis (polio) has been
eradicated in most of the world and
in a few years is expected to be
eliminated worldwide following a
vaccination campaign carried out
by the World Health Organization
(WHO) with financial support from
Rotary International. In June 2008,
the WHO reported 251 infections in
India, mostly northern India, and 3
infections in Nepal.
Vaccination of children is still
recommended in the United States,
but oral (Sabin) polio vaccine has
not been available since the year
2000 because rare cases of
paralytic polio followed its
administration.
Adults who are traveling to
areas where poliomyelitis is still
occurring and who are
unvaccinated, incompletely
vaccinated, or whose vaccination
status is unknown, should receive
inactivated polio vaccine (IPV).
Two doses should be administered
at intervals of four to eight weeks,
with a third dose six to twelve
months after the second. If three
doses of IPV cannot be
administered within the
recommended intervals before
protection is needed, alternative
schedules are available at
www.cdc.gov/travel/#hepa. A
single booster dose for adult
travelers provides lifelong
immunity.
Rabies
Rabies, a form of viral
encephalitis, is essentially always
fatal if clinical signs of infection
appear. Postexposure treatment with
wound cleansing, immune globulin,
and vaccination successfully
prevents clinical infection when
properly administered.
Preexposure vaccination for
rabies has long been recommended
by ACIP for anyone traveling to a
rabies endemic area (essentially all
of South and Central America,
Africa, and most of Asia) for more
than thirty days. However, that
recommendation has recently been
modified to include visitors, such
as travelers to remote areas, for
whom access to appropriate
medical care, including immune
globulin and vaccine, would
require more than twenty-four
hours. In addition, vaccination is
recommended for children,
particularly for preverbal children
and children so young they cannot
report or might be afraid to report
contact with a potentially infected
dog or other animal.
Intramuscular vaccination is now
exclusively recommended.
(Intradermal vaccination with
human diploid cell vaccine
[HDCV] was approved by the FDA
in 1987 but does not produce
antibody titers as high as those
produced by intramuscular
vaccination, and antibody titers do
not persist as long. The question of
intradermal versus intramuscular
vaccination is currently moot in the
United States because intradermal
HDCV, the only product licensed
for intradermal vaccination, is not
available.)
Possibly a more compelling
reason for rabies preexposure
immunization is the worldwide
shortage of rabies immune globulin.
Cleansing the wound,
administration of immune globulin,
and administration of vaccine are
considered equally essential, and
rabies deaths have resulted from
omission of any of them. Only
approximately one-third of the
immune globulin needed for
postexposure therapy worldwide is
currently being produced. In
developing countries, most
individuals exposed to rabies are
not given immune globulin unless
they knew enough about
postexposure rabies therapy to
demand its administration. Studies
have clearly demonstrated that most
travelers think rabies is not a
problem and have no knowledge of
postexposure therapy.
Individuals who have been
previously immunized do not need
postexposure immune globulin.
Vaccination on day zero and day
three after exposure is all that is
required. However, those
vaccinations are considered
essential. (Any bite or scratch by a
dog or any other animal in a rabies
endemic area must be considered a
rabies exposure, and postexposure
therapy must be instituted
regardless of the vaccination status
of the animal. Vaccines used to
vaccinate animals in areas where
rabies is endemic are not as
reliable as those used in
industrialized nations. Scratches are
considered exposures because
animals lick their paws, covering
them with infected saliva.)
Rubella
Rubella (German measles) is
one of the most widely documented
causes of birth defects. CDC
recommends that everyone, not just
women, be vaccinated unless they
have been previously infected or
have laboratory evidence of
immunity. A single injection of
attenuated live rubella virus
vaccine provides lasting immunity.
Smallpox
Smallpox has been eliminated
worldwide by a vigorous
vaccination campaign carried out
by the WHO, an outstanding
medical triumph. The last reported
case of smallpox was in Somalia in
1977. Entry requirements for recent
smallpox vaccination have been
eliminated. The vaccine is
considered more hazardous than the
risk of contracting the infection,
although threats of terrorist attacks
with microbiologic agents have
prompted reconsideration of that
policy.
Tetanus
The organisms producing tetanus
are ubiquitous, and infections can
result from trivial wounds. Because
treatment for tetanus is not
effective, the mortality rate is high.
Since immunization essentially
completely prevents the devastating
effects of such infections,
inadequate protection against this
disease is inexcusable. The initial
series of tetanus toxoid
immunizations is two injections
four to eight weeks apart. A third
inoculation should be obtained six
to twelve months later. A booster
should be obtained at least every
ten years thereafter. However, if a
booster has not been received
within five years, one should be
obtained before departing on a
wilderness outing or following a
contaminated wound.
Tetanus toxoid has been
combined with diphtheria toxoid, a
combination labeled Td. Recently,
pertussis (whooping cough) vaccine
has been added, and the
combination is labeled Tdap. That
triple combination is now
recommended for immunization and
boosters for individuals eleven to
sixty-four years old. Detailed
information about the combination
and the new recommendations is
available at
www.cdc.gov/mmwr/preview/mmwr
s_cid=rr5517a1_e.
Typhoid
Typhoid immunization is
estimated to be only about 70
percent effective in preventing
typhoid infection, but it does
significantly reduce the severity of
infections. Such immunization is
recommended, sometimes strongly,
for travelers outside of major cities
in developing countries. Two
vaccine preparations are available:
an attenuated live oral vaccine
(Vivotif Berna), and a recently
developed injectable vaccine
(Typhim Vi®). The older heat-
inactivated vaccine is no longer
available. The newer vaccines
produce fewer side effects.
The live vaccine is administered
in four capsules that are taken every
other day. The series should be
repeated every five years. Typhim
Vi is administered as a single
intramuscular injection that should
be repeated every two years.
Yellow Fever
Yellow fever can be a
devastating infection.
Approximately 20 percent of such
infections are fatal. Infants and
children are at greatest risk. The
virus is endemic in the equatorial
regions of Africa and South
America. For travelers, the risk of
illness from yellow fever is
probably ten times greater in rural
West Africa than in South America
(Figs. 5-3 and 5-4); these risks vary
greatly according to specific
location and season. In West Africa,
the most dangerous time of year is
during the late rainy and early dry
seasons (July to October). Virus
transmission is highest during the
rainy season (January to March) in
Brazil.
Yellow fever has never been
recognized in Asia, and its
introduction could result in
disastrous epidemics because
mosquitoes that could spread the
virus are abundant. For that reason,
yellow fever immunization is
required for travel in many Asian
countries, particularly for persons
arriving from countries where
yellow fever is endemic.
The low incidence of yellow
fever among travelers, generally a
few hundred reported cases per
year, has led to complacency. All
five cases of yellow fever among
travelers from the United States and
Europe between 1996 and 2002
were fatal and occurred in
unvaccinated travelers.
The attenuated live-virus
vaccine is one of the most effective
available. A single inoculation
provides immunization. Boosters
are required every ten years, but
prolonged persistence of immunity
has been documented and is
probably lifelong. Immunizations
must be obtained from a WHO
Yellow Fever Vaccination Center,
the locations of which can be
obtained from local health
departments or the CDC website.
The vaccine is prepared from
viruses cultured in eggs. Persons
allergic to eggs should not receive
the vaccine.
Historically, yellow fever
vaccine-associated adverse events
were seen primarily among infants
and presented as encephalitis. Since
1992, five cases of encephalitis
among adult recipients of yellow
fever vaccine have been reported in
the United States. In addition, ten
cases of neurologic disease have
been reported. Crude estimates of
the risk for vaccine-associated
neurologic disease in the United
States range from 4 to 6 cases per
1,000,000 doses distributed.
Figure 5-3. Distribution of yellow
fever in Africa3
Infants less than six months old

should not be vaccinated because
they are more susceptible to
encephalitis. Preferably,
immunization should be delayed
until an infant is at least nine months
old. Physicians considering
vaccinating infants younger than
nine months old in unusual
circumstances should consult with
the Division of Vector-Borne
Infectious Diseases (phone: 970-
221-6400) or the Division of
Global Migration and Quarantine
(phone: 404-498-1600) at CDC.
Another serious adverse reaction
has recently been described among
recipients of yellow fever vaccines.
This syndrome is now called
yellow fever vaccine-associated
viscerotropic disease (YELAVD).
Since 1996, nine cases of this
disorder, which resembles naturally
acquired yellow fever, have been
reported in the United States; an
additional seventeen cases have
been identified worldwide as of
October 2004. All U.S. cases
required intensive care, and six
were fatal. In several individuals
from whom tissue samples were
available, viral dissemination
throughout the body was
demonstrated. All cases reported
thus far have occurred in
individuals being vaccinated for the
first time.
Figure 5-4. Distribution of yellow
fever in South America 4
Yellow fever vaccines must be

considered a possible, but rare,
cause of YEL-AVD that is similar to
fulminant yellow fever. Crude
estimates of the incidence of
vaccine-associated viscerotropic
disease in the United States range
from 3 to 5 cases per 1,000,000
doses distributed. This frequency
appears to be higher for persons
older than sixty years of age, with
as many as 19 cases per 1,000,000
doses distributed.
Recently, a history of thymus
disease has been identified as a
contraindication to yellow fever
vaccination. Four of the twenty-six
vaccine recipients with YEL-AVD
worldwide have had a history of
diseases involving the thymus, all
of which are extremely rare,
suggesting that compromised thymic
function may be another
independent risk factor for YEL-
AVD.
Because deaths from yellow
fever have occurred among
unvaccinated travelers to areas
where yellow fever is endemic,
yellow fever vaccination of
travelers to high-risk areas is still
strongly recommended by the CDC
and the WHO as a key prevention
strategy. However, the vaccine
should be administered only to
persons truly at risk for exposure to
yellow fever.
____________
REFERENCES
1. Data from the Centers for
Disease Control and Prevention,
www.cdc.gov
2. Ibid.
3. Ibid.
4. Ibid.
CHAPTER 6
SANITATION, ARTHROPOD
AVOIDANCE, AND WATER
DISINFECTION
Sanitation and water disinfection

play vital roles in preventing
infections, particularly in
developing nations that do not have
clean water supplies and sewage
disposal facilities to which
residents of industrialized countries
are accustomed.
SANITATION
Many inhabitants of developing
countries know nothing about the
most rudimentary sanitation
procedures, such as washing their
hands after defecating. Even when
they follow such practices, many do
not understand their purpose and
consider them the idiosyncrasies of
foreigners. When local inhabitants
are employed as cooks or in similar
roles, hand washing and
disinfection; disinfection of water
for drinking, cooking, or even
washing dishes; and sanitary food
preparation must be vigorously
enforced and tightly supervised.
Everyone should wash their
hands with water and soap,
preferably an antibacterial soap,
after using the toilet, before eating,
and any time their hands become
contaminated, such as after
covering their mouth or nose when
they cough or sneeze, after contact
with animals, and after handling
money. Alcohol-based gels, such as
Purell® and Isogel-X®, are an
effective adjunct to hand washing
and kill 99.9 percent of all bacteria
on the hands. They are alcohol
based and evaporate in about fifteen
seconds, so drying with a towel that
might be contaminated is not
needed.
Locally obtained food must be
regarded with the same distrust as
the water supply. The only food that
can be regarded as safe from
contamination is that which has
been thoroughly cooked under
supervision. Eating utensils and
plates are rarely washed in water
hot enough to kill bacteria, and soap
may not have been added to the
water. The most common practice is
to simply rinse these items with
water that has not been disinfected.
However, wellcooked food served
immediately usually is safe—and
often delicious—if travelers
provide their own plate, cup, and
spoon.
Fruits that have been picked
above ground level, cleaned with
disinfected water, and peeled or
sliced by the eater should be safe
because bacteria cannot enter the
fruit as it is growing. However,
fruits that have been sliced for
display often have been cut with
contaminated knives and sprinkled
with undisinfected water to keep
them attractive for potential buyers.
Bacteria on the skin of oranges at
the time they are squeezed can
contaminate orange juice. Melons
sold by the pound may be injected
with undisinfected water to
increase their weight. Leafy
vegetables are often fertilized with
human feces and cannot be
adequately disinfected by washing.
Even soaking food in strong
chlorine solutions does not
effectively eliminate all bacteria.
All other foods must be assumed
to be dangerous, particularly
custards, cakes, bread, cold meats,
cheeses, and other dairy products.
Milk is a potential source of
tuberculosis. Bottled carbonated
drinks—water, sodas, and beer—
are generally safe, but infections
have resulted from drinking bottled
water that is not carbonated, which
occasionally has not even been
disinfected. Ice, even that served in
airport lounges, is often made from
undisinfected water.
Sites for garbage disposal and
latrines should be downstream,
downhill, downwind, and as far as
possible from water sources.
However, latrines that are too far
away are not used, which can make
campsites unpleasant and unsafe.
Local inhabitants often must be
instructed to use latrines.
Developing Southeast Asian
countries suffer epidemics of
cholera at the beginning of each
monsoon season because rain
washes human feces from the streets
into the streams that serve as the
water supply.
ARTHROPOD AVOIDANCE
Insects can be avoided by wearing

appropriate clothing, applying
insect repellents to skin, and
applying insecticides to clothing.
Currently the recommended method
for avoiding insect bites is to apply
one of the two effective insect
repellents to exposed skin and to
apply the insecticide permethrin to
clothing.
Clothing
Clothing that forms an effective
barrier to insects should be loose
fitting. Mosquitoes can bite through
snugly fitting clothing. The clothing
should be light colored because
dark colors tend to attract insects.
Shirts should have long sleeves;
pants should have long legs that can
be tucked into socks or bound with
gaiters to block access by ticks.
Broad-brimmed hats protect the
head and can support mosquito
netting that blocks out mosquitoes
and stinging insects such as bees
and wasps. In tropical areas beds
should be covered by mosquito
netting that has been treated with
permethrin. Tents should have
mosquito netting at all entrances.
Insect Repellents
The only two conventional insect
repellents currently recommended
by the Centers for Disease Control
and Prevention (CDC) are products
containing DEET—N, N-diethyl-m-
toluamide or N, N-diethyl-3-
methyl-benzamide—and products
containing picaridin—KBR 3023,
or 2-(2-hydroxyethyl)-1-
piperidinecarboxylic acid 1-
methylpropyl ester. DEET was
developed for military use in 1946
and became generally available
worldwide in 1957. Despite its age,
nothing comparable was developed
until picaridin was introduced in
the United States in 2005. (It had
been introduced earlier in Europe.)
Both agents are highly effective
against mosquitoes and are also
effective against ticks and chiggers.
They are not effective against flies.
In a comparison of mosquito
repellents carried out in 2002
(before picaridin was introduced),
DEET-based products provided
complete protection for the longest
time. A formulation containing 23.8
percent DEET had a mean
complete-protection time of 301.5
minutes (five hours.) A soybean-
oil-based repellent, the second most
effective, protected against
mosquito bites for an average of
94.6 minutes. An IR3535-based
repellent protected for an average
of 22.9 minutes. All other botanical
repellents tested provided
protection for less than twenty
minutes. Repellentimpregnated
wristbands offered no protection.
The duration of effective
protection from mosquito bites
varies with the concentration of
DEET in the preparation:
A product containing 23.8
percent DEET provided an
average of five hours of
protection.
A product containing 20 percent
DEET provided almost four
hours of protection.
A product with 6.65 percent
DEET provided almost two
A product with 4.75 percent
DEET provided roughly 1.5
DEET is available in
concentrations that range from 5 to
100 percent, although the
preparations most commonly used
have concentrations in the range of
30 percent.
DEET and picaridin are
removed by sweating, absorption,
evaporation, wiping, and rain and
must be reapplied several times a
day. However, two long-lasting
formulations of DEET have been
developed: a microencapsulated
product in which DEET is encased
in a protein shell, and a preparation
in which the agent is dissolved in a
polymerized lotion.
Ultrathon is a polymer-based
product containing 34.34 percent
DEET. It is produced by 3M
Corporation and is the standard-
issue insect repellent for the U.S.
military. It is generally accepted to
last twelve hours. The
microencapsulated product is
Sawyer® Controlled Release Insect
Repellent, a 20 percent DEET
preparation that was selected by
Consumer Reports as the most
economical lotion insect repellent
(four cents an hour) because it
lasted so long. Sawyer claims this
agent is effective for at least eleven
hours after each application but may
last longer.
DEET is absorbed through skin,
and 10 to 15 percent of the
unmodified preparations can be
recovered from urine. (Both of the
long-acting preparations are
associated with much less
absorption.) Allergic reactions to
this agent, including bullous
eruptions, contact urticaria, and
anaphylaxis, have been reported.
Toxic encephalopathy with grand
mal seizures has occurred,
particularly in infants and children.
However, in recent years extensive
investigations of DEET have been
carried out by a number of agencies
because it is used so extensively.
The Environmental Protection
Agency (EPA), which is
responsible for testing such agents,
and the CDC state that preparations
containing 30 to 35 percent
concentrations of DEET are
essentially totally safe when
applied as directed. Complications
such as those listed have followed
inappropriate use.
The American Academy of
Pediatrics changed its
recommendations in 2003. That
organization now considers 30
percent or less concentrations of
DEET safe (instead of less than 10
percent, its former
recommendation) and considers
such preparations safe for infants as
young as two months. (Its former
recommendation limited application
to children older than two years.)
In studies of picaridin required
for EPA approval, that agent was
found to be essentially nontoxic.
Picaridin is currently available in
preparations that range in
concentration from 7 to 14 percent
and would be expected to last as
long as DEET-containing products
with the same concentrations. Some
commentators state it is not as
consistently effective as DEET.
Some individuals do not like to
use DEET because they find the
product oily and the odor
objectionable. DEET also is
reported to damage plastics such as
watch lenses and eyeglass frames,
certain fabrics such as rayon and
spandex, and painted or varnished
surfaces. Boosters of picaridin
claim that it is odorless and not
sticky.
Application of Repellents
Repellents should be applied to
exposed skin but not under clothing.
A light application is effective;
increasing the amount of repellent
carries no benefit. Spray repellents
should not be applied in quantities
that drip from the skin. Spray
repellent should be applied to the
face by spraying it on the palms and
rubbing the face so that contact with
eyes and mucous membranes is
avoided.
Repellents should not be applied
over cuts; wounds; and inflamed,
irritated, or eczematous skin.
Complete skin coverage is not
required for the repellent to be
effective. After the repellent is
applied, it should be wiped from
palmar surfaces to prevent
inadvertent contact with the eyes,
mouth, and genitals.
Young children should not apply
repellents themselves. To prevent
subsequent contact with mucous
membranes, DEET should not be
applied to a child’s hands.
Simultaneous application of a
DEET repellent and a sunscreen
reduces the effectiveness of the
sunscreen by as much as one-third,
and more frequent application of the
sunscreen is required to maintain its
effectiveness. Combination
products that contain both insect
repellent and sunscreen should be
avoided. Proper use of sunscreens
requires frequent reapplication, but
insect repellents should only be
reapplied when their effectiveness
seems to be waning.
Insecticides
Permethrin (trade name:
Permanone®) is a pesticide derived
from chrysanthemums that is highly
effective against arthropods when
used on clothing. This agent kills
insects so rapidly it sometimes is
thought to be a repellent, and some
commercial products are labeled
repellents. When applied to
clothing this agent has essentially
no toxicity for humans.
A number of spray preparations
are available. Clothing should be
sprayed until damp and allowed to
dry. Sprays last two to three
washings. After the clothing has
dried it is odor free. Reportedly,
approval is being sought for
permethrin solutions in which
clothing can be soaked. Such
applications should last forty to
fifty washings.
WATER DISINFECTION
In recent years widespread
microbial contamination of
backcountry water sources in the
United States has been recognized.
The single-cell Cryptosporidium
parasite is essentially ubiquitous,
and its universal presence has
dictated changes in water
disinfection techniques previously
considered completely effective.
Developing countries build
neither water systems that reliably
supply uncontaminated water for
drinking and cooking nor sewage
systems that prevent contamination
of water sources. Many residents
are resistant to the organisms in the
water as the result of continuous
contact since infancy, but deaths
from diarrheal disease still number
in the millions. Most water in
developing countries is
contaminated. Tap water is usually
contaminated, even in the best
hotels, although some
establishments provide disinfected
bottled water for drinking. Tap
water should not be used even for
brushing teeth. Ice used to chill
drinks is usually unsafe. Even in
remote areas, herdsmen and their
cattle or sheep often contaminate
small wilderness streams. All
water that is to be consumed or
used in food preparation must be
disinfected.
Removing Particulate Material

River water, particularly glacial
streams, often contains a large
amount of suspended particulate
material that gives the water a
“muddy” or terracotta color.
(Glacial streams are milky, gray, or
grayish tan.) In the Grand Canyon
and the upstream tributaries of the
Colorado River, the condition of the
water depends on whether
thunderstorms have recently
occurred upstream. The water is
often clear. At other times, the
Colorado is described as “liquid
mud,” and the silt can be removed
from equipment only by vigorous
scrubbing. It frequently cannot be
completely removed from clothing.
Following a storm, side streams are
as muddy as the river.
If such water is placed in a
container and allowed to stand,
much of the suspended material
settles, although the process may
take hours and the water may retain
some color. Filling buckets in the
evening allows the water to be
filtered the next morning. However,
allowing the water to stand may not
be necessary. River water that
appears quite muddy can contain
surprisingly little suspended
material when viewed in small
quantities, such as in a water bottle
or bucket.
Filtration
Water can be completely cleared
by filtration. Filters used for
disinfecting water perform this
function well but do become
obstructed. A filter that can be
manually cleaned is essential. For
large groups, a large-volume filter
such as the Katadyn® Explorer (1
gal/min) serves quite well. The
filter can be removed in seconds,
and scrubbing it for twenty or thirty
seconds with a brush or scrubber
gets rid of the obstruction. (At least
one Grand Canyon rafting company
uses a battery-operated electric
filter.) Usually two to three liters
can be filtered before cleaning is
necessary. The one- or two-person
smaller filters, such as the
Sweetwater filter, also clear water
and can be easily cleaned, but they
can filter only about one liter
between cleanings.
Flocculation
Flocculation was used to remove
unpleasant colors, smells, and
tastes from water by the Egyptians
as long ago as BC 2000. Currently it
is widely used in municipal water
plants, and the technique can be
applied in the field, although it is
time consuming and rarely used.
Flocculation removes suspended
matter—colloids—that are not
settled by gravity, which includes
organic and inorganic material and
many microorganisms, including
more than 90 percent of Giardia
cysts and most bacteria and viruses.
However, it does not remove all
microorganisms and must be
followed by a second step, such as
halogenation or heat.
The best flocculant is alum
(aluminum potassium sulfate), a
common chemical used by the food
industry in baking powder and for
pickling. It can be found in food
stores or in chemical supply houses.
Other substances, such as lime or
potash, can act as flocculants.
Baking powder or even the fine
white ash from a campfire can be
used in an emergency.
The alum induces colloid
particles to coagulate, forming
larger clumps that settle by gravity
or layer on top. Approximately one-
eighth to one-quarter of a teaspoon
of alum per gallon should be added
to water and mixed well and
frequently for five minutes. (The
alum does not need to be measured
precisely.) The mixture should be
allowed to settle for thirty to sixty
minutes, then decanted or filtered
through a coffee filter or a fine
mesh cloth. Since alum is nontoxic,
if the water is not cleared by the
first flocculation, the process can
be repeated a second or third time.
Granular Activated Charcoal

Granular activated charcoal
binds (adsorbs) many chemicals to
its surface. It is used widely in
medicine to treat poisoning or
overdose by binding toxins in the
intestines. This nonspecific
adsorption also removes chemicals
from water. Charcoal
filters/purifiers for household use
are popular for removing the taste
and smell of chlorination by-
products and toxic chemical
contaminants such as pesticides.
Several field devices combine
filtration and halogenation with a
charcoal matrix. Charcoal filtration
should be used after halogen
disinfection because it removes
iodine or chlorine from water.
When the charcoal binding sites
are full, compounds pass through
unadsorbed or displace other
chemicals from the charcoal. Color
or taste in the water indicates that
the carbon is exhausted and should
be replaced. However, the capacity
is large and the filter usually clogs
before the charcoal is exhausted.
Charcoal does not adsorb all
microorganisms and does not kill
them, so it does not disinfect.
DESIRABLE
CHARACTERISTICS OF
WATER DISINFECTION
SYSTEMS
A water disinfection system for use
in the wilderness or developing
countries must have all of the
following characteristics:
Simple and convenient
Fast
Small and lightweight
Reliable
Wilderness users tend to be
young and impatient; many will not
use a system that is not simple and
convenient or will not wait for a
slow process. They may consume
water without disinfection if it
appears clear and uncontaminated.
They will not carry a system that is
not small and lightweight. A system
that is not reliable should not be
used by anyone.
Disinfection systems suitable for
wilderness use are also suitable for
urban use in countries with an
unsafe water supply. However,
long-term residents usually develop
a more convenient system,
optimally one that combines a filter
with chemical or ultraviolet
treatment.
GOALS OF WATER
DISINFECTION
The goal of water disinfection is the
elimination of waterborne
microorganisms. Unlike urban
systems, the techniques used to
disinfect small quantities of water
usually kill all organisms.
Three types of microorganisms
must be eliminated: parasites,
bacteria, and viruses. Some
parasites are single-cell organisms
such as Cryptosporidia,
Cyclospora, Giardia, and amoebae;
others are larger, multicellular
organisms, such as tapeworms or
roundworms.
When eliminated from the body,
single-cell parasites often form
thick, tough walls around
themselves—cysts—that are much
more resistant to chemical agents or
heat than the unprotected organism.
More complex parasites lay eggs
that are excreted by the host.
Bacteria, which are intermediate
in size between parasites and
viruses, make up most of the bulk of
feces. They produce a wide range
of infections, many of them
potentially lethal.
Viruses are much smaller than
bacteria and also produce a wide
variety of infections. Many cases of
“traveler’s” diarrhea result from
infection by waterborne viruses.
Hepatitis A and polio have long
been known to result from fecal
contamination of water.
TECHNIQUES FOR
WILDERNESS WATER
DISINFECTION
Only four water disinfection
methods suitable for wilderness use
are available: heat, the combination
of microfiltration and chemicals,
chemicals alone that require four
hours or more to remove
Cryptosporidia, and ultraviolet
light.
Heat
Heat is a reliable way to
disinfect water. To eliminate
Cryptosporidia, CDC and the EPA
recommend boiling water for a full
minute (three minutes above 6500 ft
or 2000 m because water boils at a
lower temperature at higher
altitude). However, simply bringing
water to a boil is just as effective.
(Milk is pasteurized, which
eliminates most organisms, by
heating it to only 160°F [71°C] for
twenty to thirty minutes.)
Table Boiling Temperature of
6-1 Water at Various Altitudes
Altitude Temperature
Sea level 212°F (100°C)
10,000 ft (3000
194°F (90°C)
m)
14,000 ft (4300
187°F (86°C)
m)
19,000 ft (5500
178°F (82°C)
m)
29,000 ft (8800
160°F (71°C)
m)
Boiling is inconvenient and time

consuming, particularly for small
quantities of water. Fuel must be
carried, particularly above tree
line. If a wood fire is built, an
unsightly residue is unavoidable
without heavy, bulky firepans.
Pressure cookers save time and fuel
at all elevations. No additional
disinfection can be achieved by
distillation.
Microfiltration
Cryptosporidia, and possibly
some other parasites such as
Cyclospora, are resistant to halide
disinfectants, which makes
microfiltration an essential element
of quickly disinfecting small
quantities of water. (The second
desirable feature of water
disinfection systems is “fast.”)
Treatment with a chemical to
destroy viruses is still needed
following filtration with filters that
do not eliminate those organisms.
As of May 2009, the following
websites for filter manufacturers
were functional:
General Ecology® (First Need®
filters): www.general-
ecology.com
Katadyn® (variety of filters):
www.katadyn.com/chen
Mountain Safety Research®
(Hyperflow and Sweetwater
Filters):
www.msrgear.com/watertreatmen
Sawyer® Products (Sawyer
filters):
www.sawyerproducts.com
The First Need® filter has an
absolute pore size of 0.4 microns;
the Sawyer® Viral Purifier has an
absolute pore size of 0.2 microns.
Both have been demonstrated to
remove viruses as well as bacteria
and parasites in studies conducted
for the EPA. (Since such devices
remove all microorganisms, they
have been called water “purifiers”
even though purification is not
synonymous with total disinfection.)
First Need® states that the
“Structured Matrix” of its filters
removes viruses electrolytically.
Data about the removal of
poliovirus type 1 and rotavirus SA-
11 are presented. Sawyer states that
its viral purifier removes viruses
and cites data about removal of the
bacteriophage Coliphage MS2.
However, the method by which the
viruses are removed is not stated.
All effectively remove Giardia,
Cryptosporidia, other parasites,
and bacteria (Table 6-2). However,
the filter pores of other filters are
too large to remove viruses. In fact,
as the pores enlarge with use, they
may allow passage of small
bacteria, such as the Vibrios that
cause cholera. After filtration the
water must be chemically treated to
destroy those organisms, and the
manufacturers’ websites
recommend treatment with iodine or
chlorine.
Size Comparison
Table
(Micrometers) of
6-2
Organisms and Filter Pores
Filter pores 0.3 to 0.4 μm
Giardia cysts 6.0 μm
Cryptosporidium
4.0 μm
cysts
Bacteria 1.5 to 3.0 μm
Viruses 0.004 to 0.06 μm
Filters are relatively bulky (for

backpacking), are somewhat
expensive, and can be obstructed by
sediment in the water. The
obstruction can be slowed or
prevented with prefilters; but
eventually the filter must be
removed and cleaned.
Chemical Disinfection Systems

Chemical disinfection systems
combined with microfiltration
provide the desired features of
simplicity, speed, small size,
lightweight, and reliability for all
organisms. Although many
chemicals are effective, only
preparations that release halides
(iodine or chlorine) are readily
available and have been proven by
extensive use. Silver compounds
are used in other countries but have
not been approved by the EPA for
the United States.
Iodine Disinfection
During World War II, a search
for a simple, reliable water
disinfectant was initiated at
Harvard University because
chlorine-based systems were too
undependable. The investigating
team found that diatomic iodine (I2)
and the various ions resulting from
the dissociation of molecular iodine
in water consistently and reliably
disinfects water containing as many
as ten million bacteria per
milliliter, a concentration
approximately ten times greater than
grossly polluted water. (The
effectiveness of iodine was
demonstrated on raw sewage from
the Cambridge, Massachusetts,
sewage system.) Unlike chlorine,
iodine is fast, resists inactivation by
organic compounds, is active over a
wide pH range, and is available in
stable preparations.
At 73°F (23°C), even in
moderately turbid water with
moderate amounts of organic color,
an iodine concentration of 8 mg/l (8
parts per million) eradicates
bacteria, viruses, parasites, and
parasitic cysts other than
Cryptosporidia. A contact time of
only ten minutes already includes a
considerable margin of safety.
(About ninety seconds is adequate
for eliminating bacteria and
viruses.)
However, an iodine
concentration of 8 mg/l (8 parts per
million) is only needed to destroy
parasitic cysts. A concentration of
0.5 to 1.0 mg/l eliminates other
microorganisms. If filters are used
to eliminate Cryptosporidia and
other parasites, only such small
concentrations are needed. The only
currently available preparation that
readily supplies such a limited
quantity of iodine is a saturated
iodine solution. Tablets could be
broken up or dissolved in much
larger quantities of water (two
gallons.)
Iodine Disinfection
Precautions
In cold water (32° to 41°F or 0°
to 5°C) the chemical activity of
iodine is slower, just as all
chemical reactions are slower at
lower temperatures. An increase in
contact time to twenty minutes has
been recommended to ensure
complete disinfection.
Cloudy, heavily contaminated
water requires more iodine to
compensate for binding of the
disinfectant by organic compounds;
however, doubling the iodine
concentration or doubling the
contact time is sufficient.
If the water has been filtered,
such precautions are probably
unnecessary, but appropriate studies
have not been published.
Masking Iodine’s Taste

In water that has been filtered
and disinfected with 0.5 to 1.0 mg/l
of iodine, the low concentration of
iodine cannot be tasted by most
people. If larger quantities of iodine
are used and individuals find the
taste objectionable, several
methods for masking its taste are
available. Because such procedures
inactivate the iodine, they must not
be used before enough time has
elapsed for microorganisms to be
destroyed.
Artificial flavorings added to
hide the taste usually contain
ascorbic acid, which reacts with
iodine and impairs its antimicrobial
activity. Potable Aqua® is now
supplied with ascorbic acid tablets
—to be added after disinfection is
complete—to eliminate the iodine
taste. A less convenient technique is
to convert the iodine to tasteless
sodium iodide with an equal weight
of sodium thiosulfate. The water
can be filtered through activated
charcoal, which, by adsorption,
physically removes the iodine (and
some odors, inorganic materials,
and microorganisms but not enough
to make the water suitable for
consumption).
In clear water, the rate at which
microorganisms are destroyed by
halogens is dependent on contact
time and iodine concentration. If
time is available for more
prolonged disinfection, lower
concentrations of iodine can be
used. One-half the standard
concentration of iodine is equally
effective as a disinfectant if
allowed to act for twice the usual
time; one-fourth the standard
concentration is an effective
disinfectant if allowed to act for
four times the usual time. Even
lower iodine concentrations could
be used, but less than 2.0 mg/l
usually cannot be tasted. (Some
individuals prefer a barely
detectable trace of iodine as
assurance that the water has been
disinfected.) A common practice is
to add a small quantity of iodine to
water that is to be disinfected and
leave it overnight.
Persons with known thyroid
dysfunction should determine how
they react to water disinfected with
iodine at home before relying on
iodine water disinfection in the
wilderness or while traveling. The
uncommon individuals who are
allergic to iodine, including iodine-
containing compounds in
radiographic contrast media, and
those with thyroid dysfunction who
react adversely must not use iodine
for water disinfection. For such
individuals a filtration system to
physically remove bacteria,
parasites, and parasitic cysts,
followed by chlorine or ultraviolet
light offers a reliable alternative to
kill viruses.
Iodine Toxicity
Several publications have
claimed that the iodine used for
water disinfection is dangerously
toxic. The skull and crossbones on
bottles of tincture of iodine is
familiar. However, iodine is only
weakly poisonous. The third edition
of Goodman and Gilman’s Textbook
of Pharmacology states, “that
iodine is highly toxic … is a
popular fallacy.” The lethal dose is
2 to 3 g, but survival after ingestion
of 10 g has been reported. Iodine in
such large quantities is a strong
gastrointestinal irritant and causes
immediate vomiting, which
eliminates most of the iodine. That
remaining in the gastrointestinal
tract is largely neutralized by the
intestinal contents. The immediate
treatment for iodine poisoning is
administration of starchy food.
Accidental iodine poisoning is
rare; almost all fatalities are
suicidal, but successful suicide is
uncommon if the person receives
medical care. Between 1915 and
1936 no deaths occurred among 327
individuals who arrived alive at
Boston City Hospital following
attempted suicide with iodine.
Ingested iodine is absorbed as
iodide, and an average adult
requires 150 to 200 μg a day. Daily
consumption of one to two liters of
water disinfected with 8 mg/l of
iodine would provide thirty to
eighty times that amount, but
individuals with normal thyroid
function probably would not be
affected by such quantities. (Only
two to ten times the normal
requirement would be produced by
0.5 to 1.0 mg/day.) The daily dose
of potassium iodide that used to be
administered as an expectorant for
asthmatics ranged from 1.2 to 8.0 g
(0.9 to 6.0 g of iodine).
Iodine can cause fetal goiters
that produce respiratory obstruction
at birth, but the mothers of infants
with iodide goiters were almost all
asthmatics who consumed a gram or
more of iodine daily for many
months or years.
Inmates of three Florida prisons
drank water disinfected with 0.5 to
1.0 mg/l of iodine for fifteen years.
No detrimental effects on the
general condition or thyroid
function of previously healthy
persons were detected with careful
medical and biochemical
monitoring. Of 101 infants born to
inmates who had been in prison for
122 to 270 days, none had
detectable thyroid enlargement.
However, all four individuals with
hyperthyroidism became more
symptomatic while consuming
iodinated water.
Iodine Preparations
Tetraglycine Hydroperiodide
Tablets containing tetraglycine
hydroperiodide are widely sold
under trade names such as
Globaline and Potable Aqua®. One
fresh tablet dissolved in a liter of
water provides an iodine
concentration of 8 mg/l, far more
than needed if the water has been
filtered. A major advantage of
tetraglycine hydroperiodide tablets
is their convenience. The very
small bottle of fifty tablets can be
carried easily. Sealed bottles can
be stored for months with little loss
of iodine. (The manufacturer of
Potable Aqua® claims four years.)
The principal disadvantage of
tetraglycine hydroperiodide is its
tendency to dissociate after
exposure to air. In studies to
document their stability,
tetraglycine hydroperiodide tablets
placed in a single layer in an open
dish at 140°F (60°C) lost 40
percent of their iodine in seven
days. At room temperature and 100
percent humidity, the tablets lost 33
percent of their iodine in four days.
Studies to determine the rate of
dissociation of tablets in a small
bottle opened several times a day
for one or two weekends a month,
the pattern of weekend outdoor
recreationalists, have not been
reported.
Tetraglycine hydroperiodide
tablets (and other iodine
preparations) add a definite brown
tinge to the water if 8 mg/l is
present, which should aid in
demonstrating their potency. Tightly
capping and refrigerating bottles of
the tablets may help retard iodine
loss, but they probably should be
discarded a few months after
opening. (The manufacturer of
Potable Aqua® recommends a
year.)
Saturated Aqueous Iodine

Solution
In 1975 Kahn and Visscher
described a procedure for
disinfecting water with a saturated
aqueous solution of iodine. Iodine
crystals (2 to 8 g, USP grade,
resublimed) are placed in a 30 ml
(1 oz) glass bottle with a paper-
lined, Bakelite cap. (The details are
important; aluminum-lined caps
must not be used.) The bottle is
filled with water, shaken
vigorously, and allowed to stand for
one hour to produce a saturated
solution.
Originally, one-half of this
saturated solution (15 ml) would be
poured into one liter of water to be
disinfected. If the temperature of the
water in the 30 ml bottle is 68°F
(20°C) or higher, which can be
achieved easily by carrying the
bottle in a shirt pocket, the iodine
concentration in the disinfected
water would be about 9 mg/l.
If the water has been filtered, a
bottle cap of the solution (2 ml)
provides an adequate amount of
iodine.
Saturated aqueous iodine
solutions have two distinct
advantages:
A bottle containing 2 grams of
iodine could disinfect up to
2000 liters of water;
If crystals can be seen in the
bottom of the bottle, enough
iodine for disinfection is known
to be present, so the system is
reliable.
This technique for water
disinfection has been denounced,
even in terms such as “It can kill
you,” because in decanting the
supernatant, iodine crystals could
be poured into the water to be
consumed. This hazard is
insignificant. Iodine is so weakly
toxic that three or four crystals do
not produce any symptoms.
Individuals who have used this
technique extensively have found
that small flakes of iodine are
commonly caught by surface tension
in the small bottle, poured into the
large bottle, and ingested without
producing any detectable ill effects.
A jar with a sleeve in its neck to
prevent decanting the iodine
crystals, marketed as Polar Pure, is
commercially available. On its
surface this jar also has a
temperature indicator and data for
calculating the volume of saturated
iodine solution that would contain 8
mg of iodine. However, this jar is
too large to comfortably fit into a
shirt pocket.
A saturated aqueous solution of
iodine has been singled out as being
uniquely ineffective at low
temperatures for eradicating
Giardia cysts. If microfiltration is
used to remove Cryptosporidia,
this question is moot.
One real problem with saturated
iodine solutions is the tendency for
the water to freeze and break the
bottle. (Such a small amount of
iodine is dissolved in the water that
the freezing temperature is not
significantly lowered.) Leaving an
air space in the bottle by not
refilling it after its last use in the
evening would allow the water to
expand as it freezes and prevent
breaking the bottle. Alternatively,
the bottle must be kept inside a
sleeping bag. (Glass is the only
satisfactory container for aqueous
iodine solutions.)
Saturated iodine solutions are
widely used for water disinfection
because they are convenient and
reliable. For informed adults,
extensive experience indicates that
the method is safe, although
children must not be entrusted with
a potentially lethal quantity of
iodine.
Tincture of Iodine
Tincture of iodine is useful for
water disinfection only because it is
so readily available. In
industrialized nations such as the
United States, tincture of iodine
would be particularly valuable
when a major disaster, such as an
earthquake, has resulted in
contamination of municipal water
supplies and the water cannot be
boiled because electrical power
has been interrupted and gas lines
have been broken.
The major disadvantages of
iodine tincture are its taste and its
iodide component. Many have
found the iodine taste imparted by
the tincture to be much stronger than
that of other preparations containing
similar quantities of iodine. The
U.S. Pharmacopeia (USP) standard
solution is 2 percent iodine and 2.4
percent sodium iodide in 50 percent
ethanol. (Different concentrations
are also sold as “tincture.”) The
iodide has no disinfectant activity
and increases total iodine intake.
Tincture of iodine resists
freezing. Also, it can be used to
disinfect skin, but aqueous solutions
are just as effective for that purpose
and do not sting. Addition of 0.5 ml
of a 2 percent solution to a liter of
water provides an iodine
concentration of 1.0 mg/l. The
tincture must be stored in glass
bottles.
Chlorine Disinfection
The effectiveness of chlorine for
water disinfection is well
documented. However, the
disinfectant action of chlorine is pH
sensitive, and if organic residues
are present, chlorine combines with
ammonia ions and amino acids to
form chloramines, which release
chlorine slowly and inconsistently.
Although most municipal water
systems in North America use
chlorine as a disinfectant, free
chlorine levels in the water must be
constantly monitored to ensure they
are adequate for disinfection.
Monitoring is not practical in the
wilderness or in developing
countries. Furthermore, chlorine
compounds that have been
advocated for wilderness water
disinfection, such as Halazone or
chlorine bleaches, are unstable and
of questionable reliability.
(Manufacture of Halazone was
discontinued in 1989.)
Hypochlorous acid and chlorine
dioxide are available in stable
forms and are reliable.
Chlorine Preparations
Liquid Bleach (Sodium
Hypochlorite)
Most liquid bleach preparations
for home laundry are 5 percent
sodium hypochlorite solutions,
which could disinfect water
effectively, at least theoretically.
Laboratory studies to evaluate the
effectiveness of such agents have
not been carried out. In addition, the
solutions are very unstable, which
renders them problematic for
wilderness water disinfection
because much of the chlorine is lost
as the solution sloshes around while
being transported. Solid or powder
beach preparations are not
available in a form that allows an
appropriate quantity for water
disinfection to be easily
determined.
If liquid bleach is used for water
disinfection, the standard procedure
is to add two drops to a liter of
water with a temperature above
60°F (16°C) and allow it to stand
for thirty minutes. If the water is
colder, it should be allowed to
stand for forty-five minutes. Liquid
bleach is a much slower
disinfectant than iodine
preparations or other chlorine
preparations.
MSR MIOX® Purifier
(Hypochlorous Acid)
In fall 2003 MIOX®
Corporation (www.MIOX.com), in
association with Mountain Safety
Research® (MSR), released a new
chlorine-based water disinfection
system for individuals. Various
much larger units that employ the
same electrolysis procedure have
been in operation since MIOX®
was formed in 1994. The U.S.
Forest Service uses these devices
in several parks, and the units have
proven quite valuable in developing
countries. (MIOX® was one of nine
companies to receive the
presidential E award for excellence
in exporting in 2002.) The Purifier
was a Grand Award winner in the
General Innovation category for
Popular Science’s “Best of What’s
New” issue that year.
The system operates by sending
an electrical current through a
saline solution (brine), which
produces a mixture of oxidants,
most importantly hypochlorous acid
(HOCl), a very effective chlorine-
based disinfectant compound. In
appropriate concentrations the
solution from the small, individual
unit effectively eliminates bacteria
and viruses from water in thirty
minutes. Parasites take longer.
Cryptosporidia—against which
hypochlorous acid is eventually
effective, unlike chlorine or iodine
—require four hours.
The device contains a small
chamber on top into which a salt
pellet—or rock salt or common
table salt—is placed. About a
quarter teaspoon of water is placed
in a second chamber underneath the
first, and the unit is shaken to mix
the salt and water and produce a
saline solution. A button is pushed
to send an electric current—
produced by two three-volt lithium
camera batteries—through the
solution. Pressing the button once
provides enough oxidants to
disinfect 0.5 liter of water. Pressing
it twice yields enough for a liter,
pressing three times provides
enough for two liters, and pressing
four times yields enough for four
liters. One salt pellet lasts for
approximately fifty liters of water,
and one set of batteries can
disinfect about two hundred liters.
A green light indicates when the
oxidant mixture has been generated,
which takes five seconds to two
minutes. Combinations of red and
green constant and blinking lights
indicate whether the solution is too
strong, too weak, too salty, or the
batteries are running low. A chart
aids in interpreting the signals.
After the solution has been stirred
into the water to be disinfected, test
strips are provided to determine
whether the water has been
adequately treated.
The solution is reported to add
no taste or odor to the water. A
number of online publications
proclaim that it eliminates pumping
water through a filter to remove
Cryptosporidia, but four hours is a
long time to wait for disinfection to
take place. Water disinfection
systems must be fast, or they will
not be used.
The unit is approximately the
size of a small Maglite® and
weighs 3.5 ounces, although the
entire kit, which includes test strips,
an instruction booklet, a reference
card, and a carrying sack, weighs 8
ounces. It is available online from a
number of companies but is
relatively expensive.
This system appears to be
particularly valuable for
individuals who have iodine
allergies and hyperthyroidism and
must use some disinfectant other
than iodine. Usually water needs to
be filtered—four hours is a long
wait. A bottle of tetraglycine
hydroperiodide tablets or saturated
aqueous iodine is smaller than this
device and far cheaper.
Chlorine Dioxide
Chlorine dioxide (ClO2) has
been used for many years as a
disinfectant in a number of
applications. It is rapidly effective
against a wide variety of organisms
including bacteria, protozoa,
viruses, molds, spores, and mildew.
It has 2.6 times the oxidizing
capacity of chlorine and is four to
seven times as biocidal as sodium
hypochlorite at equivalent
concentrations. However, for most
applications chlorine dioxide has to
be generated at the site where it is
used because it is unstable
(explosive) and large quantities
cannot be transported or stored.
Only in recent years has a
technique for producing tablets that
release chlorine dioxide been
developed. The tablets have a
highly engineered surface that
features sites at which the activator
is located and numerous pores.
When the tablet is immersed in
water, the activator reacts with
chlorite contained in the rest of the
tablet to generate chlorine dioxide.
The reaction takes place in the
pores because only in that location
is the concentration of chlorite high
enough to produce chlorine dioxide
at a sufficiently rapid rate to make
the system practical. The pH of the
water is not changed as it is in most
commercial chlorine dioxide
generating processes because the
reaction is largely limited to the
pores.
Chlorine dioxide was first used
for water disinfection in 1944. It is
effective at low concentrations and
over a wide pH range. It
biodegrades in the environment and
does not generate harmful
byproducts. It does not leave a
residual chlorine taste or smell.
Distributors claim it actually
improves the taste and smell of
water.
The tablets are distributed in foil
strips that do not allow contact with
water or the moisture in air. To use,
the foil packet should be cut open
and the tablet quickly dropped into
a liter of water, which should be
placed out of direct sunlight during
disinfection. Destruction of bacteria
and viruses requires fifteen minutes;
elimination of Cryptosporidia and
Giardia requires up to four hours.
Chlorine dioxide tablets are
being produced by at least three
manufacturers: Potable Aqua®
(Chlorine Dioxide Tablets),
Katadyne® (Micropur®), and
Aquamira® (Water Purifier
Tablets).
Aquamira® also has a liquid
preparation, Aquamira® Water
Treatment Drops, which comes in
two containers. The first (Part A)
contains 2 percent chlorine dioxide
and the second (Part B) contains 5
percent phosphoric acid. Seven
drops from each container are
mixed in a small cup (provided),
allowed to stand for five minutes,
during which the solution changes
from clear to yellow, then is added
to a liter of water. The manufacturer
recommends letting the water stand
for fifteen minutes before
consumption, but eradication of
Cryptosporidia and Giardia would
probably require longer.
Similar liquid preparations are
produced by Pristine Water
Treatment Systems, a British
Columbia company, and sold by the
name Water Purification System.
Contact times for inactivation of
Cryptosporidia listed by Pristine
range from fifteen minutes in warm
water using a triple dose to seven
hours using a single dose in 39.2°F
(4°C) water.
Ultraviolet Light
The SteriPEN®, produced by
Hydro-Photon, disinfects water
with ultraviolet light
(www.steripen.com). Time
magazine thought enough of the
original device to list it among the
“Inventions of the Year” for 2001. It
also was named the United
Kingdom Outdoor Writers Guild
product of the year. In studies
carried out at four major
universities, this product was
demonstrated to eliminate viruses,
bacteria, and protozoa. Among the
organisms against which this device
was effective were Cryptosporidia
and Giardia.
The original device, called the
SteriPEN Water Purifier®, is 7
inches long and about 1.5 inches on
each side. It weighs 6 to 8 ounces
with batteries, depending on the
battery type. The SteriPEN
Adventurer Water Purifier®, is
smaller, 6 by 1.5 by 1 inches, and
lighter, 3.6 ounces. A third device,
the SteriPEN Traveler Water
Purifier® is approximately half the
size of the original SteriPEN Water
Purifier®. All three are smaller and
no heavier than currently available
water filters.
The Water Purifier operates on
four AA batteries. Alkaline
batteries provide twenty to forty
water treatments; rechargeable
batteries provide sixty to seventy
treatments; lithium batteries provide
130 to 140 treatments.
The Adventurer and the Traveler
are supplied with two
nonrechargeable lithium CR123A
batteries. Rechargeable lithium
CR123A batteries are available,
and the SteriPEN® manufacturer
provides them with a recharger that
includes a 110/240 volt power
adapter and has a solar power
panel that recharges two batteries in
two to four days.
To disinfect water, the
ultraviolet light source on the
instrument’s tip is inserted into
water and stirred. All these devices
are capable of disinfecting 16
ounces of water in about sixty
seconds—a liter of water requires
ninety seconds—so they are far
faster than any other disinfecting
device suitable for backpacking.
The devices are not cheap, costing
about as much as the more
expensive filters. Batteries cost
extra.
The SteriPEN® is a slightly
expensive replacement for filtration
and chemical disinfection. Its
speed, ability to destroy parasites,
and ability to disinfect water
without imparting any taste are
particularly attractive features. For
individuals who cannot use iodine,
they are not more expensive than
other disinfection techniques.
How well these devices stand up
to the rigors of outdoor use,
particularly being crammed into a
backpack, is not stated. The two
newer devices have protective
sheaths; the older one had a sturdy
cover.
The devices appear uniquely
useful for travelers because a glass
of water could be disinfected in a
hotel room very easily in only sixty
seconds. They also are valuable for
individuals who are allergic to
iodine or who have
hyperthyroidism and must use some
disinfectant other than iodine.
CHAPTER 7
RESCUE AND EVACUATION
Ken Zafren, M.D.
Urs Wiget, M.D.
With satellite telephones, global

positioning system (GPS)
navigation, and modern air
transport, few major expeditions to
any area, no matter how remote, are
as isolated as famous expeditions of
the past. The days of crossing
oceans in sailing ships—except as a
novelty—are over. The epic stories,
such as Shackleton’s heroic
survival after his ship Endurance
became trapped in ice and sank, are
destined to be largely historical.
However, ships still sink, and
climbers still are lost and their
bodies never recovered.
Expeditions still entail risk of
illness, injury, and death and have
limited resources for coping with
such threats. Problems are best
prevented by minimizing the
hazards. Ascending slowly to
prevent altitude illness or sailing
judiciously to decrease the danger
of colliding with an iceberg are
prudent. If preventive measures fail,
the next link in the chain of survival
is preparation for untoward events.
The ability to recognize altitude
illness and to descend promptly, or
providing life rafts for ship
passengers and crew, are
preventive measures that can save
those who otherwise might die.
This chapter has been written to
aid in preparation for coping with
adverse events. Measures taken in
advance, such as securing
communications gear and setting up
rescue plans, are essential elements
of rescue planning. Other measures,
such as including expedition
members with search and rescue
experience and medical skills, and
bringing along rescue and medical
equipment, enhance the ability of an
expedition to care for and evacuate
ill or injured members.
DECISIONS THAT PREVENT

PROBLEMS
Expeditions cannot bring along
unlimited equipment. Expeditions in
which members must transport the
gear may be quite limited; some
may have no member with medical
or rescue training. Expeditions must
carefully consider likely hazards,
how to prevent them, and how to
provide for their successful
resolution if preventive measures
fail.
The transition of Himalayan
mountaineering from expedition
style, with fixed camps and a
supply chain, to alpine style, with
climbers moving up a mountain
quickly with limited food and
equipment, carried increased risk
for those at the “thin end” of the
rope. However, the exponents of
alpinestyle climbing justify the
increased risk as necessary to
achieve their goals and attempt to
compensate for it by reaching high
levels of fitness and ability. In some
ways, such efforts signal
reemergence of an earlier era.
Ernest Shackleton’s advertisement
for the Endurance expedition read,
“Men wanted for hazardous
journey. Small wages, bitter cold,
long months of complete darkness,
constant danger, safe return
doubtful. Honour and recognition in
case of success.”
Decisions that an expedition
must make prior to departure
include whether to bring equipment
such as backup gear, specialized
rescue equipment, and medical
supplies, and whether to include
members with rescue or medical
skills, either as full members of the
expedition or as resource members
who only have support roles such
as staying in base camp on a
mountaineering expedition or
staying on the surface in a diving
expedition. Some support personnel
may not even go on the expedition
but carry out such tasks as
coordinating resupply or launching
a rescue. With satellite telephones
and other modern communications
links, support personnel may not
need to wait until an expedition is
overdue to send help. Every backup
plan should include measures to be
taken if expedition members fail to
communicate as expected or miss a
planned rendezvous.
Some of the most important
decisions that expedition members
must make are establishing safe
operating procedures. Often these
decisions are not made consciously.
When the consequences of failure
are high, the consequences of an
inadequate safety culture can be
grave. A routine activity that clearly
exemplifies a safety culture is the
operation of commercial aircraft.
Flying has become extremely safe
in recent years because pilots and
airlines have embedded safety
cultures. The rates of human error
and equipment failure have been
minimized through checklists,
standardized procedures, repetitive
practice, and redundancy. Vertical
rescue is another example of an
inherently dangerous activity that
has been made safer by
implementation of these principles,
although the level of safety hardly
approaches that of commercial
flight.
When applied to expeditions,
safety culture has the potential to
decrease the incidence of
equipment failure, illness, and
injury. Adequate training is
essential. Even with training, fail-
safe measures are needed to
decrease human error and prevent
serious problems and include
simple basic measures such as
ensuring that all members wash
their hands after defecating and
before meals and requiring the use
of sun protection in high-exposure
areas. Ensuring safe practices,
including use of appropriate safety
equipment in such hazardous
activities as boating, diving,
mountaineering, canyoneering, and
caving also can dramatically reduce
the probability and consequences
for accidents.
Problem Recognition
When a threat to the health or
survival of one or more members of
an expedition exists, the leader or
other members must recognize the
problem and decide on a course of
action. This may seem obvious, but
human nature tends to ignore
problems until they are clearly
threatening. Workers have a natural
tendency to ignore fire alarms in
large buildings and to carry on as
usual. Many of those who died in
the destruction of the World Trade
Center were advised not to
evacuate by authoritative-sounding
but tragically misguided
announcements on the public
address system.
The existence of a problem is
not always clear. Communication
may be nonexistent or interrupted.
The famous self-rescue of Joe
Simpson (Touching the Void) was a
result of Simpson’s partner thinking
Simpson had died in a fall. Many
expeditions have suffered accidents
about which base camp or other
groups were completely unaware.
Decision Making
Once a problem has been
defined, members of the expedition
must attempt to solve it. The
ultimate success of the expedition
may depend on the solution. In many
cases, ill or injured members may
be unable to move under their own
power. In a few instances, such as
high-altitude pulmonary edema
(HAPE) or venomous snakebite,
moving under one’s own power
may worsen the prognosis.
Individuals with frostbite of the feet
often can self-evacuate, but
frostbite of the hands may make it
impossible to do necessary tasks,
such as descending technical terrain
with fixed lines. Individuals with
high-altitude cerebral edema
(HACE) are generally too ataxic,
even after recovering, to be
allowed to descend on their own.
If a member is ill or injured
enough to require evacuation, the
expedition must devote sufficient
resources to the task. On water, this
may be quite simple. On a
mountain, this may only require a
few members to lower the person,
but on trails or even on level
ground, the task of carrying a totally
disabled person any distance can be
quite daunting and require many
people. A prominent
mountaineering text proclaims—not
entirely in jest—that a successful
rescue requires a basket stretcher
and two dozen stretcher bearers.
Before proceeding with a
rescue, the team must spend
adequate time discussing the plan.
Every member should have a
defined role, and the team should
determine the techniques to be used.
A few minutes spent in planning
prevents many mistakes and delays
later on.
Search and Rescue

The emphasis in this chapter is
on improvised techniques. On large
expeditions with multiple teams in
the field and possibly a support
group in base camp, expedition
rescue may sometimes take on
aspects of organized search and
rescue. Search and rescue skills are
best acquired through formal
training and participation in rescue
missions in an organized rescue
group. These skills can be adapted
to the expedition setting. Written
resources include several useful
books. Mountain Search and
Rescue Techniques by William G.
May (Boulder, CO: Rocky
Mountain Rescue Group, 1973) was
written as a training manual for an
active mountain rescue group,
whereas Wilderness Search and
Rescue by Tim J. Setnicka (Boston:
Appalachian Mountain Club, 1980)
is a more general text and covers
related areas such as white-water
and cave rescue. Although both
books are now out of print and
somewhat dated, the basic
techniques have not changed. Other
specialized books include River
Rescue: A Manual for Whitewater
Safety, 3rd edition, by Slim Ray
and Les Bechdel (Boston:
Appalachian Mountain Club, 1997)
and On Call: A Complete
Reference for Cave Rescue by John
C. Hempel and Annette Fregeau-
Conover (Huntsville, AL: National
Speleological Society, 2001).
In the expedition setting, search
is usually limited or unnecessary,
because either the location of the
party needing rescue is known or
the party is inaccessible to the rest
of the expedition. If the expedition
is divided into teams, an injury or
equipment malfunction may break
the chain of communication and the
only knowledge that one team may
have is that another team failed to
arrive at a destination or failed to
communicate as scheduled. When
this occurs, the rest of the
expedition must initiate a search for
the missing party.
Search is an emergency. The
common admonition not to worry
because an overdue person or group
is very capable is often the opposite
of the correct interpretation, which
is that this very capable party may
be in real trouble since a
rendezvous or radio call was
missed.
Expeditions can increase safety
by frequent radio contact. With the
increasing availability of GPS,
expeditions have the potential for
keeping track of the location of
every member and every equipment
cache in real time.
The search phase of search and
rescue can be conceptualized in
many ways. A common schema
breaks search into phases of first
notice, planning or strategy, and
tactics. First notice on an
expedition may consist of a radio
call from a team that is in trouble,
or it may be inferred from the
failure of a team to arrive at a
location or communicate as
planned.
Next the expedition leader or a
designated member determines the
search strategy, which should be
mostly preplanned. For example, if
a team fails to arrive at a
rendezvous as expected, a series of
routine steps is initiated, which
could include extra radio calls,
alternate means of communications,
such as whistles or flares, or
sending out a search party to the
expected location of the missing
team.
In organized search and rescue,
individuals are often found with the
aid of a strategy that includes
determining their last known
location (“point last seen”) and
confining the search area by
defining the perimeter beyond
which the missing individual is
unlikely to be found. The next step
is to determine likely routes of
travel and to perform a “hasty”
search with small fast teams or
aircraft along these routes. A large
search often culminates in
“saturation searching” with large
numbers of searchers looking for
clues. At this phase, formal
estimates of the likelihood of
finding a lost person in each part of
the search area are made based on
the likelihood of the person being in
the given location and the
probability of detection using
different search methods.
For an isolated expedition,
search tactics would likely start
with “survey” methods, including
contacting other teams that might be
in contact with the missing team and
noise and flares to be answered in
kind. The next step, for expeditions
without motorized or airborne
resources, would likely employ
oldfashioned methods such as
sending a team or teams to the
likely location(s) of the lost team
and along likely routes of travel
(“scratch” or “hasty” search).
Scratch teams would carry a radio
and a minimum amount of survival,
rescue, and medical gear. If the
expedition has motorized resources
such as wheeled vehicles, snow
machines, or boats, they usually can
carry more gear than self-powered
teams.
Depending on the nature of the
expedition and the terrain,
saturation search may have no role.
In vegetated areas or in avalanche
debris, specialized line searches
may be needed.
CARRYING AN ILL OR
INJURED PERSON
On all but the largest expeditions,
taking specialized rescue equipment
in addition to all other necessary
equipment and supplies is hard to
justify. The bulk and weight of such
equipment—and costs—would add
a significant burden. In most
instances, the equipment is not
available where a person needs to
be rescued.
Many types of stretchers are
available. In rescue work these are
usually referred to as litters and
include basket litters, flat litters,
and soft litters. A discussion, with
specific litter examples, mostly
from North America, can be found
in the chapter “Litters and Carries”
in Wilderness Medicine, 5th
edition, edited by P.S. Auerbach
(St. Louis: Mosby, 2007). Whereas
having a litter at base camp might
conceivably be worthwhile under
unusual circumstances, most
expeditions have little use for
heavy, bulky equipment. If long,
overland evacuation with a litter
from base camp is a real
possibility, an expedition should
consider having a wheeled litter,
with which it is much easier for a
small number of rescuers to move a
disabled person over long
distances.
An item that might prove useful
under some circumstances is a
vacuum mattress (also referred to
as a full-body vacuum splint).
These devices provide the best
means of immobilizing a person for
a long transport. They are superior
to backboards for stabilizing spinal
injuries because they are far more
comfortable and much less likely to
lead to decubitus ulcers from
pressure points. A vacuum mattress
is essentially a mattress-shaped
beanbag with a valve for evacuating
air. Once the air is removed,
atmospheric pressure causes the
mattress to assume a rigid shape
that conforms to the person’s body.
A vacuum mattress can be used
alone as a stretcher in nontechnical
terrain but more commonly is
placed in a litter for ease of
transport. For a large expedition, a
vacuum mattress could be kept at a
base camp.
Improvised techniques, although
not as satisfactory in some ways as
commercial equipment, have the
advantage that they can be used
immediately where needed. The
most useful of these techniques are
discussed in “Improvised
Transportation” elsewhere in this
chapter. On most expeditions, the
initial stages of transport, if not the
entire rescue, are dependent upon
improvised techniques. The basic
improvised litter is the rucksack
stretcher, which also is described in
the “Improvised Transportation”
section of this chapter.
Packaging
No matter what type of litter is
used, individuals must be protected
from further injury. All injured
areas must be stabilized with
dressings and splints, including
traction splints and cervical collars
if needed. The person must be kept
warm, even though immobile, while
allowing for reassessment of
injuries with the least possible
interruption of transport. The
individual must be protected from
hazards of transport, including
falling objects or tree branches,
secured to the litter (except for
some forms of water transport), and
in technical terrain belayed
independently of the litter. A
vacuum mattress is easily secured
to most litters, and most
commercial litters come with tie-in
straps.
For the rucksack litter, an
improvised litter constructed with
three or four rucksacks secured end
to end, the hip belts serve as tie-in
straps. The person’s head can
usually be secured by placing the
hip belt of the pack at the end for
which the hip belt is not part of the
assembly around the forehead. Care
must be taken not to secure a hip
belt too tightly around the chest,
which would restrict breathing.
Depending on the specific injuries,
some adjustments may be necessary
to avoid placing pressure on injured
areas. Slings, short lengths of rope,
and tape can all be used to
improvise systems for immobilizing
individuals and injured areas so
they do not slide in the litter and
sustain further injury.
Rucksack stretchers containing
clothing provide some padding. If
backboards or commercial litters
are used, the person should be
placed in (or on) a sleeping bag,
preferably with sleeping pads
underneath the sleeping bag for
padding. The vacuum mattress is the
only ideal way to prevent pressure
sores, however.
A person who is vomiting or
likely to vomit ideally should be
transported on one side—the
“recovery position”—to protect
against aspiration. However, no
good method to secure a person in
that position has been developed.
Elevating injured parts, as
advocated by some writers, is
usually not feasible, although
injured areas should be protected
from excessive pressure. Most
individuals are transported in the
supine position. They must be
tightly secured in the litter and
monitored so that if they vomit the
entire unit—litter and occupant—
can be turned on its side and the
airway protected. If pelvic or leg
injuries are not present, padding
placed under the knees greatly
increases comfort in the supine
position.
Individuals who need evacuation
are usually placed in a sleeping bag
for warmth. In any case their bodies
should be covered for protection
against falling or windblown
objects, especially for helicopter
evacuations. The face and head
should be covered for the same
reason, although goggles reduce
claustrophobia. In steep terrain, the
person should wear a climbing
helmet. The arms should be
restrained in the litter for ease of
packaging and injury avoidance.
If the litter could be upended, the
person should be prevented from
sliding downward either head first
or feet first. Because vacuum
mattresses conform to the body, they
do not allow the person to shift,
either lengthwise or from side to
side. Commercial litters sometimes
have leg dividers, which help,
although they do not allow fractured
legs to be splinted by lashing the
legs together. Padding under the
knees also reduces the tendency for
the occupant to shift position.
Straps tied around each foot and
secured to the side of the litter are
sometimes used but do not work if
the knees are bent or a lower
extremity is injured.
In mountainous or glaciated
terrain, occupants should wear a
climbing harness that can secure
them to lowering or belay ropes and
prevent sliding lengthwise in the
litter.
High-Angle Terrain
In high-angle terrain (also
referred to as technical terrain), the
expedition usually would be
carrying ropes and anchors. An ill
or injured person who can assist the
rescuer can be lowered on vertical
terrain using a tragsitz (German for
“carry seat”). The original tragsitz
was made of canvas, and today the
device is available with additional
fabric choices. The method
described in “Improvised
Transportation” later in this chapter
accomplishes the same task without
a fabric seat. A rescuer splits a long
coil of rope into two joined coils
and puts the coils over his
shoulders. The injured party puts
one leg through each coil, which
can also be joined in front of the
rescuer, and the rescuer and the
injured person are lowered down a
cliff or very steep slope. This
technique is easiest in truly vertical
terrain. Both the injured person and
the rescuer must be tied into the
lowering line.
With the tragsitz technique,
single rescuers could lower
themselves and injured persons on
rappel. Rappel brakes must be
located well above both
individuals, both of whom must be
secured to the braking system.
Another method for
accomplishing the same reresult is
the single rucksack technique (also
described in “Improvised
Transportation”). Rescuing an
unconscious or severely injured
person from vertical terrain using
improvised gear can be a desperate
undertaking. Although many rope
and fabric stretchers have been
described, none provide significant
back support. Some can be stiffened
with skis or ski poles, but these are
not often available in a vertical
environment. In a pinch, an
individual could be lowered in a
sleeping bag, especially if a
bivouac sack and sleeping pad—
and preferably some other means to
stiffen the system for back support
—are available. Suspension of
some rope litters through loops as
tie-in points would be
straightforward, but fabric carriers
—sleeping bags and bivouac sacks
—typically lack tie-in points, so a
harness for the litter would still
need to be constructed. As with all
rescue systems on technical terrain,
the injured person and rescuers
must be directly secured to the
lowering line or to the suspension
system and not just to the stretcher.
The rucksack stretcher
(described in “Improvised
Transportation”) can be used.
Rucksacks are not designed to hold
a human load but are generally quite
strong, and this system provides
substantial back support. Properly
suspended horizontally from a
harness, which is often referred to
as “spiders,” the rucksack stretcher
would function like a litter on a
vertical or near-vertical evacuation.
As with all evacuations from
technical terrain, the rescuers and
the disabled person must both be
belayed, with both wearing
climbing harnesses. Both persons
are usually tied to the spider
system, never directly to the litter. If
the litter system fails, the result is
not a catastrophic fall. Although
many rescue groups use a single
rescuer to guide the litter, it is
easier to use two rescuers in all but
vertical or overhanging terrain.
Ideally, these litter bearers should
wear their own packs. If rockfall or
other falling objects threaten, the
litter bearers can attempt to lean
over the occupant for protection,
while their packs protect their
backs.
The spiders can also be
improvised. One easy method is to
use a double bowline on a bight,
with the end loop of the rope as
long as the other two loops, forming
a knot with three loops that can be
attached to two sides and an end of
the litter. A single 15-meter length
of climbing rope would suffice to
make two spiders with six points of
suspension. This would be tied into
a long loop with the spiders
suspended from the lowering rope
at the top and a shorter connection
along the long axis of the litter
between the two spiders, which
could be formed into an occupant
tie-in. Additional methods of
improvising a litter suspension are
suggested in the very useful chapter
on improvisation in the book
Mountain Search and Rescue
Techniques by William G. May.
With a rucksack stretcher, the
loops should be longer and run
completely under the rucksacks so
the rucksacks are supported by the
rope rather than by the straps of the
rucksacks. In less-than-vertical
terrain, the potential for abrading
the rope supporting the side of the
litter that faces the cliff is always a
problem. Tape can be used to
protect the rope in areas likely to
rub.
Intermediate Terrain
On steep terrain, the litter is
usually oriented vertically (parallel
to the slope angle), rather than
horizontally as on vertical terrain,
and is lowered on a rope. On very
steep terrain, two litter bearers
positioned on either side of the
litter are sufficient because much of
the weight of the litter is taken by
the rope. As the terrain becomes
less steep, it becomes very difficult
for two litter bearers to carry the
litter, since less weight can be
borne by the rope, and four litter
bearers are better than two. A
rucksack stretcher can be used for
such terrain but requires some
ingenuity for creating an
appropriate tie-in system. As in all
technical rescue systems, the
occupant must wear a climbing
harness and be secured directly to
the lowering rope in case of litter
failure.
On snow slopes, a person often
can be lowered in a sleeping bag
(with a sleeping pad underneath) in
a bivouac sack. This is a better
technique for ill than for injured
individuals. On steeper slopes, the
bivouac sack usually slides nicely
and can be lowered from a fixed
anchor. The occupant wears a
climbing harness and is tied into the
lowering line. On gentler slopes,
the bivouac sack can slide with
assistance from rescuers, usually
with a rescuer using a rope from
above to belay the occupant in case
the bivouac sack gets out of control.
This rescuer may move with the
litter on very gentle slopes and
safeguard the individual with a
short line tied to the rescuer’s
harness. However, this procedure is
safe only if the rescuer could
reliably self-arrest—even just lie
down—to stop the litter from
sliding downhill, and usually is safe
only on soft snow.
Flat Terrain and Gentle Slopes

On gentle terrain, where the risk
of the occupant and litter falling or
sliding down a slope is minimal,
the rucksack stretcher is superior to
most of the other commonly
advocated improvised techniques,
although short drags or carries still
can play a limited role.
Dragging or carrying an
unconscious individual should be
done only in the most hazardous or
dire conditions. The person can be
dragged without any special device,
especially if wearing smooth
synthetic outerwear, but a sleeping
pad, a bivouac sack, or some other
fabric, such as a tent, is preferable.
For very short carries of
individuals who are able to assist
to some extent, a simple piggyback
carry is a useful method. Even a
heavy person can be carried uphill
by a single rescuer, but only for
very short distances. It is easier if
two other rescuers are able to help
support the weight from the sides.
For longer, but still short,
carries, a four-handed technique
may be useful. The disabled person
sits between two walking rescuers,
supported on the joined right arm of
the rescuer on the right and left arm
of the rescuer on the left. The
rescuers’ other arms support the
back and the individual’s arms are
wrapped around their necks. The
disabled person can also be
supported between two rescuers on
a coil of rope suspended over the
rescuers’ shoulders, which has the
advantages of leaving the rescuers’
outer arms free and having the
person’s weight supported by the
rescuers’ shoulders rather than
forearms. The disadvantage is the
need to reposition the rope every
time the rescuers change. Two
rescuers cannot carry an adult very
far using either method.
For longer carries, the rucksack
stretcher is the most useful
improvised technique under most
circumstances. Stretchers made of
tarps, tents, or blankets without
poles provide little support for the
occupant’s back and rapidly
become uncomfortable. Rope
stretchers are usually quite
elaborate, take a long time and a lot
of practice to assemble, and also
provide little back support. Both
fabric and rope litters can be made
more rigid with poles (ski poles,
skis, or tree branches) but still are
more difficult to construct and offer
less support than the rucksack
stretcher. Rucksacks are almost
invariably present on expeditions,
whereas the other methods require
special equipment and do not solve
the problem of what to do with the
disabled person’s rucksack.
Some pole litters are designed to
be carried from the ends by two
rescuers, which is practical only for
very short distances unless the
individual is very light. However,
carrying a person in a litter in this
manner is sometimes necessary for
short stretches on narrow sections
of trails or across bridges.
Travois stretchers and
improvised sleds are theoretically
useful on quite smooth ground,
especially on snow, but are difficult
to construct. Polar expeditions and
expeditions in other glaciated areas
often have sleds available. These
can be commercial, heavy-duty
sleds or children’s plastic sleds
with additional rigging. Either type
is adaptable for transporting people
with suitable padding, even though
few are long enough to be ideal.
The occupant, like any important
load, must be tied into the main
rope in crevassed areas.
Carrying a Litter on Nontechnical

Terrain
The optimum number of litter
bearers on nontechnical terrain is
six, with three on each side. More
litter bearers just get in each other’s
way. Fewer carry too much weight
and risk dropping the litter if one
person stumbles. On level and
uphill terrain, the occupant is
carried head end first, but on
downhill terrain the litter is turned
around to keep the person’s head
higher than the feet. If the heights of
the litter bearers vary, the pairs
should be matched for height across
the litter, except on sidehill carries,
where the taller litter bearers
should be on the downhill side.
Sometimes a seventh rescuer
acts as litter captain. The captain
stays in front on level terrain,
sometimes supporting the heavier
head end, but also may steady the
litter from behind on downhill
stretches. The captain or the litter
bearers in front should call out
obstacles to those behind, who will
have difficulty seeing ahead. If
enough people are available, the
person who is providing medical
care can walk behind the litter to
monitor and comfort the occupant.
Even with six litter bearers,
carrying a litter with an adult for
any significant distance is
strenuous. If the rescue group is
large, enough members to carry the
litter in rotation may be available.
Some members should go ahead to
scout the route, stopping in pairs at
intervals of 50 to 100 meters. They
should station themselves on either
side of the trail, and as the litter
passes they replace the pair of litter
bearers at the back of the litter. This
back pair simultaneously moves
forward to become the middle pair,
the middle pair moves forward, and
the front pair walks ahead of the
litter. A leader or captain may
station the pairs, who can switch
sides so they use different muscles
in consecutive carries. In complex
terrain, such as woods or very
rocky terrain, this technique can be
modified by having the replacement
pairs in front of the litter and
performing the replacement in
reverse order. In either sequence,
the litter keeps moving
continuously, with only occasional
interruptions in complex terrain.
The litter bearers can support the
litter with a three-meter strap or
sling attached to the litter and
passed over the bearer’s shoulders
to the outside hand, which transfers
much of the weight to their
shoulders and makes carrying the
litter less strenuous. The slings can
also be used to adjust the height of
the litter to compensate for
variations in terrain. The litter
bearers should not be tied to the
litter.
Water Rescues
On flat water, such as lakes and
protected harbors, a boat or raft
may be valuable for avoiding a
long, difficult carry on land. A six-
person raft is adequate, but only a
single rescuer can row. An
eightperson raft allows two rowers
and an additional one or two
rescuers and is more stable. The
rescued and all rescuers should
wear personal flotation devices,
and the disabled person must not be
strapped into the litter.
RESCUES BY AIRPLANE AND

HELICOPTER
The sight of a horse
makes the strong man
lame.
—Old Afghan Proverb
The sight of a
helicopter makes the
strong rescuer lame.
—New Proverb
In many parts of the world, rescue
has been revolutionized by the use
of aircraft, which enable long
transports that were almost
unimaginable in the preaircraft era.
For expeditions operating in
suitable terrain, fixed wing aircraft
have many uses for rescue. Many
expeditions in remote areas arrive
and leave by airplane, which can be
adapted with skis for snow and
floats for water. Where airplanes
are unable to land, they can be used
to airdrop supplies. Rotorcraft
(helicopters) have additional
capabilities that make them useful
for expedition transport or rescue in
mountainous, canyon, or forested
terrain. A general knowledge of
aircraft operations can be crucial
for the success of expedition
rescue.
One particularly important
principle for flying in remote areas
cannot be overemphasized: Nobody
should ever be separated from
personal survival gear. Expedition
members should never board an
aircraft, take off in an aircraft, or
leave an aircraft without their
packs, even if the aircraft is
expected to return immediately or
two aircraft are flying the same
route at the same time. Aircraft can
be diverted by weather, mechanical
problems, or, most unfortunately, by
crashing.
To use aircraft successfully for
rescue, the group should have a
plan to activate air rescue, to
communicate with the pilot, to
define or construct a safe landing
zone, and to assist the pilot with the
landing. Every member of the
expedition should be familiar with
safety in aircraft operations.
Preplanning should include a
plan for activating air rescue if the
expedition does not have its own
aircraft. In many countries,
including most developing
countries, arranging air rescue
requires either prepayment or a
guarantee of payment. Expeditions
from many developed countries can
count on their embassies in the host
country to guarantee payment, but
the expedition must contact its
embassy in advance to ascertain its
policy. In the past, an alternative to
guaranteed payment was to make
funds available in the form of a
cash deposit or bond with the
embassy of the expedition’s home
country. Now credit card
authorization for the aircraft
operator is usually sufficient.
The expedition should know the
requirements for landing zones for
any aircraft likely to be used in a
rescue or evacuation. Airplanes
will need a runway for wheeled
aircraft, a large area of snow if on
skis, or a large body of water—
usually a lake—if on floats. The
pilot must know the altitude, slope,
and nature of the surface—
especially if it is uneven or if soft
snow is present that may cause a ski
to stick—and also must know about
any obstacles on the approach or
takeoff. Although helicopters can
land and take off vertically, a route
for gradual descent and takeoff is
safer. This is usually considered
two routes—one for ingress and
another for egress—although
helicopters can often turn 180
degrees while still near the ground
and follow the same path for
landing and takeoff. The larger the
landing zone, the safer it is. No
objects, such as shrubs or tree
stumps, should be sticking up, and
all loose objects must be secured so
they do not get blown about and
become hazards. Helicopter pilots
also need to know if the surface is
covered with loose snow, gravel, or
dust that could limit visibility on
takeoff or landing when blown up
by rotor wash.
Airplane and helicopter pilots
need to know the weather
conditions at the landing zone,
including visibility, temperature,
and wind speed and direction.
Ideally, at least one radio should be
available for ground-to-air
communications, but signals can be
used. A visible indicator of the
wind speed and direction is
essential and can be a brightly
colored article of clothing, a flare,
or a smoke grenade. (Smoke from a
fire is hazardous because the
burning material can be spread
about by rotor or propeller wash.)
Marking the landing zone is
helpful, particularly on snow. Dark-
colored garbage bags filled with
snow or rocks give the pilot a
visual reference that otherwise
would be lacking. Some pilots
throw these out of the airplane onto
the snow on a pass before landing.
Any object used to mark the landing
zone or give wind direction must be
well secured or heavy enough not to
blow about in propeller wash or
rotor downwash.
All personnel and equipment
should be out of the landing zone,
unless the terrain requires that a
helicopter land right next to a
rescue team. The team must crouch
and not move while the helicopter
lands. No loose equipment or
clothing should be allowed in the
landing zone. If the landing zone has
gravel, dust, or loose snow, anyone
nearby should wear eye protection
and face away from the helicopter
during landing and takeoff. In an
emergency, putting a hand in front of
the eyes and squinting helps
somewhat. A windbreaker with a
hood is also helpful.
Hot loading and unloading
(engine running and rotors turning)
is more hazardous but may be
necessary. During hot loading the
tail rotor may be nearly invisible.
People on the ground must
approach or leave helicopters only
from the front and sides (except for
rear-loading Chinook helicopters)
and only after a signal or radioed
permission from the pilot or a crew
member. They must stay in the
pilot’s line of sight during the entire
process. If the helicopter is on a
slope, ground personnel should
approach and leave from the
downhill side of the helicopter,
which helps to maintain a safe
distance below the rotor blades. If
circling around the helicopter is
necessary, it should always be done
around the front.
Individuals should crouch while
approaching or leaving the
helicopter and should carry any
objects horizontally below waist
level. On some helicopters the ends
of the rotor blades may be as little
as 5 feet (1.5 m) above level
ground. Chinook helicopters have
rear doors. Crew members assist
with approaching and leaving these
helicopters because the tail rotor is
so close.
Other safety rules for
approaching or leaving a helicopter
include removing hats, holding on
to loose objects, and never reaching
up or running after a loose object
that is blown away. A person
blinded by dust should crouch
lower or, ideally, sit down and
await help.
Individuals boarding a
helicopter should place their gear
inside first and then board, moving
over if other passengers are going
to board. The pilot or a crew
member should give instructions
about where to put gear, where to
sit, and how to put on seat belts and
shoulder harnesses. Any changes in
location of passengers or gear may
affect the helicopter’s center of
gravity and must be cleared with the
pilot or other crew member in
advance.
On occasion, boarding or exiting
a helicopter while it is hovering
just above ground or on one skid
may be necessary. Since the pilot
must compensate for any weight
shifts or changes, all movements
into and on the helicopter must be
done slowly and as gently as
possible. Passengers should gently
place packs and other equipment on
board before boarding and when
leaving should gently place (or
occasionally drop) the pack and any
other baggage on the ground.
Sometimes a short jump to the
ground is necessary, in which case
communication with the pilot is
essential. Rappeling out of a
helicopter is potentially dangerous
and must only be done by those with
special training and only when no
other method of reaching the ground
is feasible.
If an injured person is on a litter,
the method of loading depends on
the type of helicopter. In small
helicopters, the litter may fit only
longitudinally next to the pilot or in
another specified configuration.
Some helicopters have external
baskets; loads must be secured in
these by the crew. A load not
placed inside the helicopter is
referred to as an external load. In
rescue work, ropes or cables may
be used to carry a load below the
helicopter or to hoist a load into or
out of a helicopter. People or gear
can be attached to a line underneath
the helicopter and flown from one
location to another in that position,
which is referred to as “long-line”
or—confusingly—“short haul”
operation. For gear, often placed in
a net, such transport is often termed
“sling loading.” Long-line
operations differ from winch or
hoist operations in which the
external load is lowered from or
raised into the helicopter by a
winch. Members of expeditions
who are not trained for long-line or
hoist operations should await
instruction from a helicopter or
ground crew member. A load
hanging from a helicopter should
never be touched until it has
contacted the ground and
discharged the often considerable
static electricity built up in flight.
Loads hanging from helicopters
must be approached cautiously
because they can swing from side to
side or spin unexpectedly and injure
those on the ground. Some
helicopters with suitably trained
crew may be able to pick injured or
stranded climbers off cliffs or other
technical terrain. Usually, a rescuer
descends first and secures the
external load for this delicate and
potentially hazardous operation.
Airplanes are usually safer to
approach than helicopters, but
precautions must be taken around
the propellers. The pilot or another
crew member should give signals
or instructions. Usually hot loading
and unloading are avoided. In twin-
engine aircraft the engine on the
side of the aircraft opposite the
main cabin door is left running.
Most of the other safety principles
are the same as for helicopters.
Movement of people and gear in
light aircraft can change the center
of gravity just as in a helicopter and
must be avoided without approval
of the pilot or crew.
Many types of helicopters exist,
not all of which are suitable for
rescue. Most aeromedical
helicopters are not well suited for
rescue and vice versa. In certain
mountainous areas, such as the
Alps, rescue helicopters typically
have significant aeromedical
capabilities. In other areas, major
danger for helicopter crews and
those who would be rescued are
associated with the use of
aeromedical and other helicopters
in technical terrain. Any helicopter
used for rescue should meet
specific qualifications for
performance and crew training.
Wilderness rescue is the art of
the possible. Transporting an ill or
injured person in a suitable
helicopter initially and transferring
to an aeromedical helicopter is
preferable unless the aeromedical
helicopter has adequate
performance and the crew is trained
for operations in mountain terrain.
For high-altitude and mountain
operations, most helicopters,
including helicopters not routinely
used for rescue, such as news
helicopters, sightseeing helicopters,
and air taxis, are dangerous for
rescuers and should be used only
for the most limited tasks, such as
ferrying gear or equipment to
optimal landing zones that are well
within the performance capability
of the helicopter and crew. The
same principles apply to airplanes.
IMPROVISED
TRANSPORTATION
Many improvisations can be useful
for rescue. Transportation should be
easy, even in cold, windy
conditions, and should require only
material that is already carried by
the group. Following are a few very
useful techniques, some of which,
such as the rucksack stretcher, are
not usually found in printed
reference materials and have
advantages over other devices. The
selected techniques are basic, but
most require practice. They are best
learned before an outing and ideally
should be practiced periodically.
Split Coil Technique

If a climbing rope is available, it
may be used as an improvised
device for a conscious person who
does not have severe injuries. One
disadvantage of the split coil
technique is that the legs of the
person being carried can hang very
near the ground, particularly when
the rescuer is going downhill and is
shorter than the person. Another
disadvantage is the person being
carried and the rescuer can carry
only one rucksack, which must
contain all essential survival gear.
The rope is coiled into a loop
with the wrapping that holds the
coil in place around only one side
of the coil, not both. The diameter
of the coil should be based on the
rescuer’s height. The coil should be
split into two coils, and the person
to be carried puts one leg through
each coil. The rescuer slips an arm
through each coil, pulls the coils up
on his shoulders, and by standing
lifts the person to be carried. The
coil wrapping must be located at
the back of the disabled person at
the level of the rescuer’s belt (Fig.
7-1).
Figure 7-1. Split coil technique for
carrying an injured person
Rucksack Techniques
On expeditions, rucksacks are
generally available. Techniques for
carrying individuals with rucksacks
can be improvised very quickly.
Another advantage of using these
techniques is the group is able to
carry the most important survival
gear.
Single-Rescuer Technique
This technique is excellent for
individuals with lower limb
injuries or those who are ill but are
conscious and able to sit and hold
themselves on the back of a rescuer.
Both rescuer and the person being
carried can carry a rucksack with
their most important personal gear.
The rucksack with the longest
straps is chosen.
The rescuer’s shoulders are
padded.
The person to be carried puts
one leg through each strap so the
rucksack is partially under his
seat and pulls the rucksack as
high on his back as possible.
(The waist belt of the rucksack
must be located between the
thighs of the person to be
carried.)
The rescuer slips between the
legs of the person to be carried
and places the straps on his own
shoulders.
The person to be carried is
informed that he will be held
high over the head of the rescuer
and that he should secure
himself by placing his arms over
the shoulders of the rescuer.
The rescuer should stand up, if
possible with the help of another
person, and adjust the load.
The person to be carried should
be given his own rucksack by a
helper. (If the person to be
carried and the rescuer are
alone, the person may put his
rucksack on his back before the
rescuer stands up.)
While traveling, the rescuer may
search for large stones that can
be used as resting places. The
rescuer lets the person being
carried sit on the stone without
slipping out of the rucksack
straps (Fig. 7-2).
Rucksack Stretcher
For individuals who should be
carried in a horizontal position,
such as unconscious persons or
individuals with femoral, pelvic, or
vertebral fractures, a rucksack
stretcher made with fairly full
rucksacks (survival gear) and
carried by at least three rescuers on
each side, allows the occupant to be
well stabilized. While restrained
with the hip belts of the rucksacks,
the occupant will not fall from the
stretcher if one of the rescuers
slips. This stretcher can, literally,
be made in one minute and provides
good support, whereas improvised
rope stretchers take a long time to
construct and provide rather poor
support.
Three or four rucksacks
(depending on the height of the
person to be carried) are placed
on flat ground, top to bottom in a
line with the carrying sides up.
The shoulder straps of the
middle or two middle rucksacks
should be released, which may
require cutting the security
seams at the ends of the straps.
Figure 7-2. Single rucksack technique
for carrying an injured person
The shoulder straps of each

rucksack except the top one
should be run through the
shoulder straps of the one above
it and reattached (Fig. 7-3).
The straps should not be
tightened before putting the
person to be carried on the
stretcher and making sure the
waist belts of the rucksacks lie
flat and wide open.
The person to be carried should
be placed flat on the stretcher.
Lifting by clothing may be
easiest. The person’s head can
be placed between the upper
ends of the straps of the first
rucksack or can be stabilized by
the waist belt of the lowest
rucksack. If the person is
unconscious, the neck should be
stabilized with a SAM Splint®.
The occupant should be firmly
restrained with the waist belts,
and the straps under the person
should be tightened.
Figure 7-3. Rucksack stretcher
One of the rescuers should be

prepared to give commands
before lifting the stretcher.
One of the rescuers at the head
of the occupant continuously
observes the breathing of an
unconscious occupant.
When the group stops to rest, the
rucksacks should be supported
so they do not roll over with the
occupant on them.
Many improvements are
possible. Ski poles may be inserted
through the straps to clip in a
shoulder sling with a carabiner.
Without a sling and a carabiner,
carrying the rucksacks with a
person on them directly by the
straps is easier. Ski poles are too
small to be held by hand for a long
time. The occupant may be placed
in a sleeping bag.
If an unconscious occupant
vomits, the rucksack litter can be
turned (on command) by pulling up
one side and lowering the other
side. The person will be held by the
hip belts and the forearms of the
rescuers.
OTHER IMPROVISED
TECHNIQUES
Many improvised techniques may
be useful on expeditions. Eric
Weiss has coined the phrase “101
uses for a safety pin.” Twenty-two
of these are listed in a chapter on
wilderness improvisation in
Wilderness Medicine, 5th edition,
by Eric A. Weiss and Howard J.
Donner, edited by Paul S. Auerbach
(St. Louis: Mosby, St. Louis, 2007).
This useful chapter also describes a
number of other improvised
techniques, including many for
using SAM Splints®.
For mountaineering expeditions,
a number of references with
information about self-rescue are
available. Glacier Travel and
Crevasse Rescue, 2nd edition, by
Andy Selters (Seattle: The
Mountaineers Books, 1999), is a
clearly written guide to glacier
safety and rescue. Self-Rescue by
David J. Fasulo (Evergreen, CO:
Chockstone Press, 1996) is geared
to self-rescue in rock climbing and
contains many useful strategies for
self-rescue in a vertical
environment. A newer book on the
same subject is Climbing Self-
Rescue: Improvising Solutions for
Serious Situations by Andy Tyson
and Molly Loomis (Seattle: The
Mountaineers Books, 2006).
Improvised Techniques in
Mountain Rescue by Bill March
(selfpublished) is a classic text that
is now almost impossible to find.
First published as a spiral-bound
guide for mountaineering students, it
was later included in the book
Modern Rope Techniques in
Mountaineering Incorporating
Improvised Techniques in
Mountain Rescue (New York:
Hippocrene Books, 1984).
SECTION II
TRAUMATIC
DISORDERS
CHAPTER 8
HEAD AND NECK INJURIES
Philip F. Stahel, M.D.
Christoph E. Heyde, M.D.
Michael A. Flierl, M.D.
Head injuries are the major

potential cause of death in
wilderness accidents. The most
common causes are a fall from a
height or a direct blow on the head
from a falling object.
BRAIN INJURIES
Although most head injuries are of
minor nature and do not require
specific treatment, the early
identification of those individuals
who have sustained a potentially
significant brain injury is of utmost
importance. Airway protection and
immediate evacuation are the
crucial treatments for a significant
head injury in the wilderness.
Types of Brain Injuries

Most individuals who sustain a
brain injury suffer a mild cerebral
concussion, which is a diffuse brain
injury with preserved
consciousness but a certain amount
of temporary neurologic
dysfunction. In contrast, the classic
cerebral concussion results in a
reversible loss of consciousness,
which is always accompanied by a
certain degree of a memory loss
(amnesia). Approximately 3 to 10
percent of all individuals with a
mild head injury (cerebral
concussion) develop potentially
lethal bleeding inside the skull.
Localized brain injury is caused
by direct concussion or
compression forces, whereas
diffuse injuries are usually caused
by indirect trauma mechanisms,
such as sudden deceleration or
rotational acceleration. The most
severe brain injuries are the so-
called diffuse axonal injuries or
focal contusions with bleeding
inside or around the brain.
Secondary brain injury occurs after
the initial trauma as a consequence
of bleeding inside the skull and
swelling of the injured brain.
Among the brain’s unique
features is its snugly fitting
envelope of bone (the skull), which
is lined by a dense fibrous
membrane (the dura). Although the
skull is essential for protecting the
soft brain from injury, its presence
may occasionally be a
disadvantage. Bleeding or swelling,
which accompany injuries to any
tissue, compress the brain within
the rigid bony covering and
frequently produce damage and
dysfunction far out of proportion to
the original injury. A hemorrhage
that would be of no significance at
another site can cause death when
confined within the skull.
Occasionally a blow to the head,
although not severely injuring the
brain at the time, tears some of the
blood vessels around the brain.
Blood from the torn vessels pours
into the narrow space between the
brain and the skull and produces a
clot that compresses the brain,
which often results in death unless
treated by surgical decompression
in a timely fashion.
Bleeding develops either outside
the dura (epidural hematoma), due
to tearing of arteries, or inside the
dura (subdural hematoma), due to
tearing of bridging veins (Fig. 8-1).
Traumatic hemorrhage may occur
within the brain, either as bleeding
with a contusion or as a so-called
subarachnoid hemorrhage. Epidural
and subdural hematomas are
associated with the worst prognosis
of all bleeding patterns associated
with head injury. Individuals at risk
for developing a significant
hemorrhage after head trauma must
be identified and evacuated at the
earliest opportunity.
Assessment
One of the greatest pitfalls in
assessing an individual who has
sustained a head injury is
underestimating the severity of
injury. In fact, initial trauma may
represent just the beginning of the
damage, and secondary
deterioration may occur over time.
The classic example is the
individual who may be fully awake,
alert, and talking shortly after
sustaining a brain injury but
deteriorates and dies within a few
hours as a result of aggravating
circumstances, such as delayed
bleeding inside the skull. A high
level of suspicion, in conjunction
with a complete assessment and
estimation of potential risk, should
mandate early evacuation of these
individuals.
Figure 8-1. Subdural hematoma
The assessment of trauma must
include estimating the force of the
impact, including the falling height
and the presence of a short-term
loss of consciousness after the
accident. The critical falling height
for sustaining a significant head
injury is considered 20 feet (6 m)
or more, although falls from lower
heights may also result in severe
brain injuries, particularly in the
presence of individual risk factors.
Amnesia or a history of a brief
period of unconsciousness after
trauma is an important indicator of
a significant brain injury.
A major risk factor that may
aggravate traumatic brain injury is
taking blood thinner medications,
such as aspirin, new-generation
platelet inhibitors such as
clopidrogel (Plavix®) or long-term
anticoagulants such as warfarin
(Coumadin®). In addition, age is an
important risk factor for developing
a severe brain injury due to the
fragility of cerebral vessels in older
persons, which increases the risk of
significant bleeding in the injured
brain, even after minor trauma.
In contrast to the frequent blunt
head injuries resulting from falls,
individuals may rarely sustain
penetrating brain injuries in the
wilderness. Such injuries may
result from, for example, accidental
gunshot wounds, penetration of
falling sharp objects, or falls from a
height onto an edged rock. Any
penetrating head trauma must be
considered a severe brain injury,
even in the absence of a loss of
consciousness or other risk factors.
The following parameters must
be immediately assessed in an
individual who has sustained a head
injury:
Airway compromise
Alertness, awareness, and
orientation
Amnesia
Injuries to the scalp and skull
Cerebrospinal fluid or blood
seeping from ears or nose
Pupil size, symmetry, and
reactivity
History and mechanism of
trauma
Risk for aggravation of brain
injury
Significant associated injuries
Severe headache
Nausea and vomiting
Airway Compromise
The principal risk for
individuals who have sustained
head injuries is acute airway
compromise, which must be
recognized and alleviated
immediately. Anoxia or hypoxia
caused by airway obstruction after
a head injury leads to the worst
outcomes and may result in
irreversible cognitive and
functional impairment. Airway
management has the highest priority
for any person with a suspected
brain injury (Chapter 3: Life-
Threatening Problems). As a rule of
thumb, an individual who is fully
awake, alert, and able to
communicate verbally without any
signs of distress does not have a
compromised airway.
Amnesia and Level of
Consciousness
Next in priority is evaluating the
level of consciousness, awareness,
and orientation. The level of
consciousness is judged by asking
the individual specific questions
related to the accident (“What
happened?”) and inquiring about
current time, place, and personal
information, such as name and birth
date. These questions also help
determine the presence of amnesia,
with which an individual does not
remember events that occurred
shortly before (retrograde amnesia)
or after (anterograde amnesia) the
accident. Amnesia is an indirect
sign of an injury to the hippocampus
or surrounding cortices in the brain.
The level of consciousness can
be quantified with scientific grading
scales, such as the Glasgow Coma
Scale (GCS) or the simplified
AVPU (Alert, Verbal stimuli,
Painful stimuli, Unresponsive)
method (Table 8-1). Although the
assessment and calculation of the
GCS may be fairly sophisticated
and cumbersome for nonmedical
professionals, its practical use is of
crucial importance for assessing the
severity of brain injury and
communicating the information to a
rescue team. Any person with
amnesia or lack of normal level of
consciousness (GCS of 14 points or
less; lack of A in AVPU method) is
at risk of having sustained a
significant brain injury that may
become worse over time and
should, therefore, be evacuated at
the earliest possible moment.
Headache, Nausea, and

Vomiting
Other signs of a significant brain
injury include the presence of
severe headache, nausea, and
vomiting. Appearance of these
symptoms and signs some time after
the head injury are indicative of
increased intracranial pressure
resulting from swelling or bleeding
and the need for urgent evacuation.
Scalp Injuries and Skull

Fractures
The assessment of head-injured
individuals includes inspection and
palpation of the scalp and skull to
detect external wounds or a skull
fracture. Scalp wounds may be a
significant, albeit often
underestimated, external bleeding
source because the scalp contains
numerous blood vessels that may
bleed profusely, even after minor
injuries. On the other hand, the
excellent vascular supply renders
the scalp less susceptible to
infection following contaminated
wounds.
Skull fractures are often
surprisingly difficult to diagnose.
Nonfatal fractures may occur with
relatively little brain injury and no
detectable external deformity. In
contrast, many fatal brain injuries
occur without an associated skull
fracture. The main risk of skull
fractures is not the depression of
bone into the brain, which is a rare
occurrence, but the associated
rupture of arterial vessels outside
the dura, which results in an
epidural hematoma, bleeding
between the brain and skull. An
epidural hematoma is associated
with a dismal prognosis. The
affected individuals usually have a
lucid interval between the initial
trauma and subsequent deterioration
and are a paradigm of head-injured
individuals who talk and die.
Therefore, the identification of a
skull fracture, either by direct
palpation or visualization or by
indirect means, is of crucial
importance for identifying head-
injured individuals at risk of death.
Table Assessment of Level of
8-1 Consciousness After Head
Injur
GLASGOW COMA
SCALE (GCS)
CLINICAL
POINTS
PARAMETER
Eye Opening (E)
Spontaneous 4
To speech 3
To pain 2
Does not open eyes 1
Best Motor Response (M)

Obeys commands 6
Localizes pain 5
Pulls away from 4
pain
Uncoordinated
bending of 3
extremities
Uncoordinated
stretching of 2
extremities
No motor response 1
Verbal Response (V)
Fully oriented 5
Disoriented/confused 4
Inappropriate words 3
Incomprehensible
words 2
No verbal response 1
GCS Score = Sum of E + M + V
Severity of Head Injury
14–15 points Mild
9–13 points Moderate
3–8 points Severe
AVPU METHOD
Alert and fully oriented A
Responds to Verbal
V
stimuli
Responds to Painful
P
stimuli
Unresponsive U
With a skull fracture, the typical

signs of a fracture in any other bone
—pain, tenderness, swelling, and
discoloration—are often masked
(or mimicked) by contusions or
lacerations of the scalp that produce
swelling and bleeding.
Occasionally, signs typical of a
fracture are present on the opposite
side of the head from the point of
impact. In this location, pain,
tenderness, swelling, and
discoloration are indicative of a
fracture. This injury, the so-called
contre-coup fracture, is produced
by the coincidence of forces created
by an impact on the opposite side of
the skull.
A sign of a fracture of the base
of the skull (basilar skull fracture)
is drainage from the ears or nose of
cerebrospinal fluid or blood. Any
bleeding from the ears or nose in
individuals with head trauma must
be considered a sign of a basilar
fracture, until proven otherwise.
Additional indirect signs of a skull
fracture are bruises behind the ear
(battle sign) or around the eyes
(raccoon eyes). In contrast to these
subtle findings, larger depressed
skull fractures or fractures
accompanied by obvious deformity,
as well as open fractures, are easy
to diagnose but are usually
associated with a lethal outcome.
The presence of any direct or
indirect signs of a skull fracture
mandates immediate evacuation to a
trauma center.
Pupils
The pupils are the only external
“window” to the brain. Under
normal conditions, pupils are
similar in size and react to light by
constricting in a coordinated,
symmetric fashion. Any discrepancy
in pupil size or symmetry or the
presence of asymmetric or absent
light reactions is a sign of
potentially severe brain injury.
(Many individuals with such signs
are unconscious.) Pupil reaction is
tested by quickly changing light
exposure from dark to bright, either
with a flashlight or by manually
covering and uncovering one eye.
With a normal consensual reaction,
the opposite, untested pupil reacts
identically to the illuminated pupil.
Any abnormality in pupil size,
symmetry, or reaction time, or
absence of pupil reaction or
consensual reaction, mandate
immediate evacuation.
Rarely, a person may clarify the
presence of differing pupil sizes as
a known precondition. However,
when in doubt, the lack of pupil
symmetry has to be considered a
sign of brain injury until proven
otherwise.
Associated Head Injuries

Aside from a compromised
airway, which is considered a
“killing injury” in head trauma,
significant associated injuries
include the following:
Injuries to the chest (hypoxia,
blood loss)
Injuries to the abdomen and
pelvis (blood loss)
Long bone fractures (blood loss,
stress, and pain)
Spine injuries (neurological
impairment, neurogenic shock)
These injuries may significantly
aggravate the extent of a head injury
due to secondary insults related to a
diminished supply of blood and
oxygen to the brain. An isolated
traumatic brain injury never results
in shock or hypotension (Chapter 3:
Life-Threatening Problems). The
rare occurrence of neurogenic
shock is exclusively associated
with injuries to the spinal cord.
Similarly, an individual who has
sustained an isolated brain injury
does not have motor impairment of
the extremities. Thus, shock or
paralysis should never be attributed
to brain injury and warrant the
search for associated injuries to the
torso and spine.
Treatment
No specific treatment for brain
injury is possible in the field. The
therapy of choice for severely
braininjured individuals is
intensive care in conjunction with
neurosurgical intervention. The
ideal treatment for any person who
has sustained a potentially
significant head injury in the
wilderness is airway protection and
immediate evacuation to a trauma
center with neurosurgical
capabilities. Since brain injuries
tend to be underappreciated, the
decision for evacuation should be
made generously in the field. The
algorithm in Table 8-2 lists the
symptoms and risk factors that
warrant early evacuation of any
individual who has sustained head
trauma in the wilderness.
Treatment for specific injuries
includes the following:
External bleeding from scalp
wounds should be controlled
by direct pressure over a
sterile dressing.
Open skull fractures should
never be probed, and foreign
bodies embedded into the skull
or brain must not be removed.
These injuries must be
covered with a sterile
dressing. Antibiotic treatment
should be started early with
amoxicillin/clavulanate
(Augmentin®) or
trimethoprim/sulfamethoxazole
(Bactrim or Septra®).
Table Evaluating Head Trauma

8-2 in the Wilderness
Level of consciousness
A Normal, fully awake,
alert, oriented, GCS
15, AVPU
B Minimally impaired,
awake, disoriented,
GCS 14, AVPU
C Impaired, somnolent,
disoriented, GCS 13
or less, AVPU
C Comotose, GSC 8 or
less, AVPU
Presentation
B Amnesia (retro-
/anterograde)
C Abnormal pupils
(symmetry, reaction)
C Skull fracture (direct
or indirect signs)
B Severe headache
B Nausea, vomiting
Trauma mechanism
A Minor
B Fall from height
greater than 20 feet (6
m)
B Penetrating
mechanism
Risk factors
A None
B History of loss of
consciousness
B Anticoagulation
(aspirin, warfarin,
etc.)
B Age greater than sixty
years
A = Do not evacuate
B = Consider evacuation
C = Evacuate immediately
(presence of any
parameter)
GCS = GLASGOW COMA
SCALE
Signs of a basilar skull fracture,

such as bleeding or drainage of
cerebrospinal fluid from the
ears or nose, also mandate early
antibiotic treatment. Ideally,
antibiotics should be
administered intravenously, but
if this is not feasible,
medications by mouth should be
administered with only small
volumes of water.
Due to the risk of aspiration,
individuals with a suspected
brain injury must be kept sober
and take nothing by mouth
(NPO) until reaching a hospital.
Keeping individuals NPO also
facilitates any required
neurosurgical intervention.
FACIAL INJURIES
Soft-Tissue Injuries
The tissues of the face have a
greater blood supply than most
other areas, tend to heal faster, and
have greater resistance to infection.
Tags of skin around facial wounds
should not be trimmed away unless
they are so badly damaged that
survival is obviously impossible.
Many such skin fragments can be
saved and may reduce the need for
skin grafting at a later date.
Preserving these fragments may
also reduce scarring.
Fractures
Facial fractures are
uncomfortable but, except for lower
jaw fractures, do not require
splinting and seldom interfere with
locomotion. Delayed treatment is
often the preferred method of caring
for hospitalized individuals with
such injuries. Therefore, treating
facial fractures is rarely an urgent
problem. However, such fractures
can make the maintenance of an
open airway quite difficult,
particularly for unconscious
individuals. A fractured jaw may
permit the tongue to drop back into
the throat, completely obstructing
the passage of air. Extensive
fractures of the nose and adjacent
bones can allow the nasal air
passages to collapse.
Brain injuries, skull fractures,
and fractures of the neck frequently
accompany facial fractures and
must be recognized and treated.
Fractures should be suspected after
any forceful blow to the face that
produces pain, tenderness,
swelling, or discoloration.
Survivable fractures rarely cause
any obvious deformity, except for
some fractures of the nose or jaw.
Some discontinuity of the bones can
occasionally be felt. A broken nose
usually bleeds profusely. Double
vision is a sign of fractures of the
bones about the eye.
A broken jaw can be splinted
with a bandage that passes under
the chin and over the top of the
head, binding the lower jaw to the
upper. However, individuals
splinted in this manner may have
difficulty breathing, particularly if
they are stuporous or comatose.
Fractures of the jaw should not be
splinted if the person needs to
breathe through the mouth.
Furthermore, the splint has to be
instantly removable should
vomiting occur.
The maintenance of an open
airway in a person with facial
fractures may require diligence and
perseverance. A finger must be
swept through the mouth of an
unconscious individual with a
broken upper or lower jaw to
remove tooth or bone fragments and
prevent them from entering the
airway. If a tracheostomy cannot be
performed and an oral airway is
unavailable or not tolerated, the
person may have to be transported
in a face-down (prone) position,
particularly if severe bleeding or
swelling is present. Obviously, the
face must be kept free of pillows,
sleeping bags, and the stretcher
while the individual is in this
position.
Nosebleeds
Nosebleeds are very common
following minor injuries to the
nose. Fractures of the nasal bones
are usually accompanied by rather
severe bleeding. Nosebleeds
without any antecedent trauma are
even more common and may be
severe. Anyone with repeated or
severe nosebleeds should consult a
physician since such incidents may
be signs of a serious disorder.
An individual with a nosebleed
should be seated or standing in an
upright position while leaning
forward. Leaning backward or lying
down permits blood to drain back
into the throat where it is
swallowed, which often produces
nausea and vomiting.
Many different maneuvers for
stopping nosebleeds have been
devised. Almost all are equally
ineffective. However, most
nosebleeds stop spontaneously,
with no specific treatment.
Having the individual blow out
any clots, spraying generously with
a decongestant spray that contracts
the blood vessels, and pinching the
nostrils together along their full
length for ten minutes without
releasing the pressure is probably
as effective as any other maneuver
and usually controls the bleeding
from nasal fractures.
If bleeding persists, a small, flat
absorbent cotton pad (pledget) can
be moistened with phenylephrine
nose drops or spray and formed into
an elongated roll. After both
nostrils have been blown clear of
clots or mucus, the cotton roll
should be inserted in the nostril that
is bleeding. The nose should be
held closed with gentle pressure for
three to five minutes. After the
pressure has been released, another
two or three minutes should be
allowed to pass, and then the cotton
roll can be removed gently. If
bleeding persists, this procedure
can be repeated as often as
necessary until the bleeding is
controlled.
DENTAL INJURIES
Trauma can cause several different
dental injuries.
Fractured Teeth
Traumatic cracks or fractures in
teeth have different features
depending upon their depth. Small
craze lines on the surface of a tooth
require no treatment. Fragments that
have been broken away should be
found and preserved if possible.
When the crack is limited to the
enamel, the base of the defect has a
white appearance. Teeth with such
injuries are usually not tender. This
type of fracture has been labeled
Ellis type I and requires no
immediate treatment. If the edges of
the fracture are rough, they may
need to be smoothed, which usually
would be difficult or impossible in
a wilderness situation. Subsequent
treatment is primarily cosmetic.
If the fracture extends into the
dentin—an Ellis type II fracture—
the base has a yellow color. If it
extends deeper and involves the
pulp—an Ellis type III fracture—
the base has a pink, red, or bloody
appearance. Teeth with such
fractures are tender to touch and
hurt when exposed to air. The pulp
of the tooth is very prone to
infection. Furthermore, the exposed
dentin in Ellis type II fractures does
not provide adequate protection for
the pulp. Such fractures should be
covered with a protective material
such as Dycal or Intermediate
Restorative Material (IRM) to
reduce the risk of infection and
reduce thermal sensitivity.
Individuals with fractures that
involve the dentin or pulp require
analgesics and in a wilderness
situation should be treated with
penicillin, a cephalosporin such as
Keflex®, or clindamycin.
Evacuation to dental care should be
carried out promptly, and the
individuals should avoid hot and
cold food and beverages.
Some fractures involve the root
of a tooth. Typically such fractures
can only be diagnosed with dental
X-rays. The character of the
fracture determines the treatment
needed, which must be provided by
a dentist.
Loosened Teeth
One or more teeth may be
partially removed from their
sockets by trauma, an injury that is
termed an extrusion. The tooth may
be quite loose or mobile. The tooth
should be returned to its socket and
gentle pressure applied to force
blood from the socket and reseat the
tooth. After the tooth has been
restored to position, it should be
splinted—with adhesive tape if
nothing else is available.
Individuals on short outings
should seek immediate dental care.
Individuals on more extended
expeditions may have to tolerate the
injured tooth for a prolonged
period. Two to three weeks are
required for healing, and eating may
be problematic.
Lost Teeth
An injury in which a tooth is
totally removed from its socket is
termed an avulsion. The tooth
frequently can survive if replaced
in its socket promptly, preferably
within one hour, and an effort
should be made in the field to do
so. The tooth should be held by its
crown and gently rinsed with saline
or disinfected water. It should not
be scrubbed, and the roots should
not be touched. The tooth must not
be allowed to dry. (If prompt
restoration of the tooth is not
possible, it can be kept in liquid for
delayed restoration by a dentist.
Liquids in which the tooth can be
stored are, in order of preference,
whole milk, saline, the person’s
saliva, sports drinks, and water.)
The individual then should be
evacuated for definitive treatment
as quickly as possible.
Dental Care After Trauma

Following traumatic injuries,
individuals should eat a soft diet for
ten to fourteen days. They should
brush their teeth gently with a soft
toothbrush after every meal. They
should rinse their mouths twice
each day, preferably with a
chlorhexidine-containing
mouthwash but with a warm salt
solution if nothing else is available.
EAR INJURIES
Ear injuries are uncommon. Most
are simple skin injuries and should
be treated like similar injuries
located anyplace else. More severe
injuries are often associated with
severe head or brain injuries.
One important cause of ear
injuries is cleaning the external
canal with long narrow objects,
such as match stems. The
admonition “Never put anything in
your ear smaller than your elbow”
is wise, particularly in a remote
area. If an accumulation of wax, a
foreign body, or a small insect
causes problems, it should be
removed by irrigating the ear with
lukewarm water, preferably with a
soft rubber bulb designed
specifically for this purpose.
Figure 8-2. Anatomy of the ear and
eustachian tube1
Occasionally a traumatic injury

causes a blood clot beneath the skin
of the external portion of the ear. If
the clot is large enough to cover
one-third or more of the ear, it can
cause a permanent cauliflower ear
if allowed to persist. Such clots
should be drained to avoid this type
of scarring. The skin should be
cleaned and swabbed with an
antiseptic. Then one or more one-
eighth-inch (3 mm) incisions should
be made and the blood expressed
with gentle pressure. Removal of
all the blood is not necessary and
would probably aggravate the
underlying injury.
Barotrauma
The middle ear and the
paranasal sinuses are lined by thin
mucous membranes and are filled
with air. These chambers have
narrow openings to the nose or
throat through which air moves to
equalize the pressure within the
chamber with atmospheric pressure.
The opening into the middle ear, the
eustachian tube, is much longer than
the openings into the sinuses and is
more easily obstructed (Fig. 8-2).
As a result barotrauma is more
common in the ear.
As atmospheric pressure
decreases during an ascent to
altitude, air usually leaves these
chambers without difficulty.
However, increasing atmospheric
pressure during a descent to lower
elevations tends to close the
chamber openings. Active measures
such as swallowing or yawning may
be required to open the eustachian
tube. A light “pop” is often heard as
the pressure is suddenly equalized.
However, when the difference in
pressure between the middle ear
and the atmosphere is 90 mm Hg or
more, the eustachian tube can no
longer be opened by swallowing. In
air this pressure differential
requires a change in altitude of
about 3750 feet (1150 m) near sea
level and can only develop when
descent is rapid, as occurs in
aircraft or rarely in automobiles on
steep mountain roads. However,
under water, such pressure
differences can develop with a
descent of only a few feet,
particularly near the surface. Colds
or nasal allergies cause swelling of
the mucosa around the eustachian
tube or the ducts into the nasal
sinuses, which can partially
obstruct the openings and hinder
pressure equalization.
If the pressure within the
chambers is not equalized with the
atmosphere, a sense of fullness or
pain develops. Hearing is
diminished if the middle ear is
involved. As the pressure
differential increases, the ears and
sinuses become more and more
painful. Involvement of the middle
ear also can cause sensations of
noise, lightheadedness, and hearing
loss.
Immediately upon becoming
aware of symptoms in the nose or
ears, an individual should begin
trying to equalize the pressure.
Scuba divers, for whom barotrauma
is a constant threat, commonly pinch
their nose shut and forcibly exhale
against the obstruction to open their
eustachian tubes. Individuals with
colds or hay fever should be aware
of their increased risk of
barotrauma and should not dive, or
at least should use decongestants to
reduce mucosal swelling before a
dive. Oxymetazoline sprays are
usually adequate. The spray must be
applied a second time after an
interval of several minutes so it can
enter the deeper recesses of the
nose. A systemic decongestant can
also be taken in advance of the
descent. (Decongestants are often
combined with antihistamines,
which often cause drowsiness. Such
combinations should not be taken if
drowsiness is likely to create
problems.)
If precautions are not successful
or are neglected, or the individual
is unconscious, an aerotitis media
or aerosinusitis may develop. The
reduced pressure (negative
pressure) within the chamber
causes hemorrhage into the mucosa,
which usually is quite painful.
However, it rarely causes any other
problems, and the pain usually
disappears within twenty-four
hours. The person should be given a
systemic decongestant to promote
drainage. Acetaminophen,
ibuprofen, or a stronger analgesic
may be given to help relieve the
pain.
NECK INJURIES
Injuries to the neck can damage
vital structures. Massive
hemorrhage usually follows injury
of the large blood vessels.
Hoarseness, coughing up blood, or
diffuse swelling that feels spongy or
crackles (crepitance) indicates
injury to the air passages. Persons
with such injuries must be
evacuated without delay. Swelling
associated with the injury may lead
to airway obstruction, so
preparations should be made for a
tracheostomy or cricothyrotomy. If
the bandage over the wound
encircles the neck, which is
undesirable but is often the only
way to keep the bandage in place, it
must be loose enough to
accommodate subsequent swelling
that could result in obstruction of
blood flow.
VERTEBRAL FRACTURES
An injury to the vertebral column
(spine) must be suspected in any
individual who has sustained a fall
from a height, independent of the
presence of neurologic impairment.
The higher the level of the fracture,
the greater the risk for a serious
injury to the spinal cord. Pain in the
back or neck is the dominant
symptom of an acute spine injury,
which can be diagnosed with
certainty only by X-ray. In the
wilderness, the adequate
management of a person with a
suspected spine injury is complete
immobilization, exact
documentation and timing of the
findings, and immediate evacuation,
ideally by air transport.
Assessment
If an injured person is
unconscious, the presence of a
cervical fracture must be assumed.
Approximately 10 to 15 percent of
individuals with head injuries
severe enough to produce
unconsciousness have fractures of
the cervical vertebrae. If an
individual has numbness or tingling
sensations, or paralysis of any
extremity, a serious injury to the
spinal cord must be suspected. A
spinal cord injury at the level of the
neck may result in quadriplegia
(paralysis of all four extremities),
whereas an injury at lower levels of
the thoracic or lumbar cord may
result in paraplegia (paralysis of
the lower extremities). Bladder and
bowel function may be impaired as
well.
When assessing the neurologic
impairment in an individual who
has sustained a spine injury,
documenting the exact time of
assessment is crucial, since
neurologic deterioration may occur
over time.
Most individuals with spine
injuries do not have neurologic
impairment. Pain or tenderness
along the spine or anywhere in the
neck following a fall should arouse
concern about a vertebral fracture.
In the wilderness, the personnel
taking care of individuals with
suspected spine injuries must be
constantly aware that any excessive
manipulation during assessment,
particularly manipulation of the
neck, may worsen the neurological
injury and the long-term outcome.
On the other hand, individuals with
traumatic paralysis may eventually
recover some neurologic functions.
Correct handling at the accident
scene and early transport to a
trauma center with adequate
immobilization are essential.
Treatment
The neck of an unconscious
individual, or a conscious person
thought to have a cervical fracture,
must be stabilized as quickly as
possible, well before the individual
is moved or transported. If a
cervical collar is not available, one
can be improvised with a SAM
Splint® and can be applied quickly
even if the individual is lying in
deep snow. One attendant should
stabilize the injured person’s head
and neck with both hands while the
SAM Splint® is rolled snugly
around the neck like a bandage. The
chin must be outside the splint, and
the head should be in a slightly
extended position. The rim of the
splint can be folded down it if it
forms pressure points, and the end
can be secured by tape or by a short
bandage (Fig. 8-3).
No specific treatment other than
immobilization is possible in the
wilderness for individuals with
spine fractures. Proper
immobilization is generally
achieved with the injured person in
a neutral supine position without
rotating or bending the spinal
column, particularly the neck.
Unfortunately, ideal immobilization
equipment—long spine board and
cervical collar—are usually not
available at the site of injury.
Figure 8-3. Cervical collar made with
a SAM Splint®
If an individual with suspected

spine injury has to be moved, this
must be done—preferably after the
neck has been splinted—with spine
protective precautions. The thoracic
and lumbar spine must be protected
by the so-called logroll maneuver,
meaning the body must not be
torqued during the rolling
procedure for assessing the back or
for placing the person in a lateral
position to avoid aspiration while
vomiting. At the same time, the
cervical spine must be protected by
manual in-line traction that keeps
the neck in a neutral position by
avoiding rotation, flexion, or
extension. Different techniques for
the adequate transport of a spine-
injured person have been described
(Chapter 7: Rescue and
Evacuation). However, perfect
logrolling and transportation
techniques are cumbersome and
usually require at least four helpers
(Fig. 8-4).
During evacuation, a person with
a confirmed or suspected vertebral
fracture must be secured so that his
body does not roll or twist as it is
moved over rough terrain. A rigid
support, such as a metal basket or a
broad wooden board, is essential.
A rolled-up jacket or a similar
cushion should be placed under the
small of the back to support the
spine in that area. With injuries of
the neck, a cervical collar must be
installed or improvised with a
SAM Splint®, or padding must be
placed on both sides of the head
and neck to prevent the head from
rolling from side to side (Fig. 8-5).
An individual with spinal cord
damage and paralysis requires
special attention during evacuation,
particularly when evacuation takes
more than several hours. The
immobilized person must be
protected from heat loss
(hypothermia), which may occur
very fast in the outdoor
environment. Care must also be
given to the areas that support the
body’s weight, such as heels,
buttocks, shoulders, and elbows.
Pressure on these areas prevents
blood from circulating through the
tissues. Normally such deprivation
of the blood supply results in pain,
and the person shifts position.
Individuals with spinal cord
injuries may not be able to feel pain
and may not be able to shift
position. After a few hours of being
deprived of blood, the tissues in
these areas die, eventually resulting
in ulcers known as bed sores or
pressure sores. To avoid this
complication, the pressure points,
particularly the heels and buttocks,
must be carefully padded.
Furthermore, this padding must be
rearranged every couple of hours,
day and night. As mentioned, severe
vertebral fractures that damage the
spinal cord may paralyze the
urinary bladder and large intestine.
Bladder care may require repeated
catheterizations at least every eight
hours or the insertion of an
indwelling catheter.
Figure 8-4. Logroll carry of a person
suspected of having a vertebral
fracture
Figure 8-5. Technique for
immobilizing the head of a subject
with fractured cervical vertebrae
The American Red Cross

recommends that amateurs not try to
evacuate a person thought to have a
vertebral fracture. Transportation
must be postponed until cervical
collars, body boards, basket
stretchers, and appropriately
trained emergency medical
technicians have been brought to the
scene of the accident. Within
industrialized nations such advice
is excellent and should be followed
if at all possible. However, in much
of the rest of the world emergency
medical technicians and the
necessary equipment are not
available.
____________
REFERENCES
1. Adapted from Dorland’s
Illustrated Medical Dictionary,
26th ed. Philadelphia, W.B.
Saunders, 1981.
CHAPTER 9
CHEST INJURIES
Ben Eiseman, M.D.
Bruce Paton, M.D.
Chest injuries are of particular

significance because they interfere
with the vital function of
respiration. At high altitude where
the oxygen content of air is low,
chest injuries that would be of
minor consequence at low altitude
can be life threatening. In contrast
to abdominal injuries, for which
little can be done in a wilderness
setting, a well-informed person can
take steps to increase the chances of
survival for individuals with chest
injuries.
THE MECHANICS OF
RESPIRATION
During inspiration, muscles in the
chest wall pull the ribs upward.
Simultaneously the diaphragm
contracts and flattens, expanding the
chest and drawing air into the lungs.
Expiration, in contrast, is passive
and requires no muscular action.
Elastic tissue in the lung, which is
stretched as the lung expands during
inspiration, retracts and reduces the
volume of the lung during
expiration, pushing air out of the
chest. (Anatomy of the respiratory
system is described more fully in
Chapter 18: Respiratory Disorders.
Also see Fig. 9-1.)
A thin membrane, the pleura,
folds back upon itself and envelops
each lung and the inner surface of
the rib cage. The potential space
between the pleural layers is called
the pleural cavity. Normally the
lungs fill the entire thorax and,
because negative pressure is
generated in the pleural cavity, the
two layers of the pleura remain in
intimate contact. There is, therefore,
no real space in the pleural “cavity”
under normal conditions. However,
if the chest wall is perforated or a
lung is punctured, air enters the
pleural space through the defect and
the elasticity of the lungs causes
them to collapse. This condition is
known as pneumothorax (see
“Fractured Rib”).
Figure 9-1. Anatomy of the respiratory
system
Effect of Body Position

In the standing position the
diaphragm lies low in the chest,
permitting full expansion of the
lungs. When a person lies down,
however, the abdominal organs
push against the diaphragm, which
is displaced toward the head,
compressing the lungs and reducing
ventilation. When obese individuals
are in a supine position, the
abdominal organs may push the
diaphragm up to the level of the
nipples, seriously impeding gas
exchange in the lungs. Placing a
person on his side permits the
abdominal organs to shift away
from the diaphragm and can
improve ventilation, particularly in
the upper portions of the lungs. In a
sitting position the abdominal
organs tend to fall away from the
diaphragm, improving respiration.
A person with a severe chest
injury should be placed in the
position that is most comfortable,
but lying on the side or sitting may
allow for better respiration than
does lying flat. If blood loss has
been significant, the individual may
have to lie flat to maintain adequate
blood pressure (“Shock” in Chapter
3: Life-Threatening Problems).
CLOSED CHEST INJURIES

Fractured Rib
A forceful blow to the chest may
break one or more ribs, but the ribs
are so tethered by surrounding
muscles they do not need to be
splinted or realigned like other
broken bones. Other than producing
discomfort, most rib fractures are
not serious injuries. However, the
discomfort can be disabling, and
movement of almost any part of the
body causes pain at the fractured
site that is accentuated by muscle
spasm. Pain also interferes with
motion of the chest wall and limits
breathing. Furthermore, a broken
rib may be displaced inward,
puncturing the lung and producing a
pneumothorax (air in the pleural
space). As mentioned, the pleural
space surrounding the lung normally
does not contain air, but when the
lung is punctured air escapes from
the lung and enters the pleural
cavity due to the negative pressure
generated during breathing. With
increasing size, a pneumothorax
compromises air exchange through
the lungs.
A fractured rib should be
suspected when pain and tenderness
at the point of impact follow a blow
to the chest, particularly when deep
breathing or movement aggravates
the pain. Rarely can a defect be
palpated at the point of fracture
because the ends of the rib are held
in position by surrounding muscles.
The pain of a fractured rib and
associated muscle spasm may be
severe enough to require analgesics
for a few days. Almost any
movement and sleep may be
extremely uncomfortable for
several weeks, particularly when
lying on the injured side, but the
pain gradually disappears as the
bones heal. Sudden sharp pain at
the site of injury for weeks after the
injury should not arouse concern.
Relief of pain so it does not
interfere with breathing is the most
important aspect of managing
broken ribs, particularly at high
altitude, in the elderly, and in
individuals with reduced pulmonary
function such as smokers.
Adhesive strapping over the rib
is not advisable, particularly at
altitudes above 10,000 feet (3000
m). Such immobilization further
reduces movement of the chest on
that side, diminishes the capacity
for exertion, and allows secretions
to collect in the immobile lung.
Pneumonia is a potential
complication of rib fractures. At
lower elevations, if the pain cannot
be controlled with moderate
analgesics, several two-inch-wide
strips of adhesive tape can be
applied along the fractured rib from
the midline in front to the vertebral
column in back. Taping provides
some relief from pain but should be
removed as soon as the individual
has been evacuated. Wrapping the
chest circumferentially with an
elastic bandage should not be used
since both sides of the chest are
restrained, substantially reducing
respiratory function.
A blow to the lower chest may
also damage intraabdominal organs
—the liver if the blow has been
low on the right side, the spleen by
left-sided injuries, or the kidneys by
a blow to the back (Chapter 10:
Abdominal Injuries).
Pneumothorax
Pneumothorax allows the lung to
partially or totally collapse (Figs.
9-2 and 9-3). When the air is
introduced by rupture of a small
bleb or air bubble on the surface of
the lung, the pneumothorax is
considered “spontaneous.” If the air
is introduced by an injury, the
pneumothorax is “traumatic.”
Occasionally a tear in the surface of
the lung functions as a one-way
valve, allowing air to enter the
pleural space during inspiration but
closing and not allowing air to
escape during expiration. As a
result the lung collapses, tension
within the pleural space increases
with every breath, and both
respiratory and cardiac function can
be severely impaired. This
condition is called tension
pneumothorax.
Figure 9-2. Pulmonary function with a
punctured lung and intact chest wall 1
Figure 9-3. Collapse of the left lung
and shift of heart and trachea to the
right with left pneumothorax
A spontaneous pneumothorax is
heralded by the sudden onset of
chest pain associated with shortness
of breath. Such alarming symptoms
in an older person and on the left
side of the chest may suggest a heart
attack. Spontaneous pneumothorax
is rarely fatal, but can be painful
and usually compromises
respiratory capacity. Individuals
with spontaneous pneumothorax
should be evacuated promptly. If
shortness of breath is not severe,
they may be able to walk out
unassisted.
A key to the diagnosis of
pneumothorax is the absence of
audible breath sounds when
listening to the chest, preferably
with a stethoscope. With a tension
pneumothorax resulting in a shift of
the heart to the opposite side, the
neck veins become distended and
the person develops signs of shock
(Chapter 3: Life-Threatening
Problems).
Although supplemental oxygen
partially alleviates symptoms of
pneumothorax, the only definitive
treatment is removing the air
trapped in the pleural cavity and
allowing the lung to expand. To
accomplish this, a tube must be
inserted into the pleural space,
preferably by an experienced
medical professional. If the device
is left in the pleura, a one-way
valve or suction apparatus must be
applied to maintain the negative
pleural pressure and expand the
lung. This procedure, tube
thoracostomy, should not be
attempted in the wilderness except
for rare circumstances in which an
individual is dying as the result of a
tension pneumothorax. Only major
expeditions or well-equipped
rescue groups would be expected to
carry the appropriate equipment and
include medical professionals that
could perform this procedure.
Tube Thoracostomy
Inserting a tube into the chest of
an injured person in distress from a
tension pneumothorax can be life
saving but is also a potentially
hazardous procedure. The
complications include puncture of
the heart, lung, or large blood
vessel and penetration of the
diaphragm with injury to the
underlying spleen or liver, all of
which could be disastrous in the
wilderness.
Tube thoracostomy should only
be attempted when the following
conditions exist:
The individual is dying as a
result of impaired respiratory
function due to extensive air in
the chest, a condition virtually
always the result of severe
trauma.
The basic equipment, an
appropriate tube for insertion
and flutter valve (Heimlich
valve), is available.
The individual performing the
procedure has been formally
instructed or, under extreme
circumstances, is being
monitored by a physician
through telecommunication.
Optimally, a skin antiseptic and
injectable local anesthesia
should be available.
The following are the steps for
emergency tube thoracostomy in the
wilderness:
1. The injured person should be
positioned on the ground, or on a
cot, with the head supported on a
pillow and the arm on the injured
side elevated with the hand
behind the head.
2. If time permits, attendants should
scrub their hands and forearms
and the injured person’s injured
chest from the clavicle to the
lower margin of the ribs with
soap. An antiseptic, such as
Betadine® or alcohol, should be
applied to the cleansed chest
wall. The attendant should then
put on sterile gloves if available.
3. A tube entrance site should be
identified in the rib space below
the large chest wall muscle
(pectoralis), or the breast in
women, at the midaxillary level
on the chest wall (Fig. 9-4). This
site is optimal because it allows
access to the chest cavity after
traversing the least amount of
tissue and is sufficiently high to
avoid injury to the diaphragm.
The chest tube should be
introduced on the top of the rib
rather than the undersurface to
avoid the artery there.
Figure 9-4. Site of chest tube insertion
4. The position selected for tube

insertion on the chest wall should
be infiltrated with a generous
amount of a local anesthetic such
as 15 ml or more of lidocaine.
5a.If the apparatus includes a
trochar (a metal inner guide), an
approximate 0.25-inch incision
should be made on the top border
of the rib with a sterile scalpel.
The trochar should be advanced
slowly along the upper edge of
the rib until resistance is no
longer felt, indicating entrance
into the chest cavity. The depth
required for tube placement
varies with the thickness of the
individual’s fat and muscle, but
for most the tube should be in the
chest cavity within 3 inches. The
trochar should be removed, and
the tube advanced further into the
chest an additional 2 inches.
When the tube is appropriately
positioned in the chest for a
tension pneumothorax, an audible
rush of air from the tube is often
heard. The chest tube should be
connected to the flutter valve,
and the valve should be checked
to ensure it is attached in the
correct direction.
5b.To insert a chest tube without a
trochar, the chest tube should be
connected to the flutter valve
first. Inserting a chest tube
without a trochar requires a
considerably larger skin opening,
usually 1.5 inches horizontally
on the top edge of the rib. The
scalpel, or preferably sterile
scissors, used to make the skin
incision should be used to cut
through the fat and muscle of the
chest wall to enter the chest
cavity. A sterile finger should be
inserted to confirm entry into the
chest cavity, and then the tube
should be advanced through this
track. Insertion approximately 5
inches into the chest should be
sufficient for the average
individual. If a tension
pneumothorax is present, a rush
of air occurs. When a clear
plastic tube is used, breathing
should result in fogging of the
tube.
6. Once the chest tube is in the
correct position, it should be
anchored to the chest wall to
prevent it from being pulled out
of the chest or forced inward too
far.
7. Frequently a small amount of
blood is expelled through the
chest tube. If a consistent stream
of blood exits, a collection bottle
should be added to the system
(Fig. 9-5).
Successful insertion of a chest
tube to relieve a tension
pneumothorax should result in
prompt improvement in the injured
individual. However, following
rapid reexpansion of the lung, the
individual may experience transient
pain with breathing.
Hemothorax
An accumulation of blood in the
pleural cavity is known as
hemothorax. In the wilderness,
bleeding from vessels around a
broken rib is the usual source, but
may originate from a punctured or
ruptured lung. Blood in the pleural
space collapses the lung and
interferes with its function just like
trapped air does. If bleeding is
severe, the person may go into
shock and even die as the result of
blood loss. If a hemothorax of
lesser volume is left unattended, it
can become infected. The
immediate threat in a remote area is
death from blood loss or impaired
respiration. Such an event is
unlikely unless a large vessel, such
as an artery or vein in the lung or
the thoracic aorta, has been torn, in
which case the person usually dies
before help arrives. Less severe
bleeding usually stops
spontaneously within a few hours.
pneumothorax treated by tube
thoracostomy 2
The signs and symptoms of

hemothorax are similar to those of
pneumothorax: immediate pain,
increasing difficulty in breathing,
signs of decreased oxygenation
(cyanosis—purple or bluish
discoloration of the mucous
membranes lining the mouth, lips,
skin, and nail beds due to reduced
amounts of oxygen bound to
circulating red blood cells—and
increased pulse rate), and absence
of breath sounds over the involved
lung. A large hemothorax can
eventually produce signs of shock
due to blood loss. However, an
observer can seldom differentiate a
hemothorax from a pneumothorax in
the wilderness.

flail chest 3
In fact, individuals may have

both air and blood within the
pleural cavity: a
hemopneumothorax. Only a chest X-
ray can determine accurately what
has accumulated. In either case, the
person must be evacuated.
Hemothorax is treated initially the
same as pneumothorax, including
supplemental oxygen.
Flail Chest
A flail chest is a condition
produced by fracture of a number of
adjacent ribs in two or more places
that produces a mobile, freely
floating plate of chest wall that
moves back and forth during
respiration. When the chest
expands, the loosened segment of
chest wall moves inward. During
expiration the loosened plate is
forced outward: paradoxical
respiration. Since the chest wall
moves without moving air into or
out of the lungs, respiratory distress
results, even if the damaged area is
relatively small (Fig. 9-6).
The individual usually has
received a severe blow to the chest
and is fighting for air and breathing
very rapidly. His lips, skin, and
nails may be cyanotic due to
reduced oxygen availability.
Examination of the bare chest
discloses a mobile segment of chest
wall that moves paradoxically with
each respiration. A simple fractured
rib produces pain with breathing
but does not interfere with the
movement of air.
The loosened segment must be
immobilized. In an emergency, the
individual should be placed on the
injured side (despite the pain) with
a rolled-up piece of clothing
beneath the loose segment of rib
cage (Fig. 9-7). The pressure
effectively immobilizes the
loosened portion of the chest wall
and allows more effective
respiration. More secure fixation of
the rib cage can be achieved by
taping or bandaging a large pad
firmly over the mobile area, but the
dressing should be confined to the
involved side of the chest.
Figure 9-7. Subject lying on a rolled-

up garment to support a flail chest
Oxygen should be administered,

and the individual should be
evacuated immediately. A large
area of flail, particularly at high
altitudes, may be fatal.
PENETRATING CHEST
INJURIES
A fall onto a pointed object such as
an ice ax or ski pole may punch a
hole in the chest wall and then into
the lung. If the opening in the chest
is small and seals quickly but
leaves a hole in the lung, air may
leak into the pleural cavity, causing
a pneumothorax. The air leak may
cause a tension pneumothorax (Fig.
9-8).
If the defect in the chest wall is
large and air is sucked in and out of
the chest cavity with every breath,
the injury is obvious (Fig. 9-9). The
opening should be sealed as fast as
possible with a pad of sterile
dressings, preferably with an inner
layer of gauze impregnated with
petroleum jelly—or a clean cloth if
that is all that is available. The pad
should be taped securely over the
open wound, but an edge that can be
lifted to allow air to escape should
be available in case a tension
pneumothorax develops.
Supplemental oxygen should be
given immediately. Decompression
of the chest with a chest tube may
be necessary. Shock almost
invariably accompanies a large
penetrating wound of the chest and
should be anticipated. If the person
is not allergic to penicillin, a
penicillinase-resistant penicillin or
a cephalosporin should be given
every six hours until evacuation is
completed.
All individuals with penetrating
injuries of the chest must be
evacuated at the earliest possible
moment because serious underlying
injury may be present and the
potential for severe functional
impairment of respiration is great.
punctured chest wall 4
Figure 9-9. Open chest wound before
and after bandaging
____________
REFERENCES
1. Johnson J. and Kirby C.
Surgery of the Chest, 3rd ed. Year
Book Medical Publishers, Inc.,
1964. (Adapted and used by
permission.)
2. Ibid.
3. Ibid.
4. Ibid.
CHAPTER 10
ABDOMINAL INJURIES
Ben Eiseman, M.D.
Hunter B. Moore, B.A.
The definitive treatment for a

severe abdominal injury usually
consists of an operation, which is
out of the question in a wilderness
setting. Therefore, management of
severe abdominal trauma in such
situations consists of recognizing
potentially serious injury and
deciding whether immediate
evacuation is required. Under no
circumstances should pseudoheroic
attempts at operative intervention
be made. The results would be
uniformly fatal without proper
anesthesia, sterile operating
conditions, and proper instruments.
Moreover, even the most severe
trauma can occasionally be
successfully managed without
surgery.
ASSESSMENT
Before any decision can be made
concerning the care for someone
with an abdominal injury, a
systematic assessment must be
done. The first step is obtaining an
account of the accident. Exact
details of the mishap, including the
site and direction of a blow to the
abdomen, are helpful in diagnosing
an abdominal injury. A blow to the
left upper quadrant of the abdomen
or lower part of the left chest may
rupture the spleen. A blow to the
corresponding area on the right side
may injure the liver. Trauma to
either flank or the back may damage
a kidney.
The abdomen must be examined
carefully (Chapter 20: Acute
Abdominal Pain). In addition, close
attention should also be given to
signs of shock, including blood
pressure, pulse rate, respiratory
rate, color of the skin and mental
status (“Shock,” Chapter 3: Life-
Threatening Problems). The vital
signs must be recorded hourly for at
least the first twelve hours after
injury. The urine should be
examined for blood. Attention must
not focus on the abdomen to the
extent that other injuries are
overlooked or neglected. At some
time during the individual’s care,
preferably early, a complete
physical examination—including an
examination of the back—must be
performed.
If the individual is to be
evacuated, as most require, a
written account of the accident and
all diagnostic findings, along with a
detailed record of subsequent
events, should accompany the
person. The exact time of the
accident, all medications and the
time they are administered, hourly
measurements of vital signs, and
observations about the individual’s
general condition must be written
into that record.
TREATMENT
Individuals who require immediate
evacuation to a surgical facility
should be carried with all
reasonable haste to a point from
which they can be evacuated. The
sooner this can be accomplished,
the better such persons withstand
the subsequent rigors of bleeding or
peritonitis. Individuals with severe
abdominal injuries usually require
litter evacuation.
Abdominal trauma frequently
produces rather severe pain, but the
pain may not be proportional to the
severity of the injury. Even minor
abdominal trauma may be quite
painful at first, although the
discomfort usually subsides in the
hours that follow. In general, the
person should be kept comfortable
with analgesics. Intravenous
administration may be necessary if
shock is present. If injected
intramuscularly, these drugs may not
be well absorbed, and an overdose
could occur after the circulation is
restored. The individual should be
made comfortable but not overly
sedated. If evacuation is not
necessary or must be delayed, more
liberal use of analgesia,
particularly strong analgesics, is
warranted.
Severe abdominal trauma may
produce bleeding into the peritoneal
cavity, rupture of abdominal organs,
or both. Peritonitis inevitably
results, although the inflammation
following hemorrhage is due to
irritation by blood rather than
infection.
Gastric distension, absence of
bowel sounds, nausea and vomiting,
and other signs of peritonitis are
usually present (Chapter 20: Acute
Abdominal Pain, for more on
diagnosis and treatment of
peritonitis). Shock may occur when
trauma causes intraabdominal
hemorrhage, and this should be
anticipated and treated.
NONPENETRATING INJURIES
Blunt or nonpenetrating injuries to
the abdomen may produce:
Contusion of the abdominal
wall
Internal bleeding due to a
ruptured spleen, liver, or
kidney
Peritonitis due to perforated
intestines or urinary bladder
Combinations of the above
Contusion of the Abdominal Wall

Any blow to the abdomen causes
a bruise that may be painful.
Although the area of impact may be
quite tender, the abdomen around it
is not so sensitive. If the internal
organs have been injured,
tenderness is usually diffuse. In the
first hour after injury, deciding
whether a severe blow has
produced merely a bruise or serious
intraabdominal damage may be
difficult. A delay of several hours
may transpire before the severity of
the injury can be determined.
A large black-and-blue area may
blossom forth twenty-four to thirty-
six hours later as blood lost at the
time of injury works its way to the
skin. This discoloration is of no
significance, does not require
treatment, and subsides
spontaneously in time regardless of
its extent. After a tumbling fall, as
may occur on boulders or on steep
ice slopes, bruises often appear in
areas that the person had not
realized were injured. Frequently
the individual feels far more sore
and stiff a day or two after a fall
than immediately after the injury. If
no associated injuries are present,
the person usually recovers after a
few days of rest and mild to
moderate analgesia every four to
six hours.
Internal Bleeding Due to

Ruptured Liver, Spleen, or
Kidney
A blow to the abdomen may
rupture the liver, spleen, kidney, or
some combination of them. Rupture
is more likely if the blow strikes
immediately over the organ. The
liver lies in the right upper
quadrant, the spleen in the left
upper quadrant. Both are tucked
under the rib cage but can be
injured by blows to either the upper
abdomen or lower part of the chest
(Fig. 10-1). A blow from the back
may damage the kidneys, which lie
on either side of the backbone (Fig.
10-2). These organs are solid and
may shatter when hit directly. Blood
from a severely injured liver or
spleen flows unimpeded into the
abdominal cavity. The hemorrhage
often does not stop without
operative intervention.
Figure 10-1. Location of the liver and
spleen in relation to the lower ribs
anteriorly
Figure 10-2. Location of the liver,
spleen, and kidneys in relation to the
lower ribs posteriorly
A ruptured kidney is usually

manifested by a history of a blow in
the back or flank; pain, tenderness,
and discoloration at the point of
injury; and blood in the urine. The
kidney is enveloped in a tough,
fibrous sheath, and bleeding from
kidney injuries usually stops
spontaneously; rarely is an
immediate operation necessary.
However, the presence of large
amounts of blood in the urine for
more than six hours and signs of
shock are indications that bleeding
has assumed dangerous proportions.
Such an individual should be
treated for shock and evacuated as
rapidly as possible. If bleeding
from a damaged kidney stops, the
individual must still wait at least
ten days before resuming vigorous
activity since delayed bleeding may
occur.
Abdominal Pain Due to Ruptured

Liver or Spleen
A blow to the upper abdomen or
lower chest may result in pain,
tenderness, and evidence of
contusion in the area of impact, and
one or more ribs may be broken.
Shortly after the injury,
intraabdominal pain appears, first
in the region of the injury and later
more diffusely throughout the
abdomen. The pain is usually
aggravated by breathing deeply and
may be associated with pain in the
shoulder. Individuals with either of
these injuries usually appear to be
in reasonably good condition at
first, but as hours go by their
condition deteriorates. Signs of
shock progress, and the abdomen
becomes diffusely tender with
rebound tenderness, reduced bowel
sounds, and distension.
A person with an injury of the
spleen may recover from the initial
accident only to bleed massively
when a clot breaks loose from the
splenic surface several days or
even weeks later. Signs of
intraabdominal hemorrhage appear
rapidly after such events. Persons
with such injuries must be
evacuated to the care of a surgeon
as rapidly as possible. Hemorrhage
rarely stops spontaneously; most
individuals bleed to death if not
surgically treated.
Peritonitis Due to Ruptured

Intraabdominal Organ
Severe blunt abdominal trauma
may rupture one of the hollow
intraabdominal organs, such as the
intestines. The contents of the
damaged organ are spilled into the
abdominal cavity, producing
peritonitis. Following injury the
pain gradually becomes worse and
spreads over the entire abdomen as
peritonitis becomes generalized.
Diffuse tenderness, abdominal
distension, vomiting, and fever soon
appear. Treatment is the same as for
peritonitis of any cause (Chapter
20: Acute Abdominal Pain). The
urinary bladder is rarely ruptured
unless it is full at the time of injury,
and usually rupture is associated
with a fractured pelvis. If the
bladder is ruptured, no more urine
is voided except for a few drops
that are mostly blood. This injury
also demands prompt evacuation.
PENETRATING ABDOMINAL
INJURIES
Penetrating or perforating injuries
of the abdomen are unusual in the
wilderness but occasionally are
caused by a fall on a sharp object.
These injuries are extremely
serious and require operative
treatment. Not only are the
abdominal organs injured, but the
abdominal cavity is contaminated
from external sources, resulting in
severe peritonitis. The diagnosis is
usually obvious, but a penetrating
abdominal wound may be
overlooked. Attention must not be
limited to the area of most obvious
injury. The person should be
stripped of all clothes and the entire
abdomen and back carefully
checked, including the underarms
and buttocks.
Evacuation should be carried out
as quickly and rapidly as possible.
During evacuation the individual
should be treated for peritonitis,
and shock should be anticipated and
treated.
A sterile dressing should be
placed over the wound. In contrast
to the usual care given softtissue
injuries, the wound should not be
washed or cleaned, because such
efforts may introduce more
infection. Any loops of bowel
protruding through the wound
should be pushed back into the
abdomen with the cleanest
technique possible, and the wound
should be covered with a dressing
that is sufficiently snug to prevent
the bowel from extruding again.
This dressing should not be changed
once it is in place because further
contamination of the wound could
result.
CHAPTER 11
FRACTURES AND RELATED
INJURIES
Joseph B. Serra, M.D.
Wilderness accidents often result in

broken bones or joint and tendon
injuries. Care for individuals with
such injuries demands an
understanding of them and their
potential complications. The
diagnosis of a fracture—or the
absence of a fracture—without X-
rays is particularly challenging.
Fractures vary widely in
severity. Fractures of small bones
in the hands or feet may produce
little pain or disability. Bone ends
of a fractured hip may be driven
into each other (impacted) in such a
manner that the fracture is stable,
produces little deformity, and
causes little damage to the
surrounding tissues. In contrast,
bones can be so shattered the limb
feels as if no bone is present.
Fractures with a single, clean
break are simple fractures. If the
bone ends are driven into each
other with little or no displacement,
the fracture is impacted. If the bone
is broken into one or more
fragments, the fracture is
comminuted. Vertebral fractures in
which the bone simply collapses as
the result of trauma or osteoporosis
are compression fractures. When
the surrounding skin is intact, the
fractures are closed. If the skin has
been penetrated, the fracture is
open or compound.
Many bone or joint injuries are
of major significance, particularly
in situations where immobilization
without food or shelter is life
threatening. Disruption of major
blood vessels can produce severe
hemorrhage; vascular obstruction
can cause gangrene of extremities;
breaks in the skin can lead to
chronic infections; damage to
nerves may result in paralysis.
DIAGNOSIS
The following are the principal
signs of a fracture:
Pain and tenderness
Swelling and discoloration
Deformity
Most fractures are painful, the
pain is aggravated by movement or
manipulation, and the fracture site
is sensitive. Swelling and
discoloration are usually present.
However, these signs are not
diagnostic and may occur with
sprains or occasionally with simple
contusions.
Obvious deformity is diagnostic
of a fracture. Grating of the ends of
the broken bones is also diagnostic
but may be too painful to use as a
diagnostic test. One or both ends of
the bone can occasionally be seen
in open fractures. A common sign of
a fractured hip is shortening of the
extremity by one to two inches and
outward rotation of the foot.
Loss of function of the injured
extremity is not a reliable sign of a
fracture and can be an emotional
response to an injury. A few
injuries are so painful that function
is lost without fracture. Function
may persist even though a fracture
is present, particularly with
compression fractures of vertebrae
and fractures of small bones in the
feet and hands.
In a wilderness situation,
ascertaining that a fracture is
present is not essential. If a fracture
is suspected, its existence should be
assumed until X-rays prove
otherwise. Occasions commonly
arise, particularly with ankle
injuries, in which an extremity is
severely injured but does not
appear to be fractured. In a remote
area, delaying evacuation until the
character of the injury becomes
evident may be desirable. If a
fracture is present but the extremity
has been immobilized and elevated,
the delay would rarely have an
adverse effect on healing. If no
fracture is present, the person may
be able to walk out.
TREATMENT
Immobilization
The basic treatment for any
fracture is immobilization, which
minimizes further tissue damage by
the bone ends, reduces pain, and
decreases shock. Permanent
immobilization by a cast or
surgically implanted hardware
allows the fracture to heal.
Immobilizing a fracture in a
wilderness setting can be
challenging if splints must be
improvised. Any material that
stabilizes the fracture can be used.
A folded newspaper, magazine, or
map is particularly effective for
splinting fractures of the forearm
and wrist. (Cardboard arm and leg
splints are used in alpine ski areas.)
Ensolite pads may be used to splint
forearms or lower legs, and they
make excellent cylindrical splints
for knee injuries. Crosscountry skis
or ice axes can be used for lower-
leg splints. Pillows, heavy clothing,
or sleeping bags can be used to
splint ankles. Metal pack frames
can be used for splints, and the pack
straps can be used to hold the splint
in place.
Bony prominences at the wrist,
elbow, ankle, and knee must be
padded to prevent discomfort and
nerve damage from hard splint
materials. The injured person must
be given the responsibility for
reporting any symptoms, or any
change in existing symptoms, that
may herald nerve or vascular
compression.
A large and well-prepared
outing probably should carry
splints. Padded aluminum splints
(SAM splints®) are lightweight,
relatively small, and can easily be
molded to form stable splints for
fractures of the neck, arms, wrists,
lower legs, or ankles.
Inflatable splints have largely
been replaced by more versatile
SAM Splints® and are most
suitable for immobilizing fractures
of the lower leg and ankle. These
splints are lightweight although
somewhat bulky, easy to apply, and
help control hemorrhage by
applying pressure over the leg when
the splint is inflated. (The air
pressure in the splint may need to
be briefly lowered every one to two
hours to ensure the blood supply to
the skin is not impaired.) Inflatable
splints (Fig. 11-1) must be
protected from puncture during
evacuation. Changes in air pressure
within the splint with changes in
altitude and environmental
temperature must be anticipated.
Heavier splints with zipper
closures and screw-type air locks
seem to work better than lighter,
self-sealing splints, which are
affected by large temperature
changes.
To achieve immobilization, both
the joint above and the joint below
a fracture must be splinted. For a
fracture of the forearm, the wrist
and elbow should be immobilized.
For a fracture of the lower leg, the
knee and ankle must be stabilized.
Fractures of the thigh (femur) are
often associated with severe
bleeding and usually are very
painful, particularly a few hours
after injury when the surrounding
muscles go into spasm.
Immobilization of such fractures,
particularly during evacuation,
requires traction, which is
described in more detail in the
specific discussion of such injuries.
To apply a splint or to pack the
individual in a basket stretcher, a
fractured extremity must be
straightened, which can be
accomplished most readily with
traction immediately after the
fracture has occurred. Straightening
also improves the stability of the
extremity. Later, muscle spasm and
the individual’s diminished
tolerance for pain make
manipulation more painful and more
difficult but still worth doing.
A definite indication for
manipulation of a fractured limb is
loss of the blood supply to the limb
beyond the fracture site. If the ends
of fractured bones obstruct blood
flow by pressing on an artery, or
have lacerated the artery, the result
is severe pain, numbness, and
coldness in the affected limb, which
typically is cyanotic or pale. If the
bone ends are only pressing against
the artery or vein, restoration to
normal position may relieve the
obstruction. If the vessel is actually
torn, manipulation is usually not
helpful. (Loss of sensation may also
result from injury to a nerve.)
Figure 11-1. Inflatable splint for
fractures of the lower leg and ankle
Bleeding
Some bleeding occurs with all
fractures. Broken bones with sharp
ends can cause extensive
destruction of the surrounding soft
tissues and profuse blood loss.
Fractures of the pelvis or thighs are
usually associated with severe
bleeding. The hemorrhage often
causes shock and can be lethal, and
yet may produce little or no external
evidence of bleeding. Anyone
caring for an injured person with
either of these injuries—or multiple
fractures of other bones—must be
aware of the threat of shock and
should institute treatment in
anticipation of its appearance.
Open Fractures
The danger of infection makes
open or compound fractures much
more serious problems.
Osteomyelitis, an infection of bone,
can produce extensive bone
destruction and may prevent healing
of fractures. However osteomyelitis
is now uncommon due to good
wound cleansing, debridement, and
antibiotics.
Any fracture is considered open
if the skin is broken, regardless of
whether the skin was damaged by
the bone ends or in some other way.
A fracture produced by a
penetrating injury, such as a gunshot
wound, is considered open because
the skin is no longer able to keep
bacteria away from the injured
bone.
If the bone ends protrude through
a break in the skin, before any
attempt to straighten the extremity is
made. they should be cleansed with
antibacterial soap and rinsed with
disinfected water until all visible
foreign material has been removed.
Manipulation causes the bone ends
to retract beneath the skin, and
foreign material carried with them
greatly increases the severity of the
subsequent infection. The wound
should be left open and covered
with a bulky bandage. The
individual should be evacuated as
rapidly as possible. If evacuation
can be completed in a few hours,
antibiotics should not be
administered unless they can be
given intravenously. If evacuation
must be delayed, high doses of oral
or intravenous antibiotics should be
given. A cephalosporin or
(Augmentin®) are the drugs of
choice.
Control of Pain
Pain from a fracture is greatly
reduced by immobilization. Shortly
after injury, pain medications are
usually not needed during splinting.
However, analgesics may be
required for the inevitable jolts of a
prolonged evacuation over rough
ground.
If needed, morphine can be
injected intramuscularly every two
to three hours. However, absorption
of the drug from the injection site is
reduced if the person is in shock,
and repeated injections can lead to
an overdose when normal
circulation is restored. Pain
medications usually are inadvisable
for injured persons who are in
shock. If such individuals do
require analgesia, morphine should
be injected intravenously in small
amounts until any necessary
manipulation has been completed or
the pain has been reduced to a
tolerable level.
Transportation
Immobilization of fractures and
treatment for other injuries must be
completed before the person is
moved unless the injured’s location
is threatened by hazards such as
falling rock, an avalanche, or an
electrical storm. After obvious
injuries have been treated, but
before evacuation is begun, the
person must be slowly and
thoroughly examined to ensure that
no additional injuries have been
overlooked in the initial evaluation.
Attention must be directed to the
person’s back, which is often
neglected. If not treated, such
injuries could be seriously
aggravated during evacuation.
Individuals with fractures of the
upper extremity, collarbone, or ribs
and some persons with head
injuries are able to walk. Such
individuals must be closely
attended because weakness and
instability can result from the injury
or from drugs given for pain.
Persons with fractures of the lower
extremities, pelvis, or vertebral
column and individuals with severe
head injuries usually must be
carried. Considerable
resourcefulness and sheer
determination are required to
successfully evacuate individuals
with these injuries, particularly in
bad weather. Carrying a person a
significant distance often requires
twelve to fifteen people.
SPECIFIC FRACTURES OF
THE UPPER EXTREMITY
Hand and Finger

Fractures of a finger are usually
obvious; fractures of a hand may be
difficult to diagnose. If pain persists
for several days, a fracture is
probably present. The hand and
fingers should be immobilized by
bandaging the hand in the position
of function with a wad of material
in the palm. An elastic bandage or
rolled up pair of socks serves
nicely for this purpose. If the
fracture is adjacent to the wrist, a
splint should be applied to the palm
and the underside of the forearm. A
forearm sling should be used to
keep the hand elevated, preferably
higher than the heart (Fig. 11-2).
Forearm, Elbow, Upper Arm, and

Shoulder
Forearm and wrist fractures are
usually obvious. To stabilize
forearm fractures, the hand and
elbow must be included in the
splint. A wrist fracture may be
immobilized in a forearm splint.
After splinting, the injured arm
should be supported in a sling. An
improvised sling can be made from
the injured person’s shirt. The
injured arm should be held over the
abdomen with the hand higher than
the elbow. The bottom of the shirt is
rolled over the forearm and the
upper arm and pulled up as high as
possible, preferably to the shoulder.
The shirt tail can be secured with
safety pins or a small stone or
similar object placed inside the
shirt and held by a shoelace or cord
tied around it and looped around the
person’s neck.
Figure 11-2. Application of a forearm
sling
A jacket or windbreaker also

can act as a sling. The jacket should
be put on with the sleeve of the
injured arm pulled inside. A belt,
cord, or rope placed around the
lower chest holds the injured arm in
a suspended position.
Fractures of the upper arm and
shoulder can be distinguished from
dislocations of the shoulder
because the arm is held snugly
against the chest. When the shoulder
is dislocated, the forearm cannot be
brought into contact with the chest.
The bone in the upper arm
(humerus) is palpable throughout its
entire length on the inner surface of
the arm. Undisplaced fractures can
be detected by gently running a
finger along this bone.
Immobilization of fractures of
the elbow, upper arm, and shoulder
is best achieved with two slings.
One supports the elbow, forearm,
and hand. The second is tied around
the body and holds the upper arm
against the chest, which serves as
the splint (Fig. 11-3). The elbow
should not be flexed more than
ninety degrees to avoid impairment
of circulation. Should numbness of
the little and ring fingers develop,
the elbow should be padded to
relieve pressure on the nerves
located there. If only one triangular
bandage is available, webbing or
similar material can be substituted
for one of the slings. A sling can be
improvised by pinning the shirt
sleeve to the front of the shirt with
safety pins.
Figure 11-3. Forearm sling with an
upper arm binder
Figure 11-4. Figure-eight bandage for
splinting a fractured collarbone
Collarbone
Fractures of the collarbone
(clavicle) usually can be felt by
running a finger along the bone.
Such fractures are less
uncomfortable if the shoulders are
held back. The shoulders can be
splinted in this position by webbing
or rope that passes over the
shoulder and under the armpit on
opposite sides, forming a figure
eight (Fig. 11-4). The strapping
should be applied over the clothing,
and the shoulders and armpits must
be padded. However, an excellent
alternative is using a backpack as a
figure-eight splint. It is also an
excellent splint for an
acromioclavicular (shoulder)
separation. The person may carry
lightweight items in the pack. In all
cases, it is important to document
the injury, the neurovascular status,
and the treatment rendered.
THE LOWER EXTREMITY
Foot and Toe
Fractures of the small bones in
the foot may be difficult to
diagnose. Some fractures result
from accidents that seem
insignificant, such as stepping off a
curb, and are associated with
relatively little pain. If pain persists
for several weeks, the person
should consult a physician. Injuries
of the toe and foot can be splinted
by a well-fitting shoe or boot. Since
climbers or skiers are usually
wearing a boot when injured,
fractures below the ankle are
uncommon among them.
Fractures of the heel (calcaneus)
result from a jump or fall when the
individual lands flatfooted or on the
heels on a hard surface. Pain
usually prevents bearing weight on
the injured foot during evacuation.
Ankle
Fractures of the ankle are often
difficult to differentiate from
sprains if the ankle is not
dislocated. Swelling is commonly
more severe with sprains. If pain in
an injured ankle does not begin to
subside in two or three days, the
presence of a fracture should be
assumed until X-rays can prove
otherwise.
Ankle fractures can best be
immobilized with a U-shaped splint
that passes around the bottom of the
foot and extends up along both sides
of the leg. A flexible splint, such as
a SAM Splint®, would be ideal.
Straightening may be necessary
before a displaced or dislocated
fractured ankle can be splinted, and
that can best be achieved by
applying gentle traction on both the
heel and front part of the foot while
rotating the foot and ankle into a
more normal position.
Straightening should be
attempted without delay to relieve
pressure and stretching of skin and
of nerves and blood vessels that
pass through the ankle.
Straightening a dislocated ankle is
usually easy, since the only way to
dislocate an ankle is to tear the
ligaments that hold it in place.
Ankle dislocations are almost
always associated with fractures.
A person with a minor injury,
such as a fracture of the bony
protuberance on the outside of the
ankle (lateral malleolus) or a
fracture of the bone in the foot just
below the malleolus (fifth
metatarsal), may be able to walk a
considerable distance with a
walking aid, such as an ice ax, after
immobilization. Individuals with
more severe injuries may be able to
hop short distances on the uninjured
leg, but evacuation for distances
greater than a few hundred yards
usually requires a stretcher or
crutches.
Leg and Knee

Fractures of the lower leg are
usually obvious if the tibia (the
larger bone) or both bones are
broken. Fractures of the fibula (the
small bone on the outer side of the
leg) may not be so apparent. The
diagnosis may be made by
tenderness to palpation over the
fibula. Most individuals with a
fibula fracture can walk gingerly on
their injured leg.
Lower leg fractures should be
immobilized in the same manner as
fractures of the ankle, with a splint
on either side of the leg or with an
inflatable splint. Fractures that
involve the knee require
immobilization of the ankle and
knee.
Kneecap
Fractures of the kneecap
(patella) may be difficult to
distinguish from a severe bruise.
Occasionally the fracture severs the
tendons that extend the knee. To
immobilize such fractures, a splint
that extends from the ankle to the
hip should be applied. A cylindrical
splint is best, but if material to
make one is not available, SAM
Splints® placed medial and lateral
to the knee work well. With the
knee well splinted, the injured
individual should be able to walk.
Thigh
Fractures of the thigh (femur) are
usually readily apparent because
they are associated with pain and
deformity. Adequate immobilization
of a fracture of the femur requires
traction, which should be applied
as soon as possible and continued
until evacuation has been
accomplished.
Immobilization is needed to
control bleeding. The strong thigh
muscles cause the bone ends to
override and damage the
surrounding tissues, resulting in
severe hemorrhage. Traction
stretches the muscles to their
normal length and compresses the
blood vessels—particularly veins
—within them, limiting the
bleeding. Compression over the
fracture site with a circumferential
dressing, such as an elastic
bandage, may also help control
bleeding.
Traction is also required to
control muscle spasms, which
usually begin within an hour after
the fracture, move the bone ends,
and can be very painful. Spasms
also increase damage to the
surrounding muscle.
Traction splints (Fig. 11-5) can
be improvised and are
commercially available. The
Kendrick® Traction Device and the
Sager Splint® are two examples;
information about them is available
on the Internet.
When a traction splint is to be
applied, the shoe or boot should be
left in place, the ankle should be
carefully padded to prevent
obstruction of the blood supply to
the foot, and a figure-eight bandage
similar to that used for sprained
ankles should be placed over the
boot and padded ankle. The leg
should be gently lifted by pulling on
the foot, and the splint should be
slipped into place and secured at
the groin. A hitch slipped under the
figure-eight bandage should be
looped over the crosspiece of the
metal frame and tied. A rod inserted
through this hitch can be twisted to
apply traction on the leg. The pull
should only be strong enough to
prevent the foot and leg from
sagging when the splint is lifted.
Twenty to thirty pounds of traction
are usually adequate. The hitch may
need to be tightened periodically as
the thigh muscles relax and
lengthen.
Figure 11-5. Fractured thigh
immobilized by a traction splint
Bandages should be used as

hammocks to support the leg in the
splint, and one bandage must
completely surround the leg to
prevent swinging from side to side.
The lower end of the splint should
be elevated so that no pressure is
on the heel. The person is more
comfortable, particularly during a
long evacuation, if the knee is
flexed five to ten degrees.
Pain in the foot after the splint
has been applied indicates the
blood supply to the foot has been
impaired. The figure-eight bandage
must be disassembled at once and
the ankle more carefully protected.
Permanent injury, which may be
more crippling than fractures, can
result if circulation is not
adequately protected. Such injury is
more likely when traction splinting
lasts overnight or longer. In a cold
environment, careful attention to
circulation is required to avoid
frostbite.
Well-equipped rescue groups
and wilderness expeditions should
probably carry one or more
Kendrick® Traction Devices or
Sager Emergency Traction
Splints®. The Kendrick device is
lighter (20 oz or 600 gm) and packs
into a much smaller space than the
Sager Splint®. A makeshift traction
splint can be made from two ski
poles. The wrist straps can be
hooked together and slipped up
against the buttock like the half ring
of a manufactured splint. A
handkerchief or strap can be used to
tie the hand grips together across
the front of the thigh like the belt on
a standard splint. Bandages tied
between the poles support the leg,
and the hitch around the ankle is
hooked to the baskets or ends of the
ski poles. Other materials can be
used similarly to improvise a
traction splint, but improvised
traction splints almost never work
as well as a manufactured splint.
Ordinary splints that do not
apply traction, such as those for
fractures of the ankle and lower leg,
should not be used for fractures of
the thigh because they do not
control bleeding or prevent muscle
spasms. If materials to improvise a
nontraction splint are available,
they can be used for a traction
splint.
Individuals with a fractured
thigh must be evacuated, preferably
in a basket stretcher and by
mechanical means, such as a
helicopter. Since the basket
stretcher must be transported to the
accident site, a traction splint can
be transported at the same time. If
avoidable, improvised splints
should not be used during
evacuation.
Hip
Fractures of the hip are actually
fractures of the upper portion of the
femur (head, neck, or trochanteric
portion) or of the socket in the
pelvis into which the head fits: the
acetabulum. Shortening of the leg
and rotation of the foot to the
outside along with pain in the hip
are the typical signs of a fractured
hip. However, shortening and
rotation may not be present if the
fracture is not displaced. If a
fracture is suspected, the person
must not be permitted to walk on the
injured leg.
Such fractures require no
splinting other than binding the legs
together.
THE TRUNK
Pelvis
Fractures of the pelvis should be
suspected following violent
accidents, particularly if side-to-
side or front-to-back pressure over
the pelvis causes pain. Blood loss
of major proportions is inevitable
with pelvic fractures, is rarely
evident when the person is
examined, yet commonly produces
shock and may be lethal. Therapy
for shock should be instituted if a
pelvic fracture is suspected.
The source of bleeding is usually
the fracture sites and extensive vein
tears in the pelvis. Compression
and stabilization of the pelvic
fractures may facilitate spontaneous
blood clotting and cessation of
bleeding. Although commercial
compression devices are available,
these therapeutic goals can usually
be achieved by wrapping the pelvis
with a bedsheet or sleeping-bag
liner (Fig. 11-6). The sheet should
be folded to a width that covers the
entire pelvis and is centered over
the hip joints. Ideally two
individuals, one on each side of the
injured person, should apply
tension in opposite directions, and
the ends should be tied over the
midportion of the pelvis. The wrap
can be tightened by inserting a stick
or rod through the knot and rotating
it like a windlass, as is done to
tighten a tourniquet. During
tightening, the injured person may
have increased pain, but this should
resolve with pelvic stabilization.
Fracture pain, however, does
require ongoing pain medication,
often opiates.
Figure 11-6. Wrapping a pelvic
fracture to control bleeding
Splinters of bone from pelvic

fractures frequently damage the
organs within the pelvis,
particularly the urinary bladder.
This complication should be
suspected if the person fails to void
or passes only a few drops of
bloody urine after the injury.
(Injuries of the bladder are
discussed in Chapter 10:
Abdominal Injuries.)
Vertebra
Fractures of the vertebral
column (spine) in the back and neck
are particularly threatening because
they are always accompanied by the
possibility of injury to the enclosed
spinal cord. These fractures are
discussed in Chapter 8: Head and
Neck Injuries.
Other Fractures
Rib fractures are discussed in
Chapter 9: Chest Injuries; skull
fractures and fractures of the face
and jaw are discussed in Chapter 8:
Head and Neck Injuries.
DISLOCATIONS
A dislocation is an injury in which
the normal relationships of a joint
are disrupted. The bone may be
forced out of a socket, as occurs in
dislocations of the shoulder, elbow,
or hip. Some joints, like those
between the bones in the fingers,
have no socket, and the joint
surfaces are simply displaced.
Bones may be fractured and
adjacent nerves, blood vessels, and
supportive structures may be
injured.
The signs of dislocation are
similar to those of a fracture: pain
that is aggravated by motion,
tenderness, swelling, discoloration,
limitation of motion, and deformity
of the joint. The findings are
localized to the area around a joint,
but comparison with the opposite,
uninjured joint may be necessary to
be certain that a definite
abnormality is present. Frequently,
the dislocated joint appears larger
than normal due to overlapping of
the bone ends. Pain and muscle
spasm usually prevent use of the
extremity for physical activities.
Dislocations should be reduced.
The risk of causing additional
damage is quite small, and any
fractures of the joint surface are
better aligned after reduction.
Furthermore, dislocations should be
reduced as quickly as possible. The
muscles surrounding a dislocated
joint go into spasm quickly. The
chances for successful correction of
the dislocation decrease and the
risk of further injury increases with
the passage of time after injury.
Other advantages of early
reduction of a dislocation are these:
Pain relief is often dramatic.
The risk of circulatory or neural
damage is reduced.
Immobilization of the joint is
easier.
Transportation of the injured
person is easier.
Pain, pallor or cyanosis,
swelling, numbness, or the absence
of pulses beyond the dislocation are
indicative of obstruction of the
blood supply. Entrapment or
compression of arteries is
particularly likely to occur with
dislocations of the elbow or knee.
Prompt action may be required to
save the limb from gangrene.
The individual performing the
reduction should use other members
of the party if they can help and
must ensure that the injured person
understands and agrees with what is
being attempted and the technique to
be used. Strong analgesics such as
intramuscular or intravenous
morphine are helpful; medications
such as diazepam (Valium®)
promote relaxation of the muscles
and the injured individual. Traction
must be gentle and steady; forceful,
jerking maneuvers must be avoided.
After any dislocation is reduced,
the extremity should be splinted in
the same manner as for a fracture. It
may need to be immobilized for two
to three weeks—sometimes longer.
Fingers
Dislocations of the fingers,
which occur most commonly at the
second joint, are usually obvious
and may be corrected quite easily
immediately after the injury.
Reduction is best accomplished by
holding the digit in a moderately
flexed position and applying
traction while pushing the end of the
dislocated bone back into place
(Fig. 11-7).
Dislocations at the base of the
index finger and at the base of the
thumb may not be reducible. With
such injuries, surrounding ligaments
and tendons often entrap the end of
the bone, and surgery is required
for reduction. An initial effort to
reduce such dislocations should be
made, but if unsuccessful the hand
should be splinted in the position of
function and the person evacuated.
After reduction, an injured finger
can be splinted effectively by taping
it to an adjacent uninjured finger.
Figure 11-7. Technique for reducing a
finger dislocation
Elbow
Dislocations of the elbow are
usually obvious, particularly when
compared with the opposite side.
Most dislocations are posterior, and
the tip of the dislocated ulna is very
apparent. Movement of the joint is
restricted.
Elbow dislocations may be
difficult to reduce. The slightly
flexed forearm should be pulled
downward while the upper arm is
pulled upward by an assistant. A
considerable amount of force is
usually needed. As the joint
separates, any sideways
displacement of the bones should be
corrected first. The forearm may
need to be rocked back and forth
very gently. If the joint is not fully
reduced, gentle bending of the
elbow may complete the correction.
The ability to flex the elbow to
ninety degrees or more is proof of
reduction.
Immediately after the dislocation
has been reduced, the pulse at the
wrist should be checked. If the
pulse is absent but the color of the
hand is normal and pain is
diminished, the absence is probably
the result of arterial spasm for
which nothing needs to be done. If
the pulse is absent, the hand is
darkly colored or cyanotic, and
pain is increasing, the artery to the
forearm may have been entrapped
when the bones of the elbow
slipped back into position. The
joint should be slightly separated
again with traction (not dislocated
again) and gently rocked back and
forth to free the entrapped
structures.
The arm and hand should be
splinted with the elbow at a ninety-
degree angle. Pulse and sensation
should be checked again after the
splint is applied. The elbow must
not be wrapped circumferentially
with tape or bandages because
swelling does occur and, if
confined, would compress blood
vessels and nerves. Fracture of the
bones of the elbow commonly
occurs with dislocation. A
physician should be consulted as
soon as possible, particularly if
pain persists.
Shoulder
Shoulder dislocations result
from strong jerks when the arm is
rotated outward and held away
from the body. A typical situation is
a kayaker thrusting back and
downward with a paddle (Fig. 11-
8). Many individuals have recurrent
dislocations, can readily identify
the injury, and often are helpful with
reduction.
Among shoulder dislocations
(Fig. 11-9), 95 percent are anterior
(Fig. 11-10). The individuals are in
pain and hold the upper arm and
forearm away from the body in
various positions, but the arm
cannot be brought into contact with
the chest. (With a fractured
humerus, the arm is usually held
snugly against the chest.) The
absence of the end of the humerus in
the joint, which is located just
lateral to the collarbone and below
the shoulder, may be most easily
recognized by loss of the normal
roundness or fullness of the deltoid
muscle, particularly when
compared with the opposite
shoulder.
Figure 11-8. Mechanism of shoulder
dislocation by a kayaker
Figure 11-9. Normal and dislocated
shoulder joints
Figure 11-10. Appearance of a
shoulder after anterior dislocation
Posterior shoulder dislocations

are rare and often difficult to
diagnose. The forearm and upper
arm are typically held across the
chest in contact with the chest wall.
The forearm cannot be externally
rotated away from the chest. A
defect is usually present in the
normal contour of the deltoid
muscle, which forms the outer point
of the shoulder, and the head of the
bone in the upper arm (humerus)
sometimes can be palpated
posteriorly.
Of the many methods for
reducing a dislocated shoulder, two
appear to combine the best chance
for success with the least risk of
additional injury.
The first uses active traction by
an attendant (Fig. 11-11). The
person should be lying flat with the
injured arm held straight out from
the side of the body. (A table for the
individual to lie on would provide
the best positioning, but a
wilderness situation would require
improvisation, such as a log or
stone bench.) The injured arm
should be flexed at front view side
view DISLOCATED the elbow and
the forearm held in a vertical
position. A loop of webbing,
clothing, or similar material that has
been tied loosely around the
attendant’s waist should be slipped
over the arm and down to the
elbow. After padding the elbow, the
attendant can apply traction by
simply leaning backward. Another
attendant must hold the person,
preferably with a loop of clothing
around the chest, to prevent traction
moving the entire body.
Figure 11-11. Technique for reducing
a shoulder dislocation with active
traction
a shoulder dislocation with passive
traction
Figure 11-13. Technique for splinting
a dislocated shoulder that cannot be
reduced
Communication with the injured

person helps achieve maximal
relaxation. The humerus may be
gently rotated by moving the
forearm from side to side, and the
head of the humerus may be gently
pushed toward the socket with the
fingers of the opposite hand. After a
few minutes, reduction can be
recognized by the palpable settling
of the humeral head into its socket
and is heralded by the relief of the
individual, who is immediately
more comfortable. If the forearm
can be swung across the body and
can lie in contact with the chest
wall, reduction has been achieved.
A second method to restore the
dislocated bone to its normal
position is to use the prone
passivetraction method (Fig. 11-
12). The individual must be lying
prone on a table, log, or rock
surface with the injured arm
hanging downward and not touching
the ground. A backpack with ten to
fifteen pounds of weight is secured
to the upper arm with duct tape or
an Ace® wrap. After fifteen to
twenty minutes, the constant pull by
the weight tires the muscles
surrounding the shoulder, causing
them to relax enough for the
humerus to slip back into its socket.
If the dislocation is not corrected
within an hour, traction should be
discontinued, the arm splinted as
well as possible, and the person
evacuated (Fig. 11-13).
Following reduction of a
shoulder dislocation, the arm
should be immobilized for at least
two weeks, preferably three, with
two slings, one supporting the
forearm and hand and the other
holding the upper arm against the
body. A recurrent dislocation of the
shoulder may not require such long
immobilization. The ultimate
treatment of repeated shoulder
dislocations is surgical repair of the
lax ligaments that allow the
dislocation, which may occur with
disabling frequency after
insignificant trauma until reparative
surgery is performed.
Dislocated shoulders sometimes
cannot be reduced, and the
discomfort makes rapid evacuation
necessary. When the shoulder is
dislocated, the arm is held in an
awkward position that makes
splinting difficult. Successful
techniques use a strap or bandage to
anchor the hand on top of the head.
Sometimes the hand is held close to
this position spontaneously, but the
muscles would soon tire, producing
increased pain in the muscles and in
the shoulder. On ski slopes,
effective splinting has been
achieved with a rolled-up blanket
secured in a figure-eight position
like the splint for a fractured
clavicle but with the bulk of the
blanket in the armpit to support the
upper arm. In more remote
wilderness settings, a similar splint
would have to be devised.
Hip
Most hip dislocations are posterior
and result from falls with the hip
flexed. The force of impact
transmitted longitudinally through
the knee and femur drives the
femoral head backward out of its
socket. Strong forces are required
to produce such injuries. Impact of
the knees with the dashboard in an
automobile accident is a common
cause. Anterior hip dislocations are
most commonly produced by falls
in which the person lands directly
on the outer aspect of the hip and
are encountered most commonly in
children.
With a posterior dislocation, the
hip is partially flexed and the leg is
internally rotated, so the knee is
pulled upward and inward over the
opposite leg; with an anterior
dislocation the hip is externally
rotated with the knee turned
outward and away from the body
(Fig. 11-14). The key diagnostic
clue with both types of dislocation
is that returning the leg to a normal
position for splinting or
transportation in a stretcher is
impossible. The position of the leg
helps differentiate dislocations
from fractures of the hip or thigh,
with which the leg would lie flat.
Reducing a dislocated hip (Fig. 11-
15) is difficult and painful, but is
worth attempting because reduction
relieves pain, improves circulation
to the femoral head, and greatly
facilitates placing the person in a
basket stretcher for evacuation.
Figure 11-14. Posterior and anterior
hip dislocations
a hip dislocation
The technique for reduction is

the same for anterior and posterior
dislocations. Two attendants are
required. One holds the injured
person flat on the ground with hands
on both sides of the pelvis. The
other straddles the injured leg and
gently flexes the knee and hip to
ninety degrees. After bending the
knees and locking the hands behind
the injured person’s knee, the
second attendant can apply strong
upward traction by simply
straightening the legs. The weight of
the injured individual and the first
attendant provide countertraction.
Rotating the hip by moving the
lower leg gently from side to side
may help with reduction.
After reduction, the injured
extremity must be splinted to the
opposite leg. Gentle traction is
beneficial if available; the person
should be transported in a supine
position.
Knee
Knee dislocations are major,
sometimes disastrous injuries that
result from forceful impact with the
knee bent, most commonly in
automobile accidents. In most
instances, the ligaments and tendons
around the knee are so extensively
torn that dislocated knees pop back
into position spontaneously. The
nature of the injury can be
recognized by the pain and
instability of the knee. If the knee
remains dislocated, reduction can
usually be achieved quite readily
with traction on the lower leg.
Pulses and sensation in the foot
must be checked. Injury to the large
vessels behind the knee occurs
frequently. Such damage is
suggested by painful swelling
behind the knee developing
immediately or hours after
correction of the deformity and
confirmed by the absence of pulses.
The leg should be splinted as
securely as possible with
precautions not to interfere with
circulation. Dislocated knees are
too unstable for walking.
If a knee dislocation has been
reduced or instability suggests the
knee has been dislocated and has
reduced spontaneously, the
individual should be transported as
quickly as possible to a hospital
where injury to the large vessels
can be assessed. Even if the
circulation seems normal, damage
to the blood vessels may have
occurred and must be diagnosed
and repaired before irreversible
ischemic damage to the lower leg
occurs.
Kneecap
Dislocations of the kneecap
(patella) frequently are recurrent,
much like shoulder dislocations.
The kneecap is usually displaced to
the outside, and the knee is held in a
flexed position for comfort.
Comparison with the opposite knee
typically makes the abnormality
obvious.
To reduce the dislocation, the leg
should be gently straightened while
the kneecap is pushed back into
place. Straightening alone may be
adequate. Extending the knee
relaxes the thigh (quadriceps)
muscle, allowing the patella to
reduce easily. The person is usually
able to walk with a splint. SAM
Splints® folded double and placed
medially and laterally work well.
Ankle
Dislocated ankles are usually
associated with fractures of the
adjacent bones. They should be
reduced without delay and treated
in the manner described for
fractures. Reducing (realigning)
displaced fractures improves the
circulation and facilitates splinting.
Jaw
An individual can become so
completely relaxed while asleep
that the jaw falls downward and
slips out of its socket. Usually such
complete relaxation follows the use
of sleeping pills or overindulgence
in alcohol. The jaw also can be
dislocated by trauma or during
vomiting. People whose jaws have
been dislocated are unable to close
their mouth. In a remote situation,
the resulting inability to swallow
could lead to serious difficulties.
Dislocations of the jaw can be
safely reduced, usually rather easily
(Fig. 11-16). Both thumbs should be
inserted over the molars of the
lower jaw and pressed directly
downward. Considerable force is
required to overcome the spasm in
the jaw muscles, which are quite
strong, but the jaw should slip back
into place without too much
difficulty. (The thumbs should be
padded to prevent bites as the jaw
pops back into its socket.) After
reduction, persistent pain in the
joint, which is located just in front
of the ear, may be indicative of a
fracture, and a physician should be
consulted. If dislocations recur, the
individual can wear a bandage to
hold the mouth closed when asleep.
The bandage should cover the tip of
the chin and should be tied over the
top of the head and around the back
of the neck.
OTHER INJURIES OF BONE

AND RELATED STRUCTURES
Contusions of Bone and
Subperiosteal Hematomas
A blow that does not produce a
fracture or dislocation may still
cause sufficient damage to produce
swelling in the fibrous bone sheath
(periosteum) or bleeding between
that tissue and the rigid portion of
the bone (subperiosteal hematoma).
The injured person complains of
pain, the area is tender, and the
bone may appear or feel larger than
normal.
a jaw dislocation and bandaging the
jaw to prevent recurrence
Treatment consists of
immobilization and applying cold
and a pressure bandage for twenty-
four hours following injury. After
twenty-four hours, local heat should
be applied, and activity can be
allowed to the limits of pain
tolerance. However, if a fracture or
dislocation cannot be ruled out,
immobilization should be
continued.
Sprains and Strains

Sprains and strains are
stretching, tearing, or avulsing
injuries of ligaments around a joint
and often cannot be differentiated
from fractures without X-rays. They
can be as disabling as a broken
bone. The signs are similar to a
fracture, although grating of broken
bone ends and deformity are not
present. Swelling is often quite
marked, and discoloration may also
be present. If an injury is obviously
severe, the wisest course is to treat
it as a fracture.
The treatment for sprains is
summarized in the acronym RICE,
which stands for Rest, Ice,
Compression, and Elevation. An
elastic bandage can partially
immobilize a small joint such as an
ankle and provides compression
that helps limit swelling. Applying
cold immediately after an injury
reduces hemorrhage and swelling.
Absorption of blood and edema
fluid can be promoted by elevating
the injured area. Later, heat may be
helpful but should not be applied
until at least three days after the
injury. Motion and use may speed
recovery but only when resumed
after the initial swelling and
hemorrhage have subsided.
Sprained ankles are the most
common injuries of this type, and
circumstances frequently require the
individual to walk (hobble) from
the injury site. In most situations a
figure-eight bandage over the shoe
or boot should support the ankle.
Loops of the figure eight should
pass around the back of the heel and
under the sole of the foot, crossing
on top of the foot. Support must be
snug but must not obstruct the
circulation. The injured person can
no longer rely on the injured ankle,
and the risk of further damage is
significant.
If the ankle is to be taped, the
foot should be held perpendicular
to the leg while the tape is applied.
Alternate interlacing layers of tape
should be placed under the heel and
straight up the leg, and around the
back of the heel and straight out
over the foot (Fig. 11-17). Tape
must not completely surround the
leg, or swelling (which could result
just from immobilization) would
impair blood circulation to the foot.
The ankle should be taped only for
the first three or four days of use
after healing is underway.
One of the most common
downhill skiing injuries is a strain
or tear of the ligaments of the knee.
Occasionally the cartilage that
covers the joint surfaces also is
injured. The knee should be
splinted as if it were fractured, but
the person may be able to walk
after the knee has been
immobilized. If standing or walking
is painful, the individual should be
evacuated by sled or stretcher. Such
injuries frequently require a cast
and four to six weeks or more to
heal.
Figure 11-17. Technique for taping a
sprained ankle after healing has
begun
Muscle and Tendon Tears

A sudden, strong jerk with the
bones and joints fixed in position,
as occurs at the end of a fall, may
rip a muscle from its insertion or
may partially or completely tear the
body of the muscle or tendon.
Muscle tears or “pulls” can also
result from vigorous activities, such
as sprinting at top speed, and from
sudden movements or changes in
direction. A penetrating injury may
sever a muscle or tendon. Complete
separation of the muscle or its
tendon results in loss of function.
Incomplete interruption seldom
produces complete loss of function
but is painful and does predispose
structures to subsequent injury.
Insertions are the points where
muscles or tendons are attached to
bone. The most common sites at
which insertion injuries occur are
the fingertips behind the nails,
shoulder, elbow, and ankle. Rupture
of muscles and tendons more
commonly occurs in the calf, the
front and back of the thigh, and the
upper portion of the arm and
shoulder. Pain, tenderness,
swelling, and loss of motion are the
usual findings. Sometimes a defect
in the muscle or tendon can be felt.
Prehospital treatment should
include immobilization, applying
cold, and rapid evacuation.
Definitive repair of such injuries is
most successful if performed within
twenty-four hours of the accident.
Muscle Compartment Syndromes

Some muscles are enveloped in
a fibrous sheath or “compartment”
that is only slightly distensible.
Swelling of the muscle as the result
of unaccustomed exercise or trauma
can raise the compartment pressure
to a level that impairs blood flow.
When deprived of its blood supply,
the muscle dies, usually crippling
the extremity.
Compartment syndromes are
uncommon, but because they can
produce permanent disability, they
should be recognized and promptly
treated. The anterior tibialis
muscle, which is located on the
outside of the shin, is the muscle
most commonly affected by
compartmental compression. Most
individuals have an obvious leg
injury, typically a crushing injury.
However, compartmental
syndromes are insidious because
they can develop following
unaccustomed exercise.
Occasionally pressure on the leg
during a period of unconsciousness,
or injuries such as burns, can
produce this disorder. A few
individuals have experienced
previous episodes of milder pain,
particularly following vigorous
exercise.
The initial symptom is pain in
the involved muscles, which
typically is much more severe than
would be expected from the injury
or exercise by which it is preceded.
Passive movement or stretching of
the muscle is also painful. Usually
the muscle is obviously swollen
and the overlying skin is tense and
glossy. However, the most
diagnostic feature is severe
weakness or paralysis of the
involved muscle. A person with an
anterior tibial compartment
syndrome cannot flex the foot
upward or resist pressure forcing it
down. The foot may be cold and
numb, and the pulses may be weak,
but such signs are inconsistent and
their absence is not an indication
that a compartment syndrome is not
present.
Outside of a hospital, two
maneuvers may be beneficial: Any
constricting clothing or bandages
should be removed, and the
extremity should be positioned at or
above heart level. However, the
only effective treatment is to
surgically open the compartment to
relieve the pressure. Since surgeons
alone are familiar with the
technique and the anatomy,
individuals with this disorder
should be evacuated to a hospital. If
evacuation is not possible,
medically trained personnel may be
able to perform the procedure with
appropriate guidance.
Evacuation is urgent. Treatment
must be prompt to avoid permanent
paralysis. Only 31 percent of one
group of individuals treated within
twelve hours had residual
disability; 91 percent of those
decompressed later had permanent
functional deficits and 20 percent
required amputations. The usual
functional deficit is “foot drop,” an
inability to flex the foot upward,
which usually requires a brace to
support the foot when walking on a
flat surface. On a wilderness trail,
disability would be much greater.
Bursitis, Tendinitis, and Shin

Splints
Bursitis, tendinitis, and shin
splints are caused by inflammation
of tendons or the flattened, cystlike
spaces (bursae) that cushion the
movement of tendons. These
disorders are characterized by pain
and stiffness that has a gradual
onset, usually following
unaccustomed use of a muscle for
an extended time. The pain can be
quite severe and frequently is first
noticed the morning after such
activities.
Splinting may relieve the
immediate discomfort but often
prolongs the problem. Moist heat
and a mild analgesic may provide
some relief; sometimes cold is
more effective. The pain, which is
rarely disabling, may persist for
days, weeks, months, or years.
Continued use of the joint through
its full range of motion helps to
prevent stiffness.
Tenosynovitis
Inflammation and infection of the
sheaths that surround tendons and
lubricate their movements may
result from unaccustomed overuse
or a penetrating injury. In the field,
such infections may develop
several days after sustaining a small
cut or puncture wound that did not
appear significant at the time,
particularly on the hand, finger, or
foot. Pain with motion of the
involved tendon is the diagnostic
finding. When infection is present,
painful swelling, increased warmth,
and redness are apparent. A
crackling sensation in the affected
tissue may be felt with pressure or
movement of the tendon. Although
sterile inflammatory episodes
caused by overuse usually subside
with rest, an infected tenosynovitis
requires the attention of a physician,
who sometimes must surgically
drain the tendon sheath. If infection
is suspected, broad-spectrum
antibiotics should be started, and
the individual should be evacuated
without delay. Failure to obtain
surgical treatment can result in
permanent loss of mobility of the
tendon or in extension of the
infection to adjacent tendons and
body spaces and even greater loss
of function.
Joint Effusion
Swelling, mild discomfort,
increased warmth, and redness may
appear in a joint after an injury—
sometimes without any preceding
trauma. The knee is most commonly
involved, but other joints,
particularly the elbow or wrist, can
be involved. The cause may be
outside the joint, as with tennis
elbow or a similar condition
involving the insertion of the
tendons just below and to the side
of the kneecap. Within the joint,
effusions often result from
deterioration of the cartilage
following repeated injury. If
inflammation but no infection is
present, the discomfort and
swelling may respond to rest,
wrapping with an elastic bandage,
moist heat, and a mild analgesic. An
infected joint—manifested by more
obvious redness, greater pain and
swelling, and fever that is
sometimes high—requires
immediate care by a physician,
particularly when the person is
febrile.
Ingrown Toenails
Ingrown toenails are best prevented
by trimming the toenails straight
across without rounding the corners
and by wearing well-fitted boots
and socks. If pain and redness occur
during an outing, a wedge can be
cut from the outer third of the nail.
The offending sharp corner must be
removed. Warm soaks hasten
recovery; as the nail regrows,
elevating the new corner with a
pledget of gauze may prevent
recurrence.
Corns and Calluses

Corns and calluses should be
prevented by wearing well-fitted
shoes. If they cause discomfort on
an outing, they can be shaved flat
with a razor blade after they have
been softened by soaking in warm
water.
BACK INJURIES
Strain and Spasm
Back pain is produced by a wide
variety of disorders, such as
carrying heavy loads, working in an
unaccustomed stooped position, or
sleeping in an awkward position.
However, treatment is frequently
frustrating. The measure that
provides the greatest relief is
sleeping on a firm support. When
sleeping outdoors, a mat that
provides insulation but little
padding is best. Heat may help
relieve muscle spasm. Mild
analgesics such as acetaminophen
may relieve the pain, but stronger
medications may sometimes be
necessary. A few individuals have
severe, incapacitating pain from
muscle spasms.
Sciatica
Sciatica is a type of pain most
commonly caused by disc extrusion
or by bone spurs. Discs are
cushions of cartilaginous material
that separate the vertebrae of the
spinal column. A so-called ruptured
disc is an extrusion of this
semisolid material into the spinal
canal so that it compresses the
spinal cord or the nerves coming
from the cord. The basic defect is
degeneration and weakening of the
ligaments that normally hold this
cushion in place. Trauma is only the
final incident. Unless the basic
defect is present, trauma alone
usually fractures the vertebrae
instead of causing the disc to
rupture.
Similar pain can be caused by
the formation of small bony growths
known as bone spurs that impinge
on the nerves coming from the
spinal column. Such spurs are a
feature of osteoarthritis and are
common in older individuals.
Sciatica is caused by an
extruded disc or bone spurs in the
lumbosacral area. The symptoms
are highly characteristic. Pain
begins in the lower back, radiates
to one side, and passes through the
buttock and down the back of the
leg. The pain may involve the
outside of the leg but is rarely felt
in the front or inner portion of the
leg. The person frequently walks
with a decided limp. Pain when
moving to and from a supine
position is also characteristic.
As a result of the pain associated
with movement, muscles in the
lower back go into spasm. The
vertebral column in the lower back
is immobilized and does not bend
when the individual leans to either
side, which can be seen when the
person is examined from behind. An
examiner’s fingers can usually
palpate this muscle spasm. Over the
foot and lower leg on the affected
side, loss of sensation to pinprick
or the light touch of a wisp of cotton
may be present.
Prehospital treatment for sciatica
is the same as for strain of back
muscles. However, the two
conditions should be differentiated
since each has a quite different
outlook. Strain usually clears up in
a few days, or perhaps a few
weeks, with rest and proper
treatment. Although the pain of
sciatica may disappear in a few
days with rest, it may be more
prolonged and may be relieved only
by surgery. Furthermore, a disc or
bone spurs can produce permanent
nerve injury and muscle weakness.
Even though symptoms of sciatica
may disappear rather promptly, a
recurrence is likely at any time.
In expedition circumstances,
these prognostic factors must be
considered. Individuals with a
previous history of a ruptured disc
should consult an orthopedist or
neurosurgeon before undertaking
remote wilderness activities,
particularly if sensory impairment
is present.
SNOWBOARDING INJURIES
Snowboarding is a rapidly growing
winter sport that is gaining
acceptance at most ski areas. Not
many studies on injuries have been
published, but an investigation of
415 injuries in the Lake Tahoe area
has provided significant data.
Those injured were 75 percent
males; the average age was twenty
years. At least 60 percent were in
their first year of snowboarding.
Many had never skied before taking
up “boarding.” Falls produced 75
percent of all injuries, mainly to
wrists, shoulders, knees, and
ankles. The fracture rate was much
higher in snowboarders than in
skiers. Wrist fractures were most
common. Dislocations of shoulders
and elbows also occurred. Ankle
sprains and fractures predominantly
befell wearers of soft boots. Those
wearing hard-shell boots more
commonly had knee injuries,
similar to skiers. However
snowboard injuries to the knees are
mainly collateral ligament sprains,
not anterior cruciate ligament tears.
The injury rate was slightly lower
than that seen in skiers.
Prevention of injuries is directed
at learning proper technique,
including learning how to fall with
less risk. Pads for elbows and
knees and gloves with built-in wrist
splints are available.
In addition, many snowboarders
are new to the mountains and must
learn to respect the mountains in
winter, particularly the snow
patterns and residuals of mountain
storms. Many snowboarders have
been killed by falling into tree
wells filled with deep powder
snow. They generally end up upside
down and are unable to release
their bindings. Proper education
and avoiding snowboarding alone
in ungroomed or remote terrain
could prevent such tragedies.
CHAPTER 12
SOFT-TISSUE INJURIES
Lacerations, abrasions, bruises, and

blisters are the most common
injuries occurring in the wilderness.
They are called “soft-tissue”
injuries to distinguish them from
injuries to bones and ligaments.
The treatment of soft-tissue
injuries has four objectives:
Control of bleeding
Control of infection
Promotion of healing
Preservation of function in the
injured part
CONTROLLING BLEEDING
Direct pressure is the only effective
means for controlling bleeding from
a soft-tissue wound. The damaged
blood vessels must be collapsed to
obstruct blood flow and permit
clots to form. Pressure must be
applied directly over the wound.
Pressure points are not worth
considering. Tourniquets can be
dangerous and are needed or
justifiable only for severe injuries
such as amputations, open-limb
fractures complicated by arterial
injuries, or gunshot wounds that
have penetrated a major artery.
When such injuries are the result of
falls, injured individuals may bleed
to death before anyone can get to
them. (Falls severe enough to
produce amputations would often
produce fatal injuries to other parts
of the body.)
If a tourniquet is to be applied, it
must be recognized that the tissues
beyond the tourniquet are totally
deprived of blood and may die,
necessitating amputation. Pressure
from the tourniquet can also damage
nerves.
The tourniquet should be made
from fabric, such as a triangular
bandage folded to make a band one
to two inches wide. The band
should be placed around the limb
two to three inches above the injury
and tied in an overhand or square
knot. A stick, rod, or similar object
should be placed on top of the knot
and held in place with another
square knot. The stick should be
rotated like a windlass until the
bleeding stops. One end of the stick
can be tied or taped to hold it in
place. The tourniquet should not be
released until the injured individual
is in a situation where bleeding can
be controlled by an experienced
medical professional.
Bleeding from most skin wounds
is from veins and capillaries. The
pressure in these vessels is so low
that simply holding a dressing on
the wound for five minutes allows
the blood to clot and plug the
vessels. Deeper lacerations may cut
larger veins that bleed more
profusely, such as the veins visible
beneath the skin of the arms and
legs, but bleeding from these
vessels can be easily controlled by
compression because the pressure
within them is low.
Arteries have much thicker,
elastic walls and are deeper
structures. However, arterial blood
is under much higher pressure, and
blood loss is harder to control
when these vessels are damaged.
The only dependable way to
identify arterial bleeding is to see
blood spurting from the wound with
each heartbeat. The color of the
blood is not a reliable indicator of
its source. Arterial bleeding also
must be controlled by direct
pressure, but the pressure must be
maintained for a much longer time.
If bleeding persists, even after
direct pressure has been applied for
more than fifteen minutes,
particularly when an arterial injury
is suspected, the wound should be
packed with sterile gauze and
wrapped snugly with a continuous
bandage.
Bandages that completely
surround a limb may act as
tourniquets and obstruct circulation
to the rest of the limb. Absent
pulses, bluish discoloration of the
skin or nails, tingling sensations, or
pain indicate that the blood supply
to the tissues beyond the bandage is
inadequate. Since swelling at the
site of the wound can greatly
increase the pressure beneath a
circumferential bandage, the limb
beyond the bandage must be
carefully checked for circulatory
impairment every few minutes. If
the bandage initially is too tight, or
becomes too tight, it must be
loosened. After bleeding has been
controlled, the circumferential
bandage should be removed.
Movement may cause bleeding
to recur after it has been controlled.
To avoid further blood loss,
severely injured limbs should be
splinted or immobilized in some
other way before the individual is
evacuated.
CONTROLLING INFECTION
Wound infection results from
contamination, and all open wounds
are contaminated to some extent.
Preventing infection by minimizing
contamination and eliminating
conditions that promote bacterial
growth is far preferable to treating
an established infection.
Wound Cleansing
After bleeding has been
controlled, further contamination of
soft-tissue wounds must be
avoided. All persons caring for the
injured individual must wash their
hands, preferably with an
antibacterial agent such as
PhisoHex®, a povidone-iodine
preparation such as Betadine®, or
an alcohol-based skin disinfectant.
Sterile gloves, if available, should
be used but only after the hands
have been cleaned. The skin around
the wound should be vigorously
cleaned, preferably by scrubbing
with the same antibacterial agent.
Washing dirt, dried blood, or other
contaminants into the wound must
be avoided.
Finally, the wound itself must be
cleaned. A 20 ml or 50 ml syringe
with a large bore needle (18 gauge
or larger) is ideal for this purpose
because a jet of water can be
directed into the wound with
sufficient force to rinse out any
foreign material. (A plastic bag
with a pinhole can be used as an
improvised syringe.) Such rinsing
produces little pain and does not
damage the tissues. Obviously, only
disinfected water is suitable for
such cleansing. Foreign material,
dead tissue, or even clotted blood
left in the wound virtually insure
infection. Wound cleansing must be
complete. The syringe must be
repeatedly refilled and emptied into
the wound. Sterile forceps should
be used to remove any embedded
debris that cannot be rinsed away;
small tags of dead tissue may be
snipped off with sterile scissors.
For puncture wounds, bleeding
should be encouraged to help
remove bacteria and debris. The
depths of such wounds are not
reached by air, and anaerobic
bacteria that thrive in such
conditions, such as those that cause
tetanus and gas gangrene, can
produce devastating infections.
Antiseptics
Antiseptics have little value in
the control of wound infections.
They cannot compensate for
negligent wound cleansing and, for
wounds that are thoroughly cleaned,
provide little additional bacterial
control. The informed use of the
proper antiseptics, however, may
help significantly for animal bites
or other heavily contaminated
wounds.
Antiseptics placed in a wound
must be able to kill bacteria without
injuring the tissues. Minimizing
tissue damage is essential because
no agent can kill all the bacteria,
and injured tissue provides an
excellent medium for the growth of
the remaining organisms. The best
readily available antiseptic that
meets these qualification is a 10
percent solution of a povidone-
iodine preparation (Betadine® and
others). Povidone-iodine has two
advantages: It is ideal for scrubbing
hands or the skin around a wound
(which is why it is routinely used
by surgeons), and it can be
packaged in polyethylene bottles.
Povidone-iodine can be used
undiluted for cleansing skin prior to
needle punctures, but for rinsing a
wound it should be diluted 10:1 or
20:1 with disinfected water. The
wound should be flooded with the
solution.
Antiseptics such as alcohol,
tincture of iodine, or the mercurial
preparations damage tissues and
should not be placed directly in an
open wound.
Wound Closing
In the wilderness, soft-tissue
wounds never need to be sutured. If
a wound is left open, purulent
material from infected areas drains
to the outside. This purulent
material cannot escape from a
sutured wound and is extruded into
the surrounding tissues, spreading
the infection. In hospitals, softtissue
wounds are sutured under sterile
conditions to promote healing and
minimize scarring. However, such
sterile conditions rarely can be
duplicated in the wilderness, and
the damage done by an infection in
a sutured wound would greatly
prolong healing and lead to far
greater scarring and deformity.
Furthermore, if an unsutured wound
is not infected, the edges tend to fall
together, healing is rapid, and
scarring is minimal.
Minor wounds that appear to
present little risk of infection can be
held together with butterfly
bandages or tape. Such devices can
easily be removed and the wound
opened and drained should
infection develop. Wounds that are
too large to close with tape should
not be closed by anyone but a
surgeon who knows how to
obliterate the spaces beneath the
skin surface and how to avoid
producing further damage from
sutures. The danger of introducing
infection, and the far greater
destruction of tissue that results
from infection in a wound that has
been sutured, far outweigh any
benefits that might be obtained from
early closure.
Diagnosing Wound Infections

If infection occurs despite
preventive measures, early
detection minimizes tissue damage
and the threat to the person’s health.
Signs of infection should be looked
for every day, so the dressing over
any wound except a burn should be
changed daily until healing is
clearly underway. The person’s
overall condition should also be
monitored, particularly body
temperature.
The signs of infection around the
wound itself are primarily the signs
of inflammation—pain, redness,
swelling, heat, and limitation of
motion. These signs can be found
with every wound but are much
more severe in the presence of
infection. Pain from soft-tissue
injuries usually begins to subside
by the second or third day after
injury. Persistence of severe pain
beyond this period or an increase in
pain suggests infection. Redness is
usually limited to the margins of the
wound. More extensive
discoloration, particularly streaks
extending upward along a limb,
indicates infection. Severe swelling
around a wound, particularly a
simple cut with which swelling
would not be expected, is a sign of
infection, as is a detectable
increase in skin temperature.
Swelling and pain combine to limit
voluntary and involuntary motion,
which is more obvious in the
presence of infection.
An oral temperature of 100° to
101°F (37.8° to 38.3°C) can be
expected for one or two days after
any severe injury. A temperature
elevation after a minor injury, a
higher temperature, or an elevation
persisting for a longer time is
suggestive of infection.
Located throughout the body are
collections of lymph nodes that trap
bacteria and debris from a
localized infection and become
enlarged and tender (Fig. 12-1).
Tissue destruction occurs with any
injury, and the regional lymph nodes
often become enlarged, but in the
presence of infection the nodes
become more enlarged and painful.
When infection is present, lymph
nodes often are enlarged and tender
in more than one area.
Figure 12-1. Locations of the major
collections of lymph nodes
The diagnosis of a wound

infection is confirmed by the finding
of purulent material—pus—in the
wound or on its dressing. The
discharge may be cream, green,
pink, or reddish in color, depending
upon the infecting organism.
Occasionally the discharge may be
clear and straw colored. A foul
odor is often—but not always—
present. Rarely, an infected wound
produces a very scanty discharge. A
diagnosis of infection is not
necessarily incorrect just because
little purulent drainage is present.
The skin edges of an infected
wound are sometimes sealed by
coagulated serum, and exudate from
the infection cannot escape onto the
dressings. If other signs of infection
are present, the edges of the wound
should be spread apart and the
wound gently probed with a pair of
sterile forceps. (This process is
less painful if the wound is soaked
in warm, disinfected water first to
soften the coagulum.) If an infection
is present, pus usually pours out
when the wound is opened. If no
infection is present, opening the
wound usually does little harm
except for the discomfort, which is
of little consequence when
compared with the damage that
could result from an undiscovered
infection.
Treating Wound Infections

Treatment of an infected wound
consists of drainage and antibiotic
therapy. The wound should be
opened by prying apart its edges
with a pair of sterile forceps. Since
pus in an infected wound tends to
collect in pockets, the deeper parts
of the wound must be probed to
ensure all such pockets are drained.
If one is found, others should be
expected. After drainage, gauze
should be placed in the wound to
keep it open. The gauze, preferably
impregnated with petroleum jelly,
should be changed whenever the
wound is dressed. The edges of the
wound should not be allowed to
reseal as long as any evidence of
infection is present.
Infected wounds covered by a
crust of coagulated serum and pus,
particularly those on the
extremities, benefit from soaking in
warm water. Moisture softens the
crust and permits more thorough
drainage. Heat causes the blood
vessels to dilate, increasing the
flow of blood to the tissues, which
promotes healing and the
eradication of infection. For
infected small wounds on the
extremities—or for large wounds if
the person cannot be evacuated—
the dressing should be removed and
the wound immersed in warm,
sterile water for periods of twenty
to thirty minutes three to four times
a day. An antiseptic such as
povidone-iodine should be added to
the water. Afterward, the skin
should be carefully dried and a
fresh dressing applied.
Antibiotics should not be given
routinely to individuals with soft-
tissue injuries because the
probability of infection is low,
antibiotics have only a limited
ability to prevent soft-tissue
infections, and the risk of allergic
reactions and other adverse side
effects is significant. However, for
severe soft-tissue injuries or badly
contaminated wounds, antibiotics
should be administered
prophylactically before signs of
infection appear. In a remote
situation, antibiotics should also be
given to persons with major wound
infections with the understanding
that the major benefit would be to
inhibit spread of the infection and
not to eradicate the infection within
the wound.
If antibiotics are administered as
a preventive measure, they should
be given in large dosages for only
two days; such a brief course of
antibiotics does not allow the
emergence of resistant bacterial
strains. If a significant, established
soft-tissue infection is being
treated, however, high doses of
antibiotics should be given for at
least five days, or until all signs of
infection are gone.
BANDAGING
A bandage is usually composed of
three layers, each with different
functions.
Inner Layer
The inner layer of a bandage
should be material, such as
petroleum jelly–impregnated gauze,
or a plastic such as Telfa® that
does not stick to the wound and
allows the bandage to be changed
relatively painlessly without
aggravating the injury. Obviously,
this material must be sterile.
Dressings
The middle portion of a bandage
is referred to as a dressing and has
five different functions:
Prevent contamination to prevent
infection or limit the infection to
organisms already present
Absorb wound drainage, which
must not be allowed to
contaminate clothing or other
wounds
Keep the skin adjacent to the
wound dry to prevent
maceration and infection
Apply pressure on the
underlying wound to aid in the
control of bleeding or swelling
Protect the wound from further
trauma To perform these
functions, dressings must be
sterile and bulky. Although
special dressing materials are
available, simple gauze pads
that have been opened and
crumpled to increase their bulk
work almost as well and are
easier to transport into
wilderness areas.
Dressings that have been
contaminated by purulent drainage
should be handled with gloved
fingers or with forceps or similar
instruments that can be sterilized.
Such dressings should never be
touched with bare fingers and must
be disposed of by burning or in
some other manner that does not
contaminate the environment. If
more than one wound or more than
one injured person must be cared
for, attention to the infected wounds
should be put off until last, and
attendants must scrub their hands
thoroughly after dressing each
wound to prevent the spread of
infection.
Outer Wrapping
The outer portion of the bandage
also has more than one function:
Hold the dressings securely in
place
Keep the dressings from being
wet by water or perspiration,
which would inevitably carry
along bacteria
Apply pressure to help control
bleeding and swelling
Splint and immobilize portions
of the body such as the hand
Materials that have some
elasticity are easier to use and
stay in place better. Such
materials also compress the
wound slightly, but an elastic
bandage is more satisfactory if
significant compression is
needed. If the wound must be
kept dry, it should be covered
with waterproof tape, plastic, or
some other waterproof material.
However, moisture accumulates
beneath waterproof tape and
lifts it from the skin surface. If
protection from outside moisture
is not needed, porous tape
should be used to hold the
bandage in place. When the
bandage is changed, the tape can
be clipped off at the skin edges
and new tape placed on top of
the old to avoid the skin
irritation that results from
repeatedly stripping off the tape.
SPECIFIC INJURIES
Lacerations
Lacerations are slicing injuries
that may be clean and straight or
ragged. Such wounds commonly
bleed. Infections are also a threat,
particularly when small tags of
dead tissue are present in ragged
wounds. Blood vessels, nerves, or
tendons may be damaged, but
attempts to repair such structures
outside of a hospital would cause
further damage and increase the risk
of infection. Individuals with such
severe injuries should be
evacuated.
Puncture Wounds
A puncture wound may extend
deeply into underlying tissues.
Hidden structures may be damaged,
and infection is always a threat.
Bleeding to wash out dirt and
bacteria should be encouraged.
Foreign bodies should be removed.
A small wick of gauze can be
inserted into the opening of the
wound to prevent sealing and to
allow the exudate from any
infection to drain to the outside,
although no evidence supports the
value of this logical procedure.
Antibiotic therapy has not proven
beneficial except for animal bites.
The greatest danger from such
wounds is tetanus, which should be
prevented with tetanus toxoid
inoculations well before an outing
is even contemplated.
Abrasions
Abrasions are scraping injuries
produced by forceful contact with a
rough surface. Severe bleeding is
rare and the objectives of treatment
are to control infection and promote
healing. Before bandaging, large
fragments of foreign material should
be removed from the wound with
sterile forceps. Removing numerous
small embedded particles is
painful, may aggravate the injury,
and can do more harm than good;
many such particles are extruded
during healing, and the rest can be
removed under more propitious
circumstances. (In emergency
departments, such wounds are
anesthetized by applying lidocaine
jelly and scrubbing away the
particles.)
The wound should be covered
with a layer of nonadherent material
such as gauze impregnated with
petroleum jelly, over which should
be placed a bulky dressing to
absorb drainage and cushion against
further trauma. During dressing
changes, the inner layer should not
be removed until it spontaneously
separates from the wound surface.
Similarly, crusts that form during
healing should not be removed.
Infected abrasions usually
produce purulent exudate, but the
entire wound is open and drainage
is not impaired. Dressings should
be changed frequently and should
be thick enough to absorb the
exudate.
If nonadherent material is not
available, an improvised dressing
for such wounds can be made by
cutting a piece of a plastic bag a bit
larger than the surface of the
wound. The unprinted side of the
plastic should be placed directly on
the wound and a bandage applied.
The dressing should be removed
every twelve to twenty-four hours
and the wound cleaned as needed.
The wound should be dressed in
this way until the wound surface is
dry. The surgeon who developed
this technique points out that plastic
remains more or less sterile, even
when carried in a rucksack, because
the material is not a fabric but a
solid without pores.
Skin Flaps and Avulsions

Forces roughly parallel to the
skin surface tend to lift or tear out
chunks of tissue. If the tissue is
completely torn away, the injury is
considered an avulsion. (A limb
may be completely severed or
avulsed, and few people survive
accidents in which such powerful
forces are generated.) If the skin
along one side remains intact, a skin
flap is created. Small skin flaps are
rather common, but occasionally
larger flaps are produced.
If the full thickness of the skin is
avulsed, the injury should be
bandaged like an abrasion. As a
general rule, wounds of this type
that are more than one inch in
diameter require skin grafting, so
the person eventually must be
hospitalized. Large avulsions are
incapacitating.
If a thick flap of tissue with fat
or muscle attached to the
undersurface has been produced,
the person must be evacuated. Such
injuries heal poorly and tend to
become infected. The wound should
be thoroughly cleaned and the tissue
flap replaced in its original
position. If the tissue flap is large, a
strip of gauze should be placed
along the lip of the wound so that
the edges do not seal and purulent
exudate can escape if the wound
becomes infected. The wound
should be bandaged with a bulky
compression dressing, and the
entire limb should be immobilized.
The flap, which must not be
allowed to move or shift its
position, is in essence a skin graft.
If the wound is to heal, the flap must
remain stationary while new blood
vessels grow into it.
The individual must be closely
watched for signs of infection, and
any wound infection that does occur
must be promptly drained.
Antibiotic therapy should be started
at the time of the injury.
In expedition situations,
evacuation may not be necessary if
the wound appears to be healing
satisfactorily without infection. The
tissue flap is less likely to be
moved inadvertently while the
individual is lying in a tent than
when walking or being carried over
rough terrain. However, such
wounds do not usually heal without
infection, and evacuation may be
much more difficult for a person
with a severe injury that is infected.
When the flap does not survive,
it first acquires a dusky appearance
and then becomes progressively
darker until it is totally black.
Uninfected flaps are dry and hard;
infected flaps may be moist, foul
smelling, and soft. Surgical
excision and grafting are required
for both, and the infection can be
life threatening.
Small skin flaps with little or no
fat on the undersurface are an
entirely different matter. The
wounds must be cleaned and the
flaps held securely in position by
bulky bandages just as larger flaps
are, but such wounds often heal
with no complications or severe
infection. The skin flaps commonly
do not reattach to the underlying
tissue, but they protect the delicate
new skin that grows in from the
sides and allow it to cover the
wound. By the time the wound is
covered, the flap usually has dried
up and fallen off. The new skin may
need to be protected for a few days,
but no further therapy is required.
(A ruptured blister could even be
considered a small skin flap for
which the full thickness of the skin
is not removed.)
Contusions
Contusions, or bruises, are
crushing injuries that cause
bleeding into damaged tissues.
Usually the subcutaneous tissue and
muscle are injured without a break
in the overlying skin. The vast
majority of contusions are minor,
almost insignificant injuries, but
rarely the damage can be great
enough to severely incapacitate the
individual.
The ideal treatment for a severe
contusion is described by the
mnemonic ICE:
I Immobilization
C Cooling, preferably with
snow or ice
E Elevation
Ideally, such therapy should be
given immediately and should
persist until bleeding has ceased.
However, such treatment may be
impractical—even life threatening
—in some circumstances. Complete
cessation of bleeding usually
requires six to eight hours, but by
that time the muscles may be so stiff
and sore the person cannot walk.
Anyone with a severe contusion in a
remote area may need to walk out,
or at least back to camp, while still
able to do so. After the muscles
have stiffened, they often are too
painful for vigorous exercise for
three or four days, and weeks may
be required for complete recovery.
If circumstances do not require
immediate evacuation, the injured
area should be elevated and cooled
with snow, ice, or wet towels or
clothing, any of which will cause
constriction of blood vessels in the
area, reduction of bleeding into the
tissues, and lessening of pain.
(Cooling hastens disabling muscle
pain and stiffness and should not be
used for lower extremity injuries if
the person must be able to walk.) If
extensive swelling develops, the
extremity may be wrapped with an
elastic bandage that applies mild
pressure. The wrapping should
encompass the entire limb from the
toes (or fingertips) to well above
the area of injury but must not
occlude circulation.
After twelve hours, movement of
the injured area may be resumed, if
tolerated, to speed resorption of the
blood. After three days, heat may be
applied to accelerate blood
resorption and to diminish muscle
pain.
Stiffness persisting for more than
two to three weeks in a muscle that
has been severely bruised may
herald the onset of calcium
deposition in the injured tissue.
Rarely, this process can continue
until the entire clot has been
transformed into bone—up to a
year. The amount of muscle damage
varies and is sometimes significant,
so the condition should be
recognized and treated to minimize
disability.
Wounds of the Hands and Feet
Wounds of the hands and feet are
of special importance because these
structures are anatomically
complex. All wounds in these areas
must be thoroughly cleaned, but no
tissue should be trimmed away
unless it is unmistakably dead. If
fingers or toes are enclosed in a
large bandage, they must be
separated by gauze to prevent
maceration of the skin from the
dampness produced by
perspiration. Such bandages should
splint the hand in the “position of
function,” which is the position the
hand takes when holding a pencil
(Figs. 12-2 and 12-3).
Figure 12-2. “Position of function” of

the hand
The color and sensation in the

fingertips must be checked
frequently to ensure the bandage is
not too tight. For severe injuries,
antibiotic therapy should be
instituted at the time of injury and
evacuation begun immediately.
Ring Removal
For any hand injury, rings should
be removed immediately to prevent
circulatory problems in the fingers.
With the “thread technique,” rings
often can be removed from a
somewhat swollen finger. The
technique works well with fine
fishing line, dental floss, or a fine
nylon thread extracted from a
climbing rope. The more slippery
the thread, the easier is removing
the ring.
One end of a 50- to 70-cm-long
thread should be inserted carefully
under the ring (perhaps with a knife
blade) with the long end in the
direction of the fingertip. The ring
should be pulled toward the knuckle
as far as it goes and the thread
should be slowly wound around the
finger including the knuckle. The
thread must be wrapped carefully
with each layer touching the next
one. The procedure may hurt a bit
and the finger may become blue.
When the thread is completely
wrapped, the end of the thread near
the hand should be pulled slowly
and firmly while holding the end of
the thread near the fingertip. By
unrolling the thread, the ring is
forced over the knuckle, the skin of
which has been compressed by the
thread. If the ring is not freed, the
procedure can be repeated.
Blisters
Traumatic blisters are caused by
friction that pulls the skin back and
forth over underlying tissues.
Eventually a cleft or tear develops
in the midportion of the epidermis
—the most superficial portion of
the skin—and fluid collects in this
cleft.
Figure 12-3. Technique for bandaging
the hand in the “position of function”
For a blister to develop, the

epidermis must be thick and tough
enough to resist destruction by the
friction, which otherwise would
produce an abrasion. Also, the skin
and subcutaneous tissues must be
bound to the underlying bone to
some extent, or the friction would
just move the skin and no shear
stress would develop. Finally, the
skin must be moist enough for the
object producing the blister to
adhere to the skin surface instead of
sliding back and forth. Only the last
condition can be modified to
prevent blisters, but the first two
conditions explain why blisters
usually form at only a few specific
sites, such as toes and heels.
The most common cause of
blisters is new or ill-fitting boots.
Boots that are loose in the instep
allow the foot to slide forward
when going downhill, producing
“downhill blisters,” usually on the
toes or front part of the foot.
“Uphill blisters” are most common
over the heel or the Achilles tendon
at the back of the ankle.
Boots should fit properly and be
“broken in” slowly and thoroughly.
(One recommended method is to
wet the boots and walk in them on a
flat surface until they are dry.)
Areas prone to blister should be
protected, preferably with one of
the new blister coverings, but
adhesive tape, duct tape, or
moleskin can be used. Duct tape has
a smooth surface and works well
for covering blisters. Adherence
between skin and boot should be
minimized by keeping the feet dry
with powder, as well as by wearing
a thick outer sock and a thin inner
sock that allow slippage between
them. As soon as the pain or heat of
an early blister—a “hot spot”—has
been detected, the area should be
covered. (Well-fitting boots do not
provide enough space for thick
coverings, such as rings of padded
material.)
Healing is faster, pain is
diminished, and the risk of infection
is greatly reduced when the blister
roof is preserved. Blister fluid may
have to be drained to allow the roof
to become adherent to the base. To
drain the fluid, the skin should be
cleaned, preferably with povidone-
iodine, and a sterile needle inserted
underneath the skin and into the
blister from a point 3 to 5 mm
beyond its edge.
If the roof of the blister has been
torn away, the injury should be
treated just like an abrasion:
covered with a nonadherent inner
layer and protected with a thicker
outer layer. (An improvised
dressing for large, unroofed blisters
is described previously in this
chapter under “Abrasions.”)
Various proprietary products for
covering blisters are available.
These are either double-layered
products with which friction moves
one layer over the other,
hydrocolloid dressings that
eliminate friction at the skin
surface, or a combination of the
two. All are thin and very smooth.
The feet should be kept as clean
as possible to reduce the risk of
infection.
Skin Cracks
In dry or in wet and cold
conditions, skin cracks are common
on fingers and hands. Barefoot
porters often suffer from deep and
painful skin cracks on the soles of
the feet. Such cracks may not heal in
a humid and dirty milieu. They may
be closed by carefully applying a
drop of skin glue in the crack and
waiting until the glue dries. (Drops
of the glue must not be splashed in
the eyes, and the glue must not be
touched as long as it is moist
because it will stick to whatever
touches it.) The crack heals from
the inside and the glue
progressively appears at the skin
surface where it wears off.
Sometimes repeating the
application is necessary.
CHAPTER 13
BURNS
Minor burns, such as burns of the

hands or fingers from hot pots or
stoves, are common, and their care
is straightforward—although they
must not be neglected. Major burns
are rare in the wilderness. Possibly
the greatest risk is at high altitude
when food is being cooked or snow
is being melted for water inside a
tent. In these situations fuel spills or
even explosions occur due both to
the notoriously poor performance of
stoves at high elevations and to
hypoxic impairment of the
individuals using them. Such
accidents are catastrophic if
destruction of tents, sleeping bags,
and clothing leave people with
severe burns exposed to an extreme
environment.
Successful rescue of individuals
with major burns from this kind of
situation would require an
incredible combination of medical
knowledge, evacuation skills,
dedication and determination, and
sheer luck. The intravenous fluids
and other supplies needed just to
keep burn victims alive for the first
twenty-four hours would almost
never be available in such
circumstances. However, severe
burns can occur in less remote
circumstances, and few wilderness
users would not try to provide the
best care possible. Therefore, a
discussion of the basic principles of
care for major burns appears
worthwhile, even though few
opportunities for its successful
application can be expected.
EVALUATING BURN
SEVERITY
Depth, size, and location determine
the severity of a burn. In the past,
burns have been classified
according to their depth as first,
second, or third degree. First-
degree burns were superficial, did
not kill any of the tissues, and only
produced redness of the skin.
Second-degree burns damaged the
upper portion of the skin, resulting
in blisters. Third-degree burns
destroyed the full thickness of the
skin and could extend into
underlying tissues. This terminology
has been modified, and first- and
second-degree burns are lumped
together as “partial thickness”
because generally they are treated
the same. Third-degree burns are
labeled “full thickness.”
The size of the area covered by
the burn is of critical significance.
Before the development of burn
centers, few individuals have
survived fullthickness burns that
covered more than 50 percent of
their body surface. In contrast, few
burns covering less than 15 to 20
percent of the body are lethal when
given proper care.
Location is also important.
Burns of the face and neck, hands,
or feet are more incapacitating due
to the specialized organs and
complex anatomy of these areas.
Burns of the face may be associated
with burns of the air passages or
lungs, which often are lethal. Burns
of the genitalia or buttocks are
difficult to keep clean and usually
become severely infected.
BURN SHOCK
The immediate life-threatening
problem associated with major
burns is shock—specifically burn
shock. When tissues are burned, the
damaged capillaries allow blood
serum to flood burned tissues. This
fluid loss reduces blood volume
and produces shock just like a
major hemorrhage would. A person
with a major burn usually dies in
shock within twelve to eighteen
hours unless appropriate fluid
therapy is instituted. Such fluids
almost always must be administered
intravenously. Individuals with
severe burns are often unconscious
or too stuporous to swallow fluids.
If they can swallow, they often
vomit anything taken by mouth. If
they are not vomiting, the fluids
often remain in the stomach and are
not absorbed. Appropriate fluids
are rarely available in wilderness
situations; a major burn in a remote
area usually requires immediate
evacuation by the fastest means
available.
EVACUATION
As a general rule, all full-thickness
burns larger than one inch in
diameter eventually require surgical
therapy: debridement and skin
grafting. Therefore, the only
decision that must be made for
individuals with burns of that size
or larger is how urgently they
should be evacuated. Help with this
decision can be obtained from the
following criteria for the
classification of burn injuries
established by the American Burn
Association and the American
College of Surgeons:
Major
Blistering partial-thickness
burns of more than 25 percent of
the body surface
Full-thickness burns of more
than 10 percent of the body
surface
Significant burns of the critical
areas: face, eyes, ears, hands,
feet, or perineum (genitals and
buttocks)
Significant associated trauma or
coexisting disease
Moderate
burns of 15 to 25 percent of the
body surface, with less than 10
percent full-thickness burns, and
no involvement of critical areas
Mild
burns of less than 15 percent of
the body surface, with less than
2 percent full-thickness burns,
and no involvement of critical
areas
Individuals with moderate or
major burns require hospitalization
and must be evacuated. If any
question about the severity of the
burn exists, the person should be
evacuated. Experts have difficulty
determining whether a burn is
partial or full thickness immediately
after it occurs, and inexperienced
persons almost always
underestimate both the depth and the
area. Persons with major burns are
often deceptively alert for several
hours until fluid losses become
severe.
Many individuals with less
extensive burns must also be
evacuated, particularly with burns
of the hands or face, but speed is
not as crucial. Fluid loss occurs
with all burns, both partial and full
thickness, but in previously healthy
young adults does not achieve life-
threatening proportions if the burns
cover less than 10 to 15 percent of
the body surface.
Care of a seriously burned
individual demands a major
commitment of time and personnel.
Only a large group would have
enough members for some to
continue the expedition while others
take care of even one burned
individual.
TREATING THE BURN

Immediate Care
Immediately after the burn, all
clothing and jewelry around the
injury should be removed. If the
burn is small and not full thickness,
immediate application of cold helps
reduce pain. Holding a towel
soaked in ice water against the
burned area, or immersing it in
cold, soapy water usually is
effective. More extensive partial-
thickness and full-thickness burns
should not be treated in this manner.
Fullthickness burns are usually
painless because the nerves in the
skin have been destroyed.
The burn, like any other open
wound, should be cleaned and
covered with a dressing. In the
field, cleaning can be done best
with sterile cotton, liquid soap, and
warm, disinfected water. If these
materials are not available, the burn
should be cleaned in the best way
possible. All debris, dirt, and
fragments of loose skin must be
removed. These measures may be
surprisingly painless if carried out
gently.
The burn should be covered with
a thin layer of an antibacterial
ointment such as silver sulfadiazine
in a petroleum jelly base
(Silvadene®), over which should
be layered gauze, a bulky dressing,
and a snug bandage that applies
pressure but does not interfere with
blood circulation. The dressing or
slings can be used to immobilize a
burned extremity and reduce pain.
Burned hands should be splinted in
the “position of function,” the
position the hand assumes when
holding a pencil (Figs. 12-2 and 12-
3).
Ointments or creams that do not
contain appropriate antibacterial
agents increase the risk of infection
and should not be used.
Subsequent Care
The bandage on a burn should be
left undisturbed for six to eight
days. Changing the dressing
increases the risk of introducing dirt
and bacteria that could produce an
infection. Furthermore, an accurate
distinction between partial- and
fullthickness burns can be made
only about a week after the injury. If
the burn is very superficial (first
degree) and no blisters are found
when the bandage is removed, no
further treatment is required.
Subsequent bandaging would be
needed only to protect a sensitive
area from trauma.
Unbroken blisters generally
should be left intact. However, the
blister fluid is an ideal medium for
bacterial growth, and blisters larger
than 2 to 3 inches (5 to 8 cm) in
diameter probably should be
opened (without contamination) to
reduce the potential for infection. A
protective dressing should be
applied to prevent rupture of
smaller blisters and infection and
should be changed every three or
four days until healing is complete.
Full-thickness burns six to eight
days old are covered by a thick,
leathery layer of parched, dead skin
that may range in color from white
to dark brown or black. The dead
skin is usually insensitive to touch.
If the depth of the burn—whether it
is partial or full thickness—is
uncertain, gentle probing with a
sterile needle or pin is a good way
of testing.
If the burn is full thickness, it
should be rebandaged and the
person evacuated. Even under ideal
conditions these wounds essentially
always become infected. They
require operative care, including
skin grafting, which can be
provided only in a hospital.
FLUID REPLACEMENT
The most urgent aspect of treatment
for a major burn is the
administration of fluids to prevent
or treat shock.
Calculating Fluid Volumes

A convenient formula for
determining the volume of
intravenous fluids to be
administered during the first
twenty-four hours following a
major burn is:
Weight (kg) x Percent Surface Area
x 3 = Volume of Fluid to Be
Administered
The body weight in kilograms
(2.2 pounds = 1 kilogram) is
multiplied by the percentage of the
body surface covered by the burn,
and that product multiplied by three
equals the volume (in ml) of fluids
to be given. The percentage of the
body area covered by the burn can
be estimated from Figure 13-1.
The fluid requirements for the
first twenty-four hours after a burn
for a 176-pound (80-kg) man with a
30 percent body surface area burn
(approximately one arm and one
leg) would be calculated as
follows:
Figure 13-1. Percentage of total body
surface area of various portions of the
body
80 (kg) x 30 (%) x 3 = 7200 ml

Approximately half of this fluid
should be given in the first eight
hours of treatment; the remainder
should be given over the next
sixteen hours. Although opinions
differ about the ideal composition
of the fluids, in a wilderness
situation saline or Ringer’s lactate
solution are almost certain to be the
only fluids available.
Monitoring
These calculations illustrate the
tremendous volume of fluids
required, but such exact volumes
cannot be given indiscriminately
because the severity of the vascular
injury produced by the burn and the
functional capacity of the person’s
heart and kidneys vary widely. (In
some burn centers the product of
body weight times burn area is
multiplied by four instead of by
three.) Careful monitoring of the
response to the fluids is just as
essential as the calculations.
Failure to give enough fluid can
lead to shock. Administering too
much can overload the
cardiovascular system and lead to
heart failure, particularly in older
individuals who already have
reduced cardiac reserve. A fine line
separates inadequate fluid
replacement and overload, and at
high altitude the margin of safety is
even narrower.
If the person remains confused
or stuporous (in the absence of a
head injury), blood pressure is
below normal, pulse is weak and
rapid, and urinary output is below
50 ml per hour after several hours
of treatment, fluids must be
administered more rapidly and
perhaps in larger quantities.
Excessive fluid administration is
indicated by a urinary output greater
than 75 ml per hour; by
subcutaneous fluid accumulation
causing swelling in unburned
tissues, particularly in the legs or
over the sacrum; or by pooling of
fluid in the lungs producing unusual
shortness of breath. If these signs
are present, the rate of fluid
administration must be slowed,
occasionally drastically. An
indwelling urinary catheter is
helpful for monitoring urinary
output.
Other Considerations
Fluid requirements for
individuals with burns covering
more than 50 percent of the body
surface should be calculated as if
the burn were limited to that area.
Larger fluid volumes overload the
heart if given within twenty-four
hours.
A severely burned person is
usually thirsty, as are most
individuals in shock, but thirst
should be controlled with
intravenous fluids because fluids
given orally usually cause vomiting
and still greater fluid loss. (Fluids
lost by vomiting must also be
replaced with Ringer’s lactate or
saline solution.)
Subsequent Fluid Therapy

During the first twenty-four
hours after a burn, Ringer’s lactate
or saline solution should be used to
replace the fluid and sodium lost
into the burned tissues. Thereafter,
5 percent glucose should be used
for fluid replacement. (Few
expeditions would carry such
fluids, but in some popular trekking
areas, such as the southern
approach to Everest, fluids left
behind by expeditions are
available.)
Once shock has been prevented
or corrected, fluid requirements are
somewhat greater than normal but
not on the enormous scale of the
first day after the burn. Also, the
individual may be able to take
fluids by mouth with only small
(one- to twoliter) intravenous
supplements. As always, urine
volume is an excellent indicator of
fluid status.
By the second or third day after
the burn, the blood vessels in the
burned tissues begin to recover and
the fluids lost into those tissues are
reabsorbed and excreted by the
kidneys. Large volumes of urine
may be passed, but in this recovery
stage fluid intake should not be
restricted because the urinary output
is high. Fruit juices that have a high
potassium content may be
particularly beneficial at this time.
CONTROL OF PAIN
Inexperienced persons often are
horrified by the appearance of a
major burn and mistakenly
administer unneeded pain
medications, thinking the wound
must be painful. However, the pain
from a burn is quite variable.
Superficial burns hurt at first but
are usually relatively painless once
they are covered and not exposed to
air. Full-thickness burns are usually
less painful because they destroy
the nerves and produce anesthesia
in the area of injury. In addition,
shock tends to dull the pain. If the
individual complains, pain should
be controlled with as little
medication as possible. Drugs
stronger than a moderate analgesic
are rarely needed. If strong
analgesics are necessary, smaller
doses (onehalf to three-fourths the
usual dose) should be tried before
resorting to a full dose. Strong
analgesics may aggravate the
general effects of the burn and are
almost never needed. Furthermore,
if the individual is in shock when
the drugs are administered, they are
poorly absorbed. If absorbed later
when the shock is corrected, an
overdose can result.
FACIAL BURNS
Burns around the face and neck are
particularly dangerous because the
flames and hot smoke may be
inhaled, damaging the lungs.
Persons with such injuries must be
evacuated with extreme urgency.
Burns of the face, nose, mouth, and
upper respiratory tract cause
swelling and obstruction of the
airway. Treatment requires
intubation with an endotracheal or
nasotracheal tube or creation of an
alternate airway by tracheostomy or
cricothyrotomy. If the flames and
smoke reach the lower portion of
the respiratory tract and the lungs
are seared, no effective treatment is
possible in the field. If the
individual survives the initial
injury, the burn and smoke cause
fluid to collect in the lung in
quantities that are often lethal.
Subsequently, severe pneumonia is
common. Fortunately such injuries
are rare.
Burns of the upper airway
should be anticipated after any
facial burn, particularly if the skin
around the nose and mouth is
burned or the nasal hairs are singed.
The individual typically becomes
hoarse and begins to have difficulty
breathing. Wheezes may be heard
when listening to the chest. The
most critical sign of an airway burn
is coughing up black, sooty
material, which should be
considered diagnostic. Sometimes
these signs do not become
detectable until twenty-four to
forty-eight hours after the injury, so
individuals with facial burns must
be closely watched.
OXYGEN
Oxygen, if available, should
probably be administered
immediately to all individuals with
severe burns occurring at high
elevations. Burns can reduce
respiratory effectiveness, and at
high altitude such persons may not
be able to breathe rapidly and
deeply enough to compensate for
lower environmental oxygen
pressure. Fires in enclosed quarters
such as a small tent, in which air
circulation may be further reduced
by a covering of snow, produce
large amounts of carbon monoxide.
Individuals burned in such
circumstances may have to cope
with a reduced oxygen-carrying
capacity of the blood due to carbon
monoxide poisoning regardless of
the altitude. Oxygen may be
lifesaving until the individual can
be evacuated to lower altitude,
particularly for the first hour or two
after the burn while the carbon
monoxide is being eliminated.
ADDITIONAL MEASURES
Individuals with burns covering
more than 20 to 25 percent of their
body surface usually develop
paralysis of the stomach and
intestines known as ileus. As they
continue to swallow air and saliva,
the paralyzed stomach becomes
distended and they vomit. To avoid
these problems, a nasogastric tube
should be inserted and gastric
suction instituted. (Appendix B:
Therapeutic Procedures). Fluids
lost through the nasogastric tube
should be replaced with Ringer’s
lactate or saline solution.
Dehydration following a burn,
caused by the outpouring of fluids
into the tissues, greatly increases
the risk of thrombophlebitis. This
complication should be anticipated
and appropriately treated if it
occurs. However, prevention by
administering the required fluids
and avoiding dehydration is far
more desirable.
A burn that involves the entire
circumference of a body part is
called a circumferential burn. Full-
thickness circumferential burns can
present problems because the
burned area forms a hardened, dead
area (eschar). The eschar does not
stretch like normal skin. It
contracts. If the burn goes around an
arm, leg, finger, or toe, the
contraction can create a
compartment syndrome (Chapter
11: Fractures and Related Injuries).
If the burn goes around the chest,
contraction can result in inability to
expand the lungs, which causes
major breathing problems. In either
case, the solution is to use a scalpel
to make one or more cuts through
the hard eschar, allow the cut edges
to separate, and relieve the pressure
from the contracture and from fluid
accumulation on blood vessels in
the underlying tissue. Since full-
thickness burns destroy nerve
endings, this process is painless.
SECTION III
NONTRAUMATIC
DISORDERS
CHAPTER 14
NEURAL DISORDERS
The nervous system has two major

components, the central nervous
system (CNS), which consists of the
brain and spinal cord, and the
peripheral nervous system, the
numerous nerves that transmit
impulses from and to the CNS.
Almost everything that happens in
the body—voluntary and
involuntary movement, respiration,
blood circulation, even endocrine
function—is controlled or regulated
by the nervous system. The diseases
of this complex system are
numerous and often disabling.
However, most of these diseases
come on too slowly to create
problems on a wilderness outing,
even on trips lasting several
months.
SIGNS AND SYMPTOMS

The signs and symptoms produced
by diseases of the nervous system
consist of:
Altered intellectual function
Impaired control of movement
(motor disturbances)
Sensory disorders
Loss of function of specific
nerves
A group of unrelated, less
specific signs that includes
headache, nausea and vomiting,
and changes in pulse rate and
blood pressure
Altered Intellect
Alterations of intellectual
function usually produce
personality changes first, most
commonly increased irritability or
silliness. Impairment of contact
with surroundings shows up later
and is manifested initially by
forgetfulness and confusion but can
progress to hallucinations, delirium,
or complete loss of consciousness
(coma). Such alterations are typical
features of altitude disorders,
particularly highaltitude cerebral
edema.
Motor Disturbances
Motor disturbances, when early
or mild, result in loss of
coordination that causes stumbling,
falling, or the inability to perform
delicate or repetitive movements.
More severe dysfunction causes
convulsions, weakness, or total
paralysis. Paralysis is a typical
feature of vertebral fractures that
injure the spinal cord. Bell’s palsy
is a type of paralysis that involves
the facial muscles.
Sensory Disturbances
Sensory disturbances most
commonly consist of paresthesias:
tingling or prickly sensations like
those felt when a limb “goes to
sleep.” Such sensations may not be
indicative of nervous system
disease. Acetazolamide, which is
frequently administered to treat or
prevent acute mountain sickness,
commonly produces similar
symptoms. Total anesthesia is rare.
Anesthesia of an entire limb or an
entire limb below a specific level,
a “stocking” pattern, is due to
hysteria rather than organic disease.
The distribution of nerves does not
allow this pattern of anesthesia to
be produced by disorders that are
not of emotional origin.
Individual Nerve Loss

Dysfunction of nerves that
originate in the brain—cranial
nerves—causes highly varied
symptoms. Disturbed function of
nerves to the eyes may cause
blindness (occasionally limited to
only a portion of the field of
vision), paralysis of eye
movements, or double vision. The
pupils may fail to contract when
exposed to light or may differ
greatly in size. Vision may be
blurred.
Disorders of nerves to the
muscles of the face, a common
complication of Lyme disease,
cause weakness or paralysis of
facial movements and drooling on
the affected side. Swallowing is
impaired when the nerves to the
muscles of the throat are affected,
and fluids may be regurgitated
through the nose or aspirated into
the lungs. Disturbances of the
nerves to the ear cause ringing or
buzzing, vertigo, or hearing loss.
Damage to other nerves may cause
loss of smell, loss of taste, severe
facial pain, weakness of the
muscles of the neck, or impairment
of respiration.
Damage to the nerves originating
in the spinal cord causes paralysis
or sensory disturbances, commonly
anesthesia, in the portion of the
body supplied by the injured
nerve(s). Reflexes such as the knee
jerk may be lost.
Other Signs and Symptoms

Blood clots, tumors, infections,
or any disorder that increases
pressure within the skull can cause
nausea and vomiting, the latter
typically occurring without
warning. A slow pulse and a wider-
than-normal separation of diastolic
and systolic blood pressures are
also typical of increased
intracranial pressure. Headache
associated with nervous system
disease is often severe. Fever with
central nervous system infections is
often high. In other nervous system
disorders, the temperature is normal
or only slightly elevated.
COMMON NERVOUS SYSTEM

DISORDERS
The common nervous system
disorders are usually not very
serious and are frequently brief in
duration.
Headache
Headache is a very common
ailment suffered occasionally by all
but a few fortunate individuals.
Often a specific cause for a
headache cannot be identified, and
the disorder is thought of as a
disease in itself, although it is often
a symptom of another illness.
Headache after a rapid ascent to
altitude is common and is usually a
symptom of acute mountain sickness
(Chapter 24: Disorders Caused by
Altitude). Headache can also be
caused by dehydration.
The pain of a headache may be
located in the back of the neck,
behind the eyes, or all areas in
between. Little significance can be
attached to the location of the pain
except when it is limited to one side
of the head, which is typically a
sign of vascular headaches
(migraine).
A severe, persistent headache in
an individual who usually does not
suffer from headaches may be a sign
of serious disease. Headache
associated with confusion,
forgetfulness, dizziness, nausea and
vomiting, and (rarely) convulsions
or loss of consciousness may be the
result of an acute increase in blood
pressure (hypertensive
encephalopathy). This disorder
usually occurs in persons with
preexisting hypertension and
requires prompt treatment (Chapter
Disorders). Headache associated
with fever and a stiff neck are
characteristic of meningitis.
Following a head injury, increasing
severity of a headache may be
indicative of the development of a
blood clot within the skull (Chapter
8: Head and Neck Injuries).
Acetaminophen, ibuprofen, or
aspirin every three to four hours
relieves the pain of most headaches;
acetaminophen and codeine or
aspirin and codeine taken with the
same frequency are adequate for
most of the remainder. Individuals
with frequent headaches should
consult a physician. Some causes of
recurrent headaches, such as brain
tumors or high blood pressure, are
quite serious but usually come on so
slowly they would cause problems
in the wilderness only on a
protracted expedition. However, a
few individuals with brain tumors
have first experienced symptoms
when they developed high-altitude
cerebral edema (Chapter 24:
Disorders Caused by Altitude).
Fainting (Syncope)
Fainting is a common disorder
that usually is not a sign of organic
disease. It typically follows
emotional stress and sometimes
occurs without an identifiable
cause. When fainting is the result of
disease, the disorder most often
involves the heart and not the
nervous system. Therefore, this
condition is discussed in Chapter
Disorders. It can also be the result
of low blood pressure and is
discussed in Chapter 3: Life-
Threatening Problems.
Bell’s Palsy
Bell’s palsy is the most common
form of facial paralysis and
involves the muscles innervated by
the seventh cranial nerve. The
paralysis develops rapidly and
maximum weakness is present
within twentyfour to forty-eight
hours. The condition is painless,
and in its early stages the individual
may have to be told that it is
present. No etiology can be
identified for most individuals,
although persons with untreated
Lyme disease may develop this type
of paralysis. The prognosis is good;
about 80 percent of individuals
with this condition recover quickly
and completely, and another 10
percent improve somewhat over a
few weeks or months.
A typical feature of Bell’s palsy
is involvement of muscles of the
forehead along with the other facial
muscles. If forehead involvement is
not present, the individual should
be evaluated by a physician to
ensure stroke or a tumor is not the
cause of the paralysis. Evacuation
is unnecessary for Bell’s palsy.
Seizures (Convulsions)
Seizures may be a sign of
disease of the nervous system but
also occur with diseases that only
affect the brain indirectly. Many
seizures, particularly in young
people, are solitary events for
which no cause can be established
and which never recur.
Epilepsy is a condition with
which a person suffers repeated
seizures. (Seizures associated with
high fevers in young children are
not considered epilepsy.) Most
epilepsy can be controlled with
medications, and seizures rarely
recur as long as the prescribed
treatment is diligently followed. A
person with epilepsy need not
refrain from wilderness activities,
including ascents to high altitude, if
the disorder is controlled and the
individual is conscientious about
taking prescribed medications.
Outing partners should be informed
of the condition so they can learn
the measures to take should a
seizure occur. However, the stigma
once attached to epilepsy is
completely unwarranted.
The onset of a seizure is usually
sudden and may be marked by a
sound of some kind. The person
characteristically loses
consciousness and falls to the
ground twisting and writhing, the
limbs twitching, jerking, or flailing
about. The jaw may be involved,
and the person may bite the tongue.
Salivation may be profuse and
urination and defecation
uncontrollable. The eyes are usually
open.
In any single convulsive
episode, all or none of these
features may be present. Sometimes
only slight twitching of the
extremities is present. A person
who is unconscious from a head
injury may exhibit only a series of
jerking movements that gradually
increase in intensity and then
subside. Limbs paralyzed by injury
do not move.
Nothing can shorten or terminate
the convulsive episode. The only
helpful measure is to protect the
person from self-injury. Arms and
legs should be restrained only
enough to prevent striking nearby
objects as the individual flails
about. Attempts to hold the
extremities absolutely still may
produce muscular or tendinous
injuries. Clothing around the neck
should be loosened to prevent
strangulation.
Seizures usually last only one or
two minutes but can persist for five
minutes or even longer. A period of
unconsciousness almost always
follows and can last from a few
minutes to several hours. The coma
may be so deep the individual is
completely unresponsive, even to
painful stimuli, and requires the
same care as any comatose person,
particularly maintenance of an open
airway. The person should be
permitted to awaken without
stimulation and allowed to rest until
strength has returned and recovery
appears complete. The individual
must not be left alone for at least
twelve hours, the time in which
recurrences are most likely.
Individuals should consult a
physician for a first seizure. If they
are in a wilderness situation, they
should be evacuated. Following a
seizure that continues for more than
five minutes, when breathing
difficulty is present and confusion
or unconsciousness persists,
emergency care should be sought.
Occasionally, injuries sustained
during a seizure require emergency
treatment.
Meningitis and Encephalitis
Meningitis is an infection of the
membranes surrounding the brain
and spinal cord, usually caused by
bacteria. Encephalitis is an
infection of the brain itself, most
commonly caused by a virus. These
diseases produce similar signs and
symptoms, in the wilderness would
be treated the same, and are
discussed as a single category.
(Rabies, a form of encephalitis, is
discussed in Chapter 32: Rabies.)
Both meningitis and encephalitis
are spread by human contact or by
insects, particularly mosquitoes.
Meningitis can result from the
direct spread by bacteria from a
chronic infection of areas such as
the sinuses, ears, or mastoids or
from an open fracture of the skull. A
number of organisms can cause
meningitis or encephalitis, and each
organism varies in the effects it
produces. The signs, symptoms, and
severity of this group of infections
cover a wide spectrum.
Individuals with meningitis or
encephalitis often have had a recent
upper respiratory infection, such as
a cold or sore throat. Headache,
usually severe, is the most common
initial symptom. Fever is usually
present and may be high. Nausea
and vomiting sometimes occur. An
abnormal sensitivity to or
intolerance for light (photophobia)
is a common symptom. Paralysis is
rare and usually affects only one or
two nerves: those originating in the
brain more commonly than those
from the spinal cord. Seizures occur
in about one-third of individuals
with meningitis. Confusion,
delirium, or coma may ensue and
are fairly common with
encephalitis.
The most specific diagnostic
signs of central nervous system
infections result from involvement
of the fibrous membranes that cover
the brain, which are inflamed
severely with meningitis and to
some extent with encephalitis.
Movement of these membranes by
bending the neck or back causes
pain. To prevent such movement,
the muscles surrounding the
vertebral column go into spasm.
Individuals with one of these
disorders are unable to touch their
chins to their chest, although that
maneuver is normally very easy. If
placed on the back and the leg is
lifted with the knees bent,
straightening the leg causes pain in
the back. This maneuver pulls on
nerves in the leg, which produces
movement of the spinal cord and its
coverings, resulting in pain.
The treatment for meningitis and
encephalitis consists primarily of
control of the infection. Large
amounts of antibiotics are needed
and should be given intravenously if
possible, which usually would
require urgent evacuation. High
blood concentrations of the
antibiotic are required for
therapeutic quantities to get into the
brain and cerebrospinal fluid where
the infection is located. Ceftriaxone
(Rocephin®) is the drug of choice
for individuals who are not allergic
to penicillin. Penicillin or
ampicillin can be administered if
ceftriaxone is not available. If the
individual has anaphylactic
reactions to penicillin, that would
be another indication of the need for
urgent evacuation.
Fever accompanying these
infections can be high and should be
lowered if it goes above 104°F
(40°C) orally. Acetaminophen,
ibuprofen, or aspirin can be given
every four hours. Cooling by
covering the arms and legs with wet
cloths or clothing and fanning may
be required.
The headache that accompanies
these disorders is frequently severe
but can usually be controlled with
acetaminophen, ibuprofen, or
aspirin—possibly combined with
codeine—every four hours.
Medications for sleep or
medications for pain stronger than
codeine should not be given
because they depress brain function.
Fluid balance must be
maintained; intravenous fluids may
be necessary. Coma requires the
same care as unconsciousness from
any cause. Movement to low
altitudes or oxygen administration
is desirable. The person should be
isolated with a limited number of
attendants to prevent spread of the
disease. Evacuation to a hospital is
essential. Approximately 25 percent
of adult meningitis is fatal, and
survivors typically require
prolonged rehabilitation. Death
rates for encephalitis can be even
higher.
Stroke
Stroke is a term for a group of
disorders that are also called
cerebral vascular accidents
because obstruction or rupture of
arteries in the brain destroys the
tissue they supply. In the United
States stroke is the third most
common cause of death.
Approximately 80 percent of
strokes are caused by clotting of
blood within an artery, which
causes the death (necrosis or
infarction) of tissue supplied by that
blood vessel. The other 20 percent
are the result of hemorrhage, which
can obliterate significant portions
of the brain.
Most strokes result from
arteriosclerosis (hardening of the
arteries), are associated with high
blood pressure, and occur in older
people. However, strokes can occur
in young adults with severe,
untreated hypertension. The
dehydration and increased number
of red blood cells typical of high
altitudes increase the risk of stroke.
One type of stroke (subarachnoid
hemorrhage) originates from
aneurysms of the cerebral arteries.
The individuals most likely to
have strokes on wilderness
expeditions are members of support
teams, such as porters. Many of
these individuals have never had
any professional medical care, not
even a routine physical
examination, and high blood
pressure could not have been
detected. They should be screened
for hypertension, as well as other
diseases, particularly infectious
diseases such as tuberculosis, and
affected individuals should be
excluded from the expedition,
although the political situation in
many areas does not permit such
discrimination. (A physician should
examine participants in expeditions
beforehand so hypertension or other
disorders predisposing to strokes
can be detected and treated.)
Although many persons survive
strokes, frequently with surprisingly
little or no disability, the prognosis
is still serious, particularly at high
altitudes where cold and reduced
atmospheric oxygen add to the
stress.
The symptoms of stroke are
distinct because they happen
quickly and include the following,
depending upon which portion of
the brain is involved:
The sudden onset of numbness or
weakness of the face, arm, or
leg, particularly on one side of
the body
The sudden onset of confusion,
trouble speaking, or trouble
understanding speech
The sudden onset of impairment
of sight in one or both eyes
The sudden onset of difficulty
walking, dizziness, loss of
balance, or loss of coordination
The sudden onset of a severe
headache with no known cause
The sudden onset of personality
changes such as combativeness,
indecisiveness, or irritability
More severe strokes may be
preceded by a headache, but
unconsciousness follows fairly
quickly and rapidly progresses to a
deep coma in which no response to
any stimuli can be elicited. (These
events may take place almost
instantaneously.) Breathing is noisy
and may be very irregular (Cheyne-
Stokes respirations). Paralysis is
usually present, most commonly
affects one side of the body, and
may include the face as well as the
extremities. However, paralysis is
difficult to evaluate if the individual
is comatose.
The recommended course of
action for anyone suspected to be
having the onset of a stroke in an
accessible location is to have the
person transported to an emergency
care center as quickly as possible.
At the center the individual could
be immediately treated with tissue
plasminogen activator (tPA) to
dissolve the blood clot within an
artery. However, tPA is effective
only when administered within the
first three hours after the onset of a
stroke. For persons in wilderness
situations, evacuation within that
time is commonly impossible.
Regardless of the severity of
symptoms, anyone with a stroke
should be evacuated to lower
altitude without delay. Oxygen
should be administered at altitudes
above 8000 feet (2400 m). An open
airway must be maintained if the
individual is unconscious. Elevated
blood pressure should be treated if
medications are available. After a
lower elevation is reached, a
conscious individual with
hypertension should rest for several
days. A physician’s care is
essential. Such recovery as will
occur requires months.
Transient Ischemic Attack

A transient ischemic attack
(TIA) is an episode in which an
individual develops symptoms
identical to those of a stroke, but the
symptoms disappear. By definition,
the symptoms of a TIA disappear
within twenty-four hours, but for
most individuals the symptoms
disappear in a matter of minutes. A
person who has had a TIA must still
consult a physician right away,
although it does not have to be on
an emergency basis.
A TIA is a warning that a stroke
is imminent and is particularly
likely to occur in the following days
or weeks. Among untreated
individuals with a TIA, 10 percent
have a stroke within three months. If
a physician can bring blood
pressure under control, lower
cholesterol, and help with cessation
of smoking, the risk can be lowered
to 2 percent.
CHAPTER 15
EYE DISORDERS
Geoffrey C. Tabin, M.D.
Gilbert C. Wong, M.D.
In 1988, on the southwest face of

Mount Everest, two climbers died
above 26,250 feet (8000 m); their
last radio message was that they
were both totally blind. In 1996,
near Everest’s summit, a highly
publicized case of blindness, which
was blamed on a popular surgical
procedure done to correct
refractive errors, almost caused a
climber’s death from hypothermia
and frostbite. These and other less
dramatic episodes highlight the
importance of understanding the
basic anatomy and physiology of the
eye, as well as knowing about the
problems commonly encountered in
wilderness or mountaineering
environments.
The eye is like a digital camera.
Lenses focus light entering through
the pupil on a delicate and sensitive
nerve layer at the back of the eye,
the retina, which is analogous to the
light-sensitive sensor in a digital
camera. The impulses from the
nerve cells in the retina are
transmitted along the optic nerves to
the brain. These nerves can be
thought of as a messenger taking
film to be developed or the wiring
that transmits a digital image to the
viewing screen. Finally, the nerve
impulses are processed in the
visual cortex of the brain where
they are converted to images that
are interpreted in accord with the
individual’s experience with the
visual world. Sight is dependent on
the lenses, retina, optic nerves, and
brain all functioning properly. All
these structures can be adversely
affected by high altitude or
exposure to the elements.
The eye has two lenses that
focus light on the retina. Two-thirds
of the focusing power comes from
the cornea, the clear window in the
front of the eye. One-third of the
focusing comes from the crystalline
lens. The outer corneal surface and
its interaction with the lubricating
film of tears is the most important
refractive surface. If the cornea is
too wet or too dry, vision blurs. In
addition, the cornea has one of the
highest densities of sensory nerve
fibers in the body, making it
exquisitely sensitive to pain.
The colored ring visible through
the cornea is the iris, which serves
as an aperture does in a camera.
The iris expands or contracts the
pupil to increase or limit the amount
of light entering the eye.
Immediately behind it is the lens
that can be focused to see close
objects (near vision). Focusing is
not needed for distant vision by
individuals with normal vision.
Everyone slowly loses their
accommodating (focusing) power in
this lens, which is why people with
perfect vision when they are young
require reading glasses after age
fifty. People who are farsighted can
use this focusing power in the lens
to see well at a distance when they
are young but require glasses to see
both near and far as they age and
lose their accommodating power.
Nearsighted people are unable to
see at a distance without glasses but
can always see near objects that are
brought to a point in front of the eye
where accommodation is totally
relaxed.
Considering the number of
factors influencing function of the
eye, it is a remarkable instrument,
able to adapt to a variety of
environments. However, exposure
to the elements in wilderness
environments offers unique
challenges and can cause problems
ranging from bothersome to severe.
RED EYES
Eye problems result in a number of
different signs and symptoms. Often
pain, visual changes, itching,
irritation, and other symptoms
signify a problem. One of the most
common signs of a problem is a red
or inflamed eye. Individuals should
have a framework for evaluating a
red eye in outdoor situations.
First is understanding the
common causes of red eyes in such
settings. Second is identifying the
different etiologies. Last is treating
the eye based on the etiology, and
knowing when to evacuate to
professional medical care.
Conjunctivitis
One of the most common causes
of a red eye is conjunctivitis. The
conjunctiva is a thin clear
membrane that lines the inner part
of our eyelids and the sclera, the
white part of the eye. The area that
coats the inner part of our eyelids is
the palpebral conjunctiva, and the
area that coats the sclera is the
bulbar conjunctiva. Conjunctivitis
means “inflammation of the
conjunctiva.” It has four important
etiologies:
Allergies
Viral infections
Bacterial infections
Trauma
Conjunctivitis is usually
characterized by dilatation of blood
vessels causing redness, swelling,
and a discharge or tearing. The
palpebral conjunctiva is always
involved with conjunctivitis, which
helps differentiate that disorder
from other causes of red eye.
Symptoms of conjunctivitis differ
slightly depending on the etiology,
but it is not always possible or
necessary to identify the etiology.
Viral infection is the most common
cause of conjunctivitis. Usually the
bulbar conjunctiva is red, and a
watery discharge may be present.
Viral conjunctivitis often occurs at
the same time or shortly after an
upper respiratory infection. The
presence of swollen lymph nodes in
front of the ear is strongly
suggestive but rarely present with
viral conjunctivitis. It is usually a
self-limiting condition but
sometimes can move from one eye
to the other after a few days. The
condition is very contagious during
this period, and the affected
individual should try to minimize
contact with others in the party.
Bacterial conjunctivitis often
begins with an abrupt onset and
usually spreads from the initially
affected eye to the other eye within
forty-eight hours. It is characterized
by redness, tearing, and irritation
throughout its course and often
produces a purulent discharge.
Swollen lymph nodes are usually
not present, although bacterial
conjunctivitis can follow an
episode of viral conjunctivitis.
Allergic conjunctivitis is most
often characterized by redness,
itching, tearing, and sometimes
nasal congestion. It is almost
always in both eyes and will
subside once the offending agent is
removed. A variety of substances
can cause allergic conjunctivitis,
including pollen, animal dander,
and dust. It occurs more often in
people with a history of allergy
problems.
The goal of treating
conjunctivitis is to relieve the
symptoms and to prevent or treat an
infection if present. In general,
treatment for bacterial and viral
conjunctivitis should be the same—
application of artificial tears as
needed to provide comfort and
application of an antibiotic four
times a day. The antibiotic both
treats bacterial infections and
prevents a secondary bacterial
infection if the infection is viral in
origin. If the conjunctivitis appears
to be clearly allergic in nature,
artificial tears help dilute the
offending allergen and relieve some
of the itching. Antihistamine drops
or a combination
antihistamine/vasoconstrictor can
also be used in allergic
conjunctivitis to effectively relieve
symptoms. These should not be
used for more than two to three
days as they can cause a reactive
redness and itching.
Subconjunctival Hemorrhage
A subconjunctival hemorrhage is
easily differentiated from other
causes of red eye. It is a benign
condition, though it rarely may be
associated with other more serious
disorders, such as bleeding
disorders or hypertension. The
appearance is distinct from
conjunctivitis in that the redness is
uniform and possesses distinct
borders, completely obscuring the
sclera that it covers (Fig. 15-1). It
causes no pain, visual changes, or
discharge and is a selflimiting
condition that should resolve
completely within one to two weeks
depending on its size. The person
should be reassured that continuing
outdoor activities is safe.
Figure 15-1. Subconjunctival

hemorrhage
Iritis, Scleritis, and Acute Angle-

Closure Glaucoma
More serious causes of red eye
that warrant immediate attention
and evacuation of the individual to
the nearest medical facility include
iritis, scleritis, and acute angle-
closure glaucoma. These all have a
fairly distinct presentation and
should be taken very seriously as
they can result in permanent loss of
vision if not treated appropriately
and quickly.
Scleritis is characterized by
inflammation of the sclera (the
white part of the eye beneath the
bulbar conjunctiva). It causes pain
and is tender to touch. The redness
that it produces can be either in one
area or diffuse. The palpebral
conjunctiva is not involved in
scleritis, which helps differentiate
this condition from conjunctivitis.
Scleritis can pose a significant
threat to vision and may be
associated with serious disease in
other parts of the body.
Iritis (acute anterior uveitis) is
characterized by inflammation in
the front part of the inside of the
eye. Characteristic findings can be
seen with the magnification of a slit
lamp, but this is not feasible in an
outdoor environment. The following
clues may help identify iritis. It
causes pain, photophobia
(increased sensitivity or intolerance
to light), blurry vision, and redness.
The pain is often described as an
ache. The redness is usually
greatest at the limbus, where the
white part of the eye meets the clear
part, and decreases as it gets farther
away. The pupil is often slightly
constricted or irregular as well as
somewhat sluggish in its response
to light. Sometimes, if the condition
is severe, an accumulation of white,
purulent material may settle on the
inside of the cornea and be visible
without magnification.
Acute angle-closure glaucoma
can also cause a red eye and is an
ocular emergency. Normally, a
healthy eye contains fluid that keeps
the internal pressure within a
certain range. This fluid is
constantly being produced and
drained in a balanced manner that
keeps a relatively specific amount
within the eye. The area where the
fluid drains is the trabecular
meshwork located at the angle
where the iris meets the cornea. If
this angle becomes too narrow or
closes, then the outflow tract is
blocked and fluid builds up in the
eye, leading to rapidly elevated
intraocular pressure. The result is
moderate to severe pain and
redness. Most often involvement is
limited to one eye. The redness, as
in iritis, is greatest at the limbus.
If angle-closure glaucoma is
suspected, gently pressing on each
eye with the lids closed reveals that
the eye on the involved side is much
harder. As opposed to the semi-
constricted pupil in iritis, the pupil
in angle-closure glaucoma is
dilated and does not react to light.
The pupil in the unaffected eye is
normal in size and does react to
light. This condition can result in
optic nerve atrophy and permanent
loss of vision within hours if not
treated appropriately.
Iritis, scleritis, and acute angle-
closure glaucoma all require
immediate evacuation to the nearest
medical facility with an
ophthalmologist.
OCULAR SURFACE
DISORDERS
Other problems that people may
experience in outdoor settings
include damage or irritation to the
ocular surface, particularly the
cornea, the clear area on the front
surface of the eye. The cornea is
extremely important in vision; it
protects the inside of the eye from
the outside environment, and it
provides two-thirds of the focusing
power for light that eventually
reaches the retina.
Dry Eye
Dry eye can become very
troublesome for those engaged in
outdoor activities. Dry eye is a
general term describing disorders
of the film of tears that covers the
surface of the eye. These disorders
include decreased production,
increased evaporation, or an
imbalance or abnormality of the
mucin or lipid layers of the tear
film. Though a dry eye syndrome is
associated with autoimmune
disease, outdoors enthusiasts would
rarely be dealing with that disorder.
In an outdoor setting, and for those
who have no history of autoimmune
disease, dry eye is most likely
caused by increased exposure to
elements such as wind, dry air, or
ultraviolet light. Common symptoms
of dry eye include a dry or gritty
sensation, itching, pain,
photophobia, tearing, and redness.
If the symptoms are mild, they can
usually be adequately treated for
individuals to continue their
activities. Insertion of artificial
tears four times a day and a
lubricating ointment at bedtime
usually relieve the symptoms.
Snow Blindness and Other UV

Damage
The surface of the eye—the
cornea and conjunctiva—absorbs
ultraviolet radiation just as the skin
does. Excessive acute exposure can
result in sunburn of the cornea and
produce snow blindness. During the
period of exposure, no sensation
other than the intensity of the light
serves to warn that sunburn is
occurring. Symptoms may not
develop until eight to twelve hours
later. When they do develop, they
include a dry or gritty sensation,
irritation, photophobia, pain,
redness, tearing, and swelling of the
eyelids. A severe case of snow
blindness may be disabling for
several days and may even lead to
ulceration of the cornea,
permanently damaging the eye.
Snow blindness should be
prevented by consistently wearing
protective goggles or sunglasses.
Any ultraviolet blocking lens is
sufficient. Glasses should be large
and curved or have side covers to
block reflected light coming from
below and from the sides. When
ultraviolet radiation exposure is
high, as it would be on a concave
high-altitude snowfield, goggles are
safer, even though they may be less
comfortable and tend to fog. Spare
goggles or glasses should be
carried, but emergency lenses can
be made of cardboard with a thin
slit or pinhole to see through. The
eyes may be covered alternately so
that only one eye at a time is
exposed to sunlight. Eye protection
is just as necessary on a cloudy or
overcast day as it is in full sunlight.
Snow blindness can occur during a
snowstorm if the cloud cover is
thin.
Snow blindness heals
spontaneously in a few days. A
significant concern though, is the
potential for infection. The damage
to the cornea removes part or
sometimes all of the epithelial
barrier in areas of the cornea,
which is the protective barrier that
prevents infection when germs
reach the surface of the eye. If this
barrier is gone, infection is much
more likely, and the infection can
quickly extend inside and to the
back of the eye, resulting in an
ocular emergency.
Steroids must not be
administered because they increase
the susceptibility to infection.
Antibiotic drops and antibiotic
ointment should be administered to
prevent infection. If possible, the
eyes should be kept closed; a
bandage over the closed lids can
help. A topical anesthetic relieves
the pain but makes it more likely
that the person does not keep the
eyes closed, which allows germs to
reach the compromised surface of
the cornea. A topical anesthetic
must be used with great caution and
only when required to safely
evacuate the individual.
Foreign Bodies and Corneal

Abrasion
Foreign bodies and corneal
abrasions can also be significant
sources of ocular surface damage.
Both can occur in virtually any
outdoor activity. Both typically
cause severe irritation, tearing, and
redness of the eye. Common foreign
bodies include dirt, debris, and
other particulate matter that reaches
the surface of the eye.
If the foreign body remains very
superficial, then tears often wash it
out. If tears do not remove it,
sometimes the foreign body can be
washed out intentionally, ideally
with artificial tears. Occasionally a
foreign body may become
embedded deeper in the cornea in
which case the person usually needs
an ophthalmologist to remove it
under a slit lamp.
Foreign bodies can also become
lodged on the inner, conjunctival
surface of an eyelid. As the eyelid
blinks, the body rubs across the
surface of the cornea, leaving
corneal scratches. The eyelid
should be everted, and the foreign
body removed with a moist cotton-
tip applicator (Fig. 15-2). The
applicator should not be used on the
cornea itself, as it may result in a
larger defect. Besides scratches
from foreign bodies, painful corneal
abrasions that lead to flooding of
tears that blur the vision can also
occur from inadvertent trauma, such
as a fingernail or tree branch
scratch.
Figure 15-2. Technique for everting an
eyelid and removing a foreign body
Virtually all injuries by corneal

freezing and superficial abrasions
heal completely, with normal vision
restored within forty-eight hours.
During the acute period, however, a
person can be rendered totally
disabled by blindness. As with
snow blindness, the corneal surface
layer is damaged or compromised
by abrasions. Topical antibiotics
should be applied to prevent
infection.
Corneal Ulcer
A more serious condition
involving the cornea is a corneal
ulcer. A corneal ulcer is
characterized by inflammation or
infection that penetrates into the
corneal stroma, is usually very
painful, and sometimes produces a
white infiltrate in the cornea.
Most corneal ulcers are infected
and require some form of antibiotic
treatment. The cause of the infection
is most commonly a herpes virus,
bacteria, or fungi. In a clinic or
hospital, cultures are taken prior to
treatment to identify the infective
agent and the antibiotic to which it
is sensitive. In an outdoor
environment, culture is unfeasible.
Therefore, if a corneal ulcer is
suspected, antibiotic treatment
should be initiated and the person
should be evacuated to the nearest
hospital or clinic for proper
diagnosis and care.
TRAUMA
In outdoor settings the eye can be
traumatized in a number of ways.
These can range from nuisances to
emergencies and can cause a wide
range of symptoms, including visual
changes, pain, swelling,
hemorrhage, tearing, and discharge.
Lid Lacerations
Lid lacerations can happen in a
variety of ways. Projectile foreign
bodies, falls, tools, or fish hooks
are not uncommon causes. A healthy
eyelid is absolutely necessary to
protect the eye and keep it
functioning properly. Therefore, lid
lacerations should be considered
serious. First and foremost,
bleeding must be stopped and
further damage must be prevented,
which can usually be accomplished
with a pressure bandage. The lid
should be closed as much as
possible, the margins of the
laceration should be approximated
as closely as possible and a
bandage placed over it and secured
in place. The individual should be
evacuated to the nearest medical
facility as soon as possible.
Globe Injuries
Globe (eyeball) injuries often
result from penetrating foreign
bodies or blunt trauma. In an
outdoor setting, this may take many
forms including rocks, tree
branches, or fish hooks. Globe
injuries can result in severe
traumatic damage to any part of the
eye or in infection. Hemorrhages
may infiltrate the retina, resulting in
retinal detachment, or may infiltrate
the fluid that fills the eye. The lens
may be damaged or dislocated,
resulting eventually in a cataract.
The drainage system of the eye may
be damaged, leading to increased
risk of glaucoma. Finally, trauma
may result in rupture of the globe or
an orbital blowout fracture, in
which the eye is forced through the
inferior floor.
As with lid lacerations, bleeding
should be stopped and further injury
should be prevented. Only
superficial foreign bodies should be
removed. Trying to remove
embedded foreign bodies may
cause more damage or result in
more bleeding. Antibiotics should
be applied, and a covering bandage
should be secured over the eye. The
person should be evacuated
immediately to the nearest medical
facility.
Globe Rupture
Globe rupture is a specific type
of globe injury that requires slightly
different initial treatment. As
previously mentioned, it can be a
complication from a variety of
globe injuries, including foreign
bodies, lacerations, and blunt
trauma. Because pressure on a
ruptured globe absolutely should be
avoided, patching or bandaging is
not recommended.
Instead the eye should be
protected from pressure with a rigid
shield. Many authorities do not
recommend topical antibiotics for
fear of introducing high
concentrations of antibiotics inside
the eye. Therefore, the only initial
response is to secure a rigid shield
over the eye, making sure it is not
applying any pressure on the eye.
Evacuation to the nearest medical
facility must be immediate. If
evacuation requires days or longer,
a broad spectrum antibiotic should
be administered systemically.
Chemical Injuries and Burns

Chemical injuries and burns are
extremely serious traumas that often
result in permanent loss of vision.
Treatment can help salvage vision
but often must be carried out
quickly. Among chemical injuries,
alkali burns tend to be more serious
than acid burns because an elevated
pH causes disruption of cell
membranes, resulting in cell death.
The alkali usually penetrates the
cornea; on the other hand, acids
tend to cause proteins in the corneal
epithelium and stroma to coagulate,
limiting ocular penetration.
The most important concept to
remember about chemical burns is
that immediate and abundant
irrigation of the eye could save the
person’s vision. The longer a
chemical is in contact with the eye,
the more damage is done. Irrigation
can help to quickly remove any
chemical from the eye, neutralize
the pH, and prevent irreversible
damage. Ideally, the eye should be
irrigated for at least ten minutes.
Such burns are true ocular
emergencies, and the person should
be evacuated to the nearest medical
facility as quickly as possible.
RETINA AND OPTIC NERVE
DISORDERS
The retina is the photosensitive
layer that lines the back of the eye.
It contains a meshwork of
photoreceptor nerve cells that
absorb light and transform it into an
electrical signal that is sent to the
brain through the optic nerve. The
macula is an area of dense
photoreceptor cells near the center
of the retina that is responsible for
central vision, which permits a
person to read, drive, and perform
other activities that require sharp,
straight-ahead vision. Peripheral
vision is the ability to see objects
and movement outside the direct
line of vision—“out of the corner of
the eye.” Damage to the retina that
causes loss of peripheral vision
may go unnoticed for some time, but
damage to the macula usually
results in immediately noticeable
loss of central vision.
The delicate nerve cells in the
retina connect directly with nerve
cells in the brain and share a
similar physiology. Both require a
large and steady supply of oxygen.
A specialized network of blood
vessels supplies the retinal cells.
To allow clear focusing of light, a
barrier prevents blood or fluid from
escaping into the retinal spaces.
Either decreased oxygen to the
retinal cells or leakage of fluid or
blood into the retina can cause loss
of vision.
High-Altitude Retinal
Hemorrhages
High-altitude retinal
hemorrhages are disorders that
occur at altitude and are discussed
in Chapter 24: Disorders Caused by
Altitude.
Optic Neuropathy
The optic nerve is also
susceptible to damage. This vital
connection links the eye to the
brain. Increased pressure in the
brain from swelling of the nerve
cells, increased blood volume, and
edema is transmitted to the optic
nerve. This leads to papilledema, a
swelling of both optic nerves that
causes transient blackouts of vision.
Obstruction of blood flow to part of
the optic nerve can cause permanent
visual loss.
Glaucoma is a condition in
which the pressure within the eye is
increased because the secretion of
intraocular fluid exceeds
resorption. Damage to the optic
nerve is associated with the
increased intraocular pressure. The
decrease in oxygen at altitude
makes the optic nerve much more
vulnerable to damage by glaucoma.
Thus, climbers who have open-
angle glaucoma must be particularly
careful when ascending to high
altitude (acute angle-closure
glaucoma, which is not related to
altitude, is discussed in the “Red
Eyes” section).
Acetazolamide (Diamox®) is
often taken to treat acute mountain
sickness because it helps the
kidneys correct the alkalosis caused
by rapid breathing at altitude. It is
also a potent drug for glaucoma that
decreases the amount of aqueous
fluid in the eye. Individuals with
glaucoma should take all their
current medications and also
consider taking acetazolamide when
climbing high.
Retinal Vein and Artery

Occlusions
Another type of retinal condition
for which altitude may increase the
risk is occlusion of the retinal vein
or artery. People who have
experienced this in one eye at sea
level have been found to be at
increased risk for developing the
same condition in the opposite eye.
Presumably they are at increased
risk at altitude. One mechanism of
compensation for low oxygen at
altitude is increased production of
red blood cells. Red blood cells
are packed with hemoglobin, which
is the molecule responsible for
transporting oxygen from the lungs
to organs and tissues throughout the
body. As lungs bring in less oxygen,
the body creates more red blood
cells to increase its oxygen-carrying
capacity. This results in increased
blood viscosity, essentially thicker
blood, which is compounded by the
dehydration that many climbers
experience during rigorous activity.
Having thicker blood can lead to
more occlusive events, especially
in small vessels. Retinal vein and
artery occlusions can be very
serious and can result in transient or
permanent vision loss. Individuals
who have experienced these
phenomena at sea level must use
caution and keep well hydrated
when venturing to altitude.
Diabetic Retinopathy
Diabetes is a common disorder
in which the body loses its ability
to control blood sugar levels. One
of the many problems associated
with diabetes is damage to small
blood vessels (microangiopathy).
Microangiopathy results in
capillaries functioning improperly,
leading to oxygen deficiency and
nutrient depletion in surrounding
tissues. The tissues and organs that
are most affected include the eyes,
kidneys, and nerves.
Because diabetes can result in
retinal hypoxia and ischemia even
at sea level, it is presumed that
diabetics are at increased risk at
altitude. Diabetics who venture to
altitude experience additional
hypoxia to the retina, adding to the
effect of the hypoxia caused by their
diabetes. Although no studies have
investigated whether high-altitude
retinopathy and diabetic retinopathy
have a synergistic deleterious
effect, it appears likely. Diabetics
considering a trip to altitude would
be wise to be evaluated by an
ophthalmologist and discuss the
relative risks of their plans.
Retinal Detachment
Retinal detachment is a
separation of the photoreceptor
layer of the retina from the wall of
the eye. Surgeries to reattach retinas
often use gas bubbles to apply
pressure that holds the retina in
place. Since gases may expand and
contract with changes in altitude,
individuals who have recently had
this procedure should not fly or
venture to high altitude until the gas
has dissipated. Although no studies
have investigated whether people
with previous retinal detachments
are at increased risk at altitude, it is
presumed that altitude confers no
increased risk once the retina has
been reattached and the gas bubbles
have dissipated.
REFRACTIVE CORRECTION
Eyeglasses and Contact Lenses
In general contact lenses and
eyeglasses are not good options for
outdoor activities at altitude where
oxygen levels are low. Keeping
glasses clean and free of fogging in
inclement weather and cleaning
contact lenses sufficiently in an
outdoor setting, particularly at
altitude, are difficult. Contact
lenses further reduce the amount of
oxygen reaching the cornea, which
can result in corneal hypoxia. This
appears to be the principal reason
contact lenses are not well tolerated
at altitude.
Various types of contact lenses
are available. The two most
commonly used are rigid gas
permeable (RGP) and soft lenses.
RGP lenses allow oxygen to reach
the cornea surface through diffusion
and through temporarily moving
with each blink, thus briefly
exposing parts of the cornea to
ambient oxygen. Compared to soft
lenses, RGPs offer the advantages
of being relatively easy to clean and
maintain, are associated with a
lower incidence of corneal ulcers,
and provide crisper vision for
people with astigmatism. Their
disadvantages in outdoor settings
include a profound foreign body
sensation when dust or other
particles are in contact with the
lens. People may also find the
cumbersome requirement of daily
cleaning and maintenance
unfeasible. In addition, hard contact
lenses are not designed for
overnight use, tend to be dislodged
easier, and may lead to a sensation
of dryness and grittiness at altitude.
Soft lenses come in a variety of
types and designs. Some are
designed for one-day disposable
use; they come in sterile individual
packages, and after one day are
discarded. Others are designed to
be used for months, requiring
cleaning on a nightly basis. Others
are designed for extended wear,
allowing people to keep the lenses
in overnight for many days; these
offer a variety of advantages,
particularly requiring less
maintenance and cleaning.
However, extendedwear lenses also
are associated with at least a
tenfold increased risk of corneal
ulcers.
In general, contact lenses often
prove cumbersome and unfeasible
for those engaging in outdoor
activities, especially at high
altitudes. Glasses often are no
better, as they too become
cumbersome in such environments.
A better option for many outdoor
enthusiasts may be refractive
surgery.
LASIK and PRK

Laser-assisted in-situ
keratomileusis (LASIK) and
photorefractive keratectomy (PRK)
are surgical procedures that use an
excimer laser, which produces a
cold beam of ultraviolet light, to
reshape the cornea to correct
refractive errors. This laser is able
to remove corneal tissue without
creating heat or damage to
surrounding tissue, which allows
for very precise modeling of the
cornea to shape it for a very
specific refractive goal. LASIK is
currently more widely used than
PRK; it offers the benefits of more
rapid healing and visual correction
and less discomfort. One
disadvantage that LASIK and PRK
have relative to glasses or contact
lenses is that they can exacerbate
dry eye syndromes. If individuals
seeking refractive correction have
dry eyes, these procedures may not
be the best option for them,
especially if they plan on outdoor
activities in which they are exposed
to conditions that also may cause or
exacerbate dry eyes.
Though more investigation is
needed on LASIKand PRK-treated
eyes at altitude, these procedures
appear to be excellent options. A
recent study on Mount Everest of a
small number of climbers who had
undergone LASIK found relatively
stable refraction compared to those
wearing contact lenses. All the
climbers retained excellent vision
at base camp (17,600 ft; 5370 m).
Five of six reported no visual
changes up to 26,400 feet (8050 m).
Two climbers reported slight
changes at 27,000 and 28,500 feet
(8230 and 8700 m) that improved
with descent. Three of the six
experienced no visual changes up to
the collapsing dome the summit
(29,035 ft; 8850 m). As most
outdoor enthusiasts, even most
climbers, are not venturing to these
altitudes, this suggests LASIK is an
excellent and stable option for
refractive correction.
Figure 15-3. Effect of altitude on
cornea after radial keratotomy (RK):
Circumferential expansion from edema
causes peripheral steepening with
corresponding central flattening.1
Radial Keratotomy
Radial keratotomy (RK) is a
form of surgical therapy for
refractive errors that is no longer
used. Climbers over the age of
forty-five who may have undergone
this procedure when they were
younger should be aware of
possible complications at altitude
(Fig. 15-3). Hyperopic (farsighted)
vision changes in RK eyes at
altitude have been reported in a
number of individuals, including
Beck Weathers, who has said that
his well-known trouble on Mount
Everest in 1996 began when he was
blinded by the effects of high
altitude on his eyes that had been
altered by RK.
____________
REFERENCE
1. Adapted from an illustration
by Tom Mader. (Reproduced with
permission.)
CHAPTER 16
EAR, NOSE, THROAT, AND
DENTAL DISORDERS
Diseases of the ears, nose, and

throat, the most common of all
disorders if the common cold is
included, are usually inconvenient
rather than disabling and, except for
allergies, are of relatively short
duration. However, all diseases of
these organs, even colds, carry
some threat of significant
complications and must be
respected and treated carefully,
particularly in the wilderness.
DISORDERS OF THE NOSE

Common Cold
A number of viruses cause upper
respiratory infections (colds).
(Some generalized viral infections,
particularly measles, often mimic a
cold during their initial stages.) The
viruses are spread by personal
contact. Chilling may play a role in
contracting the disease by
increasing susceptibility to
infection, but in the absence of the
causative viruses, cold exposure
alone cannot produce infection.
Secondary bacterial infections and
allergy to the virus or bacteria
cause many of the symptoms of a
cold.
A sense of dryness, scratchiness,
or tickling in the throat or back of
the nose usually appears first,
although at altitude these symptoms
are sometimes encountered and are
not signs of a cold. Such early
symptoms are followed in a few
hours by nasal stuffiness, sneezing,
and a thin, watery nasal discharge.
After forty-eight hours, when the
disease is fully developed, the eyes
are often red and watery, the voice
husky, and the nose obstructed. An
abundant nasal discharge is present,
and taste and smell are diminished.
A cough is commonly present and
typically is dry at first. Later a
moderate amount of mucoid
material may be coughed up. The
individual characteristically is
uncomfortable but not seriously ill.
Fever is usually absent but may be
as high as 102°F (39°C). The throat
may be sore, but exudates (white
spots) are not present (see
“Streptococcal Pharyngitis”), and
the lymph nodes around the neck
and jaw usually are not enlarged.
No effective treatment for a cold
has been developed, although some
measures to alleviate the symptoms
are available. The disease usually
lasts seven to ten days. Strenuous
activity during the first few days
when symptoms are most severe
should probably be avoided,
particularly at higher altitudes, to
reduce the probability of
complications such as sinusitis or
bronchopneumonia. Moderate
exercise at low altitudes and
limited work at higher altitudes for
the additional three to six days
required for complete recovery are
usually well tolerated.
A decongestant nasal spray may
be used to reduce nasal congestion
and obstruction. However,
symptoms may be worse after the
decongestant wears off, particularly
after short-acting decongestants
such as phenylephrine.
Decongestant sprays should
probably be reserved for the times
when they are needed most, such as
at night to permit restful sleep.
When first administered, a
decongestant usually relieves
obstruction by reducing the
swelling of the mucous membrane
over the more prominent portions of
the nasal passages. A second spray
five to ten minutes later may be
necessary to reach the recesses of
the nasal cavity. Swelling in these
areas should be relieved to promote
drainage and reduce the risk of
bacterial sinusitis. A systemic
decongestant or a combined
decongestant and antihistamine
taken orally may be beneficial.
Antibiotics have no effect on the
viruses that cause colds and for
most individuals should not be
administered. The rare serious
complications of colds may require
antibiotic therapy, but such therapy
should not be given until the
conditions actually develop.
Prophylactic antibiotic therapy
should be avoided, even at high
altitudes, because the bacteria
producing any subsequent infection
could become resistant to the
antibiotics. However, the
uncommon individuals who almost
invariably develop a bacterial
bronchitis or bronchopneumonia
following a cold should be
considered exceptions to this rule.
Sinusitis
Sinusitis is an infection of one or
more of the paranasal sinuses (Fig.
16-1), air-filled spaces within the
bones of the face that are lined by a
thin mucous membrane similar to
that of the nose and are connected
with the nose by narrow canals. The
sinuses serve to make the skull
lighter in weight than it would be if
these areas were occupied by solid
bone.
Sinusitis most commonly results
from obstruction of the canals that
drain the sinuses, usually caused by
swelling of the mucous membrane
around the opening due to a cold or
allergy. Mucous collects within the
sinus, becomes infected, and the
infection spreads to the surrounding
tissues.
Sinusitis, although accompanied
by a headache, is rarely disabling
by itself. Complications do occur,
and spread of the infection to the
bones of the skull or to the brain
itself can result in chronic
osteomyelitis, meningitis, or a brain
abscess. However, these potentially
lethal complications usually follow
prolonged chronic sinusitis, which
should be eradicated before an
extended wilderness outing.
Acute sinusitis sometimes
accompanies or follows a cold or
hay fever. The most prominent
symptom is headache, which may
be located in the front of the head,
“behind the eyes,” or occasionally
in the back of the head. A purulent
discharge frontal frequently drains
into the nose and back into the
throat—so-called postnasal drip—
where it may be swallowed.
Figure 16-1. Location of the frontal
and maxillary sinuses
Fever rarely gets higher than

102°F (39°C) and may be entirely
absent. Tenderness may be present
over the involved sinus. Infection in
the maxillary sinuses may produce
pain or tenderness in the teeth of the
upper jaw.
The treatment of acute sinusitis
consists of drainage and antibiotic
therapy. (Treatment of chronic
sinusitis should be directed by a
physician.) A decongestant nasal
spray should be administered at
regular intervals to reduce the
swelling of the nasal mucosa and
permit drainage through the canals
that enter the sinuses. Spraying
should be repeated ten minutes after
the first application to make sure
the spray reaches the recesses
where the openings of these canals
are located. (Because rebound
swelling of the mucosa occurs when
the decongestant spray wears off,
some physicians recommend a
twelve-hour spray that is only
administered at night.) A systemic
decongestant also can be
administered. In a remote area,
(Augmentin®) should be given for
ten days. Trimethoprim-
sulfamethoxazole (TMP-SMX,
brand names Bactrim or Septra®)
is a substitute for individuals
allergic to penicillin.
Acute sinusitis usually clears up
within a few days. Symptoms
persisting for more than seven to ten
days may be indicative of a
complication and should prompt
serious consideration of evacuation.
If an individual appears very ill and
swelling is present around the eyes
or nose, which is a sign of spread
of the infection, prompt evacuation
should be considered.
Middle ear infections sometimes
accompany or follow acute sinusitis
(see “Ear Infections”).
Nosebleed
Nosebleed is commonly a result
of trauma, but many nosebleeds do
not follow an injury. Regardless of
the cause, the treatment is similar.
(Care for this problem is discussed
in Chapter 8: Head and Neck
Injuries.)
SORE THROAT
(PHARYNGITIS)
Sore throat is a common symptom
that is produced by a number of
different conditions.
Drying
Prolonged mouth breathing,
particularly in hot, dry climates, or
in cold climates at high altitudes
where air has a very low relative
humidity when warmed to body
temperature, causes drying of the
mouth and throat and can result in a
sore throat. An irritating, dry,
hacking cough is also usually
present. Recognizing the existence
of conditions causing drying of the
throat and excluding the presence of
other diseases characterized by a
sore throat can identify this
condition. Drying of the throat is not
accompanied by chills, fever, or
enlargement of the lymph nodes of
the neck or under the jaw. The
throat may be mildly inflamed (red)
but exudates (white spots) are not
present.
Treatment of any kind is usually
disappointing. Lozenges containing
anesthetics or antibiotics are
available. However, hard candy or
rock sugar melted in the mouth (not
chewed) is probably just as
effective, is much less expensive
and easier to obtain, and does not
carry the dangers associated with
indiscriminate antibiotic use.
Lozenges should be taken only
about every four hours, but candy
can be consumed freely. In addition,
the candy has nutritional value,
which is important at high altitudes
where loss of appetite makes the
ingestion of any food a problem.
Viral Pharyngitis
In conditions that do not produce
drying, viral infections are the most
common cause of sore throats. Viral
pharyngitis (viral sore throat)
commonly accompanies a cold but
may not be associated with
infection elsewhere. The person
usually does not feel or appear
seriously ill, although a few
individuals feel much worse than
most others. Fever may be present
but is rarely higher than 101°F
(38.5°C). The throat is inflamed,
but exudates are not present and
enlargement of lymph nodes is rare.
Before accepting a diagnosis of
viral pharyngitis, streptococcal
pharyngitis must be ruled out.
Viral sore throat usually clears
up in three to six days without
therapy. Lozenges may provide
some relief, but hard candies
melted in the mouth are equally
effective. Antibiotics are of no
benefit and should be avoided
unless streptococcal infection is
seriously suspected. However,
distinguishing between these two
infections without laboratory
facilities may be impossible.
Streptococcal Pharyngitis
Streptococcal pharyngitis (strep
throat) is encountered less
frequently than other causes of sore
throat but can be treated much more
satisfactorily. This infection is
caused by streptococci and is
potentially dangerous because it can
lead to rheumatic fever, which may
damage the heart valves.
Individuals with streptococcal
pharyngitis typically feel and
appear ill (malaise). Fever is
usually present and may reach
103°F (39.5°C) or higher. Chills
often occur. The throat appears
beefy red and exudates, which are
similar to the pus found in boils or
infected wounds, can be seen as
white or pale yellow points or
patches scattered over the throat,
particularly on the tonsils. The
lymph nodes in the neck and under
the jaw usually are enlarged and
tender.
Fever, exudates, enlarged lymph
nodes, and general malaise without
a cough serve to differentiate strep
throat from other forms of
pharyngitis. However, malaise may
not be marked, lymph node
enlargement may not be prominent,
and fever may not be very high. Any
sore throat should be regarded with
suspicion. In a remote area, if three
of the four signs and symptoms
listed are present, antibiotic therapy
should be instituted.
Treatment for streptococcal
pharyngitis consists of the oral
administration of penicillin.
Amoxicillin/clavulanate
(Augmentin®) is also effective.
Individuals allergic to penicillin
can be given cephalexin or
azithromycin. Symptoms and signs
of the disease usually disappear
completely within twenty-four to
forty-eight hours with or without
antibiotics. Nonetheless, therapy
must be continued for ten days to
ensure complete eradication of the
infection and the prevention of
complications, particularly
rheumatic fever.
DISORDERS OF THE MOUTH

Canker Sores
Canker sores are small painful
ulcers that appear inside the mouth
without apparent cause. They first
appear as small blisters that soon
rupture, leaving small, white ulcers
surrounded by an area of
inflammation. Such sores may be
caused by Herpes simplex
infection.
No therapy is effective for these
ulcers, but they disappear in a few
days without treatment. A
mouthwash consisting of a teaspoon
(4 ml) of sodium bicarbonate
(baking soda) in a glass of water is
soothing. A mouthwash of half
water and half 3 percent hydrogen
peroxide solution helps prevent
secondary infection.
Herpes
Herpes (also known as cold
sores or fever blisters) is a viral
infection (Herpes simplex) that
produces small, painful blisters,
most commonly on the lips and skin
around the mouth. The viruses
persist in the tissues so blisters
recur in the same location. Herpes
sores commonly are exacerbated by
sunburn of the lips or face, and
avoiding sunburn helps prevent
them. Herpes sores may accompany
severe infections such as
pneumonia or meningitis, but most
commonly cannot be associated
with any disorder.
An initial small, painful swelling
rapidly develops into one or more
small blisters containing a clear
fluid and surrounded by a thin
margin of inflamed skin. The
blisters may rupture, particularly if
they are traumatized, resulting in
bleeding and crusting. Fever or
other symptoms are rarely
experienced.
The application of a local
anesthetic ointment such as
xylocaine jelly may provide some
symptomatic relief. Individuals
with recurrent herpes should have
their physicians prescribe oral
acyclovir and have that with them in
the wilderness. The blisters usually
heal in five to ten days, and
although uncomfortable and perhaps
unsightly, they usually cause no
significant disability.
DENTAL EMERGENCIES
Prevention
Dental emergencies, except for
traumatic injuries, should be almost
entirely prevented by routine dental
care, which should include brushing
twice a day, daily flossing (which
is of greatest significance for
preventing gum disease), and visits
to a dentist every six months or so
for cleaning, periodic dental X-
rays, and treatment of any problems
that are found. Before an extended
outing to a remote area, all potential
dental problems must be treated.
The Peace Corps requires
certification of a dental examination
and treatment before assigning any
volunteers to developing countries.
The National Science Foundation
has similar requirements and also
requires that impacted and
unopposed third molars be
extracted before travel to
Antarctica.
Dental Pain
Dental pain has a number of
causes and can be severe enough to
be disabling.
Acute Pulpitis
Acute pulpitis is a common
painful condition caused by
inflammation of the dental pulp and
ranges in severity from mild
discomfort to intense, disabling
pain. Identifying the involved tooth
is often difficult because the pain
radiates to the eye, ear, or another
tooth. The tooth is rarely sensitive
to tapping or palpation. Commonly
pain may be elicited by exposure to
cold or sweets. With more severe
pulpitis, heat can cause pain.
Sometimes a significant cavity can
be found in the tooth, but more often
no abnormality can be seen.
Treatment consists of the
administration of an analgesic such
as acetaminophen. With severe
pulpitis, a stronger analgesic may
be needed and the individual may
need to be evacuated for dental
care. Ideally a nerve block for the
affected tooth could be
administered, but few individuals
who have not practiced
administering such blocks would
have the skills, equipment, or
anesthetic agents to perform that
procedure.
Periapical Osteitis
Periapical osteitis is an
inflammatory condition of the
supporting structures of the root of a
tooth that is characterized by
constant, throbbing pain. Unlike
acute pulpitis, the tooth typically
can be precisely identified. The
area over the root tip is usually
tender but not swollen. Overt
trauma can produce such symptoms,
but the most common cause is an
infection of the pulp, which should
be detected and treated before an
outing.
The inflammation causes the
tooth to be extruded slightly, which
intensifies the pressure on the tooth
during biting and increases the pain.
Treatment in a wilderness situation
consists of an analgesic and a soft
diet. Placing a piece of gauze or
similar material between the teeth
on the opposite side prevents the
involved tooth from striking
opposing teeth and reduces the pain.
Dental care should be obtained
promptly.
Cracked Tooth Syndrome

Individuals with a cracked tooth
may complain of pain when
chewing certain foods or when
releasing the bite. They may
complain that the pain is felt only
when biting something hard “in just
the right way.” No pain is felt when
chewing soft foods because the
crack in the tooth is not opened. The
condition usually progresses slowly
and can be controlled by not
chewing on the affected side.
Dental care should be obtained
promptly, but evacuation from an
extended expedition is rarely
necessary.
Open Cavity
An open cavity in a tooth may be
painful, particularly when it
becomes packed with food. Such
abnormalities should be corrected
before major expeditions—but may
result from fillings lost during an
outing—and can be expected in
locals hired as porters or for
similar tasks. Removing food from
the cavity often relieves the pain.
A well-equipped expedition
could carry a temporary filling
material such as Cavit®. Care must
be taken not to fill the cavity with
so much of the material that it
extends above the tooth surface,
which would cause pain from the
increased pressure on that tooth. If
nothing else is available, the cavity
can be filled with a small amount of
sugar-free chewing gum for a brief
time.
Maxillary Sinusitis
Sinus infections in the maxillary
sinuses sometimes produce pain in
the teeth. Such infections typically
are accompanied by fever and
discomfort. Indications that the pain
is from this source include the
normal appearance of the teeth and
the involvement of more than one
tooth. Such infections should be
treated in the same manner as all
sinus infections.
Abscesses
Abscesses are quite rare among
individuals who obtain regular
dental care. On outings to
developing countries, such
abnormalities would be much more
common among locals employed for
the expedition who do not have
access to such care. The origin of
such infections most commonly is
untreated infection or decay
(caries) in teeth from which
bacteria spread to the bone
surrounding the root.
Individuals with dental
abscesses usually have a history of
dental pain, but pain may be absent
at the time the abscess forms. They
also have swelling that is usually on
the side of the gum next to the lips
or cheek. If the infection has spread
to the surrounding soft tissue
(cellulitis), swelling may involve
the cheek and can be massive.
The treatment for an abscess is
drainage, which can be
accomplished by extracting the
tooth, incising and draining the
abscess, or a root canal. None of
these procedures should be carried
out by individuals who have no
experience with them. The
individual must be evacuated to
dental care. If swelling indicative
of cellulitis is present, the
individual should be treated with
antibiotics. Penicillin is most
commonly used in dental practice,
but a cephalosporin such as
Keflex® is acceptable.
Clindamycin is a good alternative
for individuals allergic to
penicillin, but such allergy is much
less common in residents of
developing countries who are
rarely treated with antibiotics.
Lost Fillings or Crowns

Fillings or crowns are
periodically lost from teeth.
Examination by a dentist often
cannot detect teeth from which these
structures are about to be lost.
Commonly such loss results from an
underlying infection (caries) but
occasionally occurs without
infection being present. The filling
or crown should be saved if
possible because sometimes it can
be restored.
On an extended outing a small
amount of dental cement, which is
available over the counter, can
temporarily cement a crown back in
place. If the tooth is not painful, a
dentist’s attention, removal of any
infected tissue, and permanent
replacement of the structure can be
delayed until the individual returns
home.
EAR INFECTIONS
Ear infections frequently occur in
infants and young children but are
uncommon in older persons.
Swelling of the mucous membrane
or enlargement of the adenoids in
young people easily blocks the
eustachian tube that drains the
middle ear. However, this tube is
larger in adults, and these disorders
rarely produce obstruction. In the
absence of eustachian obstruction,
ear infections are uncommon.
A cold, sinusitis, or hay fever
usually precedes the ear infection.
The principal symptom is pain in
the ear. Fever or malaise may be
present. Infrequently, a purulent
discharge from the ear can be
found.
Therapy consists of the oral
administration of
(Augmentin®). Doublestrength
trimethoprim/sulfamethoxazole
(Bactrim or Septra®) can be
substituted for individuals allergic
to penicillin. A systemic
decongestant should also be given
to help reduce swelling around the
opening of the eustachian tube. A
hot-water bottle and mild to
moderate analgesics every three to
four hours help reduce the pain.
Warm (not hot), bland oil such as
olive oil inserted into the ear also
helps relieve the pain.
CHAPTER 17
HEART AND BLOOD VESSEL
DISORDERS
Blair D. Erb, Sr., M.D.
Blair D. Erb, Jr., M.D.
The heart and blood vessels

circulate blood, which transports
oxygen and nutrients to the body
tissues and carries away carbon
dioxide and waste. The heart
consists of a four-chambered pump:
right atrium, right ventricle, left
atrium, and left ventricle. Blood
travels from the left ventricle
through the aorta and through
repeatedly branching smaller and
smaller arteries to capillaries
barely large enough to permit
passage of single red blood cells. In
the capillaries, oxygen, carbon
dioxide, and other substances are
exchanged between blood and
tissue. From the capillaries, blood
continues its journey as it flows
through larger and larger veins to
return through the right atrium into
the right ventricle. Blood is then
pumped from the right ventricle
through the lungs, where it releases
its acquired carbon dioxide and is
replenished with oxygen. It returns
through the pulmonary veins and the
left atrium to the left ventricle. The
result is a figure-eight circuit: one
loop carrying blood through the
lungs where it is capillaries venous
blood right atrium right ventricle
arterial blood left ventricle left
atrium oxygenated, the other
carrying blood to the rest of the
body (Fig. 17-1).
Four valves permit the heart to
function as an efficient pump. The
tricuspid and mitral valves in the
right and left ventricles close during
cardiac contraction (systole),
preventing reflux of blood into the
atria. Simultaneously the pulmonic
and aortic valves open, permitting
blood to be pumped into the
pulmonary artery and aorta. After
systole has been completed and the
heart muscle relaxes (diastole), the
pulmonic and aortic valves close,
preventing reflux of blood into the
ventricles, and the tricuspid and
mitral valves open, allowing the
ventricles to fill.
Peripheral veins in the legs are
compressed by the contracting
muscles during exercise such as
walking, squeezing blood toward
the chest. Low pressure in the chest
produced by the inspiratory phase
of respiration results in a pressure
gradient that moves blood from the
extremities toward the heart.
Consequently, an individual can be
said to have “two hearts”: one in
the chest that pumps blood through
the arteries to the extremities, the
second the muscles in the legs that
pump blood through the veins back
to the chest. Delicate valves located
in the veins prevent backflow
during this process.
Figure 17-1. The circulation of blood
Delicate receptors sense blood

volume and oxygen and carbon
dioxide concentrations and adjust
cardiac output by modifying heart
rate, the force of contraction, and
the volume of each heartbeat, and
hence the amount of blood supplied
to different areas of the body
(Chapter 18: Respiratory
Disorders).
PHYSICAL EXAMINATION OF
THE CARDIOVASCULAR
SYSTEM
Simple methods for examining the
functions of the heart and
circulatory system can provide
highly significant information, even
for inexperienced examiners. The
examination should include:
Determining heart rate and
rhythm
Judging arterial and venous
pressure
Evaluating the peripheral
circulation
Listening to the heart and lungs
Heart Rate and Rhythm

The heart rate can be measured
most conveniently in the wrist at the
base of the thumb, where pulsations
in the radial artery can be felt. The
pulsations are usually counted for
fifteen or twenty seconds and
multiplied by four or three to obtain
the rate per minute. (Longer counts,
sometimes as long as two or three
minutes, may be needed for
individuals with irregular rhythms.)
In some persons, particularly
those in shock, radial artery
pulsations may be too weak to
count, and the carotid or femoral
pulse must be sought. The carotid
pulse can be found on either side of
the neck in the groove between the
thyroid cartilage (Adam’s apple)
and the prominent muscle that
extends from behind the ear to the
top of the breastbone (sternum). The
femoral pulse can be found in the
fold where the leg meets the
abdomen about midway between
the center of the pubic area and the
lateral bony edge of the hip.
Clothing must be removed before
the femoral pulse can be palpated.
If shock is so severe that no
pulses can be felt, the heart rate can
be determined by listening with a
stethoscope placed between the left
nipple and the sternum. Each
heartbeat is accompanied by two
heart sounds of slightly different
tone (lub-dup, lub-dup).
Occasionally a faint third sound
may be heard (lub-dup-dup, lub-
dup-dup.) Although heart sounds in
normal persons can be heard with
the unaided ear pressed against the
chest, the heart sounds are usually
faint in shock and a stethoscope is
often needed. A little prior practice
by examiners—even listening to
their own heart—is useful.
The normal resting heart rate
ranges from fifty (in a few well-
conditioned individuals) to ninety
beats per minute. The heart rate is
slower during sleep. At high
altitude the resting heart rate may be
as high as 100 beats per minute
during the first few days of
acclimatization.
Normally the heart rhythm is
regular, but in young individuals it
may change with respiration—
speeding up during inspiration,
slowing during expiration. Such
variation is normal, and when
persons hold their breath, the
rhythm becomes completely regular.
Arterial and Venous Pressure

When the pulse is barely
palpable, the blood pressure is
usually low. Strong, “bounding”
pulses usually indicate a normal
blood pressure and normal heart
action. Arterial pulses are usually
equal in both wrists, both sides of
the neck, and both sides of the
groin. Absence of a pulse on one
side indicates arterial obstruction
or injury.
When healthy persons are lying
flat, the partially or fully filled neck
veins can be seen extending from
the middle of the collarbone
(clavicle) to just below the lower
jaw. When the person is sitting
upright or even partially upright
(semirecumbent), filled neck veins
should not be visible above the
clavicle. Visible, distended neck
veins in an upright position are
abnormal and usually indicate heart
failure or obstruction of venous
blood flow to the heart.
Accurate measurement of blood
pressure requires a blood pressure
cuff (sphygmomanometer) and
stethoscope. The cuff should be
wrapped snugly around the arm
above the elbow and inflated to a
pressure of about 180 mm Hg or
until the radial pulse disappears.
The stethoscope bell should be
placed over the inner aspect of the
elbow crease with the arm
extended. The pulsations of the
brachial artery can often be felt
here, and the best position for the
stethoscope is over the artery. As
the pressure in the inflated cuff is
allowed to fall by slowly releasing
air through the valve on or near the
bulb, a thumping sound synchronous
with the pulse appears. The
pressure indicated when the sound
is first heard is the systolic blood
pressure. The pressure at which the
sound completely disappears as the
cuff pressure continues to fall is the
diastolic blood pressure. Normal
blood pressure ranges from 105 to
140 mm Hg systolic and from 60 to
80 mm Hg diastolic.
If the radial pulse can be felt and
a stethoscope is not available, the
systolic blood pressure can be
approximated by inflating the cuff
and allowing the pressure to fall
until the radial pulse first appears.
This pressure is 10 to 20 mm lower
than the pressure determined by a
stethoscope, but the method is
reliable in an emergency.
If a blood pressure cuff is not
available and the individual is
alert, the brain is well perfused and
an adequate blood pressure is
probably present. The systolic
blood pressure, which is most
significant, can be roughly
estimated by the presence of
palpable pulses in various
locations. If a pulse is palpable at
the wrist (radial pulse), the systolic
pressure is at least 80 mm Hg. If no
radial pulse can be felt but a pulse
can be palpated in the groin
(femoral pulse), the systolic
pressure is approximately 70 mm
Hg. If the femoral pulse cannot be
detected but a carotid artery pulse
can be felt, the systolic pressure is
approximately 60 mm Hg.
Peripheral Circulation
The lips, tongue, and fingernails
(nail beds) are normally pink, but
when oxygen concentration in blood
is low, they become blue or purple.
This discoloration (cyanosis) is
common at high altitude and is
usually severe in high-altitude
pulmonary edema. At lower
elevations cyanosis usually
indicates inadequate oxygenation of
the blood by the lungs and is caused
by disorders such as airway
obstruction, pneumonia, or chest
injuries.
When blood pressure is low and
blood flow to the extremities is
decreased, the nail beds and lips
may be cyanotic even though
oxygenation of the blood in the
lungs is normal. This type of
cyanosis is due to decreased blood
flow and is commonly seen in
shock. The skin may appear
mottled.
Anemia or blood loss may give
the nails a pale color.
Edema is an accumulation of
excess water in the tissues and is
not uncommon during the first few
days at high altitude, particularly in
women. It is caused by retention of
salt and water. The face may be
puffy in the morning, and the feet or
ankles may be mildly swollen.
More severe edema, particularly if
progressive and lasting for more
than a week, suggests heart failure
or kidney disease and should be
investigated.
Individuals who have persistent
shortness of breath with mild
exertion, or who experience
shortness of breath when lying flat
that is relieved by sitting up, usually
have fluid accumulations in the
lungs (pulmonary edema). In young
individuals at high elevations, high-
altitude pulmonary edema should be
suspected. In older individuals at
lower elevations, heart failure is a
common cause. When listening to
the chest of someone with
pulmonary edema from any cause,
crackles or bubbling sounds can be
heard with each breath. (Asthma
usually produces wheezes or
squeaking or groaning sounds,
particularly during expiration.
Auscultation of the lungs is
discussed further in Chapter 18:
Respiratory Disorders.)
Written records are vital in the
care of anyone suspected of having
heart disease. All observations,
including the time of the
observations, must be recorded.
Examinations should be repeated at
frequent, regular intervals, such as
every two to four hours. Physicians
need such records when the
individual is evacuated, and a
detailed record may make possible
a prompt, accurate diagnosis by
radio or cellular telephone.
HEART DISEASE IN THE
WILDERNESS
The terms sudden cardiac death,
paroxysmal tachycardia, and acute
myocardial infarction confirm the
unpredictable nature of heart
disease. When asked to assess a
person’s risk for participating in an
adventure, physicians are being
asked to predict that which is
inherently unpredictable.
Individuals over age fifty with
multiple risk factors for heart
disease or with known heart
disease who participate in vigorous
outdoor activity without consulting
a physician place themselves, their
companions, and success of the
expedition at risk. In addition, they
burden their companions with the
possibility of having to care for an
ill person when they lack the
appropriate skills.
An appropriate assessment of
risk should be performed in persons
over fifty years of age, those with
multiple cardiac risk factors
(hypertension, diabetes mellitus,
hypercholesterolemia, a history of
smoking, or a family history of
premature heart disease), and those
with known heart disease. This
assessment should be performed by
a physician who knows the risks of
the venture, the characteristics of
the environment, and the physical
demands of the activity.
The pre-adventure assessment
should include a detailed medical
history, including careful
questioning regarding risk factors
for coronary artery disease.
Functional status can be ascertained
by reviewing daily activities and
the participant’s history of previous
adventures. A past history of
successful similar adventures is the
strongest predictor of future success
in the wilderness. The history
should be followed by a careful
physical examination for evidence
of hypertension, heart failure,
abnormal rhythm, and
atherosclerosis. Tests such as
ECGs, chest X-rays, and stress tests
have relatively little predictive
value except possibly in those with
known heart disease.
Much more important than
testing is the strict adherence to a
prescribed medical regimen. For
example, cessation of medicines
such as aspirin or statins
(cholesterol-lowering drugs) in
persons with known coronary
disease results in an increase in the
risk of heart attack at the time the
drug is halted. In addition, the most
common reason for individuals with
heart failure to decompensate is
failure to take their prescribed
medicines. A prescribed medical
regimen must be followed in the
wilderness, or risk is unnecessarily
increased. For complex adventures,
this medical history and regimen
must be reviewed with the team
leader. The participant must be
vigilant for signs and symptoms of
problems and be honest and
forthright in communicating them to
the expedition leader.
Ultimately, the decision to
participate in an activity must be a
balance between risk and desire.
The unpredictable nature of heart
disease means that although risk
may be reduced, it cannot be
eliminated. Mountaineering and
other wilderness activities remove
the security of calling 911.
Consequently, should an event
occur, a favorable outcome is less
likely.
The Physician’s Role

Individuals who have evidence
of heart disease should have their
cardiac status evaluated to
determine the risk of moderate to
severe exertion at some distance
from medical facilities (Chapter 25:
Altitude and Common Medical
Conditions). The interview phase of
the physician’s examination is
probably the most important part of
the examination before an outing.
Since a history of a previously
successful similar venture is the
best predictor of success in the new
activity, the physician must have a
clear understanding of the risks of
the venture, the characteristics of
the environment, and the health
status of the individual. An
informed decision to accept those
risks can be made only with the
assistance and recommendations of
a concerned physician who
understands the lure of wilderness
recreation.
The individual must follow the
physician’s instructions and obtain
prescribed medications. The outing
leader should be familiar with the
treatment the person is receiving
and must be alert for complications
that require additional care or
evacuation. However, the person’s
physician is responsible for
medical management, not the trip
leader. For longer trips or
expeditions, the leader should be
supplied by the physician with a
detailed description of the
individual’s condition, restrictions
on activity that should be observed,
medications to be taken, and the
anticipated signs or symptoms that
could require additional therapy or
evacuation.
The Heart and Altitude

High altitude poses little threat
for the hearts of normal individuals.
The level of exercise an individual
can maintain is limited by the tissue
oxygen supply. (Only a few highly
motivated individuals can increase
their activity beyond the level at
which tissues are fully supplied
with oxygen—anaerobic exercise—
and temporarily allow lactic acid
and other unoxidized metabolites to
accumulate.) At sea level
atmospheric oxygen is plentiful, and
consequently oxygen delivery to the
tissues is dependent predominantly
on cardiac output. To increase
tissue oxygen to a maximum, the
heart is pushed to work hard.
At high elevations, the oxygen
supply to the tissues is limited by
the smaller amount of oxygen in the
atmosphere, not by cardiac output.
The heart extracts 100 percent of
the oxygen delivered to it at rest.
Increased oxygen demand can only
be met by increased flow. As the
partial pressure of oxygen falls with
altitude, so does the heart’s
efficiency. During maximal exercise
at high altitude the heart rate, which
is a rough guide to the cardiac work
being performed, is slower than at
maximal exercise at sea level.
MAJOR HEART DISEASES

Coronary artery disease is the most
common form of heart disease in
men and women over fifty.
Progressive narrowing of the
arteries that supply the heart results
from deposits of cholesterol on the
inner surface (arteriosclerosis or
“hardening of the arteries”) and can
produce chest pain (angina
pectoris), a heart attack
(myocardial infarction), heart
failure (cardiac dyspnea), or
sudden death. Rupture of one of
these fat deposits results in clot
formation, subsequent loss of blood
flow, and myocardial infarction.
Angina Pectoris
Angina pectoris (or simply
angina) is a sensation of pressure or
deep-seated discomfort beneath the
sternum that characteristically
appears during exercise and
disappears after a few minutes of
rest. The discomfort may be
described as crushing, a sensation
of being squeezed, feeling as if a
weight were on the chest, feeling as
if a band were around the chest, or
a deep-burning sensation. It may be
felt in the neck, jaws, arms, or
midback as well as in the chest. If
exercise is continued, the
discomfort increases; pain is
relieved by rest and nitroglycerine.
The discomfort is predictable and
rarely occurs at rest except during
periods of emotional stress. If
angina occurs at rest, this suggests
an impending heart attack. Its
duration is rarely longer than fifteen
to thirty minutes. Angina is
frequently accompanied by
shortness of breath, which subsides
as the discomfort eases.
Individuals who have suffered
episodes of angina must bring
nitroglycerin tablets with them into
the wilderness. A person suffering
angina should hold one of these
tablets under the tongue until it has
dissolved. Two or three tablets
taken at three- to five-minute
intervals may be necessary for
relief. Nitroglycerin tablets should
be kept in their original brown
glass bottle with a metal screw cap
and should not be kept longer than
six months after purchase. Cotton
wads should not be kept in the
bottle, which should be tightly
capped and kept away from heat
and moisture to reduce or prevent
loss of potency.
Individuals with only mild
angina at sea level may experience
increased symptoms during the first
few days at higher altitudes. A
decrease in physical activity,
additional medications, and oxygen
may be needed to control the
symptoms. If the person has
medications such as beta blockers
or calcium channel blockers, the
dose may be cautiously increased.
However, if symptoms persist or
occur at rest, the individual should
descend (Chapter 25: Altitude and
Common Medical Conditions).
Individuals with mild angina
may take part safely in mildly
strenuous outdoor activities if they
follow their physician’s
instructions, do not overexert, and
carry nitroglycerine tablets to
relieve episodes of pain. Their low
risk for catastrophic cardiac events
must be established by a physician.
They should be able to carry out
moderately strenuous, continuous
exercise, such as hill walking for
several hours a day with minimal or
no symptoms. Trips to remote areas
far from medical facilities or
prompt evacuation are not
advisable.
Individuals who develop angina
for the first time, or who experience
unusually frequent or severe attacks
of angina, should lie down,
completely at rest, and should take
nitroglycerine if available. Because
an initial episode of angina may not
be clearly distinguishable from an
infarct, they should be given an
adult aspirin, preferably a
chewable tablet, but any form
suffices. Absolute rest should be
continued for at least six to eight
hours—longer if the anginal
episodes persist—after which the
person should be evacuated with as
little exertion as possible,
transported if that can be obtained.
Angina at rest is an indication of
severe heart disease and often is a
prelude to a more serious event,
such as an infarct.
Myocardial Infarction
Myocardial infarction may occur
in someone who has had angina, or
it may occur in an individual who
has never had chest pain. It is
caused by obstruction of one of the
arteries to the heart—the coronary
arteries—usually by a blood clot
that forms on a ruptured cholesterol
plaque and results in death
(necrosis or infarction) of part of
the heart muscle. Among persons
with coronary artery disease, 50
percent are unaware that they have
the problem until they have a heart
attack.
Myocardial infarction is a
common cause of sudden death and
a major medical emergency. Chest
pain is the most common initial
symptom and may appear at rest or
during exercise. The pain resembles
angina pectoris but is usually more
severe, may last one to six hours,
and usually is not relieved by
nitroglycerine. Other frequent
symptoms and signs are nausea,
vomiting, difficulty in breathing,
weakness, sweating, pallor,
cyanosis, and cold extremities. The
blood pressure may be low; the
heart rate may be slow and
irregular. (Elderly individuals may
have an acute infarction with
minimal or no chest pain.)
The person should lie down at
once and rest completely. An adult
aspirin tablet should be chewed and
swallowed immediately.
Nitroglycerine should be tried,
although it usually is ineffective. If
the pain is not relieved in ten to
fifteen minutes, a strong analgesic
should be administered every two
hours until the pain is relieved. If
the individual is agitated, a sedative
should be given. If oxygen is
available, it should be administered
at a flow rate of four to six liters
per minute with a face mask. If the
person is short of breath, coughing,
and can breathe more easily sitting
up, sitting should be permitted,
preferably supported by a backrest.
(Administration of oxygen should
be continued.) Prompt evacuation,
preferably by helicopter, is
essential. A physician or advanced
emergency medical technician
should accompany the helicopter;
cardiac resuscitation may be
necessary at any moment.
Cardiac Dyspnea
Cardiac dyspnea is undue
shortness of breath caused by heart
disease and is indicative of heart
failure, inadequate blood flow to
the heart, or an abnormal rhythm.
Dyspnea occurs with exercise, but
sometimes develops at night. The
person awakens with a sense of
suffocation and feels compelled to
sit up or move out into fresh air to
obtain relief. The person is usually
anxious, is breathing fast, and has a
rapid heart rate. Crackles indicative
of fluid in the lungs may be heard
when listening to the chest.
Questioning usually discloses a
history of high blood pressure,
angina, a prior heart attack, or a
heart murmur. In the few individuals
who have no history of cardiac
disease, the heart failure may be the
result of an asymptomatic (silent)
myocardial infarction, a marked
rise in blood pressure, or
development of an abnormal
rhythm. Nitroglycerine may be
helpful, particularly if blood
pressure is high. Complete rest,
sedation, oxygen, and a diuretic are
the usual methods of treatment.
Individuals should be evacuated
after twelve to twenty-four hours of
rest with as little effort on their part
as possible. If the dyspnea is
severe, oxygen and a strong
analgesic should be given even
though no pain is present.
At high elevations, high-altitude
pulmonary edema should be
considered, particularly if the
individual has no history of heart
disease and has recently ascended
to that elevation (Chapter 25:
Conditions). If high-altitude
pulmonary edema is suspected, rest,
oxygen, and assisted descent to a
lower altitude are necessary.
Sudden Cardiac Death

Sudden cardiac death—
instantaneous or within a few
minutes of the onset of symptoms—
is very rare in well-conditioned
outdoor recreationalists who have
never had symptoms of heart
disease. The underlying cause in
most cases is arteriosclerotic
coronary artery disease, which may
not have been suspected by the
individual or the physician.
Individuals who have a family
history of sudden death, have high
blood pressure, smoke, have high
blood cholesterol concentrations or
diabetes mellitus, and have a
sedentary lifestyle are predisposed
to coronary artery disease.
Adherence to strict risk factor
modification is the only real
deterrent to sudden cardiac death.
Valvular Heart Disease

Many persons who have
deformities of heart valves that
cause heart murmurs are capable of
strenuous physical effort without
difficulty. However, with some
types of valvular heart disease,
such activities may produce
complications such as cardiac
failure, atrial fibrillation, or stroke.
Individuals with heart murmurs or
valvular heart disease should
consult physicians to determine
whether or not they should take part
in wilderness activities. Leaders of
an outing must be informed of that
person’s activity limits,
medications to be taken, and
complications that might be
expected.
Noncardiac Chest Pain

Chest pain in most individuals is
not a sign of heart disease. The
following are several common
types of chest pain not related to
heart disease:
Aching and soreness due to
muscular effort. After
unaccustomed physical work
involving the arms and
shoulders, such as climbing,
crosscountry skiing, carrying a
heavy pack, or cutting wood,
pain may be present in the upper
chest muscles for two to three
days. The ache is usually
constant and may be aggravated
by motion, and the muscles may
be tender. Aspirin or
acetaminophen, codeine, and
rest are effective treatment.
Reassurance should be
provided.
Chest discomfort due to anxiety.
Nervous, anxious, or fearful
individuals may notice a
sensation of pressure in the
chest that is associated with a
sense of suffocation, trembling,
dizziness, and occasionally
numbness of the lips and fingers.
The heart rate may be increased.
Reassurance, rest, and mild
sedation are usually the only
measures needed (see
“Hyperventilation Syndrome” in
Chapter 18: Respiratory
Disorders).
Chest pain attributable to the
chest wall, lungs, or lining of the
lungs and heart that is actually
pleuritic pain and worsens with
inspiration. Such pain is usually
related to inflammation and
responds to anti-inflammatory
agents such as acetaminophen,
aspirin, or ibuprofen. If pleuritic
chest pain is associated with
marked shortness of breath or
coughing up blood, a much more
serious disorder such as
pneumonia or pulmonary
embolus (blood clots carried to
the lungs) should be suspected
and should prompt rapid
evacuation.
Heartburn. This discomfort
typically originates below the
breastbone and may extend to
the throat. It is more common
after large, fatty meals, excess
coffee or alcohol, and when
lying down, in which case
antacids usually provide prompt
relief. Heartburn may be
difficult to differentiate from
angina pectoris. Persons in
whom heartburn does not
respond to antacids should be
queried and examined for other
signs and symptoms of angina
(Chapter 19: Gastrointestinal
Disorders).
DISORDERS OF CARDIAC
RHYTHM
Cardiac rhythm can change in a
number of ways. Speeding up with
exercise or slowing with rest are
normal. Some changes are of minor
significance; others are more
serious (Fig. 17-2). Ventricular
fibrillation is lethal if not halted in
minutes.
Paroxysmal Supraventricular
Tachycardia
Paroxysmal supraventricular
tachycardia (PSVT) is
characterized by a very rapid but
regular heart rate, sudden in onset,
that is associated with a sensation
of pounding in the chest, weakness,
dizziness, and shortness of breath.
True syncope (unconsciousness) is
rare. The heart rate is very rapid
(150 to 220 or more per minute)
and completely regular. The pulses
may be so weak that listening to the
heart with a stethoscope is
necessary to determine the rate.
(When beating so rapidly, the heart
does not have time to fill between
contractions and the amount of
blood pumped with each heartbeat
decreases.) Individuals may have
previously experienced similar
attacks.
Figure 17-2. Diagrammatic
comparison of normal and abnormal
cardiac rhythms (Note: Interval ab =
interval bc)
Most episodes of PSVT resolve

spontaneously. The individual
should rest until the episode has
ended. If the episode persists
beyond a few minutes, a few simple
maneuvers to halt the episode may
be attempted. All these maneuvers
should be performed with the
person sitting or lying down. The
Valsalva maneuver—bearing down
as if straining to have a bowel
movement—may break the rhythm.
Similarly, gagging by inserting a
tongue blade to the back of the
throat may stop the rhythm.
Immersion of the hand in ice water
to the point of pain occasionally
works. The face can be immersed in
ice water or cooled with a wash
cloth wet with icy water. If these
maneuvers fail, massage of the right
carotid artery, gently at first and
then more firmly if needed may
resolve the tachycardia.
If the individual has lost
consciousness, a more serious form
of tachycardia, such as ventricular
tachycardia (a fast rhythm from the
lower chambers), is implicated.
Unconsciousness should prompt a
sharp blow or karate chop
delivered to the midpoint of the
sternum (precordial thump).
PSVT has a tendency to recur. It
is rarely life threatening and does
not imply other cardiovascular
problems such as coronary artery
disease. An episode that has been
prolonged, has been difficult to
control, or is associated with
significant chest discomfort, may
prompt evacuation.
Atrial Fibrillation
Atrial fibrillation (AF) is a
rapid but irregular heartbeat. The
heart rate may be 100 to 180 per
minute, and the onset may be sudden
and resemble PSVT. The important
difference is the totally irregular
rhythm of atrial fibrillation. Careful
palpation of the pulse and listening
to the heart may be necessary to be
sure of the irregularity. At rates
exceeding 160 beats per minute,
irregularities are difficult to detect.
Rest should be instituted. Seventy
percent of all episodes of atrial
fibrillation resolve spontaneously
within twenty-four hours. The
symptoms associated with atrial
fibrillation are essentially the same
as those of PSVT. Maneuvers that
stop PSVT may not be of value for
atrial fibrillation. If the attack does
not respond to rest and sedation
within twelve to twenty-four hours,
the individual should be evacuated.
Unlike PSVT, atrial fibrillation is
more often associated with other
more significant heart disease such
as heart failure, coronary disease,
valvular disease, or pulmonary
embolus.
Heart Rhythm Medications

Therapy for PSVT and AF in the
wilderness should include rest,
hydration, and heart rate control
with medications. The most
effective drugs for rate control are
beta blockers such as metoprolol,
atenolol, or propanolol, although
these should not be given to
individuals with asthma or chronic
lung disease. Doses should be
started low and gradually increased
at six- to eight-hour intervals to
achieve a resting heart rate of under
100 beats per minute.
Syncope (Fainting)
Syncope is a transient loss of
consciousness commonly referred
to as fainting or “passing out.” Two
general varieties are encountered:
True syncope is complete loss of
consciousness. The individual falls
down, cannot be aroused, and may
display seizure activity. The
duration may be seconds or
minutes.
Partial syncope is a condition
with which the person feels weak
or faint and slumps to a chair, bed,
or floor, but consciousness and
communication are maintained.
After a few minutes the person
recovers but remains weak and
unsteady for several minutes.
True syncope is present in only
10 to 20 percent of the individuals
referred to physicians with that
diagnosis. Partial or near syncope
makes up the rest. True syncope is a
serious symptom, particularly if it
has occurred more than once and
without warning and should be
investigated in a hospital where
sophisticated diagnostic studies can
be performed. Many serious
conditions, including brain tumors,
heart tumors, and cardiac
arrhythmias, may cause true
syncope.
Most instances of partial
syncope—and some cases of true
syncope—are postural or vasovagal
and situational in origin. Common
provocations are a crowded,
overheated room, the sight of blood,
recent arrival at high altitude,
dehydration, a large meal, or
prolonged standing. In rare
instances, partial syncope may
occur during or immediately after
heavy exertion without adequately
cooling down.
An individual with vasovagal
syncope typically becomes pale,
sweaty, nauseated, weak, and
anxious. The pulse is usually slow
and regular but may be weak. A
history of similar episodes may be
obtained.
Partial syncope can be avoided
by having the person lie down with
legs elevated. The person must
remain supine until the episode has
completely resolved. Fresh air and
a cold, wet towel for the face
usually aid recovery. If the
individual has no history of cardiac
disease or episodes of true
syncope, hospitalization is not
necessary. Precautions to prevent
subsequent episodes should be
observed.
Partial syncope may occur as a
result of postural (orthostatic)
hypotension (a fall in blood
pressure upon assuming an erect
posture). The individual
experiences faintness upon standing
after a prolonged period of lying
down or sitting, such as upon
arising in the morning or after a
large meal, particularly when
alcoholic beverages have been
consumed. Postural hypotension is a
common problem in persons who
are receiving drug therapy for high
blood pressure or coronary artery
disease, particularly if the person is
dehydrated. Reassurance and a
decrease in the medication dose are
usually the only necessary
measures.
Individuals more than sixty years
old have a higher incidence of true
syncope resulting from cardiac
disease and are less likely to have
benign, vasodepressor syncopal
attacks. Such persons also are more
susceptible to postural hypotension,
particularly if medications for
hypertension are being taken.
Cardiac Syncope
Cardiac syncope, usually a form
of true syncope, is loss of
consciousness caused by heart
disease. Two forms are recognized:
exertional and arrhythmic.
Exertional syncope occurs during a
burst of heavy effort such as
walking fast uphill.
Unconsciousness may occur
suddenly or may be preceded by a
“graying out” sensation, severe
dizziness, or weakness. Convulsive
movements may occur. Exertional
syncope most frequently occurs in
individuals with aortic stenosis
(narrowing of the outlet valve from
the left ventricle), implies severe
aortic valvular disease, and should
prompt evacuation. Most affected
individuals have a history of
similar episodes.
Arrhythmic syncope occurs as
the result of an abnormal cardiac
rhythm, either a sudden increase in
heart rate (tachycardia) or a marked
slowing or temporary cessation of
the heartbeat (heart block). The
episode may occur suddenly,
without warning, and the person
may fall and be injured.
The blood pressure should be
measured, the heart rate should be
determined, and the rhythm should
be evaluated. The individual should
rest, with sedation if needed, for six
to twelve hours and then be
evacuated to a physician’s care.
Cardiac syncope may be an early
warning of heart disease that can
cause sudden death.
MINOR DISTURBANCES OF
CARDIAC RHYTHM
Sinus Tachycardia
Anxious individuals, after heavy
exertion or at high altitude, may
become aware of a rapid, forceful
heartbeat pounding in the chest and
fear they have heart disease. If the
heart rate does not exceed
120 beats per minute and
gradually slows with rest, a
diagnosis of harmless sinus
tachycardia may be made. No
specific treatment except rest,
hydration, and reassurance is
necessary.
Extrasystoles (“Skipped Beats”)

Normal individuals may notice
occasional irregular thumping
sensations in their chests,
particularly at rest or during the
night. They may feel their pulse and
notice occasional pauses between
beats. Such irregular beats are
called extrasystoles and are of no
significance unless the person
clearly has heart disease manifested
by angina, myocardial infarction, or
cardiac dyspnea. Rest and
reassurance are usually the only
measures needed. Avoiding
stimulants such as coffee and tea or
tobacco often entirely eliminates the
extrasystoles. Sometimes the
number of extrasystoles an
individual experiences is increased
at altitude (Chapter 25: Altitude and
If a bothersome irregularity of
the heartbeat persists, or if such
irregularities have never been
experienced before, evacuation to a
physician’s care may be desirable.
DEVICES FOR HEART

RHYTHM MANAGEMENT
Implanted devices for the
management of cardiac rhythm
disturbances include pacemakers
and defibrillators. The indications
for these devices and their
utilization are steadily increasing.
Some backcountry adventurers are
likely to have one of these devices.
Pacemakers are generally implanted
for abnormally slow rhythms or
heart failure. Defibrillators (or
ICDs: implantable cardioverter-
defibrillators) are implanted to
shock the heart out of more
malignant fast rhythms from the
lower chambers (ventricles) of the
heart. Both types of devices are
typically located beneath the
collarbone, usually on the left side.
Pacemakers usually are smaller,
about the size of a silver dollar.
Defibrillators, because they have
higher energy needs, are larger,
about two-thirds the size of an iPod
Nano®. The presence of a
defibrillator implies the individual
has much more serious structural
heart disease. Any person with one
of these devices should have the
device thoroughly interrogated in a
physician’s office prior to departure
to ensure appropriate settings and
function.
HIGH BLOOD PRESSURE
(HYPERTENSION)
Thirty percent of adult Americans
have high blood pressure. Many
individuals with high blood
pressure pursue wilderness
activities. For such individuals to
be safe, the following guidelines
should be observed:
Persons with mild or drug-
controlled hypertension should
partake in wilderness activities
only after consulting a
sympathetic physician
knowledgeable about
wilderness environments. On an
outing, such individuals must
supply their own medications
and follow their physician’s
recommendations carefully.
Fluid intake should be adequate,
and they should maintain a diet
modest in sodium.
Individuals with severe,
uncontrolled hypertension or
complications of hypertension
should not venture into remote
wilderness areas. The
complications of uncontrolled
hypertension—strokes, heart
failure, coronary artery disease,
decreased visual acuity, and
kidney failure—could be
disastrous in such situations.
Individuals with moderately high
blood pressure are at higher risk for
heart attack and heart failure. These
complications include cardiac
dyspnea, angina pectoris, stroke,
and severe headache, any of which
is an indication for prompt
evacuation.
Some persons with only
moderate hypertension have
periodic episodes of severe blood
pressure elevation. Such episodes
are typically associated with severe
headache, confusion, forgetfulness,
visual impairment, slurred speech,
and other neurologic signs and
symptoms. The blood pressure
should be measured if such
symptoms appear. If the systolic
pressure exceeds 200 mm Hg, the
individual should be forced to rest
and nitroglycerine should be given
every hour to reduce the pressure.
Evacuation should be arranged after
six to twelve hours.
Some hypertensive persons
experience an increase in pressure
at high altitudes. The rise in
pressure, which usually is not
detectable unless the blood
pressure is measured, is usually
evident within one to two days at
altitudes at and above 6000 feet
(1800 m). It typically returns to its
previous level in a few days
(Chapter 25: Altitude and Common
Medical Conditions). Individuals
who have a major rise in pressure
at such moderate altitudes should
consult their physicians, who may
increase medication dosage when at
high altitudes or may advise not
going to high elevations at all.
Individuals taking certain types
of medication for high blood
pressure (such as propranolol, a
beta blocker) may not experience
the normal increase in heart rate at
high altitude. Some develop
orthostatic hypotension. Individuals
on a diuretic must continue to take
potassium supplements if
recommended by their physicians.
Diuretic-induced potassium
depletion can result in muscular
weakness but is relieved by
potassium-rich foods such as dried
fruits, nuts, soups, and fruit juices.
VASCULAR DISEASE
Claudication
Older individuals with
arteriosclerosis of the arteries in
their legs may experience pain or
burning in their calves, hips,
buttocks, or thighs while walking
uphill, particularly when carrying a
heavy load. The pain occurs during
effort, becomes more severe as
effort is continued, and is relieved
by rest. The medical term for this
condition is claudication. When
severe, it can appear while strolling
on level terrain.
Claudication should be
distinguished from common leg
cramps, which occur at rest or
during the night, are characterized
by painful contraction of the
muscles—not just pain—and
usually involve the calf or foot.
If claudication is mild, a slower
pace and a lighter load may permit
the individual to continue. Smoking
increases the severity of
claudication and should be avoided.
If claudication suddenly becomes
severe or appears for the first time
in the wilderness, the person should
be evacuated and allowed to exert
only minimal effort.
Varicose Veins
The veins of the extremities have
numerous small valves within them
to ensure that blood flows only in
the direction of the heart. The blood
pressure in veins is so low that the
increase in intrathoracic or
intraabdominal pressure associated
with straining or strenuous exercise
would reverse the direction of the
venous blood flow if these valves
were not present.
In some individuals the valves in
the leg veins become incompetent,
the direction of blood flow is no
longer controlled, and the veins
become dilated and tortuous
(varicose). The return of venous
blood from the limb to the heart
may be impaired, causing persons
with varicose veins to complain of
aching in their legs, particularly
after they have been on their feet for
a prolonged period.
The greatest significance of
varicose veins in the wilderness
lies in the tendency for this disorder
to increase fatigability of the legs
and limit endurance. A second
problem is the greater tendency for
veins in the legs to thrombose as the
result of stasis associated with the
reduced venous blood flow typical
of varicose veins. A less common
problem is caused by the presence
of greatly enlarged blood vessels
just beneath the skin. Minor injuries
that ordinarily would go unnoticed
can penetrate one of these veins and
produce relatively severe bleeding.
Although the hemorrhage can be
easily controlled, a person with
varicose veins should be aware of
this danger.
In the wilderness, persons with
painful varicose veins should be
encouraged to elevate their legs on
pillows or a soft pad during rest
stops to decrease the pressure
within the veins. The pillow must
not be placed immediately behind
the knee where it would compress
the veins and reduce circulation.
Relief may be obtained with a
smooth elastic bandage or elastic
stocking, which should be applied
when the person is lying supine and
the veins are collapsed. (The
bandages or stockings should be
removed at night.) A hard knot or
cord that is inflamed and tender
indicates that the blood in one or
more of the enlarged veins has
clotted. Thrombosis of such
superficial veins is rarely a
problem except for the discomfort.
However, swelling of the foot or
leg beyond the area where clotting
has occurred is indicative of
associated clotting of the deeper
veins. Redness, swelling, and
tenderness in the calf may be an
indication of thrombophlebitis with
its risk of clotting and embolism. To
avoid pulmonary embolism, the
individual should be treated as
described in Chapter 18:
Respiratory Disorders.
Individuals with varicose veins
should consult a physician about
proper management of their
condition.
HEART HEALTH AND

PHYSICAL ACTIVITY IN THE
WILDERNESS
The common denominator of
outdoor ventures is physical
activity, which increases the need
for blood, oxygen, and nutrients in
the muscles. The resulting demands
placed on the heart and circulation
may precipitate cardiovascular
emergencies such as angina or an
infarct, rhythm disturbance, or heart
failure, particularly in a hostile
environment such as altitude or cold
weather.
Matching individual capacities
with the characteristics of a
proposed wilderness venture is
useful. One such classification
divides ventures into four levels
according to the physiologic
demands:
Extreme-performance ventures,
such as highaltitude Himalayan
climbing
High-performance ventures, such
as hunting in the Rocky
Mountains
Recreational activities, such as
trail walking in national parks
Therapeutic activities, such as
the highly individualized
components of cardiac
rehabilitation The health status
of participants can be matched
with the nature of the venture.
The following is one such
classification:
Demonstrated high-performance
individuals
Healthy vigorous individuals
Healthy “deconditioned”
individuals
Persons at risk for the
occurrence of disease
Individuals who are manifestly
ill An experienced physician in
cooperation with the venture
leader may estimate the degree
of risk for each individual.
Safety cannot be guaranteed, of
course, but a scheme of this type
may help match individuals with
an appropriate venture and
develop a smoothly functioning
team.
CHAPTER 18
RESPIRATORY DISORDERS
Colin K. Grissom, M.D.
The respiratory system moves air in

and out of the lungs to provide
oxygen for the body and to
eliminate carbon dioxide (Fig. 9-1).
The components of this system are:
The upper respiratory tract
includes the nose, mouth, and
larynx (vocal cords and voice
box). On inspiration, air moves
through the upper respiratory
tract and is filtered to remove
foreign particles, saturated with
water, and warmed to body
temperature.
The lower respiratory tract
starts with the trachea just
below the larynx and includes
the divisions of the airways
down to the alveoli, or
microscopic air sacs, that make
up the major portion of the lung
tissue, and in which oxygen and
carbon dioxide are exchanged
between blood and air. The
trachea descends into the chest
and divides into the right and
left bronchi that supply each
lung. The bronchi then
repeatedly subdivide in each
lung until, after some twenty-
three divisions, the alveoli are
reached. In the alveoli only a
very thin membrane separates
air in the sacs and blood in
pulmonary capillaries.
The bellows: During inspiration
the diaphragm contracts and
lowers, causing the chest wall to
expand, which moves air into
the lungs. During exercise,
muscles of the neck and muscles
between the ribs may also assist
with expanding the chest.
Expiration, or movement of air
out of the lungs, occurs
passively at rest as the
diaphragm and chest wall relax.
During heavy exercise,
contraction of the abdominal
muscles may assist with
expiration by forcing air out of
the lungs. A thin membrane—the
pleura—covers the lungs, lines
the inner surface of the chest
wall, and eases the movement of
the lungs within the chest.
The control system: Sensing
cells that detect chemical
changes in the circulating blood
(chemoreceptors), detect
movements of the chest wall,
diaphragm, and lungs
(neuroreceptors); and the
network of nerves that carries
information from these receptors
to the brain, which controls the
rate and depth of respiration.
Respiratory movements are
controlled by a complex system of
receptors, transmitters, and
effectors throughout the body.
Chemical receptors respond to
lower oxygen, an increase or
decrease of carbon dioxide, and a
change in the acidity of the blood.
These receptors signal the brain to
increase or decrease the rate and
depth of breathing (ventilation). The
carotid bodies are a set of special
receptor cells in the neck. Other
receptor cells are situated deep
within the respiratory center of the
brain and respond to changes in the
blood circulating through the brain
and in the spinal fluid that bathes
the brain.
Under ordinary resting
conditions, approximately 0.5 liter
of air is inspired with each breath.
The normal respiratory rate is ten to
twelve breaths per minute, and the
corresponding normal breathing
volume—the tidal volume—is five
to six liters per minute. Vital
capacity is the total volume of air
that can be forcefully exhaled after
inhaling as deeply as possible. The
volume of air expired in the first
second is the forced expiratory
volume in one second. These three
measures are commonly used to
describe lung function. The residual
volume is air in the lungs that
cannot be exhaled even after a full
forceful expiration.
Sleep causes a decrease in the
rate and depth of breathing—
hypoventilation—that may result in
a decreased blood oxygenation,
particularly at high altitude. In
contrast, exertion greatly increases
ventilation because it increases the
need for oxygen and the need for
eliminating carbon dioxide. These
demands stimulate the respiratory
center in the brain to increase the
respiratory volume to as much as
150 liters per minute during
vigorous exercise. Even at rapid
respiratory rates, the lungs supply
oxygen to the blood and take up
carbon dioxide with extraordinary
efficiency and precision.
A variety of disorders can affect
the function of the respiratory
system. Head injuries or diseases of
the brain may increase or decrease
breathing. Airway obstruction can
result from aspirated material or
from injuries to the throat, usually
sudden, and may halt effective
breathing. Injury of the chest wall
producing rib fractures or open
wounds can impair the bellows
action of the chest wall and
diaphragm. Even chest wall injuries
without rib fractures can cause pain
with inspiration that leads to
splinting—not expanding the chest
as much on the injured side. Air,
blood, or fluid within the chest
cavity may compress the lungs and
prevent expansion during
inspiration. An injury that damages
the lung in such a way that inhaled
air continuously leaks into the space
between the lung and chest wall but
cannot be exhaled (tension
pneumothorax) is life threatening.
Collections of fluid in the alveoli
due to edema or infection can block
the exchange of gases between
inhaled air and blood.
Injury to the brain resulting in
swelling or bleeding may depress
the respiratory control system and
cause hypoventilation. Sedative or
analgesic drugs may also depress
the respiratory control system and
cause hypoventilation. In contrast,
hyperventilation, an increase in the
depth and rate of breathing, may
occur in response to increased acid
in the blood caused by kidney
disease, uncontrolled diabetes,
shock, or ingested toxic chemical
agents or drugs.
SYMPTOMS
The principal symptoms produced
by diseases of the lungs are
shortness of breath or air hunger,
cough, pain, and fever. Each must
be considered in order to diagnose
the disorder that has caused all of
them.
Shortness of Breath
How and when did it begin?
How is it affected by position?
What makes it worse—or
better?
Cough
Is the cough dry or productive
(sputum is coughed up)?
What kind of material is coughed
up?
Does it contain blood, pus, or
foreign material?
Pain
Where is the pain?
Did it begin suddenly or
gradually?
Is the pain mild or severe?
What makes it worse?
Is the pain stabbing, sharp, dull,
or crushing?
Is the pain constant or
intermittent?
How is the pain related to
breathing?
How is the pain related to other
symptoms?
Fever
How high is the temperature?
Did it rise suddenly or
gradually?
Have chills or sweating
occurred?
Many illnesses or injuries cause
shortness of breath. At altitudes
above 8000 feet (2400 m),
shortness of breath with cough may
indicate early high-altitude
pulmonary edema (HAPE). Since
HAPE may progress rapidly to a
life-threatening problem, early
detection is important.
Altitude bronchitis—a
persistent, dry, hacking cough—is
common at high altitude due to
drying and irritation of the throat.
This inflammation of the breathing
tubes is not due to infection but
rather to breathing dry air. Cough at
altitude, however, may also indicate
lung disease or the presence of fluid
in the lungs. Usually such fluid is
reabsorbed, but it may develop into
HAPE. The sputum is usually thin,
watery, and pink or bloody with
HAPE (Chapter 24: Disorders
Caused by Altitude). The cough due
to infections of the lung is deeper
and usually produces sputum that is
green, yellow, or rust colored and
thick and stringy. With pulmonary
embolism, the sputum is usually
bloody.
Pleuritic chest pain is caused by
diseases of the lung associated with
inflammation of the pleura, or
injuries of the chest wall, and
characteristically changes with
respiratory movements. Deep
inspiration typically causes sharp,
stabbing pain. Pain that is dull or
crushing and constant is more
typical of heart disease (Chapter
Disorders).
Even though the problem appears to
be in the lungs, a full physical exam
should be performed. A rapid, hard
pulse associated with fever is
indicative of significant disease.
Fever is usually a sign of infection
but may occur with pulmonary
embolism or HAPE. Serious
infection anywhere in the body
causes fever, rapid pulse, and
shortness of breath.
The first step in examining the
chest is careful observation.
Breathing difficulty, irregularities
of respiratory rhythm, and
differences in movement of the two
sides of the chest are important.
Obvious signs include rapid or
labored breathing; shallow,
irregular, or noisy breathing; and
cyanosis (bluish discoloration) of
the lips, nails, or skin. Flaring of
the nostrils and tensing of the neck
muscles are signs of severe
respiratory difficulty. Efforts to
breathe that do not move the chest
indicate upper airway obstruction.
The respiratory rhythm should be
observed while counting the rate.
Minor changes of rhythm are of no
significance; important
irregularities are hard to overlook.
In contrast, differences in the
movements of the two sides of the
chest may be subtle and should be
sought during quiet respiration as
well as during deep breathing.
Auscultation consists of listening
to the sounds made by air passing in
and out of the lung. A stethoscope
makes the sounds easier to hear and
is more convenient, but the sounds
can be heard by pressing the
unaided ear against the bare chest.
Clothing must be removed so
important sounds and signs are not
missed.
Quiet breathing by normal lungs
produces sounds so faint that they
are barely audible except with a
stethoscope. The person being
examined must be instructed to
breathe deeply through the mouth
during the examination to amplify
these sounds. All portions of the
lungs should be examined to be sure
no abnormalities are missed and the
extent of the diseased area is
recognized.
Many diseases of the lung cause
fluid to collect in the small bronchi
and alveoli, producing crackling
sounds on inspiration. Fluid
accumulation is typical of infection
or edema of the lungs. Wheezing, a
high-pitched sound heard on
expiration, is more indicative of
asthma or chronic lung disease due
to cigarette smoking (chronic
bronchitis or emphysema). With
severe pneumonia or pulmonary
embolism a portion of the lung is
often consolidated or airless due to
fluid and inflammatory exudate in
the alveolar sacs. Over these areas,
the breath sounds are harsher and
louder because consolidated lung
transmits breath sounds from the
bronchial tubes much more
effectively than air in a normal lung.
These bronchial breath sounds are
similar to the sounds, but
differentiated from, those heard
directly over the trachea.
Infection or an embolus often
produces inflammation of the pleura
overlying the involved lung, which
makes the pleural surface rough.
Since the pleural surfaces no longer
slide smoothly over each other,
movement of the lung during
respiration produces a squeaking
sound like two pieces of leather
being rubbed together. This sound is
called a friction rub or simply a
rub. Pain with a rub means pleurisy
but does not define its cause.
If no sounds whatever are heard
over a portion of the chest, fluid or
air is usually in the space between
the lung and the chest wall. Rarely,
the absence of breath sounds may
be due to obstruction of a large
airway leading to that portion of the
lung.
Auscultation of the lung,
although it requires practice and
experience, is not too difficult to
learn and can be a valuable
diagnostic aid, particularly in a
remote wilderness situation.
CHRONIC LUNG DISEASE

The most common forms of chronic
lung disease are asthma, chronic
bronchitis, and emphysema. All
these are obstructive disorders
characterized by increased
resistance to airflow.
Chronic bronchitis and
emphysema are often associated
with cigarette smoking. Chronic
bronchitis is characterized by a
chronic productive cough due to
irritation of the airways.
Emphysema, which is characterized
by progressive destruction of lung
tissue, results in loss of alveoli for
exchange of oxygen and carbon
dioxide. Asthma may occur in both
younger and older persons and is
characterized by intermittent
episodes of increased airway
obstruction clinically apparent as
coughing, wheezing, and decreased
exercise capacity. Cold air,
exercise, or allergens in the
environment may trigger asthma.
(The treatment for acute episodes of
asthma is described later in this
chapter.) The first sign of chronic
obstructive pulmonary disease
(COPD) is a decreased forced
expiratory volume in one second.
Another type of chronic lung
disease is that caused by fibrosis or
scarring. This form of lung disease
is characterized by a decreased
forced vital capacity.
Most individuals with severe
chronic lung disease do not venture
into the wilderness. Individuals
with mild or moderate lung disease,
however, may pursue such
activities, and respiratory
symptoms may occur during
exertion or at altitude because
chronic lung disease reduces the
extra breathing capacity that is
needed in these situations. In
addition, chronic lung disease
reduces the extra breathing capacity
that may be required when the body
is stressed by infection, trauma, or
shock. Persons who know they have
impaired respiratory reserve should
be cautious about ascending to
altitude, particularly about
exercising at high altitude, and
should seek the advice of a
physician before wilderness trips
Medical Conditions).
DISORDERS OF BREATHING
RHYTHM
Sleep Periodic Breathing at High
Altitude
Sleep periodic breathing is
almost universal at altitudes above
13,100 feet (4000 m) and may
occur at moderate altitudes above
6600 feet (2000 m). The typical
pattern begins with a few shallow
breaths; increases in depth to very
deep, sighing respirations; and then
falls off rapidly (Fig. 18-1).
Respirations can cease entirely for
five seconds or more before
shallow breaths resume and the
pattern is repeated and can lead an
observer to fear that the person is
not breathing at all.
During the period when
breathing has stopped, the person
often becomes restless and
sometimes awakens with a sense of
suffocation. Acetazolamide
eliminates sleep periodic breathing
at high altitude because it acts as a
respiratory stimulant. Most
sedatives worsen hypoventilation
during sleep at high altitude and
should be avoided.
Sleep periodic breathing is so
common at altitude that it should not
be considered abnormal. Periodic
breathing may be present on some
occasions and not on others.
However, it may be a sign of a
serious disorder if it occurs for the
first time during an illness or after
an injury, particularly a head injury.
Some persons have intermittent
upper airway obstruction during
sleep that may cause snoring and an
unpleasant morning headache and
lethargy at altitude. This problem is
called obstructive sleep apnea and
is not relieved by acetazolamide.
Another form of irregular breathing
during sleep is central sleep apnea.
Some defect in the respiratory
control center in the brain causes
alarming periods of absent
breathing, followed by increasing
respiration that rises to a peak and
then decreases. This disorder
resembles periodic breathing but
occurs at any altitude and is not
relieved by acetazolamide (Chapter
25: Altitude and Common Medical
Conditions).
Hyperventilation Syndrome
Hyperventilation (overbreathing)
is common. The person begins to
breathe more rapidly and deeply
than is appropriate and appears to
be suffering from serious disease.
However, this syndrome is almost
entirely psychosomatic in origin.
Individuals who hyperventilate tend
to be nervous, tense, and
apprehensive, although the disorder
can occur in apparently stable
persons. Among beginners,
apprehension about hazards or fear
of exposure might initiate this
reaction. Knowledge of the
person’s emotional status,
particularly unusual anxiety, helps
establish the diagnosis.
Figure 18-1. Actual tracings of

periodic respirations: A, increasing
and decreasing depth of respirations;
B, two to three deep inspirations
followed by total cessation of
respiration for about twelve seconds
When a person breathes too

rapidly and deeply for more than a
short time, an abnormally large
amount of carbon dioxide is
exhaled, altering the acid-base
balance and increasing the
alkalinity of the blood, which
produces the characteristic
symptoms of numbness or tingling
around the mouth and in the fingers.
Other associated signs and
symptoms include a rapid pulse,
dizziness, faintness, sweating, and
apprehension. The person often
complains that “the air doesn’t go
down far enough” and breathes in
gasps or takes frequent deep sighs.
If hyperventilation persists, these
symptoms increase to painful
cramps or spasms of the fingers,
hands, and forearms, which are
particularly frightening to the
person.
Even though the hyperventilation
syndrome is suspected, the
individual should be examined to
ensure no other problem is present.
If not, reassurance and explanation
are usually enough to reverse the
disorder. The person should be
instructed to deliberately slow the
rate of breathing. If this is not
effective, a tranquilizer may be
necessary. Once recovered, the
individual may feel weak and shaky
and have a headache. A treatment
that has been recommended in the
past is breathing into a paper bag.
Currently this is not recommended,
however, because it may cause
dangerously low blood oxygen
levels at high altitude or because an
unrecognized lung problem actually
may be present at any altitude.
INFECTIOUS DISORDERS
Tracheitis
The trachea is the large airway
leading from the throat to the
middle of the chest, where it
divides into the two main bronchi.
This structure sometimes becomes
inflamed and occasionally infected.
Usually the pain is in the throat
below the tonsils or beneath the
sternum and becomes worse with
breathing. Coughing may cause pain
in the same area and may produce
thick sputum. The treatment for
tracheitis is the same as for
bronchitis.
Bronchitis
Bronchitis, or more properly
tracheobronchitis, is an infection of
the major air passages to the lungs.
Such infections are rarely disabling
but occasionally progress to
pneumonia. This disease frequently
comes on during or after a cold, and
may be called a “chest cold.”
The predominant symptom of
bronchitis is a persistent irritating
cough that may be dry but frequently
becomes productive after one or
two days. The sputum may be green
or yellow. Slight pain may be
associated with the coughing and
easy fatigability may be present,
particularly at high altitudes.
However, the person does not
usually appear severely ill and has
only a slight fever or none at all. If
the infection involves the larynx
(voice box), the individual may be
hoarse (laryngitis). A few wheezes
and crackles may be heard
throughout the chest, but these tend
to disappear with coughing.
The treatment for tracheitis or
bronchitis begins with adequate
hydration. The person should drink
lots of warm fluids, such as soups,
and if possible should inhale steam
from a boiling kettle or pot to
moisten the airways and loosen or
liquefy the material in the bronchi
so it can be coughed up more easily.
Rest, warmth, and nonsteroidal
anti-inflammatory drugs are helpful.
If the condition persists for more
than two or three days, descent to a
lower altitude may be necessary.
Viruses cause bronchitis more often
than bacteria, and antibiotics are
not useful for treatment.
Increasing evidence suggests that
even a mild upper respiratory
infection increases the risk of
HAPE.
Pleurisy
Pleurisy is pain that is worsened
by inspiration and is caused by
inflammation of the thin membranes
that cover the lungs and the inner
surface of the chest wall. Pleurisy
may occur with pneumonia, injury
to the chest wall, collapse of the
lung (pneumothorax), or pulmonary
embolism. The principal symptom
is pain with respiration. The pain
usually is sharp and stabbing and
limited to an area on one side of the
chest. Deep inspiration may elicit a
particularly severe twinge. Pleurisy
may be particularly uncomfortable
and painful at altitude where
respirations are more rapid and
deeper than at sea level.
Physical signs are mild or
absent. Motion of the affected side
may be limited, and a few wheezes
or crackles may be heard over the
involved area. Sometimes a
leathery, rough, rubbing sound can
be heard over the area where pain
is worst. This “friction rub” is
diagnostic of pleurisy but does not
indicate its cause. The person may
be more comfortable when lying on
the affected side, limiting the
motion of that part of the chest.
The treatment of pleurisy is
dictated by the underlying cause. If
the fever is high, the pulse rapid, or
the person seems quite sick,
pneumonia or embolism should be
suspected. Pneumonia requires
antibiotic treatment, and both
pneumonia and pulmonary
embolism dictate evacuation to a
lower altitude. Recent trauma to the
chest might suggest pneumothorax
or blood in the space between the
chest wall and lung (hemothorax) as
a cause of pleurisy. Persistent
pleuritic chest pain at extreme
altitude can be caused by rib
cartilages torn by persistent
coughing and can be disabling.
Pleurisy caused by moderate trauma
to the chest wall, such as bruised or
broken ribs without pneumothorax
or hemothorax, may be treated with
analgesics. Taping or splinting the
chest increases the risk of
pneumonia or collapse of part of the
lung and is not recommended.
Pneumonia
Pneumonia is an infection of the
lung tissue involving the alveoli and
is most commonly caused by
bacteria. Persons weakened by
fatigue, exposure, or disease
elsewhere in the body are
particularly susceptible. Infected
fluid accumulates in the alveoli, and
the exchange of carbon dioxide and
oxygen is impaired. If a large
amount of lung is involved, low
blood oxygen (hypoxia), combined
with effects of toxic substances
released from the bacteria, may
cause death. Pneumonia should
always be taken seriously.
Anyone with any type of
pneumonia is oxygen deficient
above 8000 feet (2400 m).
Supplemental oxygen should be
administered if available, and
individuals should be evacuated to
lower altitude as soon as possible.
The symptoms of pneumonia
vary with the causative organisms
and the severity of the infection.
Pneumonia usually causes fever
with an oral temperature of more
than 102°F (39°C) and rapid pulse
and respiratory rates. Bacterial
pneumonia often starts with one or
more shaking chills followed by
high fever. The individual looks
quite sick and may be very weak.
Cough is a prominent symptom. The
cough may be dry at first but usually
becomes productive after one or
two days. The sputum, which is
usually green or yellow, but
sometimes has a rusty color, is thick
and mucoid and frequently
resembles pus.
Some bacteria tend to localize in
a single segment of the lung that
becomes consolidated. The
physical signs are limited to that
area of the lung and include
crackles or increased transmission
of breath sounds on chest
auscultation. Inflammation of the
overlying pleura may occur and
cause pleuritic chest pain that, when
severe, feels like a stabbing pain
with each breath and may be an
early indication of underlying
pneumonia. Pleuritic chest pain is
more severe with deeper
inspiration, which may cause
reduced inspiration on the affected
side that may be visible as
asymmetric chest expansion
(splinting).
Streptococcus pneumoniae is a
common cause of lobar pneumonia,
which is limited to one or two
lobes of the lung. Other bacteria
that may cause pneumonia include
Haemophilus influenzae,
Staphylococcus aureus, and
Klebsiella pneumoniae. Less
common organisms (atypical
organisms) that may cause localized
or widespread pneumonia include
Mycoplasma pneumoniae,
Chlamydia pneumoniae, and
Legionella. Aspiration of gastric
contents into the lung can result in
pneumonia caused by a mixed
bacterial population. All forms of
pneumonia are treated with
antibiotics. Diagnosis of the
specific causative organism often is
not possible, even in a hospital
setting. Appropriate antibiotics that
treat most or all of these common
organisms are azithromycin and the
respiratory quinolones levofloxacin
and moxifloxacin.
Pneumonia caused by viruses or
fungi does occur and is not
effectively treated with commonly
used antibiotics.
Coccidioidomycosis is a fungal
pneumonia common in the
southwestern United States;
histoplasmosis is a fungal
pneumonia common in the
Mississippi River Valley.
Recovery from pneumonia
depends on the severity of the
infection and the organism. Rarely
can a person who has had
pneumonia resume strenuous
activity in less than two to three
weeks.
OTHER PULMONARY
DISORDERS
High-Altitude Pulmonary Edema
Although high-altitude
pulmonary edema (HAPE) was
clearly described ninety years ago,
only in the last forty years has it
been recognized as a major
problem in mountaineering. Prior to
1960 this disorder was usually
mistaken for pneumonia, and acute
pulmonary edema and pneumonia
do have similarities. This serious
problem can occur, and has been
lethal, as low as 8000 feet (2400
m). It is more fully described in
Chapter 24: Disorders Caused by
Altitude.
Asthma
Asthma is a disease of the
bronchi caused by allergy, exercise,
or breathing cold air. Inhaling the
substance to which the individual is
allergic (the allergen), or inhaling
dry or cold air that irritates the
cells lining the airway, increase the
secretion of mucus into the bronchi.
Simultaneously the muscles in the
walls of the bronchi go into spasm,
constricting these air passages. The
narrowed bronchi filled with
excess mucus obstruct the passage
of air.
Asthma may be mild, severe, or
—rarely—fatal. Although a first
attack may occur at any time, most
individuals are aware of their
susceptibility long before engaging
in wilderness activities.
Asthma is a recurring disease.
Most people with this problem have
suffered previous attacks and are
under the care of a physician who
can provide the medications that
should be taken on a trip.
Fortunately, individuals with mild
asthma are not particularly limited
in the wilderness activities in
which they can participate; some
may breathe more easily at high
altitude where the air is thinner and
freer of allergens and pollutants
Medical Conditions).
The most significant sign of
asthma is difficulty in breathing,
particularly during expiration. The
expiratory phase of respiration is
considerably prolonged, is
associated with wheezing, and may
require conscious effort.
An incessant, irritating cough is
often present. Toward the end of an
asthmatic attack, considerable
quantities of very thick mucus may
be coughed up. Fever is usually
absent, but the pulse rate may be
moderately increased. The
respiratory rate is usually faster
than normal in spite of the difficulty
in breathing. When the person is
examined, the chest may appear
more expanded than normal at the
end of expiration. Wheezing on
expiration is usually audible
throughout all parts of the lung.
The most important treatment for
an acute asthma exacerbation is an
albuterol inhaler. Albuterol
occupies beta-receptors in the
smooth muscle of the bronchi and
makes the bronchial walls relax. It
also helps loosen mucus in the
airways so that it can be coughed
up. The dose is two puffs
(inhalations) every four hours. Side
effects of albuterol inhalation may
include an increased heart rate and
tremor. Most persons with asthma
carry an inhaler with them. Steroid
inhalers also are very effective in
treating asthma on a continuing
basis. For moderate or severe acute
asthmatic exacerbations, steroids
are given orally or intravenously in
addition to inhaled albuterol.
At high altitude, asthma may
further limit the amount of oxygen in
the blood, and therefore
supplemental oxygen is helpful. At
sea level, supplemental oxygen is
usually not necessary for mild or
moderate asthma exacerbations.
On both short and extended trips
asthmatics should carry adequate
medications for treatment of an
exacerbation. Asthmatics ascending
to altitude should be conservative
in allowing adequate time for
acclimatization. Although some
asthmatics do better at altitude,
others may suffer exacerbations due
to the dry, cold air. In general,
asthmatics are not known to have an
increased risk for altitude illness,
but they may be more susceptible to
HAPE during an exacerbation.
Pneumothorax
Occasionally lung tissue may
rupture spontaneously, allowing air
to leak into the chest cavity.
Lacerations of the lung can also
occur with penetrating injuries or
with nonpenetrating injuries that
fracture and displace ribs. The lung
on the side of the air leak retracts
due to its inherent elasticity and
does not expand well during
inspiration. As a result, pulmonary
function is compromised. This
condition is known as
pneumothorax, meaning “air in the
chest.”
Figure 18-2. Pulmonary function with
a tension pneumothorax1
Rarely the tear in the lung

behaves like a valve, allowing air
to enter the pleural space but not
leave, which causes the pressure
within the space to build rapidly.
The pressure collapses the lung and
can shift the heart and its
surrounding structures (the
mediastinum) toward the opposite
side of the chest. If untreated, this
disorder, called “tension
pneumothorax” because the air is
under increased pressure, may
cause shock and result in death
(Fig. 18-2).
Pneumothorax should be
suspected when unexplained
shortness of breath appears
suddenly in an otherwise healthy,
active person—particularly in the
setting of trauma to the chest.
Sometimes the onset is associated
with sudden pain. The diagnosis is
confirmed when breath sounds
cannot be heard over the entire lung
on the affected side. A tension
pneumothorax should be suspected
when shortness of breath is severe
and the person is fighting for air.
Lips and fingernails are usually
purple (cyanotic). Sometimes the
trachea just above the sternum is
shifted to the side away from the
pneumothorax; the point where the
heart is felt may be shifted in the
same direction.
No treatment is needed unless a
tension pneumothorax develops.
Then the pressure must be relieved
by inserting a needle or tube into
that side of the chest, a simple
procedure that may be life saving,
but should be done only by a
physician except in desperate
circumstances. This procedure is
discussed in greater detail in
Chapter 9: Chest Injuries.
Individuals with a spontaneous
pneumothorax need to rest for a
week or longer until the “leak” in
the lung tissue has healed, as it
usually does. Increasing the
altitude, even passively as in an
aircraft, worsens the pneumothorax.
Descent improves it. Persons who
have had one episode of
spontaneous pneumothorax are
more vulnerable to others. They
may consider surgery to try to
eliminate the condition.
VENOUS THROMBOSIS AND

PULMONARY EMBOLISM
Blood clots in the veins of the legs
(or rarely the arms)—venous
thrombosis—are not uncommon and
may result in serious complications.
Blood clots in the large central
veins of the thigh and pelvis—deep
venous thrombosis—may break off
and travel through the heart to the
lungs, producing pulmonary
embolism. The clots (emboli)
obstruct the arteries in the lung
(pulmonary arteries) and reduce
blood flow through that organ,
which interferes with the exchange
of oxygen and carbon dioxide.
Extensive embolism or obstruction
of a major pulmonary artery, such
as the artery to an entire lung, can
be immediately fatal. Ascent to high
altitude increases the risk of venous
thrombosis and pulmonary
embolism.
An increased tendency of the
blood to clot (increased
coagulability) and slowing or even
cessation of blood flow in the veins
(stasis) favor the development of
venous thrombosis. Factors that
increase the coagulability or stasis
of blood are:
Dehydration, which causes the
blood to become thicker and
more viscous
An increase in the number of red
blood cells due to high altitude,
a normal mechanism of
acclimatization that also
increases the viscosity of blood
Prolonged immobility, such as
being stormbound for days in a
small tent, immobile and resting
in cramped awkward positions
Carrying heavy packs or
standing immobile for long
periods of time, which increase
stasis in the legs
Trauma to the pelvis or legs,
which increases the tendency for
clotting
Oral contraceptives that contain
estrogen cause a slight increase in
the incidence of venous thrombosis
and pulmonary embolism, although
the increase is far less than that
associated with pregnancy.
However, no evidence indicates
that these drugs increase the risk of
thrombosis and embolism at altitude
above the risk at sea level, at least
in nonsmokers. Smokers definitely
have an increased risk. Women
taking such drugs may wish to
consider replacing them with an
oral contraceptive that contains
only progesterone several months
before a climb to altitudes above
18,000 feet (5500 m).
Diagnosis of Venous Thrombosis

The most common symptom of
venous thrombosis is deep, aching
pain in the calf, inner side of the
thigh, or back of the knee. The pain
frequently comes on suddenly and is
aggravated by walking. When the
thrombosed vein is located in the
calf, the overlying muscles are
tender. Flexing the foot upward may
cause pain in the calf. Usually the
affected leg is swollen, which can
be detected by measuring the
circumference of both legs at
identical five-inch intervals from
the ankle to the upper thigh. A
difference in circumferences of 0.5
inch is common and of no
significance; greater differences are
cause for concern. A slight fever is
sometimes present and lasts an
average of seven to ten days. Blood
clots in the veins of the thighs or
pelvis may not cause obvious
symptoms but may break off and
travel to the lung causing pulmonary
embolism. Consequently, if a
person is in pulmonary distress and
other pulmonary disorders do not
appear to be present, pulmonary
embolism must be suspected even
though signs of venous thrombosis
are absent.
Diagnosis of Pulmonary Embolism

Pulmonary embolism is heralded
by the sudden onset of pain in the
chest. The respiratory and pulse
rates are usually increased, and a
slight fever is frequently present.
Later the pain becomes pleuritic
and is aggravated by respiration,
particularly deep breathing. A
cough often is present and may
produce bloody sputum. Signs of
consolidation (increased or absent
breath sounds and dullness to
percussion) may appear over the
involved area a day or so after
onset.
If the embolus obstructs a large
pulmonary artery, the initial
symptom may be the sudden onset
of a sense of suffocation rather than
pain. More severe shortness of
breath, cyanosis, distension of neck
veins, and signs of shock follow
shortly. Pleuritic pain, cough,
bloody sputum, and signs of
consolidation usually develop a
few hours later, although the pain of
pleural involvement may be absent
if the blood clot lodges in a central
part of the lung.
A large pulmonary embolus can
produce cardiovascular collapse
and death within seconds. Smaller
emboli cause respiratory difficulty,
including shortness of breath,
decreased exercise capacity, and
sometimes hypoxia that may be
more pronounced at high altitude.
Prevention of Pulmonary
Embolism
Prevention of pulmonary
embolism is important but difficult.
Everyone confined to a tent by a
storm should change position and
exercise their feet and legs for a
few minutes every hour.
Constricting clothing should be
removed. Long-distance airline
passengers and persons
hospitalized postoperatively often
wear snug elastic stockings that
come up to the knee, but these are of
doubtful benefit and would be
impractical in the wilderness. Extra
fluids are essential at altitude
where dehydration promotes venous
thrombosis, as well as hypothermia
and other problems. An aspirin a
day may help prevent venous
thrombosis at high altitude because
it inhibits platelet aggregation.
Treatment of Venous Thrombosis

and Pulmonary Embolism
Treatment of venous thrombosis
and pulmonary embolism is the
same. Both initially require
anticoagulant drugs that are
administered intravenously
(heparin) or subcutaneously
(enoxaparin), followed by several
months of oral therapy with
warfarin. Heparin and warfarin
need to be closely monitored to
prevent too much anticoagulation
that might cause serious bleeding in
the gastrointestinal tract or brain.
Therefore, treatment of venous
thrombosis or pulmonary embolism
requires evacuation to a medical
facility. Moderate analgesics are
usually adequate for pain.
Table Features of Various
18-1 Pulmonary Disorders
Once venous thrombosis
develops, the individual should be
immobilized. Walking or other
movement may cause the clots to
break off and embolize. The feet
should be elevated slightly, and
awkward positions should be
avoided. A snug, but not tight,
elastic bandage wrapped around the
leg from toes to knees is thought by
some to decrease the risk of
embolism and is unlikely to worsen
matters. Evacuation is essential,
especially if pulmonary embolism
has occurred. During evacuation the
individual should be carried as
much as possible. If walking is
unavoidable, the affected limb
should be carefully bandaged. Not
to evacuate such persons to hospital
care is too risky, but every
precaution must be taken to ensure
that minimum activity and stress
result (Table 18-1).
____________
REFERENCE
1. Johnson J. and Kirby C.:
Surgery of the Chest, 3rd ed. Year
Book Medical Publishers, Inc.,
1964. (Adapted and used by
permission.)
CHAPTER 19
GASTROINTESTINAL
DISORDERS
Martin I. Radwin, M.D.
The gastrointestinal tract consists of

the mouth and throat, esophagus,
stomach, small and large intestines,
liver, gallbladder, and pancreas.
This system ingests food, converts
it into forms that can be absorbed
and used by the body, and excretes
the residual waste.
The esophagus functions after
swallowing by propelling food into
the stomach by peristalsis, where it
is digested for thirty to ninety
minutes by pepsin in the presence of
hydrochloric acid. The resulting
particulate food next passes into the
first part of the small intestine
(duodenum) where enzymes from
the intestinal mucosa and the
pancreas further prepare the
partially digested food for
absorption. Bile, which is produced
by the liver and stored in the
gallbladder, helps emulsify fats so
they can be absorbed. Absorption
takes place predominantly in the
middle and lower segments of the
small intestine (jejunum and ileum).
In the large intestine, water is
extracted from the residual
material. All blood from the small
intestine first goes to the liver,
where an array of complex
biochemical reactions converts the
absorbed nutrients to substances
needed by all tissues and organs.
Diseases of many organs
produce signs and symptoms
referable to the gastrointestinal
tract, particularly nausea and
vomiting. Illnesses originating in
the gastrointestinal tract produce
similar symptoms and often cannot
be distinguished without
sophisticated diagnostic facilities.
Furthermore, even when the nature
of a disorder is known, specific
therapy may not be available.
Therefore, the treatment for most
gastrointestinal disorders that
appear for the first time in a
wilderness situation or in a remote
area of a developing country is
limited to alleviating symptoms.
disease of the gastrointestinal
system are nausea and vomiting,
diarrhea, constipation, bleeding,
jaundice, and pain. Pain that comes
on suddenly is such an eminent
problem that it is discussed
separately in Chapter 20: Acute
Abdominal Pain, as are procedures
for examining the abdomen.
NAUSEA AND VOMITING

The causes of vomiting are
innumerable and include such
widely differing disorders as
motion sickness, head injuries,
metabolic disorders, infections,
pregnancy, ulcers, environmental
heat, altitude illness, and
appendicitis.
If a person is stuporous or
unconscious, a single bout of
vomiting can be disastrous because
the gastric contents can be aspirated
into the respiratory tract. Lethal
respiratory obstruction can result if
the volume of aspirated material is
large. If a smaller amount of
vomitus is aspirated into the lungs,
the resulting severe pneumonia is
difficult to treat. At the first sign of
vomiting, an unconscious person
must be rolled onto the side with
the head lowered. The waist may be
lifted if the person has not been
involved in an accident that could
have produced a fractured spine. (If
a blow to the head is responsible
for the unconsciousness, the
individual should be assumed to
have a cervical spine injury.) The
headdown position must be
maintained until vomiting has
ceased and vomitus cleared from
the mouth. The person must not be
allowed to aspirate the vomited
material.
Protracted vomiting sometimes
ruptures small blood vessels in the
lining of the lower esophagus, and
variable amounts of blood appear
in the vomitus. Chronic use of
aspirin or other nonsteroidal anti-
inflammatory drugs (NSAIDs) or
excessive alcohol consumption can
irritate the stomach and cause the
vomitus to be bloody. When ulcers
of the stomach or duodenum cause
vomiting, the vomitus may contain
large quantities of blood that may
be black or look like coffee
grounds.
Vomiting caused by minor
disorders often stops without any
treatment. After the first bout the
individual usually feels better and
is able to resume limited activity. If
vomiting does not stop within a few
hours, a serious underlying disease
must be considered. Vomiting may
be an important sign of brain injury,
an acute abdominal disorder such
as intestinal obstruction or
appendicitis, drug overdose, and
many other diseases. If a person has
one of these disorders, controlling
vomiting with medications could
delay diagnosis and definitive
treatment but may be essential if the
individual is not near a medical
facility.
When no underlying disease can
be identified, vomiting can be
treated symptomatically. If
medications can be taken orally,
prochlorperazine (Compazine®) or
ondansetron (Zofran®) can be
given. Therapy should continue
until the person has been
asymptomatic for at least four hours
and can maintain adequate oral
hydration. If oral drugs cannot be
retained, orally dissolving
ondansetron tablets (Zofran ODT®)
can be given or prochlorperazine or
promethazine (Phenergan®) rectal
suppositories can be inserted every
four to six hours until oral
medications can be kept down.
Treatment required for more than
twenty-four hours should dictate
evacuation. Drowsiness is a
common side effect of many drugs
used to treat vomiting, but not
ondansetron and related
medications. While taking
prochlorperazine orally or using
either of the recommended
suppositories, the individual must
not take part in activities in which
drowsiness or inattentiveness could
result in injury.
If vomiting is prolonged, the
body becomes depleted of fluid and
salt. On rare occasions, vomiting
cannot be stopped until the fluid and
salt have been replaced. Treating
such intractable vomiting requires
intravenous fluids. If fluids for
intravenous therapy are not
available, the person must be
evacuated.
Following recovery, fluids
should be replaced as quickly as
possible to correct dehydration.
The individual should eat bland
foods, preferably liquids, for about
twenty-four hours.
Motion Sickness
Susceptible individuals may
develop nausea and vomiting when
traveling by car on a winding road,
by airplane when turbulence is
substantial, or by boat when the
water is rough. Symptoms may be
improved by limiting the motion:
moving to the front seat of a car, the
center of a ship, or over the wing of
an airplane. Lying still with the eyes
open can sometimes reduce
symptoms of motion sickness.
Several medications can prevent
or decrease motion sickness if taken
one hour or more before the motion
is encountered. Three can be
purchased without a prescription.
Dimenhydrinate (Dramamine®) is
an old standby. Meclizine (Bonine®
and Antivert®) or cyclizine
(Marezine®) are more effective for
some individuals. Transdermal
scopolamine (Transderm Scop®),
an option that requires a
prescription, consists of a patch
placed behind the ear from which
scopolamine is absorbed through
the skin. All may cause sedation
(drowsiness) as a side effect.
Scopolamine may also cause dry
mouth and blurred vision but is
usually the most effective of these
agents.
Dimenhydrinate, meclizine, and
cyclizine should be taken every four
to six hours as long as a risk of
motion sickness exists. The
scopolamine patch lasts three days
but can be removed earlier.
Travelers taking other
medications or with existing
medical conditions should contact
their physicians before taking any of
these medications to ensure that no
drug interaction or adverse effect
on their illness is likely.
DIARRHEA
Diarrhea is the most common and
most notorious of travelers’
illnesses. The most common cause
is simply a change in food or water.
Many other causes are equally
benign, although some diseases
characterized by diarrhea can be
life threatening.
Mild Diarrhea
Mild diarrhea consisting only of
soft, unformed stools and one to
four bowel movements a day, has
many different causes. A change in
food, water, or surroundings is the
most common. Excitement or
anxiety frequently produces such
symptoms. Diseases of other organs
may be accompanied by mild
diarrhea.
These disorders may last for
days or even weeks. However, the
diarrhea is only bothersome, not
incapacitating, and usually clears
up without any therapy.
Antimicrobial agents do not help
and should be avoided. Loperamide
(Imodium®), 2–4 mg (1–2 tablets
or capsules) each morning may be
helpful.
Individuals with persistent
chronic diarrhea after returning
from a developing country should
consult a physician. The cause of
such disorders may be a parasitic
infestation such as amebiasis that
can become a major illness if
untreated.
Invasive and Noninvasive

Diarrhea
In situations where microbiology
laboratories that can identify the
causative organisms are not
available, distinguishing between
noninvasive and invasive diarrhea
allows appropriate therapy to be
administered. Noninvasive
diarrhea is caused by organisms
that do not invade the lining of the
intestinal tract (the mucosa) but
remain in the intestinal lumen and
release toxins that are absorbed and
produce diarrhea. (Viruses invade
the cells lining the intestinal tract,
but produce a noninvasive type of
diarrhea.) Most traveler’s diarrhea
is noninvasive. The diarrhea
produced by these organisms is less
severe than that caused by invasive
organisms, although an exception is
cholera, which can be lethal and is
a noninvasive infection that causes
massive fluid secretion from the
gastrointestinal tract.
In contrast, in invasive diarrhea
organisms actually penetrate the
intestinal mucosa and can spread
systemically throughout the body.
Typhoid fever, a form of invasive
diarrhea, typically involves all
body tissues. Invasive bacterial
infections often are associated with
chills and fever, and with pus,
mucus, or blood in the stool, and
should be treated with
antimicrobial agents. Antidiarrheal
agents are not recommended
because they may aggravate and
prolong the illness.
With the exception of cholera,
antimicrobial agents should not be
administered for noninvasive
diarrhea. They usually are
ineffective and, even when they are
helpful, can lead to the emergence
of antibiotic-resistant strains of
organisms. However, antidiarrheal
agents may be helpful for these
disorders.
Traveler’s Diarrhea
Most acute gastroenteritis
occurring in visitors to other
countries, particularly developing
areas, is noninvasive traveler’s
diarrhea. About one-third of
visitors from the United States,
Canada, and Europe develop
diarrhea during travel in such
countries. Residents of developing
countries coming to the United
States or Europe sometimes
develop the same disorder, which
has many colorful names: the Aztec
two-step, Delhi belly, Montezuma’s
revenge, or simply turista. Such
infections are not limited to
travelers and involve the native
population as well.
Enteropathogenic Escherichia
coli (E. coli), organisms that
secrete a toxin that causes
noninvasive diarrhea, are the most
common cause of traveler’s
diarrhea. These bacteria are
normally found in everyone’s large
bowel, and individuals develop
resistance to toxins from the strains
found in their environment.
However, exposure to strains to
which the individual has not
developed resistance often
produces illness.
Other noninvasive bacteria also
cause traveler’s diarrhea. A high
percentage of the severe diarrheal
disorders acquired in the
wilderness and in developing
countries are of viral origin. The
high incidence of parasitic
infestations such as
cryptosporidiosis was not
appreciated until the 1980s.
Giardia have occasionally been
associated with traveler’s diarrhea.
Infection is usually spread by
fecal contamination of water or
food and is more common in
countries with inadequate sewage
disposal and water disinfection.
However, the illness may be
contracted anywhere.
Traveler’s diarrhea can be
prevented in several ways.
Avoiding infection is clearly best
but is not always easy. Water is the
major source of infection. In
developing countries, even in
modern hotels, tap water is usually
contaminated and must be
disinfected before being consumed
or even used just for brushing teeth.
(Many of the better—and more
expensive—hotels provide bottled
water for drinking and brushing
teeth.) However, some of these
hotels serve drinks containing ice
prepared from undisinfected water.
Beer, bottled soft drinks, and
bottled carbonated water are safe.
Bottled noncarbonated water
usually is safe, but some
unscrupulous street vendors refill
bottles with undisinfected water.
Bringing water to a boil,
regardless of altitude, kills all
organisms that cause diarrheal
diseases. Most are destroyed by
appropriate exposure to iodine or
chlorine. Unfortunately,
Cryptosporidia and possibly
Cyclospora, two diarrhea-
producing parasitic infestations
recognized in the last twenty-five
years, are resistant to chlorine and
iodine and must be removed by
filtration (Chapter 6: Sanitation,
Arthropod Avoidance, and Water
Disinfection). Infectious bacteria
may survive well in food stored in
a refrigerator, at room temperature,
and even at temperatures too hot to
touch comfortably. Food and
beverages are safe only if they have
been brought to boiling or near
boiling temperatures prior to
consumption.
Previously peeled fruits and
salads containing leafy vegetables
are well-recognized sources of
infection. Fruits with a protective
rind that is not eaten are generally
safe, but such fruits split open for
display in markets are often
splashed with undisinfected water
so they will remain attractive.
Melons sold by the pound are often
injected with undisinfected water to
increase the weight. All fruits and
vegetables should be thoroughly
washed in disinfected water and
peeled by the consumer.
Contamination of food during
preparation must be avoided.
Modern concepts of sanitation, even
such simple measures as hand
washing after defecation, are totally
alien to many natives of developing
countries. They must be monitored
to ensure they wash before
preparing food. Stool cultures to
detect carriers of infectious
diseases are desirable for the native
personnel in large parties,
particularly those engaged in
preparing meals, but are essentially
impossible to obtain. Disinfection
of water used for food preparation
as well as for drinking may be
necessary. Unfortunately, such
precautions are not universally
effective and are difficult to sustain
for a prolonged time.
The incubation period for
traveler’s diarrhea is usually
twelve to forty-eight hours, and the
disorder usually lasts two to five
days. The onset is characterized by
rapidly developing generalized
abdominal distress culminating in
waves of cramps and diarrhea.
During spasms of pain, infected
individuals may draw their knees
up against the abdomen for relief.
However, the periods between
spasms are relatively free of pain.
Nausea is common and may be
accompanied by vomiting.
Occasionally nausea and vomiting
are the dominant features of the
illness.
Mild generalized abdominal
tenderness may be present,
particularly in the lower abdomen,
and bowel sounds are usually much
louder than normal. Chills and fever
are mild or absent.
Traveler’s diarrhea is frequently
explosive in onset and is
characterized by copious, watery,
foul-smelling stools. The number of
stools varies from three or four to
as many as twenty or more in
twenty-four hours. Mucus is
occasionally present in the stool,
particularly when stools are
numerous, but pus and blood are
absent.
Antimicrobial agents can reduce
the incidence of traveler’s diarrhea,
but physicians are justifiably
reluctant to recommend their routine
use. All antibiotics have potentially
significant side effects. They
predispose individuals to the
development of invasive bacterial
infections and can induce drug
resistance in bacteria, increasing
the risk of infection by organisms
that are antibiotic resistant and
more dangerous. However, an
antibiotic that is not absorbed and
stays in the gastrointestinal tract has
been recently developed for
traveler’s diarrhea and shortens the
duration of illness. Rifaximin
(Xifaxan®) is taken only for
noninvasive traveler’s diarrhea
typically due to enteropathogenic E.
coli. The medication has not been
evaluated in individuals under
twelve years of age or during
pregnancy and should be avoided
by such persons.
An over-the-counter drug,
bismuth subsalicylate (Pepto-
Bismol®), prevents traveler’s
diarrhea in approximately 65
percent of the individuals taking it.
The liquid form is so bulky that its
use is impractical, but the tablets
are effective (two tablets four times
a day). This drug has no major
toxicity and appears considerably
safer for prophylactic use than
antimicrobial agents. Aspirin,
which is also a salicylate, should
not be taken concomitantly with
Pepto-Bismol®.
The essential element of
treatment for vomiting and diarrhea
is fluid and salt replacement. (The
relief of other symptoms, although
desirable, is of secondary
importance.) These disorders often
produce significant dehydration,
although lethal dehydration is
uncommon in healthy adults.
Worldwide, 3.3 million deaths per
year are caused by diarrhea, 80
percent of them in children less than
two years old. Vomiting or diarrhea
would definitely aggravate the
dehydration almost invariably
encountered at high altitudes.
Urine volume and color are
reliable indicators of dehydration;
small volumes (less than 500 ml
daily) of dark yellow or orange
urine indicate substantial fluid
depletion.
To replace fluids and salts, fruit
juices, broths, and soups can be
consumed. Rehydration with a
sugar-and-salt solution may be
more effective. (The sugar is a key
ingredient because it promotes
absorption of the salts.) Packaged
rehydration salt mixtures are
available for purchase. Formulas
for replacement solutions are
provided in Table 19-1. Others can
be found in standard references.
The components of oral
replacement solutions can be
packed in small units at home, can
be purchased in prepackaged form,
or can be made up in the field. The
rather crude measurements listed
(teaspoons) are sufficiently
accurate for anyone with normally
functioning heart and kidneys,
which will retain what is needed
and excrete the rest. Furthermore,
diarrheal salt losses vary more than
such measures. Disinfected water
must be used to dissolve the salts
and glucose. Individuals with
moderate diarrhea (five to ten
watery stools per day) should drink
one to three liters of solution in
addition to their usual water intake
every twenty-four hours. Persons
with more severe diarrhea (ten or
more watery stools per day) should
drink enough solution to equal the
volume of the estimated losses and
an additional 1.5 to 2 liters per day.
No salt-free water should be
consumed until rehydration is
achieved and the diarrhea is
substantially improved.
Table Oral Fluid Replacement

19-1 Solutions
3.5 gm per liter
or
Sodium chloride
½ level teaspoon
per liter
2.5 gm per liter
Sodium or
bicarbonate ½ level teaspoon
per liter
1.5 gm per liter
Potassium or
chloride
¼ level teaspoon
per liter
20 gm per liter or
Glucose 6 level teaspoons
per liter
or
40 gm per liter or
Sucrose (table 12 level
sugar) teaspoons per
liter
U.S. PUBLIC HEALTH SERVICE
FORMULA (CENTERS FOR
DISEASE CONTROL AND
PREVENTION)
Glass no. 1
8 ounces fruit juice
½ teaspoon honey or corn syrup
1 pinch table salt
Glass no. 2
½ teaspoon baking soda
(bicarbonate)
8 ounces water (disinfected)
Drink equal amounts from each
glass, alternating between the two.
Treatment of nausea and
vomiting with orally dissolving
ondansetron tablets (Zofran
ODT®), oral prochlorperazine
(Compazine®), or prochlorperazine
or promethazine (Phenergan®)
suppositories may be required for
adequate amounts of oral fluids to
be consumed. Bismuth subsalicylate
(Pepto-Bismol®), two tablets every
six hours, may also be helpful.
Whether drugs that specifically
control diarrhea should be used is
controversial. Some evidence
suggests these agents may prolong
the illness even though the
frequency of bowel movements is
decreased. A compromise that
appears reasonable is to administer
medications only to control severe
cramps or in circumstances where
frequent bowel movements would
be hazardous or substantially
inconvenient and uncomfortable.
Certainly the need to leave a tent in
an ice and snow environment five to
ten times a night would justify the
use of a medication to lessen the
frequency of bowel movements.
Paregoric (tincture of opium),
codeine, and diphenoxylate
(Lomotil®) are effective agents but
are potentially habituating and
available only by prescription.
Loperamide (Imodium®) has
similar actions, and tablets are
available without a prescription.
These drugs vary in their
effectiveness for different
individuals. The drug most effective
for each specific individual should
be administered. If the initial drug
is not effective, one of the others
may be tried.
Individuals with severe diarrhea
(more than ten stools per day) that
has persisted for more that a few
days, particularly if chills and fever
are present and stools contain
blood, mucus, or pus, should seek a
physician for diagnostic studies and
treatment. Such infections are
probably caused by invasive
organisms. If such care is
unavailable, many authorities
recommend treating such prolonged
or severe traveler’s diarrhea with
an antidiarrheal agent such as
loperamide for two days and an
antibiotic such as ciprofloxacin
(Cipro®) or trimethoprim-
sulfamethoxazole (TMPSMX; trade
names Bactrim DS or Septra DS®),
every twelve hours for five to seven
days.
The amount of rest required
varies widely. Few are able to
continue vigorous activities. Most
must restrict physical activity until
symptoms improve or resolve.
Clostridium difficile
(Pseudomembranous) Colitis
Persons taking antibiotics for
infections not involving the
gastrointestinal tract should be
aware that diarrhea often is a side
effect of such therapy. It should
resolve a day or two after the
medication is stopped, but if
diarrhea persists or worsens and
abdominal cramps, fever,
weakness, and malaise develop,
colonic infection with organisms
such as Clostridium difficile may
be the cause. Individuals with such
infections are severely ill. Testing
for the toxin is the optimum guide
for therapy, but facilities are not
available in the wilderness. The
antibiotic should be stopped. (If the
condition for which the antibiotic is
being taken is considered life
threatening, the antibiotic should be
changed.) Metronidazole (Flagyl®)
may be administered four times a
day until a sophisticated medical
facility can be reached. Alcoholic
beverages can cause severe
vomiting for individuals receiving
metronidazole and should be
avoided while taking the drug and
for three days afterward.
SPECIFIC CAUSES OF
DIARRHEA
Staphylococcal Enteritis
Staphylococcal enteritis is a type
of acute gastroenteritis caused by a
toxin produced by staphylococci.
These bacteria are present on the
hands of about half the population,
and contamination of food during
preparation is common. Any food
may harbor the organisms, but
salads made with mayonnaise,
sweets such as custards and cream
pies, meat, and milk are the most
common sources. The
staphylococcal toxin is produced
when contaminated food is allowed
to stand unrefrigerated for several
hours, which allows the organisms
to multiply and produce toxin.
Subsequent reheating—even boiling
—does not destroy the toxin or
prevent illness. To prevent
contamination and growth of the
organism, food must be consumed
or refrigerated immediately after it
is prepared. (Food contamination
with other organisms that have a
very short incubation period can
produce an identical disorder.)
The onset of cramps and
diarrhea, with or without nausea
and vomiting, occurs one to six
hours—an average of three hours—
after contaminated food is ingested
and is frequently abrupt. The
diarrhea lasts until the
gastrointestinal tract is emptied,
rarely more than five to six hours.
Most of the individuals who have
eaten the contaminated food
develop the disease, which
establishes the diagnosis.
Antibiotics are not effective; they
do not neutralize the toxin.
Antidiarrheal and antiemetic agents
may help.
Giardiasis
For years frantic alarms about
the perils of Giardiasis have
aroused exaggerated concern about
this infestation. Governmental
agencies, particularly the U.S. Park
Service and the U.S. Forest
Service, have filtered hundreds of
gallons of water from wilderness
streams, found one or two
organisms (far less than enough to
be infective), and erected garish
signs proclaiming the water
“hazardous.”
Giardiasis is not a new problem.
Giardia have always been present
in wilderness streams and in the
water supplies for most cities. They
often have not been detected
because they are not isolated by
routine bacterial cultures. This
protozoal parasite is found all over
the world. Many animals harbor
and excrete the organisms, resulting
in contamination of wilderness
streams, but the organism has been
found in the municipal water
supplies of a number of large U.S.
cities, as well as in cities as
diverse as St. Petersburg in Russia
and Kathmandu in Nepal.
In humans, the noninvasive
parasites live in the upper intestinal
tract, where they form numerous
cysts that are passed in the stool.
The cysts do not produce active
disease but are resistant to
disinfectants and other agents in
their environment and do transmit
the infestation. Fecal contamination
of water is the most common route
of transmittal. Less common, but
significant, is direct passage of
cysts or organisms from stool to the
hands of a food preparer and to the
food itself.
Filtration removes the
organisms. Iodine in a concentration
of eight parts per million effectively
kills parasites and cysts within ten
minutes (twenty minutes if the water
is cold—32°F to 40°F or 0°C to
5°C). Bringing water to a boil and
chlorine compounds also can kill
Giardia.
Symptoms of Giardiasis vary
widely. Clearly, most infested
individuals have no symptoms at
all. In an incident carefully studied
by the Centers for Disease Control
and Prevention (CDC), disruption
in one city’s water disinfection
system allowed the entire
population to consume water
heavily contaminated with Giardia.
Only 11 percent of the exposed
population developed symptomatic
disease, although 46 percent had
organisms in their stools. In the
same study, 8.5 percent of the
population of a neighboring city
was found to have totally
asymptomatic Giardia infestations.
Characteristic symptoms, when
they occur, are mild to moderate
abdominal discomfort, abdominal
distention due to increased
intestinal gas (“rotten egg burps”
that smell like hydrogen sulfide are
typical), and mild to moderate
diarrhea. Stools are soft, may be
liquid, and are bulky and foul
smelling; they do not contain blood,
mucus, or pus. Two to four bowel
movements a day are typical. A few
individuals have more severe
symptoms. Cramps may occur. Mild
to moderate generalized symptoms
of illness—weakness, loss of
appetite or even nausea, and chilly
sensations—may appear. Without
treatment infestation lasts seven to
ten days; because symptoms and the
organisms disappear and recurrent
symptomatic infestations are rare,
apparently most people develop
some type of immunity after that
time.
Rare individuals, less than 1
percent of those with infestations,
fail to rid themselves of the
organisms and develop chronic
infestations that can cause
malabsorption, loss of weight,
ulcerlike stomach pain, and other
chronic disturbances. Such
prolonged infestations may result
from mild immunologic
deficiencies but can occur in
otherwise healthy individuals.
Sometimes Giardiasis is
associated with the explosive onset
of voluminous diarrhea like
traveler’s diarrhea, and travelers,
including physicians, often
overdiagnose Giardiasis. However,
if a laboratory is not available and
typical symptoms persisting for six
to seven days have not been
relieved by measures effective for
traveler’s diarrhea, a therapeutic
trial of one of the drugs effective
against this parasite may be
justified.
Several drugs are effective.
Metronidazole (Flagyl®) for five to
ten days is the most common and
effective therapy in the United
States. Cures have been obtained
with a single large dose of this
drug. If alcohol is consumed while
taking metronidazole, severe
vomiting results. Therefore, alcohol
must be avoided during and for
three days after taking this drug.
Tinidazole (Tindamax®) is an
agent similar to metronidazole. The
advantage of Tindamax® is its ease
of administration—with all tablets
taken at the same time. As with
Flagyl®, alcohol must be avoided
during and for three days after
taking the drug. Tindamax® is more
expensive than Flagyl®.
Cryptosporidiosis
Cryptosporidia were
discovered in laboratory mice in
1907 and have been known to
produce diarrheal disease in a
variety of animals including
domestic animals. They were not
thought to infect humans until 1976
when the first human infection was
diagnosed. In the subsequent
decade, infections by the parasite
were recognized mostly in
immunocompromised individuals,
primarily persons with acquired
immune deficiency syndrome
(AIDS) or malnutrition. Since the
early 1980s, cryptosporidiosis been
recognized as a major worldwide
cause of diarrhea in otherwise
healthy individuals.
Cryptosporidia are ubiquitous.
The organisms have been found in
up to 97 percent of the large
streams, lakes, and reservoirs in the
United States. Infections occur on
every continent but Antarctica and
cause up to 20 percent of the cases
of diarrhea severe enough for
individuals to seek medical
attention. These microorganisms are
commonly found in swimming pools
because they are resistant to the
chlorine used to disinfect the water.
Some pools do not allow babies in
diapers because they are a common
source of Cryptosporidia.
Cryptosporidia present a
particular problem in wilderness
situations because the organisms
resist iodine and chlorine
disinfectants and must be eliminated
from water by boiling, filtration, or
ultraviolet light. Hypochlorous acid
and chlorine dioxide do destroy
these parasites but require four
hours.
After ingestion, the organisms
implant in the cells lining the small
intestine. Mature organisms are
released into the intestinal lumen as
thick-walled (80 percent) or thin-
walled (20 percent) cysts. The
thick-walled cysts are excreted, but
the thin-walled cysts can reimplant
and maintain the infestation.
In immunocompetent hosts the
incubation period is two to fourteen
days. Typical symptoms are watery
diarrhea, crampy pain, anorexia,
malaise, and flatulence.
Approximately 10 to 15 percent of
infected individuals are
asymptomatic. Others may have
more than seventy stools a day. The
volume of diarrheal fluid may
exceed twenty-five liters a day,
mostly in immunocompromised
individuals. Obviously, dehydration
is common and often severe. Eating
aggravates the diarrhea and pain, so
many individuals do not eat and
lose weight.
Eradication of the infection is
dependent on the development of
immunity by the host.
Immunocompromised individuals
rid themselves of the organisms
slowly—or not at all. For persons
with HIV infection or receiving
chemotherapy that suppresses their
immune system, infestation may
prove fatal. Malnourished children
have impaired cellular immunity
and also are prone to severe
cryptosporidiosis.
The only drug found to be
effective for immunocompetent
people is nitazoxanide (Alinia®),
but this agent is not effective for
immunocompromised persons. The
drug is more effective when taken
with food. This agent is also
effective for Giardia infestations
but is more expensive than
metronidazole (Flagyl®).
Fluid replacement is a vital
aspect of therapy and can be
accomplished with bouillon,
Gatorade®, or other oral
rehydration fluids. The disorder
lasts from two days to a month,
typically about two weeks, but may
recrudesce. Infective cysts may be
shed for a longer time.
Cyclosporiasis
Cyclospora cayetanensis is a
parasite first reported in New
Guinea in 1977 and found in New
York and Peru in 1985. Among the
names it was given is blue-green
algae. Cyclosporiasis has now been
reported from all over the world.
This organism gained notoriety in
the United States in 1996 when
1465 infections were reported to
the CDC. Investigation clearly
indicated that most of the infections
were related to raspberries shipped
from Guatemala.
Waterborne outbreaks have also
occurred. In Nepal in 1992, twelve
of fourteen British soldiers were
infected by Cyclospora in their
drinking water. The water had been
chlorinated, which suggests that
Cyclospora, like Cryptosporidia,
may be halide resistant.
Cyclospora involve the small
intestine and are capable of
completing their entire life cycle
within a single host. However,
infected individuals excrete cysts
that require days to weeks to
become infectious. As a result,
direct human-to-human transmission
of infection is unlikely. Humans are
the only identified host for this
parasite.
Infection typically causes watery
diarrhea with frequent, sometimes
explosive, stools. Other symptoms
can include loss of appetite and
substantial weight loss; bloating
and increased flatus; cramps,
nausea, and vomiting; and muscle
aches, low-grade fever, and fatigue.
Untreated illness may last for a few
days to a month or longer and may
follow a remitting–relapsing
course. As would be expected,
some infected individuals are
asymptomatic. Diagnosis is
dependent upon identifying the
organism in stool.
Trimethoprim-sulfamethoxazole
(TMP-SMX, trade names Bactrim
or Septra®) is effective treatment.
No alternative drugs for individuals
who are intolerant of TMP-SMX
have been identified.
Irritable Bowel Syndrome

Irritable bowel syndrome (IBS),
previously known as mucus colitis
or spastic colon, is a common
disturbance of large intestinal
function that may result in diarrhea,
constipation, or both. The syndrome
is at least partially emotional in
origin and is often related to stress
in susceptible persons. Most
individuals with this disorder have
had a history of similar symptoms
for many years. New onset during a
wilderness outing would be very
unusual and should not be
considered.
Abdominal pain relieved by
defecation, looser stools at pain
onset, more frequent stools at pain
onset, abdominal distension, and the
passage of mucus are commonly
associated with this condition.
Stools may be thin and tapered
(pencil shaped).
Recognizing the nature of the
disorder and reassuring the person
are important aspects of treatment.
In individuals with constipation, a
high-fiber diet, possibly
supplemented with psyllium husk
fiber (Metamucil®), may be useful.
If diarrhea is the predominant
symptom, loperamide may be
helpful.
Other types of drug therapy, all
of which must be administered by a
physician, include Librax®, which
includes a benzodiazepine,
Bentyl®, and cholestyramine. Other
psychoactive drugs, such as
Elavil® and Prozac®, have been
used. Treatment is directed at the
control of symptoms since no cure
for this condition is known. All
interventions may be ineffectual.
Fortunately, the condition is mainly
a nuisance and not life threatening.
SEVERE DIARRHEAS
Severe acute diarrhea and subacute
diarrhea are mostly of bacterial
origin and, like less severe
diarrhea, are most frequently
transmitted by fecal contamination
of drinking water. In areas where
these diseases exist, all water must
be carefully disinfected. Other
precautions are described in the
discussion of traveler’s diarrhea.
Experienced physicians have
difficulty distinguishing different
invasive bacterial diarrheas in the
wilderness. Nonphysicians in this
situation cannot expect to be able to
make correct diagnoses. Individuals
in any of the following categories
who are considered to have an
invasive gastrointestinal bacterial
infection should contact a medical
center with a bacteriologic
laboratory as soon as possible:
Children under three years of
age and adults over sixty-five,
particularly those with other
significant illnesses
Individuals who are pregnant
Anyone with severe diarrhea
lasting more than forty-eight to
seventy-two hours that is
associated with any of the
following:
Stools that contain blood or
easily detected pus
Pronounced abdominal
tenderness
Fever (morning temperature
over 99°F or 37.2°C; evening
temperature over 100°F or
37.8°C)
Dehydration (loss of more than
5 percent of usual body
weight)
If timely evacuation is
impossible, appropriate
antimicrobial drugs should be
administered. Under these
circumstances, pregnant women
present a special problem since
some of the drugs normally used
may harm the developing child.
Loperamide (Imodium®) is safe.
TMP-SMX is relatively safe for the
first eight months but should be
avoided at term. The safety of
ciprofloxacin (Cipro®) during
pregnancy and the first eighteen
years of life has not been
established, but the drug is
extremely effective.
Precautions are necessary to
avoid spread of the infection. An
individual with one of these
diseases should be isolated as much
as possible. Attendants should be
limited to one or two individuals
who are scrupulous about
cleanliness.
The attendants must scrub their
hands vigorously, preferably with
an antibacterial soap such as
PhisoHex® or soap containing
Betadine®; wear protective rubber
or plastic gloves, and use a
handdisinfectant gel after any
contact with an infected person. All
feces and vomitus should be buried
where contamination of water does
not occur, preferably after being
mixed with an antiseptic such as 1
percent Cresol. All utensils and
other instruments should be
immersed in boiling water.
Indispensable items, such as
clothing or sleeping bags that
cannot be boiled, should be aired in
bright sunlight for at least one or
two days after the individual is
recovering.
Invasive Bacterial Infections

(Dysentery)
Invasive bacterial infections, or
bacillary dysentery, are caused by a
wide variety of bacteria including
Salmonella, Shigella,
Campylobacter, Yersinia,
Aeromonas, Clostridium, non-
cholera Vibrios, and occasionally
other organisms. These organisms
are found in temperate as well as
tropical areas, but severe cases of
bacillary dysentery occur most
frequently in tropical or
semitropical climates.
Salmonellae are particularly
widespread. Virtually all domestic
animals, including household pets
—dogs, cats, birds, and turtles—
and many wild animals harbor these
bacteria. The number of
asymptomatic human carriers has
been estimated at two persons per
thousand.
Contaminated water and food
spread infections. Any item of food
or drink can be contaminated. For
Salmonella the greatest single
source of human disease is poultry
products—both meat and eggs—and
raw meat of other types. Lack of
hydrochloric acid in the stomach
(the result of disease or therapy for
peptic ulcer) and alteration by
antibiotics of the normal microbial
flora in the intestinal tract increases
susceptibility to infection by these
organisms.
The incubation period varies
from one to six days with an
average of forty-eight hours
(somewhat shorter for Salmonella).
The onset is often rather abrupt and
characterized by severe,
intermittent abdominal cramps
followed by diarrhea that may be
copious and soon progresses to
watery, foul stools. The stools
contain large amounts of mucus and
pus and occasionally moderate
amounts of blood, particularly four
to five hours after the onset. Nausea
is common, but vomiting may not
occur. Infection usually is
associated with fever (100.5°F to
102°F, 38°C to 39°C, or higher) and
chilly feelings or frank, shaking
chills. Abdominal tenderness may
be pronounced, is most marked in
the lower portion of the abdomen,
and is frequently accompanied by
spasm of the abdominal muscles.
Abdominal pain may be sufficiently
intense, localized, and associated
with enough rebound tenderness to
suggest an acute abdominal
disorder requiring surgery. The
individual is obviously ill and may
be prostrate.
After six to eight hours the
symptoms abate somewhat, but the
disease may take seven to ten days
to run its course. Considerable
variation in the severity of
symptoms is observed, even among
persons infected at the same meal.
The most important aspect of
treatment for invasive bacterial
gastroenteritis is prompt correction
of dehydration. Large amounts of
fluids (such as those delineated in
Table 19-1) should be
administered. Intravenous fluids
may be necessary for more severe
cases. A bland diet may be given if
it can be tolerated.
A hot-water bottle or other
source of warmth placed on the
abdomen may reduce some of the
pain and tenderness. Drugs to stop
the diarrhea are not recommended
because they tend to produce
intestinal paralysis, which prevents
the individual from taking fluids
orally. These agents also may make
the fever and overall disability
worse. However, many individuals
take such medications.
These infections should be
treated with antibacterial agents.
Ciprofloxacin (Cipro®) is the drug
of choice; TMP-SMX is the second
choice. (In Latin America, 25
percent of Shigella are resistant to
TMP-SMX.) The usual duration of
therapy is one week. Rifaximin
should be avoided if the infection is
considered invasive.
Although antimicrobial therapy
frequently produces marked
improvement in twenty-four hours
or less, it must be continued for at
least five days—longer if symptoms
persist.
Individuals with these infections
require rest; most should be in bed.
People who have had bacillary
dysentery frequently require seven
to ten days to recover their strength
after symptoms have disappeared.
Evacuation is desirable for people
who are not on extended
expeditions.
Enterohemorrhagic E. Coli
Enterohemorrhagic E. coli,
serotype 0157:H7, produces a
severe invasive infection of the
colon that is often manifested by
colitis, bloody diarrhea, and
abdominal pain. Undercooked meat,
particularly beef, is often the source
of infection, which is sometimes
complicated by anemia, kidney
failure, and impaired brain function.
Fever, chills, and an extremely
tender abdomen can mimic an acute
surgical disorder such as
appendicitis, especially since the
colitis may predominantly involve
the colon near the appendix. No
specific treatment is available, but
antibiotics such as ciprofloxacin
(Cipro®) should be used in a
wilderness environment. Seriously
ill individuals require
hospitalization in an institution that
can provide supportive therapy.
Antimotility drugs should be
avoided because they aggravate the
illness.
Cholera
Cholera, once a scourge
throughout the world, is almost
nonexistent where modern
sanitation and water purification
methods are practiced. However,
infections that claim many lives are
common in some areas of the
world. A major outbreak recently
killed thousands in Peru, Ecuador,
and Colombia. In Southeast Asian
countries, monsoon rains wash
feces that have collected on the
ground and in the streets into
streams and rivers and regularly—
almost annually—precipitate
epidemics. Effective treatment is
unavailable for the poor in many
developing countries.
Although cholera is transmitted
primarily by contaminated water,
the infection may also be contracted
from food, particularly items that
are not cooked. Injected vaccines
are ineffective. Oral vaccines are
being developed and tested.
Vaccination is not recommended by
the CDC and other authorities, is
not available in the United States,
and is not required for entry by any
country.
Fortunately, the cholera Vibrio
cannot survive very long outside the
human body. As a result, most
outbreaks occur in areas of
significant population and thus near
areas where hospitals are
available. However, undiagnosed
individuals with mild symptoms
and carriers, although much rarer
than carriers for Salmonella that
causes typhoid fever, may spread
the organisms a considerable
distance from hospitals. The
rapidity with which prostration
appears in severe infections may
prevent evacuation and mandate
treatment in the field.
Cholera can become
overwhelming with amazing speed,
leaving the person severely
dehydrated and in shock from fluid
loss within one to three hours. An
uncooked seafood dish
contaminated with cholera
organisms served after takeoff on a
jetliner flight from Lima, Peru, to
Los Angeles, California, produced
fifty-three infections, one of which
was fatal before the flight could be
completed. However, the usual
incubation period for cholera is one
to three days, during which the
individual may notice mild
diarrhea, depression, and lassitude.
The end of the incubation period is
signaled by the explosive onset of
voluminous watery diarrhea.
The gastrointestinal tract is
quickly emptied, and the stools lose
their fecal character and foul odor.
The individual is constantly
dribbling stools consisting almost
entirely of water. Flecks of mucus
that look like grains of rice floating
in water have resulted in the name
“rice water stools” for this
material. The stools rarely contain
blood.
Frequently, no warning of the
need to defecate is felt, resulting in
repeated, often uncontrollable
bowel evacuations. Similarly,
vomiting may occur without
antecedent nausea, although
vomiting is uncommon after the
onset. As the person becomes
dehydrated, fever and a rapid pulse
appear. The blood pressure
frequently drops below normal, and
a weakened pulse becomes difficult
to feel. The features become gaunt,
the eyes shrunken, and the skin
shriveled and dry. Urinary output
falls to less than 20 ml per hour due
to the greatly reduced blood
volume, and kidney failure ensues.
The treatment for cholera is fluid
replacement. The entire volume of
stool and vomitus must be replaced
with oral or intravenous salt
solutions. Stool volumes should be
measured for replacement to be
accurate. Intravenous administration
of fluids is often necessary during
the early stages of the disease,
particularly if vomiting is
substantial, and may be lifesaving if
the person is severely dehydrated
and in shock. Two to four liters of
saline or Ringer’s lactate solution
may be required in the first hour
and as much as eight or more liters
during the first day. After
dehydration has been corrected and
individuals are no longer in shock,
they usually are able to take fluids
orally. Either of the replacement
solutions listed in Table 19-1 is
suitable.
People with cholera are severely
ill and obviously require bed rest.
A canvas cot with a hole in the
center through which the person can
defecate without having to move
improves comfort and facilitates the
collection and measuring of the
stools during the first few days of
the illness. Feces must be disposed
of carefully to avoid contamination
of water supplies and infecting
others.
Tetracycline or doxycycline is
the preferred antibiotic therapy for
adults. In areas where tetracycline
resistance is prevalent,
ciprofloxacin should be substituted.
For children, furazolidone is the
preferred medication; TMP-SMX is
the second choice. Antibiotics are
only an adjunct to therapy and
cannot substitute for fluid and
electrolyte replacement. Sedatives
make care of the individual more
difficult and are not useful.
Cholera is not very contagious if
proper precautions are followed as
it is spread principally by feces.
Sanitary disposal of feces and
vomitus must be strictly enforced,
and all contaminated articles,
including clothing, bedding, and
utensils, must be cleaned.
The acute phase of the infection
rarely lasts more than three to five
days. The individual usually is able
to eat a bland diet by the third day.
However, several weeks are
required for full recovery.
Typhoid Fever
Typhoid fever is a systemic as
well as a gastrointestinal infection
caused by Salmonella typhi. The
bacterial organisms invade the wall
of the small bowel and enter the
bloodstream, causing septicemia.
Occasionally, people who have
recovered from typhoid fever
continue to harbor the organisms
(carriers) in the gastrointestinal
tract and excrete them in their
stools. The bacteria can survive for
months under natural conditions.
Uncooked foods, salads, raw milk,
and contaminated water are the
most important sources of infection.
The incubation period is seven
to fourteen days. Symptoms during
the first week consist of fever,
headache, and abdominal pain. The
onset is usually insidious. Often
there is no change in bowel habits
during the initial ten days of illness.
Near the end of the first week,
enlargement of the spleen may be
detectable. A brief, somewhat
diagnostic rash can be seen in 70
percent of light-skinned individuals
about seven to ten days after the
onset of symptoms. The rash
consists of “rose spots” that are
deeply red, usually few in number,
2 to 4 mm in diameter and often
present in clusters, blanch on
pressure, and occur most often on
the lower chest and upper
abdominal wall. During the second
week of illness, fever becomes
more continuous and many
individuals are severely ill. A pulse
rate that is often paradoxically slow
in comparison to the severity of the
fever is an important diagnostic
feature. Cough and nosebleeds may
occur. In the third week, extreme
toxicity, irrationality or confusion,
and “pea soup” diarrhea may occur.
The latter may presage the dire
complications of perforation of the
intestine or intestinal hemorrhage.
For survivors, the fourth week often
brings improvement in their status.
However, typhoid fever is a long-
lasting and debilitating infection.
For typhoid fever, supportive
care and maintenance of fluid intake
are important. Antipyretic agents
such as aspirin, ibuprofen, or
acetaminophen may cause severe
sweating and may lower blood
pressure. Cautious use is
acceptable only if sponging with
tepid water does not control the
high fever.
Ciprofloxacin (Cipro®) is the
antimicrobial drug of choice for the
treatment of typhoid fever.
Chloramphenicol has been
relegated to second choice for two
reasons: Typhoid bacteria from
central Mexico and Vietnam are
often resistant to chloramphenicol,
and this drug may rarely cause a
potentially lethal anemia after
prolonged therapy. The usual
duration of therapy is two weeks.
Prior to travel to an area where
typhoid may be encountered,
immunization for typhoid and
paratyphoid fever should be
obtained. Although immunization
does not completely prevent
infection, it does reduce the
severity of the disease and reduces
the incidence of complications.
Oral typhoid vaccine is now
available.
Amebiasis
Amebiasis is caused by the
invasive parasite Entamoeba
histolytica. Although generally
thought of as a tropical disease,
amebiasis is by no means limited to
such areas.
These organisms invade the wall
of the large intestine. The adults
form cysts that are passed in feces
and spread the infection. The cysts
are most commonly ingested in
contaminated water. Food that has
been fertilized with human excreta,
carelessness in food preparation,
and insects—particularly flies—are
other sources of infestation. Iodine
in appropriate concentrations and
boiling destroy the cysts effectively;
filtration removes them.
Amebiasis is usually a very mild
disorder in its early stages, and
symptoms may be entirely absent
then. Mild diarrhea with soft stools
and a moderately increased number
of bowel movements are more
common. Occasional individuals
develop constipation rather than
diarrhea. A few individuals have
more severe symptoms, including
abdominal cramps and numerous
watery stools that contain mucus or
blood. However, a period of mild
gastrointestinal dysfunction usually
precedes the onset of the more
severe stage.
Easy fatigability, low fever, and
vague pains in the muscles, back, or
joints are frequently present.
Nervousness, irritability, and
dizziness occasionally develop.
Typically no abnormality can be
found on physical examination,
although slight tenderness in the
right lower quadrant of the
abdomen is sometimes present. The
chronicity and mildness of the
diarrhea and a history of exposure
to conditions in which infection is
likely suggest the diagnosis.
Laboratory facilities are required to
make a definitive diagnosis.
If amebiasis is suspected,
metronidazole (Flagyl®) should be
given. Occasionally, metronidazole
may not completely eradicate the
infection.
Persons visiting an area in which
amebiasis is prevalent should
consider examination for infestation
upon their return. The amoebae may
lie quietly within the large intestine
for years and then spread to the
liver, where they form abscesses
from which they occasionally even
invade the lung. This form of the
disease has a high mortality.
CONSTIPATION AND RECTAL

PROBLEMS
Healthy adults rarely need to be
concerned about constipation. The
concept that normal individuals
should have a bowel movement
every day is a myth perpetrated on
bowel-conscious people by remedy
peddlers and overprotective
mothers. Bowel rhythm can vary
widely. For some individuals, three
stools a day is normal; others have
one stool every three days. A
change in bowel habits for which
no cause can be identified may be
significant, but new foods,
medications, travel, or alteration in
daily schedule can produce such
changes.
The type of food consumed plays
a large part in determining the
character and frequency of stools.
Foods that are almost completely
absorbed, such as liquids or
carbohydrates, cannot be expected
to produce a copious stool. The
converse is true for foods with a
large unabsorbed residue such as
bran, fresh fruit, or vegetables.
Reduced food intake due to illness
or dieting leads to smaller stool
volume.
Constipation is more accurately
defined as the passage of hard, dry
stools rather than a specified
frequency of bowel movements.
Reduced intake of fluids and
disruption of normal schedules with
infrequent rest stops (travel by air)
all tend to cause constipation. An
adequate water intake of 1.5 to 2
quarts a day, fruits and other foods
that loosen the stools, and bran or
high-fiber cereals that provide bulk
help to maintain normal bowel
function.
In general, laxatives have very
little prophylactic or therapeutic
value. If, in an unusual situation,
laxatives become necessary, the
best and safest is Milk of
Magnesia®, one or two
tablespoonfuls or two to four
tablets at bedtime.
Fecal Impaction
Under conditions in which the
urge to defecate is resisted, such as
weather or illness that confines
individuals to their tents, the normal
bowel reflexes may become
insensitive and permit stool to
accumulate in the rectum.
Dehydration may cause the water in
the stool to be reabsorbed with such
avidity that a bulky, hard residue
that cannot be evacuated in a
normal manner results.
The best way to determine
whether impaction has occurred is
to insert a lubricated and (if
available) gloved index finger into
the rectum (Fig. 19-1). If a mass of
hard stool is found, it must be
extracted. The mass of stool should
be broken up impacted stool with
the index finger and the fragments
removed as gently as possible.
Injury of the rectal and anal tissues
should be avoided. Following
manual removal of the impaction
the causes of the impaction should
be corrected.
Figure 19-1. Digital removal of a
fecal impaction
Although breaking up and

extracting a fecal impaction is
aesthetically unpleasant, no
alternative exists. Enema fluids will
not enter the solidified fecal mass;
laxatives have no effect on the
dilated, flaccid rectal wall.
Paradoxically, fecal impaction may
be accompanied by the passage of a
number of small, watery stools—
the only material that can get past
the impacted mass.
Anal Fissure
With constipation the stool may
become so hard and bulky that its
passage causes a small tear
(fissure) in the skin of the anus.
Subsequent bowel movements are
painful and may be associated with
a small amount of bleeding.
Avoiding hard, constipated
stools by consuming adequate water
often allows the fissure to heal. A
temporary low-residue diet that is
low in fiber and consists of foods
that are almost totally absorbed,
such as milk, soups, and
carbohydrates, may avert bowel
movements for several days and
allow healing, although this diet
may be constipating. Straining at
stool should be avoided
indefinitely. Supporting the body so
its full weight is not on the toilet
seat during defecation avoids
aggravating the injury. The anal
area should be cleaned gently after
each bowel movement. Aggressive
wiping (particularly with coarse
paper), scratching, and rubbing
should be avoided.
Mineral oil, one tablespoonful
(15 ml) twice a day, lubricates the
stool and reduces the pain with
bowel movements (mineral oil is
not a laxative—only a lubricant). If
pain persists between bowel
movements, a bland anesthetic jelly
such as 1 to 2 percent lidocaine
may be applied. The jelly or a
rectal suppository may have to be
inserted into the anal canal. Healing
may also be aided by the
application of 1 percent
hydrocortisone ointment.
Persistent pain or bleeding
should be brought to the attention of
a physician as soon as possible.
Hemorrhoids
Hemorrhoids (piles) are
abnormally dilated veins that
protrude from the anus. They are
usually present before a journey
begins but can be aggravated by the
constipation that commonly
develops with new foods,
prolonged sitting, and irregular
schedules. (Individuals with
preexisting hemorrhoids should
have them assessed by a colorectal
surgeon before a major wilderness
outing.) Hemorrhoids usually are
more annoying than disabling but
can be a source of considerable
itching and discomfort and can
cause severe pain if they become
prolapsed and thrombosed.
Hemorrhoids bleed modestly
following a hard or bulky, dense
bowel movement, but serious
bleeding is rare. The blood is
usually noted on the toilet paper or
on the outside of the stool; blood
mixed within the stool could
suggest bleeding from the colon, a
much more serious problem.
If hemorrhoids become
bothersome in the field, measures to
soften and lubricate the stool—most
important, a generous water intake
—and one tablespoon of mineral oil
twice a day may provide relief.
Bearing down during bowel
movements should be avoided.
Sitting in warm water for ten to
fifteen minutes several times a day
helps relieve symptoms but
interferes with outdoor activities.
Bulk formers such as Metamucil®
may be helpful during an acute
episode. Hemorrhoidal
suppositories or creams may
relieve symptoms.
Thrombosed Hemorrhoid
The blood within a hemorrhoid
occasionally clots, resulting in
significant anal pain that may come
on gradually or suddenly. A purple
nodule that is firm and tender can
be seen protruding from the anal
opening or can be felt just inside.
Clots smaller than one-half inch
(1.25 cm) in diameter are best
allowed to resolve spontaneously.
Clots larger than one inch (2.5 cm)
may require surgical therapy to
evacuate the clot. The severity of
the pain should determine how clots
between these two sizes should be
treated.
An incision in the top of the
thrombosed hemorrhoid and
evacuation of the clot can provide
dramatic relief of pain. Days of
distress can be avoided if the
thrombosed hemorrhoid is large.
Before incision, the anus should be
washed with soap and water. A
moderate analgesic can be given
prior to incision. Ice or snow
pressed against the nodule provides
surprisingly effective anesthesia.
The incision should be left open,
and pads should be left in the
intergluteal cleft to reduce soiling
by blood. Warm baths help relieve
pain and anal muscle spasm.
Rectal Abscess
Abscesses in the tissues
surrounding the rectum and anus
usually follow long-standing anal
problems such as fissures or
hemorrhoids, which should be
corrected before a prolonged
wilderness outing. Abscesses in
this location are not basically
different from abscesses elsewhere
in the body.
The cardinal symptom of a rectal
abscess is throbbing pain in the
region of the anus. Malaise, fever,
and chills are common, and the
individual may appear acutely ill.
Examination usually reveals the
characteristic signs of an abscess—
a mass that is red, tender, and
warm. The abscess may come to a
point (head) in the skin adjacent to
the anus. A few rectal abscesses are
located deeper beneath the skin and
can only be felt during digital
examination of the rectum.
Rectal abscesses should be
treated just like abscesses
anywhere else—with incision and
drainage. If the abscess comes to a
point in the skin beside the anus, an
incision can be made in the center
of the fluctuant area. If a deeper
abscess is felt or the surrounding
inflammation is extensive, the
person should be evacuated; only a
surgeon should drain such
abscesses, and serious
complications can follow an
abscess in this location that is not
properly treated. If the individual
has a fever, amoxicillin/clavulanate
(Augmentin®) or ciprofloxacin
(Cipro®) should be administered
during evacuation.
PEPTIC ULCER AND

RELATED PROBLEMS
A peptic ulcer is an inflammatory
destruction of the lining of the
stomach or intestine produced by
the digestive action of the enzymes
and acids from the stomach (Fig.
19-2). The cause of peptic ulcers is
not completely understood, but
although stress is thought to play a
role, familial and host factors
affecting mucosal protective
mechanisms are most important.
Many ulcers are associated with
infection by Helicobacter pylori, a
ubiquitous bacteria found
worldwide that is adapted to living
in the acidic environment of the
stomach. Aggressive diagnosis and
therapy in developed countries have
produced a notable decrease in the
prevalence of stomach ulcer this
infection. However, in
underdeveloped countries, the
organism is widely disseminated
and can be contracted from infected
food, water, or persons. Chronic
infection with this organism has
been associated with two gastric
malignancies: adenocarcinomas and
lymphomas. However, the manner
in which this organism produces
these disorders is as yet unknown.
Drugs such as aspirin, ibuprofen,
nonsteroidal anti-inflammatory
agents (NSAIDs), and steroids
sharply aggravate the ulcerative
effects of the bacteria.
Figure 19-2. Peptic and duodenal
ulcers
An uncomplicated ulcer is not

usually disabling, although the pain
can be substantial, but is threatening
because it may hemorrhage or
perforate. These disabling, life-
endangering complications require
immediate evacuation to a medical
center. (Perforation is discussed in
Chapter 20: Acute Abdominal
Pain.)
The characteristic symptom of an
ulcer is gnawing pain, usually
located in the upper portion of the
abdomen near the midline. The pain
is quite localized, and the person
usually can pinpoint it with a
fingertip. Typically, the pain comes
on one to four hours after eating or
between midnight and two o’clock
in the morning. Bland food, milk, or
antacids usually relieve the pain.
The pain is thought to be caused
by the effects of stomach acid on the
ulcer. Acid is a factor in all peptic
ulcers. Food and antacids tend to
neutralize the acid and thus relieve
the pain. The characteristic times at
which the pain occurs are the
periods when there is no food in the
stomach to counteract the acid. (No
explanation has been found for the
absence of pain in the early morning
when the stomach is totally empty.)
Treatment of Peptic Ulcers

The basic therapy for ulcers
associated with H. pylori is
eradication of the infection, but
diagnosis and treatment of such
infections are complex endeavors
and should be carried out by a
physician. Supplemental ulcer
therapy is primarily directed
toward reducing the acidity of the
stomach contents. Antacids have
been used in the past and are still
valuable. However, newer, more
effective approaches include drugs
that block the secretion of acid.
Antacids are best taken between
meals. Consumption within an hour
of other anti-ulcer drugs should be
avoided. Since overdosage with
antacids is rarely a problem, more
frequent doses may be administered
if pain persists. Liquid antacids are
more effective than tablets but are
less portable. Many preparations
are available.
Antacid therapy became less
important after histamine H2
receptor antagonists (H2 blockers)
became available. Famotidine
(Pepcid®), ranitidine (Zantac®),
cimetidine (Tagamet®), and
nizatidine (Axid®) are H2 blockers
currently being used; all are equally
effective in appropriate dosage.
Famotidine, ranitidine, and
cimetidine are now available
without prescription. Famotidine
and nizatidine are best taken once a
day at bedtime and are simpler to
administer. The other two drugs
must be taken more frequently. The
most potent medications now
available are the proton pump
inhibitors (PPIs) introduced in
1989. Omeprazole (Prilosec®) was
the first drug of this class to become
available and now is available
without prescription. Esomeprazole
(Nexium®), lansoprazole
(Prevacid®), pantoprazole
(Protonix®), and rabeprazole
(Aciphex®) are other popular drugs
of this type but require a
prescription.
Any NSAID being administered
must be discontinued. Aspirin in
any form must be strictly avoided; it
increases the risk of bleeding
fifteen-fold. Smokers with ulcers
should cease smoking entirely; at
the very least, and of much less
impact, they should substantially
decrease their nicotine usage.
Alcohol and caffeine also must be
avoided. A mild tranquilizer may
help highly stressed individuals.
Symptoms normally improve
within a few days, but full healing
takes six to eight weeks. Physical
activity may continue during
treatment, but strenuous exertion,
particularly if emotionally stressful,
is best avoided for at least a week
after the institution of appropriate
therapy. Persistent symptoms in
spite of the institution of treatment
merit the care of a physician.
Individuals with active ulcers
should not take part in extended
expeditions until the ulcer has
healed.
Gastroesophageal Reflux Disease

(GERD)
GERD is caused by the reflux of
acidic gastric contents into the
esophagus. It is generally
associated with relaxation of the
lower end of the esophagus or a
hiatal hernia, a protrusion of the
stomach into the chest through the
opening in the diaphragm through
which the esophagus passes. The
symptoms of GERD include
cramping pain or burning in the
midline of the lower chest
(heartburn), a sense of fullness after
eating, excessive belching, and
regurgitating small amounts of food
or sour stomach contents.
Occasionally the chest pain is so
severe it may be difficult to
distinguish from the pain associated
with a heart attack. Some
individuals have trouble
swallowing. Sour stomach contents
may reach the back of the throat.
Symptoms usually get worse with
eating, whereas ulcer symptoms are
usually improved for an hour or so
after food consumption. The
symptoms of GERD become less
noticeable with time and the
passage of food from the stomach,
also the opposite of ulcer
symptoms.
Medications that may provide
symptomatic relief include antacids,
H2 blockers, and proton pump
inhibitors (PPIs) such as
omeprazole (Prilosec®) or
esomeprazole (Nexium®). Eating
small meals four to six times a day
may be helpful. Symptoms that are
not readily relieved by medications
should prompt consultation with a
physician to rule out the presence of
ulcers or even a malignant tumor.
Individuals with this condition
should avoid fatty foods, caffeine,
and chocolate; should not eat for
several hours before going to bed
so their stomachs are empty; and
should try to sleep with head and
shoulders elevated so that gravity
can help prevent reflux. GERD is
rarely severe enough to prevent
individuals from partaking in
wilderness activities.
Gastrointestinal Hemorrhage
One of the most serious
problems that can occur in the
wilderness is hemorrhage from the
stomach or intestines. Even with
expert treatment, about 10 percent
of elderly individuals hospitalized
with this condition die. (Death rates
in young, otherwise healthy adults
are lower.) Since blood
transfusions and other forms of
intensive medical and surgical care
are required to treat this life-
threatening disorder, every effort
must be made to get the individual
to a hospital as quickly as possible.
If, in a remote area, helicopter
transport cannot be achieved
promptly, the condition must be
managed in the field. Attempting
litter evacuation or walking out
with assistance while active
bleeding is occurring is unwise.
Fortunately, a young person usually
stops bleeding within twelve to
twenty-four hours. Six to twelve
hours after bleeding appears to
have stopped, a choice between
remaining in camp at rest for one to
three days and attempting to reach a
hospital must be made. A slow
pulse, cessation of vomiting, and a
normal brown stool color are
indications that relatively little
blood has been lost and bleeding
has stopped. However, rebleeding
can occur at any time. Careful
consideration must be given to the
unique circumstances found in
every situation.
Individuals are usually very
weak after a significant bleeding
episode and require assistance
during evacuation. They should by
no means attempt to continue
vigorous activities, even if feeling
well at rest.
Except for the occasional
individuals who bleed slightly after
prolonged retching, essentially all
gastrointestinal bleeding in
otherwise healthy young adults is
due to peptic ulcer. However, even
though the ulcer is almost always
present prior to the hemorrhage, it
may be totally asymptomatic.
serious gastrointestinal bleeding
include the following:
Faintness or weakness, which is
more prominent when erect than
when lying down
Vomiting obvious blood
Vomiting material that looks like
coffee grounds (blood that has
been partially digested in the
stomach)
Rectal passage of obvious blood
Passage of liquid or solid tarry-
black stools (blood that has
been digested in the intestines.)
(Iron, which is contained in
vitamin and mineral
preparations, and the bismuth in
Pepto-Bismol® also can cause
stools to have a dark color.)
Shock
No medications currently
available stop heavy bleeding from
peptic ulcers. However, high-doses
of a PPI often significantly reduce
the rate of bleeding. H2 blockers
may be helpful if a PPI such as
omeprazole is not available.
When the bleeding ceases, acid-
suppressive drugs lessen the
likelihood of rebleeding. In
addition, smoking must cease!
Aspirin and other NSAIDs, alcohol,
and caffeine must be avoided. The
individual should rest as much as
possible. If a substantial amount of
blood has been lost and the person
becomes lightheaded when erect,
the individual should be kept
supine. If signs of shock,
particularly low blood pressure and
rapid heart rate, appear,
appropriate treatment should be
instituted (Chapter 3: Life-
Threatening Problems).
Once the individual has
stabilized, evacuation should be
carried out in the least demanding
and least stressful way possible.
DISEASES OF THE LIVER
Jaundice
Jaundice is produced by
diseases of the liver. One of the
numerous functions of the liver is to
remove from the blood the pigment
(bilirubin) resulting from the
normal destruction of old red blood
cells. When disease severely
damages the liver, the bilirubin not
removed from the blood
accumulates in the body and imparts
a yellow or bronze color to the
whites of the eyes and later the skin.
Bilirubin is excreted into the
intestine through the bile ducts and,
following further changes in the
intestinal tract, imparts the normal
brown color to stools. If the
pigment is excreted into the
intestine in small amounts or not at
all, the stools become pale or clay
colored.
Excess bilirubin is partially
excreted by the kidneys, imparting a
brown color to the urine and
causing the foam produced by
shaking to have a yellow color
instead of the normal white
appearance.
When jaundice is suspected, the
person should be examined in
daylight. Flashlights and other
artificial lights usually produce a
yellowish color that can simulate
jaundice. Any treatment
administered should be for the
underlying disease causing
jaundice.
Hepatitis
Acute hepatitis, an inflammatory
disorder of the liver, is
predominantly caused by infection
with viruses that selectively
involve that organ. It is the most
important cause of painless
jaundice likely to occur for the first
time in wilderness conditions.
(Jaundice associated with pain is
discussed in Chapter 20: Acute
Abdominal Pain.) Untreated
malaria and other conditions cause
jaundice occasionally by the
excessive destruction of red blood
cells. However, such disorders can
usually be recognized from other
findings. Individuals with previous
attacks of jaundice should be
evaluated by a physician and
instructed in the treatment for their
condition prior to undertaking an
outing.
A number of distinct hepatitis
viruses are now recognized:
hepatitis A, B, C, the delta agent
(hepatitis D), and hepatitis E, F, and
G. Hepatitis A is an RNA virus that
is spread principally by fecal
contamination of water and food,
particularly shellfish. Infections are
common but almost never fatal;
well over 90 percent of infected
individuals have such minor
symptoms they do not realize they
are ill. If jaundice does develop, it
rarely lasts over a month. However,
such individuals are usually unable
to continue a wilderness outing.
Chronic liver disease does not
follow hepatitis A infections.
Effective vaccines are available.
Individuals not known to have been
previously infected should be
vaccinated before traveling to
developing nations, particularly if
they visit such areas frequently
(Chapter 5: Immunizations). Gamma
globulin may be advisable for
unvaccinated individuals who
cannot defer travel for the time
needed for vaccination to be
effective.
Hepatitis B is caused by a DNA
virus that is spread principally by
body fluids through personal
contact, particularly sexual contact.
As with hepatitis A, most
individuals do not realize they have
an infection, but up to 10 percent
may be quite ill, a few die, and
approximately 5 percent develop
chronic liver disease.
Approximately half the individuals
with chronic liver disease develop
cirrhosis (scarring of the liver), an
eventually lethal disorder. Hepatitis
B is directly responsible for many
cases of hepatocellular carcinoma
(a malignancy arising in the liver),
the most common malignant tumor
on a worldwide basis, although it is
relatively uncommon in the United
States. A safe and effective vaccine
for hepatitis B is available.
Everyone should be vaccinated, but
it is essential for medical workers,
others who come in contact with
blood, and travelers to developing
countries (Chapter 5:
Immunizations).
The delta agent, or hepatitis D,
is an incomplete DNA virus that can
produce infections only in
association with hepatitis B.
Therefore, immunization for
hepatitis B prevents hepatitis D.
Hepatitis D may be acquired
simultaneously with hepatitis B or
subsequently. Individuals with both
infections simultaneously have a
higher risk of more severe disease.
Acute hepatitis B infection may
become rapidly fatal, and chronic
hepatitis B is more likely to
progress to cirrhosis when
associated with hepatitis D
infection.
Many of the infections
previously termed non-A, non-B
hepatitis are now known to be
caused by hepatitis C, a viral agent
identified in 1989 that accounts for
roughly 20 percent of the cases of
acute hepatitis and a much higher
percentage of chronic, long-
standing infections in the United
States. Acute infections are often
asymptomatic and undiagnosed.
Greater than 50 percent of hepatitis
C infections result in chronic liver
disease, which is often
asymptomatic but may cause
persistent fatigue. Approximately
25 percent of individuals with
chronic hepatitis C develop
cirrhosis, an ultimately lethal
disorder, within twenty-five years
of acquiring the infection. After
twenty years, up to 5 percent of
individuals, often with cirrhosis,
develop hepatocellular carcinoma.
Significant alcohol consumption
increases the risk of such severe
complications.
For hepatitis following blood
transfusion, 90 to 95 percent has
been caused by hepatitis C,
although procedures for screening
for this infection introduced in the
early 1990s have essentially
eliminated this problem in the
United States. In developing nations
such screening procedures often are
not available or not affordable, and
the risk of hepatitis C is much
higher. Hepatitis C is also spread in
developing nations by needles and
syringes that are reused after being
washed but not sterilized.
Hepatitis C is an RNA virus that
is transmitted through broken skin
or mucous membranes mainly by
blood-to-blood contact. Prior
intravenous drug use accounts for
50 percent of the infections, sexual
contact for 10 percent, blood
transfusion (mostly before 1993)
for 5 to 10 percent, and exposure to
infected blood by nurses,
ambulance attendants, and similar
medical professionals for 5 percent.
The routes of inoculation for the
remaining one-third of the
infections are unidentified, although
homemade tattoos and sharing
cocaine devices have also been
implicated. Diagnostic blood tests
for this virus are widely available,
but development of a vaccine has
not yet been accomplished. Gamma
globulin is of no value for
preventing infection.
Another form of non-A, non-B
hepatitis—an important form
worldwide—is hepatitis E, which
is rarely encountered in the United
States. The virus was first
identified in 1989 and has been
linked to epidemics in Africa and
Asia and to two outbreaks in
Mexico. Infection usually results
from ingestion of water
contaminated with sewage and can
be prevented by routine
disinfection. Infection can also be
spread by close personal contact.
Like hepatitis A, hepatitis E usually
produces an acute infection that is
rarely fatal and heals without
producing chronic liver disease.
However, in some outbreaks the
mortality in pregnant women has
been as high as 20 percent. No
diagnostic blood test is available,
but the virus can be identified in
stool samples. No vaccine is
available. The effectiveness of
gamma globulin for preventing or
ameliorating the infection is
unknown.
Hepatitis F and G are recently
discovered bloodborne infections
about which little is known.
The onset of hepatitis may be
abrupt or insidious and follows an
incubation period ranging from
three weeks to six months. The
earliest symptoms are loss of
appetite, general malaise, and easy
fatigability. Later a low fever and
nausea and vomiting appear. Many
smokers have a peculiar loss of
taste for cigarettes. In individuals
with more severe infections, the
symptoms increase in severity.
Lightcolored stools and dark-
colored urine may precede the
appearance of jaundice by several
days. Vague upper abdominal
discomfort and tenderness may be
present, particularly in the right
upper quadrant, but severe pain is
absent. After the appearance of
jaundice, some individuals
experience ill-defined joint or
muscular pains. A highly variable
skin rash may be present, and some
have generalized itching. When
jaundice does develop, it often lasts
three to six weeks. Malaise, easy
fatigability, and loss of appetite
may persist for several more
months.
No effective treatment for the
acute episodes of any type of
hepatitis infection is available. A
study of previously healthy young
adults in the U.S. Army indicated
that restriction of exercise had no
effect on the course of the disease
for that rather select group of
individuals. Most wilderness
explorers would fall into the same
group of previously healthy,
relatively young adults. However,
most people infected with hepatitis
do not feel capable of more than
very mild exercise. A nourishing
diet, high in proteins and
carbohydrates and supplemented
with vitamins, should be provided.
All drug therapy should be
avoided if possible, including
alcohol and drugs to promote sleep.
The liver metabolizes most drugs.
When that organ’s function is
impaired by hepatitis, such
metabolism may be much slower
than normal. If the drugs are not
completely metabolized between
doses, they can accumulate in the
blood and may reach toxic
concentrations.
Most people with hepatitis
should be evacuated. Recovery
usually takes so long that delaying
evacuation until the person is well
is impossible. In addition,
complications that require a
physician’s care may develop. If the
infection is severe, important
proteins involved in the clotting
mechanism of blood are not
effectively produced by the liver,
predisposing the individual to
bleeding.
Treatment of chronic hepatitis B
with lamivudine and subsequent
newer nucleotide or nucleoside
agents has produced favorable
results and is well tolerated.
Considerable viral resistance to
lamivudine has displaced this agent
in favor of the newer medications.
Hepatitis C can be treated with
injectable interferon in combination
with oral ribavirin, producing an
agonistic antiviral effect, but
therapy is prolonged, expensive,
and only partially successful.
Prevention is of utmost importance
to avoid contracting infection in
endemic areas.
Cirrhosis
Hepatic cirrhosis is a
progressive scarring or fibrosing
process that results from chronic
hepatitis B and C infections,
prolonged alcohol abuse, and other
inflammatory disorders. It is
ultimately lethal. Jaundice and
ascites, an accumulation of fluid in
the abdomen, are common
complications. The scarring blocks
the normal flow through the liver of
blood returning from the intestines.
To return to the circulation, the
blood must find other channels,
which results in the enlargement of
veins in several areas, most
prominently the lower esophagus.
Death often results from massive
bleeding from these enlarged
esophageal veins (known as
varices), which can only be
controlled in a hospital setting.
Variceal hemorrhage in a
wilderness setting would often be
fatal. Liver failure is also a
common cause of death for
individuals with cirrhosis. Such
problems are rare in wilderness
situations because individuals with
these conditions rarely feel well
enough to visit the backcountry; in
any case, they should be
discouraged from doing so.
Acute Hepatic Necrosis

Acute hepatic necrosis is a
disorder that is usually fatal within
a week. Toxic fungi (Amanita
mushrooms); large quantities of
some drugs, such as acetaminophen
(Tylenol®), particularly when
associated with regular alcohol
consumption; rare reactions to
medication; and certain chemicals
such as carbon tetrachloride or
other toxic exposures can produce
this disorder. However, knowledge
of these hazards has become more
widespread, and the most common
cause of acute hepatic necrosis now
is probably acute hepatitis.
Individuals with acute hepatic
necrosis rapidly deteriorate,
become intensely jaundiced, and
sink into a coma that cannot be
reversed. The only effective
treatment is hepatic transplantation,
which rarely can be performed
rapidly enough, even in major
medical centers.
CHAPTER 20
ACUTE ABDOMINAL PAIN
Hunter B. Moore, B.A.
Ben Eiseman, M.D.
Travelers to remote areas who

consume food and water from
questionable sources are familiar
with the abdominal pain associated
with acute diarrhea. These
symptoms, although painful for a
few hours or days, are self-limited
and gradually subside.
Distinguishing such relatively
trivial conditions from serious
diseases that are potentially life
threatening can be difficult.
Inappropriate delay in evacuating
an individual to a medical facility
where surgical intervention is
available may seriously
compromise the outcome, but
unnecessary evacuation can disrupt
a carefully planned expedition. The
key question is whether evacuation
is warranted.
A few questions are helpful in
making a preliminary decision:
1. Do others in the party share
identical complaints? The most
common cause of abdominal pain
in wilderness conditions is
infectious gastroenteritis
(traveler’s diarrhea), which is
Gastrointestinal Disorders.
2. Has the individual had similar
attacks of abdominal pain in the
past? If so, symptoms are likely
to have the same cause and
previously effective treatment
should be repeated.
3. Does the person have a known
medical disorder? What
medications are being taken?
Individuals often fail to mention
medications that they use
routinely in their urban
environment, such as aspirin,
anticoagulants, antihypertensive
agents, bronchodilators,
antihistamines, diuretics, mood
elevators or depressants, and
even insulin. Such drugs may
produce unexpected symptoms
and alter the course of a disease
when taken in a harsh outdoor
environment.
4. Are the pain and tenderness
localized to a single point in the
abdomen? Such localization
often suggests an inflammatory
process that requires operation.
5. Is the abdomen diffusely tender
and rigid? A boardlike abdomen
commonly signals generalized
peritonitis that requires
immediate evacuation and
surgery.
6. Is the person seriously ill?
Delirious? Febrile? Dehydrated?
Thirsty? (These can be signs of
shock.) Does the individual feel
warm?
7. Does the person seem likely to
overreact to discomfort? A
wilderness environment
constitutes a severe emotional
stress for some inexperienced
persons.
DIAGNOSIS
A definitive diagnosis may be
impossible during the early phases
of a disease, but a tentative or
working diagnosis, with the
understanding that it may be altered
as signs and symptoms change, is
appropriate because it provides
guidance for the next step. Once the
abdominal pain and other evidence
of disease are well developed, an
astute examiner can usually match
the signs and symptoms with the
pattern of a known disorder.
History
Important information to be
obtained for the history includes the
following:
When did pain begin?
What is the nature of the pain
(sudden versus gradual onset,
sharp versus dull, persistent
versus intermittent)?
Where is the pain (right or left
of the midline, above or
below the umbilicus)?
How have the pain and
tenderness progressed since
onset? (Is the pain increasing
or decreasing? Has it shifted
from one part of the abdomen
to another? Has the nature of
the pain changed? For
example, has generalized
discomfort become localized
sharp pain?)
Is nausea, vomiting, or
diarrhea present?
Are chills, fever, or other
signs of infection present?
Does the urine contain blood?
Does the individual have a
history of any of the
following?
Similar episodes
Pain relieved by food or
milk
Indigestion caused by fried
or fatty food
Previous abdominal
surgery
A missed menstrual period
Physical Examination
An unhurried examination should
be performed in the quietest place
available, with the person as
comfortable and as secure as
possible. However, in the
wilderness medical emergencies
frequently arise at night, and a
frightened individual must be
examined inside a cramped tent
with a headlamp as the only light
source.
The entire abdomen from crotch
to nipple line should be bared and
examined visually first. Abdominal
surgical scars suggest intestinal
obstruction caused by postoperative
adhesions. Abdominal distention is
indicative of intestinal obstruction,
either mechanical obstruction or
paralysis of the intestinal muscles
(ileus) by inflammation. A mass or
hernia should be specifically
sought. The abdomen should be
watched to determine whether
attacks of cramping pain are
accompanied by abdominal
muscular spasm.
Detecting abnormal bowel
sounds by listening to the abdomen,
preferably with a stethoscope, may
be an exercise in futility for an
inexperienced examiner. But the
absence of bowel sounds over a
period of several minutes is an
indication of ileus, usually resulting
from peritonitis. Conversely, the
presence of hyperactive bowel
sounds is consistent with
gastroenteritis.
Figure 20-1. Organs of the abdominal
cavity
Palpation of the abdomen is

critical for localizing the disorder
but must be performed gently,
patiently and systematically (Fig.
20-1). The examiner’s hands should
be as warm as possible to avoid
inducing muscle spasm with cold
fingers. The individual should be
asked to tell where the pain is
greatest and to point with one finger
to that site. The examiner should
stay away from that point during the
initial examination; jabbing at the
tender spot usually results in tensing
the abdominal muscles, which can
block subsequent attempts to detect
subtle tenderness and muscle
guarding. Gentle pressure at a site
distant from the suspected disorder
may elicit pain referred to the site
of inflammation and clarify the
diagnosis. A typical example is
pressure in the left lower
abdominal quadrant causing pain in
the right lower quadrant in cases of
acute appendicitis (Fig. 20-2). Pain
elicited when pressure by the
examining hand is released—
rebound tenderness—is a sign of
peritoneal inflammation, which is
usually caused by infection.
Figure 20-2. The four quadrants of the
abdomen
Consultation
Progress in telecommunication
technology, particularly cellular and
satellite telephones, has simplified
obtaining medical consultation in a
wilderness environment. Those
providing medical care in such a
situation should never hesitate to
seek advice. Before a consultation,
the care provider should prepare
answers—preferably written—to
all relevant questions (“Medical
History” and “Physical
Examination” in Chapter 1:
Diagnosis). The person’s name,
address, age, and gender are also
essential facts.
If a decision to observe the
individual overnight is made, calls
should be scheduled at four- to six-
hour intervals so that any
deterioration in the person’s
condition can prompt evacuation
plans at first light (Table 20-1).
CONDITIONS THAT DO NOT

REQUIRE EVACUATION
Gastroenteritis
With acute gastroenteritis, others
who have shared the same food or
drink often have similar signs and
symptoms. The typical onset is
gradually increasing abdominal
distress that soon changes to waves
of cramping pain that may be severe
and are often associated with an
overwhelming urge to defecate. The
stools soon become watery and, in
severe cases, may contain flecks of
blood. The acute pain
characteristically subsides
following each diarrheal stool, and
the individual may be relatively
free of right upper quadrant right
lower quadrant left upper quadrant
left lower quadrant discomfort until
another episode of cramps begins.
A feeling of weakness or malaise
and a low-grade fever often appear
with the diarrhea, and the person
may become dehydrated. Vomiting
is usually not prominent.
Differentiating gastroenteritis
from appendicitis may be difficult
in the early hours of the disease.
Diarrhea is seldom associated with
appendicitis but is typical of
gastroenteritis. The pain of
appendicitis is steady and
unrelenting, whereas discomfort
with gastroenteritis is usually
intermittent and cramping in nature.
The pain or discomfort from
appendicitis may start near the
midline but characteristically shifts
to the right lower quadrant of the
abdomen. In contrast, the pain and
discomfort of gastroenteritis are
typically generalized.
Table Acute Abdominal Pain

20-1 Features
PAIN
GENDER
LOCATION
CONDITIONS NOT REQUIRING
EVACUATION
Gastroenteritis Equal Diffuse
Lower
Mittelschmerz Female
quadrant
CONDITIONS THAT MAY
REQUIRE EVACUATION
Lower
Salpingitis Female
quadrant
Kidney stone Equal Flank/back
Upper
Peptic ulcer Equal
middle
Right
Acute Female
upper
cholecystitis > Male
quadrant
Acute Upper
Equal
pancreatitis middle
CONDITIONS REQUIRING
EVACUATION
Right lower
Appendicitis Equal
quadrant
Ruptured
ectopic Female Lower
pregnancy quadrant
Intestinal
Equal Diffuse
obstruction
Incarcerated Male >
Groin
hernia Female
Left lower
Diverticulitis Equal
quadrant
Differentiating the two

conditions is important because
appendicitis must be treated by
early operation, whereas
gastroenteritis is usually self-
limited and rarely requires
evacuation. As detailed in Chapter
19: Gastrointestinal Disorders,
hydration is necessary for
gastroenteritis, but oral intake of
any kind is difficult for a nauseated
individual with appendicitis and
should be avoided unless
evacuation is expected to require
more than twenty-four hours.
Mittelschmerz
Midway between menstrual
periods, some women encounter
discomfort from the slight amount of
bleeding associated with normal
ovulation. The pain is located on
either side of the lower abdomen,
where the involved ovary is
located. The discomfort is
sometimes significant. While some
women recognize the cause of such
discomfort, younger women
unfamiliar with this symptom may
under the stress of a wilderness
environment confuse this process
with appendicitis, particularly
when ovulation is from the right
ovary.
The differential diagnosis is
usually easy; the timing of the
discomfort halfway between
menstrual periods is invariable.
Physical signs of inflammation are
minimal, and the disorder usually
disappears without treatment within
twenty-four hours.
CONDITIONS THAT MAY

REQUIRE EVACUATION
Salpingitis
This gynecologic infection, also
known as pelvic inflammatory
disease, occurs in sexually active
women of any age. Most infections
affect one of the Fallopian tubes,
through which eggs move from the
ovaries to the uterus. The organism
is usually either Chlamydia or
Gonococcus. The tipoff is that the
women are sexually active,
typically with multiple partners,
and have tenderness right above the
pubic bone, a mild fever, and
occasionally some vaginal
discharge. The characteristic
symptom is the gradual onset of
pelvic and suprapubic discomfort.
Women with this condition seldom
appear acutely ill or toxic, and
some have had previous attacks.
The treatment consists of antibiotics
(Chapter 22: Infections), and
evacuation is usually not necessary.
However, occasionally salpingitis
results in an abscess that can
rupture and produce generalized
peritonitis, and when located on the
right side it may be confused with
acute appendicitis; in either of these
situations, the condition requires
prompt evacuation.
Kidney (Renal) Stone

When minerals in the urine
precipitate to form a stone, it may
remain in the kidney or may pass
through the narrow tube (ureter) that
connects each kidney to the bladder.
The resulting pain typically is quite
severe. Renal stones are considered
by some to be the most painful
condition people encounter. The
pain usually is sudden in onset and
cramping in nature. The pain is
usually associated with nausea, and
may be accompanied by vomiting.
The pain may be localized to one of
the flanks or back but often radiates
down to the groin and into the
scrotum or labia. The diagnosis is
confirmed by identifying blood in
urine collected in a clear glass
container or passed into snow.
However, the pain of a kidney stone
can be confused with that of an
incarcerated (irreducible) inguinal
hernia or appendicitis. If the stone
does not pass through the ureter into
the bladder, pain persists, although
it may gradually diminish to a dull
ache in the side. Fever, chills, and
generalized malaise may
accompany the pain with a stone
that obstructs the ureter. In extreme
cases, the urine may contain pus if a
kidney infection supervenes
(Chapter 21: Genitourinary
Disorders).
Treatment consists of antibiotics
and consumption of large volumes
of water by mouth to increase urine
volume and help wash the stone into
the bladder. If the stone passes into
the bladder, the pain quickly
subsides and the emergency is over.
Once the stone has passed, an early
recurrence of another stone is rare,
but the individual should consult a
urologist upon completion of the
trip. On the other hand, in the rare
case of prolonged retention of the
kidney stone in the ureter with
secondary infection, evacuation is
warranted.
Peptic Ulcer
Peptic ulcer is described in
greater detail in Chapter 19:
Gastrointestinal Disorders. Ulcers
characteristically produce
discomfort in the upper part of the
abdomen, usually some hours
following a meal, when the stomach
is empty, and the pain is often
relieved by eating bland food or
milk. Duodenal or gastric ulcer
usually is a chronic disease. The
individual may have previously
been diagnosed with a peptic ulcer
and may have been taking
medications such as antacids or
proton pump inhibitors.
If the discomfort is localized and
not significantly different from
previous ulcer pain, treatment with
antacids or proton pump inhibitors
is usually all that is necessary.
However, if the pain develops
suddenly, is unusually severe, or is
associated with signs of peritonitis,
free perforation of the ulcer into the
abdomen is likely and evacuation is
mandatory.
Acute Cholecystitis
The gallbladder is a thin walled
sac that lies beneath the liver in the
right upper quadrant of the abdomen
and stores bile secreted by the
liver. When food containing fat
empties from the stomach into the
intestine, the gallbladder contracts,
forcing bile through the common
bile duct into the intestine where it
mixes with the food to assist
digestion. Bile salts in the bile can
precipitate and form stones, which
may remain in the gallbladder or
pass through the bile duct into the
intestine. Most individuals with
gallstones are middle aged, usually
obese, and may have a history of
intolerance for fried or fatty foods.
Individuals with acute
cholecystitis usually have had
uncomplicated gallstones
(cholelithiasis) for a number of
years. Acute cholecystitis develops
when one of the gallstones obstructs
the duct emptying the gallbladder.
The typical manifestations are the
sudden onset of acute right upper
quadrant stabbing pain associated
with nausea and vomiting and
abdominal tenderness that is
maximal in the right upper quadrant.
Analgesics should be
administered to relieve pain; severe
pain may require an opiate such as
morphine. Antibiotics are needed if
symptoms are prolonged, or the
attack does not resolve
spontaneously. As soon as vomiting
stops, the individual can start
drinking small amounts of water
and eating a gradually increasing
fat-free diet. If symptoms persist for
more than forty-eight hours,
evacuation is warranted.
Acute Pancreatitis
Acute pancreatitis is an
uncommon but dramatic cause of
acute abdominal pain. As the name
implies, it is inflammation (not
infection) of the pancreas, which
lies across the upper part of the
abdomen. The condition
characteristically involves middle-
aged persons who have a history of
alcohol abuse, but gallstones can
also be a cause. This disorder
typically is heralded by the sudden
appearance of severe upper
abdominal pain that is associated
with nausea and vomiting. It
frequently follows an episode of
alcohol overindulgence. The
individual is usually immobilized
by the severity of the pain.
Individuals with acute pancreatitis
may be frighteningly ill and in
severe pain.
Treatment consists of analgesics
to minimize pain and encouraging
fluid intake. For the individual
whose condition fails to improve,
evacuation is necessary to provide
intravenous fluids for hydration.
CONDITIONS REQUIRING
EVACUATION
Appendicitis
Appendicitis is the most
common acute abdominal condition
requiring immediate evacuation
from a remote region. Early surgery
is needed to avoid rupture of the
inflamed appendix and
contamination of the entire
peritoneal cavity, which can cause
life-threatening peritonitis. Acute
appendicitis can occur at any age
and in either sex. Only a previous
appendectomy excludes the
diagnosis. In the early stages this
condition may resemble influenza
or similar infections. The first
symptoms are vague and
generalized abdominal distress,
nausea, and vomiting. Rarely is
persistent diarrhea present, which
often is helpful in differentiating
appendicitis from gastroenteritis. In
the early stages the abdomen may
be soft with some generalized
lower abdominal tenderness not
greater on one side or the other. As
the disease progresses, greater
tenderness is found on the right
side.
At this stage the individual
should be kept under careful and
frequent observation to determine
whether the pain and tenderness
change location. Within six hours
the abdominal pain and tenderness
usually shift from the midline to the
right lower quadrant. Maximal pain
and tenderness usually are felt
midway between the umbilicus and
the bony protuberance of the pelvic
iliac crest (McBurney’s point);
pressure applied anywhere over the
abdomen is referred to this site,
which overlies the appendix, and
pain is felt in that location when the
individual coughs or when pressure
on the abdomen is suddenly
released (rebound tenderness).
If the appendix ruptures,
generalized peritonitis usually
develops. This complication is
manifested by high fever, vomiting
of any fluid or food taken by mouth,
and rigidity of the abdominal
muscles. By the time such advanced
signs and symptoms develop, the
astute examiner should have tried to
obtain consultation by radio or
telephone and should have decided
that evacuation is necessary. Delay
invites rupture with its severe
consequences.
As soon as the diagnosis of
appendicitis is made, a broad-
spectrum antibiotic should be
administered to minimize the spread
of the infection. The individual
should be allowed only sips of
water by mouth to relieve feelings
of dryness. Any additional fluid
taken by mouth will not be
absorbed and usually induces more
vomiting.
Ruptured Ectopic Pregnancy
A ruptured ectopic pregnancy
should be suspected in any sexually
active woman experiencing the
sudden onset of severe lower
abdominal pain who also has a
history of missing one or more
menstrual periods and who has
evidence of blood loss such as
weakness, dizziness on standing,
increased pulse rate, low blood
pressure (“Shock” in Chapter 3:
Life Threatening Problems).
Without definitive treatment, the
signs of bleeding continue to the
point of shock. The only definitive
way to stop the bleeding is to
surgically remove the Fallopian
tube, which requires immediate
evacuation to a hospital.
Intestinal Obstruction
Obstruction of the intestinal tract
produces cramping abdominal pain
and ultimately causes nausea and
vomiting. If the obstruction is in the
upper part of the small intestine
near the stomach, vomiting usually
begins soon after obstruction
occurs. An obstruction lower in the
bowel first produces an
accumulation of gas and fluid in the
obstructed segment of intestine. The
onset of vomiting occurs later, and
the abdomen is noticeably
distended by dilated loops of
intestine. The onset of acute small
bowel obstruction is usually sudden
and unexpected and is characterized
by waves of severe, sharp colicky
pain that seem to involve the entire
abdomen. Each rush of gas and fluid
propelled against the obstruction by
peristalsis is accompanied by a
spasm of acute pain felt throughout
the entire abdomen. When the flow
of intestinal contents is blocked,
diarrhea is absent. Not even gas is
passed.
Regardless of the cause of the
obstruction, the urgency of
evacuation is based on whether the
obstruction is complete or
incomplete. If the obstruction is
complete—does not permit
intestinal contents to pass beyond
the site of obstruction—immediate
evacuation is needed to avoid
perforation of the intestine and
catastrophic peritonitis.
The most common cause of small
bowel obstruction is postoperative
adhesions, followed by an
irreducible (incarcerated) hernia,
which is usually inguinal. The cause
of adhesions is tissue reaction that
occurs with any surgery in the
abdominal cavity. After certain
surgeries, particularly those
associated with infection in the
lower abdomen, fibrous adhesions
or scar tissue bind loops of
intestine together. Kinking or
narrowing of the intestine by
adhesions can obstruct the flow of
intestinal contents and is the most
common cause of small bowel
obstruction. Some individuals are
much more prone to developing
adhesions than others. A surgical
scar on the abdominal wall strongly
suggests adhesions as the cause of
an intestinal obstruction. Although
such obstructions manifest most
frequently in the weeks following
surgery, they may not occur for
months or even longer.
Almost nothing can be done in a
wilderness setting to relieve
obstruction due to adhesions. The
only decision to be made is whether
obstruction is complete and the
individual should be evacuated
immediately, or whether the
obstruction is incomplete and
evacuation may be delayed. Only a
few hours are available for this
decision. If the obstruction is
unrelieved, perforation results and
can be life threatening. A venerated
surgical maxim states, “The sun
must not rise or set on a patient with
an obstructed small intestine”
(without surgery). In a wilderness
environment, this translates into
deciding within about six hours
whether the obstruction is
incomplete—whether the individual
is passing gas, has had a bowel
movement, is experiencing less
pain, or the distention of the
abdomen is diminishing. Antibiotics
should be administered once the
decision for evacuation has been
made.
Incarcerated Hernia
Most hernias (ruptures) are
protrusions of the intestines through
an abnormal weakness or opening
in the abdominal wall. Most occur
in the groin or inguinal region (Fig.
20-3). Occasionally—particularly
in women—the hernia may be
relatively unobtrusive, appearing as
a slight bulge below the groin
crease—a femoral hernia. Some
hernias develop in surgical
incisions. Hernias are detectable by
routine physical examination and
should be repaired before a
substantial wilderness excursion,
certainly before a major expedition.
Hernias become important when the
intestine within them cannot be
reduced, that is, returned to its
proper location within the
peritoneal cavity. Obstruction of the
bowel can result and is evidenced
by pain and tenderness at the site. If
the blood supply to the intestine
caught in the hernia is obstructed,
the pain and tenderness become
intense and the bowel can perforate,
resulting in life-threatening
peritonitis.
Figure 20-3. Anatomy of an inguinal
hernia
In contrast to adhesions, if an
incarcerated hernia causes
intestinal obstruction, reducing the
hernia can relieve the obstruction,
which in some circumstances can
be life saving. When an unreduced
hernia is identified, every effort
should be made to reduce it. The
individual should lie flat, face up,
and as relaxed as possible. If much
pain is being experienced, an
analgesic, even an opiate, can be
given to maximize muscular
relaxation. The intestine should be
pushed back into the peritoneal
cavity with gentle but continuous
pressure. A quarter of an hour or
more may be required, and the
process cannot be hurried. Often the
hernia contents slip back into the
peritoneal cavity, and the
obstruction is relieved. The longer
reduction is delayed, the more
likely is compromise of the blood
supply to the entrapped bowel. If
the hernia is reduced, the individual
should be advised to evacuate as
soon as convenient. Most such
individuals can hike out, although
actions producing increased
intraabdominal pressure that may
push the intestine back into the
hernia should be avoided.
If, despite all efforts, the hernia
cannot be reduced or the person
continues to vomit and show signs
of obstruction, evacuation is
mandatory. Antibiotics should be
given in this circumstance.
Diverticulitis
Diverticulitis is inflammation of
an outpouching (diverticulum) of
the colon, most commonly in the
section of colon in the left lower
quadrant (sigmoid colon). Although
diverticulitis usually occurs in
obese individuals more than fifty
years old, it occasionally occurs in
younger people who are not obese.
diverticulitis are similar to acute
appendicitis, but they occur on the
opposite side of the abdomen.
Treatment consists of broad-
spectrum antibiotics, and such
individuals should be evacuated
because perforation of the colon
with peritonitis may occur.
Figure 20-4 presents an
algorithm that outlines the key
decision points in managing an
individual with acute abdominal
pain in the wilderness. The safest
approach is to assume the worst
scenario and avoid delay that may
risk an individual’s life.
NASOGASTRIC INTUBATION
Nasogastric intubation is a highly
desirable—almost essential—
element in the care of individuals
with intestinal paralysis (paralytic
ileus) or obstruction. All the
serious disorders associated with
severe, acute abdominal pain
produce such paralysis; the effects
are most severe with intestinal
obstruction or disorders causing
peritonitis.
Large quantities of air are
swallowed with food or liquids,
including saliva. Gas is always
present in the gastrointestinal tract,
and swallowed air is the source of
most of it. If the stomach is
paralyzed, its contents—including
gas—cannot be expelled into the
intestine, and it quickly becomes
ballooned with air. The distended
stomach impinges on the diaphragm
and interferes with respiration; it
also presses on the veins in the
abdomen and impedes the return of
blood from the lower body to the
heart.
In addition, large quantities of
fluids—digestive juices, partially
digested food, and other liquids that
have been consumed—pool in the
paralyzed stomach with the air, and
eventually lead to vomiting. Loss of
the fluids and electrolytes can
produce or aggravate dehydration,
and pneumonia or respiratory
obstruction may result if the
vomitus is aspirated.
A tube inserted through the nose
and esophagus into the stomach
permits the air that is swallowed to
escape and prevents most of these
problems. The tube is
uncomfortable and can cause a sore
throat, but it usually does not cause
gagging or related symptoms.
The use of nasogastric suction is
not without hazard because fluids,
as well as air, are removed from the
stomach. If these fluids are not
replaced intravenously with a
balanced salt solution or saline, salt
and water depletion inevitably
result. If fluids for intravenous
therapy are not available, the
nasogastric tube should be used
only to remove air that has
collected. After the air has escaped,
the tube should be clamped and
only reopened when significant
quantities of air have
reaccumulated.
Figure 20-4. Algorithm for diagnosing
acute abdominal pain
The technique for nasogastric

intubation is as follows:
1. The tube, at least a size 18
French, should have the tip
lubricated with a bland jelly,
mineral oil, or at least water
before it is inserted.
2. The person should be sitting up
and should have cold water,
crushed ice, or snow to
swallow. If available, lidocaine
jelly can be applied to the
nares, and the throat can be
sprayed with cetacaine to
relieve discomfort during
intubation and afterward.
3. The tube should be inserted
through one nostril, horizontally
along the floor of the nasal
cavity, to the back of the throat.
Then the person should be
instructed to swallow. During
swallowing, the tube should be
thrust farther so the tongue and
muscles of the throat can guide
it into the esophagus. Several
attempts are usually necessary.
When the tube does enter the
esophagus the individual should
be told to keep swallowing.
With each swallow the tube
should be thrust farther down
until a length equal to the
distance from the person’s nose
to the stomach (which should
have been previously measured
and marked) has been inserted.
4. After the tube is in place, a
small amount of air should be
injected through it with a large
syringe or bulb syringe. If the
tube is in the stomach, bubbling
sounds made by the injected air
can be clearly heard by
listening over the stomach with
a stethoscope. If the tube has
coiled in the back of the
person’s throat or turned on
itself in the esophagus and has
not entered the stomach, such
sounds are not heard, and the
tube must be partially
withdrawn and reinserted.
5. Rarely, the tube may enter the
trachea, causing the individual
to cough and sometimes to be
unable to talk. If the tube is
withdrawn promptly, no harm is
done, but the person may be
understandably reluctant to
undergo further attempts at
intubation.
Figure 20-5. Apparatus for applying
gentle suction to a nasogastric tube
6. After the tube is in place, it
should be taped to the person’s
nose or forehead to prevent its
being expelled or swallowed
entirely. Air and fluid in the
stomach can be withdrawn with
a syringe equipped with an
attachment to fit the tubing.
After the stomach is emptied,
the tube should be attached to a
suction apparatus constructed
by suspending a jar filled with
water several feet above the
person’s body, as shown in the
accompanying diagram. (A
lower bottle can collect the
drainage.) (Fig. 20-5.)
7. Nasogastric tubes have a
tendency to become obstructed
by mucus or particles of food.
Therefore, the tube should be
flushed with a small amount of
a salt solution (or water if a salt
solution is not available) every
two hours. (The fluid used to
irrigate the tube must be
subtracted from the total
volume lost through the tube
when calculating the person’s
fluid requirements.)
The total volume of fluid lost
through the nasogastric tube must be
carefully measured and recorded.
All the fluid lost in this manner
should be replaced intravenously
with a balanced salt solution or
saline.
CHAPTER 21
GENITOURINARY
DISORDERS
The urinary tract consists of the

kidneys, ureters, urinary bladder,
and urethra (Fig. 21-1). The genital
system includes the ovaries,
Fallopian tubes, uterus, vagina, and
external genitalia in females; the
testes, epididymides, vasa
deferentia, seminal vesicles,
prostate gland, and external
genitalia in males. The kidneys
filter blood and excrete unneeded
substances and water as urine.
Urine is transported by the ureters
from the kidneys to the urinary
bladder, where it is held until
voided through the urethra.
Normally hydrated adult males
of average size with normal renal
function form approximately 1 ml of
urine per minute. About 60 ml or
two ounces is formed per hour;
1500 ml or 1.5 quarts is excreted
per day. Persons with smaller or
larger bodies produce somewhat
smaller or larger urine volumes,
although urinary output does not
vary directly with size. Dehydration
reduces urine volume;
overhydration increases urinary
output.
Figure 21-1. Anatomy of the urinary
tract
ACUTE URINARY TRACT

DISORDERS
The following are the most common
symptoms or signs of acute urinary
tract disease:
◆ Pain in the back or flank
◆ Burning with urination
◆ Blood in the urine
◆ Changes in urine volume
◆ Chills and fever, sometimes a
high fever
Back pain is often indicative of
kidney disease, particularly when
located to one side of the vertebral
column at the point where the
lowest ribs join. However, the pain
frequently radiates to the sides just
above the pelvis and around to the
groin.
A burning sensation with voiding
is unmistakable, is often described
as the sensation of passing gravel,
and usually results from infection or
inflammation of the urinary bladder,
prostate, or urethra.
Bleeding can be obvious or may
produce only cloudy or “smoky”
urine. If the urine is allowed to
stand so the cells can settle out, a
red sludge often can be seen at the
bottom of the container, confirming
the presence of blood. Surprisingly
small amounts of blood can be
detected in this way.
Changes in urinary volume,
except for very large deviations,
usually go unnoticed unless the
urinary output is measured. In the
wilderness, dehydration is by far
the most common cause for a
change in urinary output. However,
some renal diseases can result in
total or near total cessation of
kidney function. Uncommonly, a
larger volume of very dilute urine is
excreted. The color of the urine is a
reliable indicator of the state of
hydration, particularly dehydration,
which typically results in dark
yellow or orange urine.
Cystitis
Cystitis is inflammation of the
urinary bladder that occurs with or
without infection. This disorder is
rare in young males but fairly
common in females. When cystitis
is associated with acute
pyelonephritis, symptoms of the
latter usually predominate.
The principal symptom of
cystitis is burning or pain during
voiding. The pain may increase
somewhat as the bladder is emptied
but disappears gradually after flow
has stopped. The frequency of
voiding may be increased because
the irritated bladder feels full with
a smaller urine volume. Fever or
other symptoms are rare. Slight
bleeding sometimes occurs; rarely,
bleeding may be severe enough to
make the urine obviously bloody.
Cystitis should be treated
because it usually is the result of an
infection. Ciprofloxacin (Cipro®)
or Trimethoprim-sulfamethoxazole
(TMP-SMX) may be administered.
Cephalexin (Keflex® and others) is
an alternative. These drugs are
excreted by the kidneys and reach
high concentrations in the urine. If
symptoms persist after three days of
drug therapy, the medication should
be changed. Abundant fluids must
be consumed.
Pyelonephritis
Pyelonephritis, an infection of
one or sometimes both kidneys, is
characterized by the rather sudden
onset of high fever, often with
chills, and pain over the kidney.
The individual often feels and
appears ill. Pain of moderate
severity is usually present. Pressing
or gentle pounding with the fist just
below the lower rib on either side
of the vertebral column reveals
tenderness. Symptoms of cystitis
are often present, and slight to
moderate bleeding may occur.
The individual should drink
large quantities of fluids. Fluid
intake and urinary output should be
recorded. Evacuation from altitudes
above 14,000 feet (4300 m) is
desirable.
Antibacterial therapy is
important. Ciprofloxacin (Cipro®)
should be given. If symptoms
persist after three days of drug
therapy, the medication should be
changed. TMP-SMX is an
acceptable alternative but requires
a longer course of treatment.
Individuals with repeated episodes
of pyelonephritis should consult a
physician because irreversible
kidney disease can result. In
addition, an underlying disorder
such as kidney stones may be
present.
Acute Urinary Retention

The most common cause for
cessation of urinary output in men
older than forty or fifty years is
acute urinary retention, which
almost always is caused by an
enlarged prostate. Urinary retention
is usually accompanied by a strong
urge to urinate along with pain in
the bladder or lower abdomen. The
diagnosis is established by
catheterization, which discloses a
large quantity of urine in the
bladder.
Sometimes a man with urinary
retention is able to void again after
a single catheterization, but more
typically an indwelling Foley
catheter must be inserted, and the
person must be evacuated for care
by a urologist. While the catheter is
in place the person should be
treated with ciprofloxacin (Cipro®)
or TMP-SMX to prevent infection.
Acute Renal Failure
Renal failure, a drastic reduction
or total cessation of kidney
function, occasionally follows a
severe injury, particularly if the
person is in shock for several hours
or longer. Certain poisons, drug
reactions, and other disorders can
also cause acute renal failure. If the
person can be kept alive through the
period of reduced renal function,
which may last from a few days to
several months, complete recovery
is usually possible.
The principal manifestation of
renal failure is reduced urinary
output. Dehydration may also cause
a low urinary output, but when a
dehydrated individual is given fluid
the urinary volume increases. An
individual with acute renal failure
cannot increase urinary output, no
matter how much fluid is given.
With dehydration the urine is
concentrated and has a deep yellow
or orange color; with acute renal
failure, the small amount of urine
produced is typically dilute. Any
adequately hydrated person with a
urinary output of less than 400 ml
per day of dilute urine following a
severe injury should be considered
to be in renal failure.
Usually few symptoms related to
diminished renal function are
present for the first two or three
days. However, weakness becomes
apparent on about the third day, and
loss of appetite, nausea, vomiting,
diarrhea, muscle twitching,
confusion, convulsions, and
eventually coma appear sometime
later during the three to ten days
following injury.
Urinary retention and rupture of
the urinary bladder simulate renal
failure because urinary output
ceases. However, such complete
cessation of urinary output is not
typical of acute renal failure.
Urinary retention is usually
accompanied by a strong urge to
urinate as well as by pain in the
bladder or lower abdomen. (If
urethral catheterization discloses
the bladder to be empty, urinary
retention can be ruled out.)
Following bladder rupture,
evidence of an abdominal or pelvic
injury, including abdominal pain
and tenderness, is usually obvious
(Chapter 10: Abdominal Injuries).
However, acute renal failure can
also be associated with an injury in
which the bladder is ruptured.
Evacuation is urgent for renal
failure. Only wellequipped medical
centers would have the dialysis
(artificial kidney) facility required
to keep someone with acute renal
failure alive for more than a few
days. During evacuation fluid intake
must be carefully controlled to
prevent overloading with water. To
establish the diagnosis of acute
renal failure the person’s previous
state of hydration must be
determined. If the person appears
dehydrated, enough fluids must be
given to correct that situation. If
renal output does not return,
subsequent fluids must be
administered very carefully. Each
day’s fluid intake should be limited
to one quart plus a quantity roughly
equal to the urine volume. Unusual
fluid losses caused by vomiting,
sweating, or high elevation must
also be replaced (Chapter 2: Basic
Medical Care).
If nausea and vomiting, which
are usually present after the third
day, prevent taking fluids orally,
intravenous fluids must be
administered. The quart of water,
the previous day’s urinary output,
and any unusual losses through the
lungs should be replaced with a 5
or 10 percent glucose solution.
Fluids lost through vomiting and
excessive sweating should be
replaced with a balanced salt
solution. To ensure that the volume
replaced matches the amounts that
have been lost, urine volume, losses
from other sources, and oral or
intravenous intake must be
measured and recorded.
While able, the individual
should be encouraged to eat sweets,
such as hard candy or glucose
tablets. However, citrus fruits and
fruit juices must be avoided
because they contain potassium,
which can be toxic for a person
with reduced renal function.
Medications should be avoided
because the kidneys excrete most
drugs. In the absence of renal
excretion, their concentration can
rapidly build to toxic levels.
URETHRAL
CATHETERIZATION
With acute urinary retention, most
commonly caused by drugs or an
enlarged prostate in older males,
but also occurring following
prolonged periods of
unconsciousness or after severe
trauma, particularly injuries in
which the lower portion of the body
is paralyzed, the urinary bladder
may be severely distended. Due to
stretching of the bladder muscles
and pressure against the opening of
the bladder, the individual may be
unable to void. As the bladder
becomes more distended, it
becomes painful. To relieve the
distension a catheter must be
inserted into the bladder through the
urethra. The discomfort from this
procedure is surprisingly small,
usually much less than that from a
distended bladder.
Urethral catheterization is rarely
required for females, whose much
shorter urethra offers far less
resistance to voiding. If urethral
catheterization is needed for a
female, it must be carried out by
someone with enough knowledge of
female anatomy to correctly identify
the urethral opening.
Rarely, an individual with a
distended bladder repeatedly voids
a small amount but does not
completely empty the bladder. For
such individuals distension requires
longer to develop but can become
much more severe because it is less
obvious. Since the individual is
voiding, the primary symptom is the
severe discomfort from the
distended bladder.
Usually about eight to ten hours
are required for the bladder to
become distended. Urethral
catheterization can often be avoided
if the person can be induced to void
before that much time has elapsed.
Having the person walk around for
a few minutes or placing the
person’s hand in warm water is
frequently helpful in achieving that
goal.
The greatest risk from urethral
catheterization is infection, but
meticulous care to avoid
contamination of the catheter
reduces this hazard.
The following procedure should
be followed for urethral
catheterization:
1. Everything needed must be
assembled before the procedure
is begun. Any break to obtain a
forgotten item invites
contamination and infection.
The required supplies consist
of a sterile urinary catheter, size
16 or 18 French, sterile rubber
or plastic gloves or sterile
instruments to handle the
catheter, sterile lubricating
ointment, and Betadine® or
soap and water. A sterile towel
on which to place the items is a
great convenience and helps
prevent contamination. The
sterile wrapper from the gloves
may be an appropriate
substitute. A receptacle to
collect the urine should also be
on hand, particularly if the
volume of urine must be
measured.
2. The glans must be cleaned with
Betadine® or just soap and
water, and the catheter must be
removed from its container
without being contaminated.
The circumstances and
assistance available should
determine which is done first,
but the glans should not touch
any nonsterile objects after it
has been cleaned. For women,
the labia should be spread and
the opening of the urethra and
surrounding mucosa should be
cleansed in a similar manner.
The labia must not be allowed
to close until the catheter has
been inserted into the bladder.
3. A small amount of a sterile
lubricant should be applied to
the catheter tip, and, with the
individual in the supine
position, the catheter should be
inserted into the urethra and
gently threaded upward until
urine begins to flow from the
open end. In men, this maneuver
is facilitated if the penis is
pulled upward to straighten the
urethra and eliminate any folds
in the mucosa lining this
passage. After the urine has
ceased to flow, the catheter
should be gently withdrawn.
Some individuals require only a
single catheterization and are
subsequently able to void without
difficulty, but in the wilderness
most individuals require multiple
catheterizations or an indwelling
Foley catheter. Predicting who
would need only a single
catheterization is infeasible, with
the possible exception of
individuals whose retention is
clearly due to a drug that is
expected to wear off.
Foley catheters with leg bags are
the treatment of choice in the
wilderness. This type of catheter
has a small balloon just below the
tip. After the catheter has been
inserted, this balloon can be
inflated by injecting fluid with a
syringe and needle into the nipple
provided for this purpose on the
external end of the catheter. The
balloon must be deflated by
clipping off the end of the nipple
before the catheter is withdrawn.
However, a catheter of this kind can
usually be left in place for up to
three days.
OTHER URINARY TRACT
DISORDERS
Kidney (Renal) Stones
Since the characteristic symptom
of kidney stones is severe pain, this
disorder is discussed in Chapter
20: Acute Abdominal Pain. Bloody
urine and burning with voiding can
also accompany the passage of a
stone.
Hematuria
In residents of developed
countries, hematuria (bloody urine)
may be associated with traumatic
injuries or tumors of the urinary
tract, as well as the disorders
previously discussed, most
commonly cystitis. Schistosomiasis
and—less commonly—tuberculosis
are causes encountered in residents
of developing countries. Traumatic
urinary disorders are discussed in
Chapter 10: Abdominal Injuries.
Adequate treatment for tumors is
impossible in the wilderness.
Visibly bloody urine produced
by cystitis usually disappears in
about twenty-four hours and is
accompanied by symptoms of
cystitis. In the absence of signs of a
specific disorder, hematuria should
prompt immediate medical
consultation to determine the cause
and institute appropriate therapy.
Hematuria can be an indication of a
serious disorder. (The loss of blood
itself is almost never of sufficient
volume to be disabling.)
Hemoglobinuria
Severe injuries, severe
infections, burns, and other
disorders can destroy red blood
cells and release hemoglobin into
the blood. This pigment is excreted
by the kidneys and imparts to the
urine a faint pink to deep red color
that resembles bloody urine.
Hemoglobinuria must be
distinguished from hematuria,
which is caused by entirely
different conditions. If urine that
contains hemoglobin is permitted to
stand, no blood settles to the bottom
of the container. Acute renal failure
sometimes follows disorders
producing hemoglobinuria if the
individual becomes dehydrated or
goes into shock. Immediate
administration of enough fluids to
significantly increase urinary output
helps prevent this complication.
Occasionally, strenuous exercise
alone results in hemoglobinuria or
myoglobinuria. (Myoglobin is a
protein similar to hemoglobin that
originates in muscle and also can be
released by crushing injuries.) Such
disorders can also cause acute renal
failure but usually disappear with
rest. Generous fluid intake must be
maintained to reduce the chances of
renal failure.
The pigment from some foods or
dyes, particularly beets,
occasionally imparts a reddish
color to urine. However, the
individual can usually remember
the ingestion of these substances,
and the pigment disappears from the
urine within a few hours or days.
Hemoglobinuria that is not
associated with renal failure
requires no therapy other than a
high fluid intake.
FEMALE GENITAL
PROBLEMS
Although gynecologic problems are
common and widely variable, few
appear so rapidly that they create
problems on a wilderness outing.
(Ectopic pregnancy, which would
usually cause serious problems, is
discussed in Chapter 20: Acute
Abdominal Pain.) An examination
by a physician before departure
should disclose any potential
disorders and permit their
correction before the outing is
underway.
Two problems that could occur
are dysmenorrhea and abnormal
bleeding.
Dysmenorrhea
Dysmenorrhea means “painful
menstruation.” The pain is caused
by many different abnormalities,
including a wrongly positioned
uterus and passage of blood clots.
Most women with dysmenorrhea
have had it most of their
postpubertal lives, and encountering
it for the first time on a wilderness
outing would be most unusual.
Exercise often relieves
dysmenorrhea.
The pain typically is cramping,
may be disabling, although it
usually is less severe, and usually
is worse the first day or two of
menstrual periods. Mild or
moderate analgesics usually mask
the pain. Prostaglandin antagonists
such as ibuprofen are most
effective.
Diminished physical activity
may be of some benefit. Women
bothered with this problem—they
are numerous—have usually
learned to deal with it long before it
could create problems in a
wilderness situation.
Abnormal Uterine Bleeding
Abnormal uterine bleeding can
take the form of excessive bleeding
with menstrual periods, bleeding
between periods, or both. Although
numerous disorders can produce
such bleeding, commonly no cause
can be identified, particularly in
perimenopausal women. No
specific treatment can be given in a
wilderness situation. The bleeding
is rarely severe enough to create
blood loss problems. If a
hemorrhage of massive proportions
does occur, packing the vagina with
tampons, gauze, or anything
available may help slow the
bleeding during evacuation,
although complete control of
bleeding by such means probably
cannot be obtained. Such problems
must be exceedingly rare; exercise
helps control abnormal bleeding for
many women.
Pregnancy
Pregnancy, at least in its early
stages, does not necessarily require
curtailment of a woman’s customary
activities, but some precautions
should be observed during
wilderness activities. Of all
pregnancies, 15 to 20 percent
terminate in spontaneous abortions,
most of which occur during the first
three months of pregnancy.
Occasionally such abortions are
associated with severe bleeding
that cannot be stopped without
hospital facilities. A woman in this
stage of pregnancy should probably
not enter an area so remote that
evacuation within twelve hours
could not be readily accomplished.
During the last three months of
pregnancy, the enlarged uterus and
the baby it contains often cause
problems with balance. Activities
that require balance would be
difficult. A fall could injure the
mother, baby, or both, even though
such falls would not injure a
woman who was not pregnant.
Premature labor, whether caused by
a fall or occurring spontaneously,
could result in the birth—in less
than optimal circumstances—of a
small, immature baby who could
not survive without the facilities
available in a hospital.
Occasionally pregnancy creates
or aggravates other medical
problems, such as diabetes,
hypertension, or cardiac disease.
The mother should consult her
physician for any special care such
problems would require on a
wilderness outing.
(The specific problem of altitude
and pregnancy is discussed in
Chapter 25: Altitude and Common
Medical Conditions.)
Contraceptives
One aspect of pregnancy, its
prevention, does have implications
for high-altitude activities. Oral
contraceptives cause a very slight
increase in the incidence of deep
vein thromboses and pulmonary
embolism. High altitudes also
predispose to the development of
these disorders (Chapter 18:
Respiratory Disorders, Chapter 24:
Disorders Caused by Altitude).
Trekkers who stay at moderate
altitudes do not have a
demonstrable increase in the
incidence of such conditions unless
they are smokers. However, female
climbers taking part in expeditions
requiring a prolonged stay at
altitudes above 18,000 feet (5500
m) should consider discontinuing
oral contraceptives or switching to
a preparation that does not contain
estrogen several months in advance.
MALE GENITAL PROBLEMS

Few male genital problems appear
with sufficient speed or at an age
young enough to cause problems in
mountaineering situations. Two
exceptions are acute epididymitis
and torsion of the testes, two
entirely different disorders that
have similar features and may be
difficult to distinguish, even for a
physician.
Epididymitis and Testicular

Torsion
Epididymitis is an inflammatory
disorder of the epididymis, an
organ adjacent to the testis in which
sperm collect before passing
through the vas deferens to the
seminal vesicle. Epididymitis
sometimes is the result of
gonorrheal infection, but cultures
are rarely taken from the inflamed
tissues. Most epididymitis probably
has no relation to sexually
transmitted infection; many cases
may not result from infection.
Torsion refers to twisting of the
testis within the scrotum. The
spermatic cord, which contains the
vas deferens and the arteries and
veins supplying the testis, also is
twisted, and the blood vessels,
particularly the veins, are occluded
(Fig. 21-2). If the occlusion is not
relieved, which usually requires
surgery, the testis is deprived of its
blood supply and “dies” within a
few hours.
Figure 21-2. Testicular disorders
Both of these disorders are quite

painful. The scrotum is often
distended and may be inflamed,
particularly with epididymitis. The
testis is usually swollen and quite
tender. The pain of testicular
torsion may appear rapidly;
epididymitis usually develops more
slowly. An enlarged, firm, nodular
epididymis may be felt with
epididymitis. Elevation of the
scrotum is frequently helpful with
epididymitis; elevation of the
scrotum usually does not help
relieve the pain of testicular
torsion. With testicular torsion, the
testis may be higher in the scrotum
than the opposite testis because
twisting shortens the cord.
Both disorders are too painful
for vigorous activity. Hot baths are
helpful for epididymitis but would
usually be impossible in a
wilderness situation. Ciprofloxacin
(Cipro®) or levofloxacin
(Levaquin®) should be
administered to individuals older
than thirty-five years for either
disorder. Younger individuals
should receive the currently
recommended therapy for
gonorrhea, which changes
frequently and is listed on the CDC
website www.cdc.gov. Persons
with testicular torsion who cannot
be evacuated right away need
antibiotics to prevent the
establishment of an infection in the
dead tissue of the testis.
Almost everyone with either of
these disorders must be evacuated.
Individuals with testicular torsion
require surgery, even if it cannot be
carried out quickly enough to save
the testis. Individuals with
epididymitis require rest and
antibiotics. Two to three weeks may
be required for complete healing.
Resumption of activity before all
symptoms have completely cleared
frequently reactivates the disease.
However, epididymitis has little
tendency to spread to other tissues
and probably could be adequately
treated in base camp in truly remote
circumstances.
SEXUALLY TRANSMITTED
INFECTIONS
Of sexually transmitted infections
(STIs or STDs), syphilis,
gonorrhea, and herpes are the most
common. Hepatitis B is spread
largely by sexual contact in
developed nations but is not
considered an STD and is
Gastrointestinal Disorders. Human
immunodeficiency virus (HIV) also
is spread by sexual contact. That
infection and the acquired
immunodeficiency syndrome
(AIDS) it produces are discussed in
Chapter 22: Infections.
All STDs are spread by intimate
personal contact. Infection from
toilet seats or similar sources
essentially does not occur because
the organisms cannot survive
outside of the body. At the present
time the only dependable way to
completely prevent such infections
is to avoid sexual contact with
infected individuals. Condoms are
helpful but do not completely
prevent infection. Prophylactic
antibiotic therapy has many
disadvantages in addition to the
significant risk of allergic reactions
to the drugs.
Syphilis
Syphilis is produced by the
spirochete Treponema pallidum.
This infection has an interesting
history. It apparently originated in
the Western Hemisphere, was
transported to Europe by members
of Columbus’ crew, and in an
amazingly short time spread all
over the world. The great variation
in its clinical features, its long
duration, and its ability to involve
any of the body’s organs and mimic
many other diseases has been
particularly fascinating. The
discovery of penicillin therapy was
a dramatic triumph.
Syphilitic infections have three
stages. The primary stage is that of
the chancre, a one-quarter- to one-
half-inch (6 to 13 mm) painless
ulcer that appears at the site of
inoculation. Most chancres appear
on the genitalia but are occasionally
found on the mouth or lips or the
skin of other parts of the body. In
women, chancres may be located
within the vagina or on the uterine
cervix, where they are not easily
seen. Sometimes primary chancres
never appear, or they go unnoticed,
particularly when hidden in a
location such as the vagina.
The secondary stage of syphilis
is characterized by the appearance
of a skin rash about six weeks after
the primary lesion. However, many
individuals do not manifest this
stage of the disease. The
appearance of this rash is highly
variable, although it does not
produce blisters, and it usually has
a wide distribution, including the
palms of the hands, soles of the feet,
and mucous membranes of the
mouth. The rash does not itch, and
infected individuals usually have no
other significant symptoms. It
usually lasts from a few days to a
few weeks.
In its third or tertiary stage,
syphilis can produce fatal cardiac
disease or disabling brain disease.
However, tertiary syphilis takes
years to develop and can be
prevented by appropriate antibiotic
therapy.
A precise diagnosis of syphilis
requires laboratory facilities not
widely available in developing
countries. Treatment in the
wilderness should be based on a
history of sexual contact and the
presence of a primary chancre or
the secondary skin rash. The
infection is most contagious during
the primary and secondary stages.
The preferred treatment for all
stages of syphilis is penicillin.
Benzathine penicillin G should be
administered for primary or
secondary disease. Alternatively,
single daily intramuscular
injections of procaine penicillin G
may be given. Individuals allergic
to penicillin can be treated with
erythromycin or tetracycline, but
follow-up care should be obtained
from a physician after a wilderness
outing to ensure the infection has
been totally eradicated.
Gonorrhea
Gonorrhea is a common,
widespread infection that in males
is usually limited to the lower
genital tract, principally the urethra.
Infection at this site is associated
with a purulent discharge, but the
diagnostic feature is pain, often
severe pain, with voiding. Residual
infection may persist, particularly
in the prostate, or the infection may
spread to other parts of the body.
In females, gonorrhea is a much
more insidious infection. Of
infected women, 75 percent have no
initial symptoms at all. The
infection must be diagnosed by
bacterial cultures taken from the
vagina or uterine cervix. Treatment
must be based on a history of sexual
contact with an infected individual
when laboratory facilities for a
definitive diagnosis are not
available.
Gonorrhea is also a much more
threatening disorder in females.
Spread of the infection to other
organs is much more common.
Extension to the Fallopian tubes
produces painful infections with
symptoms similar to those of
appendicitis (“Salpingitis,” Chapter
20: Acute Abdominal Pain).
Permanent sterility often results.
Spread to one or more joints can
produce a destructive arthritis;
involvement of the heart can cause
disabling cardiac disease.
Infections also occur in other
tissues.
Unfortunately, strains of
gonorrhea resistant to penicillin
have emerged in recent years and
are now present worldwide. In
wilderness situations all gonorrhea
should be assumed to be penicillin
resistant and treated with a single
intramuscular injection of
ceftriaxone (Rocephin®).
Alternatively, doxycycline
(Vibramycin®) can be given orally.
Genital Herpes
Despite the attention it has
attracted, genital herpes infection is
little different from herpes
occurring on the lips (fever
blisters). Although the genital
infection is transmitted by sexual
contact, it has the same tendency to
recur in the same location as oral
herpes. Because the tissues are
somewhat more sensitive,
infections on the genitalia may be
more uncomfortable than those
around the mouth. No curative
treatment has yet been developed;
acyclovir (Zovirax®) does shorten
the symptomatic period and
duration of virus shedding.
Everyone with a suspected or
known STD should consult a
physician for treatment. An
untreated infection can be
disastrous. The ease with which
syphilis and gonorrhea can be
treated has created a lack of
concern for all such infections. To
encourage individuals to obtain the
therapy they need, many states have
laws that permit physicians to treat
minors without reporting the
infection to parents or guardians.
CHAPTER 22
INFECTIONS
C. Kirk Avent, M.D.
Infections occur whenever

microorganisms invade body
tissues and multiply within them.
Humans normally have harmless
organisms, which rarely cause
disease, in such sites as the skin,
throat, and intestines. However,
when the body’s defenses against
infection are deficient, when
organisms that are not harmless are
present, or when an injury allows
organisms to enter tissues in which
they are not normally present,
infection may result.
Infections that are transmitted
directly or indirectly from one
person to another, such as influenza
and streptococcal sore throat, are
contagious. Others, such as urinary
tract infections or appendicitis,
although infectious, are not
contagious. Many of the infections
of concern to wilderness enthusiasts
are transmitted by vectors such as
mosquitoes (malaria and yellow
fever) and ticks (Rocky Mountain
spotted fever and Lyme disease).
Few infections likely to occur in the
wilderness are so contagious that
they require isolation precautions.
A boil or abscess in the skin
typifies the pain, swelling, redness,
and heat produced by the
inflammation accompanying
localized infections. An infection
confined to a small area such as the
superficial layers of skin usually
does not cause fever or other
systemic symptoms. If a localized
infection extends deeply, however,
organisms may enter the
bloodstream and disseminate
throughout the body. Individuals
with such widespread infections
normally have chills, fever, and
malaise. Additional nonspecific
symptoms may be headache, nausea,
vomiting, and back pain.
When localized signs of disease
accompany fever, identification of
its cause is not difficult. For
example, burning pain on urination,
frequent passage of small amounts
of urine, and discomfort over the
bladder or kidneys indicate a
urinary infection is probably the
cause of chills and fever. Similarly,
if pleuritic chest pain is
accompanied by a cough productive
of thick yellow sputum, the
diagnosis is pneumonia. The
infections discussed in this chapter
are those that involve the skin and
selected other generalized
infections. Infections of specific
organs are discussed in the chapters
dealing with those organs or
systems.
ANTIBIOTICS
Although a large number of
antibiotics have been developed for
the treatment of infectious diseases,
organisms vary greatly in their
sensitivity to individual drugs. An
antibiotic that is effective against
the specific causative organism
must be used for each infection. For
example, streptococci commonly
cause pharyngitis and skin
infections and are usually sensitive
to the penicillin family of
antibiotics. Bacteria resistant to
penicillins but susceptible to the
quinolone family of antibiotics
cause typhoid fever and bacillary
dysentery. Identifying the organism
causing an infection so that the most
appropriate antibiotic can be
administered is highly desirable but
usually is not possible in the
wilderness or in remote towns and
villages.
To eradicate an infection,
antibiotics must be given in
quantities large enough to produce
blood and tissue concentrations that
kill or inhibit the growth of the
causative organisms. Dose
recommendations should be
followed carefully. If nausea or
vomiting prevents oral
administration, or the antibiotic is
not effective when given orally, it
must be administered by
intramuscular or intravenous
injection. Intravenous
administration of drugs and fluids in
the field has become more feasible
with the development of
disposable, plastic administration
sets and may be necessary when
high blood concentrations of
antibiotics are required, as in
meningitis.
Once therapy with an antibiotic
has been started, it should be
continued until organisms have been
killed and until all signs and
symptoms of the infection have been
absent for several days. Treatment
usually lasts from five to twenty
days, depending on the infection.
Shorter courses of therapy may
result in relapse.
prophylactically to prevent
infections except under special
circumstances. For example, most
individuals with colds or minor
wounds should not be given an
antibiotic to prevent pneumonia or a
wound infection. Administration of
antibiotics in this manner does not
prevent subsequent infection, and it
may allow resistant organisms to
multiply and produce an infection
that becomes difficult to treat.
Two frequently used families of
antibiotics are the cephalosporins
and the penicillins. Penicillin V
(Pen Vee K® and others) and
cephalexin (Keflex® and others)
are well-absorbed orally. If
intramuscular injection is
necessary, procaine penicillin G is
used. The intravenous preparation
of penicillin is aqueous or
crystalline penicillin G, and a
frequently used intravenous
cephalosporin is ceftriaxone
(Rocephin®). Cephalexin is given
orally for less severe
staphylococcal infections, except
for those caused by strains of
staphylococci that are methicillin
resistant. Ampicillin, cephalexin,
and ciprofloxacin are usually
effective against organisms that
produce urinary tract infections.
(TMP-SMX, Bactrim, Septra®, and
others), a combination of two
agents, one of which is a
sulfonamide, is useful for treating a
wide variety of infections,
including typhoid fever and
bacillary dysentery, urinary tract
infections, skin infections, and
pneumonia. Ciprofloxacin (Cipro®)
and levofloxacin (Levaquin®) are
quinolones that have a special role
in bacillary dysentery, urinary tract
infections, and traveler’s diarrhea.
Because it affects growing bones,
ciprofloxacin should not be given to
children.
Some individuals are allergic to
the penicillins and may have
severe, even fatal, reactions to
either oral or intramuscular
administration (“Anaphylactic
Shock,” Chapter 23: Allergies).
Anyone who is to receive a
penicillin (or any other drug, for
that matter) must be carefully
questioned about previous allergic
reactions. If a person has a history
suggestive of a serious penicillin
allergy, a chemically different
antibiotic effective against the
infecting organism should be
substituted. Allergies to other
antibiotics and to sulfa drugs also
occur.
BACTERIAL INFECTIONS
Infections of the respiratory tract,
urinary tract, and skin are the most
common bacterial infections. These
disorders are usually innocuous,
although disastrous, widespread
infection can result if they are
mistreated.
Abscesses
Abscesses, boils, carbuncles,
and pimples are localized skin
infections that differ only in size.
They frequently occur at sites of
injury and around hair follicles,
particularly in the armpits and
groin. They are usually caused by
staphylococci resistant to
penicillin. Staphylococci release
enzymes that cause clotting and
obstruction of blood vessels and
lymphatics surrounding the site of
infection. Since the vascular
obstruction blocks the spread of
bacteria, the infection usually
remains localized, but the vascular
obstruction also hinders the access
of white blood cells and antibiotics.
Other enzymes released by these
bacteria destroy tissues around the
infection, producing an abscess
cavity filled with pus (a mixture of
bacteria, white blood cells, and
liquefied tissue).
The treatment for such disorders
consists primarily of drainage and
is similar to the treatment for
infected wounds. Pimples and small
abscesses do not need to be
surgically opened. They should be
covered until they rupture
spontaneously. Squeezing pimples
may force bacteria into the
surrounding tissues and tends to
spread the infection. A particularly
dangerous area for such infections
is around the nose and below the
eyes. Squeezing a pimple in this
region (sometimes referred to as the
“danger space”) may force bacteria
into veins and lymphatics of the
head, which carry them directly to
the brain.
Larger abscesses may have to be
incised to drain them. After the
surrounding and overlying skin has
been cleaned with a preparation
such as povidoneiodine
(Betadine®), alcohol, or clean
water and soap, a small incision
should be made with a sterile
scalpel or razor blade. A local
anesthetic may be necessary. When
a large abscess has been drained, it
should be probed with sterile
forceps to make certain no pockets
of infection remain. Then the skin
should be cleansed again, and a
small piece of sterile gauze should
be inserted into the opening so it
cannot seal off. Finally, the entire
area should be covered with sterile
dressings.
Antibiotics are unnecessary for a
small, uncomplicated abscess.
However, if the abscess is
surrounded by red skin that is more
than 0.8 inch (2 cm) in width, or if
fever, chills, or other symptoms are
present, oral clindamycin
(Dalacin® and others) and TMP-
SMX should be given until all
evidence of infection has been
absent for two days.
Methicillin-Resistant
Staphylococcus Aureus (MRSA)
Methicillin-resistant
Staphylococcus aureus (MRSA)
was first described in 1961 and is
currently found worldwide. It is
spread by direct contact, by sharing
personal items such as towels or
razors that have touched infected
skin, and by touching surfaces or
items such as used bandages
contaminated with MRSA.
These organisms produce
abscesses just like other
staphylococci. Because MRSA are
resistant to all penicillins and
cephalosporins, alternative agents,
such as TMP-SMX and clindamycin
should be used. Similar therapy
should be instituted, even without
signs of bloodstream or secondary
infection, if the individual has
multiple abscesses or is diabetic,
since diabetes may predispose to
severe infections.
Individuals who do not respond
promptly to incision and drainage
and appropriate antibiotics should
be evacuated to a medical center
where infectious disease specialists
and intravenous medications are
available.
Cellulitis
Cellulitis is a bacterial infection
of the skin and underlying tissues
produced by organisms that do not
cause obstruction of blood vessels.
Such infections do not tend to
remain localized, and the bacteria
can spread to other areas more
easily than can some other bacterial
infections. The site of the infection
is usually red, swollen, hot, and
tender. Fever is usually present.
Since the blood vessels remain
open, these infections can be
successfully treated without
drainage. A cephalosporin and
TMP-SMX should be administered
until all signs of infection have been
absent for two days. Clindamycin
can be substituted for either of these
agents if the individual is allergic to
that drug. The person should rest
quietly until the infection has
cleared. Due to its propensity to
spread, cellulitis can be a more
dangerous infection than an abscess,
and its potential for complications
must be respected.
Bacteremia
Bacteremia is defined as the
presence of bacteria in the
bloodstream. The organisms may
multiply in the blood and produce
infections throughout the body.
Bacteremia is usually preceded by
a localized infection such as an
infected wound, a urinary tract
infection, or an abscess but may
also accompany intestinal
infections, such as typhoid fever.
Bacterial bloodstream invasion
produces chills, high fever,
sweating, and prostration. Specific
signs may indicate spread of the
infection to other parts of the body.
Severe headache, a stiff neck, and
nausea and vomiting suggest
involvement of the brain or its
covering (meningitis). Cough,
shortness of breath, and pain with
breathing suggest pneumonia.
With such severe infections,
prompt administration of antibiotics
may be lifesaving. Ceftriaxone
(Rocephin®) combined with
ciprofloxacin is a broadly effective
regimen. If only aqueous penicillin
G is available, it should be given
intravenously. Persons with such
severe infections should be
evacuated.
Individuals with bacteremia
should be provided with rest,
warmth, a soft or liquid diet, and
adequate fluids. Medications for
pain and sleep are often helpful;
aspirin or acetaminophen may be
given to reduce fever. A record
must be kept and should include the
individual’s temperature and the
times any drugs are administered.
Rocky Mountain Spotted Fever

The triad of fever, severe
headache, and rash occurring in the
warmer seasons should suggest the
possibility of a rickettsial infection.
Rickettsiae, a bacteria with
worldwide distribution, are
transmitted to humans by the bite of
arthropod vectors, such as ticks,
lice, and fleas. Not only the most
severe of the rickettsial infections,
Rocky Mountain spotted fever
(RMSF) is also the most prevalent
rickettsial disease in the United
States. Other spotted fevers are
among the emerging infectious
diseases occurring with increasing
frequency, not only in the United
States but also around the world.
RMSF is caused by Rickettsia
rickettsii transmitted to humans by
the bite of a wood- or dog tick. Two
to fourteen days after the bite, mild
chilliness, loss of appetite, and a
general rundown feeling appear.
These mild symptoms are followed
by chills, fever, pain in the bones
and muscles, severe headache, and
confusion. Between two and six
days after the onset of symptoms,
small red spots appear on the skin
around the wrists and ankles and
spread over the entire body,
frequently including the palms of
the hands and the soles of the feet.
These spots are actually
hemorrhages into the skin; in severe
cases, large blotchy red areas may
appear all over the body. The
person appears seriously ill without
an obvious cause. Untreated
infections last about two weeks and
have a mortality rate of 20 to 30
percent; treatment reduces the rate
to 3 to 10 percent. Diagnosis is
aided by a history of a tick bite in
an endemic area. In spite of this
infection’s name, which reflects the
site where it was first identified,
the most important endemic area is
the south-Atlantic coastal states;
over half of Rocky Mountain
spotted fever infections are
reported from Delaware, Maryland,
Washington, D.C., Virginia, West
Virginia, North Carolina, South
Carolina, Georgia, and Florida
(Fig. 22-1). Infections also occur in
other parts of the United States, the
Pacific region (Washington,
Oregon, and California) and the
west south-central (Arkansas,
Louisiana, Oklahoma, and Texas)
region. The two states with the
highest incidences of Rocky
Mountain spotted fever, North
Carolina and Oklahoma, accounted
for 35 percent of the total number of
U.S. cases reported from 1993
through 1996. This infection can
occur in any of the fortyeight
contiguous states.
Tetracycline and doxycycline are
the preferred agents for
uncomplicated cases and should be
given orally. Severe cases,
particularly during pregnancy,
should be treated with
chloramphenicol under close
medical supervision. General
measures such as bed rest, fluid
replacement, antifever medication if
needed, and medication for sleep
are also important.
can be prevented when in an
endemic area by careful daily
inspection for ticks. If any ticks are
found, they should be firmly
grasped with fine-tipped tweezers
as close to the skin as possible and
pulled away with a steady motion
perpendicular to the skin. Any
remaining body parts should be
scraped away, and the wound
should be cleansed carefully.
Individuals moving about in brush
in an endemic area should keep
their shirtsleeves rolled down with
the cuffs buttoned. Shirt collars
should be buttoned, heads should be
covered, and long trousers should
be closed by gaiters or tucked into
boot tops. No reliable vaccine is
available.
More information is available at
www.cdc.gov/ticks/diseases/rocky_m
Figure 22-1. Rocky Mountain spotted
fever cases in the United States
(1994–1998)
Ehrlichiosis (Anaplasmosis)
Though generally an illness
milder than RMSF, ehrlichiosis has
many of the same symptoms and,
like RMSF, is transmitted to humans
by ticks. Two varieties of
ehrlichiosis are found in the United
States. One has roughly the same
distribution as Lyme disease, the
other is concentrated in the South
and mid-Atlantic states. Fever,
headache, nausea, and muscle aches
begin a week to ten days after a tick
bite. One-third of infected
individuals have a rash. The clue to
diagnosis is the development of the
typical symptoms following a tick
bite in one of the high-risk
geographic areas. Low white blood
cell and platelet counts are
frequently found on laboratory
testing. Doxycycline is the treatment
of choice.
The original name, ehrlichiosis,
has been replaced with
anaplasmosis. More information is
available at
www.cdc.gov/ticks/diseases/ehrlichi
Relapsing Fever (Tick Fever)

Tick fever occurs in mountainous
areas of the western and west-
central states. It is a bloodstream
infection caused by a spiral
bacterium (Borrelia recurrentis)
transmitted to humans by a tick bite
or, in some areas, by lice. The ticks
live on rodents and small animals
such as chipmunks, squirrels, and
rabbits. About two to fifteen days
after the bite, chills, fever, severe
headache, muscle aches and pains,
joint pains, a cough, and often
nausea and vomiting appear. A red
rash may appear on the body and
limbs. Bleeding from the nose,
lungs, or gastrointestinal tract may
occur but usually is not severe. The
initial attack lasts two to ten days
and may be followed by an
asymptomatic remission lasting
three to ten days. During the
remission, fever is absent and the
person feels well. A relapse, during
which the previous symptoms recur,
but in a milder form, usually
appears seven to ten days later in
untreated individuals. In such
individuals, three to ten relapses
may occur before complete
recovery. Blood smears should be
examined under a microscope
during febrile episodes to identify
the organism. Doxycycline should
be given to shorten the symptomatic
period and prevent relapses.
www.cdc.gov/ncidod/dvbid/Relapsin
Plague
Plague is a serious infection
caused by Yersinia pestis, an
organism transmitted to humans by
contact with infected rodents or
rabbits or by flea bites. The
organism, not particularly
widespread, is found chiefly in the
southwestern United States and in
rural areas of South America,
Africa, and Asia, particularly
Vietnam. After multiplying in the
skin following a bite, the organisms
spread to regional lymph nodes and
produce large swellings (buboes),
which are responsible for the name
bubonic plague. Fortunately,
involvement of the lungs is rare;
when pneumonia does occur, the
infection is termed pneumonic
rather than bubonic, and becomes
transmissible by droplets in the air.
The illness is characterized by high
fever, chills, prostration, and shock.
It may be rapidly fatal, particularly
in the pneumonic form. Treatment
with streptomycin and tetracycline
should be started whenever the
infection is even suspected and
should be administered by a
physician.
www.cdc.gov/ncidod/diseases/subme
Tularemia
Another infection transmitted to
humans from wild rodents such as
rabbits and muskrats is tularemia.
Humans acquire infection from
skinning infected animals or by the
bite of ticks. A red swelling
develops at the site of inoculation,
then enlarges and ulcerates. The
fever, chills, headache, and nausea
that accompany spread of the
organism to the bloodstream begin
suddenly two to ten days after
inoculation. An enlarged spleen,
rashes, and prostration may
complicate severe cases. Treatment
with tetracycline and gentamicin
should be given by a physician.
Lyme Disease
Lyme disease is a combination
of signs and symptoms related to
infection by Borrelia burgdorferi,
an organism transmitted to humans
from deer and mice by Ixodes ticks.
Although concentrated in the
Northeast, upper Midwest, and
Pacific coast, Lyme disease occurs
throughout the United States and in
parts of Europe (Fig. 22-2).
Approximately 20,000 cases are
diagnosed in the United States
yearly, making it the most common
vector-borne illness in the country.
Because the tick is so small, its bite
frequently goes unnoticed. The risk
of developing Lyme disease from a
tick bite in New England, where
one-quarter to one-half of all ticks
harbor the organism, is only in the
range of 1 to 5 percent. It is most
common in late spring and early
summer. Disease is rare unless ticks
remain attached for more than
twenty-four hours.
The first and most characteristic
symptom, usually occurring three to
ten days after exposure, is a flat,
red, expanding rash that sometimes
clears in its center as it grows
larger and that spontaneously fades
in two to four weeks. Fever,
malaise, and muscle aches
resembling influenza may
accompany the rash. In this stage,
treatment for fourteen to twenty-one
days with oral doxycycline,
(Augmentin®), or cefuroxime axetil
(Ceftin®, Zinacef®) is effective. In
later stages, which may be days to
months after the original illness, a
more widespread rash, headaches,
fatigue, a stiff neck, and pain and
swelling in joints and muscles may
occur. Even later, in the third stage,
serious nervous system, joint, and
skin complications may appear in
untreated individuals. The
diagnosis of Lyme disease in later
stages is based on blood tests for
antibodies to the organism.
Treatment in the later stages is
with different drugs or for longer
times and is best undertaken by a
physician.
www.cdc.gov/ncidod/dvbid/lyme/ind
Figure 22-2. Categories of risk of
Lyme disease in the United States
Leptospirosis
Leptospirosis is an infection
acquired from fresh water or soil
contaminated by urine from infected
animals. Outbreaks have been
associated with adventure travel,
particularly water sports such as
kayaking, white water rafting, and
swimming in tropical rivers. The
illness is biphasic. The first phase
is characterized by a flulike illness
typified by fever, chills, headache,
muscle pains, and nausea. It usually
lasts four to seven days.
Conjunctivitis with red eyes and
muscle tenderness help confirm the
diagnosis.
The second phase is immune
mediated and characterized by
uveitis (redness of the eye, blurred
vision, sensitivity to light or
photophobia, and eye pain), a rash,
and rarely cardiovascular collapse.
Jaundice, renal failure, severe
respiratory distress, and
hemorrhagic phenomena such as
bleeding into the skin may develop.
Pulmonary involvement occurs in
20 to 70 percent of infected
individuals. Approximately 5 to 10
percent of such severe infections
are fatal.
Doxycycline is the preferred
therapy for early disease.
Intravenous penicillin and
hospitalization in an intensive care
unit often are required for severe
infections. Doxycycline provides
effective chemoprophylaxis.
www.cdc.gov/ncidod/dbmd/diseasei
Tuberculosis
Tuberculosis is a slowly
progressive, chronic infection that
is a huge health burden and a major
cause of death worldwide. Much of
the tuberculosis in developing
countries has become resistant to
the drugs available for treatment.
Few individuals with an active
infection would feel well enough to
take part in a wilderness
expedition, and such an infection
would almost always be detected
by a physician before the outing
began. The major problem for
travelers is avoiding being infected
by individuals with active infection.
Two features characterize active
infection and should help travelers
recognize individuals harboring
them. First, pulmonary tuberculosis
is the most common form of
infection and the type that is most
often spread. Individuals with
active pulmonary tuberculosis have
a chronic cough, and material is
usually coughed up. The sputum
typically is thick and yellow and
may be bloody, but if the person
swallows the material that is
coughed up no one can see it.
The second typical feature
results from the long-standing
nature of the infection and the
debilitation that accompanies it.
Infected individuals appear
chronically ill. Most have lost a
significant amount of weight. They
look sick.
Not everyone with active
tuberculosis presents these features,
and such individuals are much more
difficult to recognize. However,
travelers should avoid close
proximity to individuals with
typical features.
Avoiding contact with infected
individuals may be easier said than
done. On city streets of developing
countries discerning travelers can
give people that appear to have
active infections a wide berth.
However, such individuals
sometimes are passengers in public
conveyances, even aircraft, and
staying a safe distance from them
may be difficult.
Travelers must be alert to this
risk and try to avoid contact with
individuals who appear possibly to
be suffering with an active
infection.
VIRAL INFECTIONS
Influenza
Influenza, or “the flu,” is a viral
infection caused by influenza
viruses A or B and produces an
acute, self-limited disease that lasts
five to six days. Spread occurs by
sneezing, coughing, or close contact
with an infected person. Epidemics
are common, particularly in winter
months. The incubation period is
one or two days. The onset is
heralded by chills, fever, weakness,
lassitude, headache, loss of
appetite, and the characteristic
aching muscle pains. A dry, hacking
cough is prominent and may be
severe. The runny nose and sinus
congestion of the common cold are
absent. Fever usually lasts two to
three days and occasionally reaches
104°F (40°C).
respiratory tract involvement
usually differentiate influenza from
other systemic infections; the fever,
muscle aches, and cough distinguish
it from a common cold. A history of
contact with other persons with
influenza is helpful in making a
diagnosis. Gastrointestinal
symptoms are usually absent, but
diarrhea may occur.
Symptoms are partially relieved
by rest, warmth, a light diet with
abundant liquids, and medications
such as acetaminophen (Tylenol®
and others) or ibuprofen (Motrin®
and others) to relieve discomfort.
Medication to promote sleep and
reduce cough may be helpful.
Specific antiviral treatment with
oral oseltamivir (Tamiflu®) or
inhaled zanamivir (Relenza®) is
expensive, is effective only if
started within forty-eight hours of
the onset of symptoms, and shortens
the length of illness by only a day.
Antibacterial drugs have no
value for the routine treatment of
influenza. If fever returns after
several days or a cough productive
of purulent sputum indicates a
secondary bacterial pneumonia has
developed, it should be treated with
an antibiotic having a broad
spectrum of activity, such as a
cephalosporin (Keflex® and
others).
Influenza vaccines prevent or
greatly reduce the severity of
influenza infections. Although
almost anyone can be immunized,
CDC specifically recommends
vaccination for the following
groups:
◆ Children ages six months
through eighteen years
◆ Pregnant women
◆ People fifty years of age and
older
◆ People of any age with certain
chronic medical conditions
◆ People who live in nursing
homes and other long-term care
facilities
◆ People who live with or care
for those at high risk for
complications from flu
More information is available
at www.cdc.gov/flu.
Infectious Mononucleosis
Infectious mononucleosis is a
common viral infection of young
adults spread through close
personal contact. Approximately 95
percent of adults forty years old
have been infected. Although
sometimes incapacitating, it is
usually a mild illness; fatal
complications such as splenic
rupture, secondary bacterial
infections, severe anemia, and low
platelet counts are rare.
The most characteristic symptom
of infectious mononucleosis is a
persistent, severe sore throat. Other
complaints are not specific: fever,
fatigue, and loss of energy. Lymph
nodes in various portions of the
body are usually enlarged,
especially those in the neck.
The triad of sore throat, lymph
node enlargement, and fever is
classic, but infectious
mononucleosis is notorious for its
great variability. A skin rash,
headache, weakness, loss of
appetite, and generalized aching
may be present. Mild liver
involvement is frequent; more
severe involvement with jaundice
occasionally occurs.
No specific treatment is
available. Antiviral and
antibacterial drugs are of no
benefit. Serious complications, such
as hepatitis or an obstructed airway
due to enlarged lymph nodes can be
treated with a five-day course of
prednisone. Saltwater gargles may
help the sore throat. An adequate
fluid intake should be stressed since
the sore throat may discourage oral
intake. Rest is important, and the
person’s activity should be limited
until fever resolves. Since minor
abdominal trauma could easily
rupture the enlarged and fragile
spleen, climbing with a waist loop
and other activities in which such
injury is likely should be avoided.
Recovery in most cases takes two
to four weeks. If jaundice or skin
hemorrhage is present, the
individual should be evacuated.
www.cdc.gov/ncidod/diseases/ebv.h
Dengue Fever
Dengue is another febrile illness
that is associated with a rash and is
transmitted to humans by Aedes
mosquitoes, the same vector that
transmits malaria. The disease is
caused by a virus in the same family
as the yellow-fever virus. In recent
years, dengue has emerged as a
major public health problem,
particularly in the Americas. The
disease has the same geographic
distribution in the tropics as
malaria and is the most important
mosquito-borne viral infection
affecting humans. Because Aedes
mosquitoes are most commonly
found near human habitation, the
disease is more common in urban
than rural environments, and the
risk of infection for wilderness
travelers is smaller. After an
incubation period of four to seven
days, infected individuals develop
the sudden onset of high fever,
headache, joint pain, nausea,
vomiting, and a blotchy, red rash.
After a brief period of
improvement, fever and symptoms
may recur. Almost everyone
recovers, but bleeding, hepatitis,
and neurologic complications may
occur and require a physician’s
care. A vaccine is under
development but is not yet
available.
Colorado Tick Fever

Colorado tick fever is a viral
disease transmitted by the wood
tick. It occurs in all western states
and is far more common there than
Rocky Mountain spotted fever.
Infections usually occur in spring
and early summer when ticks are
active. Four to six days after
exposure, chills and fever appear,
along with headache and
generalized aching. The eyes may
be unusually sensitive to light. The
initial attack lasts about two days,
at which time the fever and other
symptoms disappear, only to recur
two to five days later. The outlook
for complete recovery is good, even
though no specific treatment is
available. Bed rest, fluids, and
aspirin are helpful. A physician
should evaluate the person to be
sure that Rocky Mountain spotted
fever, a more serious disorder that
requires antibiotic treatment, is not
present.
www.oregon.gov/DHS/ph/acd/diseas
Yellow Fever
Yellow fever is an infection of
humans and primates caused by a
virus transmitted by the Aedes
mosquito. The disease occurs
chiefly in South America and in
sub-Saharan Africa. Following an
incubation period of three to six
days, chills, fever, headache, and
backache begin. The heart rate may
be slow in relation to the severity
of the fever. Most individuals
recover completely after a few days
without progressing to the severe
form of the disease. In a few,
however, fever returns and the
person becomes flushed, feels
nauseated, starts vomiting, and
appears seriously ill. The eyes may
be bloodshot and the tongue red.
Bleeding from the gums and into the
skin may occur; vomiting material
that looks like coffee grounds or
black stools indicates that bleeding
is occurring in the stomach or
intestines. Jaundice, which gives
the disease its name, develops.
The treatment of yellow fever
consists of bed rest and a liquid or
soft diet high in carbohydrates.
Fluid and salt replacement may be
necessary because of the
dehydration that accompanies
vomiting, diarrhea, and high fever.
Nonsteroidal anti-inflammatory
drugs for discomfort and bedtime
medications for sleep are helpful.
No specific treatment is available.
If travel into a yellow fever area is
planned, vaccination with the highly
effective yellow fever vaccine
should be obtained (Chapter 5:
Immunizations).
www.cdc.gov/ncidod/dvbid/yellowfe
Hantavirus Pulmonary Syndrome

The hantavirus pulmonary
syndrome (HPS) was first
recognized in the Four Corners area
of New Mexico, Arizona, Utah, and
Colorado in May 1993. Through
March 2007, 465 infections had
been reported in the United States,
35 percent of which had resulted in
death. Infections have been reported
in thirty states, including most of the
western half of the country and
some eastern states. Infections have
also been reported from Canada,
Argentina, Brazil, Chile, Paraguay,
and Uruguay.
The agent responsible has been
named Sin Nombre virus. (Other
hantaviruses—the Hantaan,
Dobrava-Belgrade, Seoul, and
Puumala varieties—cause
infections that produce renal failure
and hemorrhagic fever. These
infections have been recognized in
Europe and Asia since 1913 and
may have been observed in China
as early as AD 960). The name
hantavirus comes from the Hantan
River in Korea, although Lee Ho-
wang, who first isolated the virus,
in his original publications
transliterated the river’s name
idiosyncratically as “Hantaan.”
At onset HPS is flulike: fever,
muscle aches, headache, and cough.
Progression to respiratory failure
and death frequently is quite rapid.
Urgent hospitalization and intensive
care are usually required. No
specific treatment is available.
Therapy is supportive and includes
control of hypoxia, avoidance of
excessive fluids, and support of
blood pressure.
In the Four Corners area
hantavirus infection was found in
30 percent of the deer mice, which
do not become ill but shed the
organisms in saliva, urine, and
feces. Human infection occurs when
infected saliva or excreta that has
dried are inhaled as aerosols. Dried
rodent excreta that are introduced
directly into broken skin or the eyes
may also infect humans.
The disease is best controlled by
environmental hygiene that excludes
rodents. For campers, the CDC
recommends the following
commonsense precautions:
◆ Tents or sleeping bags should
not be placed near areas
attractive to rodents such as
garbage dumps or woodpiles.
◆ Rodent infested cabins should
be avoided.
◆ Tents with floors or cots
should be used for sleeping—
bare ground should be
avoided.
◆ Food should be kept in rodent-
proof containers.
◆ Garbage should be disposed of
properly.
◆ Water should be disinfected.
◆ Dead mice should be handled
with gloves.
More information is available
at
www.cdc.gov/ncidod/diseases/h
Hemorrhagic Fever Syndromes

The hemorrhagic fever
syndromes (HFS) are a group of
infections caused by four entirely
different families of viruses,
although all are RNA viruses and
have a fatty envelope (Table 22-1).
Most of the infections have a high
mortality rate. Ebola Zaire has a
mortality rate of 80 percent,
although this infection occurs
mostly in areas where sophisticated
medical care is rarely available.
Some are quite common. Yellow
fever is estimated to kill 30,000
individuals a year in Africa even
though most infections are mild and
the mortality rate is only about 15
percent. Only two infections each
by Ebola Tai and Ebola Sabia (or
Brazilian hemorrhagic fever) have
been recognized.
These infections share the
feature of frequent, although not
universal, bleeding into the skin,
into the gastrointestinal tract, and
from body orifices. However, the
unfortunate individuals who
contract hemorrhagic fever die as
the result of organ failure, usually
liver or kidney failure; they do not
bleed to death.
The viruses that cause these
infections have highly specific
animal reservoirs, and the
infections are limited to areas
where those animals are found. For
instance, the reservoir for Argentine
hemorrhagic fever is two species of
rat found only in cornfields in
northern Argentina, and the
infection is limited to that area.
However, hemorrhagic fevers of
one type or another are found over
most of the globe, and the reservoir
for one such infection, Seoul
hemorrhagic fever, is the common
rat or Norwegian rat, which is
found everywhere. Dengue, which
can produce dengue hemorrhagic
fever, is found throughout the
tropical world.
Table
Viral Hemorrhagic Fevers
22-1
METHOD
VIRUS CLINICAL
OF
FAMILY DISORDER SPREAD
Bunyaviruses
Hantavirus
Hemorrhagic
Rodent
Fever with
contact
Renal
Syndrome
Hantavirus Rodent
Pulmonary contact
Syndrome
Crimean-
Direct
Congo
contact or
Hemorrhagic
tick borne
Fever
Rift Valley Mosquito
Fever borne
Flaviviruses
Mosquito
Yellow Fever
borne
Dengue
Mosquito
Hemorrhagic
borne
Fever
Kyasanur Tick
Forest Disease borne
Tick-borne Tick
Encephalitis borne
Omsk
Tick
Hemorrhagic
borne
Fever
Filoviruses
Bats and
Marburg
Disease direct
contact
Bats and
Ebola Sudan direct
contact
Bats and
Ebola Zaire direct
contact
Bats and
Ebola Reston direct
contact
Bats and
Ebola Tai direct
contact
Bats and
Ebola
direct
Bundibugyo
contact
Arenaviruses
Rodent
Lassa Fever
contact
Junin Fever
(Argentine Rodent
Hemorrhagic contact
Fever)
Machupo
Fever (Bolivian Rodent
Hemorrhagic contact
Fever)
Guanarito
Fever
Rodent
(Venezuelan
contact
Hemorrhagic
Fever)
Sabia Fever
(Brazilian
Hemorrhagic
Fever)
Whitewater
Fever (United
States)
Because most of these infections

have a geographically limited
distribution, they are unlikely to
strike mountaineers and adventure
travelers who avoid centers of
infection. Precautions against
mosquito and tick bites further
reduce the risk.
www.cdc.gov/ncidod/diseases/virlfv
PARASITIC DISORDERS
Malaria
Malaria is caused by protozoa of
the genus Plasmodium and is
transmitted by the bite of infected
mosquitoes. Worldwide, 300 to 500
million clinical infections occur
each year, more than tuberculosis,
AIDS, measles, and leprosy
combined. One million persons die
from malaria every year, 90 percent
of whom are children less than six
years old.
Malarial parasites are ingested
along with the blood of an infected
person or animal when female
Anopheles mosquitoes bite. The
parasites undergo fertilization,
reproduce in the mosquito’s gut, and
are transmitted to humans when the
mosquito injects saliva into the skin
during a subsequent bite. In the
human, parasites invade red blood
cells, multiply, and release daughter
parasites, destroying red blood
cells in the process. The daughter
parasites invade other red blood
cells, and the process is repeated.
The periodic release of parasites
produces recurrent episodes of
fever; the destruction of red blood
cells can eventually result in
anemia.
The initial symptoms of malaria
are muscular soreness and a low
fever, which appear about six to ten
days after a bite by an infected
mosquito. Four to eight days later,
the typical chills and fever appear.
Shivering, chattering teeth, cold and
clammy skin, and a feeling of
chilliness that is not relieved by
heating pads or blankets
characterize this stage. An hour
later, the febrile stage begins with a
flushed face, a feeling of intense
heat, headache, often delirium, and
temperature as high as 107°F
(41.5°C). This stage lasts about two
hours and is followed by drenching
sweats and a fall in temperature.
Headache, backache, and muscular
aches may be very severe.
The repeated occurrence of
febrile episodes at regular intervals
such as every day, every other day,
every three days—occasionally at
irregular intervals—is
characteristic of malaria. In severe
cases vomiting, diarrhea, severe
anemia, dark urine containing
elements of destroyed red blood
cells, shock, and coma may occur.
Enlargement of the liver or spleen
may be present.
Treatment consists of general
supportive measures and specific
drug therapy. Rest in bed and
maintenance of body warmth during
the chill is highly desirable. Since
water losses by sweating may be
severe, a large fluid intake should
be encouraged. Fluids and salt lost
by vomiting or diarrhea also must
be replaced. A careful record of
temperature and pulse should be
kept. If possible, blood smears
should be made during the chill for
later identification of the parasites.
During an acute episode of malaria,
the subsequent period of therapy,
and for two weeks following
recovery, strenuous exercise should
be avoided to prevent rupture of the
spleen.
Specific treatment for malaria
should be given by a physician
familiar with its various types and
manifestations. The most effective
general regimen for chloroquine-
sensitive malaria consists of
chloroquine and primaquine.
Plasmodium falciparum malaria
is the most dangerous form of
malaria for two reasons: It
produces the most severe disease,
and strains resistant to chloroquine
have been found throughout the
world except for isolated pockets in
Central and South America.
Expeditions into areas where
malaria is present should consider
carrying mefloquine, quinine,
pyrimethamine, and doxycycline to
treat chloroquine-resistant
falciparum malaria. Instruction by a
physician should be obtained before
using these drugs.
Before leaving for a region in
which malaria is present, a
traveler’s clinic or the Centers for
Disease Control and Prevention
should be consulted to determine
whether chloroquine-resistant
falciparum malaria has been found
in that area. Chloroquine
prophylaxis effectively prevents
malaria caused by strains that are
not resistant. Treatment should start
two weeks before entering an
endemic area and continue for five
weeks after leaving. Any illness
occurring within five weeks after
leaving a malarial area should be
reported to a physician.
If travel is anticipated into areas
where chloroquine-resistant
malaria is present, mefloquine
(Lariam®) should be taken
beginning one week before travel
and continuing for four weeks after
return; contraindications include
pregnancy, psychiatric illness, and
seizures. A combination of
atovaquone and proguanil
(Malarone®) is an alternative
antimalarial agent that should be
started one to two days before
entering a malaria endemic area and
continued for seven days after
return. Consultation with a
physician knowledgeable about
travel medicine should be arranged
well before the anticipated date of
departure.
In cities and towns frequently
visited by tourists, malaria is
uncommon, and malaria-carrying
mosquitoes are rarely found at
elevations above 4500 feet (1500
m). In malarial areas, contact with
mosquitoes should be minimized
with screens or mosquito netting,
protective clothing, and insect
repellents. The best available
repellent is N, N-diethyl-m-
toluamide (DEET). In long-acting
preparations it remains effective for
up to eighteen hours, a considerable
advantage over other repellents,
which are effective for only two to
four hours. It may be easier to avoid
malarial areas than to take
chloroquine for multiple weeks, as
this drug does occasionally cause
itching, gastrointestinal complaints,
and a variety of other side effects.
www.cdc.gov/malaria.
Babesiosis
Babesiosis is a malarialike
parasitic disease occurring
primarily along the northeast coast
of the United States and in Mexico,
Yugoslavia, and Ireland. The
organism is transmitted from mice
and voles to humans by Ixodes tick
bites. The illness is characterized
by fever, chills, sweats, headache,
and muscle aches. Because red
blood cells are destroyed by the
parasite, anemia may result. The
disease is usually self-limited, and
most people recover uneventfully.
In a few individuals, particularly
those whose spleen has been
removed, the disease is severe,
even fatal. Treatment with quinine
and clindamycin appears to be
effective.
The tick that transmits this
parasite is the same tick that
transmits Lyme disease and
ehrlichiosis, and some individuals
are infected by two or all three of
these organisms. Laboratory studies
are required to identify ehrlichiosis
and babesiosis, and individuals
suspected to have either should be
referred to a physician.
www.cdc.gov/ncidod/parasites/babe
Schistosomiasis (Bilharziasis)
Schistosomiasis is a parasitic
infestation caused by three different
species of the genus Schistosoma. It
affects over 200 million people
worldwide, but most infested
people have no symptoms or
clinical evidence of disease.
Depending upon the particular
species, infestation can cause
complications in the liver, bowel,
or urinary tract. The life cycles of
all species are similar. After the
eggs leave the human host in stool
or urine, they hatch into tiny
miracidia that penetrate any of
several species of freshwater
snails. The absence of an
appropriate snail host in the waters
of the United States probably
accounts for the absence of disease
in this country. Within the snail the
miracidia mature into free-living
cercariae. When released from the
snail into water, the cercariae are
able to infest humans by penetrating
through intact skin, a step that
requires about thirty minutes. After
two days, the organisms spread
through the bloodstream to the lungs
and liver. A month later, the worms
mature and migrate through veins to
their final dwelling place in the
intestines or urinary bladder. Adult
worms live five to ten years.
The clinical manifestations of
schistosomiasis occur in stages and
are produced by the effects of the
organism. Skin penetration by the
cercariae usually is not associated
with any reaction, but repeated
exposure may lead to a red rash that
is called swimmer’s itch or
schistosome dermatitis where such
infestations occur.
Sometimes, with particularly
heavy infestations, fever, chills,
headache, and a cough occur when
adult worms form and eggs are first
produced. Such episodes are known
as Katayama fever or acute
schistosomiasis. The liver, spleen,
and lymph nodes are enlarged, and
eosinophilia is present.
The chronic effects of infestation
are produced when the body
responds to the eggs. S. mansoni
and S. japonicum adults live in the
intestines and release their eggs into
blood that goes to the liver.
Scarring occurs around the eggs,
producing obstruction to liver
blood flow. First the liver and then
the spleen become enlarged. In late
stages catastrophic gastrointestinal
bleeding and liver failure may
occur.
Different complications are
associated with infestation by S.
haematobium because the adults
live in the veins around the urinary
bladder instead of in the intestines.
Scarring from the eggs of these
organisms produces obstruction of
the bladder and ureters. Blood in
the urine and painful urination are
the usual symptoms. Eventually, the
chronic irritation associated with
the infestation can lead to malignant
changes. Squamous cell carcinoma
of the urinary bladder is rare in
most of the world but is one of the
most common malignancies in areas
where schistosomiasis is endemic.
The three main Schistosoma
species are found in freshwater
lakes and rivers worldwide.
Infections caused by S. mansoni are
found throughout all of Africa,
Arabia, South America (Brazil,
Venezuela, and Surinam) and the
Caribbean. S. japonicum occurs in
Southeast Asia and the Philippines,
whereas S. haematobium occurs in
Africa and the Middle East.
The diagnosis of schistosomiasis
is made by finding the characteristic
eggs in the stool or urine of
individuals with any of the clinical
manifestations of infection, such as
dermatitis, Katayama fever, or liver
disease. A blood test is available
through the CDC.
Safe and effective oral drugs
have recently been introduced for
the treatment of schistosomiasis.
The most broadly effective is
praziquantel (Biltricide®) in
differing dosages for S. mansoni, S.
haematobium, and S. japonicum.
Treatment should be undertaken
only by a physician. The drugs kill
the organisms but do not eliminate
them from the body, and they
produce inflammatory reactions
similar to—although considerably
less severe than—those produced
by living eggs.
Avoiding infestation is far more
satisfactory. Infestation can be
avoided only by staying completely
out of stagnant or slowly moving
water in areas where the parasites
are found. No swimming, bathing,
or even wading should be allowed
in infested water. No other effective
preventive measure exists. The
snails that form an essential part of
the schistosome life cycle do not
live in rapidly moving water, so the
schistosomes are not found there.
Significant infestations have
occurred among rafters on slow-
moving streams that did not occur
during flood season when the water
was flowing much faster.
Onchocerciasis
Onchocerciasis (river blindness)
is one of the most common causes
of loss of vision in developing
countries. It is caused by a filarial
parasite transmitted to humans by
the bite of black flies found near
rivers in higher elevations of
tropical Africa, Central America,
and South America. Adult worms
live in hard, painless nodules under
the skin. The adults release
microfilaria that cause intense
itching in the skin and irritation of
the eye. The diagnosis is made by
examining skin biopsies or
examining the eye for the organism.
Effective treatment is now
available with ivermectin
(Stromectol®).
www.cdc.gov/ncidod/submenus/sub_
Chagas’ Disease
Chagas’ disease, or American
trypanosomiasis, is found from
southern South America to northern
Mexico. The causative organism,
Trypanosoma cruzi, is transmitted
from infected animals to humans by
the bite of several kinds of reduviid
(kissing or assassin) bugs that
inhabit the walls and ceilings of
poorly constructed houses. After a
bite, usually at night, redness and
swelling occur locally and are
followed by fever, headache,
generalized lymph node swelling,
and enlargement of the liver and
spleen. Ten to thirty years later
signs of irreversible damage to the
heart, esophagus, or colon appear.
Although no clearly effective form
of treatment in the late stages of
disease is available, nifurtimox may
be useful early.
Preventive measures include
insecticide spraying of infested
houses. Insecticide-impregnated
bed nets may reduce the risk of
infection for travelers who cannot
avoid camping, sleeping outdoors,
or sleeping in poorly constructed
houses in endemic areas.
www.cdc.gov/chagas.
Trichinosis
Trichinosis (or trichinellosis) is
a parasitic disease caused by eating
improperly cooked meat containing
larvae of the roundworm
Trichinella spiralis. Infection is
common in wild carnivores and
may also be found in domestic pigs.
After the larvae are ingested, they
attach themselves to the wall of the
small bowel, mature, and produce
eggs. The larvae released when the
eggs hatch spread throughout the
body via the bloodstream and
localize in muscles.
If infestation is heavy,
penetration of the intestinal wall by
the larvae one to four days after
ingestion produces nausea,
vomiting, abdominal cramps, and
diarrhea that resemble food
poisoning. The migration of the
larvae to the muscles seven days
after ingestion produces fever,
chills, muscular weakness, a skin
rash, and swelling of the face and
tissues around the eyes. Headache
may be severe.
The diagnosis is based upon the
onset of characteristic symptoms
following the ingestion of poorly
cooked wild game or improperly
prepared pork or pork products
such as salami. A skin test is
available. If the Trichinella
parasite is discovered early, in the
intestinal phase, albendazole can be
effective in eliminating the
intestinal worms and larvae. There
is no specific treatment for late-
stage trichinosis. Symptomatic
treatment consists of rest, mild or
moderate analgesics, and sedatives
to promote restful sleep. Prednisone
may be beneficial in the early
stages of the disease. All pork must
be thoroughly cooked. In addition,
freezing at 0°F (−18°C) for twenty-
four hours or 5°F (−15°C) for
twenty days usually kills all
trichinae.
www.cdc.gov/ncidod/dpd/parasites/t
ACQUIRED
IMMUNODEFICIENCY
SYNDROME (AIDS)
Acquired immunodeficiency
syndrome is the result of a
susceptibility to unusual infections
and malignant tumors caused by a
defect in the immune system. The
disease results from the destruction
of normal lymphocytes by the
human immunodeficiency virus
(HIV). Since its identification in
1981, the disease has spread
worldwide. Over two-thirds of HIV
cases, and over 80 percent of
deaths, occur in sub-Saharan
Africa.
Significant Febrile Illnesses
Table Likely to Be Encountered
22-2 by Mountaineers and
Adventure Travelers
FEVER
WITH FEVER FEVE
MACULES1 WITH WITH
AND 3
PETECHIAE RASH
PAPULES2
Rocky Rocky
Mountain Mountain Typho
spotted fever spotted fever
Dengue fever Dengue fever Malar
Infect
Typhoid fever Malaria
monon
Lyme disease Meningococcal Plague
disease
Infectious Relapsing
mononucleosis fever
Hepatitis B Yellow fever
Viral
Measles hemorrhagic
fevers
Epidemic
Rubella
typhus
Tularemia
Relapsing
fever
Colorado tick
fever
Toxic shock
1A macule is a flat patch of discolored s
2A papule is a small, raised area of disc
skin.
3Petechiae are small, dark red or purple
containing blood.
The period of time between

infection by HIV and the
development of AIDS can be many
years. During this latent phase, the
infected person has no symptoms
but is capable of transmitting the
infection by sexual contact, by
blood, and from mothers to infants.
Transfusions of blood or blood
products, injections with needles or
syringes contaminated with blood,
infected mothers giving birth, and
splashing contaminated blood into
open wounds are some of the ways
blood can transmit the virus. On the
other hand, kissing, sharing utensils,
using the same toilets, drinking from
the same containers, touching, and
other nonintimate contacts do not
transmit the virus and are safe.
Persons who are infected with HIV
but otherwise are in good health do
not need to be excluded from
wilderness outings, although they
should inform other participants of
their infection.
Blood transfusions are extremely
risky in any country that does not
effectively screen blood for HIV. A
traveler’s clinic or the CDC can
supply upto-date information.
Similarly, injections from reused
syringes or needles are dangerous.
The safest ways to avoid sexual
transmission of infection are
abstinence or monogamous sexual
relations with a person known to be
uninfected. Condoms reduce, but do
not eliminate, the risk of infection.
www.cdc.gov/hiv.
CHAPTER 23
ALLERGIES
When foreign substances enter the

body, the immune system responds
by forming antibodies that combine
with the foreign materials to
facilitate their elimination. When
the foreign substances (antigens)
are bacteria or viruses, antibodies
play a large role in preventing or
eradicating infection. Other foreign
antigens also elicit an antibody
response.
Once a person has contacted an
antigen, antibodies persist in the
blood for years or even for a
lifetime. These persistent
antibodies provide permanent
immunity following infections such
as measles or mumps. Vaccines are
composed of dead or weakened
organisms that induce immunity by
eliciting an antibody response
without producing a full-blown
infection. Some vaccines do not
elicit an antibody response as
effective as that following an actual
infection and must be repeated
every few years.
Antibodies are proteins known
as immunoglobulins (Ig). Various
types of immunoglobulins are
classified as G, M, A, E, and D and
are usually abbreviated IgG, IgM,
and so on. Occasionally a person
reacts to an antigen by forming an
excessive amount of antibody,
particularly IgE, the principal
antibody responsible for allergic
reactions. Contact with that antigen
—or allergen (an antigen that
produces an allergic reaction)—
results in a strong IgE response that
releases histamine and related
substances to produce an allergic
reaction.
The periodic injection of
gradually increasing amounts of an
allergen can sometimes overwhelm
the antibody response. This
process, desensitization, eliminates
or greatly reduces the allergic
reaction. If desensitization is
stopped, the original allergic
condition usually returns.
Nonetheless, desensitization can be
useful in helping to control allergic
reactions such as hay fever.
The substances to which an
individual may become allergic are
unlimited. Foods, pollens, animal
dander, and dust are the most
frequent offenders. Reactions to
therapeutic agents are also common.
Insect stings, peanuts, and penicillin
are notorious for causing
anaphylactic reactions, an
uncommon type of allergic reaction
that is explosive in onset and can be
lethal if not effectively treated.
HAY FEVER
Pollens, dust, or other allergens in
the air and animal dander are the
most common causes of hay fever
(acute nasal allergy). Hay fever is
rare in a world of ice and snow,
whether at high altitude or extreme
latitude, but is a common problem
—occasionally a severe problem—
in warmer climates. Hay fever
caused by pollens tends to be
seasonal; hay fever caused by other
antigens such as animal dander may
be a year-round problem. The nasal
membranes are red and swollen,
causing nasal stuffiness and nasal
discharge. Frequent sneezing is
common. The eyes are often red;
excessive tearing is common.
Individuals with recurrent hay
fever so severe it hinders routine
activities should consider
desensitization and should consult a
physician or allergist to determine
the medications that are most
effective for them personally. Some
drugs and drug combinations are
more effective for certain
individuals than others.
For individuals with less than
severe hay fever, over-the-counter
antihistamines that cause little or no
drowsiness and need to be taken
only once a day are available.
Other antihistamines are effective
but do induce drowsiness.
HIVES
Hives are often caused by food
allergies—chocolate, seafood, and
fresh fruit are the most common
offenders—but can occur as an
allergic reaction to almost any
substance, including dusts and
pollen, insect bites and stings, or
drugs, occasionally even to drugs as
commonly used as aspirin. Hives
appear quickly following contact
with the allergen, are often widely
scattered, and consist of red or
white raised wheals (bumps) that
itch intensely. Hives may rapidly
appear and disappear several times
from a single allergen exposure.
Repeated exposures to the same
allergen usually reproduce the
attacks indefinitely. However, the
condition is more miserable than
serious.
The treatment for recurrent
episodes of hives consists of
antihistamines. Nonsedating
antihistamines are effective for
some people, but the standard is
diphenhydramine (Benadryl®,
Dramamine®, and others).
Cornstarch packs or baths or bland
lotions may help reduce itching.
Individuals who have hives with
other symptoms, such as hoarseness
or throat swelling, should be
evaluated by a physician and
probably need to carry epinephrine
to treat recurrent or more severe
symptoms. Spontaneous recovery
occurs without treatment if further
exposure to the allergen is avoided.
CONTACT DERMATITIS
A rash occasionally develops
following contact with jewelry, the
case of a wristwatch, or a similar
material. Often the cause cannot be
determined, and the rash may not be
located at the point of contact. The
rash is usually more annoying than
disabling, typically is composed of
multiple small blisters on a red
background, and may itch or burn.
Bothersome rashes may be treated
with 1 percent hydrocortisone
cream or ointment, which are
available over the counter.
POISON IVY, POISON OAK,

AND POISON SUMAC
Poison ivy, poison oak, and poison
sumac (Fig. 23-1) produce an acute
contact dermatitis—toxicodendron
dermatitis—due to the urushiols that
are components of their sap. Poison
ivy and poison oak are closely
related plants found throughout the
United States and Canada and grow
as shrubs or vines. Their leaves are
shiny and grow in clusters of three,
a distinctive pattern that allows
them to be easily recognized.
Poison ivy leaves tend to have
smooth edges, and poison oak
leaves tend to be more lobulated or
serrated, but the patterns overlap
and distinguishing the two is not
important. Poison sumac does not
have this identifying feature but
grows only in marshy areas east of
the Mississippi and is encountered
much less frequently.
Figure 23-1. Typical appearance of
the leaves of poison oak (A), poison
ivy (B), and poison sumac (C)
The rash typically develops at

the point of contact but may appear
at sites that are far removed. It
usually appears on the hands and
face only a few days after contact,
but as long as a week may pass
before it appears at other locations.
The rash usually disappears in the
same order it appeared after four to
seven days.
Red streaks or patches that itch
appear first but are followed in
twelve to twenty-four hours by
blisters that typically are arranged
in lines. The blisters often break,
resulting in oozing and crusting of
the surface. Usually swelling of the
underlying tissues, burning, and
itching are present. Scratching
should be avoided because it can
introduce infection or cause
scarring, but scratching does not
spread the rash; the blisters are
filled with serum, not the urushiol
that causes the dermatitis.
Treatment depends upon the
extent of the rash. If the area
covered is small, no therapy at all
may be needed. Calamine lotion
may relieve itching. For more
extensive eruptions, itching may be
relieved by cool saltwater
compresses (2 teaspoons [8 ml or 8
gm] of salt per quart of water)
applied for ten minutes four times a
day. A steroid ointment such as 1
percent hydrocortisone can be
applied in limited amounts after the
compresses. Individuals with
extensive, disabling urushiol
dermatitis require systemic steroid
therapy. In urban surroundings such
persons have been defined as those
sick enough to seek a physician’s
care; the physician should prescribe
the appropriate medication.
According to its manufacturer,
Zanfel®, a recently developed
product, binds with the urushiols
that cause the rash, removes them
from the skin, and relieves
symptoms in thirty seconds. To use
this product the area of dermatitis
should be wet with water. A 1.5-
inch strip of the cream should be
squeezed onto one palm, and the
hands should be wet and rubbed
together for ten seconds to work the
product into a paste. Then both
hands should be rubbed on the
affected area, working the product
into the skin until the itching stops,
which usually takes only about
thirty seconds. Finally, the area
should be rinsed thoroughly. If the
itching returns the application can
be repeated.
Desensitization for poison ivy
has been tried, but the side effects
are as bad as the rash. No
desensitizing agent has been
approved by the Food and Drug
Administration (FDA). Many over-
thecounter preparations for poison
ivy contain antihistamines,
analgesics, or even antibiotics that
can produce a secondary allergic
reaction that may be worse than the
original problem.
ANAPHYLACTIC SHOCK
Anaphylactic shock is an acute,
severe allergic reaction that
involves essentially the entire body.
Fortunately, such reactions are not
common, for death can occur within
five to ten minutes if treatment is
not administered immediately—nor
are they rare. An estimated 500 to
1000 fatal anaphylactic reactions
occur each year in the United
States. Deaths due to anaphylactic
reactions undoubtedly still go
unrecognized, are attributed to heart
attacks or similar disorders, and
may be significantly more common
than appreciated. The number of
milder reactions is much greater but
cannot be accurately determined
because no precise definition of the
syndrome has been accepted. Some
physicians only diagnose severe
reactions as anaphylaxis, although
others include milder disorders.
The causes of anaphylactic
shock likely to be encountered in a
wilderness situation are food
allergies, drug reactions, and insect
stings. Food allergy was
responsible for one-third of the
anaphylactic reactions in
individuals presenting to the
emergency room at the Mayo
Clinic. The foods that most
commonly cause food-induced
anaphylaxis are peanuts; tree nuts
such as pecans, walnuts, and
almonds; and shellfish, but a wide
variety of foods has caused such
reactions.
Drug reactions are an equally
common cause of anaphylaxis. Most
such reactions are caused by
penicillins or cephalosporins that
have been injected, although orally
ingested drugs occasionally cause
them. An estimated 1 in 5000
penicillin injections results in
anaphylaxis. Foreign serums, such
as horse serum-based antivenom
used to treat venomous snakebites,
cause anaphylaxis in approximately
one-fourth of the individuals
receiving them. Because the danger
of anaphylactic shock is so great,
these serums must be administered
only when absolutely essential and
must be given only in a hospital
where the allergic reaction can be
monitored and controlled.
Insect stings are a less common
cause of anaphylactic shock but
more common in wilderness
situations. In the United States,
deaths due to allergic reactions to
insect stings far outnumber those
caused by all other venomous
animals, including venomous
snakes, spiders, and scorpions
(Chapter 33: Envenomations).
Other substances, such as latex,
also cause anaphylaxis, and for a
number of reactions no cause can be
identified.
Diagnosis
The symptoms of anaphylactic
shock usually appear five to fifteen
minutes after exposure to the
allergen. Occasionally an hour or
more may pass before symptoms
appear, and very rarely twentyfour
hours can elapse, particularly after
oral ingestion of the offending
substance.
The dominant feature of
anaphylactic shock is severe
respiratory distress that appears
and progresses rapidly. Swelling of
the tissues of the upper air
passages, particularly in the larynx
where the airway is already
narrowed by the vocal cords
(laryngeal edema) narrows the air
passages and can produce lethal
respiratory obstruction. Narrowing
of the bronchi within the lungs—
bronchospasm—produces
respiratory difficulty that is similar
to asthma. The cause, spasm of
muscle in the walls of small
bronchi that results in severe
constriction, is identical. With
anaphylaxis the onset is more
abrupt and usually develops within
minutes. Sometimes a sense of
pressure beneath the sternum is
noted.
The skin is the most common
organ involved by anaphylaxis.
Hives may be present and are
widely distributed. Angioedema, a
localized swelling of the skin and
subcutaneous tissue, may occur on
an extremity or around the eyes or
mouth. Such swelling can also
involve mucous membranes and
produce respiratory obstruction.
The skin usually appears flushed
but sometimes is pale. It is rarely
normal in appearance.
Involvement of the eyes and nose
causes changes that resemble a
sudden, severe attack of hay fever.
The eyes are swollen and red, and
the flow of tears is increased. A
red, swollen mucosa and mucoid
discharge plug the nose. Nausea,
vomiting, abdominal pain, and
diarrhea reflect involvement of the
gastrointestinal system. Rarely,
involvement of the cardiovascular
system can result in shock or a
cardiac arrhythmia that can be fatal.
Treatment
Anaphylactic shock is a true
medical emergency for which
minutes may make a difference
between therapeutic success and
failure. Individuals who know they
are at risk for anaphylaxis should
wear warning bracelets and carry
auto-injectors, which they must
learn how to use before they are
needed. Time for reading the
directions, which are available on
the patient insert as well as on the
Internet, may not be available once
a reaction has begun. Individuals
who are carrying auto-injectors
should also carry an antihistamine
—diphenhydramine (Benadryl®,
Dramamine®, and others) is the
standard—and prednisone
(described below).
Treatment must be instituted
without delay and consists of
intramuscular injection of 0.3 ml of
a 1:1000 aqueous solution of
epinephrine (adrenaline).
Epinephrine in 1:1000 dilutions
is available in several forms in the
United States. EpiPen® is a
preloaded syringe that can be
injected almost instantaneously with
only one hand. The needle can be
jabbed into the thigh or any other
convenient location, through
clothing if necessary. Although the
syringe contains 2 ml of solution,
only a single 0.3 ml dose can be
delivered with each syringe.
EpiPen Jr.® is intended for children
and delivers one-half the adult
dose.
The manufacturer’s directions
state that the user should do the
following:
◆ Grasp the auto-injector with
the black tip pointing down.
◆ Pull off the gray safety release.
◆ Jab the needle, which is in the
black tip, firmly into the
midportion of the outer thigh
perpendicular to the skin until
it clicks.
◆ Hold the auto-injector firmly
against the thigh for ten
seconds.
◆ Remove the auto-injector and
massage the area for ten
seconds.
The manufacturer warns that no
one should touch the black tip, the
gray safety release should not be
removed until the unit is to be used,
no button is present under the safety
release, and the autoinjector should
not be used if the expiration date
has passed, the solution is
discolored, or a red flag appears in
the clear window in the auto-
injector body. (If nothing else is
available, the auto-injector can be
used if the expiration date has
passed or the solution is
discolored.)
The Twinject® auto-injector is a
second device that can deliver two
epinephrine injections, a distinct
advantage because a second
injection is often needed, although
this device is more expensive. The
Twinject 0.3® delivers an adult
dose; the Twinject 0.15® delivers a
pediatric dose.
The manufacturer’s directions
for the first injection are as
follows:
◆ Remove the green tip labeled
“1” to expose a red, rounded
tip; do not touch the tip.
◆ Remove the green tip labeled
“2” on the opposite end of the
auto-injector.
◆ Jab the needle, which is in the
red tip, firmly into the
midportion of the outer thigh
perpendicular to the skin.
◆ Hold the auto-injector firmly
against the thigh for ten
seconds.
◆ Remove the auto-injector and
examine the red tip; if the
needle is exposed the
epinephrine has been injected.
To make a second injection the
manufacturer directs:
◆ Unscrew and remove the red,
rounded tip; avoid the needle.
◆ Grab the blue plastic and pull
the syringe out of the barrel;
avoid touching the needle.
◆ Slide the yellow collar off the
plunger without pulling on the
plunger.
◆ Insert the needle into the skin
of the thigh and push the
plunger down as far as it will
go.
◆ Remove the needle.
Both types of devices should be
stored at room temperature. They
should not be exposed to sunlight,
refrigerated, or exposed to
excessive heat, as would occur in
the glove compartment of a motor
vehicle. They should be replaced
by the expiration date or if the
solution becomes discolored. Both
should be disposed of as hazardous
waste and should not be discarded
in ordinary trash.
Epinephrine is made by several
pharmaceutical manufacturers. It
comes in glass vials that must be
opened, and the solution must be
aspirated into a syringe, which is
time consuming. However, for
individuals who know how to use
them and can obtain the needles and
syringes, the vials are cheaper,
smaller, and lighter in weight.
Some inhalers for asthmatics
contain epinephrine. Such
preparations are not recommended
for anaphylactic shock because the
response to them is inconsistent.
Although they are cheaper than the
injectable preparations and
undoubtedly better than nothing,
they are not totally reliable for the
treatment of severe anaphylactic
reactions—the type that most needs
reliable therapy.
Injections of epinephrine should
be repeated every five minutes if
needed. In fact, individuals must be
closely watched because many
relapse in a very few minutes as the
epinephrine wears off.
Antihistamines help control the
itching of hives and other symptoms
but should be administered only
after anaphylaxis has been
controlled. Any H1 blocker would
be effective, but diphenhydramine
(Benadryl®, Dramamine®, and
others) administered orally is
widely recommended.
An albuterol inhaler can be used
to relieve residual respiratory
obstruction if wheezes are heard in
the chest.
The administration of
corticosteroids to reduce the
possibility of late reactions is
widely recommended. The standard
therapy is oral prednisone for
several days.
Respiratory obstruction due to
laryngeal edema usually responds
to epinephrine but may require
tracheostomy or cricothyrotomy.
Other steps can help an
individual with anaphylaxis, but
none can substitute for epinephrine.
Following insect stings on an
extremity, placing a venous
tourniquet above the site can
provide more time for the
individual to be transported to a
medical facility where epinephrine
is available. Oxygen should be
administered during the period of
respiratory difficulty regardless of
altitude. Other forms of treatment
for shock should be instituted.
Appropriate care should be given if
the person is unconscious.
Individuals who have had a mild
to moderate anaphylactic reaction
to a known allergen that can be
avoided do not need to be
evacuated, particularly if additional
supplies of epinephrine are
available. They should be treated
with prednisone. Persons who have
had more severe reactions or who
have not completely recovered
should be transported to medical
care without delay.
Prevention of anaphylactic shock
by avoiding the allergen or by
desensitization is far safer than
treatment. Desensitization for insect
sting allergy with purified venoms
is effective for some individuals.
However, even after
desensitization, individuals subject
to anaphylactic shock from insect
stings or similar uncontrollable
allergens should always carry
epinephrine.
SECTION IV
ENVIRONMENTAL
INJURIES
CHAPTER 24
DISORDERS CAUSED
BY ALTITUDE
Charles S. Houston, M.D.
Ken Zafren, M.D.
For centuries travelers returning

from high mountains have reported
unpleasant symptoms, even
fatalities, and have ascribed them to
poisonous shrubs, emanations from
ores—even the breath of dragons.
Only one hundred years ago was the
real cause shown to be lack of
oxygen, which had been isolated a
century earlier.
Although 21 percent of air is
oxygen, no matter what pressure it
is under, the weight of the overlying
atmosphere—atmospheric or
barometric pressure—decreases as
altitude above Earth’s surface
increases. When a person goes
higher, fewer molecules of oxygen
—or any of the other gases that
comprise air—are available in the
atmosphere. At 18,000 feet (5500
m) the atmospheric pressure and the
pressure of oxygen in the air are
approximately half those at sea
level. On top of Mount Everest
(29,035 feet or 8850 m)
atmospheric pressure and the
amount of oxygen available are
one-third of those at sea level.
Because the atmosphere is flattened
at the poles by the centrifugal effect
of Earth’s rotation, the atmosphere
is thinner and the atmospheric
pressure is lower nearer the poles,
which makes the physiologic
altitude higher. For example, on
Denali (Mount McKinley) in
Alaska, barometric pressure equal
to half that at sea level occurs at
about 16,000 feet (4900 m), rather
than at 18,000 feet (5500 m) as it
does in more equatorial mountain
ranges.
Lack of oxygen, or hypoxia, is
the primary cause of problems at
high altitude known as mountain or
altitude sickness. The manner in
which the body takes in oxygen,
circulates it throughout the body,
and gets rid of carbon dioxide is
described in Chapter 18:
The rate of ascent is the most
important determinant of whether an
individual develops mountain
sickness. The faster the ascent, the
more likely is illness to develop.
(Going up very fast in an
unpressurized aircraft, a balloon, or
a decompression chamber produces
acute hypoxia, which causes
problems quite different from
mountain sickness.)
Significant differences between
individuals exist, and a schedule of
ascent that suits most members of a
group may be too fast for some.
Only some of these differences are
known, but among them are recently
recognized genetic variations.
These differences are inherent and
have nothing to do with an
individual’s physical condition,
determination, or courage. The
effects of hypoxia are also
influenced by factors such as cold
(hypothermia,) low blood sugar
(hypoglycemia), exhaustion, and
dehydration. Furthermore, these and
other conditions, including carbon
monoxide poisoning, often mimic
mountain sickness. Nevertheless, on
a high mountain, hypoxia should be
assumed to be the cause of any
symptoms. “Waiting to see what
happens” when symptoms are
severe all too often makes the
situation worse and can lead to
death that could have been
prevented.
Table Conversions Between Feet

24-1 and Meters
MOUNTAIN ALTITUDES
Mountain altitudes can be divided
into three levels that are
physiologically significant. (Table
24-1 lists conversions between feet
and meters.)
6500 to 11,500 Feet (2000 to 3500

M)
In the United States hundreds of
thousands of tourists—skiers,
climbers, and others—ascend to
these altitudes, at which most
altitude illnesses occur. Although
newcomers ascending above 5000
feet (1500 m) may notice a
decrease in athletic performance,
not many have any other symptoms.
Some unusually susceptible
individuals may have mild mountain
sickness as low as 6500 feet (2000
m), but serious altitude illnesses—
pulmonary or cerebral edema—are
rare at that altitude. The incidence
of mountain sicknesses in new
arrivals increases from 25 percent
to 40 percent as altitude increases
from 8000 to 11,500 feet (2400 to
3500 m).
11,500 to 18,000 Feet (3500 to

5500 M)
Several hundred mountains in
North America reach these altitudes
and are visited by hundreds of
climbers, many of whom get sick.
Most highaltitude base camps in the
Andes, Himalaya, and other Asian
ranges are above 14,000 feet (4200
m), but the experienced climbers
who attempt these peaks usually
know how to avoid mountain
sickness. This is not true of
trekkers, and a great many fall ill. A
few die. Rapid ascent to such
altitudes without prior
acclimatization is dangerous and
can cause all the different types of
altitude illness. (In this text these
altitudes generally are referred to
as “high” altitude).
18,000 to 29,000 Feet (5500 to

8800 M)
The great mountains of Asia and
South America attract experienced
mountaineers who know to avoid
illness by careful acclimatization.
Those susceptible to mountain
sickness infrequently go too high.
These individuals do occasionally
succumb to severe altitude-related
illness, but most of their difficulty
comes from prolonged stays above
20,000 feet (6100 m) that cause
loss of physical and mental fitness
rather than acclimatization
problems. Humans live permanently
at altitudes up to 17,500 feet (5400
m), where the pressure of oxygen in
the atmosphere is about 80 mm Hg
(Table 24-2), but above this they do
not thrive. Above 20,000 feet (6100
m) humans deteriorate rapidly over
days to weeks.
Table Gas Pressures at Various
24-2 Altitudes (mm Hg)
RESPONSES TO INCREASING
ALTITUDE
As individuals ascend to higher
elevations, the body makes
adjustments to sustain its supply of
oxygen. These alterations begin
almost immediately but evolve over
days into changes that comprise the
process of acclimatization.
Short-Term Changes
Increased Breathing
An early and important response
to lack of oxygen is an increase in
both the rate and depth of breathing.
This natural and logical response
brings air deeper into the lung,
flushes out the carbon dioxide and
the oxygen-depleted air in the
alveoli (air sacs of the lung), and
brings the alveolar oxygen pressure
closer to that of the outside
atmosphere. Persons whose
breathing response to low inhaled
oxygen (hypoxic ventilatory
response) is brisk appear to be less
susceptible to mountain sicknesses.
Those with a blunted response,
which includes some world-class
distance runners, may be slightly
more susceptible or may simply
take longer to adjust. However,
increased depth and rate of
breathing is the first and most
important response to oxygen
deficiency.
At sea level the work of
breathing requires only about 5
percent of the oxygen used by the
body. At higher altitude the
respiratory muscles must work
harder and require a larger share of
the inhaled oxygen. Near the summit
of Everest, climbers who are not
using supplemental oxygen are
estimated to be consuming
approximately two-thirds of their
inhaled oxygen just in the work of
respiration.
At very high altitudes the lungs
and lack of oxygen, rather than the
heart, fail to keep up with demand
and limit the amount of work that
can be done. The decreased ability
to perform physical work is
proportional to the altitude. The
rate of decline in maximum exercise
capacity is approximately 3 percent
per 1000 feet (300 m) of elevation
gain, but the decline is even faster
at extreme altitude. Acclimatization
improves the ability to work
somewhat, but even the most well-
acclimatized persons cannot reach
their sea-level work capacity.
Decreased Oxygen Saturation

At sea level the hemoglobin in
arterial blood leaving the lungs
carries almost its full capacity of
oxygen and is 95 percent or more
saturated. As altitude increases, the
saturation decreases proportionally.
Resting arterial oxygen saturation at
15,000 feet (4500 m) is
approximately 85 percent.
During exercise at sea level,
arterial saturation remains normal,
though it may fall slightly with very
strenuous effort, such as running a
440-yard (400-m) race. During
exercise at high altitude, the lower
alveolar oxygen pressure causes
incomplete loading of red blood
cells with oxygen, and saturation
falls dramatically (Fig. 24-1). The
decrease is proportional to the
exercise level and altitude. Since
the working muscles do not get as
much oxygen as they need, climbers
take more frequent rests, allowing
the saturation to rise again. At
extreme altitudes the muscles of
respiration may tire more rapidly
than those of the legs and arms.
Changes in pH
Increased breathing depletes
carbon dioxide from blood, making
the pH higher and the blood more
alkaline. Increased alkalinity
stimulates the excretion of
bicarbonate in the urine, which
tends to restore the pH of the blood
toward normal, a process called
renal (kidney) compensation. The
drug acetazolamide (Diamox®)
increases bicarbonate excretion,
and the lungs compensate by
increasing breathing.
Acetazolamide has been called the
“artificial acclimatizer” because it
causes the same physiologic
responses as acclimatization but in
reverse order (the kidneys excrete
bicarbonate and then the lungs
increase breathing, instead of the
lungs increasing breathing and then
the kidneys excreting bicarbonate).
Figure 24-1. Blood oxygen content
(saturation) under varying working
conditions at an altitude of 19,000 feet
Figure 24-2. Decline of maximum
heart rate with altitude
Pulse Rate and Cardiac Output

During a climb the pulse rate
rises with the workload but
subsides during rest. The increase
and speed with which it returns to
normal are a function of altitude
and, to a certain degree, an
indicator of acclimatization. A slow
resting pulse that increases little
during work and rapidly returns to
resting level is a sign of physical
fitness at sea level and also
indicates that an individual is
adjusting well to altitude, but the
resting pulse increases with
increasing altitude and is higher at
altitude than at sea level. Maximum
heart rate with maximum exercise
decreases at high altitude (Fig. 24-
2) because the lower amount of
oxygen available results in lower
maximum exercise capacity. The
maximum achievable heart rate at
sea level decreases with age and is
roughly 220 minus a person’s age.
For a short while after reaching
altitude, the volume of blood
pumped by the heart (the cardiac
output) at any level of exercise is
greater than normal. However, it
very soon decreases to normal and
remains normal at rest, or for a
given level of exercise, throughout
a stay at high altitude.
A crude but useful indication of
the load on the heart is the double
product: the systolic blood pressure
(the top number in a blood pressure
reading) multiplied by the pulse
rate. Obviously these increase with
work and with altitude. The double
product can estimate the combined
effect and can be helpful in
deciding whether a person with
heart disease can safely go to
altitude.
Blood Volume
Rapid ascent to high altitude is
accompanied by a prompt decrease
in blood volume because fluid is
excreted in the urine during normal
acclimatization. Acutely, fluid may
move out of the blood vessels into
the tissues and cells, resulting in
tissue swelling (edema). The
severity of fluid retention is related
to risk of altitude illness. During
acclimatization the decrease in
blood plasma volume is 5 to 10
percent of the sea level blood
volume, which is equivalent to
removing about a pint of blood
plasma. This loss of fluid causes an
increase in the concentration of red
blood cells, although the actual
number of circulating red cells does
not increase for many days.
Inadequate fluid intake at altitude
may further decrease blood volume
and result in a decreased maximal
exercise capacity.
Sleep Hypoxia
During sleep at altitude,
ventilation is often decreased and
wide fluctuations in the respiratory
rate—periodic breathing—may
occur. Sometimes alarming periods
(ten to twelve seconds) of not
breathing (apnea) are followed by a
period during which the depth and
rate of breathing increase. Often the
depth and rate rapidly increase to a
level greatly above normal but then
subside until apnea intervenes
again.
The generally accepted
explanation for periodic breathing
is that the brain’s respiratory
control centers become less
sensitive during sleep so that
respiration decreases or stops. Very
soon blood carbon dioxide rises so
high—and oxygen falls so low—
that breathing starts up again with
ever-increasing depth until the
blood carbon dioxide level
decreases and the blood oxygen
level increases to more normal
levels. At that point respirations tail
off again. Periodic breathing often
begins as a person reaches a
moderate elevation, persists or
even becomes more marked with
acclimatization, and may be an
important cause of deterioration
during prolonged stays at extreme
altitude.
At 14,000 feet (4200 m), where
resting oxygen saturation is about
86 percent in people who are
awake, periodic breathing, which is
almost universal, may cause
saturation to fall as low 60 percent.
Acetazolamide almost
completely eliminates the wide
swings caused by periodic
breathing. At 14,000 feet (4200 m),
for example, acetazolamide limits
the lower level of saturation during
sleep to about 82 percent. Sedatives
and tranquilizers make sleep
hypoxia worse and should be
avoided at high altitudes. On the
other hand, a small dose of
acetazolamide (62.5-125 mg taken
by mouth at dinner time) is a simple
and safe way to improve sleep
despite the increased urination it
may cause.
Sleep hypoxia may account, in
part, for the inability of many
individuals to sleep well at high
altitude. It may also explain why
headache and other symptoms of
acute mountain sickness are more
severe in the morning hours and
why both high-altitude pulmonary
edema (HAPE) and high-altitude
cerebral edema (HACE) often
become worse during the night. Part
of the beneficial effect
acetazolamide has for acute
mountain sickness probably results
from decreased sleep hypoxia.
Sleep hypoxia may cause
disturbed sleep, resulting in sleep
deprivation and a decrease in
physical working capacity during
the day. This provides one
physiologic explanation for the
wisdom behind the mountaineer’s
dictum “Climb high, sleep low.”
Climbers have noted better physical
performance when low-flow
oxygen has been used during sleep
because this decreases the fall in
arterial oxygen saturation. Chronic
lack of sleep on a mountain, like
hypoxia, interferes with intellectual
function, particularly at extreme
altitude, and increases the
likelihood of mistakes.
Acclimatization
The evolution of short-term
changes to longterm adjustments
constitutes acclimatization.
Survival and effective functioning
at 18,000 feet (5500 m), and the
ability of some persons to work
without supplemental oxygen as
high as 29,000 feet (8800 m), are
dependent upon the ability to adjust
or acclimatize to oxygen lack.
Taken abruptly from sea level to the
summit of Everest, an
unacclimatized person would have
only five to ten minutes of
decreasing consciousness before
lapsing into coma and dying in
about thirty minutes. Birds can fly
higher for much longer periods, but
no mammals, including man, live
permanently above 17,500 feet
(5300 m), suggesting that this is the
upper limit to which they can
acclimatize.
Acclimatization can best be
described as a series of integrated
changes by which the partial
pressure of oxygen in the blood
reaching the tissues is brought
closer to that in the ambient air. It is
a gradual process, taking days to
weeks, but a well-acclimatized
person can tolerate altitudes that
would soon incapacitate and might
kill a person newly arrived from
sea level. It is also a remarkable
process that allows many persons
who are hypoxic at sea level as the
result of lung or heart disease to
lead nearly normal lives.
The most important changes in
acclimatization are those that occur
upon first arrival at altitude:
◆ Increased respiratory volume
◆ Increased cardiac output
◆ Elevation of pulmonary artery
pressure
◆ Apparent increase in red blood
cells due to a shift of fluid
from blood to tissues and loss
of fluid in the urine
In addition, complex changes in
the way cells use oxygen, hormonal
changes that control electrolyte
migration, changes in urine output,
and redistribution of blood flow to
more critical parts of the body all
promote normal function at low
oxygen pressures.
Increased Respiratory Volume
(Ventilation)
An increase in the depth and, to
a lesser extent, the rate of
respiration—increased ventilation
—brings more outside air into the
alveoli, increasing the oxygen
available to diffuse into blood. The
increase is most obvious during
exercise. Those who have just
arrived at even moderate altitude
may experience unusual shortness
of breath during only moderate
exertion. Ventilation is the function
that limits exercise at extreme
altitudes.
Increased Pulmonary Artery
Pressure
Many conditions that reduce the
oxygen pressure in the lungs,
whether at altitude or at sea level,
increase the blood pressure in the
pulmonary arteries. The elevated
pressure tends to open more
capillaries in all parts of the lung
(many of which are closed during
quiet respiration at sea level) to
maximize the capacity of the
pulmonary circulation to absorb
oxygen. One explanation offered for
high-altitude pulmonary edema is
that increased arterial pressure,
transmitted directly to the
capillaries, forces fluid through thin
capillary walls into the alveoli.
Lack of tissue oxygen due to
anemia or carbon monoxide
poisoning (carbon monoxide reacts
with hemoglobin to prevent it from
carrying oxygen) does not increase
pulmonary arterial pressure
because the alveolar oxygen is
normal. On the other hand, sleep
apnea, which can lower alveolar
oxygen several times each minute,
can increase pulmonary arterial
pressure permanently and is thought
to increase systemic blood
pressure, too.
Increased Cardiac Output
As stated, during the first few
days at high altitude the volume of
blood pumped by the heart at rest or
at any exercise level is higher than
at sea level, which increases the
amount of oxygen delivered to the
tissues. However, after seven to ten
days the cardiac output becomes
less than at sea level, and more time
is required for any specific amount
of work, whether brisk exercise
such as running or more prolonged
activities such as carrying a load.
With a longer stay at altitude,
cardiac output rises again and, at
extreme altitude, is above sea level
values. Again the ability of the heart
to pump blood does not limit work
at extreme altitude, even during
heavy exercise. The ability—or
inability—to move air restricts
work at great heights.
Increased Number of Red Blood

Cells
Shortly after arrival at high
altitude, an apparent increase in the
concentration of red cells in the
blood results from movement of
water out of the blood into the
tissues. However, hypoxia
stimulates release of the hormone
erythropoietin, which is formed in
the lungs and kidneys. This hormone
is a powerful bone marrow
stimulant, and within the first few
days after arrival red blood cell
production actually increases. The
blood eventually may contain many
more cells than at sea level. This
increase in red cells, measured as
the percentage of whole blood
volume occupied by cells
(hematocrit), is the best known and
historically was the earliest
described change in
acclimatization, although it is not
the most important.
The increased number of red
cells enables blood to carry more
oxygen, but this increased capacity
may be offset by the increase in
blood viscosity. A serious danger of
clot formation in the veins
(thrombophlebitis) appears when
the hematocrit rises above 60
percent. (Normal at sea level in
males is 47 ± 5 percent; in females
42 ± 5 percent.)
Changes in Oxygen-Carrying
Capacity
Red blood cells contain the
enzyme 2, 3-diphosphoglycerate
(DPG), which facilitates the release
of oxygen from hemoglobin to the
tissues. The concentration of DPG
in the blood increases at higher
altitudes and allows release of a
larger volume of transported oxygen
for a smaller drop in oxygen
pressure, at least below 20,000 feet
(6100 m). At higher elevations, the
increased alkalinity caused by loss
of carbon dioxide helps blood take
on oxygen in the lungs.
Changes in Body Tissues

Acclimatization by long
residence at altitude causes more
subtle changes that enable near
normal function by the oxygen-
consuming tissues, particularly
muscle, despite low oxygen
pressures. These changes include
the following:
◆ An increase in the number of
capillaries within the muscle
◆ An increase in myoglobin, the
intramuscular oxygen-carrying
protein
◆ An increase in the
concentration of intracellular
oxidative enzymes
◆ An increase in the size and
number of mitochondria, the
tiny structures that contain
oxidative enzymes within cells
Figure 24-3. Oxygen–hemoglobin
dissociation curves: normal and the
effects of carbon dioxide, pH, and
temperature
Thanks to these changes several

million people throughout the world
are able to live at high altitudes.
Some populations that have
lived at high altitude for many
generations (for example, in the
high Andes, Caucasus, or Ethiopia)
develop physical changes
characteristic of their specific
genetic heritage. These generational
changes are better called adaptation
than acclimatization, and they
convey a few special abilities, such
as prolonged endurance at altitude,
and some superiority in endurance
sports, such as marathon running at
sea level.
Acclimatization is an ongoing
process that takes place over many
weeks. The time required for
different processes varies greatly
and also varies between
individuals. The respiratory and
biochemical changes level off in a
few weeks, but more time is needed
for the number of red blood cells to
reach a maximum; at that time,
secretion of erythropoietin
decreases, but the bone marrow
continues to produce the same
number of red cells.
Above 20,000 feet (6100 m)
deterioration outstrips
acclimatization, and after ten to
fifteen days at such altitudes
climbers cannot continue without
great risk.
Achieving Acclimatization
Individuals vary so widely in
their ability to acclimatize, not only
in the degree of acclimatization they
can achieve but also in the time
required, that no program fits
everyone. Generally speaking, the
slower the climb, the better the
acclimatization.
Using “siege tactics,” climbers
attempting a very high mountain
climb to a higher camp, return to
rest at base camp, carry supplies to
a higher camp, and repeat the
process, stocking successively
higher camps. After a few weeks, a
summit attempt can be made from
the highest camp. Most accept the
adage “Climb high, sleep low” and,
after carrying a load to a higher
camp, prefer to go down for the
night.
Other experienced mountaineers
prefer “alpine style.” The
individuals live at base camp, each
day climbing a little higher on a
nearby mountain and returning to
base. A high degree of
acclimatization can be achieved this
way. After two to six weeks, when
the weather looks promising, the
party can move up rapidly,
sometimes straight through to the
summit unless the climb is
technically very difficult. This
approach has the obvious
advantages of minimizing the
carrying of loads and consumption
of supplies, and it allows an attempt
to be made whenever the weather is
promising. Little altitude
deterioration occurs.
Popular today is a modification
of these two approaches: a small
party, stocking camps as it climbs,
acclimatizing by occasional rest
days, and then going to the summit
at an auspicious time. Another
refinement, which is useful in the
case of very high base camps, such
as Everest Base Camp at 17,500
feet (5300 m), is for the party to
spend a few days recovering at a
lower level of 13,000 feet (4000 m)
or so for a few days. Very little
acclimatization is lost, while the
body has time to recover from some
of the deterioration of the higher
altitude.
All these protocols keep
climbers high on a mountain for
relatively short periods so they are
less likely to suffer from altitude
deterioration and are less likely to
be caught by bad weather.
However, if one or more of the
party becomes ill or is injured in a
pure alpine-style climb, no stocked
camps to which the group can
retreat are available.
On modest mountains,
acclimatization is not necessary, but
to avoid mountain illnesses,
tourists, climbers, skiers, and other
visitors sleeping above 8000 to
10,000 feet (2400 to 3000 m)
should not exercise vigorously for a
day or two after arrival. Highly
susceptible individuals would be
wise to spend one or two nights at
an intermediate altitude, perhaps
5000 feet (1500 m).
The customary advice to take
one day to climb each 1000 feet
(300 m) above 10,000 feet (3000
m) is conservative and does not
apply to everyone. Above 12,000
feet (3700 m) people should find
their own pace. A good expedition
leader should pace the party to take
care of the slowest—or perhaps
send that person down.
Persons who have only a short
time to vacation at a mountain
resort are reluctant to apportion any
of their time to acclimatizing. Some
experience mountain sickness,
sometimes quite severe; others
notice little. Acetazolamide can be
a safe and effective way to speed
acclimatization for those who
cannot or will not take time, and
perhaps that is wiser than spoiling a
short vacation.
Those going to bigger mountains
usually need a number of days to
walk to base camp, gaining altitude
en route. This is a good way to
acclimatize if heat, exertion, or the
diarrheal and other illnesses so
common in developing countries do
not lead to dehydration and wasting.
Such illnesses commonly have a
greater impact on an expedition than
weather or terrain.
Acclimatization is thought to be
lost at about the same rate it is
gained. Once acclimatized, not
descending for more than a week or
ten days appears prudent.
Furthermore, a fully acclimatized
individual who goes down to a low
altitude for longer than a week or
ten days is at increased risk of
developing high-altitude pulmonary
edema upon returning (“High-
Altitude Pulmonary Edema,” this
chapter).
In recent years many persons
planning a trip to moderate altitude
have tried to acclimatize by
spending an hour once or twice a
day in a low-oxygen room or
breathing a low-oxygen gas mixture.
A number of sports clubs and hotels
in several countries offer such
facilities, and the process has been
studied in a few research
laboratories. Repeated short
exposures are not effective in
stimulating acclimatization,
although some regimens involving
longer exposure time may have
some beneficial effects.
Some climbers who have made
many trips to high mountains
believe the body acclimatizes more
rapidly and completely on later
climbs. Some evidence supports the
theory that stays at high altitude
within recent months speed
acclimatization on subsequent
ascents. Others feel that increased
familiarity with living and climbing
at high altitudes is responsible for
the apparent greater
acclimatization.
Apart from acetazolamide, no
artificial aids to acclimatization are
known. Susceptibility to mountain
sicknesses decreases with
increasing age (one of the few
benefits of aging), but the ability to
acclimatize also seems to decline
slightly as people get older.
Increased physical fitness at sea
level, however, increases exercise
capacity at altitude and can make a
trip less physically stressful and
more enjoyable.
Climbers who have reached the
summit of very high mountains—
8000 meters—without supplemental
oxygen have some inherent
physiologic advantages that cannot
be entirely predicted by sea level
studies. They are able to sustain
very heavy exercise much longer
than others, and their maximum
exercise capacity is higher than
most athletes, although not as high
as Olympic endurance athletes such
as cross-country skiers. They are
experienced mountaineers with
highly developed skills that enable
them to climb efficiently and fast
with minimal energy expenditure.
Endurance athletes have lungs with
a higher-than-normal diffusing
capacity, and they usually have a
normal or increased ventilatory
response to hypoxia. Experience
has given them confidence, reducing
the anxiety felt by novices, which
also gives them an increased
tolerance for hypoxia. Even when
made acutely hypoxic at sea level,
they seem to fare better. However,
some who have gone the highest
without illness actually have a
lower-than-normal hypoxic
ventilatory response and must take
longer to acclimatize.
Summit of Mount Everest

The barometric pressure on the
summit of Everest (29,035 feet or
8850 m), as measured directly in
1981, is 253 mm Hg or one-third
sea level atmospheric pressure.
That pressure is 17 mm Hg higher
than had been predicted, apparently
due to the greater thickness of the
atmosphere near the equator. Mount
Everest is located at 27° 59’ N
latitude, about the same latitude as
Tampa, Florida. The pressure may
vary by the equivalent of 100 to 300
feet (30 to 90 m) due to weather-
related changes in atmospheric
pressure, which means that on days
when the barometric pressure is
high, the summit is physiologically
a few hundred feet lower. In the
winter, the barometric pressure is
lower and the summit is
physiologically several hundred
feet higher. On the summit of
Everest, during the spring and fall
climbing seasons, climbers have an
arterial oxygen pressure of about 28
to 32 mm Hg, approximately one-
third of that at sea level. The
arterial carbon dioxide pressure is
about 10 to 13 mm Hg (normal at
sea level is 35 to 45 mm Hg for
adult males).
ALTITUDE ILLNESS
Most people can avoid getting
serious altitude illness. A few
simple measures prevent it in most
healthy individuals, and prudent
individuals should experience no
more than minor, temporary
discomfort. Some persons with
specific conditions are extremely
susceptible to altitude illness and
need to take special precautions to
go safely to altitude (Chapter 25:
Conditions).
Acute Mountain Sickness

Acute mountain sickness (AMS),
the most common disorder that
afflicts those who go too high too
fast, results from the effects of
lowered atmospheric oxygen on the
brain. Brain cells are probably
damaged only by extreme hypoxia,
and changes in the circulation of the
brain and the accumulation of fluid
(edema) are thought to be
responsible for the symptoms of
AMS. Low oxygen pressure dilates
cerebral blood vessels, which
occurs despite the constricting
effect of low carbon dioxide levels
resulting from increased ventilation.
The symptoms of mild or
moderate AMS are quite
realistically described as those of a
bad hangover: headache, nausea,
sometimes vomiting. The severity
of symptoms depends upon the rate
of ascent, the altitude reached, and
individual susceptibility. Symptoms
usually start twelve to twentyfour
hours after arrival and begin to
subside by the third day. The
headache is throbbing, tends to be
at the back of the head, and is
worse on awakening in the morning.
Dizziness, fatigue, loss of appetite,
disturbed sleep, and general
malaise are common. The
individual feels miserable.
One normal response to ascent is
a temporary increase in urine
output, but in AMS the output is
usually decreased and the person
retains fluid. Broadly speaking,
those people who have the least
increase in ventilation and the
lowest oxygen levels retain the
most water and are the sickest. One
attractive but oversimplified
explanation for the symptoms of
AMS is that rapid ascent causes
generalized water retention, but in
susceptible people more fluid
collects in the brain.
A few individuals develop an
unsteady gait (ataxia), an important
sign of brain involvement. If a
person begins to stumble and fall or
becomes drowsy and apathetic, he
or she should be considered to have
(HACE). (High-altitude pulmonary
edema—fluid in the lungs—may be
present, too, increasing the
hypoxia.) Such individuals are in
great danger, and rapid descent—
with supplemental oxygen if
possible—is essential.
AMS can be prevented by
gradual acclimatization at
intermediate altitudes, or, to some
extent, by medication. The
incidence or frequency of AMS
increases with altitude as shown in
Table 24-3. Only a few persons
have AMS at 6500 feet (2000 m),
but after going rapidly from near
sea level to over 14,000 feet (4300
m) more than half have symptoms.
Children and adults are equally
susceptible to AMS, but
recognizing symptoms in infants or
young children who cannot
verbalize their symptoms requires
awareness of the problem. The
incidence of AMS is decreased in
the elderly, possibly because the
normal cerebral atrophy of aging
leaves more space for a swollen,
edematous brain.
None of the symptoms of AMS is
specific. They also occur in people
who are exhausted, dehydrated,
hypoglycemic, hypothermic,
suffering from carbon monoxide
poisoning, taking prescription or
recreational drugs, or developing
an infection. Usually the
individual’s history of rapid ascent,
together with absence of other
causes, makes the diagnosis likely.
A high fever suggests infection;
AMS does not cause a high fever
unless complicated by another
condition.
Table Incidence of Acute

24-3 Mountain Sickness
Anyone who has recently come
to high altitude and has the listed
symptoms should be treated for
AMS, unless another cause is
strongly suspected. Anyone who
continues to get worse in spite of
rest should be taken to a lower
altitude. Supplemental oxygen is
helpful for providing restful sleep
but is not a substitute for descent if
a person is ill. In the hands of
medically trained personnel,
simulated descent in a portable
hyperbaric chamber, such as a
Gamow Bag, may be a safe
alternative to actual descent. (This
is discussed in more detail in
“High-Altitude Cerebral Edema,”
this chapter.)
AMS, like all altitude illnesses,
can lead to disordered thinking.
Decisions may have to be made for
the individual, who may have to be
forced to accept them. Problems
have developed when persons—
particularly trip leaders—have
refused to accept the decision of a
medical professional. When the
affected individual is a physician,
problems may become even worse.
Carbon monoxide combines
preferentially with hemoglobin and
displaces oxygen. Using a stove in a
small tent or an inadequately vented
snow cave can lead to carbon
monoxide poisoning, which not only
adds to altitude hypoxia but has
caused a number of deaths. This
possibility must always be
considered, even though the
treatment—rapid descent and
oxygen—is the same as that for
altitude illnesses.
Individuals with AMS should
avoid heavy exertion, although light
activity is better than complete rest.
Sleep is not helpful because
respirations are slower during
sleep, which may make symptoms
worse. Sedatives, including
alcohol, should be avoided at night
since they also decrease
respiration. Low-flow oxygen at
night is very helpful.
Affected persons should drink
adequate fluids and eat a light, high-
carbohydrate diet. Acetaminophen
or ibuprofen is helpful for
headache. Tobacco and alcohol
should be avoided.
Acetazolamide, for which a
prescription is required, can help to
prevent AMS and speed
acclimatization. The dose
recommended by most authorities is
125 mg twice daily, beginning one
day before ascent and continuing for
two days after arrival. If 125 mg
tablets are not available; the correct
dosage can be achieved by breaking
250 mg tablets in half. Extended
release capsules, which come in a
500 mg size, are also effective. The
dose is one capsule daily, which is
twice the currently recommended
dose, but because of slower
release, the side effects are less
than would be expected.
Tingling in the lips, fingers, or
toes is a common side effect.
Carbonated beverages (including
beer) taste flat because the drug
affects taste buds, and urine volume
is increased. These symptoms
subside when the drug is stopped.
Because acetazolamide is
chemically related to sulfa drugs,
rare individuals sensitive to sulfa
may not be able to take it. Some
individuals are more sensitive to
sunlight while taking it.
Another medication,
dexamethasone, can also be used
for treating AMS, but unlike
acetazolamide it masks symptoms,
does not speed acclimatization, and
has more side effects, including
emotional changes of euphoria and
depression after stopping. Rebound
acute mountain sickness can occur
when dexamethasone is stopped
after ascent to high altitude.
The most effective treatment for
AMS after it has developed is
descent. Mild AMS can be safely
treated by waiting for
acclimatization to occur. This
generally takes two to four days,
although rare individuals take
longer to acclimatize, and a few
continue to have symptoms of AMS
for an indefinite period.
Acetazolamide is also helpful for
treatment and works by speeding
acclimatization. Tylenol or
ibuprofen can be given for
headaches, and any anti-nausea
medicine may relieve the nausea.
Prochlorperizine (Compazine® in
the United States, Stemetil in many
other countries) is the anti-nausea
medicine usually recommended
because it is known to be a
respiratory stimulant, unlike some
others.
AMS is common and usually
self-limited, but it deserves
attention because it can evolve into
a more serious illness: high-altitude
cerebral edema. Once AMS has
resolved, it is safe to ascend further
with caution. If dexamethasone is
used, it should be discontinued for a
day or so before it is safe to ascend.
If AMS causes a person to descend,
reascending after a day or two at a
lower altitude free of symptoms is
safe.
High-Altitude Cerebral Edema

High-altitude cerebral edema
(HACE) represents the severe end
of the spectrum of acute mountain
sickness. In a few people with
AMS, usually at altitudes above
12,000 feet (3700 m), symptoms of
brain edema become worse,
sometimes with alarming speed.
Ataxia or staggering gait, which can
be demonstrated early by having the
individual try to walk a straight line
heel to toe, can become so bad that
the person cannot stand or get into a
tent or sleeping bag. The afflicted
person may not be able to get
dressed, tie shoelaces, or handle a
knife and spoon.
The individual becomes
confused, may have hallucinations,
loses memory, and develops
impaired judgment. These
disabilities may rapidly worsen to
bizarre behavior, coma, and death.
In an extreme case, a person
with a worsening headache,
vomiting, and lassitude for several
days may retire to a tent to sleep
and lapse into a coma. Companions
may become aware of the condition
only when they cannot wake the
person. Indeed, some individuals
may not respond even to painful
stimuli. The person looks pale and
blue (cyanotic) and, if crackles can
be heard in the lungs, HAPE is also
present. Autopsies on individuals
who have died of HACE have
disclosed swelling of the brain and
the presence of bleeding.
Because HACE can kill, early
diagnosis and treatment are
essential. Recent arrivals at altitude
—and, occasionally, someone who
has been at altitude for several days
—who develop confusion or ataxia
combined with a persistent
headache should be considered to
have HACE. They should be given
oxygen and taken to a lower altitude
immediately. They should be
accompanied during descent
because ataxia may progress
rapidly and individuals may fall
and be injured. Usually a descent of
a few thousand feet brings relief if
accomplished promptly. Leaving a
person with HACE alone is risky—
even at a lower altitude.
Some individuals appear to be
unusually susceptible to HACE and
other altitude-related disorders and
have suffered more than one
episode. Once HACE has occurred,
even if recovery is rapid at a lower
altitude, it may recur. Most
individuals who have had HACE
are unable to reascend for several
days or longer due to difficulty
walking. They would be prudent to
wait at least a week or two after
complete return to normal before
reascending. Some authorities
recommend against reascent for
weeks to months.
Dexamethasone is the preferred
drug for treating HACE but is not a
substitute for descent and oxygen. It
should be administered promptly by
mouth if the person is still
conscious, or intravenously.
HACE may occur without any
signs of HAPE. Some people with
severe HAPE lose consciousness
and develop signs and symptoms of
cerebral edema, occasionally with
little cough or shortness of breath.
Apparently the additional hypoxia
caused by pulmonary edema leads
to cerebral edema. For this reason
the lungs should be examined
carefully in all persons with central
nervous system signs at high
altitude.
Other neurologic disorders may
occur at high altitude and can
confuse the diagnosis of cerebral
edema (Chapter 25: Altitude and
Sometimes changes in vision, like
the flashing lights that often occur
during or before a migraine attack,
are noticed. Gradual or sudden
blindness, usually lasting only a
few minutes to an hour, has been
described. These episodes are
probably migraine equivalents,
even without headache or a history
of migraine, but are not well
understood. Brief spells of
dizziness, double vision, and
weakness in a hand, arm, or leg
have also been described at
altitude, and they may be migraine
or a transient ischemic attack (TIA;
Chapter 14: Neural Disorders).
Strokes do occur in the mountains
but are uncommon.
When descent is difficult or
impossible due to nightfall or
weather, a portable hyperbaric
chamber may be used for treatment
of HACE by simulating descent.
These chambers are inflatable bags
in which the pressure can be
increased to simulate descent of
several thousand feet. The original
device of this type was the Gamow
Bag, but several other brands of
hyperbaric bags are now available.
Treatment in a hyperbaric bag is not
an alternative to descent or
continuous oxygen but may be
lifesaving when weather or terrain
preclude descent. Once removed
from a hyperbaric bag, the person’s
symptoms may return. The treatment
for this is another session in the
bag. Hyperbaric bags are heavy and
expensive. Whether to include one
in the medical equipment on an
expedition requires careful thought.
High-Altitude Pulmonary Edema
High-altitude pulmonary edema
(HAPE) is the second common type
of severe altitude illness. It usually
occurs in the same context as AMS:
a healthy person goes up too rapidly
from low altitude. It occasionally
complicates AMS and sometimes is
associated with HACE. HAPE is a
condition in which the alveoli of the
lungs are filled with fluid that has
leaked through the walls of the
pulmonary capillaries. As more
alveoli fill with fluid, oxygen
exchange is decreased and blood
oxygen pressure falls, decreasing
oxygen supply to all cells, most
dangerously to the brain. The
individual is drowning in his own
fluids and, unless effectively and
promptly treated, may lapse into
coma and suffocate.
Symptoms of HAPE usually
begin two to four days after arrival
at altitude and consist of excessive
shortness of breath on moderate
exertion and decreased exercise
tolerance. In addition, there may be
a sense of tightness in the chest
(especially at night), weakness, and
often—but not always—an irritated
dry cough. In the late stages the
cough may produce frothy pink
sputum. A person with HAPE is
typically much more tired than other
members of the party, an important
early symptom. Since the hypoxia of
altitude is made more severe by the
fluid in the alveoli, the symptoms of
AMS are often worsened. Shortness
of breath at rest is an important
early sign. A dry cough may also be
due to irritation from overbreathing
dry air.
The pulse rate is usually rapid
(over 110 beats per minute), even
after several hours of rest, and
respirations are fast and labored
(over twenty per minute). The lips
and nails are bluish (cyanotic) and
the skin pale and cold. Bubbling or
crackling sounds may be heard
when listening to the lungs with the
unaided ear or with a stethoscope.
Sometimes crackles are heard on
one side only, usually in the middle
of the right lung (best heard just
below the armpit); occasionally
they are almost inaudible.
Symptoms and signs usually
become worse during the night.
Due to the further decrease in
oxygen reaching the brain, a person
with HAPE does not think clearly
and may become confused or even
delirious, which suggests that some
degree of HACE is also present.
When this occurs, the outlook is
poor. Unless treated quickly and
effectively, the person is likely to
die.
HAPE is not due to heart failure
or pneumonia, although years ago it
was mistaken for those disorders.
HAPE does cause a fever but not
usually a high one. The cause lies in
alterations in the pulmonary
circulation. High altitude, sleep
apnea, or hypoxia from any cause,
including heavy exercise, causes a
rise in pulmonary artery blood
pressure (PAP). Normally, the
smallest pulmonary arteries
(arterioles) constrict, protecting
capillaries from excessive pressure
and flow rates. One theory
concerning the cause of HAPE is
that individuals who develop
HAPE may not have uniform
arteriolar constriction throughout
the lungs. Arterioles constrict in
some areas but not in others.
Consequently, in those parts of the
lung where no constriction occurs,
high pressure and flow are
transmitted directly to the
capillaries, which leak fluid into
the alveoli.
Probably no one is completely
immune; HAPE occurs even in
experienced and acclimatized
mountaineers if they go too high too
fast and work too hard. Individuals
who are HAPE susceptible and
have repeated episodes of HAPE
have been recognized. These
unfortunate people respond to high
altitude—or to the hypoxia of sleep
apnea—with an abnormally large
increase in pulmonary artery
pressure, particularly during
exercise. This susceptibility may be
genetic, perhaps due to failure of
certain tissues to generate nitric
oxide (NO), one of the most
important compounds controlling
the tone of small blood vessels. The
defect may be an absent or
abnormal gene sequence or some
other defect in nitric oxide
formation.
Most persons going to moderate
altitude accumulate a small amount
of fluid between the thin layers of
the membrane lining the alveoli
(interstitial edema), which hinders
the diffusion of oxygen. Such edema
may also develop during strenuous
exertion. Usually this fluid is
absorbed as fast as it forms, but if
not, HAPE or the exercise
equivalent begins. The evolution of
interstitial to alveolar edema is
caused by rapid ascent, particularly
when associated with strenuous
exercise.
For reasons that are not
understood, some wellacclimatized
high-altitude residents, even though
not unusually susceptible, develop
HAPE when they return to altitude
after a week or ten days near sea
level. Such reentry HAPE is most
frequent in children.
The incidence of HAPE and
HACE varies with geographical
conditions. A climber living in
Seattle can be up and down Mount
Rainier (14,410 feet or 4400 m) in
a weekend. Since that climber will
be climbing fast, AMS is likely—
the incidence is over 50 percent—
but a fast descent is possible if
symptoms become bad. On Denali
(Mount McKinley), which is much
larger and higher (20,300 feet or
6200 m), deep snow, heavier packs,
severe weather, and longer
distances not only demand greater
work but also increase the
likelihood of HAPE and HACE and
make rapid descent to safety much
harder. The risk of developing
HAPE after a rapid ascent to
12,000 feet (3700 m) is about one
in two hundred (0.5 percent) in
adults—higher in children.
The diagnosis of HAPE depends
on a history of rapid ascent, often
with strenuous exertion, and on the
signs and symptoms described
above. High-altitude pulmonary
edema may progress very rapidly,
particularly during the night. Any
worsening of the condition demands
prompt descent.
The most important treatment is
getting down to a lower altitude,
either by evacuation or by treatment
with a portable hyperbaric
chamber. If the individual cannot
walk, he or she must be carried.
Since exercise can make HAPE
worse, the ill person should not be
allowed to carry a pack and should
be allowed to walk down only on
easy terrain. Descent of as little as
2000 to 3000 feet (600 to 900 m)
often results in prompt relief. The
speed with which individuals can
recover from HAPE is remarkable.
If oxygen is available, it should
be given without delay. Rescue
parties should bring oxygen or a
portable hyperbaric chamber if the
person cannot be moved, for
example if a major injury is present.
Deaths have occurred when the
seriously ill person has worked too
hard during evacuation.
Most cases of HAPE occurring
below 15,000 feet (4600 m) and
possibly higher can be treated using
a portable hyperbaric chamber
without evacuation if pulse
oximetry (the ability to measure the
saturation of oxygen in the blood) is
available. If the oxygen saturation
can be maintained above 90
percent, the individual can be
treated with multiple chamber
sessions. The head of the chamber
should be raised because fluids
pool in the lungs and a person lying
flat has trouble breathing. In some
cases, additional oxygen must be
provided inside the chamber to
keep the oxygen saturation high
enough. A number of different
protocols have been suggested. One
protocol that works is to treat the
person in the chamber for hour-long
sessions, with brief respites (five to
ten minutes) out of the chamber
between sessions, until the
individual is no longer short of
breath and can maintain an oxygen
saturation that is appropriate for the
altitude.
THE GOLDEN RULES OF

ALTITUDE ILLNESS
Mountaineers who climb to
high altitude experience AMS
if their ascent rate exceeds the
ability of their body to
acclimatize. Since AMS is
usually self-limited, waiting at
altitude is a reasonable option,
unless symptoms are severe. It
is a mistake to ascend higher
with symptoms of AMS. The
Himalayan Rescue Association
has encouraged following the
“Golden Rules of Altitude
Illness.” Nobody who heeds
these rules should ever die
from altitude illness.
Golden Rule 1: If you have
symptoms at altitude,
they are due to altitude
illness unless proven
otherwise.
◆ The symptoms include
headache plus any
additional symptoms of
AMS.
Golden Rule 2: If you have
symptoms at altitude, do
not ascend farther.
◆ Treating symptoms at
altitude with
medications such as
acetaminophen, anti-
nausea formulations,
and acetazolamide is
certainly acceptable. If
symptoms resolve with
these, ascending farther
at a slower rate is
reasonable.
Golden Rule 3: If the
symptoms are severe or
getting worse, descend.
◆ Anyone who has a
decreased level of
consciousness or cannot
walk a straight line,
must descend
immediately.
◆ Anyone with HACE or
HAPE has a life-
threatening condition,
for which the treatment
is descent. Descent
should be continued
until symptoms are
improving and the level
of consciousness is
normal. Difficulty
walking does not
usually improve right
away with descent and
often persists for
several days.
Golden Rule 4: No one with
altitude illness should
descend alone.
◆ Individuals with AMS
may still be worsening
even with descent.
◆ Persons with HACE
need, at the very least,
supervision and help
walking; most need to
be carried.
◆ Individuals with HAPE
should avoid exertion,
although if descent is
easy enough, persons
with mild HAPE can
sometimes walk down
with assistance. They
should not carry a pack.
If their condition
worsens, they need to be
carried.
Studies have shown that

nifedipine, which relaxes the
pulmonary arterioles and reduces
pulmonary artery pressure, is an
effective adjunct to descent and
supplemental oxygen for treating
HAPE. Nifedipine should not be
used alone to treat HAPE. It may
lower the systemic as well as the
pulmonary artery blood pressure
and cause faintness—even collapse
—and should be given only by
medical professionals familiar with
its effects. In the past, furosemide
was used to remove fluid from the
lungs, but this strong diuretic can
cause a large urine output, resulting
in a drop in blood volume and
collapse. Persons who could walk
with a little help have required
litter evacuation after furosemide
administration.
Recovery from HAPE usually is
surprisingly rapid. Individuals with
HAPE may reascend gradually after
a few days spent recovering at a
lower altitude.
Prevention of HAPE is the same
as for AMS: gradual ascent with
time for acclimatization. Heavy
physical exertion should be avoided
for the first few days after a rapid
ascent to high altitude. Nifedipine
starting one day before ascent, and
then continued during ascent, is
recommended for prevention in
individuals with a prior history of
HAPE. Nifedipine is the drug with
the longest history of use for
prevention of HAPE. Other drugs
that have been shown in more
recent studies to prevent HAPE
include inhaled salmeterol
(Serevent®), a drug used for
treating asthma; the corticosteroid
drug dexamethasone; and tadalafil
(Cialis®). All these drugs require a
physician’s prescription and could
be used for prevention of HAPE in
susceptible persons, but
consultation from a physician
knowledgeable about high-altitude
illness should be obtained.
Individuals who have pulmonary
vascular disorders such as primary
pulmonary hypertension or the
congenital absence of one of the
pulmonary arteries are very
susceptible to HAPE, and they
develop this disorder at much
lower altitudes. If such persons
wish to go to higher altitudes, they
must consult their physician, obtain
drugs such as nifedipine (although
this drug has not yet been tested in
such individuals), and be prepared
to descend immediately.
Table 24-4 lists the common
high-altitude illnesses.
Table The Spectrum of Common

24-4 Altitude Illness
ACUTE MOUNTAIN
SICKNESS (AMS)
• Headache with any of these
symptoms:
• Poor appetite, nausea, or
vomiting
• Fatigue and/or weakness
• Dizziness/lightheadedness
• Difficulty sleeping
HIGH-ALTITUDE CEREBRAL
EDEMA (HACE)
• Increasing headache
• Confusion
• Ataxia (trouble walking—
tested by heel-to-toe walking)
• Progressing disorientation
• Coma and death
HIGH-ALTITUDE
PULMONARY EDEMA
(HAPE)
• Increasing shortness of breath,
particularly on exertion
• Dry cough later producing
pink sputum
• Extreme fatigue progressing to
unconsciousness
HIGH-ALTITUDE RETINAL
HEMORRHAGES (HARH)
• Rarely cause symptoms except
when in macula
• Macular hemorrhage causes
central blind spot
• Visible only with an
ophthalmoscope
• Most resolve in ten to twenty
days
PERIPHERAL EDEMA (also
caused by exercise at low
altitude)
• Painless swelling of face,
ankles, and hands
• Scanty dark yellow urine
• Subsides with passage of
more urine
OTHER HIGH-ALTITUDE
CONDITIONS
High-Altitude Retinal
Hemorrhage
Hemorrhage into the retina (the
layer of sensitive light receptors in
the eye) is common above 14,000
feet (4300 m). The incidence
increases with altitude but is rare
below 12,000 feet (3600 m).
Usually the hemorrhages are small
and cause no symptoms, but rarely
the bleeding involves the macula
(the area of most acute central
vision) and can cause blurred
vision or even a tiny area of
blindness.
The hemorrhages are painless
and usually can be detected only by
looking at the retina with an
ophthalmoscope. Occasionally the
hemorrhages are larger, involve
more of the retina, and cause
blurring or loss of vision in
portions of the visual field for that
eye.
No evidence of a relationship
between hemorrhages and other
forms of altitude illness has been
found. The hemorrhages do not
appear identical to retinal
hemorrhages associated with
conditions such as diabetes or
hypertension at sea level. The
exudates that often occur in these
conditions are extremely rare with
high-altitude hemorrhages.
Most hemorrhages disappear in
a week or two, even at altitude, but
bleeding into the macula can leave
small central blind spots that persist
for many years. Persons who have
hemorrhages on one climb are
neither more nor less likely to have
them again. Because a blind spot
can persist after a macular
hemorrhage, some specialists
advise individuals with such
defects not to go to high altitude
again.
No treatment is available, nor
does a need to treat exist. Most
high-altitude retinal hemorrhages
absorb in a week or two.
Nevertheless, persons with very
large hemorrhages or macular
bleeding should descend to a lower
elevation since further exposure
may worsen the condition.
At high altitude less oxygen is
present in the bloodstream. Because
the retina and brain require a
constant amount of oxygen, one of
the responses to a lower oxygen
saturation is an increase in the flow
of blood to these vital structures.
Elsewhere in the body, arteries
have muscular coats to deal with
flow increases, but the retinal
vessels are designed to remain
clear and not obstruct light signals
with big, beefy muscles. Instead,
they have delicate support cells
(pericytes) that surround the
vessels. These pericytes are
sensitive to damage from lack of
oxygen and can rupture in high-flow
situations. The result is leaking of
blood into the retina (retinal
hemorrhaging). Such hemorrhages
also occur with severe carbon
monoxide poisoning and severe
hypoxia from other causes at sea
level.
High-Altitude Peripheral Edema
Swelling of the feet and hands
may occur during or after ascent to
high altitude. Considerable
swelling of the face and eyelids is
often present in the morning. This
edema is usually accompanied by a
decrease in urine output but may not
be associated with symptoms of
AMS. Although this condition
sometimes is a nuisance, it is
harmless and clears up within a few
days.
Almost identical edema and
fluid retention can develop
following strenuous exertion near
sea level, which makes it difficult
to assign it to altitude alone. Salty
foods and salt tablets should be
avoided because an increased
sodium intake aggravates the
condition. Nevertheless a high fluid
intake is necessary to avoid
dehydration. It is ironic that the
blood may be concentrated due to
edema and the body may be
dehydrated despite the fluid in the
tissues. Acetazolamide given for
acute mountain sickness may
diminish the edema through its mild
diuretic action. Some experts give a
small dose of the strong diuretic
furosemide to help this condition;
this should be done with caution.
Nutrition at Altitude
Almost all extreme-altitude
climbers lose weight during a
climb. Losses of as much as forty
pounds occur in a few individuals.
Since these individuals usually are
physically fit with little excess
body fat, most of the weight loss is
from muscle. The cause of such
weight loss is not well understood.
The maintenance of adequate
food and water intake is difficult at
extreme altitudes. Appetites are
poor, and high-altitude climbers
usually eat and drink much less than
they need. At least some of the
fatigue and weakness experienced
at such altitudes is due to
inadequate nutrition, dehydration,
and possibly potassium loss
accompanying high energy
expenditure.
Impairment of food absorption in
the gastrointestinal tract has been
suggested but not confirmed as a
cause for the weight loss, which
reportedly cannot be prevented by
forced feeding. The tastelessness of
the freeze-dried foods carried by
most expeditions may be more
significant. Climbers often go
hungry at high altitude rather than
eat food that they do not crave.
Menus should consist largely of
foods that all party members enjoy,
but foods should also be carried to
satisfy individual tastes. Diets
should contain large amounts of
sweets, which are usually
consumed in large quantities at high
altitudes. Fatty foods or highly
condensed rations may not be well
tolerated. During days of heavy
exertion, many climbers find that
frequent small high-carbohydrate
snacks are better than less frequent
larger meals.
On prolonged expeditions when
fresh vegetables and fruits are not
available, possible vitamin C
deficiency can be prevented with
ascorbic acid. However, most
packaged drinks such as lemonade
or orange juice contain some
vitamin C. Furthermore, several
months are required for signs of
vitamin deficiency to appear in
individuals previously in good
nutritional condition.
If vitamin intake appears
inadequate, one or two multivitamin
tablets per day can be taken. A
higher vitamin intake or special
vitamins such as E or B complex
are of no benefit at high altitudes
and may be harmful. Vitamin
requirements are only minimally
increased by the rigors of an
expedition, and a standard diet
contains much more vitamins than
are needed. Any excess is simply
excreted in the urine. Excess
vitamin A and D—possibly others
—are definitely harmful.
High-Altitude Deterioration
Acclimatized people can live a
normal life span at elevations as
high as 17,500 feet (5300 m) and
can live and work for several
weeks up to 20,000 feet (6100 m).
At higher elevations deterioration
rather than further acclimatization
occurs.
Spending as little time as
possible at extreme altitudes and
periodically descending for
recovery at lower altitudes for
several days can minimize high-
altitude deterioration. Adequate
fluid intake is essential. The urine
volume must be greater than 500 ml
every day, preferably two to three
times greater, and urine color
should be clear or light yellow, not
deep yellow or orange. Efforts must
be made to eat an adequate amount
of food in spite of a poor appetite.
An adequate caloric intake is
needed more than specific nutrients.
Nutritional deficiencies do not
develop in healthy individuals
during the short periods expeditions
are at high altitudes.
Oxygen during sleep—two liters
per minute through a face mask—is
beneficial. No drugs are known to
minimize deterioration, but sleeping
with low-flow oxygen does make a
difference.
Removing blood and replacing it
with fluid to reduce viscosity may
extend stays at high altitude, but
such extreme measures are not
justified when simple descent can
solve the problem safely.
Table Less Common Disorders at

24-5 Altitude
ALTITUDE DETERIORATION
• Slowly develops after ten to
fifteen days above 20,000 ft
(6100 m)
• Loss of appetite and weight
loss
• Exhaustion
• Impairment of memory and
judgment
CHRONIC MOUNTAIN
SICKNESS
• Develops only in long term
residents above 15,000 ft
(4500 m)
• Bluish, ruddy coloration
• Excessive red blood cells
• Various aches and pains
• Gradual heart failure
THROMBOPHLEBITIS AND
PULMONARY EMBOLISM
• Caused by dehydration and
inactivity
• Painful swelling of leg or arm
• Sharp pain in chest and
bloody sputum
TRANSIENT ISCHEMIC
ATTACK (TIA)
• Brief weakness, paralysis,
numbness or vision change
• Clears within an hour or less
• May be migraine equivalent
CEREBRAL VASCULAR
ACCIDENT (STROKE)
• Numbness or paralysis,
including one-sided facial
droop
• Difficulty with speech
(slurred speech, nonsense
speech or unable to speak)
• May progress to severe
paralysis or unconsciousness
• Slow, if any, improvement
Pulmonary Embolism
After a period of immobility,
such as being confined in a tent by a
storm, associated with dehydration
and exhaustion, blood clots may
form in the leg or pelvic veins or,
rarely, in arm veins. Occasionally
such clots break free and are
carried to the lungs where they
lodge in a pulmonary artery, a
condition known as pulmonary
embolism. Warning signs are a
swollen, painful leg or arm,
followed by the sudden onset of
chest pain, cough, and worsening
shortness of breath. Sudden death is
not uncommon in pulmonary
embolism, which is discussed at
greater length in Chapter 18:
Table 24-5 lists less common
disorders at altitude.
PREEXISTING MEDICAL
PROBLEMS AND ALTITUDE
Many people considering a trip to a
big mountain—sometimes to a
lower mountain—ask about medical
conditions that may become worse
at altitude and whether the risk is
unacceptable. Generally any
condition that causes hypoxia at sea
level is aggravated by going above
5000 feet (1500 m), but several
specific conditions may cause
problems (Chapter 25: Altitude and
Common Medical Conditions):
◆ Chronic lung disease with low
arterial oxygen saturation
◆ Pulmonary hypertension
◆ Congenital absence of a
pulmonary artery
◆ Cyanotic congenital heart
disease
◆ Previous pulmonary embolus
◆ Heart failure
◆ Severe angina
◆ Sickle cell disease
Individuals searching for
adventure and trying to “get away
from it all” must remember that they
are also getting away from prompt,
sophisticated medical care and must
assume responsibility for
themselves.
CHAPTER 25
ALTITUDE AND
COMMON MEDICAL
CONDITIONS
Peter H. Hackett, M.D.
More and more people with a

variety of medical conditions are
traveling to altitude for recreation
or work. Many are choosing to live
at altitude, particularly retirees. The
increased need for knowledge about
the mix of illness and altitude has
stimulated investigation, but for
many conditions not enough
information is available for
conclusions about the risks. This
chapter considers the effect of
altitude on preexisting illnesses,
pregnancy, children, and the elderly,
as well as the converse effect of
illnesses on altitude
acclimatization.
ALTITUDE STRESS
Ascent to altitude affects people in
various ways. Expansion of air
from the reduced pressure can
cause problems in any space that
contains air or gas, such as sinuses,
middle ears, lungs, the intestines,
even a pneumothorax. Dysbarism,
as such problems are called, is
more common with rapid ascent in
airplanes, but even gradual ascent
to terrestrial elevations can be
associated with problems such as
dental pain produced by expansion
of gas trapped beneath a filling.
In contrast, less dense air may
flow through airways more easily
and improve lung function.
Decreased air resistance improves
performance in athletic events such
as jumping, vaulting, and sprinting,
and allows balls to travel farther.
The major physiologic stress of
altitude is, of course, hypoxia. As
barometric pressure falls with
increasing altitude, the partial
pressure of oxygen declines.
Compared to sea level, Denver,
Colorado, has 17 percent less
atmospheric oxygen pressure,
Aspen has 25 percent less, and only
half the sea level pressure of
oxygen is present at approximately
18,000 feet (5500 m). In addition,
weather, season, and latitude affect
barometric pressure. Low
atmospheric pressure produces bad
weather. Pressure at high altitude is
lower in winter, and lower farther
from the equator for any given
altitude. Environmental hypoxia is
directly related to barometric
pressure, not altitude.
Many individuals experience
hypoxemia—lower arterial blood
oxygen—in everyday life, such as
during sleep, during airline travel,
or as the result of lung disease.
Commercial aircraft have cabin
pressures equivalent to altitudes as
high as 8500 feet (2600 m) and
airline crew members experience
hypoxemia. Oxygen saturations of
80 to 93 percent (normal at sea
level is 95 percent or higher) and
an average low point of 89 percent
were found in a recent study. The
effects of such hypoxemia are
inconsequential in healthy
individuals, but persons with
illnesses affecting oxygen transport
could suffer adverse effects.
Temperature decreases at a rate
of approximately 3.5°F per 1000
feet (6.5°C per 1000 m) gain in
altitude. Cold and hypoxia combine
to produce hypothermia and
frostbite, and cold may contribute to
high-altitude pulmonary edema.
Because particulate matter,
water vapor, and cloud cover
diminish with increasing altitude,
solar ultraviolet radiation increases
by approximately 4 percent per
1000 feet (300 m) gain in altitude,
increasing the risk of sunburn,
photosensitive reactions, snow
blindness, and, with lifetime
exposures, skin cancer and
cataracts. On windless days,
reflection of sunlight from snow can
produce intense heat, and heat-
related illnesses are more common
at high altitudes than generally
appreciated.
Because smaller amounts of
airborne particulate matter are
present, altitude can be beneficial
for those with allergic asthma or
other allergic conditions, and for
individuals whose reactive airway
disease is aggravated by pollutants.
However, air pollution at high
altitude is now increasing
throughout the world.
Humidity is decreased at
altitude, particularly at high
altitudes, because the air is cool.
(The vapor pressure of water at
5°F, or −15°C, is only 1.24 mm
Hg.) Furthermore, in wilderness
situations water can only be
obtained above snowline by melting
snow or ice. Such difficulty
obtaining water combined with
increased water loss from the skin
and lungs often leads to dehydration
in healthy climbers. Compromised
cardiovascular systems, diuretics
taken for heart failure or
hypertension, and pregnancy
(perhaps) aggravate this problem.
Drying of the airways increases the
risk of tracheal and bronchial
plugging, particularly in those with
chronic lung disease.
THE EFFECT OF ALTITUDE

ON RESPIRATORY
DISORDERS
Movement of oxygen from air to
blood, the first stage of oxygen
transport, is the function of the
respiratory system. Components of
this system include the controls of
ventilation (the movement of air
into and out of the lung), the
mechanics of respiration, matching
of ventilation and perfusion by
blood in the lung, and gas exchange
across the alveolar-capillary
membrane.
Disorders of Ventilatory Control

Any disorder that diminishes
ventilation or the ventilatory
response to lowered oxygen or
increased carbon dioxide—such as
stroke, trauma that injures the brain,
neuromuscular diseases, obesity
resulting in diminished respiration
(hypoventilation), chronic
obstructive pulmonary diseases
(COPD) including asthma, and
sleep apnea—pose a greater risk at
altitude. Medications may have the
same effect. Long-acting
benzodiazepines such as diazepam
(Valium®) reduce nocturnal arterial
oxygen saturation at high altitude.
Carotid Surgery
Carotid body responsiveness to
hypoxia is necessary for optimal
acclimatization to altitude, and a
lessened response to hypoxia has
been linked to susceptibility to
altitude illness. The carotid body is
commonly damaged or ablated
during carotid artery surgery
(usually for arteriosclerotic
narrowing or occlusion).
Investigative studies have found that
the ventilatory response to the
hypoxia of 5000 feet (1500 m)
observed prior to surgery was
abolished by the procedure.
Similarly, individuals with bilateral
carotid body resection for treatment
of asthma or emphysema lack
adequate ventilatory responses to
acute altitude hypoxia. However,
although altitude acclimatization
might be impaired in such persons,
whether the relative hypoventilation
leads to altitude illness remains to
be determined. Nonetheless, these
individuals can be easily identified,
and should be cautioned about
altitude exposure.
Sleep Disordered Breathing and

Apnea
Persons with abnormal breathing
rhythms during sleep at sea level,
such as snoring, obstructive apnea,
or sleep disordered breathing
(SDB), particularly the elderly, may
have greater nocturnal hypoxemia at
altitude and a consequent increase
in abnormal cardiac rhythms, an
increased pulmonary artery
pressure, and a greater
susceptibility to altitude illness. A
period of apnea at altitude would
certainly produce greater
hypoxemia than at sea level.
However, altitude-induced changes
in ventilatory control and breathing
conceivably could improve certain
apnea syndromes. Unfortunately,
virtually nothing is known about the
interaction of SDB with altitude,
even though SDB has been invoked
in the pathogenesis of acute altitude
illnesses, including high-altitude
pulmonary edema. (In contrast,
normal periodic breathing at
altitude has not been related to
development of acute mountain
sickness [AMS], and, in fact, is
associated with a brisk hypoxic
ventilatory response, which is
generally considered beneficial at
altitude.)
At altitude individuals using a
continuous positive airway pressure
(CPAP) machine without pressure-
compensating features as treatment
for SDB need to make adjustments
because altitude decreases the
delivered pressure. The error is
greater with higher altitudes and
higher initial pressure settings.
Lung Disorders
Impairment of gas exchange by
hypoventilation leaves those
afflicted with a lower arterial
oxygen pressure than their healthy
counterparts. Physiologically,
individuals with lung disease
breathe as if they are already at a
higher altitude and may suffer even
greater effects with ascent. In
addition, greater hypoxemia may
exacerbate their underlying lung
disease—increasing pulmonary
artery pressure by exaggerating
hypoxic pulmonary
vasoconstriction, for instance.
High-Altitude Residents
Lung disease is the most
common cause of impaired oxygen
transport and would be expected to
impact those living at altitude.
Studies of high-altitude residents
have found an increased morbidity
from COPD, as well as a
propensity to migrate to lower
altitude.
In South America and Asia, the
problem of acquired lung disease is
greater. A high incidence of
pneumoconiosis—lung disease
resulting from inhalation of
particulate foreign material—is
found at high altitude in central
Ladakh, located at the base of the
Korakorum range in Pakistan and
Kashmir. This disorder is attributed
to dust storms that stir up silica and
the absence of chimneys in
residents’ homes.
Cigarette smoking is also a
major cause of lung disease.
Altitude and smoking are
independently associated with
mortality from COPD in the United
States. In an analysis by states,
COPD mortality rose by 1 per
100,000 population for every
additional 5.4 packs of cigarettes
smoked per person per year, and for
each 300 feet (95 m) increase in
altitude.
Stable Hypoxemic Disease in

Lowlanders
Sea-level and low-altitude
residents—lowlanders for short—
with lung disease would be
expected to tolerate high altitude
less well. In addition, altitude might
unmask lung disease that has gone
undetected. Acute hypoxemia
associated with air travel has
received considerable attention, but
much less is known about more
prolonged hypoxia, such as a stay at
a ski resort. In one study of eight
hypoxemic individuals with
moderate, uncomplicated COPD
who ascended to 6300 feet (1920
m) for four days, the persons had
only mild symptoms on ascent,
primarily mild fatigue and
insomnia. However, arterial oxygen
pressure declined from 66 at sea
level to 51 mm Hg while at rest and
from 63 to 47 mm Hg with exercise.
(Normal resting arterial oxygen
pressure at sea level for healthy
young adults is 85 to 100 mm Hg.)
The individuals did acclimatize.
Their arterial carbon dioxide
pressures dropped abruptly and
declined further over four days, and
their arterial oxygen pressures
increased, the responses seen in
healthy persons. The authors
concluded that travel to this
moderate altitude is safe for such
persons and speculated that their
preexisting hypoxemia may have
produced the equivalent of altitude
acclimatization, decreasing the
likelihood of AMS. Despite the
authors’ plea for further
investigations with sicker
individuals at higher altitudes,
subsequent studies have not been
done.
In studies of acute hypoxia and
air travel, the ability to blow out a
match to ensure adequate expiratory
flow, and the ability to walk up a
flight of stairs without distress,
have been recommended as simple
screening tests. Supplemental
oxygen during flight has been
suggested for those who “failed.”
These and other much more
sophisticated tests may predict
oxygenation during transient (up to
four hours) modest hypoxia, but
their usefulness is limited because
sea-level arterial oxygen levels do
not correlate well with how people
fare at altitude. These studies also
did not address how individuals
might do with longer stays at
altitude and with associated
stresses such as sleeping, physical
activity, smoking, angina,
hypertension, or other problems.
Despite these limitations, a
physician attempting to evaluate the
risk of altitude for a person with
COPD may want to use the
predicted initial resting arterial
oxygen pressure at altitude as a way
to determine the need for
supplemental oxygen (Fig. 25-1).
Efforts to predict oxygenation at
high altitude in children with
hypoxemic lung disease have found
that hypoxic challenge with air
containing 15 percent oxygen is a
better way to identify individuals
who might require supplemental
oxygen during flight or in the
mountains than measuring breathing
capacity and oxygen saturation. The
main value of provocative testing is
to determine the need for oxygen
while at rest at altitude, but further
assessment of oxygen saturation
during activity and sleep is needed
to ensure a correct oxygen
prescription.
Oxygen therapy may be required
for persons who are symptomatic at
altitude or for those predicted to
become severely hypoxemic. For
those already on supplemental
oxygen, the amount of inspired
oxygen should be increased by the
ratio of higher to lower barometric
pressures. Whether acetazolamide
and medroxyprogesterone acetate,
both of which aid acclimatization
by stimulating ventilation, might be
useful (or harmful) in individuals
with COPD, especially with
elevated blood carbon dioxide
concentrations, is unknown.
Individuals should have pulmonary
function optimized prior to ascent to
altitude and should receive
instructions on medication use
(including oxygen) if problems
develop.
In summary, information
regarding the effect of altitude on
chronic lung disease is extremely
limited. Predicting who will
tolerate and who may be harmed by
the additional hypoxia of altitude
often is a difficult, possibly futile
undertaking, leaving old-fashioned
clinical judgment based upon the
overall health and capacity to
function of each individual as the
best guidance available.
Asthma
Data on mortality and morbidity
from asthma in high-altitude
residents are scant. The available
information suggests that asthma
may be less of a problem at high
altitude than at sea level, both for
residents and sojourners, because
allergens and pollution are
decreased. Studies worldwide have
reported improvement in childhood
asthma at altitude, which has been a
popular treatment for asthma in
Europe for many decades.
Surprisingly, in view of the
possibility of greater hypoxemia
during asthmatic
bronchoconstriction at altitude, no
association between asthma and
highaltitude pulmonary edema or
AMS has been reported, nor has
unexpected asthma exacerbation in
lowlanders at altitude been
described. Likewise, no
information documents the value of
a variety of logical clinical aids for
prevention, including increased
hydration or the use of an airway
warming mask.
Whether a severe asthma attack
at high altitude puts a person at
greater risk than at low altitude—an
important question—is unanswered.

ON CARDIOVASCULAR
PROBLEMS
During ascent and the first few days
of residence at altitude, the
cardiovascular systems of healthy
individuals make important
adjustments. These physiologic
changes may be limited in those
with underlying disease, or these
adjustments may stress the
compromised cardiovascular
system and aggravate illness. The
principal initial adjustments are
increases in resting and exercise
heart rate, increases in blood
pressure and systemic vascular
resistance, increases in cardiac
output and velocity of contraction,
along with contraction of the veins
in the skin, muscles, and intestines
resulting in increased central blood
volume. Largely mediated by
increased sympathetic nerve
activity, the net effect is an increase
in cardiac work, cardiac muscle
oxygen consumption, and coronary
blood flow. After four to eight days
at altitude most of these changes
diminish, and with prolonged
exposure, cardiac output, coronary
blood flow, and eventually blood
pressure may fall to below sea-
level values. An elevated
pulmonary blood pressure,
however, persists.
Figure 25-1. Nomogram for predicting
PaO2 at altitude based on sea-level
PaO2
Hypertension
The effect of altitude on blood
pressure depends on many
variables: length of exposure,
degree of hypoxemia, genetic and
dietary variables, and cold
exposure. Long-term altitude
residence has been associated with
lower systemic arterial pressures
than sea-level residence in South
America, North America, Africa,
and Asia. Prolonged altitude
exposure has also been found to
inhibit progression of hypertension.
A preliminary survey in Tibet found
an incidence of hypertension higher
(9.4 percent) than that in South
American high-altitude natives (4.5
percent), but that difference is
attributed to ingestion of large
amounts of salted tea by Tibetans.
The effect of acute exposure to
altitude on blood pressure is not
entirely clear, in part due to
differences in study methodologies.
Many studies indicate that blood
pressure increases during the first
week or two at high altitude, more
so with greater altitude. However, a
few investigations have reported no
significant change in blood
pressure, or even a slight decrease.
Whether individuals who have
high blood pressure at sea level
have an exaggerated hypertensive
response on initial ascent to altitude
has not been systematically
evaluated. Anecdotally, some
individuals have developed severe
hypertension. Such occurrences,
whatever their frequency, are not
trivial problems in view of the
large number of hypertensive
persons visiting ski resorts and
trekking at high altitude.
The magnitude of the blood
pressure change in hypertensive
individuals may depend upon the
hypoxic stress. At low altitudes, the
average increase appears to be
minimal, although individual
variability is great. Heart rates also
increase. The authors of one study
concluded that the blood pressure
increase in individuals with normal
and elevated pressures was not
important at 4000 feet (1200 m) but
could become so at 10,000 feet
(3000 m).
With acute exposure to higher
altitudes, hypertensive individuals
do have a greater blood pressure
response than normotensives
(individuals with normal blood
pressure). Importantly, individual
variation is considerable, and a few
hypertensives have an exaggerated
pressure increase. Unfortunately,
the studies that have been done have
not been continued after the first
hours at altitude, so whether blood
pressure continues to increase over
a period of days, as it does in
normotensive persons, is an
important unanswered question.
Also unknown is whether more
prolonged stay at altitude might
reliably reduce arterial pressure to
below sea-level values, as has been
reported in normotensives after five
to ten years.
Clearly the scientific basis for
advising individuals with
hypertension about ascent to
altitude is limited. Because some
individuals may become markedly
hypertensive, and because there is
no way at present to predict an
individual’s response, careful
blood pressure monitoring appears
prudent.
Which medication is best for
altitude-aggravated or induced
hypertension and whether
antihypertensive medication
regimens effective at low altitude
may be insufficient upon ascent to
high altitude are two more
significant questions not yet
answered.
Individuals with hypertension
may experience other untoward
effects of altitude in addition to
increased blood pressure. They
have a greater increase in
pulmonary blood pressure in
response to hypoxia, which could
predispose to high-altitude
pulmonary edema, a relationship yet
to be explored. In addition, the
central nervous systems of
hypertensives respond in an
exaggerated manner to hypoxia. The
prevalence of periodic breathing at
altitude could cause hypertensives
to experience very high levels of
sympathetic stimulation during
sleep, increasing their risk of
exaggerated systemic hypertension,
pulmonary hypertension, and
abnormal cardiac rhythms.
Normotensives were recently found
to have elevated nocturnal blood
pressure at altitude. Although these
concerns about hypertensive
individuals are hypothetical, the
issues of untoward events during
sleep and susceptibility to high-
altitude pulmonary edema certainly
warrant further attention.
Coronary Artery Disease

High-Altitude Residents
Various studies suggest that the
incidence of coronary artery
disease and consequent death rates
is lower in persons living lifelong
at high altitude. Firm conclusions
are difficult because such variables
as age, genetics, smoking, exercise,
diet, and migration to lower altitude
due to illness have not been
controlled, but the evidence is not
to be discounted. No study has ever
suggested an increased incidence of
ischemic heart disease in high-
altitude residents.
Lowlanders Going to High

Altitude
With acclimatization, a normal
heart can tolerate even extreme
hypoxemia without ischemic
changes or impaired function. A
theoretical basis for exacerbation of
coronary artery disease at altitude
exists, however. Cardiac work is
slightly increased, and the usual
compensatory increase in coronary
blood flow may not be attained in
those with arteriosclerotic coronary
artery disease. In fact,
arteriosclerotic coronary vessels
that cannot dilate may actually
constrict, resulting in ischemia
(inadequate blood supply).
To assess whether these
concerns are significant, four
questions need to be examined
(Chapter 17: Heart and Blood
Vessel Disorders):
1. Does altitude unmask
previously unknown coronary
artery disease?
2. Does altitude exacerbate
stable cardiac ischemia?
3. Does altitude increase the risk
for myocardial infarction or
sudden death?
4. Does altitude provoke
abnormal cardiac rhythms?
Anecdotal reports make it clear
that these events may all occur at
high altitude as they do at sea level,
but whether altitude is a contributor
is unclear. Additional
considerations are the possible
influence of cold and the risk of
ischemia in those who have no
signs or symptoms of coronary
artery disease, particularly the
elderly. Finally, what
recommendations make ascent to
altitude safer for those with known
or unknown coronary artery
disease?
Does Altitude Unmask Previously

Unknown Coronary Artery
Disease?
Investigation decades ago found
that severe hypoxia is stressful for a
heart with coronary artery disease
but is less stressful than exercise. In
a direct comparison, sea-level
exercise produced more ischemia-
related electrocardiographic (ECG)
changes in individuals with known
coronary artery disease than did
inhalation of 10 percent oxygen
while at rest. (Normal air contains
20 percent oxygen.) As a result,
exercise testing has become the
preferred way to screen. Of several
thousand individuals with suspected
coronary disease who were tested
for twenty minutes with 10 percent
oxygen, none developed serious
cardiac events or died. When
hypoxia and exercise were
combined, however, the results
were different. When seventy
asymptomatic soldiers (ages thirty
to fifty) who already had
nonspecific ECG changes were
evaluated, hypoxia at rest resulted
in further ECG changes in four.
However, ten individuals
developed changes with exercise at
sea level, and twenty developed
changes with the combination of
hypoxia and exercise. Although
these studies are interesting, they
assessed only ECG changes and
only in persons with pretesting
ECG abnormalities. Nonetheless,
hypoxic exercise appears better
able to unmask coronary artery
disease (by ECG) than hypoxia at
rest or exercise while breathing air
containing a normal amount of
oxygen. If acute hypoxic exercise
can unmask ECG evidence of
coronary artery disease, altitude
exposure may do so as well.
A stay at high altitude may stress
the coronary circulation as much or
more than acute hypoxic exercise
because the blood concentrations of
catecholamines such as adrenaline
are increased during the first few
days at altitude, exertion varies,
sleep may exaggerate hypoxemia,
temperatures are lower, and other
stresses are present.
Does Altitude Exacerbate Stable

Cardiac Ischemia?
Small increases in heart rate and
blood pressure on initial ascent to
altitude may cause angina or induce
angina in those with coronary artery
disease (Chapter 17: Heart and
Blood Vessel Disorders). Altitude
alone may aggravate angina, at least
immediately after ascent. Several
investigators have concluded that
individuals with coronary artery
disease who are well compensated
at sea level do well at a moderate
altitude after a few days of
acclimatization, but during that
period their threshold for angina
may be lower and activity should
be limited. However, two
individuals had untoward events (a
relatively high incidence of
complications): one an increase in
angina and a second a myocardial
infarct. Further study to better
define those who are at risk is
needed.
A reunion of the U.S. Army 10th
Mountain Division in Vail,
Colorado (8250 feet, or 2500 m),
provided an opportunity to observe
a number of elderly individuals
(mean age 69.8 ± 4.4 years) over a
period of four days after ascent
from near sea level. Of seventy-
seven men and twenty women,
twenty were known to have
significant coronary artery disease.
Thirty-eight had abnormal ECGs on
arrival at high altitude. Over the
four days at high altitude, no
clinically significant ECG changes
or clinical events suggestive of
ischemia occurred. These elderly
individuals with both symptomatic
and presumed asymptomatic
coronary artery disease (and
frequently hypertension) tolerated
moderate altitude well and had no
exacerbation of their stable
ischemia.
Does Altitude Increase the Risk of

Myocardial Infarction or Sudden
Death?
Data are inadequate to draw firm
conclusions about the risk of
myocardial infarction and sudden
death at altitude in those with
coronary artery disease. The
limited available evidence does not
identify an increased risk,
particularly in individuals who
have been exercising regularly at
low altitude.
Does Altitude Provoke Abnormal

Cardiac Rhythms?
In older individuals who ascend
to altitude, a number of
investigators have noted an
increased number of extrasystoles
(premature beats, paroxysmal
ventricular contractions, or PVCs)
Vessel Disorders). However, the
PVCs appeared benign and did not
suggest a propensity to life-
threatening abnormal rhythms.
Biochemical studies indicated that
increased secretion of adrenaline
and related compounds was the
most likely cause. Most persons
returned to normal after a few days,
and no dire events have been
reported.
Persons with troublesome or
severe rhythm disorders have not
been evaluated systematically at
high altitude. No anecdotal reports
of exacerbations of supraventricular
tachycardia or other common
rhythm abnormalities have been
published, and no information about
whether or to what extent ascent to
high altitude increases risk for those
with specific rhythm disorders at
sea level is available.
Cold, Altitude, and Ischemia

Whether cold provokes
myocardial ischemia at altitude has
not been studied but seems likely.
At sea level, breathing cold air
and/or exercising in a cold
environment by individuals who
already had exercise-induced
angina limited their exercise
tolerance even more. The cold-
induced increase in heart rate and
blood pressure was similar to that
reported at moderate altitude in
temperate conditions. Therefore,
cold and altitude might interact to
incite effort-induced angina.
Because high-altitude locations are
commonly cold, this question of
interaction deserves pursuit.
The Risk of Acute Ischemic

Events in Those Without
Coronary Artery Disease
In addition to arteriosclerosis,
coronary artery spasm has also
been invoked as a possible
mechanism for cardiac ischemia at
altitude. Spasm would not be
surprising at altitude since the
sympathetic stimulation and
respiratory alkalosis that typically
occur are known coronary
vasoconstrictors. However, only
one individual with altitude-
induced coronary artery spasm has
been identified.
Advice for Persons with Coronary

Artery Disease Regarding Altitude
The stress of high altitude on the
coronary circulation appears to be
minimal at rest but significant in
conjunction with exercise. Persons
exercising at altitude are more at
risk than those merely sitting in a
car or an airplane. European studies
imply that an exercise program at
sea level prior to exercising at
altitude is essential for reducing the
risk of sudden death.
Ideally, no one with any of the
following risk factors for coronary
artery disease should undertake
unaccustomed exercise at high
altitude without a physician’s
supervision—certainly not those
with known coronary artery
disease:
◆ Family history of coronary
artery disease before age fifty-
five
◆ History or presence of
hypertension
◆ Resting ECG changes
indicative of ischemia (ST
depression of any magnitude)
◆ Prior episode of chest pain
Asymptomatic males over age
fifty with any risk factors should
have an exercise treadmill test prior
to altitude exposure. Individuals
with low risk of coronary artery
disease as determined by the
exercise test can be reassured and
given such medical management as
they may need. (Individuals who
have had myocardial infarcts or
coronary artery surgery are
considered high risk only if they
have abnormal results from the
exercise test.) Persons at high risk
may require radiographic
examination of the coronary arteries
(coronary angiography) to
determine appropriate management.
An increasingly frequent
question is whether individuals
who have had coronary artery
surgery are at increased (or perhaps
decreased) risk at altitude (Table
25-1). The complete lack of data
makes advising a person difficult.
Conservative physicians may
follow the adage “Better safe than
sorry,” but others argue that
forbidding such adventure is
unwarranted and without scientific
basis. Advice for such individuals
requires individual evaluation; a
trial at an intermediate altitude at
the expected workload may be
useful. As always, nothing
substitutes for sound clinical
judgment.
Possible Beneficial Effects of

Altitude for Coronary Artery
Disease
Some studies have suggested
potential benefits from high-altitude
exposure for those with coronary
artery disease. In experimental
animals, and in studies of cardiac
rehabilitation programs at 12,375
feet (3750 m) for sea-level
dwellers with heart disease carried
out in Russia and Kyrgyzstan, and in
Peru, definite benefits have been
found and no adverse effects have
been encountered. A French group
has suggested skiing at moderate
altitude as part of a program to
lower cardiovascular risk. Given
the physiologic and biochemical
similarities of altitude
acclimatization and aerobic
conditioning, these proposals merit
attention.
Evaluation of Coronary
Artery Disease in
Table Individuals Over Age Fifty
25-1 Who Wish to Go to
Altitude
Heart Failure
A tendency toward acute
decompensation in individuals with
a history of heart failure upon
arrival to altitude has been
observed, but systematic studies
have not been made. Although the
hypoxemia of moderate altitude
does not depress myocardial
contractility, the tendency toward
fluid retention in some individuals
at altitude—sometimes manifested
as AMS—could aggravate heart
failure. Because such fluid balance
changes may occur, persons with
heart failure must be cautious about
altitude exposure. However, no data
on the magnitude of the risk or who
would be most at risk are available.
Presumably, prevention and
treatment at altitude would be the
same as at sea level, although low-
flow oxygen would probably have
greater benefit by reducing hypoxic
stress. Persons who know they have
heart failure should consult their
physician about increasing their
diuretic medication at altitude and
should monitor their blood pressure
as well as their weight, peripheral
edema, and chest congestion.
Congenital Heart Disease

The hypoxia of high altitude
elevates pulmonary arterial
pressure and resistance. As a result,
individuals with disorders such as
atrial and ventricular septal defects
(abnormal openings between the
right and left atria or ventricles),
patent ductus arteriosus (an opening
between the aorta and pulmonary
artery), and partially corrected
tetrology of Fallot (a complex
congenital heart defect) might have
increased pulmonary hypertension
and shunting from the pulmonary to
the systemic circulation at high
altitude. Children born at altitude
with atrial and ventricular septal
defects have greater pulmonary
hypertension than those born at
lower altitude. Whether such
individuals develop greater arterial
oxygen desaturation at high altitude
because the pulmonary hypertension
of altitude increases shunting
depends on the severity of
preexisting pulmonary hypertension
and that induced by altitude
hypoxia. Shunting would be
expected to contribute to altitude
illness, including high-altitude
pulmonary edema, as well as to
dyspnea, although these individuals
tend to have a lower hypoxic
ventilatory response as a result of
their chronic hypoxia. An
interesting related question is
whether defects resulting in reduced
pulmonary blood flow, such as
tetrology of Fallot, might be
protective for HAPE.
Whether individuals with
persistent pulmonary hypertension
after corrective surgery for septal
defects may have problems at high
altitude is unknown. When patent
foramen ovale (a type of atrial
septal defect) was noticed in
persons with HAPE, it raised the
suspicion that shunting and
hypoxemia may have contributed to
the illness, but further investigation
disclosed others with patent
foramen ovale who did not develop
HAPE.

ON PULMONARY VASCULAR
DISORDERS
In addition to congenital cardiac
defects, any illness resulting in
pulmonary hypertension (increased
blood pressure in the lungs, which
normally is much lower than the
pressure in the rest of the body)
may be a relative contraindication
to high-altitude exposure. Hypoxic
pulmonary vasoconstriction would
probably exaggerate pulmonary
hypertension. Given the prominent
role of pulmonary hypertension in
the pathophysiology of HAPE, any
such illness may predispose to that
disorder. Conditions for which this
caution would apply include
unilateral absent pulmonary artery
and restrictive lung diseases, both
of which have been associated with
HAPE.
Persons with primary pulmonary
hypertension (PPH) would be
expected to be more symptomatic—
to be more short of breath, to have
more frequent fainting episodes,
and to be weaker on exertion.
However, some individuals with
this disorder are able to tolerate
high altitude. Hypoxic gas breathing
can be used to identify an
individual’s response to hypoxia.
Persons with PPH who must
travel to high altitude may benefit
from calcium channel blockers,
isoproterenol, or low-flow oxygen.
These individuals must also be
aware of a probable increased
susceptibility to HAPE. A lowland
woman with pulmonary
hypertension as the result of taking
fenfluramine developed two
episodes of HAPE: the first at 7600
feet (2300 m) and subsequently at
only 6100 feet (1850 m), although
she skied up to 7750 feet (2350 m).
Other conditions that may
produce pulmonary hypertension
include bronchopulmonary
dysplasia, recurrent pulmonary
emboli, and mitral stenosis.
Whether pulmonary hypertension is
primary or secondary to some other
disorder, individuals with this
condition should be aware of the
hazards of high altitude, including
right heart failure and HAPE.
Pulmonary hypertension is at least a
moderate contraindication to ascent
to altitude.

ON HEMATOLOGIC
PROBLEMS
Abnormal Hemoglobin
The hypoxia of high altitude is a
well-recognized problem for those
with sickle cell disease. Even
pressurized aircraft cabin altitudes
(up to 8250 feet or 2500 m) will
cause 20 percent of those with
hemoglobin SS, SC, and sickle-
thalassemia to have a thrombotic
vaso-occlusive crisis. Indeed,
ascent to altitude for some has
triggered their first awareness of
their condition. People with sickle
cell disease living at high altitude
(10,000 feet or 3000 m) in Saudi
Arabia have twice the incidence of
crises, hospitalizations, and
complications as their counterparts
at low altitude.
Splenic infarction at altitude may
be more common in those with
sickle cell trait (hemoglobin AS)
than those with homozygous disease
(hemoglobin SS), who totally
infarct their spleens early in life.
The differential diagnosis of left
upper quadrant pain at altitude
(even as low as 5000 feet or 1500
m) should include splenic infarction
—in Caucasians as well as those of
African ancestry. The incidence of
problems in individuals with sickle
cell trait, however, is quite low,
and ascent to altitude, even with
vigorous exercise, is not
contraindicated, in contrast to those
with sickle cell disease. The U.S.
Army, for example, does not
consider soldiers with the trait unfit
for duty at high altitude.
Oxygen Affinity
Hemoglobin with altered oxygen
affinity may affect acclimatization
to high altitude. When individuals
with genetically left-shifted oxygen
dissociation curves were taken to
10,200 feet (3100 m), surprisingly
they did not develop a fast pulse or
rapid respirations and were
superior in their exercise
performance. At least at this
altitude, increased loading of the
hemoglobin in the lung presumably
resulted in improved oxygen
transport. Whether a decreased
oxygen affinity would be
detrimental has not been addressed.
Anemia
Given the central role of
hemoglobin in oxygen transport, a
low hemoglobin level might be
expected to affect tolerance to high
altitude. However, neither the extent
of ventilatory acclimatization or the
incidence or severity of AMS has
been found to correlate with
hemoglobin concentration.
Persons with iron deficiency,
even without frank anemia, have
reduced exercise performance at
high altitude (as at sea level), as
well as reduced erythropoietic
(bone marrow stimulation)
response. Iron deficiency is
particularly common in women who
are not careful about replacing iron
lost in menstrual blood. No data are
available on the role of anemia in
susceptibility to high-altitude
illness.

ON NEUROLOGIC
CONDITIONS
Migraine
The important question of
whether high altitude aggravates
migraine has not received sufficient
attention. That the headache of
AMS and that of common migraine
may be nearly indistinguishable
presents obvious problems in
diagnosis and determination of
incidence. The mechanisms for
migraine and the headache of AMS
could be similar. To test this
hypothesis, sumatriptin, a drug
(5HT1-receptor agonist) effective
for migraine, was evaluated as
therapy for the headache of AMS.
The results were mixed, and further
study is required.
One population in which
migraine is easier to identify at
altitude is the high-altitude native, a
population that does not suffer from
AMS. When Peruvian high-altitude
natives were compared to
lowlanders, 12.4 percent of a
general population at 14,200 feet
(4300 m) suffered migraine
headaches, but only 3.6 percent of a
similar population at sea level had
that problem.
In a group of 379 adult men
subsequently studied at 14,200 feet
(4300 m) by the same investigators,
the incidence of migraine headaches
was 32.2 percent and correlated
with increasing age, hemoglobin
values, and chronic mountain
sickness. For all types of headaches
the incidence was 54.6 percent, far
higher than reported in Peruvian
and other populations living at low
altitude. The authors postulated that
migraine in this population might be
higher due to the combined effects
of hypoxia, polycythemia, and
reduced cerebral blood flow. Since
migraine in this population may be
related to chronic mountain
sickness, a disorder that develops
over a period of years, the
implications for high-altitude
sojourners are unclear.
Whether ascent to high altitude
increases the frequency or severity
of headaches in lowlanders with
migraine is not yet determined, but
clearly ascent can trigger migraine
in both those with and those without
a prior history of migraine at sea
level. In one study, migraine
developed repeatedly in susceptible
individuals during simulated
altitude exposure between 9000 and
11,000 feet (2750 and 3400 m). For
others, although frequency may
remain stable, the severity may
change. Migraine must be included
in the differential diagnosis of a
severe headache at altitude, even
with apparent AMS, particularly
when associated with visual or
other focal neurologic deficits.
Whether hypoxic gas breathing at
sea level can identify individuals in
whom high altitude may trigger an
attack has not been investigated.
STROKE, TIA,
CEREBROVASCULAR
DISORDERS, AND ALTITUDE
Whether the incidence or severity
of cerebrovascular disease (CVD)
and stroke is different in
highaltitude natives than in sea-
level populations is unclear.
Surveys conducted in rural areas of
South America and Asia over a
range of 5100 to 14,200 feet (1550
to 4300 m) have suggested a lower
incidence of CVD. However, an
epidemiological study reported that
the prevalence ratio for CVD at
11,200 feet (3400 m) in Peru was
close to the worldwide average.
Discerning the true relationship
between altitude and
cerebrovascular disease requires
careful control for racial
characteristics and lifestyle while
comparing low- and high-altitude
populations.
Rarely, stroke has been reported
in previously healthy sojourners at
altitude and typically has been
ascribed to dehydration, forced
inactivity, and polycythemia. Stroke
may also be a complication of
highaltitude cerebral edema
(HACE); clotting in cerebral blood
vessels is a common finding at
autopsy.
Clinically, cerebral venous
thrombosis (most strokes are
arterial occlusions) is easily
confused with HACE. A number of
reports emphasize the need for
physicians to consider this
diagnosis in individuals with
persistent neurologic symptoms
after descent from altitude. In a
recent series of individuals
eventually diagnosed with cerebral
venous thrombosis, all had recently
been on long air flights and one had
been mountaineering. An
accompanying editorial suggested
hypercoagulability or increased
viscosity might be responsible and
emphasized that this condition is
relatively easy to treat and must not
be missed.
Whether acute high-altitude
exposure contributes to a
hypercoagulable state that
predisposes individuals to strokes
is a subject of debate. The
interesting question of whether high
altitude might unmask cerebral
arteriosclerosis and vascular
insufficiency in asymptomatic
individuals has not been addressed.
Transient, focal neurologic
abnormalities in the absence of
HACE have been attributed to
transient ischemic attacks (TIAs).
However, other possible etiologies
include cerebrovascular spasm
(migraine equivalent), focal edema,
and hypoxia in zones of minimal
cerebral blood flow. Most of these
individuals have been young,
healthy mountaineers, not older
individuals who would be expected
to have arteriosclerotic vascular
disease, the usual cause of TIAs.
One report described six cases of
transient blindness that appeared to
result from a cerebral rather than an
ocular process. Supplemental
oxygen or carbon dioxide breathing
promptly reversed the condition,
which suggested vascular spasm
rather than occlusion. Descent
provided slower relief. Others have
described similar incidents as well
as other problems suggestive of
TIAs. In all cases, recovery was
complete, and the few individuals
subsequently evaluated by MRI had
no detectable abnormalities. The
exact etiology of these focal
neurologic events remains a
mystery and certainly warrants
further study.
Because cerebral blood vessels
dilate during ascent to altitude,
persons with cerebrovascular
structural abnormalities, such as
arteriovenous malformations or
aneurysms, may be at risk.
Individuals with such abnormalities
that have hemorrhaged have been
encountered. Persons with known
cerebrovascular malformations
should perhaps be advised to avoid
significant altitude exposure.
Brain Tumors
Brain tumors can be unmasked
upon ascent to high altitude,
presumably because the intracranial
blood flow changes and the brain
volume increases. Four such
individuals have now been
recognized. In none of the persons
had the tumors been previously
diagnosed.
Seizures
Acute, severe hypoxia may cause
seizures, a fact more relevant and
better known to aviation medicine
and of questionable relevance for
sojourners who take time to
acclimatize and go to more
moderate altitudes. In fact, seizures
appearing for the first time in
sojourners at altitude without an
underlying seizure focus—with or
without HACE—appear to be rare.
In persons with seizure
disorders, exacerbation due to
altitude has been anecdotally
observed when they were not taking
their medication. The mechanism of
exacerbation might be related to
either the respiratory alkalosis of
altitude, similar to the
hyperventilation used in EEG labs
to trigger seizure events, or to the
hypoxia. Persons with seizure
disorders have had no increase in
frequency or severity of seizures
when medications were continued
at high altitude.
In contrast to these apparently
unusual events, syncope (fainting) is
common at altitude. Since syncope
of any cause may be associated
with seizure activity (convulsive
syncope), confusion of convulsive
syncope with a true seizure is
inevitable. Systematic studies of
individuals with seizure disorders
are sorely needed to determine
whether high altitude is a risk for
these individuals.
Whether an individual with a
grand mal seizure at very high
altitude might be at greater risk for
residual brain injury is another
unanswered question.

ON DIABETES MELLITUS
Do diabetics have more problems

at high altitude? The onset of severe
diabetic ketoacidosis in five
trekkers at high altitude, three of
whom died, raises suspicion of a
problem, but whether incidence or
severity is increased at high altitude
is unknown. Some reports have
questioned the reliability of
selfmonitoring blood glucose
devices at high altitude, but a recent
study demonstrated reliability of
one system at 8800 and 12,100 feet
(2668 and 3665 m) in Colorado.

ON PREGNANCY
A normal mother breathing room air
at sea level has an arterial oxygen
pressure (PO2) of 85 to 100 mm Hg.
The PO2 in the uterine veins is
approximately 40 mm Hg. The PO2
in the umbilical vein going to the
fetus (analogous to a systemic
artery in the adult) is 30 to 35 mm
Hg. The PO2 in the umbilical artery
coming from the fetus (similar to the
pulmonary artery) is 10 to 15 mm
Hg. Such low oxygen pressures are
normal for a fetus and this “low
oxygen” environment is remarkably
stable. The shape of the fetus’
oxygen dissociation curve and the
high affinity of its hemoglobin for
oxygen minimize changes in
maternal arterial oxygenation.
The placenta acts as a buffer in
several ways: It maintains a
constant carbon dioxide gradient
(10 mm Hg), is relatively
impermeable to bicarbonate ions
(to protect the fetus from maternal
changes in acid-base balance), and
maintains the fetal oxygen
environment. Additional changes
that maintain fetal stability include
increased ventilation by the mother
(even in high-altitude residents who
normally are insensitive to chronic
hypoxia) and increased oxygen
extraction by the fetus. As a result,
oxygen consumption remains stable
even when stressed with a 50
percent reduction in either placental
blood flow or blood oxygen
content. (The fetus must avoid a
high PO2 because that triggers the
drop in pulmonary vascular
resistance and closure of the ductus
arteriosus that normally occurs
following birth.)
Given a stable fetal environment,
what degree of maternal hypoxia
can be detrimental, and what
evidence is there for compromise of
the lowland fetus or mother upon
ascent to high altitude?
Studies of High-Altitude
Residents: Implications for
Pregnant Lowlanders
In native residents at an altitude
of 6000 feet (1830 m) umbilical
cord arterial and venous oxygen
tensions are the same as at sea
level. A slightly lower carbon
dioxide pressure reflects mild
maternal hyperventilation. At
altitudes over 10,000 feet (3000 m),
fetal response to hypoxia is
evidenced by an increased
hematocrit (2 to 3 percent higher),
increased fraction of fetal
hemoglobin, and increased
erythropoietin in the umbilical cord
blood.
Studies from all the world’s
high-altitude regions have identified
various effects of high-altitude
residence on pregnancy. The best
documented is intrauterine growth
retardation, which leads to healthy,
full-term infants that are small for
gestational age. Where
sophisticated medical care is
accessible, intrauterine growth
retardation is not associated with
increased morbidity or mortality
unless the infants are also
premature. Intrauterine growth
retardation, however, does indicate
an apparent effect of hypoxia on the
developing fetus.
Similar reductions in birth
weight are seen with mothers who
smoke, but unlike the altitude
infants, the infants of mothers who
smoke have higher perinatal
mortality at every birth weight. This
important difference indicates that
effects on fetal growth can occur
independently of effects on
mortality and also that smoking
produces more abnormalities that
affect fetal growth and wellbeing
than just reduced oxygen transport.
Reduced size for gestational age at
sea level is also associated with
pre-eclampsia, maternal hypoxic
lung disease, maternal cyanotic
congenital heart disease, and
various anemias, all of which have
diminished fetal oxygen/nutrient
delivery as a common pathway.
Unlike some of these other
conditions, particularly pre-
eclampsia, low birth weight due to
high altitude does not appear to be
associated with increased
morbidity and mortality for full-
term infants.
Various investigations suggest
that the mechanism of intrauterine
growth retardation at high altitude
is in large part lower uteroplacental
blood flow and “relative ischemia”
of the placenta. Three factors seem
to explain this decreased placental
blood flow: a smaller maternal
blood volume increase, less uterine
artery dilatation, and lack of
appropriate redistribution of blood
flow to the uteroplacental
circulation. How hypoxia could
produce these changes in unknown
but impaired placentation (the
process by which the placenta
“invades” the uterus to establish its
blood supply) has been suggested.
Recent studies have indicated that
hypoxia causes shallower
placentation and higher vascular
resistance like that seen in pre-
eclampsia. Although this finding
needs to be confirmed in normal
highaltitude placentas, this work
does question whether during
placentation (the first nine to twelve
weeks of pregnancy) hypoxic
exposure could be detrimental. A
corollary question is whether
altitude exposure is advisable for
lowland women with any
suggestion of impaired placentation
or fetal compromise, such as
hypertension or pre-eclampsia, at
any time during pregnancy.
In high-altitude residents,
intrauterine growth retardation is
not linear throughout pregnancy.
Only after thirty-two weeks of
gestation does fetal growth at
altitude become appreciably slower
than at sea level. Does this
observation mean that the otherwise
healthy pregnant lowlander need not
worry about impaired fetal growth
at altitude until after thirty-two
weeks gestation? Or is the stage set
for intrauterine growth retardation
earlier in the pregnancy, such as
during placentation, so that altitude
exposure afterward has no effect on
growth? Is the intrauterine growth
retardation of altitude residents
even relevant to lowlanders?
Without answers to these questions,
admonishing all women to avoid
altitude exposure throughout
pregnancy, as some have done
because of concerns about
intrauterine growth retardation,
seems premature.
At the present time, no evidence
indicates that altitude exposure, at
least to moderate altitudes,
increases risk to the healthy
pregnant lowlander or her fetus.
Acute Ascent for Pregnant

Lowlanders
Clinical and physiologic
investigations of pregnant
lowlanders ascending to altitude
are conspicuously missing,
particularly to altitudes over 8250
feet (2500 m). Thousands of
pregnant women travel to the
moderate altitude of ski resorts for
recreation. The absence of any
reported adverse effects is
reassuring, but the safety of altitude
exposure during pregnancy has not
been systematically evaluated. Is
adding the stress of exercise
(skiing) to that of hypoxia a cause
for concern?
The few studies available are
encouraging. A study of submaximal
and maximal aerobic work at sea
level and 6000 feet (1830 m) after
two to four days of acclimatization
found that fetal heart rate responses
were not changed from sea level. A
study of pregnant individuals who
exercised after ascent to 7350 feet
(2225 m) produced similar results.
The experience of the airline
industry is also reassuring.
Exposures are brief, but cumulative
time at cabin altitudes up to 8000
feet (2400 m) is high. Pregnant
cabin crew are generally permitted
to fly until seven months gestation.
Untoward effects have not yet been
demonstrated in this large
population, though studies are
continuing.
In summary, the only available
data, though rather inadequate,
suggest that short-term exposure to
altitudes up to 8250 feet (2500 m)
with exercise is safe for lowland
women with normal pregnancies.
Effect of Acute Hypoxia on

Fetuses
The only observed effect of
acute hypoxia on the fetus is an
increase in heart rate. Results have
been variable, but only a slight
increase (tachycardia) is the usual
response to moderate maternal
hypoxia (12 percent or 15 percent
inhaled oxygen). A slower heart
rate (bradycardia) is the response
to more severe hypoxia (10 percent
oxygen). In experimental animals,
severe acute hypoxia (10 percent
oxygen), with an average maternal
arterial PO2 of 40 mm Hg, resulted
in no change in uterine or umbilical
blood flow but substantial increases
in fetal heart rate.
Investigators have suggested that
hypoxic gas breathing could detect
placental insufficiency and potential
labor and delivery problems
because fetuses with abnormal
responses, such as prolonged
recovery from tachycardia, would
be more likely to have fetal distress
during labor. Another way to assess
relative hypoxia or ischemia of the
uteroplacental unit is to determine
the fetal response to breathing
oxygen. An improved physiologic
function with oxygen would imply
correction of a deficit. Although no
reports of this intervention at high
altitude can be found, breathing air
with a higher concentration of
oxygen at sea level had no effect in
normal pregnancy or mild pre-
eclampsia. However, it did cause
observable changes (increased
heart rate and increased fetal
breathing movements) in severe
pre-eclampsia, in fetal growth
retardation, and in small-for-
gestational-age infants.
These studies suggest that a
compromised placental-fetal
circulation could be unmasked at
altitude. In the absence of such
complications, the fetus seems to
tolerate a level of acute hypoxia far
exceeding moderate altitude
exposure.
Recommending that women with
any complication of pregnancy
avoid unnecessary altitude exposure
seems prudent. An ultrasound or
other assessment may help to
reassure the clinician and mother
about the absence of the more
common complications. For women
with no known abnormalities, there
appears to be little risk to the fetus
or the mother undertaking a sojourn
to an altitude at which oxygen
saturation remains above 85 percent
most of the time (up to 10,000 feet
or 3000 m), but the data are very
limited. Altitude alone does not
determine whether the fetus
becomes stressed. The maternal
(and fetal) arterial oxygen pressure
and arterial oxygen saturation are
critical. A woman with HAPE at
8250 feet (2500 m), for example, is
much more hypoxic than a healthy
woman at 16,500 feet (5000 m).
Altitude illness, especially
pulmonary edema, must be carefully
avoided. Similarly, smoking, lung
disease, and other disorders of
oxygen transport render the
pregnant woman at altitude more
hypoxemic, and physiologically at a
higher altitude.
Clinicians concerned about
unmasking placental insufficiency at
high altitude may find that having
pregnant women breath air with
only 15 percent oxygen is a useful
but uncalibrated tool. The safety of
modest hypoxia on the fetus and
mother at different stages of
pregnancy and at different altitudes
(different levels of hypoxia),
whether persons at risk for
untoward effects can be identified
prior to exposure, and the
interaction of hypoxia with other
stresses such as exercise clearly
require more investigation. Studies
comparing large populations of
women with and without high-
altitude exposure during pregnancy
would be particularly useful for
pregnant lowlanders trying to make
informed decisions about the
potential risks of altitude.
CHILDREN AT ALTITUDE
In general, children tolerate
moderate altitude well. Children
born and raised at high altitudes
seem to have no more problems
than adults. Whether the incidence
of acute mountain sickness (AMS)
and other altitude disorders in
infants and young children is about
the same as adults or somewhat
higher is somewhat controversial.
In one study fourteen children aged
three to thirty-six months ascended
from 5275 feet (1609 m) to 11,440
feet (3488 m). About 20 percent
developed AMS, an incidence
comparable to that in adults. As in
adults, the higher the altitude and
the faster the ascent, the greater the
incidence of AMS. A few observers
have thought that children
acclimatize somewhat more slowly.
Identifying children with AMS
can be a problem. Children
frequently become ill with vague
viral illnesses that create symptoms
similar to those of AMS—
headaches, irritability, loss of
appetite, inability to sleep, and
fatigue. Infants and young children
cannot verbalize what is bothering
them. Parents are advised to avoid
high altitudes with children so
young. If they go to such altitudes
and their children become ill,
parents should assume the children
have AMS and descend
immediately.
Air travel appears safe for
children with upper respiratory
infections, nasal allergies, and ear
infections. Children may experience
pain in flight, but permanent damage
from barotrauma appears to be
extremely rare. Nasal sprays and
decongestants may decrease the risk
of discomfort, but some studies
suggest these agents have limited
effectiveness in children. Middle
ear infections seem to protect
children from pain because fluid
obliterates the middle ear space and
pressure differences cannot
develop. Flying is safe for children
with tympanic membrane tubes.
Conventional wisdom
recommends nursing infants or
giving them bottles during ascent
and descent and when they cry
during flight. The rationale is that
the infants are crying because they
are experiencing barotrauma or are
dehydrated. No data support these
recommendations, and feeding may
make the infants more
uncomfortable. Air in the intestines
expands 20 percent during flight.
Sucking and eating introduces more
air. Infants probably should be fed
no more often when flying than
when at home.
One study has suggested that the
lower oxygen pressure in airliner
cabins at cruising altitudes may be
hazardous to infants. When forty
infants were subject to the oxygen
levels found at about 6000 feet
(1800 m) in aircraft, four
developed irregular breathing and
such decreased blood oxygen levels
that the study was interrupted.
However, these studies were
carried out in a laboratory. Millions
of infants travel on airliners without
apparent adverse effects.
ALCOHOL AT ALTITUDE
Alcohol ingestion at altitude is
widespread. A recent
epidemiological study indicated
that 64 percent of tourists ingest
alcohol during the first few days at
9240 feet (2800 m). Two questions
regarding alcohol are frequently
asked: (1) Does alcohol affect
acclimatization? (2) Does altitude
potentiate the effects of alcohol?
In regard to acclimatization,
determination of blood gases in ten
individuals one hour after ingestion
of 50 gm of alcohol (equivalent to 1
liter of beer) at 550 feet (171 m)
and again after four hours at 10,000
feet (3000 m) disclosed that alcohol
had no effect on ventilation at the
low altitude. However, at higher
altitude alcohol depressed
ventilation as gauged by a
decreased arterial oxygen pressure
(from 69 to 64 mm Hg) and
increased carbon dioxide pressure
(from 32.5. to 34 mm Hg).
Whether this amount of
ventilatory depression would
contribute to AMS and whether
repeated doses would have greater
effect was not tested. Nonetheless,
alcohol might impede ventilatory
acclimatization and should be used
with caution at high altitude (as
elsewhere).
Conventional wisdom proffers
an additive effect of altitude and
alcohol on brain function. However,
in a variety of studies mostly
related to aviation, no influence by
altitude was detectable.
The possibility of interactions
between alcohol and altitude
deserves more study. The limited
data on blood gases at altitude after
alcohol ingestion support the
popular notion that alcohol may
slow ventilatory acclimatization.
Considerable data, however, refute
the belief that at least up to 12,000
feet (3660 m) altitude increases the
effect of alcohol. How altitude and
alcohol might interact at higher
altitudes is unknown.
FUTURE DIRECTIONS
Assessing the effect of high altitude
on myriad medical conditions is a
difficult task requiring multiple
approaches. The most fruitful
avenue of research would be a
large, ongoing epidemiological data
system, similar to the surveillance
systems used for detecting adverse
drug reactions or environmental
toxicity. Many of the questions
regarding the interaction of altitude
with age, disease, and pregnancy
require such a large-scale
approach. Physicians and other
health professionals in high-altitude
regions of North America and other
continents that attract tourists are
ideally situated for this type of
investigation.
In addition to recognizing
impacts of altitude on preexisting
conditions, focused surveys of hotel
and resort guests can yield data on
prevalence of medical conditions in
a general population. Occupational
health personnel, as well as local
health care providers, could make
valuable contributions to an
epidemiological survey assessing
the health of individuals who live at
high-altitude locations, particularly
in the high-altitude locations of
South America and Asia. Focused,
detailed studies of selected medical
conditions or populations, such as
the elderly and those with coronary
artery disease investigated in the
10th Mountain Division Study, play
an important role in understanding
how specific conditions are
affected by altitude hypoxia. This
model can be applied to neonatal
and pediatric age groups,
pregnancy, and migraine sufferers,
to name but a few of the more
pressing problems needing
investigation. Such groups are also
well suited for outcome studies.
Acute hypoxic stress tests need
to be correlated with the effects of
intermediate and long-term
acclimatization. Study of high-
altitude natives will continue to
provide information of importance
for sojourners. For example,
intrauterine growth retardation in
high-altitude natives alerts us to the
possible effects of hypoxia on the
fetus of the sojourner; understanding
its mechanism would help assess its
relevance for altitude visitors and
help determine whether such effects
can be prevented or minimized.
Finally, as the molecular bases
of adaptation to hypoxia and to
disease unfold, new breakthroughs
might minimize hypoxic stress and
maximize wellness in those persons
with medical conditions who
choose to visit altitude because it
adds to their enjoyment or quality of
life.
CHAPTER 26
COLD INJURIES
The common disorders produced by

cold are hypothermia and frostbite.
Hypothermia is a decrease in the
core temperature of the body that
impairs intellectual and muscular
function, including cardiac function.
Frostbite is a localized injury
characterized by freezing of tissues.
Preventing and treating these
disorders requires knowledge of the
way heat is lost or gained and the
body’s responses to cold.
MECHANISMS OF HEAT
EXCHANGE
Heat is lost or gained from the
environment by four routes:
◆ Radiation
◆ Evaporation
◆ Convection
◆ Conduction
Radiation
Radiation, by far the largest
source of heat loss in temperate
climates, is a form of direct energy
emission, much of it as infrared
radiation. Heat is exchanged
directly with the environment, and
heat loss is determined by the
difference in temperature between
the skin and the atmosphere or
surrounding objects such as rocks,
trees, snow, or ice. Radiant heat
loss increases as the environment
grows colder.
In an environment that is warmer
than the skin surface temperature
(about 95°F or 35°C), radiant heat
is absorbed by the body. The
inability to lose heat by radiation in
such environments can contribute to
heat illness.
Clothing has little effect on heat
loss by radiation. The heat radiates
from the body to the clothing and
from there to the atmosphere.
Efforts to develop clothing
materials that reflect heat back to
the body have met with little
success. However, radiant heat loss
becomes a major problem only in
extremely cold situations (below
−20°to −30°F or −29° to −35°C). If
clothing adequately limits heat loss
by other routes, particularly
convection, the body can
compensate for the increased
radiant heat loss encountered in
most cold wilderness environments
(Fig. 26-1).
Evaporation
Perspiration is continuously
produced in small amounts, even in
cold climates. This “insensible”
perspiration evaporates from the
skin, extracting approximately 575
calories of heat for each cubic
centimeter lost. Additional heat is
lost from the respiratory passages
as inspired air is warmed to body
temperature and moistened to 100
percent relative humidity. In
temperate conditions 20 to 30
percent of all heat loss results from
evaporation, about twothirds of
which takes place on the skin.
Heat and water losses from the
lungs become much larger at high
elevations where breathing is
deeper and more rapid to
compensate for the lower quantity
of oxygen in the atmosphere. As
much as four liters of water and
2300 kilocalories of heat can be
lost daily through the lungs at high
altitudes (1000 calories = 1
kilocalorie; the calories listed for
foods are actually kilocalories).
Heat loss from the respiratory
tract cannot be reduced in any
practical manner. Mouth breathing
increases fluid and heat loss
somewhat, but the amount is
insignificant in comparison with the
quantity of heat lost through other
sources. Outdoor recreationalists
must be aware that this heat and
water loss are occurring, must eat
enough food to regenerate the heat,
and must drink enough liquids to
replace the water.
Heat loss from insensible
perspiration also cannot be
effectively limited. Vapor barrier
systems, which consist of a layer of
material impermeable to water
vapor (usually plastic) between
layers of insulation, have been
tried. Since the barrier prevents
water vapor loss, the air beneath
the barrier quickly becomes
saturated, perspiration cannot
evaporate, and heat loss by that
route should be eliminated.
However, perspiration does not
cease, and the clothing underneath
the barrier becomes saturated with
water. Wet clothing is hazardous
because it no longer limits
convective heat loss.
Figure 26-1. Heat loss by radiation
No vapor barrier system works

well at temperatures above freezing
because too much water
accumulates. Even at lower
temperatures the only vapor barrier
system widely used is in footwear.
Although such boots do keep feet
warm, application of
antiperspirants to the feet and
frequent sock changes are needed to
avoid problems related to perpetual
wetness.
Convection
Air in contact with skin is
warmed to the skin’s temperature.
When the warmed air is displaced,
cool air that replaces it is also
warmed. Since the heat that warms
the air comes from the skin, body
heat is lost as the warmed air
moves away.
Convective heat loss is an
almost continuous process, but the
amount of heat required to warm air
(the specific heat of air) is so small
that little heat is lost by this route in
temperate climates. In a cold
atmosphere, convective heat loss is
greater because more heat is
required to warm the colder air.
However, the greatest convective
heat losses occur in wind, when the
air is constantly moving. Even a
mild breeze greatly increases heat
loss because the layer of warmed
air next to the skin is constantly
being replaced with cooler air.
The amount of heat extracted by
moving air increases as the square
of the velocity, not in direct
proportion to its speed. A wind of
eight miles per hour removes four
times as much heat, not twice as
much, as a wind of four miles per
hour. A strong wind can remove
tremendous amounts of heat. The
increased heat loss that occurs with
moving air is called wind chill.
Table 26-1 illustrates the additional
cooling produced by wind in a cold
environment. For instance, a
temperature that poses little threat
in still air, such as 15°F (−9.5°C,)
can be life threatening in a wind of
20 to 25 miles per hour (mph) or 32
to 40 kilometers per hour (kph).
Table
Wind Chill Chart
26-1
Because convective heat loss
can increase so enormously, it is the
major cause of terrestrial
hypothermia in the wilderness.
Fortunately, clothing can greatly
reduce this type of heat loss.
Insulating clothing, such as down or
wool, forms a myriad of small
pockets in which air is trapped—
the essence of thermal insulation.
Windproof outer garments prevent
displacement of the air within and
between layers of clothing.
Convection also is a major route
of heat loss in cold water. The
water next to the skin extracts heat
and is warmed, but any movement,
such as swimming, displaces the
warmed water, which is replaced
by more cold water. Because the
specific heat of water is so high,
tremendous amounts of heat can be
lost through convection, much more
than can be generated by physical
activity, even by the strongest, most
well-conditioned swimmers.
Individuals accidentally immersed
in cold water can stay warmer by
holding still to reduce water
movement and limit heat loss than
they can by swimming to generate
heat. (Unless the shore or a boat is
a very short distance away, active
swimming in cold water should be
avoided.) Positions that limit the
area of the body surface exposed to
water also help reduce heat loss.
Two or more persons should huddle
together to limit their contact with
water (Fig. 26-2).
Conduction
Heat is conducted from the body
when it is in contact with water,
snow, rocks, or any cold object that
is a good conductor. Air is not a
good conductor. Water is an
excellent conductor, and conductive
heat loss is a major contributor to
hypothermia during immersion in
cold water.
Conductive heat losses can
become significant in the
wilderness when a person is seated
or lying on ice, snow, or a cold
rock. Another cause of conductive
heat loss is lying or sleeping on the
ground without adequate insulation;
foam pads eliminate much of the
conductive heat loss by this route.
(Air mattresses, which allow air to
circulate freely, provide less
insulation.) Although conductive
heat loss alone is rarely a major
cause of hypothermia, heat loss by
this route can aggravate convective
heat losses and should be avoided.
Conductive heat losses can
become large when clothing is wet.
Figure 26-2. Methods for reducing the
body surface exposed to cold water
PHYSIOLOGIC LIMITATION
OF HEAT LOSS
Physiologic mechanisms for
limiting heat loss are largely
limited to constriction of blood
vessels in the skin, arms, and legs.
(Humans evolved in a tropical
climate, and the body’s mechanisms
for increasing heat loss are much
better developed than those for
reducing heat loss.)
Vasoconstriction reduces cutaneous
blood flow, which allows tissues to
cool. Since the skin temperature is
lower, less heat is lost by radiation
and by convection.
The arms and legs, as the result
of their long narrow shape, have a
greater relative surface area than
the body and tend to lose heat more
readily. Narrowing of blood
vessels in the extremities reduces
blood flow and heat loss and also
tends to keep the heart and brain
supplied with warm blood so they
can function after the rest of the
body has become significantly
chilled.
PREVENTING HYPOTHERMIA
A human’s greatest protection
against the cold is the intellect. An
ambient temperature of about 82°F
(28°C) is the thermoneutral
temperature for an unclothed human
body, which means that a nude
individual at rest at lower
temperatures loses more heat to the
environment than heat-generating
processes are producing and heat-
preserving mechanisms can retain.
Almost everywhere they live,
humans are dependent upon
intellectually devised clothing and
shelter to protect them from the
environment and reduce heat loss to
levels for which metabolism and
physiology can compensate.
Informed, intelligent behavior is
more necessary in the severe cold
of high altitude and extreme
latitude.
Threatening situations must be
recognized in time for effective
countermeasures. Preparation is
essential because clothing adequate
for such climates can rarely be
improvised. Even when available,
such clothing must be worn
properly. Shelter often can be
improvised, but a skier with a snow
shovel is far more capable of
improvising a satisfactory shelter
than a skier without one.
Water and Food

Avoiding hypothermia in a cold
climate requires water, food, and
clothing. Failure to replace normal
water losses through the kidneys,
skin, and lungs, or abnormal losses
by other routes, results in
dehydration, which decreases the
blood volume and, in a cold
environment, impairs heat
production by exercise.
Dehydration can be accompanied
by weakness, fatigue, dizziness, and
even a tendency to faint when
standing, which impede efforts to
deal rationally with a threatening
environment.
Dehydration also contributes to
other problems. Constriction of
peripheral blood vessels so the
smaller volume of blood goes to
vital organs increases the risk of
frostbite. Severe shock may
develop following minor injuries.
Clots tend to form in the legs and
can result in pulmonary embolism
(Chapter 18: Respiratory
Disorders).
In a dehydrated state the
sensation of thirst is diminished or
absent, and a conscious effort to
consume adequate fluids must be
made. Water intake with mild
exertion should be at least two
quarts per day. With heavier
exertion or at high altitude, three to
five quarts are needed. In a world
of snow and ice, fuel is required to
melt snow for drinking water.
Eating snow does not provide an
adequate volume of water, and body
heat is lost in warming ingested
snow to body temperature.
An adequate fluid intake is
indicated by urine that has a light
yellow color and a volume of at
least one liter every twenty-four
hours. Few outdoor recreationalists
would measure urine volume, but
they should be able to appreciate a
reduced frequency for voiding,
particularly the absence of a need to
void after a night’s sleep. They
certainly can recognize the deep
yellow or orange color of
concentrated urine indicative of
dehydration. When voiding into
snow, orange “snow flowers” are
an ominous sign.
Food is needed for physical
activity and heat production. Eating
small amounts of food at frequent
intervals helps prevent depletion of
energy stores during the day. Some
experienced outdoor
recreationalists seem to be
munching almost continuously and
often have developed mixtures of
nuts, dried fruits, candies, and other
high-calorie food. Such mixtures
are sold as gorp or trail mix.
In a survival situation,
experience has demonstrated that
food is one of the most important
ingredients of success. Any source
of food, even wild animals such as
birds or rodents, which may have to
be eaten uncooked, is preferable to
the fatigue and depression that
result from not eating and can
contribute significantly to
hypothermia.
Clothing
Clothing for cold climates must
not only protect from the cold but
also must be able to compensate for
changes in environmental
temperature and for heat production
by exercise. The most flexible cold
weather clothing systems are
composed of three layers: an inner
layer (underwear), one or more
middle insulating layers, and an
outer windproof (and perhaps water
repellent) shell. The middle and
outer layers can be opened or
removed when environmental
temperature or heat production
increases. Additional insulating
layers can be added as the
temperature falls or the person
becomes inactive.
In a multilayered clothing
system, each succeeding layer must
be slightly larger than the one
beneath. If the layers are the same
size, the outer layers compress the
deeper layers and reduce their
insulation value.
However, the outer layer must
not be too large. It must be snug
enough to be warmed by the
wearer’s body so that its inner
surface temperature does not fall to
the dew point. If that occurs,
moisture collects on the inner
surface and wets the insulating
layers, greatly reducing their
effectiveness.
Sweating must be avoided.
Sweat moistens the clothing, greatly
reducing its insulation value, and
more heat is lost as the perspiration
evaporates. Outer layers must be
opened or taken off as soon as
activity begins, not after the
individual has become hot and
begun to perspire. These layers
must be put back on or closed as
soon as activity ceases, not after the
individual has become cold and
requires more heat to rewarm.
Clothing Materials
No third-party testing facility,
such as Underwriters Laboratory,
exists for clothing. Buyers are at the
mercy of advertising agents serving
the manufacturers and sellers. The
most reliable indicator of a fabric
or garment’s performance is its
persistence in the marketplace for
two to three years or more.
Effective cold weather clothing
must have two properties:
insulation and permeability.
Insulation basically is the ability of
the clothing to entrap air and
prevent convective heat loss. The
insulating properties of a material
are dependent upon its thickness
and how well it inhibits the
movement of air. Permeability
refers to the ability of water vapor
to move through the fabric. Water
vapor resulting from the
evaporation of sensible or
insensible perspiration on the skin
must be able to move through
clothing to the atmosphere. If the
clothing is impermeable, the vapor
condenses and the clothing becomes
wet.
A variety of natural materials are
used in clothing for outdoor wear.
Wool, cotton, silk, and goose down
are the most popular. All but down
are usually combined with synthetic
materials such as nylon,
polypropylene, polyester, and
acrylics to impart specific
desirable characteristics to the
fabric.
Underwear
Polypropylene became popular
for underwear in the 1970s.
Because it is hydrophobic and
allows moisture to wick from the
skin surface to the surface of the
fabric where it evaporates without
cooling the skin, it provides a
greater sensation of warmth.
Furthermore, polypropylene retains
most of its insulating properties
when wet. The disadvantages of
polypropylene include its retention
of body odors—it can become quite
foul after repeated use—its
tendencies to become brittle when
heated and to pill when dried in a
clothes dryer, and its tendency to
become baggy. The last problem
has been corrected to some extent
by adding nylon to the fabric.
Polyester fabrics have to a large
extent replaced polypropylene
because, in spite of being slightly
more expensive, they do not have
the same disadvantages.
(Capilene®, Coolmax®,
Thermax®, and Thermostat are the
trademarks of polyester fabrics.)
These fabrics keep the skin cool
and dry through a wide range of
activity, but to achieve this effect
they must be worn next to the skin,
not over cotton underwear or as a
jacket.
Wool remains an excellent fabric
for underwear but has fallen from
popularity and is difficult to find.
Adding a small amount (a
tablespoon) of olive oil to the wash
water can eliminate the scratchiness
that wool tends to develop after
repeating washings. Merino wool
has much finer fibers and feels
more comfortable against skin.
Some people like the feel of dry
silk, but when silk becomes wet it
feels unpleasant. The fabric holds
25 percent of its weight in water.
Insulation
Wool is the oldest and one of the
best insulating materials for cold
weather clothing. Its major
disadvantage is its greater weight
than pile or fleece, but it is still
popular for caps and gloves. Wool
is one of the few materials that
maintains its insulating properties
when wet. However, with
prolonged wetness the inner core of
wool fibers can absorb water,
which makes the fabric
considerably heavier. Totally drying
this core requires a large amount of
heat—generally extracted from the
wearer’s body.
Synthetic fabrics have largely
replaced wool. Pile fabrics,
introduced in the 1970s, are lighter
and are hydrophobic. However,
they tend to loose their pile and to
pill badly with wear and
laundering, so they have largely
been replaced by fleece.
Fleece is a similar polyester
fabric, but with stiffer fibers than
pile and superior qualities. It is
produced in different thicknesses:
microfleece for underwear and 100,
200, and 300 weights for outer
garments. This material breathes
well and is lightweight, durable,
and fast drying. It is easy to cut and
sew and has largely replaced pile
as a fabric for outdoor clothing.
Goose down is the best
available insulating material for its
weight—when it is dry. True down
is the philoplume of geese or ducks
and historically was handpicked
from those animals, but that
material is no longer available.
Down now comes from killed
animals and is composed of less
mature plumes that do not loft as
well. However, down garments
drape well, do not constrict
movement, loft after compression,
and are comfortable. When wet,
down mats together and loses most
of its insulating properties.
However, when precipitation is in
the form of dry snow, which is
typical of high altitudes, down is
the insulating material of choice.
Synthetic fibers can provide
insulation similar to down and
retain their insulating properties
when wet. Although various
materials have been tried,
manufacturers currently are using a
blend of three different deniers
(thicknesses) to gain high loft.
(Primaloft® and Lightloft are the
trade names of two down
replacements.) The disadvantages
of such materials are their greater
weight (about 50 percent heavier
than down) and their bulk or lack of
compressibility.
Mat materials are extruded,
densely packed fine fibers. Because
the fibers are so thin, they slightly
limit radiant heat loss but lose this
advantage when laundered. These
materials resist compression and do
not drape well. (Thinsulate® is the
dominant brand of this type of
fabric, the use of which is limited
largely to ski clothing.)
Outer Shell
The outer shell must be
windproof to protect the insulating
qualities of the underlying clothing.
Tightly woven fabrics made of
synthetic fibers are most commonly
used. The shell usually also must be
water repellent. The ideal fabric
that would allow all water vapor to
pass through freely but keep out all
liquid water has yet to be
developed. The best available
fabrics are laminates such as Gore-
Tex® and urethane-coated
materials, which have small pores
close enough together to resist
penetration by liquid water but
large enough for most water vapor
to pass through. Soiling limits the
functionality of these fabrics,
although the layer with the
perforations is now protected by
overlying layers that protect them
from body oils.
Protecting Hands and Feet

When the body is cool, the blood
vessels in the hands and feet
constrict, reducing heat loss through
those tissues but also reducing their
temperature and commonly causing
discomfort, which can be severe.
The most effective way to prevent
cold extremities is to keep the body
warm, a lesson some outdoor
enthusiasts seem to have difficulty
learning.
For the hands, mittens are much
warmer than gloves. Radiant heat is
lost from the surface of protective
garments; the larger the surface
area, the greater the heat loss.
Because the fingers are such narrow
cylinders, increasing the thickness
of gloves by more than one-quarter
inch increases the surface area to
such an extent that the increased
heat loss eliminates any benefit
from the increased insulation.
Because mittens do not have such a
large relative surface area, their
thickness can be increased to a
much greater extent without a
concomitant increase in heat loss.
The basic components of mittens
are an outer shell and an insulating
layer. A third inner layer of a thin
fabric such as nylon or silk—
usually a glove—is useful if the
mittens have to be removed to
manipulate clothing or equipment.
The outer shell should be an
abrasion-resistant material,
typically nylon. Wool works well
for insulation, but down and
synthetic materials are also used.
Many different types of one-piece
mittens have been developed,
particularly for skiing. Many are
quite expensive but are not more
effective than a simple, inexpensive
wool mitten with an outer nylon
shell.
One of the warmest types of
footgear yet devised is the U.S.
Army double-vapor-barrier boot
known as the white Korean (Mickey
Mouse) boot. However, this type of
footwear is too soft for kicking
steps in hard snow and is difficult
to fit with crampons. For the
severely cold climates typical of
high altitudes, double or triple
boots are best for climbers. The
outer boot is usually constructed of
hard, protective plastic, and the
inner boots are made of softer
insulating material. Older double
boots were made of leather, which
is heavier than plastic. Leather is
porous, which allows moisture to
escape, and leather can expand to
accommodate swelling of feet and
ankles due to an upright position or
altitude. It remains the best material
for single boots in moderately cold
climates.
Head Protection
The voluminous blood flow to
the head is a potential source of
major heat loss. In cold weather,
effective headgear such as wool
caps is essential. Balaclavas that
cover the neck and lower face are
desirable for severe conditions.
Hoods do not fit closely enough to
be as effective but do provide
additional protection when worn
over caps, particularly if the hood
is insulated.
Insulating scarves and neck
gaiters (wool, usually) reduce heat
loss from the large blood vessels
that are close to the skin surface in
the neck.
RECOGNIZING
HYPOTHERMIA
Hypothermia is usually divided into
three levels: mild, moderate, and
severe (Table 26-2). By definition
it begins when the body temperature
falls to 95°F (35°C). Individuals
who are mildly hypothermic are not
so incapacitated that they cannot
stand or walk with assistance.
Usually their temperature is in the
range of 90° to 92°F (32° to 33°C).
A person with moderate
hypothermia has stopped shivering,
is intellectually impaired, and may
be unable to walk. The body
temperature is typically below 90°F
(32°C), although the temperature at
which such severe impairment
appears varies significantly. A
severely hypothermic individual is
unconscious and usually has a body
temperature below 82°F (28°C).
Temperature is not a practical
basis for recognizing hypothermia
in the wilderness because obtaining
a temperature is so difficult.
Profoundly hypothermic individuals
usually have their jaws clamped so
tightly that oral measurements are
impossible. Rescue personnel
uniformly refuse to try rectal
measurements, particularly in a
threatening environment. Such
reluctance is probably fortunate
because much of the time moving a
person to take such measurements
could precipitate ventricular
fibrillation (explained in the
following section).
Table
Stages Of Hypothermia
26-2.
MILD HYPOTHERMIA
Sensation of chilliness;
98°– skin numbness; minor
95°F impairment in muscular
37°– performance, particularly
35°C in fine movements with the
hands; shivering begins
95°– More obvious
93°F incoordination and
35°– weakness; stumbling; slow
34°C pace; mild confusion and
apathy
Gross incoordination with
frequent stumbling, falling,
93°–
and inability to use hands;
90°F
mental sluggishness with
34°–
slow thought and speech;
32°C
retrograde amnesia;
uncontrollable shivering
MODERATE HYPOTHERMIA
Slowing and cessation of
shivering; severe
90°– incoordination with
86°F stiffness and inability to
32°– walk or stand;
30°C incoherence, confusion,
irrationality
Severe muscular rigidity;

86°–
semiconsciousness;
82°F
dilatation of pupils;
30°–
inapparent heartbeat or
28°C
respirations
SEVERE HYPOTHERMIA
Unconsciousness;
Below
eventually death due to
82°F
cessation of heart action at
Below
temperatures of 77°F
28°C
(25°C) or below
Mild Hypothermia
The key to early recognition of
mild hypothermia is awareness of
the risk of hypothermia and the
speed with which it can develop.
Close observation of each other by
members of the group is a vital
element of hypothermia prevention.
Every member of a party must be
responsible for observing everyone
else.
Cold, wet conditions can be
dangerous even in summer,
particularly when a wind is
blowing. Individuals who are
physically active and generating
heat but still feel cold, must realize
they are going to become even
colder when that activity ceases. If
they cannot produce enough heat to
warm themselves while exercising,
they certainly cannot do so when
resting and must have more clothing
or shelter to provide protection
from the environment—or an
external heat source.
Feeling cold is the most typical
early symptom of hypothermia.
Painfully cold hands or feet are
common. As body temperature
continues to fall, muscular
coordination is lost. Fine
movements cannot be performed
with the hands, but if the individual
is walking and not using the hands,
such loss may not be detectable.
The first signs of incoordination
typically are slowing of pace and
stumbling, particularly on rough
ground or loose rock. As
hypothermia becomes more severe,
stumbling becomes worse and
individuals may fall.
Characteristically they lag behind,
which should be an unmistakable
warning for the rest of the group. If
left unattended, subsequent
deterioration in their condition goes
unobserved. Shivering may further
impair the ability to walk over
rough terrain.
The intellect is also impaired as
hypothermia develops. Personality
changes, particularly irritability, are
typical. A common early sign is
refusal to admit that anything is
wrong. Some individuals are
apathetic and unconcerned about
their deteriorating condition. Slow
thought and speech may manifest
mental sluggishness. Confusion and
retrograde amnesia subsequently
indicate a greater decline in body
temperature.
A mnemonic for remembering
the signs of mild hypothermia is
“umbles”: The hypothermic person
mumbles and grumbles (personality
changes), fumbles, stumbles, and
tumbles (loss of coordination).
At this point the presence of
hypothermia should be obvious—
unless other members of the group
also are hypothermic. Failure to
institute corrective measures can
result in progression to more severe
hypothermia.
Moderate Hypothermia
Moderate hypothermia should be
defined by the person’s condition,
not by a specific body temperature.
However, the signs typical of
moderate hypothermia usually
appear when body temperature has
fallen to about 90° to 92°F (32° to
33°C) or below.
The hallmark of moderate
hypothermia is the disappearance of
shivering. When body temperature
has dropped to 93° to 94°F (34°C),
shivering typically becomes
uncontrollable As the temperature
drops lower, usually about 2°F
(1°C) lower, shivering gradually
disappears. This sign is usually
easy to recognize and serves as a
clear, unmistakable warning that the
group must stop and begin
rewarming the affected individual
or individuals. Once shivering has
ceased, individuals so affected can
no longer rewarm themselves and
an external heat source is required.
As body temperature drops further,
muscular incoordination becomes
so severe that the individual cannot
walk without assistance and
eventually becomes unable to stand
without support.
Intellectual impairment is
greater, but the impairment may be
subtle. A common and important
sign of severe hypothermia is
neglect or carelessness about
protection from the cold. Coats are
left unzipped; hoods are not pulled
up; caps or mittens are not worn.
Sleeping bags or blankets are not
snug around the head; fires are
neglected. Sometimes severely
hypothermic individuals urinate in
their clothing.
Individuals who seemed to be
acting quite sensibly have made
gross errors in judgment that have
caused problems for an entire
group. A typical pattern is the
individual who appears to be
capable of cooperating with other
members of the group but does not.
Severe Hypothermia
Severe hypothermia has been
defined as a temperature below
82°F (28°C). Eventually confusion
and irrationality progress to
incoherence, semiconsciousness,
and finally total unconsciousness
and a failure to respond to any
stimuli. At this temperature, death is
imminent. Rough handling can
precipitate ventricular fibrillation,
so these individuals must be
handled as gently as possible. At a
temperature below 77°F (25°C) the
heart may go into ventricular
fibrillation spontaneously. When the
temperature drops into the low 70s,
heart activity usually ceases, either
as the result of ventricular
fibrillation or asystole.
As an individual begins to lose
consciousness, a sensation of
extreme warmth may develop, and
if unattended, the person may
actually remove clothing or climb
out of a sleeping bag. Such bizarre
behavior is not uncommon, and its
occurrence in urban surroundings
has aroused suspicion that the
person has been assaulted,
particularly when the person has
been female. (Sometimes the
individual’s clothing has been
neatly folded, an unlikely
occurrence during an assault.)
Although the reason for such
behavior is not really known, one
proposed mechanism is dilatation
of the blood vessels in the skin,
producing a sensation of warmth
that prompts the semicomatose
person to disrobe or climb out of a
sleeping bag. The diversion of
blood flow from the brain to the
skin by the cutaneous vasodilatation
is probably the last straw that drops
the person into complete
unconsciousness.
As a severely hypothermic
individual’s condition deteriorates,
body functions slow drastically. A
comatose person’s breathing may be
so slow and shallow that it appears
absent. The heart rate also slows
dramatically and can become so
weak that it cannot be palpated.
Unquestionably, a number of
individuals with severe
hypothermia who were actually still
alive have been pronounced dead
and denied medical assistance. In
the wilderness, few hypothermic
individuals should be declared
dead unless their measured body
temperature has fallen to
environmental levels. Only after
unsuccessful rewarming can death
be certain.
No one should be considered
cold and dead until he has been
warm and dead!
TREATING MILD
HYPOTHERMIA
Recognizing mild hypothermia is
critical. Its treatment is simple:
“All those things your mother told
you to do when you went outside in
the cold.” Effective measures
decrease heat loss and increase heat
production.
Decreasing heat loss by
convection can be achieved by
putting on more clothing: sweaters,
caps, mittens, jackets, parkas,
windpants, or whatever is
available. Protection from the wind
by parkas or windpants, rocks or
trees, natural shelters such as caves
or even crevasses, or shelters such
as cabins, tents, or snow caves
reduces convective heat loss or
wind chill. Replacing wet clothing
with dry clothing restores insulation
and reduces evaporative heat loss.
The warmer environment provided
by a fire—or just body heat within
a windproof shelter—reduces
radiant heat loss.
Heat production can be
increased significantly. Shivering is
an involuntary muscle activity that
generates heat at a rate equivalent
to walking fast. More heat can be
generated by vigorously exercising
the large muscles in the legs and
back if the individual is not
shivering uncontrollably. Such
exercise is even more useful if it
helps a hypothermic person get out
of a hostile environment. However,
if escape from the predicament is
not possible, then purposeless
exercise, such as repeatedly
stepping up onto a stone or log, can
generate heat. A metabolic energy
source—food—is needed if
increased heat production is to be
maintained.
Heat-producing exercise cannot
be continued indefinitely. Nor can
enough heat be produced by
exercise to compensate for the large
quantity of heat lost in cold water
or in a snowstorm if the individual
is inadequately protected.
Once hypothermia has been
corrected, measures to prevent its
recurrence are essential. It would
probably recur faster because
energy stores would be depleted. A
rewarmed person must not be
returned to the hypothermia-
inducing environment without
additional protection.
TREATING MODERATE AND

SEVERE HYPOTHERMIA
Moderate and severe hypothermia
are complex disorders for which
the simple measures that effectively
treat mild hypothermia are
inadequate because severely
hypothermic individuals cannot
generate enough heat to rewarm
themselves. An external heat source
must be provided. In addition,
ventricular fibrillation must be
avoided while the individual is
being rewarmed.
Ventricular Fibrillation
Ventricular fibrillation is a life-
threatening condition in which the
thousands of muscle fibers that
make up the heart contract
independently. Since all the muscle
fibers must contract together for the
cardiac chambers to squeeze out
blood, no blood is pumped when
the fibers are not synchronized. The
effect would be the same if the heart
were not beating at all.
The hypothermic heart is
extremely prone to ventricular
fibrillation. It has appropriately
been compared to a mousetrap,
ready to snap with the slightest
bump or jolt—often without a
recognizable precipitating event.
Hypothermic individuals have
begun fibrillating in hospital
emergency rooms even though the
possibility of that event was well
recognized and every effort to
avoid it was being made.
Severely hypothermic
individuals cannot be placed in a
basket stretcher and carried out of
the wilderness. The unavoidable
jarring and bouncing associated
with evacuation over rough terrain
almost inevitably provokes
fibrillation. Although profound
hypothermia prolongs the time an
individual can survive the absence
of effective blood circulation
without sustaining significant
neurologic damage, that time is
limited to one hour or slightly
longer.
Rescuers must realize that a
severely hypothermic individual in
ventricular fibrillation who cannot
be evacuated by helicopter, or in
less than an hour by stretcher, may
be in a hopeless situation. The
individual must receive CPR to
avoid neurologic damage, but CPR
can only be administered
intermittently while the person is
being carried on a stretcher.
Cardioversion (defibrillation with
electrical shocks) is almost never
effective until the heart has been
warmed to 90°F (32°C). In a
situation threatened by hazardous
weather, avalanche, or other danger,
rescue leaders may be achieving the
greatest benefit by extracting their
team and—although difficult—
abandoning the unfortunate
hypothermic person.
Individuals with severe
hypothermia in the wilderness
usually must either be evacuated by
helicopter or rewarmed on the spot.
Leaders of major rescue
organizations have realized that
almost none of the severely
hypothermic individuals carried out
of the wilderness by hand without
rewarming have survived. They
now try to rewarm such individuals
where they are found.
Rewarming
Severely hypothermic persons
require external heat sources for
rewarming because their
metabolism is so slow they cannot
generate enough heat to rewarm
themselves, even if completely
protected from the environment.
Theoretically, the most effective
rewarming methods would rewarm
the core of the body first (central
rewarming). Since the heart would
be among the first tissues
rewarmed, it would be protected
from fibrillation. In hospitals,
central rewarming can be achieved
with heated peritoneal dialysis
fluids and similar techniques.
Heart-lung machines or other
devices that remove blood from the
body, warm it, and return it are only
needed for individuals who do not
have effective cardiac function and
must be rewarmed rapidly.
However, experience has
demonstrated that central
rewarming is not essential for most
individuals who have functioning
hearts. They have gotten
hypothermic slowly and can be
rewarmed slowly. Many hospitals
that commonly treat hypothermic
individuals, which includes most
northern and high-altitude U.S.
areas, rely primarily on external
forced-air rewarming devices such
as the Bair Hugger® combined with
recirculating water mattresses.
The development of wilderness
rewarming techniques has met with
limited success. Two components
are essential:
◆ Protection from the
environment
◆ External rewarming
Protection from the environment
can be achieved by placing the
individual in a tent and in a
sleeping bag. To avoid precipitating
ventricular fibrillation, an
insulating pad should be gently
slipped under the person, who then
can be carefully placed in a
sleeping bag and slid into a tent.
(The sleeping bag only insulates the
person; the body is producing so
little heat that the sleeping bag does
not rewarm the person.) To reduce
heat loss due to warming and
humidifying inhaled cold air in the
lungs, the air within the tent can be
warmed and humidified by boiling
water on a portable stove.
External rewarming transfers so
little heat that all available
techniques must be employed. One
rewarming method is to place
folded sheets or blankets soaked in
hot water and placed in plastic
bags, hot-water bottles, or similar
warming devices along the sides of
the neck and chest where the body
wall is thin. (Obviously, if enough
warming instruments are available,
they can be placed anywhere.) Hot-
water bottles and similar devices
must not be so hot they burn the
person. They should be wrapped in
fabric and the temperature checked
by holding them under the arm of a
person with normal temperature for
a full minute.
The most effective portable
device for external rewarming is a
charcoal heater, which should be
carried by rescue teams. It contains
a slowly burning charcoal fuel
canister and a fan that circulates the
generated heat through flexible
tubing. It distributes 250 watts of
heat directly to the skin for eight to
twelve hours and requires only a D-
cell battery to power the fan.
Obviously extra fuel and batteries
—and more than one warming
device—can be carried.
Placing a normothermic
individual in the sleeping bag with
a hypothermic person transfers only
a minimal amount of heat through
body-to-body contact. Heated,
humidified aerosols also transfer
only a minimal amount of heat.
Severely hypothermic
individuals are inevitably
dehydrated, and all benefit from
correction of the dehydration. Since
most are unable to ingest fluids
orally, rehydration fluids must be
given intravenously. However, the
peripheral veins of a dehydrated,
severely hypothermic person are
collapsed, and accessing a vein is
quite difficult even for experienced
individuals.
Administration of heated
intravenous fluids has been
suggested as a means of rewarming.
However, the greatest benefit from
heating intravenous fluids is
avoiding further cooling by the
administration of fluids that are at
the temperature of the environment.
Four liters of fluids heated to 104°F
(40°C) and administered over a
period of two hours to an individual
with a temperature of 77°F (25°C)
could not transfer more than 60
kilocalories (kcal) of heat per hour
to the person. That would raise the
body temperature of a 176-pound
(80-kg) individual less than 1.8°F
(1°C) per hour. More fluids would
result in fluid overload and must not
be given. At below-freezing
temperatures, more heat would be
lost by radiation to the environment.
The person would benefit more
from evacuation to a warm shelter.
In a hospital, severely
hypothermic individuals being
rewarmed with noninvasive
techniques increase their
temperature at a rate of 0.9° to
2.7°F (0.5 to 1.5°C) per hour. In the
wilderness, rewarming would be
slower. Rescuers must be prepared
to spend many hours—perhaps one
or more days—rewarming before
moving a person. Stoves and
abundant fuel for heating water must
be available so heating devices can
be renewed as they cool.
Cardiopulmonary Resuscitation
(CPR)
Cardiopulmonary resuscitation
(CPR) is essential for supporting
profoundly hypothermic persons
who have no effective blood
circulation and can survive for only
about an hour without sustaining
significant neurologic damage,
particularly when evacuation is
prolonged. However, the
probability of success is limited,
and risks to rescuers or other
members of the party cannot be
justified. CPR should be initiated in
the wilderness only by a team of
experienced individuals in a safe,
relatively protected environment. If
a hostile environment poses a major
threat to the team, CPR should be
postponed or abandoned entirely.
Individuals with a detectable
heartbeat, no matter how slow,
should not receive CPR or assisted
ventilation because ventricular
fibrillation would almost certainly
result. Three minutes or longer
should be spent trying to detect a
carotid pulse before assuming a
severely hypothermic person has no
effective cardiac activity. The pulse
rate may be as slow as fifteen beats
a minute.
Individuals who do not have a
detectable heartbeat cannot be
assumed to be in ventricular
fibrillation. They could have weak
but otherwise normal cardiac
action, and starting CPR would
almost certainly cause them to go
into ventricular fibrillation. A
portable ECG monitor to detect
cardiac activity in persons with
severe hypothermia may be
necessary, and rescue groups should
carry such units. (In a wilderness
environment, portable ECG
monitors cannot be relied upon for
distinguishing abnormalities—such
as asystole, ventricular fibrillation,
or baseline artifacts—but they do
reliably indicate the presence of a
heartbeat by portraying QRS
complexes.)
Attempting to take a blood
pressure may not be helpful because
hypothermic persons with a
functioning heart commonly have
reduced blood pressure, and blood
pressure determination may be
further hindered by the absence of
the Korotkoff sounds used when
measuring pressure.
CPR should be given at one-half
the usual rate to severely
hypothermic persons, who have
such a slow metabolism that they
need limited amounts of oxygen and
are producing little carbon dioxide.
A slower rate of ventilation avoids
excessive carbon dioxide loss and
respiratory alkalosis, which
predisposes hypothermic
individuals to ventricular
fibrillation. A slower rate of
cardiac compression provides a
longer interval for the heart to be
filled with blood by the slow
circulation.
CPR should be instituted
immediately following a witnessed
cardiac arrest or fibrillation,
particularly when transportation to
a hospital is expected to require
more than a few minutes. CPR
probably should be administered
for individuals with unwitnessed
cardiac arrest who appear
resuscitatable, but each situation
can be expected to be so unique that
more definitive recommendations
are not possible. CPR should not be
initiated if a severely hypothermic
individual can be transported to a
hospital in minutes.
CPR should not be initiated for
fibrillating hypothermic individuals
considered unsuitable for
resuscitation due to their situation
or for fibrillating individuals with
extremely low body temperature,
associated severe illness or
injuries, a noncompressible chest,
prolonged cardiac inactivity, or
drowning with more than one hour
of witnessed submersion.
No clear role for drugs in
preventing fibrillation is known.
COLD WATER IMMERSION

Cold water immersion is poorly
understood by the general public
and even some outdoor medical
experts. A common belief is that
immersion in very cold water, even
with protective clothing, results in
death from hypothermia within
minutes. Although most cold water
immersion fatalities do occur
within less than twenty minutes, the
deaths occur while the persons are
still normothermic. These incorrect
assumptions have serious
implications because believing that
death from hypothermia is imminent
can result in panic and poor
decision making.
Cold water has been defined as
water temperature below 68° to
77°F (20° to 25°C). Immersion in
cold water has been divided into
four phases:
◆ Cold shock response
◆ Cold incapacitation
◆ Hypothermia
◆ Circumrescue collapse
Cold Shock Response

Sudden immersion into cold
water stimulates one or more large
inspiratory gasps, which is usually
followed by hyperventilation and
also may be associated with a
substantial increase in blood
pressure and heart rate. Individuals
with cardiac disease may
experience cardiac arrest or
ventricular fibrillation. If the head
is submerged, the gasp reflex could
result in aspiration of water and
immediate drowning.
Subsequent hyperventilation
usually diminishes within seconds
to minutes but could be exaggerated
and prolonged by emotional stress
and panic. Uncontrolled
hyperventilation makes
coordinating breathing with
swimming strokes very difficult,
which could lead to drowning.
Theoretically, cold shock can occur
in water warmer than 68°F (20°C),
although these effects are more life
threatening at temperatures below
59°F (15°C) and worsen as water
temperature decreases.
The best way to minimize cold
shock is to enter cold water in a
slow and controlled manner and to
keep the head from being
submersed. Individuals should
focus on getting through the first
minute, suppressing panic, and
consciously getting breathing under
control. Once breathing is
controlled, individuals usually have
time to evaluate the situation and
make proper survival choices.
Cold Incapacitation
When exposed to cold, the body
attempts to preserve a normal core
temperature of 98.6°F (37°C) by
decreasing heat loss. Constriction
of the blood vessels in the limbs
shunts blood from the extremities to
the core and decreases heat loss
through the limbs, but this allows
limb tissues to cool rapidly. The
intense cooling of muscle and nerve
tissues results in muscular failure,
and the individual progressively
loses the ability to swim, to
maintain posture in the water, or to
use the hands to perform other
survival tasks. In water near
freezing, incapacitation can occur
within five to ten minutes but takes
progressively longer at higher
water temperatures.
Once physical strength and
dexterity start to diminish, the trend
continues and does not reverse
itself. Therefore, the best course of
action must be determined promptly
and followed immediately. Such
actions could include the following:
◆ Pulling oneself out of the
water, or inflating and
boarding a life raft
◆ Getting as much of the body as
possible out of the water and
onto a floating object
◆ Ensuring flotation by inflating
a personal flotation device
(PFD), which should have
been put on before entering the
water
◆ Attracting assistance
Executing these actions while the
cold shock responses predominate
may be difficult. However, once
breathing is under control,
immediate action should be taken. If
self-rescue is not possible, actions
to minimize heat loss (Fig. 26-2),
such as assuming the H.E.L.P (Heat
Escape Lessening Posture) and
huddling, should be initiated.
Clothing should be tightened to
decrease the flow of cold water
within clothing layers.
Hypothermia
The individual who survives the
immediate and short-term phases of
cold water immersion faces the
possible onset of hypothermia
because continuous heat loss
eventually decreases core
temperature. However, hypothermia
only becomes a significant
contributor to death if immersion
lasts more than thirty minutes in ice-
cold water, and this period
lengthens as water temperature
increases.
Even in ice-cold water, an hour
or more may be required for a
person to become unconscious due
to hypothermia, which occurs at a
core temperature at or below 86°F
(30°C), if a PFD, flotation
snowmobile suit, or some other
device eliminates the need for
vigorous exercise to keep from
drowning. Once a person is
unconscious, another hour or more
may be required for the heart to
stop if the head is kept above water
(if a PFD is worn and water is calm
enough for waves not to wash over
the mouth or if the arms are frozen
to the ice).
One Minute—Ten Minutes—One

Hour
The slogan “one minute—ten
minutes—one hour” helps increase
the chances of surviving cold water
immersion by providing a simple
way to remember the first three
stages of cold water immersion and
what to do during each of them.
After falling into very cold
water people have:
◆ One minute to get breathing
under control (Panic must be
avoided!)
◆ Ten minutes of useful
movement (Time is available
for getting out of the water or
creating a stable situation.)
◆ One hour until
unconsciousness from
hypothermia (A person
wearing a PFD may have
another hour until the heart is
stopped by hypothermia.)
Without flotation, remaining
afloat long enough to die from
hypothermia is virtually impossible,
and death occurs from drowning as
the result of cold shock or cold
incapacitation. Wearing a PFD
accomplishes two objectives:
survival time is increased
tremendously, and the contributions
of cold shock and cold
incapacitation are decreased
substantially.
Circumrescue Collapse
An estimated 20 percent of
individuals recovered alive from
cold water die as a result of
circumrescue complications, either
before, during, or within hours after
rescue. Prior to imminent rescue,
mental relaxation and decreased
output of stress hormones may
cause a drop of blood pressure,
resulting in fainting and drowning.
The act of rescue may cause
sudden collapse. Pulling a person
out of the water in a vertical
position removes the hydrostatic
squeeze on the person’s body and
lower limbs, allowing blood to
pool in the extremities and causing
decreased blood pressure. The
extra cardiac work—or rough
handling—may induce arrest or
fibrillation of a cold heart. If
possible a person should be gently
removed from the water in a
horizontal position.
Death may also occur within
minutes to hours after rescue. A
rescued individual may be severely
compromised by acidic metabolic
by-products accumulating in the
extremities, a heart prone to
dysrhythmias, decreased or absent
consciousness, and low blood
volume. Sudden redistribution of
blood to the extremities,
particularly the lower extremities,
may cause collapse as a result of
decreased blood pressure, sudden
return of metabolites to an irritable
heart, or continued decrease in
temperature (afterdrop) of an
unstable heart. In addition,
individuals often aspirate water
during long periods of immersion,
which may produce delayed lethal
hypoxia because gas exchange in
the lungs is compromised.
Wet clothing becomes a major
source of heat loss. Rescued
individuals with immersion
hypothermia may be warmer with
no clothes on, particularly if they
can be protected from the wind. In
any case, wet clothing should be
removed at least temporarily and as
much water wrung out as possible.
Staying Alive
If a person survives the initial
stages of cold water immersion,
heat loss must be minimized, and
energy must be conserved. Large
people cool more slowly than small
people; fat people cool more
slowly than thin people; children
cool more rapidly than adults.
Activity also affects core cooling.
Exercise heat production can almost
never equal the increased heat loss
to the water caused by increased
peripheral blood flow and limb
movement through cold water.
Water has high heat conductivity
and drains heat from the body
twenty-five times faster than air at
the same temperature.
If no flotation is worn, valuable
energy is lost keeping the head
above water. Survival depends on
swimming to safety or obtaining
some other form of flotation. When
swimming or treading water, a
person cools much faster than when
remaining still, and cold
incapacitation eventually results in
swimming failure.
If a PFD is worn, it has the
immediate benefit of maintaining a
person’s airway without the effort
of swimming. It can keep even an
unconscious person afloat. An
average-size person wearing
lightweight clothing and a PFD may
survive three to six hours in 50°F
(10°C) water by remaining still.
During cold water immersion,
more than 95 percent of the heat
loss is to the water. Since most
boats float even when capsized or
swamped, getting into or onto the
boat to get as far out of the water as
possible is usually advisable. If the
body cannot be raised out of the
water, the Heat Escape Lessening
Position (H.E.L.P.) can be adopted.
A group of immersed individuals
should keep together for
psychological support and possibly
for increased thermal insulation.
The group may try to adopt a huddle
position, but it can be difficult to
maintain in rough water because
some in the group have their backs
to the waves and movement through
the water is limited. At the very
least, individuals should tether
themselves together with ropes or
straps, and individually adopt the
H.E.L.P. position (Fig. 26-2).
FROSTBITE
Frostbite is a cold injury produced
by freezing of tissues. The hands
and feet, ears, and face are most
commonly injured. The hands and
feet are farthest from the heart, and
their blood supply is further
reduced by vascular constriction
when the body is cold. The ears are
thin and have a meager blood
supply; the rims are often frozen.
Portions of the face, particularly the
tip of the nose, are often exposed.
Constriction of blood vessels in
the extremities to conserve heat for
the central portion of the body can
be so rigorous that circulation to
those areas almost ceases. Cold
also damages the endothelial cells
that line blood vessels, causing
plasma to leak through their walls.
Loss of plasma causes the blood to
sludge inside the vessels, further
impairing circulation.
As the circulation is diminished,
the tissues begin to freeze. Ice
crystals form within and between
the cells and grow by extracting
water from the cells. However,
freezing does not necessarily kill
cells. In laboratories, cells frozen
for long periods of time can be
thawed and grown in cultures.
The ultimate damage from
frostbite results from the damage to
vascular endothelial cells. When
the tissues are warmed, blood
exposed to these damaged cells
clots and completely obstructs the
circulation. The result is identical
to the effects of thrombosis in
arteriosclerotic arteries—the tissue
supplied by that artery dies (is
infarcted).
Prevention
Frostbite usually occurs in an
environment in which the
temperature is significantly below
freezing. Of 812 U.S. Army
frostbite injuries during the Korean
conflict, 80 percent occurred at
temperatures between −0.4° and
18.5°F (−18 ° to −7.5 °C). Frostbite
is usually associated with
hypothermia. When a contributing
condition can be identified, it is
most commonly impaired
circulation. Immobility contributes
to impairment of the circulation,
particularly in soldiers under fire or
in substance abusers, but boots that
are too tight or encircling, tightly
fitting garments are common
offenders.
On rare occasions, frostbite can
result from unprotected contact with
cold metals or with liquids that
remain liquid at temperatures far
below the freezing temperature of
water, most commonly gasoline or
ethyl alcohol.
Avoiding the conditions by
which it is produced, particularly
hypothermia, is the best way to
prevent frostbite. Clothing that
keeps the trunk warm also keeps the
extremities warm by eliminating the
need for blood vessel constriction
to preserve heat. Also essential is
footgear that does not constrict the
circulation.
Cigarette smoking constricts the
blood vessels in the skin and
aggravates local cold injuries such
as frostbite.
Diagnosis and Prognosis

The early signs of frostbite are
cold, pain, and pallor of the
affected tissues. Some individuals
suffer little pain. Pain disappears as
tissues begin to freeze, a highly
significant warning sign. As
freezing progresses, tissues become
even whiter, all sensation is lost,
and tissues become quite hard. With
extensive frostbite, such as an entire
hand or foot, tissues often have a
dull purple color. Frostbite of the
face, tip of the nose, or ears can be
recognized by the pain and pallor of
the affected tissues.
The extent and severity of
frostbite are notoriously difficult to
judge accurately while tissues are
still frozen or immediately after
thawing. However, a few hours
after thawing prognostic signs begin
to appear. Minor frostbite (frostnip)
that involves only the tips of the
fingers or toes, the tip of the nose,
or small areas of the face or ears
produces redness and swelling that
lasts for a few days but leaves no
permanent damage.
With more severe injuries,
blisters develop after rewarming
and may cover entire digits (Figs.
26-3 and 26-4). If the blisters
contain clear fluid and extend to the
tips of the digits, the underlying
tissues can be expected to recover.
If the blisters do not extend to the
tips of the digits, the unblistered
tissues are usually lost. When the
blisters are filled with bloody fluid,
much of the underlying tissues
cannot recover. The most severe
frostbite injuries are not followed
by blisters and retain a deep purple
color.
Figure 26-3. Frostbite of the thumb
and fingertips one and eight days after
injury
Figure 26-4. Frostbite of the feet

manifested by blisters that do not
reach the tips of the toes
After a week or ten days the

dead frostbitten tissues develop a
thick black covering (eschar).
Eventually, usually four to six
weeks, the dead tissue, including
entire fingers or toes, separates
spontaneously.
Treatment
The preferred treatment for
frostbite is rapid rewarming in a
water bath. However, opportunities
for such therapy are rare because
most frostbite injuries have thawed
before the individual arrives at a
site where rewarming can be
performed. Climbers or cross-
country skiers often have to be
evacuated before they can be
rewarmed. Thawing of the
frostbitten tissues during evacuation
often is unavoidable. Individuals
with urban frostbite, who greatly
outnumber those with wilderness
frostbite, delay an average of
twelve hours before seeking
medical care.
Rewarming can best be carried
out in a hospital where the person
can be kept warm, and supplies for
rewarming and later care are
available. Treatment in a
wilderness environment should be
attempted only when the following
conditions can be met:
◆ The person does not need to
use the frostbitten extremity
until healing is complete.
Specifically, the person does
not need to walk on a foot that
has been frostbitten and
thawed. The greatest damage
from frostbite occurs when
frozen tissues are thawed and
refrozen. Walking on a frozen
foot produces far less damage.
◆ The person can be kept warm
during rewarming and
afterward for as long as
recovery requires. If the
person’s body is cold, the
blood vessels in his
extremities are constricted.
Rewarming in such
circumstances leaves badly
injured tissues without an
adequate blood supply at the
time it is most needed.
◆ Adequate facilities for prompt
rewarming, including
abundant supplies of warm
water and accurate methods
for maintaining the
temperature of the rewarming
bath, are available.
If the frostbitten extremity has
completely thawed, rewarming has
no beneficial effects, but if the
completeness of thawing is
uncertain, brief rewarming may be
helpful.
During rewarming the water
temperature should be maintained
between 99° and 102°F (37° and
39°C). Higher temperatures damage
the tissues and are more painful.
The water must not feel
uncomfortable to an uninjured
person’s hand. A large water bath
permits more accurate temperature
control and warms the frozen
extremity more rapidly, often
resulting in less tissue loss,
particularly when freezing has been
deep and extensive.
The extremity should be stripped
of all clothing and any constricting
bands, straps, or other objects that
might impair the circulation. The
injured foot or hand should be
suspended in the center of the water
bath and not permitted to rest
against the side or bottom.
During rewarming, hot water
must be added to the bath
periodically to keep the temperature
at the desired level. (A frozen hand
or foot is essentially a block of ice
and cools the water.) The injured
extremity should be removed from
the bath and not returned until the
water has been thoroughly mixed
and the temperature measured.
An open flame should not be
used to keep the water bath warm.
The frostbitten extremity may come
in contact with the heated area and
be seriously burned because
sensation in the tissues has been
lost.
Warming usually requires thirty
to sixty minutes; it should be
continued until the tissues are soft
and pliable or no further changes in
color are seen.
During rewarming, the
frostbitten tissues usually feel quite
painful. Strong analgesics may be
needed during or after rewarming.
Following rewarming, the
individual must be kept warm and
the injured tissues must be elevated
and protected from any kind of
trauma or irritation. A framework
should support bedclothes to avoid
pressure or rubbing on the injured
area. To avoid infection, blisters
should not be ruptured.
The individual should be
evacuated immediately. Healing
requires weeks to months,
depending upon the severity of the
injury. Subsequent care in the field
should be directed primarily
toward preventing infection.
Cleanliness of the frostbitten area is
extremely important. Soaking the
extremity in disinfected, lukewarm
water to which a germicidal soap
has been added may be helpful. A
small amount of dry, sterile cotton
or gauze should be placed between
fingers or toes to avoid maceration.
routinely, but if infection appears to
be present, ampicillin or cloxacillin
should be administered until a
physician’s care is obtained.
Smoking should be strictly
avoided because it reduces the
already deficient blood supply to
the damaged area. Movement of the
extremities should be encouraged
but should be limited to movements
that can be carried out without
manipulation or assistance from
others. Most individuals with
frostbite need continuing
reassurance and emotional support.
Surgery has little or no role in
the immediate therapy of frostbite.
Unfortunately, occasional surgeons
with no experience with this injury
are so alarmed by the appearance of
frostbitten extremities that they
insist upon immediate amputation.
Tragic mutilations have occurred.
Many individuals have refused
amputation and recovered with
minimal or no tissue loss.
With essentially no exceptions,
surgery must be delayed until
demarcation of the dead tissues is
complete and unmistakable. At that
time minor surgical debridement of
infected eschars or incision of
constricting eschars that completely
surround a digit and are obstructing
circulation may be needed.
However, surgery is usually not
required until long after the initial
injury, and then only to complete
amputation of frostbitten tissues or
to reconstruct hands or feet.
“Frozen in January, amputate in
June” is a time-proven adage.
Individuals who have suffered
frostbite usually have increased
sensitivity to cold and are more
susceptible to cold injury because
the blood vessels in the injured
tissues have been permanently
damaged.
TRENCHFOOT
Trenchfoot is a nonfreezing cold
injury that is almost entirely a
military problem, although rare
instances in civilians are
encountered. In the Falkland Islands
fighting in 1982, 14 percent (70 of
516) of the hospitalized British
battle casualties had trenchfoot.
Only soldiers with the most severe
injuries were hospitalized;
estimates of the number with lesser
injuries ranged as high as 2000.
Trenchfoot results from feet
being wet and cold without
interruption for days or weeks. The
feet do not have to be immersed in
water; simply being wet produces
the condition. Symptoms rarely
appear in less than four or five
days, and even then only in severely
cold, windy weather—as was
encountered in the Falklands.
The disorder was first described
during the Napoleonic campaigns,
particularly during the retreat from
Moscow, but received its name
during World War I from the
infantrymen who spent weeks with
their feet in the cold water that
flooded the trenches. The British
had over 115,000 casualties from
trenchfoot and frostbite in that
conflict. Similar injuries in
individuals who spent weeks with
their feet in cold water in rafts or
lifeboats after their ships had been
sunk or their aircraft had crashed
led to the name “immersion foot.”
Other names exist, but trenchfoot is
the most clearly and widely
recognized.
The cold induces intense
vasoconstriction, which deprives
the feet of adequate blood supply.
(The separate roles of cold and
poor circulation in producing injury
have not been distinguished.) After
five to seven days (or longer) the
feet become red, swollen, and quite
painful. British soldiers with
trenchfoot in the Falklands
screamed in pain when putting their
boots on in the morning (but
stormed into battle anyway!).
Treatment is simple except for
severe cases. It consists of keeping
the individual warm with feet dry,
elevated, and protected from
bedclothes. Nothing more. Severe
cases should be treated like
frostbite, although the tissues do not
need to be rewarmed.
Nerve damage can cause
persistent pain so severe that
amputation is required, but such
injuries are rare. The British had no
immediate amputations in the
Falklands. Sensitivity to cold is
usually lifelong and can disqualify
troops for continued military
service.
Prevention of trenchfoot is also
simple. World War I commanders
ordered their troops to dry their feet
and put on dry socks every day,
which reduced their trenchfoot
casualties to very low numbers,
even though the men returned
immediately to flooded trenches.
Outdoor recreationalists,
particularly participants in water-
based activities, must be aware of
the potential for injury in wet,
nonfreezing weather. They must
carry dry socks and must take time
to dry their feet, change their socks,
and dry their boots. However, they
should encounter much fewer
distractions while attending to such
precautions than do soldiers in
combat.
CHAPTER 27
HEAT AND SOLAR

INJURIES
HEAT ILLNESS
Heat illnesses cover a spectrum that
ranges from mild disability that is
more of a nuisance than a health
threat to lethal heat strokes.
Normal Heat Loss

Normal human body temperature
is maintained within a narrow range
by sensitive temperature control
centers in the hypothalamus. Heat
produced within the body is
dissipated to the environment so
that a temperature between 97° and
100°F (36° and 38°C) is
maintained.
Largely through muscular
activity, most individuals generate
2000 to 5000 kilocalories of heat
per day depending upon their size,
physical activity, and state of
nutrition. The body must get rid of
this heat to prevent a devastating
increase in temperature. If no heat
were lost, the body temperature of a
sedentary individual weighing 154
pounds (70 kg) producing only
2000 kilocalories per day would
climb approximately 62°F (34°C)
to 160°F (71.4°C) in twenty-four
hours. (The temperature would
climb at that rate as long as the
person was alive!)
Humans lose heat largely through
their skin. The lungs are the
principal route of heat loss
(panting) for hairy animals. At high
altitudes deeper, more rapid
breathing of cold, relatively dry air
causes significant heat loss in
humans, but in temperate or hot
climates much less heat is lost
through the lungs. The skin acts
much like the radiator of a liquid-
cooled engine. Blood is warmed as
it passes through exercising muscles
and cooled as it circulates through
the skin. The thermostat on the
engine increases the flow of coolant
through the radiator when the engine
is hot; comparable mechanisms
increase blood flow to the skin by
dilating cutaneous blood vessels
when exercise heats the body.
The radiator for an engine is
cooled only by air passing over it.
Heat is lost from the skin in this
way also (convection), but in a hot
climate by far the largest heat loss
is through evaporation of
perspiration. Evaporative cooling
is highly effective because a large
amount of heat is required to change
water from a liquid to a vapor. The
evaporation of 1 cubic centimeter
(1 ml) of water at a skin
temperature of 95°F (35°C)
requires 577 calories, enough to
reduce the temperature of 1 liter
(1000 ml) of water approximately
1°F. Most of this heat is extracted
from the body.
Evaporative cooling is limited
because the maximal sweating rate
for individuals not acclimatized to
heat is about 1500 ml per hour.
Evaporation of that much
perspiration would eliminate the
heat produced by running six miles
at a pace of ten minutes per mile,
which is not a particularly fast
pace.
Acclimatization to heat takes
about one week, results in an
increased tolerance for exercise in
a hot environment, and is produced
by mechanisms that increase the
maximum sweating rate but reduce
salt loss. Water deprivation does
not accelerate or otherwise
contribute to the acclimatization
process.
Exertional and Nonexertional
Heat Illness
Heat illness results from the
inability of the body to get rid of
heat it has produced. Two variants
are recognized. Exertional heat
illness results from an increase in
heat production so large that all the
heat cannot be dissipated even
though the heat losing mechanisms
are functioning well. Nonexertional
heat illness results from impairment
of heat-losing processes by disease
and can occur even though heat
production is low or normal. Heat
illnesses occurring in healthy
individuals participating in
vigorous wilderness activities are
essentially all the result of exertion,
but the initial treatment for both
disorders is the same.
A fever raises body temperature
essentially by resetting the body’s
“thermostat” at a higher level and
can be controlled with drugs such
as aspirin, ibuprofen, or
acetaminophen. Such drugs have no
effect upon the elevated temperature
associated with heat illness because
the thermostat has not been changed.
Only heat production has changed.
Preventing Exertional Heat

Illness
The only way exertional heat
injuries can be prevented is by
recognizing climatic conditions in
which heat cannot be dissipated and
curtailing physical activity. Those
conditions are easily defined: an
environmental temperature of 95°F
(35°C) or higher and a high relative
humidity.
The average skin temperature is
95°F (35°C), slightly lower than
core temperature. At environmental
temperatures above this level, heat
cannot be lost by convection
because the air temperature is
higher than skin temperature. Heat
cannot be lost by radiation because
the environment is hotter than the
skin surface. (Heat would be gained
by radiation.) The only way heat
can be lost in such circumstances is
by evaporation. (Mechanisms of
heat loss are described in Chapter
26: Cold Injuries.)
At a high relative humidity,
evaporation is greatly diminished
and heat cannot be lost by that
route. In fact, in humid conditions
at temperatures greater than 95°F
(35°C), heat cannot be lost
effectively by any route. In the
southeastern United States, where
hot, humid conditions are common
in the summer, experienced
residents know that a person
dripping with perspiration is in
danger of heat illness. If
perspiration were evaporating and
providing cooling, it would not
accumulate on the skin.
To avoid heat illness in such
circumstances, heat production must
be reduced to the lowest possible
level. Vigorous exercise must
cease. In tropical areas, where
temperatures and humidity are
usually high, the midday siesta is a
sensible way to minimize the risk of
heat illness during the time when
the threat is greatest.
In past years the most frequent
causes of exertional hyperthermia in
the United States have been
distance running (including jogging)
and football practice in late
summer, which combines vigorous
physical activity, a uniform that
inhibits evaporation of sweat, and a
hot, often humid environment.
Recognition of the hazard
associated with these activities has
led to scheduling such events in
early morning when temperatures
are lower. Wearing plastic or
rubberized suits while exercising to
lose weight is another dangerous
practice. Such suits increase body
temperature, sometimes to high
levels, because they do not allow
perspiration to evaporate.
Fortunately, this practice also has
been largely abandoned in recent
years, possibly more from the
realization that only water—not fat
—was being lost than recognition
of the danger of heat illness.
Individuals taking certain
therapeutic drugs also have an
increased risk of heat illness.
Anticholinergic drugs taken for
irritable bowel syndrome and other
disorders impair sweating. Any of
the diuretics used to treat
hypertension and heart failure can
lead to dehydration. Individuals
taking these and other medications
must be particularly cautious in hot
environments.
Water Replacement
Staggering quantities of water
must be consumed to replace
perspiration losses in desert
conditions. During 1964 U.S. Army
maneuvers in the deserts of southern
California, for which daytime
temperatures of 100° to 110°F (38°
to 43°C) were expected,
participants were required to drink
eight quarts of water every day. Not
a single case of heat illness
occurred, which was considered
almost miraculous at the time.
Israeli soldiers operating in the
Sinai Desert during the 1967 war
with Egypt were allotted ten liters
of water a day and had no heat
illnesses, which is punishable by
court martial in that army. The
Egyptians, who received only three
liters a day, suffered numerous
fatalities due to heat illness.
Thirst alone does not provide
adequate fluid intake. Individuals
must make a conscious effort to
consume the quantities needed.
During desert operations, military
commanders are held responsible
for ensuring their charges meet the
daily intake requirements.
Dehydration is a major contributor
to all forms of heat illness—mild
and severe.
In the past, an augmented salt
intake has been considered
essential for preventing heat illness.
Soldiers in the California desert
were required to take three to five
grams of salt—six to ten tablets—
every day. That recommendation
was abandoned because the diet of
residents of most industrialized
nations was thought to contain
enough salt for stressful heat
conditions. However, the pendulum
appears to be swinging in the other
direction, and a generous salt intake
seems advisable.
Consuming water alone can lead
to the condition known as exercise-
induced hyponatremia (low blood
sodium), so in addition to drinking
water, individuals should eat,
particularly salty foods, or drink
one of the sport beverages that
contain salt.
Heat Syncope and Heat

Exhaustion
Heat illnesses range in severity
from very mild to lethal. Typical
patterns of illness have been given
specific names, but the types of heat
injury must be recognized as
different manifestations of the same
basic disorder. Mild heat illnesses
have the potential for becoming
severe and must be treated with
care.
Heat syncope and heat
exhaustion are milder forms of heat
illness. Heat syncope is a disorder
similar to ordinary fainting
(syncope) except for its cause. In an
effort to increase heat loss, the
blood vessels in the skin dilate to
such an extent that the blood supply
to the brain is diminished.
Reduction in blood volume by
dehydration contributes to the lower
cerebral blood flow. Initially a
person with heat syncope feels faint
and is usually aware of a rapid
heart rate. Nausea, vomiting,
headache, dizziness, and
restlessness, even brief loss of
consciousness, are not uncommon.
Skin color and the presence of
sweating are variable.
Heat exhaustion is a more severe
disorder. Some investigators have
separated these two disorders on
the basis of body temperature,
which is normal with syncope but
elevated to 102° to 104°F (39° to
40°C) with heat exhaustion. Heavy
sweating is present, and symptoms
such as nausea, vomiting, and
headache tend to be more severe.
Individuals with heat exhaustion
have faster respirations and a fast
heart rate.
Heat syncope should be treated
just like fainting. An individual who
recognizes preliminary symptoms
should lie down, or at least sit
down, to avoid injury and, if lying
down, should elevate the feet. A
cooler environment is desirable,
and the individual should at least be
protected from direct sunlight. The
person should be given fluids,
particularly fluids like the sports
beverages that contain salt, and
should not engage in vigorous
activity for at least the rest of that
day. Only after complete restoration
of body fluids and resumption of a
normal urine output should exercise
in a hot environment be cautiously
resumed.
An individual with heat
exhaustion should be treated in the
same way, but body temperature
must be closely monitored. If the
temperature is above 104°F (40°C),
or continues to climb after the
person has been taken out of the sun
and is at rest, active cooling should
be started. If a clinical thermometer
is not available and the individual
feels warmer than others do, active
cooling should be started and
maintained until the person feels
comfortable. Individuals with heat
exhaustion have an even greater
fluid deficit that must be corrected,
which may be difficult if the
individual is nauseated or vomiting.
Such persons must be very careful
about resuming physical activity
and usually should be examined by
a physician before doing so.
Heat Stroke
Heat stroke (sunstroke) is the
most severe form of heat illness.
Fatalities are common, as are
permanent residual disabilities. The
onset typically is very rapid and is
characterized by changes in mental
function. Confusion and irrational
behavior are most frequent, but
incoordination, delirium, and
unconsciousness often follow.
Seizures occur commonly. The
pupils may be dilated and
unresponsive to light.
The body temperature during
heat stroke is almost always above
104°F (40°C) and may be above
107°F (42°C), which is the upper
limit for most clinical
thermometers. A rectal thermometer
reading to 113°F (45°C) is usually
needed to measure the temperature
of individuals with heat stroke, but
that would not be carried unless
severe heat stress had been
anticipated, in which case effective
preventive measures should have
been instituted. If the temperature is
not measured for some time after
the onset of the illness, it may have
fallen.
The skin feels hot. It is usually
covered with perspiration if the
person has been exercising at the
time of collapse. Later the skin may
dry, particularly if cooling has been
instituted. The hot, dry skin long
associated with heat stroke is
typical of individuals with the
abnormal heat loss typical of
nonexertional heat illness, not
exertional heat illness. However,
sweating does decrease during
exercise and can fall to quite small
volumes, particularly when
exercise has been prolonged and the
individual has become dehydrated.
Pulse and respiratory rates both
are increased. The heart rate may
be as high as 130. Shock is usually
present.
If a clinical thermometer to
measure temperature is not
available but typical signs and
symptoms of heat stroke are
present, cooling should be instituted
as rapidly as possible. Heat stroke
is one of the few true medical
emergencies in which a delay of
only a few minutes may
significantly alter the outcome. If
the person is unconscious, an open
airway must be maintained. Shock
should be treated by elevating the
feet and by any other methods that
are feasible.
The individual should be moved
to the coolest spot possible and
shaded from sunlight. One way of
cooling persons with heat stroke in
hospital emergency rooms is to
remove their clothing, cover them
with wet sheets, and place large
fans blowing directly across their
body from two directions. In the
wilderness, similar methods should
be devised. Clothing should be
soaked with water. If the clothing is
removed—or is scanty—the
extremities and trunk should be
covered with wet towels or other
absorbent fabric and the body
should be fanned to increase air
circulation and evaporation.
Immersion in water is also used in
hospital emergency rooms and
would be useful in a wilderness
situation. Any reasonable method
for cooling the individual should be
employed.
In a wilderness environment that
produced heat stroke, ice or snow
would not be available. In an urban
environment, they probably should
not be used. A person with heat
stroke should be cooled by
evaporation. Alcohol sponging
should not be used because
isopropyl alcohol may be absorbed
through the skin, particularly by
children, and is toxic.
During cooling, the extremities
should be massaged to help propel
cooled blood back into the organs
of the body and head. Oxygen
should be administered if available.
After the temperature has been
reduced to 102°F (39°C), active
cooling should be slowed to avoid
hypothermia, but the individual
must be closely monitored to ensure
that the temperature does not climb
back to higher levels. Rebound is
particularly common three to four
hours after cooling. Drugs do not
effectively reduce body
temperature, may aggravate
complications, and should not be
administered.
As soon as possible the person
should be evacuated to a hospital,
particularly if unconscious for more
than a few minutes. The
complications of heat stroke include
failure of essentially every organ
system—particularly the heart,
liver, and kidneys. Blood clotting
abnormalities, gastrointestinal
ulceration with bleeding,
biochemical alterations, and
extensive brain damage also occur.
Unconsciousness lasting more than
two hours is a poor prognostic sign
that is usually followed by
permanent disability or death.
Heat Cramps
Heat cramps are severe,
spasmodic contractions of one or
more muscles, most commonly the
leg muscles. Cramps may last up to
fifteen minutes or even longer, and
the muscles are usually painful for
several days afterward.
Stretching the muscle usually can
stop cramps almost immediately.
For example, extending the leg and
pulling the foot upward can stretch
the calf muscle. Kneading or
pounding the muscle is less
effective and probably contributes
to residual soreness.
Cramps usually appear in the
most heavily worked muscles and
may be produced, in part, by an
excessive water intake without
accompanying salt, resulting in
dilution of the salt in the
extracellular fluid. Cramps are
more common in circumstances that
tend to cause salt depletion; they
can be prevented to a large extent
by consuming large quantities of
salt and water.
INJURY BY SOLAR
RADIATION
Sunlight has been considered
beneficial because it plays a
significant role in Vitamin D
synthesis. However, questions
about that assumption are being
raised. Some investigators argue
that all sun exposure is harmful, not
just excessive exposure, because
DNA can be damaged by any
amount of ultraviolet radiation.
Everyone is familiar with sunburn,
but many individuals are not as
well aware of—or choose to ignore
—the degenerative changes
associated with repeated exposure
that eventually lead to skin cancer.
Three hundred thousand new skin
cancers are diagnosed every year in
the United States, and the incidence
is increasing.
Much of the energy in solar
radiation has shorter (ultraviolet) or
longer wavelengths (infrared) than
visible light (Fig. 27-1). Most
biologic damage is caused by
ultraviolet radiation, which has
wavelengths less than 400
nanometers (nm) (1 centimeter =
107 nanometers = 108 angstroms).
Ultraviolet (UV) radiation is
divided into UVA, which has a
wavelength of 315 to 400 nm, and
UVB, which has a wavelength of
280 to 315 nm. For many years only
UVB was considered harmful, but
that is now known to be incorrect.
Even when a person is shielded
from the direct rays of the sun, much
ultraviolet radiation can still reach
him due to atmospheric scattering
This atmospheric radiation may
contribute half of the total
ultraviolet radiation and tends to be
greater when high, thin cirrus
clouds are present. Indeed, total
ultraviolet radiation can be greater
on an overcast day than on a
cloudless day. Such radiation is
particularly insidious because it is
so unapparent.
Figure 27-1. Quantity of light of
different wavelengths in sunlight
Ultraviolet exposure at high

altitudes is greater than at sea level
because the atmosphere is thinner
and filters out less sunlight,
particularly in the harmful
wavelengths. The rate of increase is
4 percent/1000 feet (300 m).
Snowfields and glaciers reflect
about 75 percent of the incident
ultraviolet radiation; in a cirque or
bowl, reflection can increase the
radiation even more. Individuals
participating in water sports are
exposed to direct radiation and
large quantities (up to 100 percent)
of reflected radiation. High-altitude
sailboarding can result in major
ultraviolet exposures.
Sensitivity to Sunlight
Individuals vary widely in their
sensitivity to sunlight. Redheads are
particularly sensitive. Blueeyed
blondes are more susceptible to
sunburn than brunettes. Individuals
of northern European ancestry are
more sensitive than Mediterranean,
Indian, African, or other people
whose skin contains more
protective pigment (melanin).
Children are more susceptible than
adults.
Sensitivity to sunlight may be
increased by a wide variety of
drugs, such as sulfonamides and
their derivatives (trimethoprim-
sulfamethoxazole—brand names
Bactrim and Septra®); oral
antidiabetic agents; thiazide
diuretics such as
hydrochlorothiazide; most
tetracyclines, particularly
doxycycline, which may be used for
malaria prophylaxis; and the
fluoroquinolones such as
ciprofloxacin (Cipro®). Many other
substances such as biothionol,
which is used in soaps; many first-
aid creams and cosmetics; green
soap; many plants and grasses such
as fig leaf, certain meadow grasses,
wild parsnip, celery, and others;
dyes used in lipstick; and coal tar
or coal tar derivatives increase
sensitivity to sunlight.
UVA and UVB

UVA makes up 95 percent of all
solar ultraviolet radiation and
varies less with altitude and time of
day than UVB. UVA increases
pigmentation and thickness of the
outer layer of the skin, producing a
suntan that is protective because the
pigment and the thickened skin
reduce the penetration of ultraviolet
radiation. UVA penetrates the skin
more deeply than UVB and
potentiates the changes produced by
UVB. UVA damages the elastic
fibers in the skin and is primarily
responsible for such aging changes
as wrinkling.
UVB, although it makes up only
5 percent of all solar ultraviolet
radiation and penetrates less deeply
than UVA, is the major cause of
sunburn and skin cancer. This type
of ultraviolet radiation damages the
DNA in skin cells, which ultimately
leads to malignancy.
Sunburn
Mildly excessive exposure to
UVB produces redness (due to
dilatation of cutaneous blood
vessels) and slight swelling and
induration. Greater exposure causes
pain and blistering. Severe burns
may be associated with chills,
fever, or headache. Sunburn of the
lips is often followed by painful
Herpes simplex infections (fever
blisters or cold sores).
Gradually increasing exposure to
sunlight permits natural tanning and
thickening of the skin and helps
avoid sunburn, although sunscreens
should still be applied. For many
redheads and some other light-
skinned individuals, adequate
tanning is impossible.
The sun protection factor (SPF)
is a value that indicates how much
longer an individual can tolerate
direct sunlight when protected by a
sunscreen than with no protection.
When protected by a sunscreen with
an SPF of 12, a person whose skin
would begin to turn red after five
minutes of unprotected sun exposure
could stay in the sun for twelve
times longer or sixty minutes before
the skin would begin to redden.
Clothing is protective against
UVB, but the level of protection is
dependent upon how tightly the
fabric is woven. If the fabric is held
up to a light bulb and images can be
seen through it, the SPF is less than
15. If light gets through but no
images, the SPF is 15 to 50. If no
light comes through the SPF is
greater than 50. If the fabric is wet,
it does not provide as much
protection. Clothing made from sun-
protective fabric can be purchased
from several sources. Hats with
wide brims (three inches) provide
protection of the face and neck.
Baseball-style caps protect only the
forehead or, if worn backward, only
the back of the neck.
Protective creams or lotions that
contain sunscreens are the typical
methods for protecting exposed skin
from sunlight. They should be
applied liberally and frequently.
Most individuals do not use enough
—about one ounce per day is
required—nor do they apply
sunscreens as often as needed—
every one to two hours. SPF
determinations are based on thick
applications of sunscreens. The
cream or ointment should be clearly
visible on the person’s skin, not
rubbed in until it disappears.
The face and neck should be
carefully protected because they are
essentially always exposed. The
nose, cheeks, neck, and ears are
most frequently sunburned. The
lower surfaces of the nose and chin
are commonly burned by reflected
radiation, particularly around water
or on snow.
Larger and more frequent
applications are needed when
sweating; immersion in water, and
wiping the neck and face tend to
remove the preparation. Sunscreens
labeled “water-resistant” are
effective after forty minutes or less
of immersion. Products labeled
“water-proof” are effective after
eighty minutes of immersion. No
products resist immersion
indefinitely.
The earliest chemical sunscreen,
para-aminobenzoic acid (PABA),
was introduced in the 1970s. It
caused contact dermatitis (Chapter
23: Allergies), particularly in young
children, was water soluble and
short lasting, and stained clothing; it
is rarely used now. Cinnamates or
salicylates, which cause sensitivity
reactions and are highly water
insoluble, are used in most
currently available preparations.
Price has little relation to the
effectiveness of sunscreens.
Investigators for Consumers Union,
publisher of Consumer Reports,
found equally effective adult
sunscreens to range in price from
$0.66 to $4.28 per ounce.
Most of the day’s UVB radiation
is received during the four hours in
the middle of the day, and
protection from solar injury is
particularly needed during this
interval—the time when a person’s
shadow is shorter than the person’s
height. Protection from UVA is
needed during essentially all hours
of sunlight.
A group of protective agents that
block out all ultraviolet radiation
contain opaque pigments such as
titanium dioxide (A-Fil®) or zinc
oxide (Zincofax cream). Red
veterinary petrolatum (R.V.P., Paul
B. Elder Co.) is also effective.
Such agents should be used on the
nose, lips, and ears, which are
easily sunburned and are not
covered by clothing. (Products
containing benzophenones, such as
Uval and Solbar®, also screen out
all ultraviolet radiation but were
developed primarily for individuals
with skin diseases that require such
complete protection. These agents
are easily removed by sweating and
are not suitable for protection
during recreational sun exposure.)
Treating Sunburn
If started before exposure to the
sun or before the skin has reddened,
oral nonsteroidal
antiinflammatories (NSAIDs) such
as ibuprofen (Motrin® and others)
or topical steroids such as 1 percent
hydrocortisone may slightly reduce
redness during the first twenty-four
hours after sunburn. Once sunburn
has developed, no effective
treatment is available. Nothing
speeds healing. Soothing creams,
cold compresses, topical
anesthetics, oral acetaminophen
(Tylenol® and others), or NSAIDS
may provide some symptom relief.
Extensive or unusually severe
sunburn must be treated as a
seconddegree burn and may require
hospitalization.
Skin Cancer
Repeated sun exposure over a
period of many years, even for
individuals who are darkly
pigmented, produces degenerative
skin changes that are cosmetically
unattractive and commonly lead to
cancer. Degenerative skin changes
are particularly likely in persons
who spend much time in intense
sunlight, such as ski patrol
members, lifeguards, and boaters.
Tanning clearly provides
incomplete protection.
Melanoma is the most aggressive
form of skin cancer, and the
incidence of this malignancy has
almost tripled in the last four
decades, a faster increase than any
other malignant tumor.
Approximately 32,000 new cases
and 7000 deaths from melanoma
occur annually in the United States.
This tumor has become the most
common cancer in Caucasians
between the ages of twenty-five and
twenty-nine. Sunlight is the most
significant environmental element
causing this tumor. Intermittent
exposure, particularly early in life,
appears to increase risk more than
cumulative exposure. Three or more
episodes of blistering sunburn
during childhood or adolescence
predispose individuals to
melanoma.
The incidence of basal cell and
squamous cell carcinomas of the
skin is also greatly increased by sun
exposure. Although these tumors, or
the surgery or radiation required to
remove them, are occasionally
disfiguring, they rarely cause
fatalities, unlike melanomas.
Individuals who spend much of
their time in sunlight must reduce
the severity of such changes by
conscientiously applying sunscreens
whenever they are exposed,
regardless of the risk of sunburn.
However, the best protection is
clothing, particularly long-sleeved
shirts and wide-brimmed hats that
shade the face.
Snow Blindness
The surface of the eye (cornea
and conjunctiva) absorbs ultraviolet
radiation just like the skin does.
Excessive exposure can result in
sunburn of these tissues, producing
snow blindness (photophthalmia).
This condition is discussed in
Chapter 15: Eye Disorders.
CHAPTER 28
DROWNING
Andrea R. Gravatt, M.D.
Gordon G. Giesbrecht, Ph.D.
Oceans with sun-drenched beaches,

streams and rivers cascading over
boulders, thundering waterfalls,
tree-lined swimming holes,
peaceful lakes and ponds teeming
with fish, sparkling swimming
pools, romantic hot tubs—all of
these are favorite places for
relaxation not usually thought of as
death scenes, but they can be.
Buckets filled with water, bathtubs,
and toilets are more practical
facilities but also are associated
with a significant drowning
mortality.
Drowning is a major world
health problem that causes
significant morbidity and mortality.
The Centers for Disease Control
and Prevention (CDC) reported
3582 drowning deaths in the United
States during 2005, an average of
ten per day. More than one in four
were in children younger than
fifteen years. (These numbers may
be low as the result of
underreporting.) That statistic does
not include boating-related
accidents that, according to the U.S.
Coast Guard, accounted for
approximately 710 additional
drownings in 2005.
Drowning is the second most
common cause (after motor vehicle
accidents) of accidental death in
children between the ages of one
and fourteen years and the third
most common cause of accidental
death overall. It ranks fourth among
all causes of childhood death. Of
individuals who drown, 40 to 50
percent are four years old or
younger; the only other large group
is teenage males.
For every child fourteen years
and younger who died from
drowning, four received emergency
department care for nonfatal
submersion injuries. More than half
these children required
hospitalization. Nonfatal drownings
can cause brain damage that results
in long-term disability ranging from
memory problems and learning
disabilities to the permanent loss of
all sensible brain function
(permanent vegetative state).
The financial cost of drowning is
one of the highest for any injury
group because many who have
drowned require prolonged
hospitalization and long-term care.
One series reported that for every
three deaths one individual suffers
brain damage from drowning.
DEFINITIONS RELATED TO
DROWNING
Many terms are used in the
drowning literature. For this
chapter drowning is defined as
water submersion resulting in
asphyxia and death. Individuals
who have been submerged in water
and require cardiopulmonary
resuscitation (CPR) have drowned.
Though not used in this chapter,
the term near-drowning has been
applied to situations in which
individuals survive drowning more
than twenty-four hours, after which
they may die or may survive in a
normal or impaired neurological
state. Such terminology is not used
for any other medical condition. (A
person who has been successfully
resuscitated from a cardiac arrest is
not said to have had a near-cardiac
arrest.)
A submersion incident is an
event, usually unintentional or
accidental, in which an individual
is submersed in water and is at
least at risk of drowning, may
aspirate water, but does not suffer
cardiopulmonary arrest.
Sophisticated medical care
including hospitalization may be
needed, but CPR is unnecessary.
The terms wet drowning and dry
drowning are applied to lung
changes that result from aspiration
or lack of aspiration of water. Wet
drowning refers to fluid in the lungs
after an individual aspirates water.
Dry drowning refers to a
submersion event in which spasm of
the vocal cords closes the airway
and prevents the individual from
aspirating water. About 10 to 15
percent of drownings are dry.
Immersion syndrome is sudden
death resulting from ventricular
fibrillation or cardiac arrest
immediately after sudden
immersion in cold water.
Immersion hypothermia occurs
as the core temperature gradually
falls through surface cooling when a
person is immersed in cold water.
However, even in ice-cold water
death from hypothermia does not
occur in minutes. Incapacitation by
the cold may lead to drowning in
just a few minutes, but lethal
cooling requires approximately two
hours.
Acute submersion hypothermia
is the rapid development of
hypothermia during drowning due to
core cooling from aspiration and
absorption of cold water.
EPIDEMIOLOGY OF
DROWNING
Young children are most vulnerable
to drowning due to their lack of
awareness of danger, poor
swimming techniques, and the size
of their heads in relation to body
size, which makes them susceptible
to falling into containers. Children
under one year of age drown most
frequently in bathtubs, toilets, and
buckets. Children aged one to four
years drown most commonly in
residential swimming pools. Teen
drowning is often the result of risk-
taking behaviors and lack of
supervision, compounded by drug
and alcohol intake. In 2005 males
accounted for 80 percent of all U.S.
drownings, largely due to risk-
taking behaviors characteristic of
the adolescent male group. Beyond
the toddler age group, boys have a
three times greater risk of
drowning.
Although swimming programs
for very young children have
proliferated, no studies demonstrate
that they prevent drowning. Such
programs may produce a false sense
of security, and good swimmers are
not immune to drowning.
Competitive swimmers and divers
can drown as a result of
hyperventilation prior to
competition. Deliberately “blowing
off” carbon dioxide (hypocapnia)
delays onset of the drive to breathe
produced by rising blood
concentrations of carbon dioxide,
which can allow the development
of low oxygen levels (hypoxia) that
result in unconsciousness and
underwater attempts to breathe.
MECHANISMS OF DROWNING
A few individuals who drown, such
as white-water rafters and
kayakers, get pinned or trapped
underwater. Some people dive into
shallow water, strike their heads on
the bottom or on submerged objects,
and are knocked unconscious or
suffer cervical fractures.
Individuals competing to determine
who can stay underwater the longest
or swim the greatest distance
underwater may lose
consciousness, particularly if they
have hyperventilated beforehand.
The mechanism of death for
others is less obvious. Many dive
or jump into cold water and simply
do not come up. No struggle of any
kind is witnessed. Some individuals
plunged into cold water suffer a
cardiac death, usually an abnormal
rhythm such as cardiac arrest or
ventricular fibrillation (immersion
syndrome). In recent studies of the
hearts of a teenage girl and a nine-
year-old boy who died by
drowning, Mayo Clinic College of
Medicine investigators found a
genetic defect in the electrical
conduction system of the hearts that
apparently led to an abnormal
cardiac rhythm, unconsciousness,
and death. They warned that such
defects could be more widespread.
In many accidents of this type,
the sudden contact with cold water
apparently prompts a sudden,
uncontrollable gasp that results in
aspiration of water. This response
(the gasp reflex) is essentially
universal, although it sometimes can
be controlled. Many have observed
that response upon stepping into a
cold shower.
Individuals temporarily trapped
underwater have experienced an
overwhelming compulsion to
breathe. (The time anyone can hold
their breath when submerged in
cold water is much shorter than
when submerged in warm water or
on land—usually one-fourth to one-
third as long.) Apparently some
individuals give in to this urge,
perhaps thinking they can safely
take a single breath to relieve the
respiratory drive until they reach
the surface.
One inhalation or gasp of water
may stop all efforts to reach the
surface; complete asphyxia may not
be necessary. Possibly the water
passes without delay through the
lungs into the blood, and the
reduced osmotic pressure or some
other altered characteristic of the
diluted blood has an immediate
effect on the brain. Individuals who
have been resuscitated after
drowning have described the
sensation as enjoyable, even
“orgasmic.” This hypothetical
mechanism would explain the
drowning of individuals after water
washes over their head in a
turbulent stream or ocean surf but
does not explain the deaths of
individuals who suffer vocal cord
spasm and cannot aspirate water,
which account for approximately 15
percent of all drownings.
Cold shock is the most common
cause of drowning in water colder
than approximately 50°F (10°C)
and affects both the respiratory and
cardiac systems. Upon immersion in
such cold water gasping occurs,
may be uncontrollable, and lasts
approximately one minute. Lack of
understanding of this phenomenon
may result in panic and the
aspiration of more water unless the
head is kept above water.
The sudden cooling of the skin
results in increased peripheral
vascular resistance of superficial
blood vessels. The heart rate and
cardiac output increase. The
outpouring of catecholamines
(epinephrine and related hormones)
increases the risk for fatal cardiac
arrthymias. Hyperventilation causes
the loss of carbon dioxide and
metabolic alkalosis. The subsequent
decrease in cerebral blood flow
can result in disorientation.
In witnessed drownings,
individuals typically pass through
three stages (Table 28-1). The first
is characterized by panic and
struggling, often portrayed as
flailing with the arms. The person is
trying to swim and often is
coughing, sputtering, and calling for
help.
The second stage is
characterized by breath holding or
the absence of breathing (apnea).
The individuals swallow large
amounts of water and often vomit.
During this stage they aspirate
water if laryngospasm is not
present. They may aspirate gastric
contents if they vomit, which can
produce serious lung damage.
During the third stage the
individual loses consciousness. The
airway reflexes are lost and
coughing no longer occurs. Agonal
respirations may move some water
into and out of the lungs. Seizures
may occur as the result of cerebral
hypoxia. Eventually anoxia leads to
ventricular fibrillation or cardiac
arrest.
In cold water local cooling
decreases nerve conduction and
muscle control becomes
uncoordinated and inefficient. After
approximately ten minutes of cold
water immersion, any reasonable
attempt at swimming or self-rescue
becomes almost impossible. At this
point individuals who do not have
flotation devices or a source of
support such as clinging to surface
ice usually drown. (They do not die
from hypothermia.)
Persons who are supported with
the head above water lose
consciousness as the result of
hypothermia in about an hour.
However, they do not die from
hypothermia until approximately
two hours have elapsed.
Table
Stages of Drowning
28-1
PATHOPHYSIOLOGY OF
DROWNING
The common pathway for organ
system failure, morbidity, and
mortality is reduced blood oxygen
concentrations (hypoxemia). The
sequence of events (Table 28-2) is
typically an initial period of panic
and struggle with breath holding.
Subsequently water is inhaled.
Once asphyxia occurs, the person
becomes unconscious and water
passively enters the airways as
airway reflexes disappear.
Cardiopulmonary arrest follows.
Irreversible brain damage may
occur in as little as six minutes.
Electrolyte Abnormalities
In both saltwater and freshwater
drowning, blood concentrations of
electrolytes (sodium, potassium,
chloride, and carbon dioxide) are
usually normal. In freshwater
drowning, elevated potassium
concentrations may result from
breakdown of red blood cells
(lysis.)
Table
Sequence of Drowning
28-2
A unique situation occurs with
drowning in the Dead Sea, which
has an unusually large solute load.
Deaths result from pulmonary
complications as well as the
arrhythmias induced by severe
imbalances of sodium, calcium, and
magnesium. The mortality rate in
one study of Dead Sea drowning
was 50 percent.
Freshwater Drowning
Aspirated fresh water washes
out surfactant, which alters surface
tension in the lungs, resulting in
alveolar collapse and instability.
The capillary and alveolar
membrane damage results in fluid
leakage and subsequent pulmonary
edema. As little as 1 to 3 ml/kg of
aspirated water (approximately 3 to
8 ounces for a 175-pound
individual) has been associated
with significant falls in arterial
oxygen. Fresh water aspirated into
the lungs is rapidly absorbed into
the circulation; however, the
volumes are seldom large enough to
cause significant changes in
electrolyte concentration and
increases in venous pressure are
transitory.
Saltwater Drowning
Seawater is hypertonic; it has
three to four times greater
osmolality than blood. The salt
(sodium chloride) concentration in
seawater is approximately 3.5
percent; blood has a sodium
chloride concentration of 0.9
percent. This hypertonicity is
irritating to the terminal bronchioles
and produces an osmotic gradient
resulting in alveolar fluid
accumulation (pulmonary edema).
Pulmonary edema is compounded
by injury of the alveolar-capillary
membrane produced by the
hypertonic saline.
Increased concentrations of
magnesium have also been
associated with seawater aspiration
and may contribute to low blood
pressure (hypotension),
neuromuscular malfunction,
respiratory depression, and cardiac
abnormalities.
In spite of these differences, the
resuscitative techniques and
subsequent care for individuals
who have drowned in saltwater
usually are not significantly
different from the care of
individuals who have drowned in
fresh water.
COLD WATER DROWNING

Few rescue stories arouse as much
excitement as the “miraculous
survival” of individuals who were
submersed for long periods and
lived. Most have been submerged in
water colder than 50°F (10°C) for
less than thirty minutes:
◆ A five-year-old boy fell into
the waters of a frozen lake and
was submerged for forty
minutes. Upon arrival at the
hospital his temperature was
75.2°F (24°C). He survived
neurologically intact.
◆ A three-year-old girl was
admitted to a hospital after
drowning with a core
temperature of 65.1°F
(18.4°C). After rewarming on
cardiopulmonary bypass, she
survived and had no neurologic
deficits twenty months later.
◆ A seven-year-old boy fell into
a culvert and was found fifteen
minutes later. His temperature
was 80.6°F (27°C). After an
initial period of gross and fine
motor deficits and
psychometric delays, he
ultimately was found to be
above average in school
performance.
◆ The longest submersion
followed by successful
resuscitation to date is sixty-
six minutes. CPR was started
for that two-and-one-half-year-
old girl by an experienced
professional rescue team as
soon as she was retrieved from
41°F (5°C) water. She was
transported in minutes to a
hospital that was prepared for
her arrival and was
immediately rewarmed with
cardiopulmonary bypass.
Adults have also survived such
submersion incidents. One young
lady fell through the ice of a fast-
moving river while skiing. She
struggled for almost forty-five
minutes before she finally became
unconscious. Rescue crews
required another sixty minutes to
remove her from beneath the ice.
Her core temperature had fallen to
55.4°F (13°C) yet she survived. (To
date, hers was the lowest core
temperature resulting from
accidental hypothermia that was
followed by successful
resuscitation.)
The understanding of why
individuals can survive cold water
submersion for as long as sixty-six
minutes with full or partial
neurological recovery has been
advanced by several recent
findings. Explanations for this
phenomenon relate to both the
mechanisms for, and extent of, brain
and body cooling that occurs, as
well as the manner in which this
cooling is protective.
Mechanisms of Cooling
For years children commonly
have been thought to have an
advantage in cold water submersion
incidents because their greater
surface-area-to-mass ratio allows
faster conductive cooling, which
provides cerebral protection due to
the decreased cerebral metabolic
requirements for oxygen. In
addition, the mammalian dive reflex
that produces a slower heart rate
(bradycardia) and shunts blood
flow to important core organs such
as the heart and brain was thought
to be protective. A third possibility
that has recently been explored is
that aspirating cold water may
result in a rapid and deep cooling
during submersion (acute
submersion hypothermia).
The dive reflex is elicited in
diving mammals such as seals by
contact of the face with cold water
and consists of breath holding,
intense constriction of peripheral
blood vessels, bradycardia,
decreased cardiac output, and an
increased mean arterial pressure.
Breath holding prevents drowning
and provides an oxygen reservoir in
the lungs. Selective blood vessel
constriction and progressive
hypertension ensure that the heart
and brain, which are the most
sensitive to hypoxia, are adequately
oxygenated at the expense of less
sensitive organs.
The effectiveness of this reflex
in humans, especially the breath
holding response, is doubtful.
Immersing adults suddenly in 32°F
(0°C) to 95°F (35°C) water
disclosed that colder water greatly
decreased breath holding duration
and that bradycardia was
independent of water temperature.
These studies documented a
reduced effectiveness of the dive
reflex that would actually promote
drowning.
In a second study, children four
to thirteen years old and adults
twenty to sixty-eight years old were
immersed in 84.2°F (29°C) water.
Breath holding duration was shorter
in children than adults, decreased
progressively with age for children
(ten seconds in four-year-olds), and
would be expected to be even
shorter in colder water. The
relative bradycardia was similar—
a 37 percent decrease in heart rate
—in both children and adults. This
led the investigators to conclude
that their findings did not support
the postulate that the dive response
has an important role in the
enhanced resuscitability associated
with cold water drowning and
shifted emphasis to hypothermia as
the mechanism for this phenomenon.
Subsequent studies have
confirmed the distinct bradycardia
induced by facial immersion in cold
water. Bradycardia is inversely
proportional to water temperature,
and the heart rate reduction reaches
about eighteen beats per minute in
50°F (10°C) water.
Interestingly, voluntary breath
holding consists of two phases. The
first “easy phase” is not associated
with breathing movements.
However, increasing arterial
carbon dioxide levels reach a
physiologic breakpoint and begin to
stimulate respiratory movements, so
that during the second “struggle
phase” progressive involuntary
breathing movements do occur.
The protective effect of cooling
depends on the core temperature at
the cessation of oxygen delivery
(asphyxia), and the subsequent rate
and extent of the decrease in core
temperature. Since the early 1960s
surgeons have taken advantage of
the first of these principles by using
cardiopulmonary bypass to cool
neurosurgical patients to a core
temperature of 48°F (9°C), which
allows arrest of brain blood flow
for at least fifty-five minutes with
full neurologic recovery.
Since core temperature is likely
to be near normal at the onset of an
accidental submersion, the second
principle, rapid cooling after the
onset of ischemia, is more
significant. Children have a greater
surface-area-to-mass ratio than
adults, which is well-known to
result in greater rates of core
cooling. However, whether cooling
due to conduction alone could be
responsible for a significant core
cooling is doubtful.
When cold water (38.2°F or
4°C) drowning was studied in
shaved, anesthetized dogs, core
temperatures decreased 20°F
(11°C) in four minutes in the
completely submersed dogs
compared to only 5.4°F (3°C) in
control dogs that were immersed
with their heads out of the water.
Body weight and blood
measurements indicated that water
was actually inhaled and absorbed
by the submersed dogs and that
rapid cooling was produced by
convective heat exchange in the
lungs. Dogs immersed with their
heads out were cooled only by
surface conduction.
Although these studies have
clearly demonstrated continued
ventilation of cold water after
submersion in dogs, this response in
humans has not been documented.
However, reaching the struggle
phase of breath holding during
which involuntary breathing
movements predominate, coupled
with unconsciousness, would be
expected to result in inhalation of
water in at least some
circumstances. Experimental and
anecdotal evidence in humans is
rare. However, one helicopter crash
survivor reported that, after being
trapped underwater for some time,
he recalled feeling he was about to
die and that he was breathing water
in and out just prior to escaping the
cockpit.
Protection from Anoxia by
Cooling
Hypothermia provides an
advantage during anoxic periods
such as cold water submersion
because it produces a situation
called a “metabolic ice-box.”
Whole body or focal hypothermia
has been used to extend the survival
time during surgery under ischemic
conditions for years. For heart
surgery to repair congenital defects,
circulatory arrest has been induced
for sixty minutes at core
temperatures of 59° to 64°F (15° to
18°C) without any subsequent
cerebral dysfunction.
This cerebral protection has
commonly been attributed to the
decreased cerebral metabolic
requirements for oxygen that follow
the Q10 principle, the change of
physical and chemical rates of
reaction with an 18°F (10°C)
change of temperature. The Q10 of
the whole body is about 2, although
higher values are attributed to the
brain. One investigator has shown
that the Q10 of the brain increases
from ~3 between 98° and 80°F (37°
and 27°C) to 4.8 between 80° and
64°F (27° and 18°C). Based on
these values, if the brain could
survive an ischemic insult for five
minutes at 97.6°F (37°C), cooling
to 81°F (27°C) and 63°F (17°C)
would provide fifteen and seventy-
two minutes of protection, based
solely on the decreased cerebral
metabolic requirements for oxygen.
Although long survival times at
brain temperatures below 68°F
(20°C) may be predicted on the
basis of increasing Q10 and
diminishing cerebral metabolic
requirements for oxygen, additional
mechanisms may be required to
explain intact survival after
prolonged submersion in which
core temperatures are above 86°F
(30°C). Over the past decade
several studies directed mainly
toward protection of the brain
during or following cerebral
ischemic events such as strokes
have demonstrated that moderate
brain cooling provides substantial
cerebral protection from ischemic
insult. Various groups of
investigators have demonstrated
that moderate cooling of the rat
brain to 95°F (35°C) and 91°F
(33°C) greatly reduces or even
eliminates neuronal damage caused
by ten to twenty minutes of total
cerebral ischemia. Functional
outcome is improved by cooling;
the response to electrical
stimulation and the performance in
a maze are much better when ten
minutes of ischemia occurs at a
brain temperature of 86°F (30°C)
instead of 99°F (37°C).
Various findings indicate that
when the brain cools only 5.4° to
9°F (3° to 5°C), it is protected
more than would be predicted from
decreased cerebral metabolic
oxygen requirements alone.
Furthermore, even though the
mammalian dive reflex in humans
has limited or no effectiveness, any
cold-induced circulatory
adjustments would favor
conservation of oxygen for the heart
and brain. Finally, cold water
ventilation could accelerate brain
cooling and provide further
protection.
These conclusions are supported
by the limited number of adult case
reports available. Three individuals
aged twenty-one to thirty-one years
were submersed for seventeen to
twenty-five minutes and were
admitted to the hospital with rectal
temperatures ranging from 73° to
90°F (23° to 32°C). All were
resuscitated and rewarmed
successfully. For each of these
individuals, submersion times were
almost double (triple in the
warmest person) the survival times
predicted by the
temperature/cerebral metabolic
oxygen requirements relationship.
These incidents implicate one or
both of the following mechanisms:
the existence of additional
protective cooling mechanisms, or
selective cooling of the brain below
the measured rectal temperatures.
This cooling could be the result of
ventilation of cold water with
limiting of the cooling to central
organs (heart, lungs and brain), not
peripheral tissues. Alternatively,
direct conductive cooling of the
brain by cold water could have
occurred following cardiac arrest.
The skier described a few pages
back encountered circumstances
that helped her survive and
complete her training as a
physician. Brain cooling is
necessary for surviving such a long
anoxic insult, but both the degree of
cooling and the speed of cooling
are protective. This young lady’s
face was in an air pocket that
allowed her to continue breathing
for her first forty-five minutes under
the ice. During this time she became
very hypothermic. As a result her
brain was already cold when she
became unconscious and drowned,
which helped her survive such a
long subsequent period of anoxia.
PRESENTATION OF
SURVIVORS
Individuals who have drowned
and have been successfully
resuscitated present with a
spectrum of findings that range from
a totally normal, asymptomatic
appearance to severe distress. The
heart rate may be normal or rapid
and weak. An abnormal rhythm may
be present. Pulmonary findings
range from normal to shortness of
breath, cyanosis (bluish
discoloration of the skin, lips, and
nails), wheezing, crackling sounds
heard when listening to the chest,
and profound respiratory distress.
Neurologic findings range from an
alert and oriented person to one
who is combative, stuporous, or
comatose.
Traumatic injuries, particularly
head and neck injuries, should be
sought. The head should be
immobilized. Conditions or
circumstances consistent with child
abuse, seizures, or a cardiac
disorder should be ascertained.
MANAGEMENT OF
SURVIVORS
At the Scene
Pressure from the water
produces a 32 to 66 percent
increase in cardiac output in an
individual immersed in it,
particularly if the person is in an
upright position. Individuals
removed from the water suddenly
lose this pressure, and pooling of
blood in the lower extremities
combined with this loss of pressure
can result in circulatory collapse.
Keeping individuals horizontal as
they are lifted from the water helps
prevent this hypotensive
phenomenon.
Initial management should focus
on assessment of the pulmonary,
cardiovascular, and central nervous
systems. If the individual is not
breathing spontaneously and does
not have a pulse, the airway should
be cleared and CPR begun
immediately. Any delay increases
the risk of neurologic damage and
death. Although CPR provided by
nonprofessional bystanders yields
inconsistent results, early CPR is
still recommended.
In studies of hospitalized
individuals who have drowned, no
emergency room or hospital
treatment has been found to be
nearly as effective as competent
CPR administered at the scene of
the accident. By the time the person
has reached a medical facility, the
die has been cast.
Cervical spine injury may be a
precipitating factor in drowning,
particularly when individuals dive
into the water. Attention to head and
neck trauma with appropriate
immobilization is essential.
Additional fractures or internal
injuries can be sought after CPR is
underway.
Recent studies have found that
chest compressions alone provide
better results than CPR that includes
mouth-to-mouth ventilation for
individuals who have suffered heart
attacks. However, individuals who
have had a cardiac arrest due to
asphyxia, which includes people
who have drowned, do require
ventilation as well as chest
compressions.
Mouth-to-mouth ventilation
should be performed with the head
in a neutral position (jaw thrust). If
airway obstruction by a foreign
body is suspected, the Heimlich
maneuver should be implemented.
No evidence supports performing
the Heimlich maneuver to remove
water from the airways.
Mouth-to-mouth ventilation can
be attempted while the drowned
individual is still in the water, but
buoyancy problems usually prevent
effective chest compressions.
Many people who have drowned
are hypothermic as the result of
immersion in cold water. Although
hypothermia helps protect the brain
from anoxia association with the
asphyxia of drowning, heat loss
should be minimized as soon as
effective CPR is underway. Heat
loss through evaporation and
convection should be limited by
sheltering individuals from the
wind, removing wet clothing, and
covering them with insulating
materials such as blankets or
clothing.
Defibrillation is ineffective if
the heart is colder than about 90°F
(32°C).
Distinction Between Drowning

and Hypothermia
For individuals immersed in
very cold water with a personal
flotation device (PFD) for long
enough to be rendered unconscious
by hypothermia, determining
whether they have drowned or are
only severely hypothermic can be
difficult. If they have drowned, they
need CPR. However, if they are
hypothermic, CPR would probably
initiate ventricular fibrillation, and
the hearts of individuals cold
enough to be unconscious do not
respond to electric shocks.
If the individuals are supported
by their PFDs with their heads out
of the water and their hair is not
wet, they are probably hypothermic
and only need rewarming. Their
heart rate commonly is so slow and
weak that it is difficult to detect.
Before such individuals are
assumed to have drowned, the
carotid artery should be palpated
for a pulse. Palpation should be
continued for at least a minute,
preferably three minutes. In a
suitable situation such palpation
could be performed while the
individuals are still in the water
and their circulation is supported by
the pressure of the water. If the
situation does not permit palpation
while the individuals are in the
water, they should be gently lifted
from the water in a horizontal
position and carotid palpation
performed in the rescue vessel.
If an ambulance or similar
source of medical support is
nearby, taking an electrocardiogram
to determine whether the heart is
beating is probably worth the time
it would require. The delay
probably would not have an
adverse effect on an individual who
had drowned and could avoid
initiating ventricular fibrillation for
a person who was only
hypothermic.
Treatment en Route to a Medical

Facility
If the individual has not
responded to CPR, efforts usually
should be continued while en route
to a medical facility. The person
should be kept warm, but
overzealous warming should be
avoided. Shivering, although a good
prognostic sign, does increase
tissue oxygen demands.
If the person is conscious and
able to swallow, warm drinks
containing sugar may provide some
benefit. Supplemental oxygen can
be administered if available.
A medical facility that has the
ability to provide cardiac bypass
rewarming and circulatory support
is ideal if the individual is still not
breathing and is pulseless.
PREVENTING DROWNING
Passive strategies appear to be
the most successful for preventing
drowning in young people.
Unfortunately, passive strategies
tend to have little benefit for
adolescents. Primary strategies that
require thought and judgment have
also usually not been effective in
adolescents.
Fences
Probably the largest impact of
passive strategies has been with
residential swimming pools. Fences
have been shown to reduce the
incidence of drowning by
approximately 50 percent.
However, fences may not be
effective if the pool is open to the
house or a wall of the house with
openable windows forms part of the
fence.
Supervision
Supervision has a major impact
on the incidence of drowning. The
quality and proximity of
supervision are both significant.
The case fatality rate for swimmers
supervised by adults is 30 percent,
by lifeguards 42 percent, and by
peers 71 percent.
Among children aged one to four
years, most drownings occur in
residential swimming pools. Most
young children who drown in pools
were last seen inside the home, had
been out of sight less than five
minutes, and were in the care of one
or both parents. Young children
should never be left alone, even
momentarily, where they have
access to standing water.
Lifeguards
No studies document the
effectiveness of lifeguards, but they
are widely considered to have
prevented many drownings and
effectively resuscitated many
drowned individuals. However,
CPR competency is not mandated
for lifeguards in all localities.
Upgrading lifeguard effectiveness
has been recommended.
Swimming Techniques
In a review of studies of the
impact of swimming lessons in the
prevention of drowning, the ability
to swim was found sometimes to
lead to overconfidence and
swimming in hazardous situations.
Although swimming lessons are
recommended for ages five and
older, educational programs that
explain high-risk situations and
avoidance activities may be more
beneficial.
Personal Flotation Devices

Coast Guard studies in 2003
indicated that over 90 percent of
boating-related drowning could
have been prevented by personal
flotation devices.
Alcohol and Other Drugs

Legal and societal acceptance of
imbibing alcohol during
recreational activities is lax when
compared to driving.
Advertisements widely promote its
appeal. Any drinking or use of other
recreational drugs in an aquatic
environment is risky and should be
discouraged.
AAP Recommendations
The American Academy of
Pediatrics (AAP) has issued
recommendations for various age
groups.
Infants and children

◆ Careful supervision
◆ Emptying all water containers
such as buckets and kiddie
pools
◆ Not allowing swimming
lessons to provide a false
sense of security
◆ Four-sided fences around
swimming pools
◆ CPR instruction and 911 phone
access
◆ Flotation devices
Children five to twelve years
◆ Swimming instruction
◆ Buddy swimming with
supervision
◆ Personal flotation devices
◆ Knowing the depth of the water
◆ Recognizing drowning risks
such as skating on thin ice
Adolescents
◆ Avoidance of alcohol and drug
use
◆ CPR instruction
◆ Prohibiting alcohol during boat
operation
EFFECTS ON FAMILIES
Fatal drownings have a
devastating effect on families. After
such deaths 24 percent of the
parents separate. Posttraumatic
stress disorder persists for years—
perhaps forever—in family
members. Substance abuse, alcohol
and drugs, and sleep disturbances
are common. Siblings may
experience incapacitating
survivor’s guilt.
The responsibility for preventing
or, at least, ameliorating such
distress in family members rests
with the medical personnel
providing the initial care,
particularly emergency room
physicians who are in a position to
summon professionals to provide
counseling. No one else is in a
position to know about the need for
psychological care until much later.
Counseling should be obtained
immediately. Any delay aggravates
feelings of guilt and makes full
recovery more difficult.
One tragedy must not be allowed
to generate more.
CHAPTER 29
LIGHTNING
INJURIES
Eric L. Johnson, M.D.
From the beginning of time to

today’s fast-paced, high-tech world,
the phenomenon known as lightning
has continually amazed, amused,
and at times abused. It is an
astounding natural event. Scientists
who study lightning have a better
understanding today of the process
by which it is produced, but more
needs to be learned. The cloud
conditions that generate lightning
are well known, but no one can
forecast the location or time of the
next stroke.
This presentation focuses on
what is known about the science of
lightning, injury prevention,
particularly while out-of-doors, and
treatment of individuals who have
been injured by lightning. However,
once individuals have been
“struck,” they enter a sequence over
which they have little control.
Prevention is the key! Lightning
must be respected for its power,
beauty, and devastating potential.
LIGHTNING FATALITIES
Lightning was the second most
common cause of weather-related
death over the forty-year period
from 1962 to 2002. Only floods,
many of which are also produced
by thunderstorms, killed more
people during this time. Lightning
kills more people than hurricanes
and tornados combined. During the
ten-year period 1940 through 1949
approximately 330 people were
killed each year by lightning in the
United States. Now, approximately
one hundred people lose their lives
that way each year. Of equal note,
however, only about 10 percent of
the individuals hit by lightning are
killed. The remaining 90 percent
may suffer long-lasting injuries or
disabilities, and lightning may even
have a lifetime impact.
Many think that the chances of
being struck are very remote. The
data say otherwise. Lightning
strikes the ground in the United
States about 25 million times a
year. The National Weather Service
estimates the chance of being struck
as 1 in 240,000 per year, hence
over an eighty-year lifespan the
odds become 1 in 3000. Assuming
ten family members or close friends
per individual, the chance is 1 in
300 that someone well known will
be affected by a lightning strike.
The individual risk will obviously
be greater in higher-risk situations
such as a summer afternoon in the
Rocky Mountains.
PHYSICS OF LIGHTNING
Lightning is a natural event that
occurs mostly during thunderstorms.
(On rare occasions lightning has
also been seen in volcanic
eruptions, extremely intense forest
fires, surface nuclear detonations,
heavy snowstorms, and large
hurricanes.) Over 2000
thunderstorms are in progress
above Earth’s surface at any one
time, and they generate
approximately 8 million lightning
strikes each day, or about 100
cloud-to-ground discharges every
second. Understanding the life cycle
of thunderstorms and the risks
associated with them is essential.
The basic ingredients required for a
thunderstorm to develop are
moisture, instability, and a lifting
mechanism. Each thunderstorm has
three phases (Fig. 29-1):
1. Growth
2. Maturation
3. Dissipation
During the development, growth,
or towering cumulonimbus stage,
the thunderstorm cloud is dominated
by updrafts that may carry it up to
20,000 feet (6 km) and create
turbulence around the periphery.
With maturation, the storm cell
has both updrafts and downdrafts,
and may rise as high as 40,000 to
60,000 feet (12 to 18 km). This
phase is the most dangerous for
hail, flooding, and damaging winds.
The dissolution phase heralds
the death of the thunderstorm. This
last stage is highlighted by
downdrafts, and as the storm no
longer has moisture uplifting, it
begins to dissipate. Light winds and
rain dominate, and the cloud has a
classic anvil top.
Figure 29-1. Growth, maturation, and
dissipation of a thunderstorm 1
Lightning can strike well outside

the rain area, miles away from the
storm, even beyond sight, and can
also strike from debris clouds tens
of minutes after the decay of the
thunderstorm. Safety requires time
and distance before the storm,
during the storm, and after the
storm’s dissipation.
As ice and water particles
within a cloud (hydrometeors) grow
and interact, some become charged,
possibly through collisions. The
smaller particles are thought to
acquire a positive charge, whereas
the larger particles acquire a more
negative charge. These particles
tend to separate under the
influences of updrafts and gravity
until the upper portion of the cloud
acquires a net positive charge and
the lower portion of the cloud
becomes negatively charged. The
separation of charges produces an
enormous electric potential—
millions of volts—both within the
cloud and between the cloud and
ground. Eventually the electrical
resistance of the air breaks down
and a flash begins. Lightning is an
electrical discharge between
positive and negative regions of a
thundercloud.
With the initial breakdown of the
aerial resistance, a streamer begins
to propagate downward toward
Earth’s surface. The streamer,
which cannot be seen, moves in
discrete steps of about 50 meters, in
what is called a stepped leader. As
it grows, it creates an ionized path,
depositing charge along the channel.
As the stepped leader nears Earth’s
surface, a large potential difference
is generated between the end of the
leader and the surface. Typically, a
streamer is launched from the
surface and intercepts the
descending stepped leader just
before it reaches the ground. Once a
connecting path is achieved, a
return stroke flies up the already
ionized path at half the speed of
light. This return stroke releases
tremendous energy, bright light, and
thunder. The average number of
strokes in each bolt of lightning is
four, each lasting about thirty
milliseconds, which causes
lightning to flicker.
Occasionally, when a
thunderstorm grows over a tall,
earth-grounded object, such as a
radio antenna, an upward leader
may propagate from the object
toward the cloud. This “ground-to-
cloud” flash generally transfers a
net positive charge to earth and is
characterized by upward-pointing
branches.
The initial breakdown and
propagation are similar for cloud-
to-cloud or intracloud lightning, but
the discharge occurs between
regions of opposite charge. Without
the benefit of air conducting the
strike to Earth’s surface, intracloud
lightning does not produce a return
stroke. Nevertheless, tremendous
energy, bright light, and thunder are
still produced by intracloud
lightning.
Table
Facts about Lightning
29-1
The spot where lightning is

going to strike is not determined
until the bolt is about 30 meters
from the ground or object. Shorter
objects may be struck even though a
taller object is nearby. Associated
step voltages and surface arcs may
be fatal more than 40 meters from
the initial strike point. Lightning is
unpredictable!
Lightning channels as long as 10
miles have been observed. These
can produce a “bolt from the blue,”
a lightning strike that occurs without
thunderclouds overhead or even
nearby. Lightning is very
unpredictable! (Table 29-1)
AREAS WITH GREATEST

LIGHTNING RISK
Thunderstorms can occur almost
anywhere, but individuals enjoying
outdoor activities should be aware
of the geographic, seasonal, and
diurnal tendencies. Those who live
in the Rocky Mountains clearly
understand that during any summer
afternoon, the chance of
thunderstorm development with
associated lightning risk exists. In
the United States, the National
Lightning Detection Network
(NLDN) measures lightning strike
densities, which are greatest over
central Florida (more than ten
strikes/km2). The Southeast and
Midwest have the next greatest
lightning strike frequency. The risk
starts primarily in May, peaks in
July, and falls abruptly in
September. The lowest frequency is
in January. The peak daytime hours
are afternoons and evenings. With
seasonal variations, during certain
weeks of the summer the front range
of the Rockies equals the flash
density of central Florida.
The number of lightning
casualties is dependent upon many
elements, such as the severity of the
thunderstorm and lightning strike
density, population density,
popularity of outdoor activities,
awareness of lightning risk, and
safety precautions utilized. One
major factor for those who enjoy
the mountains is higher elevation.
Sunday has the most casualties;
Saturday is next—the days more
people are outdoors. The most
common hours are July between
noon and 6:00 PM local time. Males
are struck more often than females
because more men take part in
outdoor activities.
Even though the highest numbers
of lightning deaths are in Florida,
Texas, Michigan, Pennsylvania,
North Carolina, and New York, the
highest per capita states are
Wyoming, New Mexico, Florida,
Arkansas, and Colorado (Table 29-
2). The Rocky Mountain States have
a low population and lightning flash
density but have a number of people
at high risk because they are outside
at times of high strike numbers.
More Facts About Lightning

◆ From National Center for
Health Statistics data: From
1980 to 1995, 85 percent of
lightning fatalities were men,
and 68 percent were fifteento
forty-year-olds. The annual
death rate from lightning was
highest among persons fifteen
to nineteen years old.
Table Lightning Casualty

29-2 Demographics
• 92 percent of casualties
occur between May and
September, peak in July
• 73 percent of casualties
occurred in the afternoon
from noon to 6:00 PM
• Highest numbers of deaths
occur in Florida and Texas
(National Center for
Health Statistics [NCHS])
From population normalized
data, Wyoming has the highest
lightning casualty rate
(0.196/100,000 inhabitants),
followed by New Mexico,
Florida, Arkansas, and
Colorado.
◆ From Colorado data: 66
percent of incidents had only
one casualty; the maximum
number of casualties in a single
incident was twelve.
◆ In Colorado: More people
became casualties during
recreation (52 percent) than
during employment (25
percent).
◆ In Florida: More people
became casualties during
employment (38 percent) than
during recreation (32 percent).
◆ In Colorado: More people
were injured by lightning near
or at the summit of a mountain
ridge (18 percent) and in the
vicinity of trees (16 percent).
◆ In Florida: A location close to
water was the most common
site (25 percent), followed by
proximity to trees (22 percent),
and during transportation (10
percent).
◆ Analyses for Colorado and
Florida found a high number of
injured individuals on golf
courses. However, the golf-
related frequency was equaled
or exceeded by several other
activities and locations.
◆ Military data from 1998 to
2001 found that 142 lightning
strikes caused 350 injuries and
one death of service members.
In October 1997, the National
Oceanic and Atmospheric
Administration (NOAA) published
thirty-five years of U.S. lightning
statistics. The locations at which
individuals were injured or killed
were as follows:
40 percent: site not reported
27 percent: open fields and
recreation areas
14 percent: under trees
8 percent: water related
5 percent: golfing or golfers
under trees
3 percent: heavy equipment and
machinery related
2.4 percent: corded telephone
related
MECHANISMS OF
LIGHTNING INJURY
Lightning can strike a human body
in several ways:
Direct strike: Initial contact is with
a human body. This type of
strike produces the most severe
injuries and is associated with
a high level of mortality and
morbidity because voltages and
current are high and flow
through the person. Carrying an
ice ax, golf club, or umbrella
increases the risk of a strike.
Side or splash strike: Initial
contact is with a tree or some
other object and is discharged
through the air to the person.
This type of strike is most
common and can be associated
with multiple fatalities.
Contact strike: A person is in
contact with an object that is
struck by lightning. If the object
is a metal rail or fence and a
number of people are in contact
with it, the number of injured
or killed can be high.
Step, stride, or ground strike:
Initial contact is with the
ground or flows to ground from
another object, but ripples of
current travel outward.
Electrical current enters one
leg and exits though the other
because the path of least
resistance is through the body,
not through the ground.
Discharges that strike a human
body follow two routes: Electricity
can spread over the skin, or it can
enter the body. Usually both paths
are followed, but the voltage of a
lightning bolt is so great that most
of the charge passes to ground on
the outside and does not pass
through the body.
If a significant amount of
moisture is on the person’s skin—
perspiration or rain—it may be
instantly vaporized. The resulting
water vapor, a gas, can explosively
rip the clothing from a person’s
body(flashover effect).
Many variables can affect the
person’s ultimate outcome. They
include these:
◆ Type of strike
◆ Amperage and voltage of the
lightning strike
◆ Current pathway through or
over the body
◆ Resistance of tissues
◆ Duration
◆ Blunt trauma from being
knocked about by the strike
◆ Environmental factors
One major difference between
lightning and high-voltage electrical
injuries is the very high current, yet
very short duration, of lightning.
These facts indicate that
accurately predicting the
consequence of being struck is
challenging at best and usually
nearly impossible.
EFFECTS OF LIGHTNING
STRIKES
Direct lightning strikes often
produce immediately lethal, global
cardiac injuries. If the electrical
charge is less severe, as occurs
with splash injuries or ground
currents, it may only depolarize the
cardiac conduction system, causing
the heart to stop beating (asystole).
(Asystole is more common than
ventricular fibrillation following a
lightning strike.) However, the
innate rhythmicity of the heart
usually causes it to resume rhythmic
contractions.
Subsequently, as the result of
hypoxia caused by the absence of
breathing, the heart may go into
terminal ventricular fibrillation.
The nervous system is
particularly vulnerable to lightning.
Immediate as well as prolonged
abnormalities occur. The most
significant functional disruption is
cessation of breathing. Cardiac
contractions may be resumed
promptly, but resumption of
respiratory function often is delayed
from thirty minutes to two hours. If
resuscitation is not available, the
resulting hypoxia leads to
ventricular fibrillation and death.
Several cutaneous injuries are
characteristic of lightning strikes.
Feathering is the diagnostic change.
This fernlike pattern branches away
from a central spot, can extend 5 to
20 cm, appears within an hour after
the incident, and resolves the same
day. The pattern is very similar to
the experimentally induced
electrical changes called
Lichtenberg figures that were
described in the eighteenth century.
Experimental studies have led
investigators to deduce that these
lesions are caused by positive
discharges over the skin and are not
actually burns.
A flowerlike pattern produced
by punctate burns is a less common
skin manifestation of a lightning
strike. The burns may be partial or
full thickness. Linear partial-
thickness burns may occur in areas
that are moist, such as the armpit or
groin. In contrast to injuries from
high-voltage, humanmade
electricity, distinct entrance and exit
points may not be apparent.
Thermal burns may result from
ignition of clothing or from metal
objects in contact with the skin,
such as bracelets or necklaces.
The path of the current as it
passes through the point of contact
to the ground often determines the
type of injury:
◆ Hand-to-hand current can
produce transection of the
spinal cord in the lower neck
and also can cause current-
induced cardiac rhythm
abnormalities, particularly
asystole. (Mortality rate > 60
percent)
◆ Hand-to-foot current produces
current-induced cardiac rhythm
abnormalities. (Mortality rate
> 20 percent)
◆ Foot-to-foot current produces
fewer major problems.
(Mortality rate < 5 percent)
CARE FOR INDIVIDUALS

STRUCK BY LIGHTNING
If the lightning strike is not
witnessed, determining what has
happened to the person or persons
is often difficult. The differential
diagnoses include trauma and
assault, heart attack, stroke, seizure,
diabetes, and all the other disorders
that must be considered for an
unconscious person with an
unknown history. The presence of
typical burn patterns, outdoor
location with a thunderstorm
present, or rupture of the eardrums
are diagnostic clues.
The major cause of death in
lightning injuries is
cardiopulmonary arrest. Initial
assessment and treatment must be
instituted as quickly as possible.
Most lightning strikes involve
single individuals; however, groups
are sometimes involved. Reverse
triage is a term applied to the
appraisal of multiple individuals
injured by lightning. Persons who
appear dead following the strike
should be treated before those who
show signs of life because the
person who appears dead may be
undergoing a secondary cardiac
arrest caused by respiratory arrest.
If people hit by lightning show signs
of life, they have survived. If they
appear dead, they should be given
an opportunity to outlast the period
of respiratory arrest, either by being
given basic life support through
(CPR) or, if they have a heartbeat,
through mouth-to-mouth
resuscitation.
Steps to be taken include the
following:
◆ The scene should be surveyed
for safety and the injured
individual(s) should be
assessed. (People who have
been hit by lightning are not
“electrified” and are safe to
touch and treat.)
◆ Emergency services (911)
should be telephoned as soon
as possible in urban situations.
◆ Those who appear dead should
be treated first. Others should
be made safe and stabilized
whenever possible.
◆ CPR or mouth-to-mouth
ventilation should be initiated
with precautions for the
presence of blunt injuries such
as fractures of the cervical
spine, back, and long bones.
◆ Care should be taken to avoid
hypothermia in a wet, cool
environment.
◆ Rescuers must be prepared to
provide prolonged
resuscitation but should
probably stop after thirty
minutes of chest compressions
if cardiac function has not
resumed.
PREVENTING LIGHTNING
INJURIES
When thunder roars, go
indoors!
Obviously lightning injuries should

be prevented, and yet no absolutely
safe refuge exists. With basic safety
measures, including going indoors
when possible, the risk of harm can
be minimized.
Flash-to-Bang
Thunder from a lightning flash
travels 1 mile (1.6 km) every five
seconds. (The appearance of the
lightning bolt is virtually
instantaneous.) Counting the
seconds from the visible flash to the
audible bang and dividing by five
provides an approximation of the
distance in miles to the last strike.
In urban areas or mountains, this
may prove difficult.
30-30 Rule
If the flash-to-bang is thirty
seconds or less (hence 6 miles or
less), shelter should be sought and
stayed in for a minimum of thirty
minutes, or until the storm has
clearly passed. Shelter should be
entered immediately. Half the
flashes in a thunderstorm are about
5.6 miles (9 km) apart. The
National Severe Storms Laboratory
has concluded, “It appears the
safety rules need to be modified to
increase the distance from a
previous flash that can be
considered relatively safe to at
least 10 to 13 km (6 to 8 miles).”
Although the 30-30 rule is an
excellent plan, it cannot predict the
first lightning strike.
Many casualties occur before the
thunderstorm has started, fewer
during the rain. However, more
deaths occur after the storm has
passed. Many people ignore the
threat once precipitation has
stopped and leave shelter too early.
Lightning Safe Shelters

No place is absolutely safe from
lightning, but some places are much
safer than others. The safest
location during lightning activity is
a large enclosed building that has
wiring and plumbing. If lightning
strikes such buildings, or an outside
tree or telephone pole, the
electrical current from the flash
travels through the wiring or the
plumbing into the ground. Because
the current may be traveling through
pipes or wires, individuals in the
building must stay away from
showers, tubs, and sinks and
electronic equipment such as
televisions, radios, computers, and
electric tools. If electrical devices
are to be unplugged, this should be
accomplished before the storm
arrives. Land-line telephones must
not be used, although cellular
telephones are safe. Inhabitants
should also stay away from
windows and doors because
lightning tends to enter through
those portals. Although the
basements of buildings are safe,
individuals should not lie on
concrete floors or lean against
concrete walls. These structures
usually contain metal reinforcing
rods that conduct electricity.
Buildings that are unsafe include
carports, covered but open garages,
covered patios, picnic shelters,
beach shacks and pavilions, golf
shelters, tents of any type, and small
buildings such as sheds and
greenhouses that do not have
electricity or plumbing.
The second safest location is an
enclosed metal vehicle—car, truck,
SUV, minivan, or bus—but not a
convertible, bike, or other topless
or softtop vehicle. All doors must
be closed and windows rolled up.
People inside the vehicle must not
touch any metal surfaces.
Another relatively safe location
recommended by the National
Weather Service is below a bridge
or an overpass. The steel girders
must not be touched. Individuals
should move away from bicycles or
motorcycles and remain on dry
surfaces if possible. Overpasses
are engineered structures and are
likely to be properly grounded.
Although they may be higher than
the surrounding landscape, if struck
by lightning the electrical current is
usually channeled safely into the
ground. Individuals under a bridge
should stay away from water but
must be alert for rapidly rising
water.
The National Weather Service
also suggests shelter directly
underneath high voltage electrical
as a relatively safe location.
Individuals should stay at least 50
feet away from the large metal
towers from which wires are
suspended. These wires and towers
are designed to accommodate
lightning strikes by conducting the
current safely deep into the ground.
Boats with cabins offer a safer
but not a perfect environment.
Safety is increased if the boat has a
properly installed lightning
protection system. Individuals
inside the cabin must stay away
from metal and all electrical
components. They must stay off the
radio unless in an absolute
emergency!
Individuals in small vessels
when lightning becomes a threat
should anchor the boat if an anchor
is available and should get as low
as possible. If scuba divers are
diving from a boat with a safe
cabin, they are safest there.
Otherwise they should dive deep
into the water for the duration of the
storm—or as long as possible.
However, the first choice is to head
for shore and get into a safe
building or vehicle.
When Shelter Is Unavailable

Individuals who cannot flee to a
safer location must minimize the
threat of being struck. They should
move from higher to lower
elevations, get off ridges, and avoid
open areas such as meadows, sports
fields, beaches, and golf courses.
They should avoid tall, isolated
objects, such as trees, poles, and
light posts. They should not remain
in open vehicles such as farm
tractors, riding lawnmowers, and
golf carts. (Sunroofs offer no
protection.) All water-related
activities, such as swimming
(including indoor pools), boating,
and fishing, should be terminated.
Unprotected open structures such
as picnic pavilions, rain shelters,
and bus stops must be avoided.
Contact with metal fences, metal
bleachers, or other long metal
structures also must be avoided.
Sheltering under trees to keep dry
during a thunderstorm is an
invitation for disaster.
If lightning is about to strike, it
sometimes provides a very few
seconds of warning. Sometimes hair
may stand on end, skin tingle, light
metal objects vibrate, or a crackling
or “kee-kee” sound can be heard. If
this happens and more than one
person is present, they should
spread out so several body lengths
are between each person to reduce
the risk of having a strike jump from
one person to another. Once spread
out, they should use the “lightning
crouch” by putting their feet
together, squatting down, tucking
their heads, and covering their ears.
When the immediate threat of
lightning has passed, they should
continue to the safest place
possible.
Handheld lightning detectors
have become more affordable and
more popular in recent years.
Although potentially helpful, their
performances may not been have
been independently, rigorously, and
objectively verified. Some may fail
to detect weak or intermittent, but
still deadly, lightning. Many
detectors have been installed and
used incorrectly. These devices
should be used only as a back-up to
the 30-30 rule.
Commercial services that
provide automatic notification when
lightning has been detected by the
National Lightning Detection
Network (NLDN) within user-
specified distances to an activity or
site are available. The alert can be
sent via pager, email, or cell phone.
These services are reasonably
priced and can be a useful
component of a lightning safety plan
for organized outdoor activities.
The best detection technology,
however, cannot provide long lead
times from a thunderstorm forming
rapidly overhead. Individuals who
are outdoors must still watch the
sky and be ready to proceed to a
safer location, hopefully before the
first lightning.
Lightning Safety Levels

Level 1: The weather should be
watched. Anyone planning an
outdoor activity should get a
weather forecast and know
local weather patterns.
Level 2: Individuals should start
thinking about shelter and, if a
thunderstorm is present, use the
30-30 rule.
Level 3: With lightning near,
everyone should enter a safe
shelter.
Level 4: If no safe locations are
available, the best actions to
avoid being struck should be
taken.
Level 5: If a strike is imminent, the
lightning safety position should
be assumed. If more than one
person is present, the group
should spread out to prevent
lightning that has struck one
member of the group from
striking another.
Level 6: If someone has been
struck, active treatment should
begin.
(More information about
lightning is available at the
websites of the American
Meteorological Society,
www.ametsoc.org/pilicy/Lightning_S
and the National Weather Service,
www.lightningsafety.noaa.gof/index.h
____________
REFERENCE
1. Adapted from the National
Weather Service,
www.nws.noaa.gov
CHAPTER 30
AVALANCHE
INJURIES
Martin I. Radwin, M.D.
Avalanches cause a significant

number of deaths among skiers,
snowboarders, skimobilers,
snowshoers, and hikers. According
to the Colorado Avalanche
Information Center, avalanches
have killed an average of twenty-
five people a year in the United
States over the last ten winters.
Over the last three years, thirty-
eight snowmobilers, twenty-two
backcountry skiers, nine in-bounds
skiers, eight snowshoers and hikers,
and six snowboarders have been
killed by avalanches. In Canada
from 1984 to 2005, 204 avalanche
deaths occurred. More avalanche
deaths occur every year in the
European Alps, although many of
the deaths in that area stem from
avalanches that enter villages.
AVALANCHE MORTALITY
Asphyxiation is the most
common cause of death during
avalanche burial. About 75 percent
of avalanche deaths are the result of
asphyxiation, about 25 percent are
caused by trauma, and very few
result from hypothermia. Because
asphyxiation occurs rapidly during
avalanche burial, time to extrication
is a major determinant of survival.
Individuals fully buried in an
avalanche have a greater than 90
percent chance of survival if
extricated within fifteen minutes,
but only 30 percent after about
thirtyfive minutes, emphasizing the
need for companion rescue at the
avalanche site. Survival beyond
thirty minutes of burial requires an
adequate air pocket for breathing,
and if the air pocket is large
enough, buried individuals may
survive for hours and develop
severe hypothermia.
AVALANCHE SURVIVAL
PROBABILITY
Because death during avalanche
burial most commonly occurs from
asphyxiation within the first fifteen
to thirty-five minutes, rapid access
to the airway is the most important
determinant of survival. Other
factors that influence survival
include burial depth, exposed body
parts or attached objects, and
ability to self-rescue in a partial
burial. If people buried by
avalanches are unable to extricate
themselves, then the greatest chance
of survival rests with companion
rescue experienced with an
avalanche transceiver, a probe, and
a shovel (after a hasty search for
surface clues). Organized rescue
teams usually arrive on the scene
after thirty-five minutes have
elapsed, and chances of survival
are markedly reduced.
In avalanche burials in the
United States since 1950, the
survival rate has been 63 percent
for companion rescue but only 19
percent for organized rescue (Table
30-1). In the United States overall
survival of avalanche burials has
been 40 percent, which is identical
to the 40 percent survival rate from
Austria. The Austrian study found
an increased survival rate of 46
percent when avalanche
transceivers were used for rescue,
as compared to 32 percent for other
methods of rescue. Another study
combining data from Switzerland
and Austria confirmed these
findings: a 45 percent survival rate
when transceivers were used to
locate totally buried persons as
compared to 30 percent survival
without transceivers. The difference
in survival was primarily the result
of shorter burial time: 25 minutes as
compared to 125 minutes.
Rescue transceivers are an
efficient method to locate buried
individuals, but two problems have
limited the number of survivors
who were wearing transceivers.
First, few who wear transceivers
are well practiced in using them
instantly and efficiently for rapid
localization; and second, even with
a quick pinpointing of the burial
location, extricating the person from
deeper burials may take too long.
Survival by Type of Rescue
Table
for Individuals Buried by
30-1
Avalanches 1950–2004
Recovering a person buried 3

feet deep (1 meter) requires
removal of at least 1.5 tons of
snow. Recent attention has focused
on developing an efficient
shoveling technique to decrease the
time consumed by this stage of
rescue. The current technique calls
for at least two to three shovelers to
work slightly downslope of the
probe strike to create a stairlike or
platform approach to the buried
individual and to optimize work
efficiency. The final shape of the
rescue pit allows access for more
rescuers and a reasonable work
area for medical assistance. As
with transceivers, this method
requires some practice but can be
learned easily. It avoids the
tendency to dig straight down into a
tight hole that excludes multiple
rescuers.
Since the first transceiver rescue
in 1974, only 40 percent (55 of
138) of buried individuals in the
United States found with
transceivers have been recovered
alive. However, prior to the year
2000 only 30 percent of transceiver
users survived; since 2000, 57
percent have survived. The year
2000 marked the beginning of
widespread employment of digital
avalanche rescue transceivers that
most inexperienced people find
easier to use. Increased awareness,
access to automated transceiver
parks, and teaching seminars have
also contributed to this statistic.
Transceivers give no guarantee of
live rescue. Regular practice and
training are essential for saving a
life with a transceiver with a target
of localization in under five
minutes.
AVALANCHE TRAUMA
Traumatic injury to persons caught
in avalanches is dependent on the
terrain where the avalanche occurs.
If a person is carried through trees
or over rock bands, then traumatic
injury is more likely and may result
in death. In one study traumatic
injuries occurred in 25 percent of
survivors of avalanche accidents
that included both partial and
complete burials in Utah and
Europe (Table 30-2). The most
common traumatic injuries were
major orthopedic, soft-tissue, and
head and neck injuries.
Injuries in Survivors of
Table
Avalanche Accidents
30-2
(Partial and Total Burials)
In a review of autopsy reports

from twenty-eight avalanche deaths
in Utah over a seven-year period,
half of twenty-two people caught in
avalanches who died from
asphyxiation had mild or moderate
traumatic brain injury, which could
have caused a depressed level of
consciousness and contributed to
death from asphyxiation. All six of
the avalanche deaths caused by
trauma had severe head injuries.
Recent data from Utah covering
a period from 1989 to 2006 and
involving fifty-six avalanche
fatalities found a mere 5 percent
mortality from trauma alone and 9
percent from combined trauma and
asphyxiation. A total of 86 percent
of the fatalities were felt to be
primarily asphyxiation.
In a European study of 105
avalanche accident burials that
produced a 34 percent mortality in
Austria, the most common traumatic
injuries were lower-extremity
fractures and shoulder dislocations
that did not contribute to mortality.
Only two of thirty-six deaths were
caused by trauma, in both cases
isolated cervical spine fracture
dislocations. Asphyxiation was the
cause of death in thirty-three,
hypothermia in one. This study
emphasized the concept of
geographic terrain variability and
its relationship to the differing
contributions of trauma to
avalanche mortality.
PREVENTION OF AVALANCHE
ASPHYXIA
Asphyxiation occurs during
avalanche burial because the person
either inhales snow that occludes
the upper airway or because
expired air is rebreathed. Acute
upper airway obstruction resulting
in asphyxiation is one of the causes
of early asphyxiation during the first
fifteen to thirty minutes of
avalanche burial. Asphyxiation due
to rebreathing expired air may also
occur during the first fifteen to thirty
minutes of avalanche burial if there
is no air pocket for breathing, or it
may be delayed if an air pocket is
present. Inspired air contains 21
percent oxygen (O2) and less than
0.03 percent carbon dioxide (CO2),
whereas expired air contains about
16 percent O2 and 5 percent CO2.
Rebreathing expired air in an
enclosed space results in
progressive hypoxia (decreased
blood oxygen concentrations) and
hypercapnia (increased blood
carbon dioxide concentrations) that
eventually cause death from
asphyxiation. The larger the air
pocket, the greater the surface area
for diffusion of expired air into the
snowpack and diffusion of air from
the snowpack into the air pocket,
and the longer the survival time
before death occurs from
asphyxiation.
Ice mask formation around the
buried person’s face or air pocket
surface accelerates asphyxiation by
preventing diffusion of expired air
away from the air pocket. Ice mask
formation occurs when water in
heated and humidified expired air
condenses, freezes on the snow
surface in front of the face, and
forms a barrier that is impermeable
to diffusion of air.
Utah investigators demonstrated
that sufficient air is present in
densely packed snow to permit
normal oxygenation and ventilation
as long as all expired air is
diverted out of the snowpack. They
studied individuals totally buried in
densely compacted snow while
inhaling air directly from the
snowpack (density 300 to 680
kg/m3 or 30 to 68 percent water)
through a two-way nonrebreathing
valve attached to respiratory tubing
that diverted all expired air to the
snow surface. Individuals
maintained normal oxygenation and
ventilation for up to the protocol
target of ninety minutes. This study
demonstrated that sufficient air for
breathing is present in snow of
similar density to avalanche debris,
as long as expired air is not
rebreathed.
This is the principle behind a
breathing device designed to
prolong survival during avalanche
burial, the AvaLung® (Black
Diamond Equipment, Ltd., Salt
Lake City, Utah,
www/bdel.com/gear/avalung_ii.php
(Fig. 30-1). This breathing device
allows inspiration of air from the
snowpack through a one-way
inspiratory valve and diverts
expired air around to the buried
person’s back through a one-way
expiratory valve. The device also
prevents ice mask formation. The
limitation of the device is that
expired air permeates around the
buried person’s body and through
the snow and eventually
contaminates inspired air.
Figure 30-1. AvaLung. The device is
worn over all other clothing. The
subject breathes in and out through the
mouthpiece (A). Inhaled air enters
from the snowpack through the one-
way inspiratory valve on the side of
the housing (B) inside the mesh-
protected harness on the chest.
Expired air leaves the lungs through
the mouthpiece, travels down the
respiratory tubing to an expiratory
one-way valve located at the bottom of
the housing, and exits via respiratory
tubing inside the harness around to
the back (C).
Breathing with the AvaLung®

while buried in dense snow was
compared to breathing without the
device but with a 500 ml air pocket
in the snow. Mean burial times
before the development of hypoxia
and hypercapnia were fifty-eight
minutes with the device and ten
minutes with a 500 ml air pocket in
the snow. This device has resulted
in survival from actual avalanche
burials by prolonging the time to
asphyxiation, and allowing rescuers
time to reach their companions.
However, its use and acceptance
have not been widespread even as
the device has evolved into user-
friendly equipment incorporated
into a backpack. The AvaLung’s®
full potential for reducing death by
asphyxiation requires several years
of analysis with increased usage.
PREVENTION OF AVALANCHE
BURIAL
Absolute prevention of avalanche
burial can only be accomplished by
complete avoidance of avalanche
terrain. All backcountry enthusiasts,
including over-snow travelers and
climbers, are at risk. The current
attitude in Europe, aside from wise
and proper backcountry travel and
the use of transceivers, probes, and
shovels, is supportive of proactive
devices to prevent burial when
caught in an avalanche. The
avalanche air bag system (ABS) has
proven extremely effective for more
than fifteen years throughout the
alpine countries of Europe by
greatly increasing the odds of a
surface or near-surface burial, in
addition to making rapid visual
localization of the air bags
possible. The ABS is triggered by
pulling a ripcord on the front strap.
From February 1991 to April
2006, 106 persons deployed the
system in an active avalanche
accident. Of these, fifty-two
finished on the surface, forty-two
were only partially buried and were
easily extricated, and eleven were
completely buried but with the
balloon visible on the surface for
rapid localization and recovery.
Only one person with a deployed
balloon died because a second
avalanche buried the balloon
deeply into a terrain trap.
The system works by the
principle of inverse segregation of
particles in a laminar flow, such as
occurs in avalanches. The larger-
volume particles rise to the surface,
whereas smaller volumes are
forced to the bottom. The balloons
effectively increase the size and
volume of the wearer which favors
dynamic movement into the upper
flow and a greater chance of a
surface burial.
Unfortunately, neither the ABS
device nor the AvaLung®
effectively prevents trauma. To
date, the ABS has been difficult to
obtain in the United States due to
shipping regulations involving the
pressurized canister.
TREATMENT OF
INDIVIDUALS BURIED BY
AVALANCHES
As the buried person’s head is
exposed and cleared of snow an
initial impression of the level of
consciousness and presence of an
air pocket should be obtained.
Opening the airway and ensuring
adequate breathing are the first
medical interventions. Every effort
should be made to clear the airway
of snow as soon as possible.
Ideally, ventilation should be
assisted with a bag-valve-mask
device or a pocket mask if
breathing is absent or ineffective,
and an oral or nasal airway should
be inserted if the person is
unconscious. These measures
should not be delayed until the
entire body is extricated.
If traumatic injury of the spinal
column is suspected, or if there is
evidence of head or facial trauma,
the spinal column must be
immobilized as the airway is
opened, adequate breathing
ensured, and oxygen provided. For
unconscious persons, maintenance
of the airway may be challenging in
the limited space of a snow hole
while the person is being
extricated. Improved shoveling
strategies have addressed this issue
by creating a platform toward the
airway.
After an adequate airway and
breathing are established and
supplemental oxygen provided, the
circulation should be assessed. A
conscious individual should be
assumed to have a perfusing rhythm,
and further treatment should be
directed at treating mild
hypothermia and traumatic injuries.
A person who is unconscious but
has an obtainable pulse may have
moderate or severe hypothermia
and should be handled gently to
avoid precipitating ventricular
fibrillation.
If a pulse is not detectable after
opening the airway, ventilating, and
full extrication of the individual,
(CPR) should be considered.
Before CPR is initiated, however,
careful evaluation for the presence
of a pulse should be carried out.
Individuals who have been buried
by an avalanche with an air pocket
may be hypothermic, which causes
peripheral vasoconstriction and
makes the pulse difficult to palpate.
In addition, moderate to severe
hypothermia depresses respiration
and slows the heart rate, which can
simulate full cardiopulmonary
arrest. Before initiating CPR,
palpation for a pulse should be
done for at least a full minute after
the airway is opened and assisted
ventilation has begun. The pulse
may be easier to detect after a few
rescue breaths. A stethoscope for
determining the presence of a
heartbeat is much more sensitive.
CPR for a severely hypothermic
person who actually has an
undetectable perfusing rhythm may
cause ventricular fibrillation.
Therefore, once CPR is initiated in
a potentially hypothermic
individual (long burial time, core
body temperature less than 86°F
[36°C] if available, and the
presence of an air pocket), it must
continue until transport to the
medical facility.
Figure 30-2. Assessment and care of
persons buried in an avalanche
Automatic external defibrillators

(AEDs) are available to members
of the ski patrol in ski resorts. An
AED applied to the chest can
determine whether the person has a
cardiac rhythm or is fibrillating. If
the rhythm is ventricular
fibrillation, only one defibrillation
should be attempted if an
esophageal probe or tympanic
membrane thermometer can
determine that the individual has a
body temperature below 86°F
(30°C). If this is unsuccessful,
further attempts at defibrillation
should be made only after
rewarming in a medical facility. If
the person is hypothermic but has a
core body temperature greater than
86°F (30°C), the standard
CPR/advanced cardiac life support
(ACLS) protocol should be
followed for at least twenty
minutes.
Unfortunately, the probability of
successful resuscitation of a person
buried in an avalanche who is in
cardiac arrest at the time of
extrication is generally poor and
depends on whether the arrest
occurred from asphyxiation or from
hypothermia. For burials of less
than one hour when the core
temperature is greater than 86°F
(30°C), resuscitation is unlikely to
be successful because death
probably has resulted from
asphyxiation or lethal trauma.
Persons extricated from avalanche
burials of greater than one hour who
have no signs of life but who are
severely hypothermic—a core
temperature less than 86°F (30°C)
—and for whom an air pocket for
breathing was detected upon
extrication, may be considered for
transport to a medical facility with
the capability for rapid
extracorporeal blood rewarming
(Fig. 30-2).
Determining whether an air
pocket for breathing has been
present as a person buried by an
avalanche is extricated is essential,
can be challengingø, and is often
impossible, in which case an air
pocket should be assumed to have
been present.
Most individuals buried in
avalanches and extricated in
cardiac arrest, however, have died
from asphyxiation. Continuing
resuscitation efforts until
rewarming occurs for such persons
is unlikely to result in survival,
particularly if no air pocket is
present or if the upper airway is
obstructed by snow. In one study of
thirteen individuals buried by
avalanches and found in cardiac
arrest after 30 to 165 minutes, none
survived after resuscitation efforts,
suggesting that cardiac arrest was
due to asphyxiation rather than
hypothermia. However, despite
these grim statistics, a twenty-
minute attempt at CPR is
reasonable.
HYPOTHERMIA
For persons buried in avalanches
who are extricated alive, trauma
and hypothermia are the most urgent
medical problems that require
treatment. The therapy administered
depends upon the severity of the
hypothermia and is described in
Chapter 26: Cold Injuries.
Traumatic injuries exacerbate
the onset and progression of
hypothermia. Even relatively short
burial times can result in a more
severe level of hypothermia. Figure
30-2 is an algorithm for the triage
of individuals who have been
buried that guides rescuers about
whether to discontinue efforts,
whether to make a maximum effort,
possibly at some risk, and whether
to transport for treatment of severe
hypothermia.
CHAPTER 31
LARGE ANIMAL
ATTACKS
Attacks by large animals other than

dogs are uncommon in North
America, at least in comparison
with Africa or southern Asia.
However, a significant number of
injuries and a few deaths are
caused by such encounters each
year. A number of North American
animals may be encountered in the
wilderness:
◆ Bears (black bears, brown
bears, and polar bears)
◆ Canines (dogs, coyotes, and
wolves)
◆ Bison
◆ Cougars
◆ Alligators
◆ Ungulates (moose, elk, and
deer)
Large animals in Europe are
similar to large animals in the
United States, are limited in
number, and consist mostly of
ungulates, rare bears, and rare
wolves. In addition, the following
large animals may be encountered
in Asia and Africa:
◆ Bears (brown bears, pandas,
spectacled bears, sloth bears,
Asiatic black bears)
◆ Big cats (tigers, lions,
leopards, jaguars)
◆ Pachyderms (elephants,
rhinoceroses, and
hippopotamuses)
◆ Crocodiles
◆ Cape buffalos
◆ Hyenas
◆ Primates
◆ Kangaroos
LARGE ANIMAL ATTACKS:

NORTH AMERICA
Bear Attacks
For years, approximately ten
bear attacks on humans and one
fatality were reported in North
America—including Canada—each
year, but the incidence is
increasing, apparently because
more humans are encroaching on
bear habitat. Brown bears have
been thought to be responsible for
most of the attacks and fatalities,
but black bears and occasionally
polar bears also kill humans. In his
book Bear Attacks: Their Causes
and Avoidance (Guilford, CT:
Lyons Press, 2002), Stephen
Herrero reported that during the
1990s twenty-nine people were
killed by bears, an average of three
a year. Eighteen were killed by
brown bears and eleven by black
bears. (To put these data in
perspective, between 1979 and
1998 dogs killed an average of
twenty-two humans each year in the
United States.)
Black Bears
Black bears, which have many
color variations including brown
and honey, are numerous in the
forested areas of the United States.
They have no natural enemies and
have become a nuisance for
campers in a number of national
parks.
Because these animals have
evolved in forested areas, they have
learned to hide or climb trees when
threatened. Therefore, truly wild
bears infrequently attack humans. In
contrast to brown bears, black bear
sows with cubs rarely behave
aggressively. Black bears that have
a sudden encounter with humans
almost never attack. Aggressive
behavior by humans—shouting,
waving arms, walking toward the
bear, and making threatening
gestures—almost always frightens
away black bears. Whether greater
precautions are needed deserves
consideration.
Bears that have become
habituated to humans do
occasionally attack them,
particularly individuals who
approach too closely—trying to
feed them or take pictures. Herrero
found more than five hundred
incidents in which black bears
attacked humans between 1960 and
1980. Of the injuries produced by
such attacks, 90 percent were
minor, but major injuries were
inflicted in thirty-five attacks.
A number of humans have been
killed. Herrero was able to find
reliable accounts of twenty-three
humans killed by black bears
between 1900 and 1980. According
to the bear statistics compiled by
the Canadian Conservation Office
Service, between 1978 and 1996
ten people were killed by black
bears and seventy-eight people
were injured in British Columbia.
In recent years the number of
attacks appears to have increased.
In early September of 2005 a thirty-
one-year-old female physician was
killed by a black bear in Missinaibi
Lake Provincial Park in Ontario.
One week later a sixty-nine-
yearold-man was killed while
picking plums in Selkirk, Manitoba,
a village north of Winnipeg. This
was the third time a black bear had
killed a human in the province of
Manitoba.
Herrero concluded that 90
percent of lethal black bear attacks
have been predatory. Furthermore,
90 percent of such predatory attacks
have been made by truly wild bears
that were not habituated to humans.
Only one of the predatory attacks
occurred in a national park where
most food conditioning and
habituation occur. Most of the
predatory attacks have been made
during daylight in contrast to the
night hours during which most
predatory brown bear attacks occur.
Most attacks appear to be
associated with a failure of the wild
berry crop, a vital source of food
for black bears.
Control of black bears in
national parks has been greatly
improved by making human food
and garbage inaccessible.
Brown Bears
Brown bears, also known as
grizzly bears, and Kodiak bears,
which are considered the same
species, are larger and more
aggressive than black bears.
Attacks on humans, a number of
which are fatal, are periodically
reported from areas inside and
surrounding Yellowstone and
Glacier National Parks and from the
northern Rocky Mountains in the
continental United States, Alaska,
and Canada. Unlike most black
bears, brown bears do behave
aggressively when they perceive a
human threat. Sows with cubs are
very aggressive and are responsible
for 80 percent of brown bear
attacks.
A possible reason for the
aggressive behavior of sows with
cubs is that sows stay with their
cubs for three years and will not
mate during that time. Male
grizzlies sometimes will kill cubs
so they can mate with the mother.
Therefore, the mother has to be very
aggressive in caring for her young.
Herrero, recording only reports
that he considered highly reliable,
found that brown bears had inflicted
165 injuries in 143 incidents from
the time records began in 1872
through 1979. He estimated that the
true number of incidents and
injuries was probably twice those
numbers. Of the injuries, 50 percent
were considered major. He
calculated that during the 1970s
brown bears inflicted one injury for
each 1.3 million visitors in Glacier
National Park and one injury for
each 1.5 million visitors in
Yellowstone. Injury rates were
higher for backcountry visitors and
ranged from one injury for each
2620 backcountry-use days in
Glacier and Mount Revelstoke
National Parks in Canada to one
injury for each 59,300 backcountry-
use days in Yellowstone.
Approximately half the brown
bear incidents have involved hikers
who surprised a bear. In 83 percent
of the thirty-five incidents in which
the distance from the hiker to the
bear was known, the bear was fifty-
five or fewer yards away.
Avoiding Encounters with Brown

Bears
Brown bears usually try to avoid
interacting with humans. Hikers in
the wilderness are advised to make
noise by shouting, talking loudly, or
singing as they hike to avoid
surprising brown bears. The
effectiveness of bear bells is
unproven. Police whistles, which
are usually louder than a human
voice, or high-frequency whistles
have not been proven effective,
probably because they are not loud
enough. The bear has to hear the
noise while still far enough away
not to feel threatened. Running
water or a strong wind render
noisemakers less effective.
One effective mechanism is an
air horn powered by a canister of
gas. Salmon tagging crews in
Alaska who sounded such horns
periodically, particularly when near
dense brush, never encountered
bears. When they assumed bears
were not present because they had
never seen them and stopped
sounding the horns, they came upon
a number of bears.
Particular vigilance must be
exercised when traveling into the
wind because bears may not smell
approaching humans even though
they have a keen sense of smell.
Signs of a bear’s presence, such
as tracks or scat, must be carefully
sought. Partially eaten carcasses
should be given a wide berth
because bears usually return to
finish their meal. Vultures circling
over such a carcass indicate its
presence and also warn that a bear
may be near.
One of the best ways to avoid
injury by brown bears is to travel in
a group. No serious attacks on
groups of four or more people have
been reported, and attacks on two
or three individuals are less
common than attacks on persons
traveling alone. Herrero found that
in 88 percent of brown bear
incidents only one person was
injured, in 8 percent two people
were injured, and in only 3 percent
were three persons injured.
Campers should observe the
following precautions:
◆ Bear trails or feeding grounds
should be avoided.
◆ Sites with bear signs such as
droppings or tracks should be
avoided.
◆ Sites where food or garbage
has been left should be
avoided.
◆ The cooking area should be
100 yards or more downwind
of the tent.
◆ All food and strongly scented
materials should be stored at
least 100 yards from the tent,
preferably suspended in a tree
in a manner a bear cannot
reach them, or in a bearproof
container.
◆ In brown bear territory, camp
should be near an escape tree
or well in the open away from
cover.
◆ Packs should be left outside
the tent with the flaps open.
◆ In bear country, all campers
should use tents. The danger of
brown bear predation appears
definitely to be reduced by
sleeping in a tent.
Dealing with Encounters with

Brown Bears
Brown bears have evolved in
open environments, not in forests,
and have not learned to be
frightened by aggression, as have
black bears. During a “provoked”
encounter (when a human surprises
a brown bear), a human should
attempt to be as unthreatening as
possible.
A brown bear who stands on its
hind legs is only trying to evaluate
the situation, probably trying to get
a better smell. A bear on all four
legs may show agitation by
salivating, swaying its head from
side to side, making huffing noises,
or making clacking noises with its
teeth. Charges are common, but
many are false charges in which no
contact is made with humans.
Herrero considers the position of
the bear’s ears to be a significant
indication of the bear’s intentions;
like a dog, the farther back the ears
are, the more aroused is the bear.
Eye-to-eye contact should be
avoided. Backing away slowly is
the best way to get away. Running is
not advisable because it attracts the
bear’s attention, and bears can run
much faster than humans,
approximately one-third faster than
a world-class sprinter.
“Playing dead” if the bear
approaches is often—although not
always—successful. Individuals
should curl up on the ground with
their arms over their heads and
necks. If they are wearing a pack
they can try to shoulder it over their
head. Brown bears often make only
one bite or one swipe with a paw,
and injuries to an arm are far more
survivable than injuries to the head.
One common mistake made by
individuals playing dead is getting
up too quickly. People using this
protective maneuver must be
absolutely certain the bear has left.
“Wait until you’re sure he’s gone
and then wait some more.” When
bears return to someone who has
played dead, they often are more
aggressive than during the first
curious examination.
Bear sprays (pepper sprays)
have been shown to be effective in
stopping both brown and black bear
attacks. Sprays can be used before
contact is made or during an attack.
Anyone considering carrying a
gun for protection must remember
that only a large caliber round,
precisely aimed at an area of the
bear’s head that is approximately
three by four inches in size in a
minimal amount of time, would be
effective against a charging bear.
Wounding the bear makes it angry,
and inaccurate use of a handgun
results in more serious injury and
death to the human.
Occasionally brown bears make
predatory attacks on humans, almost
always at night. When faced with
such an attack, the only recourse is
to fight back with whatever
weapons are on hand. Fighting back
is effective with surprising
frequency, probably because the
bear is looking for an easy meal,
not one for which it has to fight.
Brown bears habituated to humans
and conditioned to eating human
food and garbage initiate most
predatory attacks and consume the
bodies of those they have killed,
which supports rigorous human
food and trash management policies
in bear territory.
Polar Bears
Human encounters with polar
bears are uncommon because, with
the exception of a few towns like
Churchill, Manitoba, few humans
live in the areas where these bears
are found. The human population of
Nunavut, the huge northeastern
Canadian territory, is only about
29,500.
Polar bears are among the
largest carnivores in the world.
They are strong, fast, and agile—on
ice and land and in water.
Descriptions of polar bear
behavior range from animals that
attack without provocation—“The
polar bear is the most deadly of all.
They are known to stalk and hunt
humans.”—to animals that appear to
largely ignore humans. However,
when attacks on humans do occur,
most are predatory.
Churchill is known as the “Polar
Bear Capital of the World” because
scores of bears gather there to
await the freezing of Hudson Bay.
The town was established in 1717,
and since that time attacks by polar
bears have been infrequent. Only
two townspeople have been killed,
despite numerous encounters. The
first death occurred in 1968. Native
teenagers followed polar bear
tracks through a fresh snowfall,
found the animal, and proceeded to
molest it. The bear attacked and
killed one of the teenagers. (This
incident has also been reported as a
twelve-year-old who blundered
into a den of polar bears.)
The second took place in 1983
when a man scavenging the newly
burned ruins of the Churchill Hotel
found some unspoiled meat in the
freezer and stuffed his pockets with
it. (Reports have also stated he was
carrying the roast beef under his
arm.) Unfortunately, a polar bear in
the vicinity was intent on
scavenging and killed the man.
Churchill’s “polar bear jail”
was built in 1982 to house problem
animals—any bear that has entered
the town of Churchill is considered
a problem bear—and has reduced
bear–human encounters. Problem
bears are housed in this facility
until they can be tranquilized and
helicoptered to another location.
Although one review of bear
attacks considered only the two
Churchill fatalities to be well
documented, other lethal attacks
have probably occurred. According
to Internet sources the last person
killed by a polar bear in Canada
was a Baker Lake, Nunavut, woman
in 1999. According to a similar
source, only seven people have
been killed by polar bears in
Canada in the past thirty years. In
the same period only one person
has been killed by a polar bear in
Alaska. In all of recorded history,
only nineteen people are known to
have been killed by polar bears in
Russia.
Polar bears can be found from
the permanent pack ice and coasts
of the Arctic Ocean and Arctic
islands to southern Hudson Bay.
They live mainly on sea ice or on
land within a few kilometers of the
coast and are uncommon in inland
areas.
In fall, winter, and spring, polar
bears hunt seals on the sea ice near
open water and areas of pushedup
sea ice. They also hunt for seals in
places where sea ice is thin or
cracked, such as at tide cracks in
land-fast ice or at the toes of
glaciers.
In summer, polar bears are
forced ashore when sea ice melts.
They live in semistarvation, feeding
on birds, eggs, and small mammals
along coastlines, beaches, and
rocky islands near the coast. They
also scavenge anything from
wildlife carcasses to human
garbage.
The insulating fur and underlying
fat that allow polar bears to
comfortably survive arctic
temperatures in winter are a major
disadvantage in summer because the
bears cannot readily lose heat. To
minimize heat generation, they walk
slowly and do not pursue vigorous
activities. Bears look for sites
where the permafrost is close to the
surface and lie on the cool area to
get rid of heat.
In fall, winter, and spring,
maternity dens are located in
snowdrifts along slopes of coastal
hills and valleys. Maternity dens
can also be found at higher
elevations on snowfields and
glaciers. Dens are inconspicuous,
but bear tracks leading into or away
from snowdrifts, as well as
ventilation holes, may indicate den
locations.
In winter, temporary dens and
daybeds are dug into snowdrifts or
pushed-up sea ice. These are used
as resting places or as temporary
shelter from bad weather for a few
days up to several months.
Avoiding Encounters with Polar

Bears
Individuals in polar bear country
must stay alert. Seeing bears before
they are a problem decreases
chances of a dangerous encounter.
Humans should always travel in
groups of at least four people and
should stay together to increase
their safety. As in brown bear
territory, travelers should make
noise as they move along to
communicate their presence. They
should only travel in daylight and
must be aware of their
surroundings. Polar bears may be
hard to see, and scanning with
binoculars at regular intervals is
advisable. Areas of restricted
visibility, pushed-up sea ice,
boulders, driftwood, or vegetation
should be avoided. Tracks,
droppings, and diggings should be
carefully sought as warning signs.
Bears should never be
approached. They defend their
space and may consider humans a
threat. Bears should never be fed. A
bear that associates humans with
food is dangerous. A wildlife
carcass should never be
approached because a bear may be
in the area.
Camping on beaches and along
coastlines should be avoided. Polar
bears often travel along coastlines
using points of land and rocky islets
near the coast to navigate. Narrow
valleys and passes that may be used
by bears to cross peninsulas and to
move from one valley to another
should be avoided. Camps should
be inland on high ground with a
good view of the surroundings.
Bear tracks should be sought before
camp is established, and the camp
should be moved if a bear is in the
area.
Cooking and cleaning gear—
including stoves, pots, stored food,
food scraps and garbage, and the
clothes that are worn for cooking—
as well as any scented products
should be stored at least 100 meters
from the sleeping area. Bearproof
canisters or airtight containers
should be used for storage.
Feces should be packed out or
buried under rocks away from
trails, at least 100 meters from
camp (and away from all water
sources). All used toilet paper and
feminine hygiene products should
be placed in a sealed bag with the
garbage, all of which should be
packed out. Packaging should not be
burned because lingering food
odors may attract bears. Any
spilled food should be picked up
from cooking and eating areas.
Camping, cooking, storage, and
human waste areas should be
positioned so that a clear escape
route from a bear is available.
Campers should never sleep in
the open without a tent, should
never bring strong-smelling foods
or scented products of any kind into
a tent, and should never cook or
store food or scented products in a
tent.
Dealing with Encounters with

Polar Bears
Polar bears are curious and may
investigate any strange object,
smell, or noise. Individuals who are
objects of such curiosity should stay
calm and assess the situation. Each
encounter with a polar bear is
unique. Good judgment, common
sense, and familiarity with polar
bear behavior are important.
A bear who knows a human is
present may shows signs of
curiosity, such as moving slowly
with frequent stops, standing on
hind legs and sniffing the air,
holding its head high with ears
forward or to the side, moving its
head from side to side, or trying to
catch a scent by circling downwind
and approaching from behind.
Individuals should not run but
should back away slowly. They can
help the bear identify them as
human by talking in low tones.
Moving slowly upwind of the bear
can allow it to get the person’s
scent, although an escape route for
the bear must always be provided.
If a bear has been surprised at
close range or shows signs of being
agitated or threatened, such as
huffing, panting, hissing, growling,
jaw snapping, stomping its feet,
staring directly at a person, or
lowering its head with ears laid
back, the individual should not run
but should back away slowly.
Shouting or sudden movements and
direct eye contact should be
avoided. Individuals should act
nonthreatening while being
prepared to use deterrents.
If a bear shows signs of stalking
or hunting, such as following or
circling a person, approaching
directly, intent and unafraid, or
returning after being scared away,
or appears wounded, old, or thin,
individuals still should not run.
Rather, they should form a group,
make loud noises, and be prepared
to use deterrents and fight back.
Humans should never get
between a bear and her cubs. If a
bear with cubs is encountered,
individuals should not run but
should form a group and leave the
area immediately. They should be
prepared to fight back if the bear
attacks. If a polar bear attack does
occur, any available weapon, such
as rocks, blocks of ice, knives, skis,
or poles, should be used.
Many websites advise carrying
guns in areas where polar bears
live. The advisability of carrying
such weapons is questionable,
unless individuals are quite
proficient. Killing a charging bear
requires a carefully placed, high-
caliber shot—often more than one.
A wounded bear is far more
aggressive than one who is not.
Dealing with a Polar Bear
Emergency
Search-and-rescue capabilities
may be limited by terrain, weather,
and availability of aircraft. Aircraft
are limited in areas inhabited by
polar bears. Planes and helicopters
are rarely stationed in small
communities. Air access can be
delayed, sometimes for many days,
by poor visibility, weather
conditions, or high winds. Aircraft
can only land if the terrain is safe.
Emergency communication
devices such as satellite phones
should be carried, and users should
be conversant with their operation.
Local topography and weather
conditions can limit reception. A
global positioning system (GPS)
navigation unit also should be
carried for relaying accurate
location coordinates in case of
emergency. Batteries do not last as
long in cold weather and should be
kept warm and used only when
necessary.
Additional information is
available at polarbearsalive.org
and
www.nunavutparks.com/english/visit
information/polar-bear-safety.html.
Injuries Produced by Bears
Bears often attack the face or
head first. Injuries are produced by
biting and by clawing and batting
with the forelegs. Claws and teeth
produce lacerations that sometimes
are extensive. Body cavities are
often punctured or opened. The
lungs may be punctured. Fractures,
including skull fractures, are
common.
Dogs
In 2001, an estimated 68 million
canines were kept as pets in the
United States. These animals inflict
approximately 4.5 million bites
each year, and approximately
885,000 persons require medical
care. In 2006 more than 31,000
people underwent reconstructive
surgery to repair dog-inflicted
injuries.
More than 330 fatalities were
documented during the twenty-year
period 1979 to 1998. However,
only about three-fourths of all dog
bite-related fatalities were
identified, indicating that an
average of twenty-two fatalities
result from such bites each year.
Most are in young children, and
most result from hemorrhage from
the large blood vessels in the neck.
The number of attacks on humans
by dogs, the number of injuries, and
the number of fatalities from dog
bites in the United States clearly are
far higher than those for all other
large animals combined.
Injury rates are highest for
children five- to nine-years-old and
decrease with increasing age.
Approximately 42 percent of all
dog bites occurred among children
less than fourteen years old, and the
rate is significantly higher for boys
than for girls.
Injuries occur most commonly to
the arm and hand (45.3 percent), leg
and foot (25.8 percent), and head
and neck (22.8 percent). However,
most injuries among children less
than four years old are to the head
and neck (64.9 percent).
Although many injuries are
described in medical records as
“dog bite,” other diagnoses indicate
the types of injuries that are
produced by dog bites: puncture
(40.2 percent), laceration (24.7
percent), contusion, abrasion, or
hematoma (6 percent), cellulitis or
infection (1.5 percent), amputation,
avulsion, or crushing injury (0.8
percent), and fracture or dislocation
(0.4 percent). (Bites by wolves and
coyotes produce similar injuries.)
Most dog bites (80 percent)
incurred by persons less than
eighteen years old are inflicted by a
family dog (30 percent) or a
neighbor’s dog (50 percent). From
1979 to 1998, 75 percent of fatal
dog bites were inflicted on family
members or guests on the family’s
property. In 2001, an estimated 8
percent of dog bites to persons
more than sixteen years old were
work related, including some that
occurred while persons were
visiting homes as part of their work
activities.
At least twenty-five breeds of
dogs, including a dachshund and a
cocker spaniel, have been involved
in 238 human fatalities for which a
breed could be identified during the
1979–1998 period. Pit bulls and
rottweilers were involved in more
than half of these deaths, but the
investigators who developed these
data did not feel that breed-specific
control legislation would be
justified or effective.
In 160 human deaths, only one
dog was involved; in forty-nine
deaths two dogs were involved; and
in fifteen deaths, three dogs were
involved. From four to fourteen
dogs were involved in an additional
fourteen deaths.
To reduce the risk of infection,
closing—particularly suturing—dog
bites should be delayed for hand
and foot wounds; bites involving
joints, ligaments, tendons, and
bones; bites that have not been
treated for more than twelve hours;
and bites in immunocompromised
individuals. (Human and cat bites
should never be closed, and some
authorities think no animal bites
should be closed, particularly
outside of a hospital or emergency
room.) Tetanus immunization should
be administered if a booster shot
has not been received within five
years. The need for rabies
postexposure therapy must be
carefully considered.
and Prevention (CDC) and other
public health agencies have
established programs to reduce the
frequency of dog bites. More
details about those programs,
particularly about teaching children
to avoid dog bites, are available at
www.cdc.gov/ncipc/duip/biteprevent
Wolves
Currently the wolf population of
North America is estimated to be
60,000 to 70,000, the wolf
population in Europe is estimated at
10,000 to 20,000, and the
population in Russia is 60,000.
Wolves in North America are
limited largely to Canada, although
they do live in northern Minnesota
and have been reintroduced into
Yellowstone National Park.
Jack London notwithstanding,
healthy wolves that are not
habituated to humans almost never
attack them. Wolves are one of the
few animals that will desert their
young when approached by humans.
Until recently no instances of
humans being killed by wolves in
North America had been recorded.
A 2002 study of wolf attacks in
Alaska and Canada done by the
Alaska Fish and Game Department
found no examples of people being
killed by wild wolves going back
more than 100 years.
However, a twenty-two-year-old
man may have been killed by a wolf
pack in Saskatchewan in 2005,
although that conclusion has been
challenged. He unquestionably was
killed by an animal attack, but the
animal could not be specified at
autopsy. His body had been
scavenged, and wolf footprints
were present around the body.
In studies of wolf attacks on
humans, four conditions have been
found. Many attacks were made by
rabid wolves; many attacks were
made by wolves that had become
habituated to humans; some attacks
were provoked when humans
cornered or trapped wolves or
entered their dens; and many attacks
occurred in areas where humans
had greatly altered the environment.
No other animal becomes as
ferociously aggressive when
infected by rabies. It seems likely
that this species’ reputation for
savagery is based largely on the
behavior of rabid animals.
To avoid wolf encounters when
camping in wolf country,
individuals should cook, wash
dishes, and store food away from
sleeping areas; pack out garbage
and leftover food; suspend food,
toiletries, and garbage out of reach
of any wildlife, preferably in
bearproof containers; and keep pets
close at all times. When watching
wolves, the animals should not be
fed, they should not be approached
or enticed to come closer, and they
must be left a path to escape. BC
Parks in British Columbia, Canada,
recommends that wolves should not
be allowed to approach any closer
than 300 feet. The same agency
recommends that if a wolf acts
aggressively (growls or snarls) or
fearlessly (approaches humans
closely without fear), the following
actions should be taken:
◆ The arms, preferably with a
coat, should be raised and
waved to make the individual
appear larger.
◆ The person should back away
slowly, without turning his
back on the wolf.
◆ The individual should make
noise and throw things at the
wolf.
More information about wolf
attacks is available at the
International Wolf Center
(www.cdc.gov/ncipc/duip/bitepreven
Coyotes
Coyotes have thrived and
multiplied despite the onslaught of
civilization, and their range has
expanded to cover almost all of
North America. They have also
extended into cities. The greater
Chicago area has been estimated to
have a coyote population of
approximately 2000 animals.
Coyote attacks are uncommon,
rarely cause serious injuries, and,
because these animals are relatively
small, are usually directed at
children. A number of attacks have
occurred in urban surroundings
ranging from Los Angeles to Cape
Cod. Some of the attacking animals
have had rabies, but a number have
not.
Coyote attacks on humans have
increased since 1998 in California.
Several sources report that forty-
one attacks occurred between 1988
and 1997, but forty-eight attacks
were verified from 1998 through
2003. Most of these incidents
occurred in southern California
near the suburban-wildland
interface. Because they are not
harassed by residents, urban
coyotes lose their fear of humans,
which is worsened by people
feeding coyotes. In such situations,
some coyotes begin to act
aggressively, chasing joggers and
bicyclists, confronting people
walking their dogs, and stalking
small children.
Only one fatal attack on a human
has been recorded. In 1981 in
Glendale, California, a city of
approximately 200,000 residents
that is part of greater Los Angeles,
a coyote attacked a three-year-old
girl who was playing alone in her
front yard. She died in surgery as
the result of blood loss and a
broken neck.
Individuals under attack should
fight back. They should not appear
docile or try to pet coyotes, no
matter how tame they may appear.
Children should not be left
unattended in areas accessible to
coyotes.
Bison
Most attacks by bison occur in
Yellowstone National Park, the
home of the largest free-ranging
bison herd. The number of attacks
averages three a year. Four
fatalities have resulted from these
attacks since 1975.
Most bison attacks are
provoked, most commonly by
tourists who approach the animals
too closely for photographs.
However, totally unprovoked
attacks also occur. Bison can weigh
as much as 2000 pounds (900 kg)
and can run as fast as 35 miles per
hour (57 kph). Their potential for
injury must be respected.
Injuries from bison attacks
include gorings and blunt trauma.
The bison’s horns may appear
inconspicuous but can produce
deeply penetrating injuries. Gorings
usually involve the buttocks,
posterior thighs, and back because
the individual is running away from
the bison. However, cardiac
punctures and evisceration have
occurred. Stomping, butting, and
tossing by the bison produce blunt
injuries that include fractures and
other injuries associated with a fall.
Cougars
Over eighty attacks by cougars,
also known as mountain lions,
pumas, panthers, and some forty
other names in English alone, have
been reported in North America
since 1970, mostly in Colorado and
California, and the incidence and
fatality rates appear to be
increasing, in part because humans
are encroaching on cougar habitat.
However, cougars no longer have
natural enemies and in most areas
are protected from hunting, so the
population is growing.
Cougars are territorial. Older,
more mature animals drive young
animals out of their territory—even
killing them—as soon as the young
are ready to leave their mothers.
Many of the attacks on humans have
been inflicted by young cougars that
have been driven into less desirable
territory, closer to human
habitation.
Attacks are usually unprovoked
and predatory. Cougars usually
consume humans they have killed.
Over 25 percent of the individuals
killed by cougars have been
children.
When faced by a cougar,
threatening behavior is best for
warding off attacks. Individuals
should make noise and open their
coats so they look as large as
possible. Eye contact should not be
avoided. Running only invites
attack. If actually assaulted, humans
should fight back. Cougars are
looking for a meal, not a fight.
Humans who live near cougar
habitat should avoid making their
homes attractive for cougars. Not
only are pets such as dogs and cats
an enticement for hungry cougars,
residents must not plant vegetation
that is attractive for rabbits or other
small animals on which these large
cats prey.
Injuries are produced by biting
and by clawing and are mostly
lacerations and punctures. Like
other big cats, cougars will try to
break a person’s neck by biting the
back of the neck and shaking their
prey’s head.
Alligators
In a recent period of seventeen
years, 127 attacks by alligators and
five fatalities—a rate of 4 percent
—were reported. Alligator attacks
are predatory. Typically the animal
grabs its intended prey with its
jaws and rolls underwater to drown
it. These beasts can move with
surprising speed on land, and
individuals standing on the shore
also have been attacked.
Individuals who have been
attacked should fight back. The 4
percent success rate for animals
trying to obtain a meal is not very
high. Poking the animals in the eyes,
or in the ears or nose, has been
recommended, apparently on the
basis of a few instances in which
individuals were released after
jabbing the attacking animal in the
eye. Prying open the glottis, the flap
of tissue that prevents water from
entering the alligator’s airway, has
also been recommended, but
success with such a maneuver when
a large animal is trying to roll the
person underwater seems unlikely.
To avoid alligator attacks,
individuals should not swim at dusk
when alligators are active, should
not swim with a dog that would
attract alligators, and should not
swim alone. Totally avoiding
swimming in bodies of water or
streams inhabited by alligators
seems eminently reasonable.
Alligator teeth produce large
lacerations, commonly located on
the torso as well as the limbs. Their
efforts to roll their prey underwater
produce fractures, many of which
are open. Wounds become infected,
and injured individuals should
receive prophylactic antibiotics.
Moose
Attacks by ungulates (moose,
elk, and deer) are generally
considered provoked, although the
provocation often consists of
nothing more than entering the
animal’s territory. These animals
are herbivorous, and the attacks are
not predatory.
Moose are large animals. Mature
bulls weigh between 800 and 1200
pounds, and their antlers can have a
spread of sixty inches. Cows are
smaller, weighing between 500 and
900 pounds, and are still very large
animals. Even calves, which weigh
200 to 400 pounds by their first
winter, are large enough to injure
humans. Moose can run as fast as
thirty miles per hour. An adult
moose can defend itself against a
mature grizzly bear; a moose attack
on a human can be devastating.
Most attacks occur during the
spring calving season or during the
fall rutting season. Typically an
individual inadvertently gets
between a female and her calf or
walks or jogs into the animal’s
territory. During the rutting season,
male ungulates commonly go
without food, and the combination
of hunger and elevated hormone
levels makes them irascible.
Dogs that harass moose are
another source of human attacks.
Moose equate dogs with wolves
and attack them. When the dog runs
back to—or behind—its owner, the
moose attacks the owner.
According to the website of a
moose conservation organization,
moose injure more people than
bears do each year in Alaska. Each
year five to ten moose-related
injuries occur just in the Anchorage
area, and in a recent ten-year period
two people died from moose
attacks in that area.
The first indication that a moose
attack may be imminent is the
animal stops feeding or walking and
looks at the individual who has
approached. Its ears are up, and it
is listening. If the moose puts down
its head, lowers its ears, and the
hair on its back and neck go up, it
often is preparing to charge. The
moose may begin to lick its lips and
walk toward the person, which can
be an indication that it has been fed
by humans in the past. Moose that
have been fed may become angry
and attack when food is not
forthcoming.
If these signs appear, the
individual should start backing
away and looking for an escape
route. An escape route for the
moose should also be ensured.
Fortunately most moose charges
are bluffs, but they must be taken
seriously. A person chased by a
moose should try to get behind
something solid, a large rock or a
tree. A human can run around a tree
faster than a moose can. Individuals
knocked down by a moose should
curl up in a ball, protect their head
with their arms, and lie still. They
must not move until the moose is a
safe distance away, or it may renew
its attack.
When a moose knocks a person
down, it may continue running or
start stomping and kicking with all
four feet. Moose attack with their
hooves, even though bulls may
carry an impressive set of antlers.
Elk
Elk are the second-largest
ungulate. Bulls weigh an average of
700 pounds, stand about 5 feet high
at the shoulder, and are 8 feet long.
Cows average 500 pounds,
measuring 4.5 feet at the shoulder
and 6.5 feet from nose to tail.
Attacks on humans by elk are
less common than attacks by moose.
However, in 1999 more than 100
people were attacked by elk in
Banff, Canada. The following year,
Parks Canada shipped to a remote
area a major portion of Banff’s elk
population of some 500 animals.
However, elk remain a problem in
Banff.
Visitors to Banff National Park
of Canada are warned that “(Elk)
Attacks have occurred at any time
of the year.” The brochure for the
Canmore area in Alberta’s Bow
Valley Wildland Provincial Park
warns that “All elk can be
dangerous. Female elk can be
especially aggressive during
calving season in May and June.
During autumn rut (September to
November) male elk can also be
aggressive. Do not approach elk or
their calves. Give elk plenty of
room. Keep at a distance of at least
three bus lengths. Keep your dog on
a leash.”
A woman in Estes Park,
Colorado, received major
abdominal injuries from the hooves
of a female elk when she
inadvertently came between the
animal and its calf in the backyard
of her home.
At least two individuals working
on domestic elk ranches, one in
Colorado and one in Vermont, have
been killed by elk gorings. Such
attacks by wild elk appear to be
rare. Two individuals attacked by a
700-pound bull elk in Yellowstone
National Park received only cuts
and bruises. However, elk have
been videotaped attacking cars in
Yellowstone. Anecdotal accounts of
elk attacks abound but are not well
documented.
Little information is available
about dealing with attacking elk, but
individuals under attack have gotten
behind trees and used them as a
shield from the animal. People
should not invade the animals’
territory, particularly during spring,
when females are protecting calves,
and in fall, when these animals are
in rut.
Deer
Attacks by deer are even less
common but do occur occasionally.
A seventy-nine-year-old man was
fatally gored by a pet buck in
Alabama in 2003.
A sixty-six-year-old Georgia
man was found dead after being
gored by a deer inside the deer’s
pen on his property.
A fifty-six-year old California
woman was hospitalized for twelve
days with head injuries from an
attack by a buck outside her home.
Her husband, who came to her aid,
received bruises from the animal’s
antlers.
More typically, when a
California couple returned to their
pickup after watering a friend’s
vegetable garden, a buck ran up to
the truck, knocked the man on his
back, and pinned him to the ground
with his antlers, although the man
was not injured. His wife swung at
the animal with a piece of
firewood, and the deer turned on
her and gored her arm.
Six individuals were attacked by
deer on the campus of Southern
Illinois University in Carbondale in
2005 but received only bruises.
Wildlife biologists say the
attacks are unusual but could be a
sign that deer populations are
getting too large and the animals are
becoming too accustomed to
humans and their pets. Deer
populations throughout the United
States have increased exponentially
in recent decades, and the number
of white-tailed deer is now greater
than at any time in recorded U.S.
history. For the most part, predators
are gone, and even major
expansions of hunting seasons have
not kept the population under
control.
LARGE ANIMAL ATTACKS:

AFRICA, ASIA, AND
ELSEWHERE
Bears
Bears are among the most
widely distributed animals and are
found on every continent except
Africa and Antarctica. The
European and Asian brown bear is
genetically the same species as the
American brown or grizzly bear. In
Europe, the number of brown bears
is small, and these animals have
coexisted with humans much longer.
They have become nocturnal to
avoid humans and are rarely seen.
Human injury by these bears is
extremely rare.
In the former Soviet Union
brown bears live in vast,
undeveloped areas and have
maintained their aggressive
tendencies toward humans.
However, encounters are
uncommon. Human injuries from
bear attacks may result from
animals that have been wounded by
hunters.
Pandas are vegetarians, and
their diet consists almost entirely of
stalks, leaves, and shoots of only
two bamboo species. Because the
nutrient content of this material is
so small, pandas spend as much as
twelve hours a day eating. These
animals are shy and reclusive and
are a minimal threat to humans in
the wild.
Spectacled bears live in the
tropical Andes Mountains in
northwest South America. They
spend most of their time in trees
eating fruit. The bears are small and
shy, human encounters are rare, and
they pose very little threat to
humans.
Sloth bears live in subtropical
forests of Nepal, Bangladesh,
Bhutan, India, and Sri Lanka. Their
diet consists largely of ants and
termites. After Russian brown
bears, sloth bears appear to be the
most dangerous bear species in
Europe and Asia. Its aggression is
considered intermediate between
American black bears and grizzly
bears, but it is not predatory. An
average of one person a year is
killed in Nepal’s Chitwan National
Park, and one individual in western
Nepal is seriously injured
approximately every other year.
Asiatic black bears live in
broadleaf forests from Pakistan to
China and Southeast Asia. Small
pockets of them live in other areas.
These bears are omnivorous and
good climbers. They make
approximately two attacks per year
that produce injuries requiring
hospitalization on humans, mostly
as a result of close encounters.
Sun bears live in Malaysia,
Thailand, and Indonesia and are the
smallest of all bear species. Adults
weigh approximately 100 pounds.
They are proficient tree climbers,
are rarely seen, and present almost
no threat to humans.
Tigers
Tigers are the largest of the big
cats. They can reach thirteen feet in
total length and weigh as much as
660 pounds. A century ago, the
world’s tiger population was
estimated to be 100,000 or more
animals, but the population has
dwindled to between 5000 and
7000. According to some estimates
the population is even lower, some
2500 or fewer mature breeding
individuals. Of the nine subspecies
of modern tiger, three are extinct
and the remaining six are
endangered, some critically,
primarily as the result of habitat
destruction due to enlarging human
populations and poaching.
The threat of extinction is
mitigated somewhat by the presence
of some 20,000 tigers in captivity.
The Association of Zoos and
Aquariums estimates that as many
as 12,000 tigers are being kept as
private pets in the United States,
4000 in Texas alone. However,
parts of the captive population, such
as the 4000 to 5000 animals in
China’s commercial tiger farms, are
of low genetic diversity.
Tigers kill between 600 and 800
humans a year. In spite of their
dwindling numbers they are the
world’s number one “man killer,” at
least on land. Over the last five
centuries, an estimated 1,000,000
people have been killed by tigers.
Between 1800 and 1900, tigers are
estimated to have killed over
300,000 people in India alone.
Man-eating tigers in India
between 1906 and 1941 killed and
ate an estimated 125 persons each.
One notorious man-eating tigress
known as Champawat killed 436
individuals in India and Nepal
before she was killed in 1907 by
Jim Corbett, a famous tiger hunter.
Examination of the tigress disclosed
that the upper and lower canine
teeth on the right side of her mouth
were broken, which had prevented
her from killing her usual prey and
had caused her to become a man-
eater.
Tigers are normally wary of
humans and have shown no
preference for human flesh. Most
maneating tigers have disabilities
or are old, or their habitat and usual
prey have been destroyed. They
become man-eaters because humans
are easy prey once a taste is
acquired. Taste for human flesh may
be acquired by the consumption of
corpses that have lain unburied.
During the Vietnam and Korean
Wars, soldiers were killed and
injured by tigers who had acquired
a taste for human flesh.
Currently most man-eating
occurs in the Sundarbans Tiger
Reserve in India and Bangladesh,
where an estimated 5 percent of the
tigers are believed to be man-
eaters. Some of the tigers are
entirely healthy. Hundreds of honey
collectors, woodcutters, and
fishermen have been killed in the
reserve’s mangrove jungles even
though entering the reserve without
a permit is illegal.
Unlike man-eating leopards,
man-eating tigers seldom enter
human settlements, usually sticking
to village outskirts. They typically
stalk their prey from behind and,
reportedly, rarely press an attack if
they are seen before their ambush is
mounted. Tigers are known to stalk
groups of people bending down
while working in a field or cutting
grass but lose interest as soon as the
people stand upright, leading to the
hypothesis that some attacks are
instances of mistaken identity.
An adult tiger is so powerful that
a human is often killed instantly. A
blow to the head often has sufficient
force to produce skull fractures.
Like other big cats, a tiger prefers
to strike without warning from
behind, biting the head and neck and
often shaking its head violently to
sever the person’s spinal cord. The
resulting wounds can include
lacerations, sometimes penetrating
body cavities, deep puncture
wounds, fractures that may be
extensive, and contusions. In
addition the wounds are
contaminated by bacteria on the
teeth and claws of these animals.
Individuals who survive an attack
require appropriate antibiotic
therapy as well as attention to the
trauma they have received.
Lions
Lions are the second largest of
the big cats. Adult males range from
330 to 550 pounds. Lions used to
roam all over the world, including
North America and South America
but are now limited to sub-Saharan
Africa, except for a small
population in the Gir Forest of
northwest India. Their numbers are
declining, and they are in danger of
extinction, particularly the small
Indian population, as the result of
habitat loss and conflicts with
humans. The lions around
Kilimanjaro face extermination
from poisoning by Maasai
protecting their cattle.
Male lions with their prominent
manes are among the world’s most
spectacular animals. Reportedly a
lion’s roar can be heard as far as
five miles away. They can run as
fast as thirty miles per hour,
perhaps faster, and are so strong
they can take down prey three times
their size. They can break the neck
of an ox with a single swipe of a
forepaw. However, females are
more accomplished hunters. Males
tend to be scavengers and may
consume animals killed by a female
before allowing the female to eat.
According to some authorities,
hyenas kill more animals than lions.
In the late 1930s through the late
1940s, in what is now Tanzania, a
pride of lions over three
generations was thought to have
killed and eaten 1500 to 2000
humans. Now lions are responsible
for 300 to 500 human deaths a year
in Africa, and the numbers are
increasing. A sophisticated study in
Tanzania found the human death rate
has increased from forty a year to
seventy or more. Between 1990 and
2005, 563 Tanzanians were killed
and at least 308 were injured.
Attacks are most common in areas
with the lowest abundance of
natural prey and with the largest
numbers of bush pigs, which eat the
farmers’ crops.
Mozambican refugees crossing
South Africa’s Kruger National
Park at night are regularly attacked
and eaten by lions. Thousands may
have been killed in the decades
after apartheid sealed the park and
forced the refugees to cross the park
at night. Before that, Mozambicans
had regularly walked across the
park in daytime with little harm.
The lure of the easy kill even
attracts lions in the prime of life,
contrary to the finding that most
man-eaters are elderly or impaired
animals with diminished hunting
abilities. A man-eater in the Rufiji
district of Tanzania thought to have
consumed approximately forty
people was found to be only about
four years old when it was finally
destroyed.
Lions, like other big cats, prefer
to stalk their prey and attack from
behind. According to some hunters,
a lion will break off its attack if the
human turns and challenges it. Once
under attack, the most protective
behavior has not been determined.
Some survivors have claimed that
allowing the lion to chew on an arm
or a leg may distract them from
attacking an individual’s body.
Leopards
Most leopards are now found in
sub-Saharan Africa, most often in
humid forest habitats, but
fragmented populations exist in
India, Southeast Asia, and China.
Despite the loss of range and
continual declines in population,
their numbers are greater than the
other big cats, all of which face
more acute conservation concerns.
Males normally grow to a
weight between 90 and 200 pounds,
and females are about 50 percent
smaller than males. Most leopards
are spotted, but in a few the spots
run together and they appear black,
a condition referred to as melanism.
These animals have been referred
to as black panthers, but they are the
same species.
Leopards kill about 400
individuals each year. A number of
the persons are killed by the attack,
but many die afterward from
infection. Most healthy leopards
prefer wild prey, but cats who are
old, disabled, or struggling with a
shortage of regular prey often turn
to hunting people and may become
habituated to it. In two extreme
cases, both in India, a leopard
dubbed “the Leopard of
Rudraprayag” is claimed to have
killed over 125 people, and the
infamous beast called Panar
Leopard killed over 400 after being
injured by a poacher and rendered
unable to hunt normal prey.
Man-eating leopards are bold by
feline standards and enter human
settlements for prey more
commonly than their lion and tiger
counterparts. One well-known
hunter, who had experience with
many man-eating leopards,
described them as far more
threatening than tigers. Because of
the leopard’s smaller size it can
conceal itself in places impossible
for a tiger, its need for water is far
less, and in devilish cunning and
daring, coupled with an uncanny
sense of self-preservation and the
ability to disappear stealthily when
danger threatens, it has no equal.
Jaguars
Jaguars range primarily in
Mexico, Central America, and
South America, but infrequent
sightings have been recorded in
Texas, Arizona, southern California,
and New Mexico. These animals
vary significantly in size: Weights
are normally in the range of 125 to
210 pounds, but males as large as
350 pounds—roughly matching a
tigress or lioness—or as small as
80 pounds have been recorded.
Females are typically 10 to 20
percent smaller than males.
These animals were threatened
with extinction as the result of
hunting for their pelts. They are
now being protected in many areas
but are rarely seen. Attacks on
humans occur but are uncommon.
Jaguars have extremely strong jaws
and often grab prey—including
humans—by the head, which they
can crush. They also seize the necks
of prey and break them like other
large cats.
Elephants
Attacks by elephants, the largest
of the “large animals,” produce
approximately 500 fatalities a year
in Africa and southern Asia. The
number of attacks has increased so
much in recent years that a new
statistical category, known as
Human-Elephant Conflict, or
H.E.C, has been created. Most
attacks are considered provoked,
although the provocation required
to initiate an attack has diminished
greatly.
In Assam in northeast India,
elephants have killed 605 people in
twelve years, 239 since 2001. In the
Indian state of Jharkhand near
Bangladesh, 300 people were
killed by elephants between 2000
and 2004. During this period 265
elephants died, most killed by
villagers using a variety of poisons.
Other bizarre elephant behavior
also has been occurring. Since the
early 1990s, young male elephants
in Pilanesberg National Park and
the Hluhluwe-Umfolozi Game
Reserve, both in South Africa, and
in other game preserves have been
raping and killing rhinoceroses.
Officials in Pilanesberg shot three
young male elephants that were
responsible for killing sixty-three
rhinos, as well as attacking people
in safari vehicles. In Addo Elephant
National Park, also in South Africa,
up to 90 percent of male elephant
deaths are now attributable to other
male elephants, compared with a
rate of 6 percent in stable elephant
communities.
In normal elephant societies,
young elephants are raised within
an extended network of doting
female caregivers that includes the
mother, grandmothers, aunts, and
friends. These relations are
maintained over a life span that may
be as long as seventy years.
However, faced with diminishing
park land to accommodate these
animals and increasing human
populations that vigorously object
to the damage to farms and crops
elephants produce, park managers
have “culled” herds by shooting
animals en masse. In some areas,
ivory-seeking poachers are known
to prefer grenades over guns to kill
animals.
As a result, the normal network
of caregivers in a herd has been
destroyed, and young elephants
grow to maturity without the
support they normally have. Young
elephants relocated to “societies”
without parental figures are
traumatized and grow to be
aggressive creatures. The resulting
behavioral disorders have been
compared by investigators to post-
traumatic stress disorder in humans.
A more detailed discussion of this
problem is available at
http://www.nytimes.com/2006/10/08
pagewanted=print.
A ranger in South Africa’s
Kruger National Park has set forth a
list of ten rules to prevent or avoid
elephant attacks:
1. The vehicle engine should
never be turned off when
elephants are spotted. If the
elephant becomes aggressive, it
can cover a lot of ground
surprisingly quickly, which may
not leave time to start the
vehicle.
2. Elephants should be given
space. If they are so close that
accelerating very quickly does
not allow escape, they are too
close. At least 60 to 70 feet is
needed.
3. Bulls in musth, an annual
period of heightened
aggressiveness and sexual
activity in male elephants,
during which violent frenzies
occur, should be identified and
given even more space. The
signs of musth include
moisture, like tears, running
down the head, an engorged
penis, moisture on the legs, and
dripping. A distance of 150 feet
or more is required to be safe.
4. Individuals in an area where
elephants are known to be must
stay alert. Elephants are well
camouflaged; they disappear in
the bush, and sudden encounters
in thick bush can surprise both
humans and elephants.
5. Elephants should never be fed
… anything.
6. An elephant shaking its head
and flapping its ears is
uncomfortable. Humans should
back off immediately. They
should not try to pass the
animal if space is not adequate.
(If the elephant can be passed
at the same speed individuals
would normally travel in the
park, and they can accelerate
away without disturbing it, they
have enough space.)
7. If baby elephants are present,
extra vigilance is required.
Female elephants are very
protective, and male elephants
are likely to attack because
females are unhappy.
8. Individuals must watch where
the elephants are going. Getting
the road closed behind them
can be very scary.
9. Individuals must stay inside the
vehicle. Climbing out of a
window changes the profile of
the vehicle and draws interest,
which should be avoided.
10. Real charges by an elephant
usually can be identified
because the ears flatten against
the body and the trunk is rolled
up underneath the head. When
that occurs, it is time to get
away fast.
Trampling, goring with tusks,
and tossing or striking the
individual with the trunk produce
most injuries. When a human is
immobilized, an elephant
sometimes drops on the person with
its knees, crushing the person.
Rhinoceroses
Five species of rhinoceroses
still exist: two in Africa, the white
and black rhinoceroses (which
cannot be distinguished by their
color); and three in southern Asia,
the Indian, Javan, and Sumatran
rhinoceroses. Three of the species
—the Javan, Sumatran, and black
rhinoceroses—are critically
endangered. The Indian is
endangered, with fewer than 2700
animals remaining in the wild, and
the white is considered vulnerable,
with roughly 14,500 remaining.
Rhinos are the third largest
mammal; only elephants and hippos
are larger. The white rhino can
exceed 6600 pounds and can have a
head-and-body length of 11 to 13.9
feet and a shoulder height of
60 to 73 inches. The largest
white rhinoceros was about 10,000
pounds. Its protective skin ranges
from 0.6 to 2 inches in thickness.
The Indian rhino is comparable
in size to the white rhino. It has only
a single horn, as does the Javan. All
others have two horns.
Rhinos have a reputation for
being ill tempered and aggressive
and have become more so in areas
where they are constantly disturbed.
They are notorious for charging
without reason. Some observers
have suggested that they are
aggressive because they get
frightened easily, and mothers are
known to charge readily to protect
their calves. In addition, rhinos
have poor eyesight. (Reportedly
they have even attacked a moving
train.) They rely on their strong
sense of smell to tell them anyone is
approaching, but if they are upwind
they may not know that humans are
nearby until they are close.
When attacking, the rhino lowers
its head, snorts, and breaks into a
gallop, reaching speeds of thirty to
thirty-five miles per hour. It gores
its prey or strikes powerful blows
with its horns. In spite of its bulk,
rhinos are agile and can quickly
turn in a small space. Waiting until
the last second then jumping aside
has been suggested as a means for
avoiding rhino gorings, but most
rhinos are in protective parks and
reserves and individuals are not
allowed to leave their vehicles (or
the backs of elephants in India and
Nepal), where they are reasonably
safe. However, these beasts kill a
number of individuals, particularly
in areas where their ranges overlap
sites of human habitation.
Hippopotamuses
The hippopotamus is a large
mammal found in rivers and lakes
throughout much of Africa,
although, like most large African
animals, its population is declining
and its existence is threatened,
primarily as the result of habitat
loss and hunting. It is semiaquatic
and more closely related to whales
than to other hoofed animals. The
average weight for adult males
ranges between 3300 and 4000
pounds. However, male hippos
appear to continue growing
throughout their lives, and older
males can get much larger, reaching
at least 7000 pounds and
occasionally 8000 pounds. Females
are smaller than their male
counterparts, with average weights
between 2900 and 3300 pounds.
They reach a maximum weight
around age twenty-five and have
been known to live up to forty-five
years in the wild.
The hippopotamus is
characterized by its stout body,
stubby legs, and large bulbous head.
The jaws can open up to 150
degrees, a display indicative of
anger. The tusklike canine teeth are
long, and the incisors are sharp.
The bite force of an adult female
hippo has been measured at 1821
pounds. (An attempt to measure the
bite of an adult male had to be
abandoned due to the animal’s
aggressiveness.)
Though ungainly in appearance,
the hippopotamus can run as fast as
thirty miles per hour, which is faster
than an Olympic sprinter.
Hippos leave the water at dusk
and travel inland, sometimes up to
five miles, to graze on short grass,
their main source of food. They
spend four to five hours grazing and
can consume 150 pounds of grass
each night. Although primarily
herbivores, they have been known
to consume meat, usually when their
normal diet was not available.
Hippos are responsible for 200
to 300 human deaths a year and are
another animal credited with killing
more humans in Africa than any
other. They are known to attack
boats, coming up under canoes and
biting them in half. However, most
attacks occur on land and are
inflicted on individuals who get
between an animal and the water in
which it spends most of its time.
Refusing to believe how rapidly
hippos can run contributes to the
death of many individuals.
Crocodiles
In Australia sixteen attacks and
four deaths from attacks by
crocodiles were recorded over a
ten-year period. In contrast,
crocodiles are reputed to kill over a
thousand individuals a year in
Africa and are another of the
animals of Africa credited with
killing more humans than any other.
Unlike other man-eating crocodiles,
the Nile crocodile lives in close
proximity to large human
populations, so contact is more
frequent. However, this figure has
been disputed, and some
investigators think the number is
limited to several hundred, which is
more than all the other crocodiles
combined. Crocodiles have been
witnessed scavenging for babies
and young children in the Nile.
Attacks by crocodiles and the
injuries they produce are similar to
attacks by American alligators.
To avoid attacks, individuals are
advised to:
◆ Stay away from infested
waters, particularly at dusk or
at night, when the animals are
harder to see and when they
most actively hunt.
◆ Be aware of surroundings.
They should not dangle arms or
legs off a boat and must keep
some distance from the water
when walking on shore—
crocodilians frequently attack
fishermen and people gathering
on the shore—and should
avoid thick vegetation that
provides these animals with
good cover.
◆ Stay a safe distance from
alligators or crocodiles.
Fifteen feet is usually adequate
on land, but during mating
season a greater distance is
advisable. Nests or baby
crocodilians must be widely
avoided. Mothers are fiercely
defensive.
◆ Avoid surprising the animals.
When boating, making noise by
slapping the water with
paddles or oars, or blowing a
whistle can alert these animals.
Riverbanks should be avoided
when coming around bends in a
river.
◆ Run away from the animal.
Crocodilians rely on surprise
to capture prey, and it is
unusual for one of these
animals to pursue a person on
land. Crocodiles are not
sluggish on land, but they are
not fast either. They can run
about ten miles per hour, and
they quickly grow tired.
◆ Run away from the water.
Crocodiles seldom run on land
unless they’re trying to get
back into the water. The
commonly repeated instruction
to run in zigzags is useless; the
fastest way to get away from
the animal is to run in a straight
line.
◆ Pets should not be allowed to
swim in water inhabited by
alligators. Dogs should be kept
on a leash. Pets are frequently
attacked by crocodilians, and
their owners may be attacked if
the pet harasses one of these
animals or catches its attention
as potential prey.
Crocodilians are capable of
memorizing traveling routes and
campsites. When camping in these
animals’ habitat, the camp should be
well away from water, and the area
must not be littered with food
scraps. If the water must be
approached or entered to collect
water, wash dishes, or bathe, it
must be done with caution. Entering
the same place each time must be
avoided.
Cape Buffalo
The cape, or African, buffalo is
a large animal that weighs 1100 to
2000 pounds. The closely related
forest buffalo is only half that size.
The African buffalo is not closely
related to the slightly larger Asian
water buffalo, and its nature is so
unpredictable that it is highly
dangerous to humans and has not
been domesticated like its Asian
counterpart.
The African buffalo is one of the
most successful grazers in Africa. It
lives in swamps and floodplains, as
well as grasslands and forests of
the major mountains of Africa.
Buffalo can be found from the
highest mountains to sea level and
prefer habitat with dense cover,
such as reeds and thickets.
However, herds are also found in
open woodlands and grasslands.
These animals are notorious for
unprovoked attacks but usually do
not attack unless cornered. They can
run as fast as thirty-five miles per
hour. They kill twenty to a hundred
humans each year. Reportedly, more
big game hunters have been killed
by African buffalo than by any other
African animal. Wounded animals
are reputed to stalk the hunter,
sometimes circling behind them and
attacking.
Hyenas
Although hyenas bear some
physical resemblance to dogs, they
are most closely related to
mongooses. All hyena species have
a distinctly bearlike gait because
their front legs are longer than their
back legs. Hyenas, in particular the
spotted hyena, are highly intelligent
animals, and some studies have
indicated that they have
independently evolved traits similar
to primates as a result of having to
adapt to similar environments.
Spotted hyena societies are more
complex than those of other
carnivorous mammals and have
been reported to be remarkably
similar to those of baboons,
macaques, and green monkeys in
group size, structure, competition,
and cooperation.
Hyenas have extremely strong
jaws for their body size and a very
powerful digestive system with
highly acidic fluids, making them
capable of eating and digesting their
entire prey, including skin, teeth,
horns, and bones. They eat carrion,
so their digestive system must deal
very well with bacteria.
The spotted hyenas are primarily
predators and successful pack
hunters of small and large
ungulates. They are the most
abundant carnivore on the African
continent. Some observers consider
them more successful predators and
less dependent upon scavenging
than lions.
Hyenas attack natives sleeping
outside their huts in warm weather,
commonly decapitating them or
producing massive facial trauma.
They have been known to attack
campers sleeping with their heads
at the open end of a tent. They are
more consistent man-eaters than
lions or tigers.
Primates
Bites by monkeys and other
primates are common and occur
most frequently in urban sites and in
animal preserves where the
monkeys and other primates have
become accustomed to humans,
particularly to being fed by humans.
In Rohtak, India, monkey bites
accounted for 8.8 percent of all
animal bites treated at the
Postgraduate Institute of Medical
Sciences, and monkeys are
becoming the second most common
animal to inflict bites. In Nepal,
monkeys are responsible for 25
percent of the animal bites that
require postexposure rabies
therapy.
One small neighborhood in New
Delhi reported more than thirty-five
monkey attacks on humans in only
one month’s time. The attacks
included bites, breaking into
people’s homes, and vandalism. In
that city monkeys often attack in
packs, making them much harder to
fight off. In a New Delhi hospital
monkeys have attacked doctors and
have even tried to run off with
newborn babies.
Monkeys attack humans in an
effort to get food. Monkeys at the
Swayambunath Temple in
Kathmandu, Nepal, are notorious
for attacking humans—and for being
infected with rabies. In Malaysia
over 300 monkey attacks on humans
were reported in one year. Most of
the humans were carrying colorful,
transparent plastic bags, and the
monkeys apparently thought the
bags contained food.
Other primates attack humans for
food, too. According to a bulletin
from Cape Point, South Africa,
baboons are not a threat to humans
until they get fed. Then they can
become aggressive and attack
humans to get food. In Taung, a
small town in South Africa, a
baboon broke into a home and
killed a three-month-old infant by
biting its head. The area was
suffering from a drought, and the
baboon apparently was searching
for food. It bit the infant when
threatened by adults in the house.
Larger primates, such as
chimpanzees, which are incredibly
strong, go on rampages that do not
appear to be related to food. A
chimp that had escaped from the
Tacugama Chimpanzee Sanctuary in
Sierra Leone attacked a car
carrying four adult men, killed one
of the men, and bit away half of the
hand of another. Two chimps that
escaped from a southern California
animal preserve attacked a man and
his wife. They chewed off most of
the man’s face, tore off his foot, and
attacked his limbs and genitals. A
psychobiologist who studies
primate behavior suggested that the
aggression might have been related
to the presence of sexually
receptive females.
Interestingly, gorillas, are
herbivores and—in spite of the way
they are portrayed in fiction and
movies—are placid animals and
almost never attack humans.
Bites by smaller primates can be
avoided by behaving in a
threatening manner: waving sticks
or clubs, pretending to throw or
actually throwing stones, or even
exploding firecrackers. Large
primates would not be deterred by
such actions and can be escaped
only by seeking shelter. A motor
vehicle may not suffice because
chimpanzees can break through the
windows.
Monkey bites commonly produce
significant injuries. Loss of one or
more fingers is not uncommon.
Furthermore, the bite wounds
typically become severely infected.
All such wounds must be thoroughly
irrigated, then rinsed with a
bactericidal agent such as
Betadine®. The wounds should not
be sutured. Prophylactic antibiotics,
tetanus immunization, and
postexposure rabies therapy all
must be carefully considered.
Kangaroos
Kangaroos are shy and retiring
and present little threat to humans.
Male kangaroos often “box” for
dominance or in competition for
mates. Their forepaws are used for
punching and grappling. A real
danger exists with a kick by a
hindleg because sharp toenails
could disembowel an opponent.
Kangaroos rarely attack humans
without provocation, although more
pummelings have occurred in recent
years as an expanding human
population has encroached on
kangaroo territory. The only
reliably documented fatal kangaroo
attack occurred in New South
Wales in 1936 when a hunter was
killed trying to rescue his two dogs.
CARE FOR INDIVIDUALS

ATTACKED BY ANIMALS
The wounds inflicted by attacking
animals are not significantly
different from the soft-tissue
injuries and fractures produced by
other traumatic incidents, except for
the greater risk of infection.
Prehospital care for individuals
who have been attacked is
complicated: Is the scene safe? Is
the attacking animal likely to
return? Since each situation is
different, no specific rules can be
made, but these details must not be
overlooked or ignored.
Otherwise, care for individuals
who have been attacked by animals
is little different from care for those
injured in other accidents. Rescuers
first on the scene should check the
ABCs: airway, breathing,
circulation. The severity of the
individual’s disability must be
ascertained, and at some point all
clothing should be removed to
ensure no wounds go undetected
and untreated.
Individuals with severe wounds
should be evacuated as fast as
possible.
Bacteria almost always heavily
contaminate animal bite wounds.
Lacerations and puncture wounds
must be carefully explored,
debrided, and vigorously irrigated
with disinfected water. Foreign
material is often introduced by
animal wounds and must be
carefully sought. Only after
thorough cleaning can wounds be
dressed and splinted.
High-risk wounds, including
wounds of individuals who are
immunocompromised, constitute
dangerous situations. Such wounds
should be sutured only by
experienced physicians.
Hand wounds are common
because the hands are used to
defend against the attacking animal.
Such wounds deserve special
consideration because the structures
are anatomically complex and hand
function is so much a part of day-to-
day activities.
Puncture wounds are common in
bites and must be appropriately
treated.
Everyone bitten by a wild
animal should be offered
postexposure rabies therapy
(Chapter 32: Rabies). Tetanus
immunization should be
administered if the individual has
not had a booster within five years.
Antibiotic therapy is particularly
significant following an animal bite
because the wounds are so
contaminated. The organisms
typically found in bite wounds are
specific to the source:
◆ Bears—Micrococcus and
Streptococcus
◆ Cats—Pasteurella and
Pseudomonas
◆ Ungulates—Pasteurella and
Acinetobacillus
◆ Crocodiles—Aeromonas
If possible, antibiotic therapy
should be directed toward the
specific pathogens associated with
the attacking animal species.
Otherwise, broadspectrum
antibiotics should be administered.
Amoxicillin/clavulanate
(Augmentin®) is probably the drug
of choice in most cases. A
cephalosporin with metronidazole,
clindamycin and doxycycline,
gatifloxacin, or moxifloxacin are
other alternatives.
CHAPTER 32
RABIES
Rabies is a catastrophic viral

infection that has been known and
justifiably feared since antiquity. In
all of history, only six humans who
have developed clinical signs and
symptoms of rabies are known to
have survived. All but one were
vaccination failures, and three had
severe residual neurologic damage.
(One was blind, quadriplegic, and
dead only thirty-four months after
he became ill.) Although rare in
industrialized nations, rabies
remains a scourge in developing
countries that cannot afford the
canine vaccination programs
required to keep the infection under
control. In India approximately
25,000 people die every year from
rabies. The incidence is probably
similar in Africa—Ethiopia has a
high incidence of rabies—but
surveillance and reporting are so
inadequate the true rate is unknown.
The World Health Organization
(WHO) estimates that 55,000
individuals die every year from
rabies. This infection ranks
eleventh among infectious causes of
death worldwide.
RABIES WITHIN THE UNITED

STATES
Within the United States, human
rabies has been controlled to a
large extent by vaccinating
domestic animals, mostly dogs and
cats, and eliminating stray animals.
Dog rabies diminished from 6949
cases in 1947 to 79 in 2006.
(Rabies is now more common in
cats, with 318 cases reported in
2006.) Human rabies has
concomitantly declined from
approximately 350 cases from 1940
to 1949 to 10 cases from 1980 to
1989, seven of which were
acquired outside the United States.
Two of the other three were of bat
origin, and the third was from a
skunk. From 1990 through 2006, an
additional forty rabies infections
were acquired within the United
States; all but three were caused by
rabies virus strains associated with
bats (Figs. 32-1 and 32-2).
Figure 32-1. Human rabies acquired
from bats in the United States, 1980–
2006 (39 cases total)
Figure 32-2. Rabies in bats, 1998
(989 cases total)
Essentially all mammals are

susceptible to rabies and capable of
transmitting the infection, but
transmission by rodents has not
been documented. The United States
and Canada are unique in that
rabies epizootics (rabies epidemics
in animals) are recognized in a
number of wild animals: raccoons,
skunks, foxes, and bats. Bat rabies
is endemic in all areas of the
continental United States, both
urban and rural, including Alaska.
An epizootic in raccoons that
began in the late 1970s has spread
to involve the entire U.S. East
Coast (Fig. 32-3). Only one human
rabies infection has resulted from
this epizootic, although extensive
vaccination programs have been
required after humans contacted
animals infected with the raccoon
virus.
A coyote and gray fox epizootic
in southern Texas originated from
unvaccinated dogs crossing the Rio
Grande from Mexico. It spread to
dogs in Texas, resulting in two
human rabies deaths in 1991 and
1994 and over 2000 humans having
to be vaccinated. This epizootic has
been controlled with baits
containing an oral rabies vaccine,
most of which were dropped from
aircraft, the largest program of this
type every accomplished.
TRANSMISSION OF RABIES
In infected animals, the rabies virus
travels through nerves from the
central nervous system to the
salivary glands and is present in the
saliva. Transmission of the
infection occurs when a bite wound,
a preexisting wound, or a weeping
skin rash is contaminated with the
saliva of a rabid animal. The
infection can also be transmitted by
scratches because animals lick their
paws and their claws are
contaminated with saliva containing
the rabies virus. The virus cannot
penetrate intact skin but can pass
through intact mucous membranes
such as the lining of the mouth,
nose, or eyelids. Licking alone can
transmit the infection if saliva
contacts these surfaces.
The average incubation period
between the time of the bite and the
appearance of a clinically evident
infection is thirty-five days.
(Approximately 1 percent of human
rabies infections appear following
an incubation period of a year or
more.) The virus travels along
nerves at 15 to 100 mm a day to
reach the brain. Bites on the
extremities allow more time for
treatment than bites about the face,
which are particularly dangerous
and must be treated urgently.
Figure 32-3. Rabies in raccoons, 1998
(2872 cases total)
Bat rabies is thought to be

transmitted to humans by bites,
although bat teeth are so small and
so sharp that bites go undetected,
particularly when individuals are
sleeping when the bite occurs. Four
infections have been spread by
aerosols, two in laboratories and
two in Frio Cave near Uvalde,
Texas. Only six of the thirty-seven
individuals infected with rabies of
bat origin from 1990 to 2006 had a
clear history of a bite by a bat,
although two had a history
suggestive of a bat, and fifteen had
reported physical contact with a
bat. Eleven individuals did not
know of any contact with a bat.
TREATING THE BITE OF A

RABID ANIMAL
The treatment for rabies
(immunoprophylaxis) is a race to
develop protective immunity before
clinical infection appears.
Treatment must be initiated at the
time the bite is inflicted. Therapy
begun after the individual begins to
show signs of rabies is ineffective.
The treatment of any animal bite
has three components:
◆ Cleansing the bite wound
◆ Passive immunization with
rabies immune globulin
◆ Active immunization with
rabies vaccine
Within the United States, if the
attacking animal is a domestic dog,
cat, or ferret that has been
vaccinated for rabies within the
past year and can be captured, it
should be confined under
observation for ten days following
the bite. If the animal is healthy at
the end of that time, it is safe to
assume the animal did not have
transmissible rabies at the time the
bite was inflicted, and
immunotherapy is not required.
All other animals, including
wolf hybrids, should be killed
(euthanized) and their heads
shipped under refrigeration to a
laboratory where the brain can be
examined to determine whether
rabies virus is present. Public
health services are responsible for
maintaining reliable laboratories
and for transporting the heads.
If the animal cannot be killed or
captured, or if the encounter occurs
in a developing country, the animal
must be assumed to be rabid
regardless of the manner in which it
was behaving or whether it has
been vaccinated. Rabies in animals
follows a highly variable course.
The notorious “mad dog” foaming
at the mouth is almost never seen.
Unprovoked attacks are the most
common indication of rabies.
The behavior associated with
rabies by animals other than dogs or
cats is not well known.
Occasionally the only sign of rabies
is the absence of fear of humans,
which may even appear to be a
show of friendliness. Animals such
as skunks, which usually scurry
away from any threatening situation,
may actually pursue humans.
Because rabid behavior of such
animals is unknown, quarantining
for ten days is not a reliable way to
determine whether they are
infected.
The only exceptions to this
caveat would be those few areas
where rabies does not occur.
Hawaii, for example, is free of all
forms of rabies. (To prevent the
introduction of this infection any
mammal brought into the Islands is
quarantined, unless the animal can
be positively identified by an
implanted microchip, has been
vaccinated for rabies, and
laboratory studies have
demonstrated that the vaccination
was effective.)
Cleansing of the bite wound is
just as vital as administration of
immune globulin and vaccine in the
care for persons exposed to rabies.
The severity and speed of onset of
any infection is dependent upon the
number of viruses or bacteria
introduced. Rinsing saliva out of a
bite wound reduces the number of
rabies viruses that can enter the
tissues and slows the onset of
infection, which allows time for
vaccination to be effective.
Washing should be done with
large quantities of soap and water
—the WHO recommends fifteen
minutes of continuous washing—
and the wound subsequently should
be flushed with a povidoneiodine
preparation such as Betadine®.
Washing is of such urgency that it
should be instituted without delay.
If soap and water are not available,
anything on hand—even a favorite
whiskey—should be used.
Immunotherapy for rabies
consists of administering immune
serum from an individual or horse
immune to rabies, followed by
vaccine to build up immunity to the
rabies virus. The immune globulin
provides passive immunization
while the body is building active
immunity in response to the
vaccine. In the United States and
Canada only immune globulin of
human origin is licensed. In
developing nations, usually only
equine (horse) globulin is
available.
Twenty international units per
kilogram of body weight (20 IU/kg;
2.2 lb = 1 kg) of rabies immune
globulin of human origin or 40
IU/kg for equine globulin should be
injected around the wound. If a
single bite is on a finger or toe, as
much globulin as possible should
be infiltrated immediately around
the wound; the rest should be
injected deeply in the nearest large
muscle. (Infiltration of large
volumes of globulin into a finger is
painful.) If multiple wounds are
present, the globulin can be diluted
with saline and injected around all
the wounds. (Additional globulin
should not be given because it
interferes with active immunization
by vaccine.)
Following an exposure, one
milliliter (1 ml) of rabies vaccine
should be injected into the deltoid
muscle on the day of the bite (day
zero) and on days three, seven,
fourteen, and twenty-eight. The
injections must be made into the
deltoid (shoulder) muscle for adults
and the anterior thigh for small
children. Rabies has developed
following gluteal (buttock)
injections of vaccine.
The WHO has approved three
rabies vaccines:
◆ Human Diploid Cell Vaccine
—Rabivac®, Imovax®
◆ Purified Chick Embryo Cell
Vaccine—Rabipur®,
RabAvert®
◆ Purified Vero Cell Vaccine—
Verorab®, Imovax®, Rabies
Vero®, TRC Verorab®
Only the first two are available
in the United States and Canada.
Because a few cases of human
rabies develop following prolonged
incubation periods—at least two
were six years—postexposure
therapy should be administered
regardless of the time that has
elapsed since the bite.
BAT EXPOSURES
Because the manner in which rabies
is transmitted by bats is uncertain,
the following four measures have
been recommended:
◆ Dwellings should be bat-
proofed by carefully covering
all possible entrances,
particularly roof ventilation
openings, with wire screens.
Protection from bats in
unscreened dwellings or when
sleeping outdoors can be
achieved with mosquito
netting.
◆ Contact with bats should be
assiduously avoided,
particularly bats that are
behaving unusually. Bats are
nocturnal, and any activity
during daylight hours should be
considered abnormal.
Diseased bats often are unable
to fly. Bats should be caught
with nets; disabled bats should
be scooped into a container.
These animals must never be
picked up or handled with
unprotected hands.
◆ Anyone who has contact with
a bat, regardless of whether a
bite is thought to have been
inflicted, should receive
postexposure rabies therapy
unless the bat can be caught
and tested for rabies.
◆ Anyone, particularly a child,
who awakens from sleep and
finds a bat in the room should
receive postexposure
prophylaxis unless the bat can
be caught and tested for rabies.
A number of U.S. rabies
infections in children have
followed this type of exposure.
(A tennis racket may be useful
for capturing a bat. Injuring the
animal is not a consideration
because it must be killed to
examine its brain for rabies.)
The problem of rabies
transmission by bats is best
addressed through education.
Reducing the bat population is not
an acceptable approach, is
probably impossible, and would
almost certainly be an ecological
disaster because bats play such a
major role in insect control.
RABIES IN DEVELOPING
COUNTRIES
Any bite or contact with saliva from
any animal in a developing country
should be considered an exposure
to rabies, regardless of the animal’s
vaccination history. The vast
majority of such exposures are to
dogs, although in Nepal monkeys
are responsible for approximately
25 percent of exposures, commonly
monkeys leaping for food held by
tourists visiting the Swayambunath
Temple.
Individuals exposed to rabies
while visiting developing countries
cannot depend upon local
physicians or institutions for
reliable treatment. In many areas
vaccine prepared from infected
animal brains is used to immunize
individuals exposed to rabid
animals because it is inexpensive.
This vaccine has been described as
the “crudest” biological preparation
administered to humans. It varies
considerably in its potency and
effectiveness and probably is not
effective for severe exposures with
multiple bites about the head and
neck. Twentyfour injections are
required and are quite painful, and
the vaccine is associated with a
high incidence of side effects, a
number of which are disastrous.
Vaccination should be refused
unless the recipient is certain the
preparation is one of the
WHOapproved vaccines.
The amount of rabies immune
globulin being produced worldwide
is estimated to be about one-third
the quantity needed for treating all
individuals exposed to rabies. In
developing countries, immune
globulin is rarely administered.
Travelers to those countries treated
in local facilities are not given
immune globulin unless they know
enough about rabies postexposure
therapy to insist upon its
administration.
If a reliable source of therapy,
such as the CIWEC Clinic in
Kathmandu, Nepal, or the Queen
Saovabha Memorial Institute in
Bangkok, Thailand, is not available,
U.S. citizens exposed to rabies
should go immediately to the
nearest American embassy. These
embassies have physicians on their
staffs or available to them and are
required to be able to obtain
reliable immune globulin and
vaccine within an appropriate
period of time. (Citizens should not
allow themselves to be turned away
in off-duty hours by uninformed
duty personnel.) In addition, the
embassies of Canada and Britain
have usually welcomed the
opportunity to assist citizens of the
United States in an emergency.
PREEXPOSURE RABIES
VACCINATION
Preexposure rabies vaccination of
humans consists of the three
intramuscular injections of 1.0 ml
of vaccine on days zero, seven, and
twenty-one or twentyeight. Rabies
vaccines are so reliable that
serologic testing for antibody levels
is recommended only for
individuals known to be
immunodeficient.
In 1987 the Food and Drug
Administration (FDA) approved
vaccinations with only 0.1 ml of
vaccine intradermally on the same
schedule. (The volume injected is
only one-tenth that administered
intramuscularly.) However, the
antibody level produced by
intradermal injections is not as
high, and does not last as long, as
that produced by intramuscular
injections. Some authorities are
recommending that only
intramuscular injections be
administered, and the vaccine for
intradermal injections has not been
available for a number of years.
If a vaccinated individual
subsequently has contact with a
rabid animal, treatment with
vaccine is still necessary. However,
rabies immune globulin is not
needed, and only two vaccine
injections (1.0 ml injected in the
deltoid muscle) on day zero and day
three after exposure are required.
The duration of therapy is much
shorter, but at a time when rabies
immune globulin may be difficult or
impossible to find in many areas,
eliminating the need for immune
globulin is a more significant
consideration.
and Prevention (CDC) divides
individuals at risk of developing
rabies into three groups. Group I
has the highest risk and consists of
rabies laboratory workers. Group II
has a lower but significant risk and
includes spelunkers, as well as
veterinarians, animal control
workers, and fish and game
wardens in areas of high rabies
incidence. For these individuals,
CDC recommends vaccination and
serologic testing or boosters every
two years.
Group III, which has a definite
but still lower risk, includes
travelers to areas with a high
incidence of rabies, veterinarians
and animal control workers in areas
of low rabies incidence, and
veterinary students. The Advisory
Committee for Immunization
Practices recommends preexposure
vaccination only for individuals
who are planning to reside in rabies
endemic areas for thirty days or
more. However, CDC and many
other authorities recommend such
vaccination for anyone visiting
remote areas from which they
cannot reach a center where
appropriate therapy can be given in
less than twenty-four hours. These
authorities also recommend
preexposure vaccination for young
children who cannot be relied on to
stay away from dogs or to report
any contact with dogs.
RELIABILITY OF RABIES
POSTEXPOSURE THERAPY
In its 1992 Eighth Report, the World
Health Organization Expert
Committee on Rabies made the
remarkable statement, “Prompt and
thorough cleansing of the wound,
and administration of purified
equine or human rabies
immunoglobulins and cell-culture
rabies vaccine immediately after
exposure virtually guarantee
complete protection.” They added,
“Pregnancy and infancy are never
contraindications to post-exposure
rabies vaccination.”1 Since rabies
is essentially always fatal, no
contraindication can exist.
____________
REFERENCE
1. WHO Expert Committee on
Rabies, Eighth Report. Geneva,
World Health Organization, 1992
(WHO Technical Report Series,
No. 824).
CHAPTER 33
ENVENOMATIONS
A wide variety of animals employ

venoms aggressively or
defensively. Best known are
venomous snakes and lizards and
arthropods such as spiders,
scorpions, and insects. However,
cartilaginous and teleost fish and
jelly fish are venomous. The box
jelly fish is considered by many to
be the most venomous creature in
the world. Even a few mammals are
venomous. Some species of shrew
are capable of delivering venomous
bites, and male platypuses have a
venomous spur on their hind legs.
VENOMOUS SNAKEBITES
Venomous snakebites are
unquestionably serious, potentially
deadly accidents. Nonetheless, the
danger from a single bite has been
greatly exaggerated, particularly in
the United States, where
approximately five to ten people
(some of whom have refused
therapy) die each year as the result
of bites by venomous snakes. Less
than 1 percent of venomous
snakebites in the United States are
lethal. In other parts of the world,
where many snakes have much more
toxic venom and sophisticated
medical care is not available,
venomous snakebites are a more
serious problem.
Worldwide the treatment of
venomous snakebites remains a
subject of controversy and
confusion. (Even the material used
to treat snakebites is referred to
variously in the English literature as
antivenom, antivenin, or
antivenene.)
No venom is injected in
approximately 25 percent of
venomous snakebites (reportedly 80
percent of king cobra bites). In
another 25 percent venom has been
injected but the envenomation is
mild. Individuals with such bites
recover regardless of how they are
treated (unless they are killed by the
therapy or complications such as an
infection). In addition, many
nonvenomous snakes are incorrectly
identified as venomous. Recovery
of individuals from bites with
which little or no venom was
injected, or bites by nonvenomous
snakes following many types of
therapy, some of which—like
electrical shock—seem bizarre, has
led to acceptance of some
ineffective or unnecessary
treatments as beneficial. A
sensationalist press has aided the
wide dissemination of
misinformation.
Families of Venomous Snakes

The world’s venomous snakes
are divided into three families.
Within the family Elapidae are the
North American coral snakes
(eastern, western, and Sonoran); the
Indian krait found in India and
Pakistan; the tiger snake of
Australia; the death adder of
Australia and New Guinea; the
Indian king cobra, which occurs in
most of Southeast Asia, including
Indonesia and Formosa, and
reportedly is responsible for more
deaths than any other species; the
mamba of East Africa; and the
ringhals of South Africa.
The Viperidae include the puff
adder found in most of Africa and
southern Arabia; the saw-scaled
viper that occurs from northern and
western Africa to northern India;
the Palestine viper of the Middle
East; and the Russell’s viper found
from west Pakistan to Formosa. No
members of this family are found in
North America or South America.
The Crotalidae are of major
importance in North America and
South America. They include all the
North American rattlesnakes; the
copperheads and cottonmouth
moccasins; the fer-de-lance and
neotropical rattlesnakes found from
Mexico to Argentina; the
bushmaster found from Costa Rica
to the Amazon River basin; and the
habu that occurs in the Ryukyu
Islands of Japan, along with closely
related species in Formosa and the
southeastern part of the People’s
Republic of China.
Identification of Venomous
Snakes in the United States
The venomous snakes of the
United States are the rattlesnakes,
the copperheads, the cottonmouth or
water moccasin, and the coral
snakes. All U.S. venomous snakes
except the coral snakes are pit
vipers and have a characteristic
triangular head and heavy body. The
body markings are sufficiently
unique for species identification by
inexperienced individuals for only
a few of the rattlesnakes.
These snakes are called pit
vipers because they have a small pit
located between the eye and the
nostril—a feature found only in
these venomous species—that is an
infrared-sensing organ instrumental
in detecting the small, warm-
blooded animals these snakes eat
(Fig. 33-1). The pit vipers are also
characterized by single scales
reaching across the undersurface of
the body posterior to the anus. Most
other snakes have double scales
(Fig. 33-2).
If fangs are present, a snake is
undoubtedly venomous, but
searching for fangs is a hazardous
venture. The fangs may be folded
back against the roof of the mouth,
which makes them difficult to
identify. One or both fangs may be
broken off; three or four are
occasionally found. Rattles are of
obvious significance, but the
absence of rattles is not, because
sometimes they also may have
broken off. The Catalina Island
rattlesnake sheds its rattles with its
skin and never has more than one.
Coral snakes are small, thin,
brightly colored snakes with small
heads and are quite different from
the pit vipers. Adjacent red and
yellow bands identify them. The
nonvenomous king snakes and other
harmless species with similar
coloration have adjacent red and
black bands. A helpful mnemonic is
“Red and yellow—kill a fellow;
red and black—venom lack.”
Figure 33-1. Comparison of the heads
of pit vipers and nonpoisonous snakes
Figure 33-2. Comparison of the scales
on the undersurface of tails of
poisonous and nonpoisonous snakes
Identification of Venomous
Snakes in the Eastern
Hemisphere
Vipers (Viperidae) have large
heads and heavy bodies and tend to
resemble pit vipers, but they lack
the pits of the crotalids
(Crotalidae). Elapids do not at all
resemble pit vipers. Elapids have
small heads and thin bodies like the
coral snakes, but few have such
brilliant coloring. Except for a few
species with distinctive hoods
(mostly cobras,) they have an
appearance similar to many
nonvenomous snakes. The
venomous snakes of Australia,
including the innocently named
brown snake and the more
appropriately named death adder
and tiger snake, are elapids. Many
of the venomous snakes of Africa,
including the notorious black
mamba, also are elapids. To
individuals accustomed to the
heavy-bodied American crotalids
or pit vipers, these snakes appear
harmless, but their venoms are
vicious. Travelers who are not
knowledgeable should avoid all
snakes in areas inhabited by these
reptiles.
Snake Venoms
The venoms of all venomous
snakes contain similar toxins. To
classify snakes according to a
single target for their toxin is
misleading and can result in
inadequate medical therapy.
Vascular toxins damage the
walls of blood vessels and inhibit
blood clotting. The combination of
the two results in bleeding into the
tissues at the site of the bite as well
as spontaneous bleeding from the
gums, nose, or gastrointestinal tract.
The damaged blood vessels allow
proteins and fluid to leak into the
tissues, which produces swelling at
the point where the bite occurs.
Such fluid loss in combination with
the destruction of red blood cells
and blood proteins reduces the
circulating blood volume and leads
to shock, a consistent feature of
severe envenomation by snakes of
all species.
The ultimate effect of the
neurotoxins is paralysis, most
importantly respiratory paralysis.
However, abnormal sensations such
as tingling or prickly feelings and
partial paralysis of the eyelids are
more common. Although pit vipers
have been described as having
predominantly hemolytic toxins,
characteristic early symptoms
following the bites of some
rattlesnakes are numbness and
tingling of the lips and a metallic
taste, both of which result from the
effects of the toxin on neural
tissues.
Crotalid venoms do tend to have
higher concentrations of hemolytic
toxins; elapid and viper toxins tend
to have higher concentrations of
neurotoxins. However, more than a
dozen different venom components
have been identified. Different
species within the same family have
venoms of different composition.
Venom concentrations also vary.
Some, like that of the copperhead,
are rather weak, whereas others,
like that of the Mojave rattlesnake,
are concentrated and quite potent. In
addition, larger snakes are able to
inject a larger volume of venom
than smaller snakes. The
concentration of the venom, the
concentrations of its individual
components, and the venom’s total
volume are different in the same
snake at different times of the year.
Snakes tend to have more
concentrated venom when they have
just come out of winter hibernation.
Because the venom of a
copperhead is so mild, persons
bitten by these snakes often require
little more than supportive therapy.
Antivenom may not be needed for
adults bitten by a single snake. In a
compilation of over 400
copperhead bites in eastern North
Carolina, only two deaths could be
found. In both instances, the
unfortunate individuals had been
bitten simultaneously by three or
more snakes.
In contrast, the eastern
diamondback rattlesnake, a large
species that is more aggressive than
most snakes, produces venom that is
only moderately toxic, but the
volume is so great that bites by this
snake require vigorous treatment. In
the United States this species is
responsible for more venomous
snakebite deaths than any other.
Most of the bites occur in Florida.
The Mojave rattlesnake is small
but has very potent venom with a
high concentration of neurotoxins.
The effects of envenomation by this
species tend to be delayed, may not
become fully apparent until twelve
hours after the bite, and may be
much more severe than indicated by
the initial reaction.
Diagnosis of Envenomation
Although identifying the species
of snake inflicting a bite is
desirable, it is not essential. In the
United States catching or killing the
snake is not advisable because the
risks are greater than the benefits. In
some areas of the world, broad-
spectrum antiserum is not available
(for some species it is not
effective), and specific antiserum
must be administered. If the snake
cannot be precisely identified,
specific therapy may be impossible.
Inspecting the bite occasionally
helps in determining that the snake
is venomous. Typically the fangs of
a pit viper produce two small
puncture marks, which are a
reliable indication that the snake
was a member of this family.
However, characteristic fang marks
are distinctly uncommon. The target
is usually moving, and the snake’s
strike is rarely accurate. Only one
fang may strike, or the fangs may
only graze or scratch the skin. The
snake may be missing a fang, and
occasional snakes have three or
even four fangs. The fang marks
may be hidden among the marks
from the other teeth if the snake has
embedded its fangs so deeply that
the other teeth have also penetrated
the skin. Although only the fangs
have entered the skin, a U-shaped
row of teeth marks from the bottom
jaw may be present.
Even though an attacking snake
can be positively identified as
venomous, the individual it has
bitten does not require specific
treatment unless envenomation has
occurred. Venomous snakes attack
humans in sheer terror, not for food.
Sometimes snakes strike without
opening their mouths or extending
their fangs. Occasionally venom is
only sprayed on the surface of the
skin or clothing. Even when the
fangs pierce the skin, no venom or
only a very small quantity is
injected in approximately 25
percent of the bites by venomous
snakes occurring in the United
States. Reportedly, for king cobra
and sea snake bites the incidence of
nonenvenomation is about 80
percent, but reliable data are
probably not available.
If the individual has been bitten
but not envenomated, the bite
should be treated like any other
animal bite to reduce the risk of
infection. It must be thoroughly
cleaned. Since the wound is a
puncture wound, bleeding should be
encouraged and tetanus prophylaxis
should be administered.
Crotalid Envenomation
The reaction following the bite
of a crotalid (pit viper) is one of the
best indications that the snake was
venomous and is the only indication
that envenomation has occurred and
treatment may be needed. This
reaction begins within minutes after
the bite, typically is severe
following an eastern diamondback
rattlesnake bite, but may be less
marked after other pit viper bites.
The reaction may be deceptively
mild following the bite of a Mojave
rattlesnake and almost nonexistent
after a massagua or pygmy
rattlesnake bite.
The earliest symptom is pain or
burning at the site of the bite,
although some people experience
relatively little pain. Shortly
afterward the area begins to swell
as fluid pours out into the tissues.
Bleeding usually produces a purple
or green discoloration, but this
change may take several hours to
appear.
If no further symptoms develop,
the envenomation is mild and
antiserum therapy is rarely needed.
However, the individual should be
taken to a hospital, even though the
reaction appears mild. Evidence of
more severe envenomation may take
several hours to develop.
Numbness or a tingling sensation
about the mouth or tongue,
sometimes extending into the scalp
or involving the fingers and toes,
and often associated with a metallic
or rubbery taste, commonly follows
the bite of eastern diamondback and
some western rattlesnakes.
Following moderate
envenomation, the swelling and
discoloration extend farther from
the site of the bite, blisters
(sometimes large) that contain clear
or bloody fluid appear, and the
regional lymph nodes (particularly
in the armpit or the inguinal crease)
become enlarged and tender.
Severe envenomation is
heralded by systemic reactions. The
individual becomes weak and dizzy
and develops signs of shock,
particularly cold and clammy skin
and a weak pulse.
Prehospital Care for Crotalid

Bites
Most of the venomous snakebites
within the United States occur in
situations where hospitalization is
less than two hours away. The
average interval between bite and
hospitalization has been reported to
be thirty-five minutes. When a
person can be hospitalized in such a
short time, the only treatment
needed is limiting the spread of the
venom and immobilizing the
individual and the extremity.
Tourniquets have been
recommended to help reduce spread
of the venom, but no evidence
supports their effectiveness. They
are potentially harmful and should
not be used.
Wrapping the bitten extremity
snugly and immobilizing it with a
splint is a technique devised by
Struan Sutherland in 1978 for
inhibiting the spread of venom from
Australian elapids. This procedure
is not recommended for crotalid
bites. Most bites by crotalids are
not life threatening, and the primary
goal of therapy is to limit local
tissue damage. Immobilizing the
venom allows it to continue to
digest the tissues in that area and
significantly increases the resulting
destruction.
Incision and suction should not
be attempted. Both procedures
injure the tissues, and experimental
studies have clearly demonstrated
that suction does not remove a
significant amount of venom.
The skin around the snakebite
should be cleaned, the extremity
should be immobilized and kept at
the same level as the heart, and the
person should be transported to a
hospital. Movement, even just
walking, increases the circulation
of blood and speeds the spread of
venom through the rest of the body.
Furthermore, the effects of activity
are frequently worse than would be
expected from this consideration
alone. The person should be lying
still if possible. No drugs, including
alcohol, should be administered.
No other treatment should be
attempted.
An individual bitten by a
venomous snake who is alone in a
remote area has no choice but to
walk out. If a companion is present,
the companion could make sure the
person is warm and comfortable
and could go for help, preferably a
helicopter. If the party is large
enough, the person can be carried
out. Even jostling on a makeshift
stretcher probably stimulates blood
flow and venom absorption less
than attempting to walk out.
However, stretcher evacuation
would be slower than walking out.
Every situation is different.
Antivenom Therapy
Antivenom is the only specific
treatment for venomous snakebite.
The administration of antivenom
should not be attempted by anyone
other than a physician, and even
then only in situations such as
hospital emergency rooms or
intensive care units where reactions
can be monitored and treated. The
antivenom used currently is
CroFab®, which is produced in
sheep and treated with papain to
split the antibody portion (Fab)
from the rest of the immunoglobulin
molecule (Fc). The Fc is
eliminated, which significantly
reduces the incidence of allergic
reactions (as does preparing the
antivenom in sheep), particularly
anaphylactic reactions. Treated
individuals do have a variety of
other problems, particularly failure
of the blood to clot normally.
A few individuals carry single
vials of antivenom when traveling
in snake-infested areas so they can
be prepared to treat themselves
should they be bitten. This practice
is not only useless but dangerous:
◆ A person bitten by a snake who
needs crotalid antivenom needs
a number of vials, not one.
◆ If the antivenom was
administered and a major
allergic reaction occurred, the
individual or others in the
party might not be able to
provide effective therapy.
◆ Carrying antivenom could
impart a false sense of security
that could lead to inadequate
precautions to avoid venomous
snakes.
The antivenom that used to be
most widely available in the United
States was a polyvalent or general-
purpose crotalid antivenom made
by Wyeth Laboratories that was
effective against all North
American pit vipers. A specific
Micrurus fulvius antivenom, which
was the proper one to use for coral
snake bites, was made by the same
company. However, that company
has ceased manufacturing both
antivenoms.
Coral Snake Bites
Coral snakes are the only
elapids native to the United States.
They are found mostly in the coastal
states from southern North Carolina
to Texas. The eastern coral snake
inhabits this area from Mississippi
eastward; the western coral snake
is found in Louisiana and Texas.
The Sonoran coral snake is found in
a limited portion of southern
Arizona.
These North American elapids
are shy and rarely seen; bites are
even less common. Reportedly,
children may play with these snakes
for hours without being bitten.
Envenomation appears to occur in
less than 40 percent of the bites that
are inflicted. Coral snake bites
make up less than 2 percent of all
snakebites in the United States.
Fatalities from coral snake bites
apparently have not occurred since
the development of specific
Micrurus fulvius antivenom. This
antivenom is effective for bites of
the eastern coral snake (Micrurus
fulvius fulvius) and the western
coral snake (Micrurus fulvius
tenere). It is of little value for bites
by the Sonoran coral snake
(Micruroides euryxanthus), but
envenomation by this species is not
severe. No deaths following its bite
have been reported.
Coral snakes tend to bite and
hang on, sometimes chewing for as
long as a minute, which contrasts
strikingly with the lightning strike of
pit vipers. The bites are rarely
associated with the local reaction—
severe pain and swelling—typical
of crotalid bites. Puncture marks
from the fangs usually cannot be
identified, particularly if the person
is intoxicated and cannot provide a
reliable account of the bite, which
is a common occurrence. Some pain
may be present and may radiate up
the limb. Often the first sign of
coral snake and other elapid
envenomation is painful
enlargement of the regional lymph
nodes. With severe envenomation,
numbness and weakness of the limb
appear within one to two hours,
sometimes less. Later signs and
symptoms include drowsiness,
apprehension, weakness, tremors of
the tongue or other muscles,
difficulty swallowing, nausea, and
vomiting. Pronounced weakness of
the eye or eyelid muscles may
occur; pupils may be pinpoint in
size. Breathing may be labored.
Convulsions may occur. Eventually,
in inadequately treated, severely
envenomated individuals
unconsciousness and paralysis are
followed by death in shock from
respiratory and cardiac failure.
Antivenom is the only effective
therapy for coral snake bites and
should be administered as quickly
as possible without waiting for
signs and symptoms of
envenomation. The limb can be
wrapped to immobilize the venom
and should be splinted. Travelers to
Asia and Africa should learn the
technique so it could be used for
treating snakebites inflicted in those
areas.
The object of pressure
immobilization is to hold venom at
the site of the bite and prevent it
from moving through lymphatics to
other parts of the body. The
technique has two components:
pressure to block lymphatic
drainage, and immobilization to
prevent the pumping action of
muscles. Pressure is preferably
applied with an elastic bandage, but
any fabric suffices in an emergency.
Bandaging should begin two to four
inches above the bite (between the
bite and the heart), wind around in
overlapping layers toward the
heart, then wind back down over
the bite and past it toward the hand
or foot.
The bandage should be about as
tight as the wrap for a sprained
ankle. It must not obstruct blood
flow, or even be uncomfortable; if it
is uncomfortable, the person flexes
the limb, defeating the purpose of
immobilization. The location of the
bite should be clearly marked on
the outside of the bandage. Some
swelling of the tissues beyond the
wrap can be expected.
The limb must be immobilized,
if possible with a splint and sling,
and pressure immobilization should
be applied as quickly as possible.
Waiting until symptoms become
noticeable allows the best time for
treatment to pass. Once a pressure
bandage has been applied, it must
never be removed until after
administration of antivenom has
begun. The combination of pressure
and immobilization can contain
venom so effectively that no signs
or symptoms are apparent for more
than twenty-four hours, producing
the illusion of a dry bite.
The individual should be rapidly
transported to a hospital while he
or she exerts as little effort as
possible. Incision and suction or
other forms of nonhospital treatment
are of no value. The Wyeth
antivenom is no longer available.
Antivenom now must be imported,
probably from Mexico or Costa
Rica, and antivenoms produced in
those countries are considered
reliable.
Exotic Venomous Snake Bites

Bites by snakes that are not
native to the United States
occasionally occur among
collectors, amateur and
professional herpetologists, and
exhibitors. The treatment for such
bites is essentially identical to that
for coral snake bites:
immobilization of the venom by
wrapping the limb, splinting, and
transportation to a medical center.
Incision and suction or cooling have
no value in treating such bites.
Antivenoms for bites by exotic
species of snakes and physicians
experienced in treating such bites
may be available through zoos.
Poison control centers can be
valuable sources of information and
assistance, and a nationwide
telephone system at 800-222-1222
can route calls to the appropriate
poison control center. In other
countries, such information and
antivenoms may not be so easy to
obtain. The nearest hospital would
probably be the most reliable
source of information and
assistance, particularly in areas
where snakebites are common.
However, India now has a national
snakebite protocol. Australia has
antivenoms for the tiger and brown
snakes and a snakebite detection kit
that can be used to determine which
antivenom should be used to treat
the bite even if the type of snake is
unknown.
If a person who has been bitten
by a venomous snake in a
wilderness area cannot be
evacuated for several days (after
which evacuation may not be
needed), antibiotics may be needed
to combat wound infection. A
sedative/hypnotic every four to six
hours may help keep the individual
quiet and allay anxiety but must not
be given to a stuporous or
unconscious person. Pain should be
controlled with moderate
analgesics. Strong analgesics may
have harmful effects and should not
be administered. Alcohol, which
increases absorption of the venom
and physical activity by the person,
must be avoided.
Most snakebite fatalities result
from shock, regardless of the
species of snake or whether the
venom is primarily hemolytic or
neurotoxic. This complication
should be anticipated and treated.
Every person with a venomous
snakebite is different and the
treatment for each must be
individualized. Children and
elderly persons tolerate venomous
snakebites poorly and require more
vigorous treatment. Children can
require huge quantities of
antivenom. Bites occurring in the
spring, when the snake has just
emerged from hibernation and its
venom is more concentrated, are
more severe than bites occurring at
other times of the year. Bites about
the head or trunk are more
dangerous than bites on the
extremities and require more
aggressive treatment.
Avoiding Venomous Snakes

Venomous snakes and their bites
are best avoided, not treated.
Several simple measures would
prevent almost half of all
envenomations:
◆ Venomous snakes should not be
teased or handled, even after
they are dead. Reflex strikes
with envenomation can occur
for several hours after death.
◆ Unprotected hands should not
be inserted under logs or
stones or into cracks or
crevices that have not first
been visually inspected.
◆ After dark special care must be
taken to avoid snakes. Walking
barefoot or collecting
firewood after dark are two
activities that contribute to
venomous snakebites.
◆ Snakes rarely strike higher than
the ankle. Loosely fitting long
pants and hiking boots that
cover the ankles prevent many
bites.
SPIDER, SCORPION, ANT,
AND OTHER BITES AND
STINGS
Allergic Reactions to Insect
Stings
Between 50 and 150 deaths
result annually from allergic
reactions to Hymenoptera stings
(bees, wasps, hornets, and fire ants)
in the United States, which is more
than the deaths from rabies, large
animal attacks, venomous snakes,
spiders, and scorpions combined.
Approximately 1 of every 200
people in the United States has
experienced a severe reaction to
such stings. Fatal reactions can be
prevented or successfully treated in
individuals known to have such
allergies, but many deaths still
occur in persons whose allergic
status has not been recognized. The
problem of allergies and the severe,
lethal allergic reactions known as
anaphylactic shock are discussed in
Chapter 23: Allergies.
An individual allergic to insect
stings usually experiences milder
allergic reactions before having a
potentially fatal reaction. Two types
of nonlethal reactions occur: local
reactions and systemic reactions.
Local reactions are
characterized by severe swelling
limited to the limb or portion of the
limb that is the site of the insect
sting. Almost all insect stings are
associated with some swelling, but
the area of swelling is usually three
inches (7.5 cm) or less in diameter.
With severe local reactions, a
major portion of an extremity, such
as the entire forearm, is swollen
and may be painful, associated with
itching, or mildly discolored.
Systemic reactions occur in
areas of the body some distance
from the site of the sting. Most
typical are hives, which may be
scattered over much of the body.
Generalized itching or reddening of
the skin also occur. Persons with
more severe reactions may
experience hypotension (low blood
pressure) and difficulty breathing,
either of which clearly could be
fatal if severe.
Investigators of insect
hypersensitivity reactions have
recommended that individuals who
have had a systemic reaction to an
insect sting undergo skin testing
with Hymenoptera venoms. (If the
results of skin tests are
inconclusive, more sophisticated
measurement of venom specific IgE
antibodies can be carried out.)
About half of those who have had a
systemic reaction and also have a
positive skin test would be
expected to have a severe, possibly
fatal reaction if stung again.
Desensitization with purified insect
venoms—not whole body extracts
—is recommended for these
individuals. (In one study of
children who had experienced an
anaphylactic reaction following a
sting, only 9 percent of subsequent
accidental stings led to severe
reactions. None of the reactions
were more severe than the original
reaction, which led to the
conclusion that immunotherapy was
unnecessary for such individuals.)
Desensitization can be a drawn-
out, uncomfortable procedure but
also can be life saving. Starting
with very small quantities,
increasingly larger amounts of the
insect venoms are injected
subcutaneously until the allergic
reaction is neutralized. The
individual is still allergic to the
Hymenoptera venoms, but the
antibodies responsible for
producing the allergic reactions are
used up by the repeated injections
of the material with which they
react. Generally, even after
successful desensitization,
injections must be continued at
approximately monthly intervals for
years or indefinitely. If the
desensitization injections are
stopped, the former allergic
condition often reappears.
Desensitization must be carried
out under the close supervision of a
physician experienced with the
procedure. Severe, life-threatening
allergic reactions to the
desensitization injections occur, and
a physician must be on hand to deal
with them. However, a physician
watching for a reaction can treat it
effectively. Allergic reactions to
insect stings in a wilderness
environment without a physician in
attendance are a far greater threat.
Desensitization, or even skin
testing, is not recommended for
individuals who have large local
reactions because these are rarely
followed by systemic reactions.
However, carrying epinephrine
(adrenaline) is recommended for
individuals who have had either
type of reaction.
Rock climbers and some other
wilderness users who have
systemic allergic reactions to insect
stings have a unique risk of fatal
reactions because they are subject
to stings in locations such as rock
walls where others cannot treat
them immediately and they can treat
themselves only with difficulty.
Such persons should seriously
consider desensitization. They also
must be prepared to treat an
anaphylactic reaction at any time
(Chapter 23: Allergies).
Spider Bites
Almost all spiders produce toxic
venoms, but their fangs are too
small and weak to penetrate the
skin, the venom is too weak, or the
volume of venom is too small to
pose a significant threat for humans.
The black widow, Latrodectus
mactans, is the only spider found in
the United States that is capable of
routinely producing serious illness
by its bite. The tarantula native to
the U.S. Southwest bites only after
extreme provocation. Its weak and
ineffective fangs can only penetrate
thin skin, such as that on the sides of
the fingers, and the effects of the
bite are no worse than an insect
sting.
In other parts of the world, some
spiders can cause severe, even fatal
poisoning in humans. Other species
of Latrodectus produce effects
similar to the black widow, as do
the bites of large, hairy tarantulas
found in areas such as Brazil or
Peru. The Sydney funnel web
spider, a species limited in
distribution to the area within a
hundred miles of Sydney, Australia,
is capable of inflicting a bite that
can be lethal within minutes for
infants, a couple of hours for
children, and twenty-four hours for
healthy young adults.
The bites of some spiders, most
notoriously the brown recluse or
violin spider, Loxosceles reclusa,
on rare occasions cause extensive
damage at the site. However, all but
a few bites are insignificant. The
jumping spider, Phidippus, is the
most common biting spider in the
United States. Bites by this spider,
trapdoor spiders, orbweavers,
spiders of the Chiracanthium
species such as the garden spider,
and over a hundred other species
produce local reactions that
ulcerate and less often produce
systemic symptoms. However,
individuals with these bites almost
never require hospitalization.
Spiders usually cling to the site of
the bite. (If the spider cannot be
found, some other arachnid such as
a bedbug should be suspected.)
Anyone who has been bitten should
bring the spider to be identified.
Rarely an individual may be
bitten repeatedly by a relatively
harmless spider or insect and
develop an allergy to the toxin
produced by that species.
Subsequent bites can produce
severe, even fatal allergic
reactions. Fortunately such events
are rare. The treatment for such
reactions would be identical to the
treatment for allergic reactions to
insect stings.
Black Widow Spider Bites

The female black widow
typically is coal black and has a
prominent, spherical abdomen that
may be as large as one-half inch
(1.25 cm) in diameter. This
appearance is so distinctive that
finding the characteristic markings
on the undersurface of the abdomen
is rarely necessary. The typical
markings consist of red or orange
figures that usually resemble an
hourglass but may be round, broken
into two figures, or have some other
configuration. Markings of the same
color but in varying patterns are
sometimes present on the back,
although only the undersurface
markings are considered
characteristic. In some parts of the
U.S. Southwest black widow
spiders have irregular white
patches on their abdomens.
Different species of Latrodectus in
other countries have a similar
appearance. (The male is smaller,
has a brown color, and is
harmless.)
Black widows weave coarse,
crudely constructed webs in dark
corners, both indoors and out. A
number of the black widow bites
reported in the medical literature in
the first four decades of the
twentieth century were inflicted on
male genitalia by spiders on the
underside of outdoor toilet seats.
However, this spider is timid and
would rather run than attack an
intruder.
Forty to fifty years ago five to
ten deaths a year resulted from
black widow spider bites, although
they were limited almost entirely to
small children or elderly
individuals in poor health.
Recognition and treatment of such
bites have improved so much that
deaths are rare within the United
States. (Bites in children weighing
thirty pounds or less would still
have a mortality of about 50 percent
if untreated.) In healthy adults,
black widow spider bites cause
painful muscle spasms and
prostration for two to four days, but
complete recovery essentially
always follows. Antivenom
treatment usually is not
recommended for adults.
The bite may feel like a
pinprick, may produce a mild
burning sensation, or may not be
noticed at all. Small puncture
wounds, slight redness, or no
visible marks may be found at the
site of the bite. Within about fifteen
minutes, painful muscle cramps
develop at the point of the bite and
rapidly spread to involve the entire
body. The characteristic pattern of
spread is by continuity. From a bite
on the forearm the cramps spread to
the upper arm, to the shoulder, and
over the chest to involve the rest of
the body, including the legs. The
abdominal muscles are
characteristically rigid and hard,
although the abdomen is not tender.
Weakness and tremors are also
present.
Typically, a person who has
been bitten is anxious and restless.
A feeble pulse and cold clammy
skin suggest shock. Labored
breathing, slurred speech, impaired
coordination, mild stupor, and rare
seizures (in children) suggest a
disease involving the brain. Bitten
individuals are often covered with
perspiration. Dizziness, nausea, and
vomiting are common. If the spider
or its bite has not been observed,
the signs and symptoms may lead to
an erroneous diagnosis of an acute
abdominal emergency.
Symptoms typically increase in
severity for several hours,
occasionally as long as twenty-four
hours, and then gradually subside.
After two to three days essentially
all symptoms have disappeared,
although a few minor residua may
persist for weeks or months.
Treatment consists of efforts to
relieve the painful muscle spasms
and antivenom for small children.
No treatment at all should be
directed to the site of the bite, with
the possible exception of applying
an ice cube to relieve pain. Incision
and suction are damaging and
useless and should not be
performed.
Essentially nothing can be done
outside of a hospital, and small
children always must be
hospitalized. Antivenom is
produced by Merck. Antivenom is
usually not administered to healthy
adults between the ages of sixteen
and sixty, and only to individuals of
small body size with severe
symptoms who are twelve to fifteen
years old. Instructions with the vial
of antivenom should be followed.
Periodic injections of calcium
gluconate solution or
methocarbamol to reduce muscle
spasms have been recommended in
the past but have been shown to be
no better than placebo. A
tranquilizer such as diazepam
(Valium®) may help relieve less
severe muscle spasms. Hot baths
are occasionally helpful. Strong
analgesics are helpful but rarely
provide complete pain relief.
Brown Recluse Spider Bites

The brown recluse or violin
spider (Loxosceles reclusa) has
received widespread attention as
the cause of necrotic arachnidism.
However, the threat by this spider
is greatly overblown. Its
distribution extends from the New
Mexico–Texas border east to
Alabama and northern Georgia and
north to western Kentucky, southern
Indiana, Illinois, and Iowa and the
eastern portion of Kansas. Reports
of bites outside this area are
numerous, but most are considered
erroneous by arachnoidologists.
Occasional bites by spiders
transported by travelers probably
occur, but such bites should not be
accepted as brown recluse bites
unless the spider has been captured
and identified by an
arachnoidologist. Other Loxosceles
species are found along the southern
borders of New Mexico, Arizona,
and California.
In the area of their distribution
the spiders are numerous and once
established within a house are quite
difficult to eliminate. However,
bites by the brown recluse are
distinctly uncommon. Most
individuals living in houses with
hundreds of these spiders never
report a bite. Bites usually occur
when the spider is tightly pressed
against human skin, either while
putting on clothes that have been
scattered on the floor at night or by
rolling over the spider while
asleep.
Furthermore, 90 percent of the
bites are innocuous and produce
only a small red spot or no mark at
all. (Red skin lesions with a central
pustule or necrotic center are
almost never spider bites, although
some individuals claim they are.
They are typical of methicillin-
resistant Staphylococcus aureus
[MRSA] infections.) The other 10
percent of the bites, which are the
ones that have earned this spider
notoriety, produce a blister
surrounded by an area of intense
inflammation about one-half inch
(1.25 cm) in diameter. Pain is mild
at first but may become quite severe
within about eight hours. Over the
next ten to fourteen days the blister
ruptures and the involved skin turns
dark brown or black. Eventually the
black, dead tissue drops away,
leaving a crater that heals with
scarring.
A few individuals have skin
losses large enough to require grafts
to cover the defect. Generalized
symptoms may appear within thirty-
six hours of the bite and include
chills and fever, nausea and
vomiting, joint pain, and a skin rash
or hives. With severe reactions,
destruction of red blood cells
(hemolysis) and platelets
(thrombocytopenia), resulting in a
significant anemia and bleeding
tendency, has been described. Rare
fatalities have been reported in
children, but the website for the
Department of Entomology of the
University of California Riverside
claims that bites by brown recluse
spiders have never been
documented for such individuals
(http://spiders.ucr.edu/dermatol.html
Routine care should include
elevation and immobilization of the
affected limb, application of ice,
local wound care, tetanus
prophylaxis, and other supportive
care as needed. No effective,
specific therapy for brown recluse
bites has been established,
particularly in wilderness situations
where appropriate injectable
medications would rarely be
carried. According to a review in
the New England Journal of
Medicine in 2005, reported
therapies have included hyperbaric
oxygen, dapsone, antihistamines,
antibiotics, dextran,
glucocorticoids, vasodilators,
heparin, nitroglycerin, electric
shock, curettage, surgical excision,
and antivenom. None have been
subjected to controlled, randomized
trials; many are costly, painful, or
potentially toxic.
Scorpion Stings
Scorpions are invertebrates
found throughout most of the United
States, but the species lethal for
humans, the bark scorpion
(Centruroides), is limited to
Arizona, New Mexico, Texas,
southern California, and northern
Mexico. In this area scorpions are a
significant problem. Sixty-nine
deaths resulted from scorpion stings
in Arizona between 1929 and 1954.
During the same period, only twenty
deaths resulted from venomous
snakebites. With improved medical
management of the complications of
scorpion stings, no deaths have
occurred in Arizona for well over
twenty years.
These eight-legged arachnids
range in length from three to eight
inches (7.5 to 20 cm) and have a
rather plump body, thin tail with a
stinger at the end, and large pincers,
They are found mostly in dry
climates under rocks and logs;
buried in the sand; in collections of
lumber, bricks, or brush; and in the
attics, walls, or understructures of
houses or deserted buildings. The
problems with scorpions in Arizona
are clearly related to their tendency
to live in the vicinity of human
habitation where children are
frequently playing.
Stings can be avoided by
exercising care when picking up
stones, logs, or similar objects
under which scorpions hide during
the day. Since scorpions are
nocturnal, walking barefoot after
dark is inadvisable. Shoes and
clothing should be shaken
vigorously before dressing in the
morning, particularly when camping
outdoors. Tents or tarps should be
lifted with caution because
scorpions frequently crawl
underneath them at night.
The lethal species of scorpions
are often found under loose bark or
around old tree stumps. They have a
yellow to greenish-yellow color
and can be distinguished from other
species by a small knoblike
projection at the base of their
stingers (Fig. 33-3). Adults measure
three inches (7.5 cm) in length and
three-eighths inch (1 cm) in width.
One subspecies has two irregular
dark stripes down its back.
The sting of a nonlethal scorpion
is similar to that of a wasp or
hornet, although it may be
somewhat more severe and should
be treated in an identical manner.
(Scorpion venom is not identical to
insect venom, and individuals
allergic to insect stings usually are
not allergic to scorpion stings.)
Figure 33-3. Centruroides scorpion.
Enlargement: typical bulb and stinger
Initially the sting of a

Centruroides species produces
only a pricking sensation and may
not be noticed. Nothing can be seen
at the site of the sting. (Swelling
and red or purple discoloration are
indications that the sting has been
inflicted by a nonlethal species.)
Pain follows in five to sixty minutes
and may be quite severe. The sting
site is quite sensitive to touch and is
the last part of the body to recover.
Tapping the site produces a painful,
tingling, or burning sensation that
travels up the extremity toward the
torso. (Stings by other species of
scorpions can occasionally produce
a similar sensation.) Sensitivity
may persist as long as ten days,
although other symptoms usually
disappear within ten hours.
Individuals who have been stung
typically are extremely restless and
jittery. Young children writhe, jerk,
or flail about in a bizarre manner
that suggests a seizure. Their
movements are completely
involuntary. However, in spite of
their constantly moving bodies, the
children can talk. Although they
appear to be writhing in pain, they
usually state that they do not hurt.
Seizures have been described, but
the true nature of these events is
questionable. Visual disturbances
such as roving eye movements or a
fluttering type of movement known
as nystagmus are common.
Occasionally children complain that
they cannot see, but nothing
abnormal can be found when
examining their eyes and sight
returns spontaneously in a few
minutes. Children under six years of
age may develop respiratory
problems such as wheezing and
stridor, and a few may need
assisted respiration.
Persons who have been stung
typically have an elevated blood
pressure, which may be an
important diagnostic sign since
hypertension is rare in children.
The blood pressure usually returns
to normal within four to six hours
and becomes life threatening only in
infants.
Elderly individuals with
preexisting health problems and
small children stung by
Centruroides species should be
taken to a medical facility
sufficiently sophisticated to have
the equipment and supplies
necessary to monitor these
individuals and deal with any
complications that may arise. No
other therapy is possible outside of
a hospital. In locations such as the
Grand Canyon, where prompt
evacuation is not possible,
diazepam (Valium®) can be given
to children to control the
purposeless movements.
Until a few years ago an
antivenom made in goats was
available only in Arizona.
However, problems were
associated with administration of
that antivenom and production has
ceased. Investigators in Arizona are
trying to get FDA approval for an
antivenom made from horses.
Other countries are home to
species of lethal scorpions much
more deadly than those of the
southwestern United States. Mexico
reportedly has had as many as
76,000 scorpion stings resulting in
1500 deaths in a single year. The
stings of such scorpions must be
treated with antivenom, which is
rarely available outside of a
hospital, particularly for someone
who is not fluent in the local
language. Furthermore, scorpion
venom is poorly antigenic, and the
antivenoms are largely species
specific. Twenty-two different
antivenoms are now being
produced.
Death from the stings of such
scorpions is often the result of
sudden, very severe high blood
pressure. Adrenergic blocking
agents such as propranolol may be
an effective method for treating
such stings and could be carried by
visitors to the countries where such
lethal species of scorpions exist.
Fire Ant Stings

Both the black fire ant
(Solenopsis richteri) and the red
fire ant (Solenopsis invicta) appear
to have entered the United States in
the early twentieth century through
the port of Mobile, Alabama. These
insects were originally expected to
occupy most areas where the
average minimum annual
temperature was higher than 10°F
(−12°C), but identification of
hybrids that are more tolerant of
cold indicates these insects can
ultimately infest one-quarter of the
U.S. land area. As recently as 1950
fire ants were limited to the western
half of southern Alabama and the
adjacent eastern part of southern
Mississippi. In 1989 they were
found in most of South Carolina,
Georgia, Alabama, Florida,
Mississippi, and Louisiana; the
southeastern two-thirds of Texas;
and parts of Missouri and North
Carolina. They are expected
eventually to occupy the rest of
Texas, most of California, sparing
only the northern and central Sierra
Nevada, and to occupy the coastal
areas of Oregon and Washington.
In infested urban areas, 30 to 60
percent of the inhabitants are stung
by fire ants every year. Stings are
more common among children, on
the legs, and during summer. The
ant grabs the skin with powerful
mandibles and, if undisturbed,
stings repeatedly, twisting its body
so it can reach different sites.
Almost everyone stung by an ant
develops a wheal-and-flare
reaction—a pale bump that itches
and is surrounded by a thin rim of
skin that has turned red. This
reaction resolves in about thirty to
sixty minutes, but within twenty-
four hours evolves into a sterile
pustule (a pimple or small boil).
The skin over the pustule sloughs in
two to three days. No therapy is
effective for the pustule, but
scratching can lead to infection that
may require antibiotic therapy.
One-fourth to one-half of the
individuals who have been stung
develop large local reactions that
are red, swollen, firm, and “itch
like crazy!” In extreme cases,
compression of nerves or blood
vessels develops, and a few
individuals have required
amputation. Elevation of the
extremity, steroid therapy, and
antihistamines can largely prevent
such extreme reactions. Topical
steroid ointments such as 0.25
percent hydrocortisone, local
anesthetic creams, and oral
antihistamines reduce the itching
associated with more common, less
severe reactions.
About 0.5 to 1 percent of stings
are followed by anaphylactic
reactions, and a number of deaths
have resulted. Most of the fatalities
occurred in individuals who had
been stung less than five times.
Anaphylactic reactions can occur
hours after a sting. Such reactions
should be treated like any other
anaphylactic reaction (Chapter 23:
Allergies).
No method for controlling the
population of fire ants over a large
area is currently available.
Avoiding contact with the insects is
virtually impossible for individuals
who live in infested sites. Those
who develop anaphylaxis following
a sting should consult a physician
about desensitization. Whole-body
extracts of fire ants, unlike whole
body extracts of other hymenoptera,
contain substantial (although
variable) quantities of venom and
are effective for desensitization.
Thousands of residents of infested
areas are receiving such therapy.
APPENDIXES
APPENDIXE A
MEDICATIONS
Essentially all drugs have two
names: a generic name and a trade
name. Some drugs have multiple
trade names. (Drugs also have
names based on the chemical
structure, and official names listed
in the United States Pharmacopeia
or National Formulary, but these
are rarely used.) Generic names,
assigned by the United States
Pharmacopeia Nomenclature
Committee of the American
Medical Association, are widely
used. Some generic names are
similar to chemical or official
names; many are not.
In the United States a drug has
only a single generic name
regardless of the number of
companies that manufacture it. In
contrast, if the drug is produced and
sold by more than one manufacturer,
each gives it a different trade name.
Trade names and trademarks that
are registered can be used only by
the manufacturer that has developed
them. Trade names are devised to
be more easily remembered than the
generic name so that physicians
prescribe that manufacturer’s
product. Some are similar to
generic names; many are not.
In this text, medications have
been listed by their generic names
with some of the better known trade
names in parentheses to help with
identification. (For some agents—
aspirin or penicillin, for instance—
generic names are more familiar
and are the only ones listed.) Many
generic names are unfamiliar to
people who are not medical
professionals but are known by
pharmacists and by most physicians
through whom these drugs must be
obtained. Generic names used in
countries other than the United
States may be totally different, even
in other English-speaking nations.
(A U.S. committee assigns U.S.
generic names.)
MEDICATIONS FOR THE

RELIEF OF PAIN
Drugs that relive pain are known as
analgesics. Analgesics can be
classified as mild, moderate, or
strong. The best-known mild
analgesics are aspirin,
acetaminophen, ibuprofen, and
codeine. Ibuprofen and a number of
more recently developed mild
analgesics are called nonsteroidal
antiinflammatory drugs (NSAIDs).
Moderate analgesia is provided by
codeine combined with
acetaminophen, by a combination of
acetaminophen and hydrocodone
(Vicodin®), or by a combination of
acetaminophen with oxycontin
(Percocet®). The commonly used
strong analgesics are morphine,
hydromorphone (Dilaudid®), and
other opiates, so-called because
most of them were originally
derived from opium.
The strong analgesics used to be
called narcotics, a vague term that
has no basis in chemical or
pharmacologic properties. That
term has fallen out of favor and has
been replaced by opiates.
The major hazard associated
with strong painrelieving drugs is
cerebral depression that impairs
respiration. No one with a known
or suspected head injury or
neurologic illness that impairs
consciousness should be given
strong pain medications.
Addiction is not a major hazard
of these agents—possibly not even
a significant hazard for individuals
receiving analgesics for legitimate
reasons. Almost everyone who
undergoes major surgery—
thousands of people every day—
receives strong analgesics
postoperatively to control pain.
Subsequent addiction is vanishingly
rare. Many of the drugs that relieve
severe pain also produce euphoria,
which is clearly beneficial for
someone who has suffered a major
accident or undergone major
surgery. Addiction results when
these drugs are taken for euphoria
alone.
Codeine and the strong
analgesics (and other agents) are
classified as controlled substances
in the United States, and the Drug
Enforcement Agency, an arm of the
U.S. Treasury Department, not the
Public Health Service, regulates
their distribution. They are difficult
to obtain for anyone who is not a
licensed physician (or a habitual
drug user). Problems with
regulatory agencies, particularly for
individuals who are not physicians,
can be lessened by precise records
that detail the total amount of such
agents on hand, where they are
stored, the security of that location,
persons authorized to remove the
agents from storage, the names of
individuals treated, and the time,
place, quantity, and reason for
administering the drugs.
To minimize the risk of
addiction, the following precautions
should be observed:
◆ Strong analgesics should not
be administered except when
clearly needed for the relief of
pain.
◆ A less potent analgesic should
be substituted for a strong
agent as soon as pain has
diminished to a level at which
the milder drugs can provide
relief.
◆ Strong analgesic
administration should not be
continued for more than twelve
to fourteen days except in
extraordinary circumstances,
but such circumstances could
occur in the wilderness.
Evacuation of a person with a
painful fracture from a remote
area such as the Himalaya
could take more than two
weeks. Failure to provide
analgesia, even if addiction
resulted, could be devastating.
If a potent analgesic is needed,
one should be used, and it should
be given in adequate quantities to
relieve pain. A person with severe
pain desperately needs the rest
and relief these drugs alone can
provide. Halfway measures, such
as inadequate doses or inadequate
drugs, are of almost no value.
Aspirin
Aspirin (acetylsalicylic acid) is
best known as a mild analgesic.
Willow bark, which contains
salicin, a precursor of aspirin, is
reported to have been
recommended for pain relief by
Hippocrates in approximately BC
400. Powdered acetylsalicylic acid,
which was made from purified
salicin, was first widely distributed
in 1899. Tablets became available
in 1915. This drug was considered
such an important product that the
German company Bayer, which
gave the compound its name, was
forced to give up its trademark by
the Treaty of Versailles in 1919.
However, aspirin is no more
effective than acetaminophen or
ibuprofen and cannot be
recommended as a mild analgesic,
particularly for wilderness use,
because it is such a strong gastric
irritant. A study at a major
university medical center found that
over 90 percent of the individuals
hospitalized for gastrointestinal
bleeding had been taking aspirin.
Combination with other drugs,
except codeine, offers no significant
analgesic benefits, but
acetaminophen and codeine is just
as effective and does not have such
adverse gastric effects.
Aspirin is a prostaglandin
inhibitor that helps prevent the
aggregation of platelets and the
formation of blood clots. Doses of
approximately 81 mg (“baby
aspirin”) once a day have been
found to clearly reduce the
incidence of myocardial infarction,
but that dose is too small to provide
significant analgesia for adults. All
aspirin, even baby aspirin, should
be enteric coated to reduce damage
to the stomach.
The other use for which aspirin
can be clearly recommended is one-
half to one adult aspirin tablet after
the onset of angina or one adult
tablet after the onset of a
myocardial infarct or a stroke
Vessel Disorders).
Precautions: Aspirin is
poisonous when taken in large
quantities. In the United States it is
one of the two most common causes
of poisoning in children (the other
is acetaminophen, Tylenol®).
Aspirin, particularly flavored
“children’s aspirin,” must be
inaccessible to children, as must all
medications.
Because aspirin is such a strong
gastric irritant, persons with peptic
ulcers or related disorders,
including indigestion and
gastroesophageal reflux disease
(GERD), should not use this drug.
The addition of buffering agents or
antacids does not increase
analgesic potency and reduces
gastric irritation only slightly.
Acetaminophen
Acetaminophen (Tylenol® and
others, and known as paracetamol
outside the United States) is a minor
analgesic that is just as effective as
aspirin for relieving minor pain and
reducing fever. However,
acetaminophen has much less
tendency to cause stomach irritation
and does not increase the risk of
gastric bleeding. Increasing the
dose above three standard or two
extra-strength tablets does not
provide additional analgesia.
Precautions: Acetaminophen in
large quantities (10 to 15 gm)
produces severe liver damage. At
one time it was the drug most
commonly used for suicide in Great
Britain. These deaths are
distressing because the individuals
linger for about a week before
dying of liver failure and no
effective therapy is available.
Treatment for an overdose must be
initiated within a few hours after
the drug has been ingested to be
effective. This medication should
be used with caution for individuals
known to have liver disease.
Many over-the-counter
preparations for colds or sinus
problems include acetaminophen,
but this information is often
provided only in very small print in
the list of contents. To avoid the
possibility of an overdose, such
preparations should not be
combined with acetaminophen
alone.
Ibuprofen
Ibuprofen (Motrin®, Advil®,
Nuprin®, and others) is a
nonsteroidal anti-inflammatory drug
(a prostaglandin antagonist) that is
used primarily as a minor
analgesic. Its analgesic properties
are essentially the same as
acetaminophen. It is a gastric
irritant like aspirin but is usually
sold in enteric-coated forms that
reduce such irritation.
This agent has been found useful
for dysmenorrhea (painful
menstrual cramps) because its
antagonism to prostaglandins tends
to make the uterine muscle relax.
Ibuprofen also is an effective
fever-reducing (antipyretic) agent.
Precautions: Ibuprofen is a
gastric irritant, like aspirin,
although some persons who cannot
tolerate aspirin have no problems
with ibuprofen. Persons with a
history of peptic ulcer or severe
indigestion should not take this
drug. All individuals receiving this
drug must be aware of its potential
to produce gastrointestinal
ulceration and bleeding and must be
alert for signs or symptoms of those
disorders.
Although many people prefer
ibuprofen to acetaminophen, the
latter is the safer drug for acute pain
and should be preferred except for
the relief of painful menstrual
cramps.
Codeine
Codeine is an opium derivative
that can be considered for inclusion
in wilderness medical kits because
it has three actions. It is a minor
analgesic, although when
administered alone it is no more
effective than acetaminophen alone.
However, the analgesia produced
by combining codeine with
acetaminophen is approximately
twice that of either alone. Codeine
is one of the most effective cough
suppressants and is a component in
many cough syrups. Codeine is also
an antidiarrheal agent that for a
number of people is as effective as
Imodium®.
Codeine has almost none of the
euphoric effect of other narcotics,
and addiction is rare. It is legally
classified as a controlled substance
in the United States.
Precautions: Symptoms of
indigestion or heartburn occur
frequently in individuals who have
such symptoms with other drugs,
alcohol, or spicy foods. Some
individuals experience nausea and a
small number may vomit.
Constipation is common
following codeine administration.
Hydrocodone and Acetaminophen

Hydrocodone and
acetaminophen, a combination sold
as Vicodin®, is an analgesic
somewhat stronger than the
combination of codeine and
acetaminophen.
Precautions: Like other
moderate to strong analgesics,
Vicodin should not be given to
persons with head injuries or other
disorders affecting the brain. It is
habit forming when used
excessively or inappropriately.
Oxycontin and Acetaminophen

Oxycontin (OxyCodone) is an
opiate that has properties similar to
hydrocodone. When combined with
acetaminophen it is known as
Percocet and is approximately the
same strength as Vicodin.
Precautions: Like other
moderate to strong analgesics,
Percocet should not be given to
persons with head injuries or other
disorders affecting the brain. It is
habit forming when used
excessively or inappropriately.
Morphine
Morphine is a potent analgesic
that has been so widely used for so
long, and so effectively relieves
severe pain, that it has been called
“God’s own medicine.” It is one of
the oldest and most valuable agents
in a physician’s armamentarium.
In addition to its analgesic
properties, morphine has a strong
sedative effect that helps calm
injured persons and limits thrashing
about, which could aggravate
wounds or hinder evacuation. This
sedation and morphine’s euphoric
effect also help relieve the anxiety
that would be expected to follow an
accident.
Precautions: Morphine, like all
sedatives, depresses brain function.
Morphine must never be given to a
person with a central nervous
system injury or disease, even a
mild disorder, because morphine
would usually further impair
cerebral function. After the
administration of morphine or a
related drug, determining whether
subsequent changes in the person’s
condition are the result of
progression of the disorder or the
effects of the drug would be
impossible. A person who is
unconscious does not require
analgesia.
Since the brain controls
respiration, morphine also
depresses respiratory function and
must be used cautiously for persons
with chest injuries or pulmonary
diseases, particularly at higher
altitudes. However, relieving the
pain of a severe chest injury may
allow a person to cough and breathe
more deeply (in the absence of an
accompanying brain disorder).
Morphine causes nausea and
vomiting in some individuals. It is
constipating for almost everyone
and can contribute to the
development of fecal impaction.
This drug may cause spasm of
the muscles controlling outflow
from the urinary bladder, resulting
in acute urinary retention,
particularly following abdominal
injuries.
Morphine is addicting, should be
used only when specifically needed
for the relief of severe pain, and
should be discontinued when less
potent drugs can provide adequate
analgesia.
Oral administration can produce
satisfactory analgesia if enough of
the drug is given (orally
administered morphine is only one-
third to one-sixth as effective as the
injected drugs), but absorption is
slower and thirty to sixty minutes
are required for the drug to take
effect.
Following intramuscular
injection, analgesia can be expected
after ten to fifteen minutes; the onset
following intravenous injection is
almost immediate. Individuals with
previous experience with
intravenous drug administration
should use the intravenous route of
administration for persons in shock.
The drug must be injected slowly
over a period of several minutes
and the injection should be stopped
if pain relief is achieved before the
full dose is administered.
Hydromorphone
Hydromorphone (Dilaudid®) is
an opiate that has properties similar
to morphine. Oral and injectable
forms are available.
Precautions: The precautions
that should be followed when
administering hydromorphone are
essentially identical to those for
morphine.
Lidocaine
Lidocaine (Xylocaine®) is an
injectable local anesthetic that is
widely used for dental procedures
and for minor surgery, including
suturing lacerations. Lidocaine jelly
is a preparation of the same drug
that can be applied directly to the
site where anesthesia is needed.
Although the ointment can provide
temporary relief from the pain and
discomfort of many minor
disorders, it is used most commonly
for hemorrhoids and related anal
problems.
Precautions: For the uncommon
individuals who are allergic to
lidocaine, this drug must not be
used. Adverse reactions include
anaphylaxis (Chapter 23: Allergies)
and convulsions.
MEDICATIONS FOR SLEEP
OR SEDATION
Conventional sleeping medications
should not be taken at altitudes
above 10,000 feet (3000 m). Under
the influence of these drugs,
respirations can be slowed to such
an extent that the blood oxygen
level falls drastically, aggravating
the symptoms of acute mountain
sickness. Acetazolamide is the drug
of choice for promoting sleep at
higher elevations where most sleep
disturbances are related to periodic
breathing. Zolpidem (Ambien®) is
safe and effective at high altitude.
Benzodiazepines also seem safe in
low doses, but have more potential
for producing side effects.
Sleep-promoting medications
may be useful for individuals who
have difficulty sleeping the first
night or two away from the comfort
of a warm, soft bed but should not
be taken routinely. Persistent
insomnia may be the result of a
psychiatric disorder and should be
treated only by a physician.
Benzodiazepines
The benzodiazepines are a group
of drugs with almost identical
pharmacologic properties, but
diazepam (Valium®) and lorazepam
(Ativan) are most commonly used
to treat anxiety, and temazepan
(Restoril®), a short-acting agent, is
most commonly used for promoting
sleep. Diazepam also is used to
relieve muscle spasm, particularly
in the back muscles.
Precautions: Unusual
drowsiness may persist the day
following ingestion of any of these
drugs.
Like the moderate and strong
analgesics, benzodiazepines
depress brain function and should
not be given to individuals with
head injuries or central nervous
system disease.
Benzodiazepines potentiate the
depressive effects of alcohol.
Zolpidem
Zolpidem (Ambien®) is an agent
administered to help individuals
fall asleep.
Precautions: Ambien® may
cause a severe allergic reaction that
may be manifested by difficulty
breathing or by swelling of the face,
lips, tongue, or throat.
This drug should not be taken
unless a full seven to eight hours for
sleeping are available.
Some people using this medicine
have engaged in activity such as
driving, eating, or making telephone
calls and later have no memory of
the activity.
Some individuals still feel
sleepy the morning after taking the
medication and must be careful
about driving a car, operating
machinery, or any activity that
requires them to be awake and
alert.
Alcohol should not be consumed
while taking Zolpidem.
Other Sleep Medications

Diphenhydramine
(Dramamine®, Benadryl®, and
others) is an antihistamine but is
approved by the FDA for use as a
sleeping medication. It is frequently
included in over-the-counter
sleeping preparations and is safe.
ANTIPSYCHOTIC AGENTS
Haloperidol
Haloperidol (Haldol®) is an older
antipsychotic drug that has been
used to treat schizophrenia. In
wilderness situations it could be
needed to allow evacuation of an
individual in an acute psychotic
state, such as drug psychosis or
delirium associated with
hyperactivity and aggressive
behavior.
Oral and injectable preparations
are available; persuading an
irrational person to take an oral
medication could be problematic.
Precautions: Haloperidol must
not be given to individuals who are
severely intoxicated by alcohol or
other central nervous system
depressants.
This drug must not be given to
people with known heart disease; it
tends to produce cardiac arrest.
ANTIMICROBIAL AGENTS
Antimicrobial agents are used to
treat established infections;
antiseptics such as povidone-iodine
kill microorganisms on contact.
Bacteria are classified as gram
positive or gram negative according
to their reaction with the gram stain;
as cocci (spheres), bacilli (rods),
or spirochetes (spirals); and as
aerobic if they are able to grow in
the presence of oxygen or anaerobic
if they cannot.
The Penicillins
Penicillin, the first antibiotic to
be discovered, is still widely used
and is effective treatment for many
common infections. Chemical
modifications to penicillin have
produced a family of compounds,
the penicillins. Penicillins actively
kill bacteria (are bactericidal);
some antibiotics just keep them
from multiplying (are
bacteriostatic). Organisms usually
susceptible to penicillins include
streptococci (strep throat, cellulitis,
and impetigo); Streptococcus
pneumoniae (conjunctivitis,
pneumonia); Neisseria meningitidis
(meningitis); and the spirochete that
causes syphilis.
As antibiotic use has increased
over time, some organisms formerly
sensitive to penicillins are now
resistant. In the developed world,
for example, staphylococci (boils,
abscesses, and wound infections)
are frequently resistant. Penicillins,
including ampicillin and
(Augmentin®), are no longer
predictably effective against the
organisms likely to cause
gastrointestinal infections such as
traveler’s diarrhea, dysentery, or
typhoid fever.
Penicillin V is the penicillin
most suitable for oral
administration because it is
resistant to destruction by acid in
the stomach. Aqueous crystalline
penicillin G is used for intravenous
administration.
Infections should be treated with
penicillin only if the causative
organism is known to be
susceptible. Some bacteria produce
the enzyme penicillinase (or beta-
lactamase), which destroys
penicillin, but some penicillin
preparations are resistant to
penicillinase. In recent years
staphylococci have developed
resistance even to these penicillins.
These organisms are known as
methicillin-resistant
Staphylococcus aureus (MRSA)
even though methicillin is no longer
produced and the bacteria are
resistant to the large group of
antibiotics called the beta-lactams,
which include the penicillins and
the cephalosporins. Such bacteria
are susceptible to a limited number
of other antimicrobial agents such
as trimethoprimsulfamethoxazole
(TMP-SMX), clindamycin, and
vancomycin.
Precautions: The penicillins are
usually very safe, but allergic
reactions occur in a significant
number of the individuals receiving
them. Most of these reactions
consist of skin rashes, a low fever,
or other minor problems, but a few
individuals develop severe
anaphylactic reactions that may be
lethal within minutes (Chapter 23:
Allergies).
Anyone who has suffered
anaphylaxis to any of the penicillins
must never be treated with any of
them again because a potentially
lethal reaction could occur. A
history of previous minor allergic
reactions is not predictive of such a
life-threatening event, but
penicillins should be avoided for
individuals who have had minor
reactions.
If signs of anaphylaxis develop
in a person receiving a penicillin,
the drug should be discontinued
immediately. The individual should
be warned of the allergy to
penicillin and must tell any future
physician or caregiver about it. A
bracelet or a tag warning of the
allergy must be worn. Participants
with allergies to penicillin on a
wilderness outing should inform
other members of the party and must
make preparations in advance to
have other antibiotics available.
Amoxicillin/Clavulanate
This combination of drugs
(Augmentin®) combines
amoxicillin (a broad-spectrum
penicillin analog) with clavulanic
acid. The acid inactivates a wide
variety of lactamases by blocking
active sites of theses enzymes,
which are transmitted by plasmids
and are responsible for bacterial
resistance to the penicillins and
cephalosporins. One of the major
uses for Augmentin® is the
treatment of animal bites.
Precautions: The principal risk
associated with administration of
this drug is allergic reactions,
which have occasionally been fatal.
Anyone who has had an allergic
reaction to any of the penicillins
should not receive Augmentin®.
The Cephalosporins
The cephalosporins are a group
of antibiotics chemically and
therapeutically similar to the
penicillins. They are classified as
first, second, and third generation.
The organisms against which the
first-generation cephalosporins and
penicillins are effective are
virtually the same. Second- and
thirdgeneration cephalosporins are
effective against a different
spectrum of organisms.
Cephalexin (Keflex® and
others) is an orally administered,
first-generation cephalosporin used
to treat staphylococcal and
streptococcal skin- and soft-tissue
infections and urinary tract
infections. Ceftriaxone
(Rocephin®) is a third-generation
cephalosporin administered
intramuscularly and intravenously
for treating systemic infections,
including meningitis.
Precautions: A few of the
individuals allergic to penicillin
are also allergic to the
cephalosporins. Anyone who has
had a severe reaction to penicillin,
particularly an anaphylactic
reaction, must be treated carefully
with cephalosporins.
Azithromycin
Azithromycin (Zithromax®) is
generally effective against
pneumococci, streptococci, and
mycoplasma. It is not effective for
most staphylococcal infections.
This drug is now available
generically and is used primarily to
treat the more common causes of
pneumonia.
Precautions: Very few adverse
reactions to azithromycin occur, and
those that do appear are mild.
Clindamycin
Clindamycin is another
antibiotic with antibacterial effects
similar to penicillin and is a
suitable substitute for individuals
allergic to penicillin. In addition,
clindamycin is effective against
staphylococci, particularly
methicillin-sensitive
Staphylococcus aureus, and a
number of anaerobic organisms,
particularly Bacteroides fragilis,
one of the most common of the
anaerobic organisms that cause
peritonitis.
Precautions: A significant
number of the individuals being
treated with clindamycin develop
diarrhea. Usually the diarrhea is
mild, and treatment can be
continued. However, rare
individuals develop a life-
threatening colitis from overgrowth
of toxin-producing bacteria,
Clostridium difficile, in the colon.
Such infections can develop with
therapy by other antibiotics
Disorders). Copious fluids and
electrolytes are lost and large
amounts of blood and mucus appear
in the stools. Clindamycin must be
stopped at once if this type of
diarrhea appears, the lost fluids
must be restored—intravenously if
necessary—and metronidazole
should be administered.
The Tetracyclines
The tetracyclines—tetracycline
and doxycycline (Vibramycin®)—
are effective treatment for
infections produced by a broad
spectrum of organisms that includes
rickettsia and some viruslike
organisms as well as a large
number of gram-positive and gram-
negative bacteria. However, the
tetracyclines are bacteriostatic
drugs, and a number of more
effective agents have replaced them
for the treatment of many infections.
Currently the disorders for which
tetracyclines are the antibiotic of
choice are the early stage of Lyme
disease, ehrlichiosis
(anaplasmosis), certain
mycoplasmal and rickettsial
infections, and cholera.
Precautions: Tetracycline
therapy may cause mild diarrhea
due to the suppression of normal
intestinal bacteria. The diarrhea is
rarely severe and usually ends
when the drug has been stopped.
Nausea and vomiting sometimes
occur in persons receiving
tetracyclines.
All tetracyclines increase
sensitivity to ultraviolet light and
predispose individuals receiving
them to severe sunburn.
Tetracyclines can permanently
stain the dental enamel in young
children. It should not be
administered to children and
pregnant women when other agents
are available.
Tetracyclines are poorly
absorbed from the stomach when
given with milk or other dairy
products, with antacids, or with
bismuth (PeptoBismol®). They
should be given one hour before or
two hours after meals.
After their expiration date
tetracyclines may become toxic,
unlike most drugs that just become
less potent.
The Quinolones: Levofloxacin,
Ciprofloxacin, Moxifloxacin, and
Ofloxacin
Levofloxacin (Levaquin®),
ciprofloxacin (Cipro®),
moxifloxacin (Avelox®), and
ofloxacin (Floxin®) are
quinolones: antimicrobial agents
effective against a broad range of
bacteria. Levofloxacin is
particularly useful for treating
pulmonary infections; ciprofloxacin
is much less effective for such
disorders. Both are useful for
urinary tract and gastrointestinal
infections, although resistance to
ciprofloxacin is developing in
southern and Southeast Asia.
Quinolone eyedrops are made
with ciprofloxacin as well as
moxifloxacin and ofloxacin, two
similar agents. Such eyedrops are
the preferred therapy for
conjunctivitis.
Precautions: Quinolones should
not be administered to children or
pregnant women. High doses given
to immature animals produced
permanent cartilage damage.
However, in emergencies
ciprofloxacin has been given to
children with no adverse results.
Trimethoprim-Sulfamethoxazole
(TMP-SMX)
(Bactrim, Septra®, trimethoprim-
sulfa, TMP-SMX, or cotrimoxazole
[the latter is the British-approved
name]) is a combination of two
agents, one of which is a
sulfonamide. Sulfonamides are
useful for treating many
gastrointestinal and urinary tract
infections because they can be
administered in preparations that
produce high concentrations of the
drugs in these organs. In addition,
some organisms resistant to
antibiotics, particularly methicillin
resistant Staphylococcus aureus
(MRSA), are readily destroyed by
sulfonamides.
Precautions: Sulfonamides in
general are not very soluble in
water and tend to precipitate in the
urine, in effect forming small kidney
stones that can cause significant
damage. To prevent such damage,
persons receiving these drugs must
consume large quantities of fluids to
maintain a high urinary volume.
Some persons are allergic to
sulfonamides and should not be
treated with them. Sulfonamides
should not be taken by individuals
with glucose-6-phosphatase
deficiency. (This disorder, which
must be diagnosed by a physician,
usually causes mild anemia and is
aggravated by certain drugs,
particularly some sulfonamides.)
Sulfonamides cross the placenta,
are excreted in milk, and can have
harmful effects on a fetus or
newborn. Only a physician should
administer them during the last
months of pregnancy and to nursing
mothers.
Silver Sulfadiazine Cream

Silver sulfadiazine cream is a
sulfonamide in an ointment
(Silvadene®, SSD Cream®, and
others) that is applied to burns to
help control bacterial infections
(Chapter 13: Burns). It is effective
against a wide variety of organisms,
particularly the organisms that most
commonly infect burns.
Precautions: Since silver
sulfadiazine is a sulfonamide, the
precautions described for TMP-
SMX should be observed.
Application: A thin layer of the
cream should be applied sterilely to
the burn twice a day if the burn is
exposed. Dressings covering a burn
should not be removed just to apply
the cream if no evidence of
infection is present.
Metronidazole
Metronidazole (Flagyl® and
others) is a drug used to treat a
variety of parasitic infestations and
bacterial infections. Its principal
use in wilderness circumstances
would be for treating Giardiasis
and amebiasis, but this drug is also
used to treat Clostridium difficile
colitis (Chapter 19: Gastrointestinal
Disorders).
Precautions: Alcoholic
beverages taken during therapy with
metronidazole can cause severe
vomiting and should be avoided
while the drug is being taken and
for one day afterward.
Metronidazole should be
administered only by a physician
during the first trimester of
pregnancy and to anyone with
concomitant disease, particularly
liver, blood, or neurologic
disorders.
Metronidazole should not be
given to children except to treat
amebiasis.
Tinidazole
Tinidazole (Tindamax® or
Tiniba®) is an antiparasitic drug
used widely throughout Europe and
the developing world as treatment
for a variety of parasitic infections.
It is chemically similar to
metronidazole but has a shorter
treatment course with a more
convenient dosage schedule.
Precautions: The precautions
for tinidazole are the same as those
for metronidazole.
ANTIFUNGAL AGENTS
Clotrimazole Cream
Clotrimazole is a broad-
spectrum antifungal agent that is
applied for skin infections,
particularly tinea pedis (athlete’s
foot), tinea cruris (jock itch), and
ringworm caused by various
species of fungi and yeasts.
Precautions: Clotrimazole is
poorly absorbed through the skin,
and toxic reactions are uncommon.
Administration: The cream
should be gently massaged into the
affected and surrounding skin twice
a day, in the morning and evening.
Improvement with relief of itching
usually occurs within the first week
of treatment.
ANTIMALARIAL AGENTS
Various antimalarial drugs are
available. Chloroquine, mefloquine,
and malarone are used most
commonly. Travelers to malaria-
endemic areas should consult a
travel medicine specialist because
recommendations for drugs for
specific areas change so frequently.
Chloroquine
Chloroquine is highly effective
for both prevention and treatment
for chloroquine-sensitive malaria.
Unfortunately, chloroquine-resistant
falciparum malaria is widespread.
As a result, mefloquine (Lariam®)
or atovaquone/proguanil
(Malarone®) are the prophylactic
agents of choice for travel to most
malarious areas. Chloroquine is
also effective to some extent in the
treatment of amebiasis.
Precautions: In the dosages
used for preventing or treating
malaria, chloroquine has few
serious side effects. Therapeutic
doses may cause minor
gastrointestinal disturbances. Skin
rashes or itching occur
occasionally. However, these
symptoms often do not require
interruption of therapy or
prophylaxis and rapidly disappear
when administration is ended.
Dose: 0.5 gm orally once
weekly on the same day of the
week, starting one week before
entering a malaria endemic area and
continuing for four weeks after
leaving.
Mefloquine
Mefloquine (Lariam®) is
administered for preventing or
treating chloroquine-resistant
falciparum malaria.
Precautions: Individuals
allergic to mefloquine or related
agents, particularly quinine or
quinidine, should not take this drug.
Because dizziness occasionally
follows mefloquine ingestion,
individuals taking it must be careful
with activities such as driving a car,
piloting an aircraft, or using
machinery in which injury could
occur.
Psychiatric reactions such as
anxiety, depression, restlessness,
hallucinations, or confusion occur
occasionally with mefloquine, and
the drug should be stopped if these
appear. Persons with significant,
preexisting psychiatric illness,
particularly those on psychiatric
medication, should take mefloquine
with caution, preferably after
consulting a physician.
Animal studies have shown
serious complications from
mefloquine taken during pregnancy.
There are no studies of the safety of
mefloquine in pregnant women. The
drug should only be taken by
pregnant women if the potential
benefits justify the potential risk to
the fetus.
Dose: 250 mg once weekly
beginning one week before entering
an area in which
chloroquineresistant falciparum
malaria is known to exist, and
continuing for four weeks after
leaving the area.
Malarone®
Malarone® is a combination of
the antimalarial agents atovaquone
and proguanil. Malarone® is
indicated for the prevention of
falciparum malaria, including areas
where chloroquine resistance has
been reported. It is also useful for
the treatment of acute,
uncomplicated falciparum malaria.
Although no adequate, well-
controlled studies of atovaquone or
proguanil in pregnant women have
been performed, Malarone® may
be used if the potential benefit
justifies the potential risk to the
fetus.
Dose: Prophylactic treatment
with one tablet daily started one or
two days before entering a malaria
endemic area and continued daily
during the stay and for seven days
upon return.
ANTISEPTICS
Povidone-Iodine
Povidone-iodine, an iodophor
and a loose complex of iodine with
polyvinylpyrrolidone, was patented
in 1956 and subsequently has
become widely available as a 10
percent solution under the trade
names Betadine®, Povidine®,
Pharmadine, and others. These
preparations offer two significant
advantages for wilderness use:
They can be kept in polyethylene
containers, which avoids glass
containers, and they are effective
disinfectants in dilute solutions so
that less must be carried.
Povidone-iodine retains the
strong bactericidal activity of
iodine but eliminates many of the
disadvantages, such as skin
irritation, staining of the skin, and
some of the odor. A 1:100 dilution
of a 10 percent solution has been
found to have much greater
bactericidal action than the original
stock solution, and 1:1000 dilutions
are almost equally effective.
Precautions: Rare individuals
are allergic to iodine; a chronic
skin rash is the usual manifestation.
Such individuals should not use
povidone-iodine.
Povidone-iodine has been
recommended for water
disinfection, but no substantiating
data have been provided. The
1:10,000 dilution that would result
has been found to have no
significant antimicrobial activity. At
present, these agents cannot be
considered reliable for water
disinfection.
Application: For skin
disinfection prior to injections, the
undiluted solution is suitable and
convenient. For rinsing a larger
wound, the original solution should
be diluted several hundred times
and the wound thoroughly rinsed
with large quantities of the solution,
particularly following the bite of a
possibly rabid animal.
MEDICATIONS AFFECTING
THE HEART, BLOOD
VESSELS, AND RESPIRATORY
SYSTEM
Acetazolamide
Acetazolamide (Diamox®)
inhibits the enzyme carbonic
anhydrase, which catalyses the
reversible combination of carbon
dioxide with water to form
carbonic acid. This drug promotes
renal bicarbonate excretion and
tends to reduce the respiratory
alkalosis (increase in blood pH)
resulting from carbon dioxide loss
at high altitudes as the result of
faster and deeper breathing.
Acetazolamide reduces the
severity of acute mountain sickness
symptoms in individuals who must
ascend from sea level to 12,000 to
14,000 feet (3700 to 4300 m)
without adequate time for
acclimatization. It may not eliminate
such symptoms entirely. In addition,
it promotes acclimatization.
A significant effect of
acetazolamide on highaltitude
pulmonary edema has not been
demonstrated.
Perhaps the greatest benefit from
acetazolamide is relief of sleep
problems at high altitude.
Elimination of episodes of severe
hypoxia during sleep may be
responsible for better tolerance of
high altitude during waking hours.
Precautions: Acetazolamide is
a sulfonamide, although it does not
have any antibacterial actions.
Persons allergic to sulfonamides
may be allergic to this drug.
Persons with liver or kidney
disease should not be treated with
acetazolamide, and the drug should
not be given during the last months
of pregnancy or to nursing mothers.
Many individuals, perhaps most
individuals, develop tingling
sensations in the lips, fingers or
hands, toes or feet, or occasionally
other areas; blurring of vision; and
alterations of taste when taking this
drug. These sensations disappear
when the medication is stopped.
Dose: To promote sleep at high
altitude, 62.5 to 250 mg orally at
dinnertime.
Dexamethasone
Dexamethasone (Decadron and
others), a synthetic glucocorticoid,
is a potent steroid that is used to
treat a variety of disorders, but its
value in the wilderness is quite
limited. The ability of this agent to
reduce the edema associated with
the spread of malignant tumors from
other organs to the brain led to
therapeutic trials for high-altitude
cerebral edema. In the wilderness,
its value is largely limited to the
treatment of severe acute mountain
sickness and high-altitude cerebral
edema.
Dexamethasone is as effective as
acetazolamide for treating acute
mountain sickness. However, it
does not promote acclimatization.
Symptoms of acute mountain
sickness relieved by dexamethasone
therapy recur when treatment is
stopped. Dexamethasone is
recommended only when symptoms
have developed after preventive
measures have been neglected or
have been impossible, such as in
emergency rescue situations.
However, recreational skiers
susceptible to acute mountain
sickness at 8000 to 10,000 feet
(2400 to 3000 m) altitudes
commonly take dexamethasone
instead of acetazolamide because
they want to enjoy carbonated
beverages, principally beer.
Precautions: Significant side
effects from dexamethasone
administered for the short time
periods required to evacuate
individuals with acute mountain
sickness or high-altitude cerebral
edema—evacuation should be the
principal therapy—are rare. The
primary risk is relying on
dexamethasone alone and not
evacuating the affected individual
to a lower altitude.
Rarely side effects such as
euphoria or cloudy judgment have
developed after therapy with
dexamethasone.
Prolonged therapy with
dexamethasone is associated with
major side effects, but such
prolonged therapy should never be
needed for altitude problems.
Skiers should not take
dexamethasone for more than five
or six days.
Nifedipine
Nifedipine (Procardia® and
Adalat®) is a member of a class of
drugs, the calcium channel
blockers, used primarily to treat
hypertension and coronary artery
disease. Because this drug lowers
pulmonary artery pressure, it has
been given to some individuals with
high-altitude pulmonary edema. In
studies of individuals with unusual
susceptibility to highaltitude
pulmonary edema, nifedipine
reduced the incidence of that
disorder. However, its usefulness in
other persons has not been
established.
Precautions: Nifedipine
administered for the time required
to evacuate an individual with
highaltitude pulmonary edema
would produce few side effects.
However, the therapy for high-
altitude pulmonary edema is
descent to lower altitude. Oxygen
may be helpful and should be
administered during descent.
Nifedipine alone cannot substitute
for those measures.
Nitroglycerin
Nitroglycerin (the explosive
compound) relaxes the walls of
small blood vessels, permitting
them to dilate and increase the flow
of blood. It is most commonly used
to treat angina pectoris (severe
chest pain associated with
inadequacy of the blood supply to
the heart) but dilates all small
arteries and can be used to increase
the blood flow to other organs or
tissues. As the result of dilatation of
cerebral arteries, throbbing
headaches frequently follow the use
of nitroglycerin.
Precautions: The most serious
side effect of nitroglycerin therapy
is a drop in blood pressure due to
the dilatation of blood vessels.
Fainting or—even worse—
aggravation of the cardiac damage
could result. Therefore, a person
receiving this drug must be closely
attended. The individual should lie
down with head lowered if
symptoms of faintness or dizziness
appear.
The tablets should be kept in
their original brown bottle and
should not be kept longer than six
months after purchase as they begin
to lose their potency. Cotton wads
should not be kept in the bottle,
which must be kept tightly
stoppered.
Epinephrine
Epinephrine (adrenaline) is a
hormone secreted by the medulla of
the adrenal gland. It is used to treat
spasm of the bronchi due to
anaphylactic shock or severe
asthma or to relieve the spasm and
respiratory obstruction of laryngeal
edema. Epinephrine is effective
when injected or when applied
directly to the involved tissues. It is
destroyed by the acid and digestive
enzymes in the stomach and is
ineffective when administered
orally.
Precautions: Epinephrine must
be administered slowly and
carefully to elderly individuals or
to persons with heart disease of any
kind, high blood pressure, thyroid
disease, or diabetes. It also should
not be given to persons in shock
from blood loss. Epinephrine is a
powerful cardiac stimulant; its
effect on individuals with these
disorders could be lethal.
The epinephrine preparation
must be discarded without being
used if it is outdated, has turned
brown, or contains a precipitate.
DECONGESTANTS
Decongestant Sprays
These agents cause the blood
vessels in the nasal mucosa to
contract, reducing their volume but
also reducing the amount of fluid
collected in the tissue (edema)
around the vessels. Decongestants
shrink the swollen mucosa of the
nose for persons with colds, hay
fever, or sinusitis. Importantly,
these drugs not only relieve
obstruction to the passage of air but
also promote drainage from the
small canals opening into the
sinuses.
Phenylephrine hydrochloride, a
widely used decongestant and well
known as Neo-Synephrine®, has
been found to increase the
incidence of cerebrovascular
accidents (strokes). It has been
replaced in most decongestants,
including Neo-Synephrine®.
Oxymetazoline, a decongestant
that is equally effective, is much
longer acting and lasts up to twelve
hours after a single application.
(Because the onset of its action is
slower, some individuals have
gained the impression that
oxymetazoline is not as effective as
phenylephrine.) A 0.05 percent
solution is contained in a number of
preparations such as Afrin® and
Dristan® long-acting nasal sprays,
but many drugstore and grocery
chains sell identical preparations
under their own label at a price 40
to 50 percent below that of the
established brands.
Precautions: Individuals with
severe hypertension should not use
nasal sprays.
Administration of the nasal spray
should be repeated ten minutes after
the first application. Initially the
spray only reaches the mucosa over
the more prominent structures in the
nasal cavity. Not until this portion
of the mucosa has been shrunken
can a subsequent application extend
into the recesses where the small
canals draining the sinuses open.
After the effects of the nasal
spray have worn off, swelling of the
nasal mucosa and airway
obstruction recur. Such rebound
symptoms are often worse than the
initial symptoms. With each
subsequent application, the duration
of the spray’s effects tends to
become shorter. For this reason, use
of the spray should be limited to the
hours when decongestant action is
needed to promote restful sleep.
When used in this manner rebound
is much less severe or absent.
Pseudoephedrine
Pseudoephedrine (Sudafed® and
others) is a systemic decongestant.
The drug acts through the nerves
supplying the blood vessels in the
mucosa of the upper respiratory
tract, causing those vessels to
contract. Excess fluid in the mucosa
(edema) is reduced, the mucosa
shrinks to normal thickness, and
obstruction to the passage of air is
relieved. This drug also shrinks the
mucosa lining the small canals that
drain the sinuses and the eustachian
tubes that drain the middle ears,
allowing air or fluid to move
through these structures and helping
to avoid aerotitis media,
aerosinusitis, or infectious sinusitis.
Precautions: Only a physician
should give pseudoephedrine to
individuals with high blood
pressure, heart disease, thyroid
disease, or diabetes.
Pseudoephedrine acts as a mild
stimulant and makes some
individuals restless or jumpy,
which can inhibit restful sleep.
Reducing the dose of the drug by
only taking part of a tablet usually
prevents these side effects.
ANTIHISTAMINES
Antihistamines are a group of drugs
that block the effects of histamine, a
substance released during allergic
and inflammatory reactions and
considered responsible for many
symptoms of allergy. In addition,
some of these agents can prevent or
reduce symptoms of motion
sickness.
Precautions: All antihistamines
have a tendency to cause
drowsiness, although individual
susceptibility varies. Some more
recently developed agents produce
much less drowsiness, but even
those drugs are not completely free
of this side effect. Some are
available over the counter. Anyone
who has taken an antihistamine must
be very careful about engaging in
activities for which drowsiness
could be a hazard, particularly
driving a car.
Dimenhydrinate, Meclizine, and

Cyclizine
Dimenhydrinate (Dramamine®,
Benadryl®, and others), meclizine
(Bonine® and Antivert®), and
cyclizine (Marezine®) are
antihistamines used primarily to
control motion sickness. All should
be taken about one hour before
embarking on a trip. All are fairly
effective against allergies.
Precautions: All antihistamines
have a tendency to cause
drowsiness, although individual
susceptibility varies. Anyone who
has taken an antihistamine must be
very careful about engaging in
activities for which drowsiness
could be a hazard, particularly
driving a car.
MEDICATIONS FOR
GASTROINTESTINAL
DISORDERS
Paregoric
Paregoric (camphorated tincture
of opium) is a mixture of several
compounds, the most important of
which is morphine. This mixture is
used to control diarrhea through the
immobilizing action of opium
derivatives on the lower
gastrointestinal tract.
Precautions: The problems
related to using any drug to control
diarrhea are discussed in Chapter
19: Gastrointestinal Disorders.
Paregoric is classified as a
controlled substance because it
contains opium. Addiction to
paregoric does occur but is
uncommon.
Diphenoxylate with Atropine

Diphenoxylate with atropine
(Lomotil®) is a combination of two
compounds used to control diarrhea
through slowing of intestinal
mobility.
Precautions: The most
important complications resulting
from the administration of
diphenoxylate are those from using
any drug to control diarrhea.
Addiction is at least
theoretically possible, and
diphenoxylate is classified as a
controlled substance.
Loperamide
Loperamide (Imodium®) helps
control diarrhea by reducing
intestinal mobility. The suspension
and tablets are now available over
the counter.
Precautions: The most
important complications associated
with the administration of
loperamide are those resulting from
using any drug to control diarrhea
Disorders).
Prochlorperazine and
Promethazine
Prochlorperazine (Compazine®)
was one of the first tranquilizers
and is quite similar to
chlorpromazine (Thorazine), which
is better known. Although these
agents were major therapeutic
advances, more effective drugs
have largely replaced them, and the
principal use of prochlorperazine
currently is treating severe nausea
and vomiting. It is useful at high
altitudes because it is a mild
respiratory stimulant.
Promethazine (Phenergan®) is a
chemically closely related drug that
also has significant antihistamine
activity. However, a more common
use is treating severe nausea and
vomiting.
Individuals who are vomiting
repeatedly often are unable to retain
oral medications and rectal
suppositories must be substituted.
Precautions: Prochlorperazine
and promethazine must not be given
to individuals who are comatose or
whose consciousness is
significantly impaired.
Only a physician should give
either of these agents to children
younger than two years old. In
wilderness situations
prochlorperazine probably should
not be given to pre-teenage
children.
Ondansetron
Odansetron (Zofran® and Zofran
ODT®) is a medication
administered to control nausea and
vomiting. The orally disintegrating
tablets (Zofran ODT®) can be
placed on the tongue where they
break down in two to three minutes
and can be more easily swallowed
than tablets by individuals who are
nauseated.
Precautions: The instructions
for removing Zofran ODT® from
the blister pack in which it is
provided should be closely
followed.
Antacids
Antacids are preparations that
contain combinations of aluminum
hydroxide, calcium carbonate,
magnesium carbonate, magnesium
hydroxide, and magnesium
trisilicate. They are administered to
neutralize acids in the stomach in
the treatment of peptic ulcers,
GERD, and for relief of symptoms
of indigestion. Some of the
preparations are flavored. Alkets,
Titralac®, Robalate, Alka-
Seltzer®, Alka-2®, Amphojel®,
Gaviscon®, Gelusil®, Maalox®,
WinGel, Rolaids®, and Tums® are
well-known antacids.
Precautions: Magnesium-
containing antacids sometimes
produce a mild diarrhea, but this
side effect rarely requires treatment
or interruption of therapy. These
drugs are absorbed from the
gastrointestinal tract in minimal
amounts, if at all, and have no
effects on the rest of the body. They
are of no value in preventing acute
mountain sickness.
Antacids should not be taken
indiscriminately over a long time.
Prolonged consumption of antacids
taken with calcium-containing foods
such as milk can lead to calcium
deposits in the kidneys and
impaired renal function.
H2 Blockers
Several agents, one of which is
histamine (H2) stimulate the cells
that secrete acid in the stomach. The
H2 blockers inhibit the secretion of
acid in the stomach by blocking the
sites at which histamine attaches to
the walls of the acid-secreting
cells. These agents were first
introduced in 1976 and were a
major advance in the treatment of
peptic ulcers, drastically
decreasing the need for surgical
treatment for this disorder. Most of
these agents are now available over
the counter.
Proton Pump Inhibitors

Proton pump inhibitors, of which
the best known are omeprazole
(Prilosec®) and esomeprazole
(Nexium®), block secretion by the
acidproducing cells of the stomach.
These agents are the most effective
yet developed for treating peptic
ulcer and gastroesophageal reflux
(heartburn). No contraindications
exist, although the safety of the drug
during pregnancy and in children
has not been established. No
significant side effects occur during
administration for the short
intervals that would typify
wilderness outings.
Omeprazole is available over
the counter. A physician’s
prescription is required for
esomeprazole.
Speed of Action
Antacids provide the most rapid
relief for symptoms of indigestion
and heartburn. H2 blockers take
effect relatively quickly. Proton
pump inhibitors take longer to take
effect but are the best for long-term
care.
APPENDIXE B
THERAPEUTIC
PROCEDURES
ADMINISTERING
MEDICATIONS
Oral Medications
The oral route is the easiest,
most convenient, and safest method
for administering drugs but has two
major disadvantages: the time
required for a drug to be absorbed,
and variations in the rate and
completeness of absorption. Acid
and enzymes in the stomach
completely inactivate some
therapeutic agents, and they must be
given by another route.
Individuals who are not fully
conscious may aspirate oral
medications and must never receive
them.
Oral therapy is much less
effective for a person who is
nauseous or vomiting. Even if the
drugs are not expelled, emptying of
the stomach is greatly retarded and
the onset of action by the agent is
delayed because orally
administered drugs are usually
absorbed only in the small intestine.
With the exception of agents that
are irritating to the stomach, such as
aspirin or ibuprofen, oral
medications should be taken at least
thirty minutes before meals. The
stomach empties more slowly and
irregularly when it is filled with
food, which delays onset of the
drug’s actions. Food interferes with
the absorption of some medications.
Intramuscular Injections
The intramuscular route for
administering drugs avoids the
vagaries of intestinal absorption but
must be used cautiously because
injected medications cannot be
retrieved.
Intramuscular injections are
associated with a slight risk of
injecting the drug directly into a
blood vessel inside the muscle,
which would produce higher and
more toxic blood concentrations of
the agent than the slower absorption
from a true intramuscular site.
Intramuscular injections are
usually not absorbed well by
individuals who are in shock or are
hypothermic. If several injections of
an agent were given and the
medication was not absorbed until
the person recovered, all would be
absorbed at once, producing an
overdose and possibly serious
toxicity.
The needle used for an
intramuscular injection may injure
nerves, blood vessels, or other
structures if the site for the injection
is not carefully chosen.
The most common complication
of intramuscular injections is an
infection produced by bacteria
introduced with the needle.
Although the needle may be free of
bacteria, the skin through which it
passes cannot be completely
sterilized. Cleansing the skin and
avoiding needle contamination
usually limit the quantity of bacteria
introduced to a number that the
body’s defenses can destroy.
The following steps should be
followed in administering any
therapeutic agent intramuscularly:
1. The skin over the injection site
should be cleaned with soap
and water, swabbed with
alcohol or preferably a
povidone-iodine disinfectant
such as Betadine®, and
permitted to dry.
2. The label on the drug container
should be read closely to
ensure the proper medication in
the correct dose is being
administered.
3. A syringe of appropriate size
should be fitted with a 25-
gauge needle that is at least one
inch long.
4. The rubber top of the vial
through which the needle is to
be inserted should be swabbed
with alcohol or a disinfectant.
5. The drug should be extracted
by inverting the vial, inserting
the needle through the rubber
top, injecting a volume of air
equal to the volume of fluid to
be removed, and withdrawing
the medication. While the
needle is still in the vial, air
bubbles or excess medication
should be expressed from the
syringe.
6. The label on the container must
be reexamined to ensure no
mistakes have occurred. Such
errors are far easier to prevent
than to correct.
7. An injection site should be
selected at which the muscle is
thick enough to prevent striking
the underlying bone. The
deltoid muscle of the shoulder,
gluteus muscle of the buttock,
or quadriceps muscle of the
anterior thigh are the usual sites
(Fig. B-1). The deltoid is used
most commonly because it is
easily accessible; the gluteus is
not as reliable for injections of
vaccine, particularly rabies and
hepatitis vaccines. The needle
should be inserted with a jab.
Figure B-1. Sites for the
administration of intramuscular
injections (A, shoulder; B, thigh; C,
buttock)
8. Before injecting the

medication, the plunger of the
syringe must be pulled back to
make certain the needle is not
in a blood vessel. If blood is
pulled back into the syringe, the
needle must be removed and
inserted in a different location.
9. The contents of the syringe
should be injected slowly to
minimize discomfort, but the
needle should be withdrawn
quickly.
Intravenous Medications
Intravenous drug administration
is required in a few medical
emergencies, may be the only
effective way to administer drugs to
individuals who are in shock, and is
the most effective method to treat
some severe infections because
higher blood concentrations of a
therapeutic agent can be attained. In
addition, a more constant blood
concentration of the drug can be
maintained without the swings
associated with intermittent
intramuscular or oral
administration.
However, intravenous injections
may be hazardous because high
drug concentrations in the blood can
develop quite rapidly. If some
medications are injected too
rapidly, severe complications can
result. Like intramuscular
injections, once an agent has been
injected intravenously it cannot be
recovered. If the person has an
allergic reaction to the drug, little
can be done to reverse the process
and it must be treated. Such
injections must be given only when
necessary and specified rates of
injection must be closely observed.
The technique for administering
intravenous medications over a long
period of time is the same as
intravenous fluid administration.
Intravenous antibiotics are usually
administered by injecting the
antibiotic directly into a bag of
intravenous fluids. Drugs also may
be injected through a port on the
tubing.
If the person is in shock and
veins in the forearm cannot be
identified, or if intravenous fluids
and the equipment to administer
them are not available, intermittent
injections such as the periodic
injections of morphine to provide
analgesia for a person in shock, can
be given in the large veins located
in the fold of the arm at the elbow
or those on the back of the hand.
Preparation of the injection site
should be the same as for
intramuscular injections. After the
needle has been inserted into a
vein, a small amount of blood
should be withdrawn to dilute the
drug and make certain the needle is
in the proper location.
Subsequently, the drug should be
injected slowly, but continuously,
over a period of two to three
minutes.
Intravenous Fluid Therapy

Intravenous fluid therapy is
required to replace normal and
abnormal fluid losses for
individuals who are not able to take
fluids orally, to administer fluids
following a severe hemorrhage, and
for the intravenous administration
of some medications.
Currently, plastic catheters are
used in most U.S. medical centers
for the administration of
intravenous fluids because they
rarely puncture the vein walls after
they have been inserted, as do sharp
needle tips, and they do not become
dislodged as easily.
The technique for administering
fluids intravenously is basically
simple. Individuals planning outings
to wilderness areas where
intravenous fluids might be required
should learn the technique
beforehand from an experienced
individual who regularly inserts
IVs.
Although minor details in the
way intravenous fluids are
administered by different
individuals vary, the basic
technique is as follows:
1. The protective cap should be
removed from the container of
fluids to be administered, the
tubing on the dispensing
apparatus should be clamped
below the drip chamber, and
the apparatus should be
inserted into the proper
opening. The drip chamber, a
small reservoir that keeps air
bubbles from being carried into
the person’s vein by the fluid,
should be half filled by
squeezing it repeatedly.
(Compressing the drip chamber
forces air out of the tubing
between the chamber and the
fluid container. When the
pressure is released, the
chamber expands and draws
fluid back into the space
previously occupied by air.)
After the chamber is half full,
the tubing should be filled by
briefly releasing the clamp. The
container (with its tubing)
should be suspended two to
three feet above the body of the
person who is to receive them
(Fig. B-2).
2. The person should be placed in
a supine position and a
tourniquet that blocks venous
but not arterial blood flow
should be placed around the
upper arm. (The pulse must be
palpable at the wrist.) The
person should open and close
his or her fist several times to
engorge the superficial veins.
Letting the arm hang down for a
few minutes or covering it with
a warm, moist towel helps
make the veins more prominent
if they are small or obscured by
subcutaneous fat.
3. A large, prominent vein in the
lower arm, preferably on the
inner, flat surface, should be
selected, and the overlying skin
should be cleaned with soap
and water and swabbed with
alcohol or a disinfectant. After
the skin has dried, the person’s
arm should be held in one hand
with the thumb stretching the
skin over the vein into which
the catheter is to be inserted.
(Intravenous catheters consist
of an outer thin sheath—the
catheter—that has a hub into
which the intravenous solution
drip chamber injection port
intravenous tubing is inserted,
and an inner metal needle that
protrudes beyond the tip of the
catheter and has a handle but no
hub.) The apparatus should be
held almost parallel with the
vein, with the bevel of the
needle upward. The needle
should be inserted through the
skin, into the vein, and the
catheter threaded up the vein
for about one inch (Fig. B-3). A
slight “give” can be felt as the
vein is entered, and blood
flows back into the needle.
Figure B-2. Apparatus for
administration of intravenous fluids
4. After the needle has been
threaded into the vein, the hub
of the catheter should be
grasped securely to ensure it is
not pulled out, and the needle
should be extracted. The end of
the intravenous tubing should
be inserted into the hub of the
catheter, the clamp on the
tubing should be released, and
the tourniquet should be
removed from the person’s arm.
Alternately a saline lock, which
will keep the catheter open, can
be attached to the catheter.
5. Once the fluids are flowing
satisfactorily, the catheter
should be anchored with tape,
and the last eight to ten inches
of tubing should be formed into
an S or U and taped to the
person’s arm. Such loops
absorb any accidental pulls on
the apparatus and prevent
dislodging of the catheter. If the
individual is not fully
conscious or is thrashing about,
the arm should be anchored in
some manner—possibly a
splint—while fluids are being
given.
Figure B-3. Technique for inserting a
needle for intravenous therapy
6. In a hospital the clamp on the

tubing is usually partially
closed so that the fluid is
flowing at about 200 ml per
hour (approximately fifty drops
per minute). In wilderness
situations, particularly for fluid
administration following a
severe hemorrhage or fluid
replacement for disorders such
as cholera, fluid should be
given as rapidly as possible.
When administration is
finished, the tubing should be
removed from the catheter and
a saline lock inserted to keep
the catheter open. (Intravenous
lines and the rate at which they
are running need to be checked
at least every thirty minutes.)
7. Swelling at the site of the
catheter indicates that the vein
has been punctured and fluids
are infiltrating into the tissue.
The catheter must be
withdrawn, discarded, and
another catheter inserted at
another site. No effort should
be made to reinsert the catheter
in the original vein until all
swelling has disappeared,
which requires several hours.
The swelling usually produces
little or no discomfort and
requires no specific treatment.
Such events are much less
common when fluids are given
through a catheter than when
fluids are administered through
a needle.
8. If the fluid fails to flow when
the tubing is unclamped, the
catheter may be obstructed.
Changing its position slightly
may move the tip away from the
wall of the vein and restart the
flow. Squeezing the tubing may
force out small clots or plugs of
tissue blocking the catheter. If
the tourniquet on the upper arm
has not been removed, or a
similar venous obstruction (by
tight clothing, for instance) is
present, the fluid cannot flow.
Occasionally such measures
are not successful in starting or
restarting flow, the catheter
must be withdrawn, and a new
catheter must be inserted at
another site.
9. The veins used for intravenous
fluid therapy usually clot after
the catheter is withdrawn and
are not suitable for subsequent
use. In situations where
intravenous fluid therapy at
more than one site is
anticipated, the first catheters
should be placed near the
person’s wrists and subsequent
catheters placed higher up the
arms as the veins become
obstructed.
10. The veins on the back of the
hands should not be used for
intravenous therapy if other
sites are available as this area
is quite sensitive. However, for
individuals who are in shock or
hypothermic, or who are obese,
particularly if they have darkly
pigmented skin, such veins may
be the only ones that can be
found.
11. Occasionally veins for
intravenous therapy are
impossible to access,
particularly in obese people or
individuals who are in shock,
hypothermic, or severely
dehydrated. In an emergency
fluids can be administered by
inserting the needle beneath the
skin of the back, abdomen, or
upper thighs and letting the
fluid infiltrate the subcutaneous
space. Absorption from such
sites is erratic, and
administration may produce
some discomfort, but when
fluids are needed, this route is
better than not giving fluids at
all. Medications should not be
administered in this manner.
INSTRUMENT
STERILIZATION
Most instruments that must be
sterile are either packaged sterilely
by the manufacturer, or they are
available from hospital central
supply units in plastic sterile packs
(individual instruments) or in
autoclaved sterile packages that can
be kept dry in plastic bags.
Dressings and instruments that have
been wrapped in paper and
autoclaved remain sterile for
several months if they are
undisturbed and stay dry. If the
items become wet, sterility is lost.
However, sterilization of
instruments before they can be used
is sometimes necessary. At sea
level, boiling in water for fifteen
minutes provides adequate
sterilization, but equipment must be
available for removing the items
from the water without
contaminating them. At higher
elevations the boiling temperature
of water is lower and the time
required for sterilization is
prolonged, but the additional time
required is not easily determined.
Boiling in a pressure cooker for
fifteen minutes under fifteen pounds
pressure should be adequate at
almost any altitude.
Scalpels, forceps, scissors, and
other metal instruments can be
sterilized by washing them
thoroughly, dipping them in alcohol,
and lighting the alcohol. The
instruments must be permitted to
cool before they are used. (Blowing
on the items to cool them produces
contamination with bacteria from
the nose and mouth.)
Since sterilization of needles
and syringes is unreliable, syringes
and needles used for one individual
must never be used to administer
injections to another. The methods
of sterilization in the field are too
uncertain and the risk of
transmitting hepatitis or human
immunodeficiency virus are too
great to chance in this manner.
Most needles and syringes
currently available are disposable
—designed to be used only once
and then discarded. Items such as
forceps and scalpels are also
available in sterile, disposable kits
that are convenient and relatively
inexpensive. Supplies of this type
should be secured for wilderness
outings and, once used, should
never be used again. They must be
carried out.
APPENDIXE C
MEDICAL SUPPLIES
Ken Zafren, M.D.
No wilderness party can be

completely prepared for every
medical problem. Only the
materials needed to care for
common medical problems can be
carried. The materials needed for
severe accidents or major illnesses
should be available at a base camp
or similar central location.
However, no two individuals,
including physicians and the
editors of this book, completely
agree about the items that should
be in a wilderness medical kit.
Following are three lists of
suggested medical supplies.
“Personal Medical Supplies” are
items that probably should be
carried by everyone on almost any
outing. “Outing Medical Kit” are
items that should be available in
popular wilderness areas and on
expeditions to remote areas.
(Obviously, larger parties can carry
a larger quantity and a greater
variety of medical supplies.) The
“Expedition Medical Kit” suggests
items that should be carried by
major expeditions and in some
areas could be made available by
air drop or similar means.
Physicians should be consulted
about the dosages and quantities of
the items to be included.
Medications for preexisting
disorders, such as diabetes or
asthma, must be supplied by the
individuals with such conditions.
PERSONAL MEDICAL
SUPPLIES
Personal water-free hand sanitizer
(Purell® or others)
Personal protective equipment
(nonsterile gloves, nitrile)
Personal medications
Medications
Acetaminophen or ibuprofen–25 or
more
Hydrocodone and acetaminophen
(Vicodin®)–20 to 30
or
OxyCodone and acetaminophen
(Percocet®)–20 to 30
Epinephrine auto-injector (if
temperatures are above
freezing)–2 per party
Diphenhydramine (Dramamine®,
Benadryl®, others)–10 per
party
Prednisone–5 per party
Supplies and Equipment

Adhesive pads (Band-Aids®),
large–10 or more
Sterile gauze pads, four-inch
squares–6 or more
Porous adhesive tape, two-inch
width–1 roll
Moleskin, four-inch squares or
proprietary blister covers–4 to
6
Elastic bandage, three-inch width–1
Triangular bandage–1
Tweezers–1 per party
Sunscreen–Generous supply
Wound antiseptic such as
Betadine®–2 to 4 ounces
or
Betadine® Swabs–10
Oxygen saturation monitor (for
high-altitude outings)–1 per
party
OUTING MEDICAL KIT

Medications (Oral Except Where
Specified)
Analgesics
Acetaminophen and/or ibuprofen
Hydrocodone and acetaminophen
(Vicodin®) Morphine
(injectable)
Lidocaine jelly (topical)
Antimicrobial Preparations
Levofloxacin
Tetracycline (in tropical areas and
sites where tickborne diseases
are common)
(TMP-SMX®)
Cephalexin
Azithromycin (for traveler’s
diarrhea in areas where
resistance to quinolones is
common, such as south and
Southeast Asia)
Metranidazole (for suspected
gastrointestinal infections)
Ofloxacin ophthalmic drops
Clotrimazole antifungal cream
Antimalarials appropriate for area
Betadine®
Gastrointestinal Medications
Antiemetics (Zofran ODT®)
An antacid (liquids are more
effective; tablets are easier to
carry)
A motion-sickness agent
A laxative (MiraLAX® powder is
light and easy to carry)
An antidiarrheal agent (Lomotil®)
An H2 blocker (Zantac® or
Pepcid®)
Cardiac and Respiratory Agents
A systemic decongestant
A local decongestant spray,
preferably long-acting
oxymetazoline
Epinephrine auto-injectors with
diphenhydramine (Benadryl®)
and prednisone
Albuterol inhaler
Acetazolamide
Dexamethasone (oral and
parenteral)
Nifedipine
Other Medications
An antihistamine (diphenhydramine
oral and parenteral; possibly a
less sedating oral agent)
An anti-anxiety medication (Ativan
or Valium®)
A sleeping medication (Ambien®)
Antipsychotic (Haldol®)
Sunscreens
Bandages and Dressings

Sterile gauze pads
Nonadherent gauze pads
Proprietary blister coverings
Bandaging materials (Kling®)
Adhesive strips (Band-Aids®)
Butterfly strips (Steri-Strips®)
Sterile absorbent cotton
Cotton swabs (Q-tips®)
Eye pads
Triangular bandages
Adhesive tape, two-inch width
(porous)
Hypoallergenic tape
Elastic bandages, two- or three-
inch width
Moleskin
Safety pins, duct tape
Equipment
Surgical forceps and tweezers
Magnifying glass
Penlight or LED headlamp
Scissors
Scalpels with replaceable blades
Syringes and needles
Oral thermometer
Stethoscope
Sphygmomanometer
Plastic oral airway(s)
Tongue blades
SAM splints®
Traction splint (KTD—Kendrick®
Traction Device; also known
as OTD—Optimum Traction
Device)
Foley catheters
EXPEDITION MEDICAL KIT

Items in Outing Medical Kit
Intravenous Fluids (in plastic
containers)
Normal or hypertonic saline
5 or 10 percent glucose
Ampoules of glucose to be added to
intravenous fluids
Tubing and needles for
administration
Intravenous starter kits
Intravenous antibiotics
Oxygen bottles, masks, valves, and
tubing
Equipment for Therapeutic

Procedures
Sterile gloves
Lidocaine
Syringes and needles
Chest tubes and valves for
thoracostomy
Tubes, bottles, and syringes for
nasogastric intubation
Catheters and lubricant for urethral
catheterization
Airway equipment suitable for
skills of expedition personnel
Splints
SAM splints®
Traction splints (KTD or
Kendrick® Traction Device
Other Items
Additional medications for known
medical problems
Two-way radio, aircraft radio,
and/or satellite telephone
APPENDIXE D
LEGAL AND
ETHICAL
CONSIDERATIONS
Forrest C. Wilkerson, Attorney-
at-Law
Charles S. Houston, M.D.
LEGAL CONSIDERATIONS
Few participants in wilderness

activities would hesitate to provide
medical care or to assist with the
evacuation of an ill or injured
individual, whether a member of
their party or another. None of the
following should raise doubts about
that ethical—not legal—obligation.
However, persons who do elect to
render medical aid to others do
have certain legal responsibilities
as well as definite legal rights.
The following are general
principles of the applicable laws in
the United States and Canada.
However, each state, province, and
nation makes its own laws, which
vary considerably. Anyone
involved with such legal problems
must obtain specific information
about the law in the relevant
geographic area.
Personal Liability
Almost no country has laws that
require anyone to help a stranger in
distress. An outdoor recreationalist
can decline, with legal impunity, to
provide medical assistance to
anyone. Any obligation that exists in
wilderness circumstances is ethical
or traditional, not legal.
In contrast, a legal obligation to
provide medical care or other
assistance does exist if the
individual has negligently caused
the injury.
If medical assistance is
provided, even though not required
by law, it must be given reasonably
and carefully. The diligence that
would be exercised by an
ordinarily prudent person under
similar circumstances must be
exercised. Anyone providing
medical care is legally liable for
harming the injured person if the
injury could have been avoided by
reasonable care. In addition, more
severe injuries or diseases are
recognized to require closer
attention and more extensive and
sophisticated treatment.
The need for wilderness users to
be familiar with first aid is well
recognized. An outdoor
recreationalist could be held liable
for injuries resulting from lack of
familiarity with techniques
generally known to others,
particularly if the person had
indicated in some manner
beforehand possession of such
knowledge. Physicians are held to a
higher standard and must conduct
themselves as ordinarily prudent
doctors of medicine.
The circumstances in which
assistance is rendered are also
significant. The care legally
required is that which is reasonable
under the circumstances. The law
takes into account the location of
the individual, hazards for the
person rendering aid, the equipment
available, and the physical
condition of the parties.
Finally, although a legal basis
for claims sometimes does exist,
lawsuits arising from voluntary
medical assistance are rare. Few
claims have followed voluntary
assistance for individuals involved
in wilderness accidents or
illnesses.
Establishing Death
The problem of establishing that
a person is dead is primarily
medical, not legal. A death
certificate signed by a physician is
the customary method. If a
physician is not available, a
statement by persons who have
actually seen the body and checked
it for life usually suffices. If the
body cannot be found or recovered
following accidents such as
drownings, avalanches, or debris
flows, the statements of those who
witnessed the accident are
ordinarily adequate. If no one saw
the accident, death may still be
established satisfactorily by
circumstantial evidence, such as
abandoned equipment, a deserted
automobile or campsite, or the last
statements of the deceased.
However, when such evidence
cannot be found, and only the
disappearance of the missing
person into a wilderness area can
be documented, particularly if the
wilderness area is one from which
the person could usually escape
without difficulty, death might be
impossible to establish. In such
instances, enough time must pass for
legal “presumption” of death,
usually seven years.
Disposal of the Body

The next of kin and local law
enforcement agencies both have a
legal interest in the body. The next
of kin has the right to determine the
disposal of the body (usually
cremation or burial), where this
shall be done, and what religious
ceremony or other customs are to be
followed. Law enforcement
agencies must determine the cause
of death to ensure that no crime has
been committed and no public
health hazard exists and must ensure
that disposal of the body does not
offend public sensibilities.
The next of kin and the law
enforcement officials may decide to
leave a body in a remote,
inaccessible location. Following a
wilderness death, the members of a
party are not legally obligated to
retrieve or even to find the body.
Estate Administration and Life

Insurance
Death occurring in the
wilderness, even if the body is not
recoverable, does not pose
insurmountable problems in the
administration of an estate or the
settlement of life insurance claims.
For administration of the estate,
death must be proven, but the
testimony of persons who actually
saw the body is usually sufficient to
establish the fact of death. If the
deceased had life insurance, proof
of death is a necessary condition for
the payment of benefits. In general,
proof of death that is adequate for
administration of the estate is
sufficient for life insurance.
A different problem is
associated with insurance that had a
double indemnity clause that pays
twice the face amount of insurance
if death is accidental. Often an
exact cause of death must be
ascertained. For example, after a
fall the question of whether death
resulted from a heart attack that
precipitated the fall might be
raised. If a heart attack caused the
fall, but injuries incurred in the fall
killed the person, death usually
would be considered accidental and
the double indemnity provision
would apply. If the individual died
before the fall as the result of a
heart attack, death would not have
been accidental and the double
indemnity provision would not
apply. Deciding which occurred
may be impossible. For automobile
accident deaths in which the injured
person has a heart attack and then
crashes a vehicle, double indemnity
is commonly paid because injuries
from the wreck cannot be proven
not to have caused the person’s
death. (Many individuals survive
heart attacks.)
The best method for answering
such questions is to carefully
examine the accident site and the
injured persons, thoroughly
question all witnesses to the
accident, and write down the
details as soon as possible. The
body still may have to be evacuated
for an autopsy to establish the cause
of death.
ETHICAL AND LEGAL

RESPONSIBILITY
With hundreds of thousands—even
millions—of persons of all ages
and abilities going to altitudes that
may present hazards for their health,
an inevitable question arises: Who
is responsible for their safety? The
obvious and overly simple answer
is the individual, which is correct
in the final analysis. Whoever
decides to go in harm’s way should
do so with foreknowledge and with
reasonable preparation and
understanding.
Risk is an important part of life.
Testing limits fuels growth.
Challenge has led people to use
fire, to traverse oceans and deserts,
to climb the highest mountains, and
to journey into space. The risk-free
life may not be worth living, but
those who take risks and expect to
survive must plan ahead and
prepare as well as possible.
What about the naïve individual
who seeks a simple adventure—
perhaps a visit to a mountain resort
and a chairlift ride up a mountain.
The person who pays has a right to
expect the chair not to fall. If it does
fall, the person blames the owner or
operator. But if that person
develops altitude illness and must
be hospitalized—perhaps even dies
—who is at fault? Failure to know
in advance that one might get sick
should no longer be an excuse after
all that has been written on the
subject. Failure to seek help is
more the fault of the individual than
anyone else, but absence of an
adequate help facility may be
blamed on the owner of the resort.
Hundreds of damage suits for such
errors have been filed. Some are
justified; many are not.
When a climber goes with a few
friends to an alpine peak and falls,
or is stranded by storm or illness,
where should that person turn for
help? In areas where thousands of
climbers are active, local
authorities have established systems
staffed by highly skilled
professionals who can provide
rapid rescue, often saving lives.
Who should pay the costs for such
systems and for expensive rescues?
Who is responsible when a rescuer
is injured or killed? If the outcome
is not what might reasonably be
expected, should the injured have
recourse? If the ski patrol responds
too slowly, or is inept, is someone
liable under law?
Such questions arise over and
over again, and precedents are set
every day, most blaming the agency
that has directly or indirectly been
paid for a service used by the
injured. Courts seem increasingly to
discount the fact that the individual
has voluntarily taken risk and to
blame the party with “deep
pockets.”
The highest and most difficult
mountains pose more serious and
complex issues, which are changing
rapidly. Fifty years ago, those who
went to remote mountains knew they
were completely on their own.
Radio contact was difficult or
impossible, rescues would take
many days or weeks, and the party
expected to rely on its own strength.
This has changed over the last
few decades. Many more people,
both experienced and
inexperienced, are undertaking
major climbs and explorations.
Radio communications or instant
worldwide telephone contacts make
possible consultations and rescues
that previously were out of the
question. Helicopters may pluck
individuals from high places that
are difficult or impossible for
rescue teams on foot to reach. Who
is responsible for such services? If
they are unavailable, is someone to
blame?
More and more novice climbers
are paying large sums to be taken up
great mountains. Explicit or implied
is the responsibility of the
contractor to safeguard the
customer. Failure to have made
adequate plans for likely
contingencies is an appropriate
reason for litigation, but how
extensive and detailed should the
contingency plans be? Should a
physician with specific
responsibility for the health of the
clients be included in the party?
How elaborate should the medical
equipment be? Should it include
aids such as a hyperbaric bag or
medical oxygen? Should equipment
to communicate with others and
within the party be required?
Should the availability of helicopter
rescue be part of the preparations?
Who is to pay for these and other
more extreme situations?
Most recently the capacity of any
professional, however experienced,
to guide a party or individual above
22,000 feet (6700 m), the so-called
“Death Zone,” has been challenged.
Who is responsible if not the
contractor? What safeguards should
be taken in advance? Should a
medical certificate be required? If
so, from whom and at what level of
expertise? What about a waiver of
liability (that may not be recognized
by a court)? Should clients
purchase their own insurance or be
required to satisfy criteria for
ability and experience? Should
persons contracting to guide others
be certified? If so, by whom and by
what standards?
Throughout the history of
mountaineering, climbers have
come to the aid of others, usually
strangers, in emergency situations.
That has been inherent in the
brotherhood of climbing. Is there a
real obligation or only traditional
ethic? What risks should an
individual or party be expected to
take in an effort to rescue another?
What if the rescuer further injures
the person? Or suppose a party
ignores cries for help from a
stranger in a crisis of his own
making?
Property owners have been
denying access to tempting cliffs
and mountains for fear of lawsuits.
Recently some protective
arrangements have been made for
individual owners of attractive
sites, and such restrictions are
improving, but they are yet to be
tested in court.
These are thorny issues, and they
are being made even more complex
by the great number of persons
going into danger, as well as the
flood of lawsuits, both justified and
frivolous. Unfortunately, little help
in solving them can be expected
from a judicial industry that absorbs
as much as half the money that
changes hands as a result of such
proceedings.
APPENDIXE E
GLOSSARY
Abrasion: A wound of the skin—
and sometimes the underlying
tissue—caused by scraping or
rubbing.
Abscess: A localized collection of
pus caused by infection and
inflammation that destroy
tissue. (Pimples and boils are
small abscesses in the skin.)
Acute: 1. Appearing after or
persisting for a relatively brief
period of time. (Does not
indicate a specific time
interval, but a short period of
time in relation to the
condition for which it is used.
An acute onset would be
minutes for some disorders,
weeks for others.) 2.
Requiring immediate or urgent
attention.
Aerosinusitis: A painful condition
of the paranasal sinuses
produced by a rapid increase
in external pressure (due to
water submersion or a rapid
descent from altitude) while
the openings into the sinuses
are closed and the pressure
within the sinuses remains
lower than external pressure.
Aerotitis: A painful condition of
the middle ear, similar to
aerosinusitis but produced by
pressure changes while the
eustachian tube is closed.
Airway: Passages through which
air enters and leaves the lungs.
Alveoli: The smallest functional
units of the lungs.
Analgesia: Relief of pain.
Analgesic: A medication that
relieves pain.
Anemia: A reduced number of red
blood cells in the circulating
blood.
Aneurysm: A localized dilatation
of an artery that can rupture
and hemorrhage. Caused by
weakening of the arterial wall.
Angina pectoris: Crushing or
squeezing chest pain caused by
a reduction in coronary artery
blood flow due to
arteriosclerosis.
Anoxia: Total absence of oxygen.
Arrhythmia: An abnormal rhythm,
usually referring to the
heartbeat.
Arteriosclerosis: A disease of
arteries characterized by
deposits of material that
narrows the lumens (most
significantly) and also stiffens
or “hardens” the arterial
walls.
Aspirate: To inspire (air is
aspirated into the lungs); to
draw in by suction (fluid is
aspirated into a syringe).
Asthma: A disorder, typically
allergic in origin,
characterized by respiratory
difficulty and caused by spasm
of the muscle in small
bronchioles that narrows their
lumens.
Ataxia: Loss of the ability to
coordinate muscular
movement.
Automated external defibrillator
(AED): A portable electronic
device that automatically
diagnoses the life-threatening
cardiac arrhythmias of
ventricular fibrillation and
ventricular tachycardia and is
able to treat them with
defibrillation, an electrical
shock that stops the arrhythmia
and allows the heart to
reestablish an effective
rhythm.
Avulsion: An injury in which tissue
is torn away or forcibly
separated.
Bacteriostatic: Stopping the
multiplication and growth of
bacteria.
Bleb: A large blister.
Boil: An abscess located in the skin
and subcutaneous tissue.
Bronchi: Air passages between the
trachea and the smaller
bronchioles.
Bronchioles: Air passages between
the bronchi and the alveoli, the
smallest sac-like units of the
lung.
Bronchitis: Inflammation of the
bronchi and bronchioles, must
often resulting from infection,
but also caused by cold
injuries or burns of the
bronchial mucosa.
Cardiac: Pertaining to the heart.
Cardiac output: Volume of blood
pumped by the heart over a
specific period of time,
usually one minute.
Cardiogenic shock: Shock
resulting from the inability of
the heart to pump blood; in the
wilderness the most common
cause is probably tension
pneumothorax.
Cardiopulmonary resuscitation
(CPR): An emergency
procedure consisting of
external cardiac massage and
mouth-to-mouth artificial
respiration used to revive
someone whose heart has
ceased functioning or who has
stopped breathing.
Carrier: A person who is immune
to an infection but transmits it
to others by carrying the
organisms within his or her
body.
Catheter: A tube introduced into
an internal organ or structure;
a urethral or urinary catheter
passed into the urinary
bladder.
Central nervous system: The
brain and spinal cord.
Cerebral: Pertaining to the brain.
Cervical: Pertaining to the neck.
Cholera: An infection
characterized by watery
diarrhea so profuse that death
from dehydration can result in
less than a day.
Chronic: Appearing after or
persisting for a relatively long
time; opposite of acute.
Coma: A state of total
unconsciousness.
Comatose: Totally unconscious.
Conjunctiva: Thin membrane that
covers the white, visible
surface of the eye and the inner
surface of the eyelid.
Contusion: A bruise.
Convulsion: An intense,
paroxysmal muscular
contraction, commonly
involving the entire body.
Crepitant: Producing crackling
sounds or having a crackling
sensation.
Cricothyroid: Area between the
thyroid cartilage (Adam’s
apple) and the large
cartilaginous ring (cricoid
cartilage) just below.
Cricothyrotomy: A surgical
opening in the cricothyroid
membrane that allows air to
enter the trachea; created when
the airway above that site is
obstructed.
Cyanosis: A purple or bluish
discoloration of the lips, nails,
and skin that typically results
from reduced oxygen in the
blood.
Cystitis: An inflammatory disorder
of the urinary bladder.
Debridement: Removal of foreign
material and dead tissue from
a wound.
Dehydration: Loss of excessive
quantities of (body) water.
Delirium: A state of temporary
mental confusion and clouded
consciousness characterized
by anxiety, tremors,
hallucinations, delusions, and
incoherence.
Diabetes mellitus or diabetes: A
disorder of glucose
metabolism that results in
increased urinary output,
glucose (sugar) in the urine, a
tendency to develop severe
infections, and other disorders,
including accelerated
arteriosclerosis and renal
failure.
Diagnose: To distinguish one
disease or injury from another;
to identify an illness or injury.
Diagnosis: Identification of an
illness or injury.
Dissociation: Separation of related
psychologic activities into
autonomously functioning
units, as in the generation of
multiple personalities
(abnormal), or shutting out the
emotional aspects of an injury
scene while concentrating on
the measures necessary to
carry out a rescue (normal).
Dysentery: A bacterial infection of
the gastrointestinal tract that
results in diarrhea, mucus and
pus in the stools, and fever.
Dysmenorrhea: Painful cramps
associated with menstruation.
Dyspnea: Abnormal shortness of
breath; awareness of the need
to breathe.
Edema: An abnormal collection of
fluid within body tissue;
pulmonary edema is fluid
within the lungs.
Electrocardiogram: A recording of
the electrical activity of the
heart.
Electrolyte: One of the four major
ions, sodium, potassium,
chloride, or bicarbonate
(HCO3) in serum.
Embolism: Sudden obstruction of a
blood vessel by an embolus,
often resulting in death of the
tissue supplied by that vessel.
Embolus: A clot or similar tissue
carried by the bloodstream
from a peripheral site, such as
a leg vein, through larger,
more proximal vessels and the
heart, until it is forced into a
smaller artery, usually in the
lung.
Encephalitis: An infection of the
brain, most commonly caused
by a virus, and often spread by
mosquitoes.
Endemic: Peculiar to or prevailing
in or among a (specified)
country or people.
Epididymitis: An infection of the
epididymis, the structure in
which sperm collect before
being transported to the
seminal vesicles.
Epilepsy: A neurologic disorder
characterized by repeated
convulsions.
Epizootic: An infectious epidemic
in animals.
Eschar: A dry, leathery crust or
scab formed at the site of skin
injuries such as thermal burns,
corrosive burns, or frostbite.
Etiology: The cause or origin of a
medical disorder.
Extrasystole: An abnormal cardiac
rhythm in which a normally
beating heart suddenly
contracts after a shorter
interval than usual; sometimes
called “skipped beats.”
Extravasate: To force a material
such as blood out of its normal
channel (a blood vessel) into
surrounding tissue.
Exudate: Any substance, most
commonly inflammatory cells
and protein, that passes
through blood vessel walls in
living tissue and can be
removed or extracted; most
frequently associated with
inflammation.
Fascia: A sheet or membrane of
fibrous connective tissue that
envelops muscles or various
other structures.
Fever: A higher-than-normal body
temperature, most commonly
the result of infection but also
caused by other disorders.
Fibrillation: An abnormal cardiac
rhythm in which cardiac
muscle fibers contract
independently of each other
instead of in synchrony. When
only the atrium is involved, the
cardiac rhythm is completely
irregular. If the ventricle is
involved, the condition is
lethal if not corrected within
minutes because cardiac output
falls to very low levels.
Flaccid: Completely lacking in
muscle tone; totally relaxed.
Flatus: Gas or air expelled from
the intestines.
Gamow Bag: An airtight bag, large
enough to hold a person, that
can be inflated with a pump to
decrease the effective altitude
by approximately 2000 feet
(600 m) to treat illnesses.
Gangrene: Death of a part of the
body, such as an arm or leg,
usually the result of an
inadequate blood supply but
sometimes due to infection.
Gasp reflex: Involuntary tendency
to gasp or inspire when
suddenly immersed in cold
water.
Generalized: Spread throughout
the body; opposite of
localized.
Globe: The entire eye.
Gonorrhea: A sexually transmitted
infection that typically
produces painful urethral
inflammation and a discharge
in men but often produces no
symptoms in women.
Hallucination: A sound, sight, or
other sensation perceived as
real in the absence of an
actually existing object or
source.
HACE: High-altitude cerebral
edema.
HAPE: High-altitude pulmonary
edema.
Heart failure: Inability of the heart
to pump out all the blood
returned, which causes fluid to
pool (edema) in the peripheral
tissues or lungs, depending
upon which ventricle is
damaged.
Heart valves: Valves that maintain
the forward flow of blood
within the heart.
Heimlich maneuver: A maneuver
for dislodging obstructing
material, usually aspirated
food, from the larynx or
trachea.
Hematoma: A mass formed by
clotted blood within tissue.
Hematuria: Blood (intact red
blood cells) in the urine.
Hemoglobinuria: Hemoglobin in
the urine, a reflection of
disorders distinctly different
from those that cause
hematuria.
Hemorrhoids: Enlarged veins
beneath the skin of the anus.
Hemothorax: Blood in the chest.
High-altitude cerebral edema: A
high-altitude illness caused by
swelling (edema) of the brain.
High-altitude pulmonary edema:
A high-altitude illness
characterized by the
accumulation of fluid (edema)
in the lungs.
Hydrated: Containing water.
(Normally hydrated means
containing a normal amount of
water.)
Hyperoxia: A higher-than-normal
blood oxygen.
Hypertension: High blood
pressure.
Hyperthermia: A higher-than-
normal body temperature.
Hypoglycemia: A lower-than-
normal concentration of
glucose in the blood.
Hypothermia: A lower-than-
normal body temperature.
Hypoxemia: A lower-than-normal
quantity of oxygen in arterial
blood.
Hypoxemic: Having a lower-than-
normal quantity of oxygen in
arterial blood.
Hypoxia: Presence of a lower-
than-normal or lower-than-
sea-level quantity of oxygen or
lower-than-normal availability
of oxygen; can refer to the
entire body, body tissues, or
the atmosphere.
Hypoxic: Having a lower-than-
normal or lower-than-sea-
level quantity of oxygen.
Ileus: Intestinal paralysis procucing
obstruction; most often caused
by peritonitis.
Immunization: Production of an
immune condition by
administration of an agent that
stimulates a protective
response.
Incubation period: Period of time
between infection by
microorganisms and the onset
of detectable signs or
symptoms of the disease.
Infarct: Death of tissue caused by
arterial obstruction, or dead
tissue resulting from arterial
obstruction.
Intramuscular: Within muscle; the
site for injection of a
medication.
Intravenous: Within a vein; the site
for injection of a medication
or fluids.
Intubate: To place a tube into a
passage such as the trachea,
usually to keep the passage
open.
Jaundice: Accumulation of bile
pigments in the blood, usually
resulting from liver disease,
that produces yellow
discoloration of the skin and
eyes.
Ketoacidosis: An abnormal acidic
condition of the blood that may
be produced by a metabolic
disorder such as diabetes
mellitus or by severe
accidental hypothermia.
Ketone body: A product of fat
metabolism.
Ketosis: Accumulation of ketone
bodies in the blood, most
commonly as the result of
anaerobic exercise,
uncontrolled diabetes, or
starvation (dieting).
Laceration: A traumatic injury
characterized by cutting or
tearing.
Larynx: Upper part of the trachea;
the voice box.
Lumen: Open passage within a
tubular organ such as the
intestines or a blood vessel.
Lymph nodes: Collections of tissue
that trap bacteria and debris
and help retard the spread of
infection or other disease
processes.
Macerate: To reduce to a soft mass
by soaking; to digest.
Malaise: A generalized feeling of
discomfort or indisposition;
feeling ill.
Malaria: A parasitic infectious
disorder characterized by
cyclic chills, fever and
sweating, that is transmitted
through the bite of female
anopheles mosquitoes.
Meningitis: Inflammation of the
thin membranes that surround
the brain and spinal cord,
usually as the result of
infection.
Metabolism: Processes in living
organisms that use energy to
construct compounds from
assimilated materials or that
break down such materials to
release energy.
Necrosis: Death of tissue as the
result of disease.
Nervous system: The cells,
tissues, and organs that
regulate the body’s responses
to internal and external stimuli.
In vertebrates it includes the
brain, spinal cord, nerves,
ganglia, and sense organs.
Neurogenic shock: Shock resulting
from transaction of the spinal
cord.
Neurologic: Of or pertaining to the
nervous system.
Nontraumatic: Not caused or
associated with physical
injury.
Nutrient: Any component of food
that aids growth, development,
or replacement of tissues.
Osmosis: Diffusion of water
through a semipermeable
membrane.
Osmotic pressure: Hydrostatic
pressure created by diffusion
through a semipermeable
membrane.
Palpate: To feel or examine by
touch.
Palpation: Examination by touch.
Palpitation: A rapid or irregular
heartbeat of which a person is
aware.
Paralytic: Causing paralysis.
Paresthesias: Abnormal
sensations, commonly tingling
or buzzing; sensations felt
when a limb “goes to sleep.”
Paroxysmal tachycardia: An
abnormal cardiac rhythm
characterized by a heartbeat
that is quite fast but entirely
regular.
Pathogenic: Producing disease.
Penicillinase: An enzyme produced
by some bacteria that
inactivates penicillin and
produces resistance to that
drug.
Peptic ulcer: A crater in the
mucosa of the stomach or
duodenum produced by the
combined digestive action of
gastric acid and digestive
enzymes.
Peritonitis: Inflammation of the thin
membrane lining the
abdominal cavity that results
from infection or irritation by
intestinal contents or blood.
Pharyngitis: Inflammation of the
pharynx, the space behind the
mouth and nose; a “sore
throat.”
Pleurisy: Inflammation of the
pleura, the thin membrane that
covers the lung and the chest
wall.
Pneumonia: Infection of the lung.
Pneumothorax: Air in the pleural
space.
Polycythemia: An increased
number of red blood cells in
the blood.
Prognosis: A prediction or
conclusion regarding the
course and termination of a
disease or injury.
Prone: Lying flat in a face-down
position.
Prophylaxis: Preventive treatment
for disease.
Proteinuria: Protein in the urine.
Pulmonary: Of or pertaining to the
lungs.
Puncture wound: A wound, usually
produced by an object such as
a nail or thorn, that is deep but
has a narrow, constricted
opening.
Purulent: Consisting of or
containing pus.
Pustule: A pimple or small boil.
Pyelonephritis: An infection of the
kidney.
Radial pulse: Pulse felt at the wrist
on the thumb side routinely
used to determine heart rate.
Radiation of pain: Diverging or
spreading of pain from a
central point.
Rebound tenderness: Pain
produced by releasing
pressure with the fingers on
the abdomen and allowing the
abdominal wall to rebound;
almost always an indication of
an intraabdominal condition
that requires surgical
treatment.
Referred pain: Sensation of pain
experienced in an area other
than the anatomical site of the
injury or disease where it is
produced.
Renal: Pertaining to the kidneys.
Resorb: To reabsorb.
Respiratory: Pertaining to the
lungs or their function.
Resuscitate: To revive; to restore
to life or consciousness.
Retrograde amnesia: Loss of
memory of events occurring
before an accident or incident.
Rheumatic fever: An inflammatory
disorder associated with
streptococcal infections in
which the valves of the heart
are damaged, often
irreversibly.
Rigor mortis: Stiffening of muscles
after death.
Roughage: Food that is high in
fiber and adds bulk to the
gastrointestinal contents.
Salpingitis: An inflammatory
disorder, usually infectious,
that involves the fallopian
tubes and may mimic
appendicitis and other
intraabdominal disorders that
require surgical therapy.
SAM splint®: A padded metal
splint that can be molded to fit
different areas of the body.
Shock: A condition characterized
by low blood pressure, fast but
weak pulse, pallor, cold
sweats, and mental impairment
that commonly results from
trauma or other disorders that
produce severe bleeding.
Signs: Physical evidence of disease
discovered by examination.
Sinus: A mucosal-lined space in the
bones of the skull.
Sinusitis: An infection of one of the
sinuses in the skull.
Soft tissue: Non-osseous tissues of
the body. (The ligaments and
internal organs usually are not
included when referring to
soft-tissue injuries.)
Somnolence: Oppressive
drowsiness or sleepiness.
Spasm: An involuntary muscular
contraction, usually painful.
Sphygmomanometer: A device for
measuring blood pressure.
Spinal canal: Canal within the
vertebral column through
which the spinal cord passes.
Sprain: An injury characterized by
incomplete rupture of the
supporting ligaments around a
joint.
Stethoscope: A device that aids
listening to body sounds,
particularly those of the heart
and lungs.
Strain: An injury characterized by
stretching, with or without
mild tearing, of a muscle or
tendon.
Stress: An emotionally or
physically disruptive or
disquieting event or condition.
Stridor: Noisy breathing in general;
specifically a high-pitched
crowing sound associated with
croup, respiratory infection,
and airway obstruction.
Stroke: Death of brain tissue
caused by hemorrhage or
arterial obstruction.
Subacute: Appearing after or
persisting for a period of time
that is intermediate between
acute and chronic in duration.
(See Acute.)
Subcutaneous: Beneath the skin.
Subdural: Beneath the dura, the
fibrotic membrane covering
the brain; most commonly used
in reference to a hematoma.
Supine: Lying flat in a face-up
position.
Suture: 1. To unite parts by
stitching; to sew together the
edges of lacerated tissue. 2.
The joints between the bones
of the skull.
Symptom: Any abnormal function,
sensation, or experience that
indicates the presence of
disease.
Syncope: A brief episode of
unconsciousness, usually not
associated with a significant
illness; fainting.
Syndrome: A group of signs and
symptoms that occur together
and comprise a disease entity.
Synergist: An agent that enhances
the effectiveness of an active
agent.
Synergistic: Producing an effect
greater than the sum of
independent effects.
Syphilis: A sexually transmitted
infection that may produce no
early symptoms but if
untreated can be devastating
years later.
Tachycardia: An abnormally fast
heart rate.
Tension pneumothorax: A
pneumothorax with which the
intrapleural pressure is
increased so greatly that the
organs in the chest are
displaced and respiration is
compromised.
Thoracostomy: A surgical
procedure that creates an
opening into the chest.
Thrombophlebitis: Thrombosis
within veins that produces
inflammation and pain.
Thrombosis: Clotting of blood,
typically within a blood
vessel, that does not follow an
identifiable traumatic injury.
Torsion: Twisting an organ or
tissue in such a manner that the
flow of blood to the tissue is
obstructed.
Toxic: Having a poisonous or
noxious effect.
Toxin: A noxious or poisonous
substance.
Trachea: Large air passage
between the mouth or nose and
the bronchi and lungs.
Tracheostomy: An opening in the
trachea through which air can
flow; produced to bypass an
obstruction above that site.
Trauma: 1. A physical force that
injures the body; an injury
produced by physical force. 2.
Any external force that
produces injury, including
emotional trauma.
Traumatic: Of or pertaining to
trauma.
Tuberculosis: A chronic infection,
most often pulmonary,
characterized by extensive
tissue destruction and death if
untreated.
Varicose veins: Dilated, tortuous
veins, most commonly in the
legs.
Vascular: Of or pertaining to blood
vessels.
Vasovagal attack: A transient
vascular and neural reaction in
humans characterized by a fall
in blood pressure that can
result in loss of consciousness.
Vertigo: A feeling that one’s self or
one’s environment is whirling
around; not synonymous with
dizziness.
INDEX
The index that appeared in the print
version of this title was
intentionally removed from the
eBook. Please use the search
function on your eReading device to
search for terms of interest. For
your reference, the terms that
appear in the print index are listed
below.
A
abdomen
injuries to
palpation of
abdominal pain
algorithm for
appendicitis
diagnosis of
diverticulitis
ectopic pregnancy
features of
gastroenteritis
hernia
intestinal obstruction
mittelschmerz
renal stones
salpingitis
abdominal wall contusion
abrasions
corneal
soft-tissue
abscess
dental
rectal
treatment of
accidents
abnormal responses to
stress caused by
victims of
acclimatization
acellular pertussis
acetaminophen
acetazolamide
acquired immunodeficiency syndrome
activated charcoal, granular
active traction
acute angle-closure glaucoma
acute cholecystitis
acute hepatic necrosis
acute mountain sickness
acute renal failure
adhesions
adverse stress reactions
airplane rescue
airway
burns to
cricothyrotomy to create
in facial-injured person
in head-injured person
obstruction of
opening of
oropharyngeal
albuterol
alcohol
allergies
alligators
altitude
dehydration at
disorders caused by
fluid requirements at
heart affected by
mountain
nutrition considerations
respiratory disorders affected by
responses to
sleep-promoting medications and
altitude bronchitis
altitude deterioration
altitude illness
acute mountain sickness
high-altitude peripheral edema
high-altitude retinal hemorrhage
altitude stress
alum
ambulation
amebiasis
amnesia
anal fissure
analgesia
anaphylactic shock
anaplasmosis
anemia
angina pectoris
angioedema
animal attacks
ankle
dislocation of
fracture of
sprain of
anoxia
antacids
antibiotics
anticoagulants
antifungal agents
antihistamines
antimalarial agents
antimicrobial agents
antipsychotic agents
antiseptics
antivenom
apnea
appendicitis
arterial pressure
arteries
arthropods
asphyxiation
aspiration of food
aspirin
asthma
ataxia
atrial fibrillation
automated external defibrillator
avalanches
avulsions
azithromycin
B
babesiosis
back injuries
bacteremia
bacteria
bacterial infections
bandages
bandaging
barotrauma
basilar skull fracture
bats
battle sign
bears
Bell’s palsy
benzodiazepines
bereavement
bilirubin
bismuth subsalicylate
bison
bites
animal
snakebites
spider
bivouac sack
black bears
black widow spider bites
bleeding
blisters
blood
circulation of
volume of
blood pressure
body temperature
cooling of
in heat stroke
normal
boiling of water
bone contusions
bowel care
bowel sounds
brain
injuries to
tumors of
breathing
altitude-related changes
assessment of
See also respiration
bronchitis
brown bears
brown recluse spider bites
burns
bursitis
C
calcaneal fracture
calluses
canker sores
cape buffalo
carbon monoxide
cardiac dyspnea
cardiac output
cardiac syncope
cardiogenic shock
in avalanches
in drowning
in hypothermia
indications for
learning about
starting and stopping
cardiovascular disorders
cardiovascular system
carrying an ill or injured person
cellulitis
cephalosporins
cerebral concussion
cerebrovascular disease
Chagas’ disease
chemical burns
chemical disinfection
chest compressions
chest injuries
flail chest
penetrating
pneumothorax
rib fractures
chest pain
Cheyne-Stokes respirations
children
chills
chlorine dioxide
chlorine disinfection
chloroquine
cholecystitis, acute
cholera
chronic lung disease
chronic mountain sickness
chronic obstructive pulmonary disease
ciprofloxacin
circulation
circumrescue collapse
cirrhosis
claudication
clindamycin
clothing
coccidioidomycosis
codeine
cold water
drowning in
hypothermia caused by
collarbone fracture
Colorado tick fever
coma
comfort
common cold
compartment syndromes
compound fracture
compression fracture
concussion
conduction
congenital heart disease
conjunctivitis
consciousness, level of
constipation
contact dermatitis
contact lenses
contraceptives
contusions
convalescence
convection
conversions
cooling
coral snakes
cornea
abrasion of
anatomy of
ulcer of
corns
coronary artery disease
cougars
coughing
counselors
coyotes
cracked tooth syndrome
cricothyrotomy
crocodiles
crotalid envenomation
Cryptosporidia
cryptosporidiosis
cyclizine
cyclosporiasis
cystitis
D
death
debriefing
decision making
decompensation
decongestants
deep venous thrombosis
deer
defibrillators
dehydration
after burns
at altitude
in hypothermia
venous thrombosis risks
delayed stress syndrome
delirium
dengue fever
dental injuries
dependent lividity
derangement
detachment, retinal
dexamethasone
diabetes mellitus
diabetic retinopathy
diagnosis
diarrhea
causes of
fluid replacement for
invasive
mild
noninvasive
severe types of
“traveler’s”
diet
diffuse axonal injuries
dimenhydrinate
diphenoxylate with atropine
dislocation(s)
ankle
definition of
elbow
fingers
hip
jaw
knee
patellar
reduction of
shoulder
signs of
dissociation
diverticulitis
dogs
dressings
drowning
dry eye
duodenal ulcers
dysentery
dysmenorrhea
dyspnea
E
ear(s)
infection of
injuries to
ectopic pregnancy
edema
ehrlichiosis
elbow
dislocation of
fracture of
electrolytes
elephants
elk
embolism
emergencies
empathy
emphysema
encephalitis
endotracheal tube
enterohemorrhagic E. coli
envenomations
epididymitis
epidural hematoma
epilepsy
epinephrine
erythropoietin
eschar
Escherichia coli
estate
ethics
eustachian tube
evacuation
of burn individuals
description of
for hemorrhagic shock
from low altitude
for vertebral fracture
evaporation
exertional heat illness
expeditions
extrasystoles
eye/eye disorders
anatomy of
blindness
conjunctivitis
dry
foreign bodies
glaucoma
iritis
ocular surface
red eyes
refractive correction
retina
scleritis
subconjunctival hemorrhage
traumatic injuries
eyeglasses
F
face
burns of
injuries to
fainting
fecal impaction
female genital disorders
femoral pulse
fetus
fever
fibular fracture
figure-eight bandage
filtration
fingers
dislocation of
fracture of
fire ant stings
first-degree burns
flail chest
flat terrain
flocculation
fluid(s)
balance of
insensible losses
intravenous administration of
lung accumulation of
monitoring of
volume calculations
fluid replacement
in burn individuals
description of
diarrhea treated with
food
allergies to
aspiration of
contamination of
sanitation concerns
foot
fracture of
hypothermia protection
wounds of
foot drop
forced expiratory volume in one second
forearm fractures
foreign bodies, ocular
fractures
ankle
bleeding caused by
calcaneal
collarbone
diagnosis of
elbow
facial
fibula
finger
foot
forearm
hand
hip
immobilization of
knee
leg
lower extremity
manipulation of
nasal
pain caused by
patellar
pelvic
rib
severity of
shoulder
skull
snowboarding
splinting of
teeth
thigh
transportation considerations
treatment of
trunk
upper extremity
vertebral
wrist
frostbite
fruits
full-thickness burns
G
gas pressures
gastric ulcers
gastroenteritis
gastroesophageal reflux disease
gastrointestinal disorders
amebiasis
anal fissure
cholera
constipation
cyclosporiasis
diarrhea. See diarrhea
dysentery
enterohemorrhagic E. coli
fecal impaction
hemorrhoids
hepatitis
irritable bowel syndrome
motion sickness
nausea and vomiting
peptic ulcers
rectal abscess
typhoid fever
gastrointestinal hemorrhage
genitourinary disorders
Giardia
giardiasis
Glasgow Coma Scale
glaucoma
globe injuries
gonorrhea
granular activated charcoal
grief
H
haloperidol
hand
fracture of
hypothermia protection
wounds of
hantavirus pulmonary syndrome
hay fever
headache
head immobilization
head injuries
brain
ears
face
teeth
heart
altitude effects on
anatomy of
physical activity effects
heartburn
heart disease
heart failure
heart rate
heart rhythm
description of
disturbances of
management of
heat
heat cramps
heat exchange
heat exhaustion
heat illness
heat loss
mechanisms of
normal
physiologic limitation of
heat stroke
heat syncope
Heimlich maneuver
helicopter rescue
hematologic disorders
hematuria
hemoglobin
hemoglobinuria
hemopneumothorax
hemorrhage
control of
gastrointestinal
subconjunctival
hemorrhagic fever syndromes
hemorrhagic shock
hemorrhoids
hemothorax
hepatitis
hernia
herpes
high-altitude peripheral edema
high-altitude retinal hemorrhage
high-angle terrain
hip
dislocation of
fracture of
hippopotamuses
histamine H2
blockers
hives
human diploid cell vaccine
human immunodeficiency virus
hydrocodone/acetaminophen
hydromorphone
hyenas
Hymenoptera stings
hypertension
hyperthermia
hyperventilation
hypochlorous acid
hypoglycemia
hypothermia
in avalanche victims
cardiopulmonary resuscitation for
cold water immersion
description of
drowning vs.
prevention of
stages of
treatment of
hypoventilation
hypoxemia
hypoxia
I
ibuprofen
immersion syndrome
immobilization
of fractures
of head and neck
pressure, for snakebites
respiration during
immunizations
cholera
hepatitis A
hepatitis B
influenza
information sources
Japanese encephalitis
live-virus
Lyme disease
measles
meningococcus
poliomyelitis
rabies
rubella
scheduling of
smallpox
tetanus
typhoid
yellow fever
immunoglobulins
impacted fracture
inactivated polio vaccine
infections
antibiotics for
bacterial
control of
ear
invasive bacterial
respiratory
sexually transmitted
viral
wound
infectious mononucleosis
influenza
ingrown toenails
insecticides
insect repellents
insect stings
insensible fluid loss
intermediate terrain
International Association for Medical
Assistance to Travelers
intestinal obstruction
intramuscular injections
intrauterine growth retardation
intravenous fluid therapy
intravenous injections
invasive bacterial infections
invasive diarrhea
iodine
iritis
irritable bowel syndrome
J
jaguars
Japanese encephalitis
jaundice
jaw dislocation
jaw thrust technique
joint effusion
K
kangaroos
kidneys
acute failure of
compensation by
ruptured
knee
dislocation of
fracture of
ligament tears
L
lacerations
laser-assisted in-situ keratomileusis
latrines
laxatives
leadership
legal considerations
leg fractures
leopards
leptospirosis
level of consciousness
levofloxacin
lid lacerations
lidocaine
lightning
lions
liquid bleach
litters
liver
diseases of
rupture of
live-virus vaccines
“long-line” operation
loosened teeth
loperamide
lower extremities
fractures of
immobilization of
lung(s)
auscultation of
chronic disease of
fluid accumulation in
lacerations of
respiratory functions of
warming of air in
lung disease
Lyme disease
lymph nodes
M
malaria
malarone
male genital disorders
mask
measles
meclizine
medical history
medical record
medical supplies
medications
administration of
types of
mefloquine
melanoma
meningitis
meningococcal meningitis
meningococcus
methicillin-resistant Staphylo-
coccus aureus
metronidazole
microfiltration
mittelschmerz
moose
morphine
mosquitoes
motion sickness
mountain altitudes
Mount Everest
mouth disorders
mouth-to-mouth rescue breathing
muscle tears
myocardial infarction
myoglobinuria
N
nasogastric intubation
nausea
near-drowning
neck injuries
nerve dysfunction
neural disorders
neurogenic shock
neurologic disorders
nifedipine
nightmares
nitazoxanide
nitroglycerin
noninvasive diarrhea
nosebleeds
nose disorders
nursing care
nutrition
O
obstructive sleep apnea
onchocerciasis
ondansetron
open fracture
open wounds
opiates
optic neuropathy
oral contraceptives
oral medications
oropharyngeal airway
osteomyelitis
oxycontin/acetaminophen
oxygen
delivery of
at high altitude
supplemental
P
pain
chest
control of
fracture-related
medications for
sciatica
pancreatitis, acute
panda bears
parasites
paregoric
paroxysmal supraventricular
tachycardia
partial-thickness burns
particulate material
passive traction
past illnesses
patella
dislocation of
fracture of
pelvic fracture
penetrating injuries
abdominal
brain
chest
penicillin
peptic ulcers
periapical osteitis
periodic breathing
peripheral circulation
peritonitis
personal flotation device
personal liability
pH
pharyngitis
photophobia
photorefractive keratectomy
physical examination
picaridin
plague
pleurisy
pleuritic chest pain
pneumoconiosis
pneumonia
pneumothorax
poisoning
poison ivy/oak/sumac
polar bears
poliomyelitis
position of function
posttraumatic stress disorder
potassium
povidone-iodine
pregnancy
premature ventricular contractions
primary pulmonary hypertension
primates
prochlorperazine
promethazine
proton pump inhibitors
pseudoephedrine
pseudomembranous colitis
psychological aid
psychological responses
of accident victims
of rescuers
pulmonary artery pressure
pulmonary edema, high-altitude
pulmonary embolism
pulmonary vascular disorders
pulpitis, acute
pulse
pulse rate
puncture wounds
pupils
pus
pyelonephritis
Q
quinolones
R
rabies
raccoons
radial keratotomy
radial pulse
radiation
rectal abscess
reduction
of hip dislocation
of shoulder dislocation
relapsing fever
renal failure, acute
renal stones
rescue
by airplane
carrying an ill or injured person
by helicopter
litters
search and
water
rescue breathing
rescuers
psychological responses of
qualifications of
rescue trauma threshold
respiration
body position effects on
depression of
during immobilization
mechanics of
periodic
See also breathing
respiratory disorders
altitude effects
chronic lung disease
infectious
overview of
physical examination of
symptoms of
respiratory system
rest
retinal disorders
rewarming
rhinoceroses
rib fractures
rifaximin
rigor mortis
ring removal
rubella
rucksack stretcher
S
safety
Salmonella
salpingitis
sanitation
saturated aqueous iodine solution
scalp wounds
schistosomiasis
sciatica
scleritis
scorpion stings
scratch teams
search and rescue
second-degree burns
sedation
seizures
self-esteem
sensory disturbances
septic shock
sexually transmitted infections
shin splints
shivering
shock
anaphylactic
burn
cardiogenic
causes of
cold
definition of
hemorrhagic
neurogenic
septic
treatment for
shoulder
dislocation of
fracture of
silver sulfadiazine
simple fracture
single rucksack technique
sinusitis
sinus tachycardia
skin cancer
skin cracks
skin flaps
skull fractures
sleep apnea
sleep disordered breathing
sleep hypoxia
sleep periodic breathing
sling
smallpox
smoking
snakebites
snow blindness
snowboarding injuries
sodium hypochlorite
soft-tissue injuries
abrasions. See abrasions avulsions
bandaging
bleeding control
blisters
contusions. See contusions
infection control
lacerations
skin flaps
wounds. See wounds
solar radiation
sore throat
spasms, back
spider bites
“spiders,”
spleen
infarction of
rupture of
splints/splinting
split coil technique
splitting
spontaneous pneumothorax
sprain
staphylococcal enteritis
sterilization of instruments
stings
strains
streptococcal pharyngitis
Streptococcus pneumoniae
stress
accident-related
adverse reactions to
altitude
normal reactions to
rescue
stress overload
stroke
subarachnoid hemorrhage
subconjunctival hemorrhage
subdural hematoma
submersion incident
subperiosteal hematomas
sudden cardiac death
sumatriptan
sunburn
sunlight
sunscreen
syncope
syphilis
T
teeth injuries
tendinitis
tendon tears
tenosynovitis
tension pneumothorax
testicular torsion
tetanus
tetracyclines
tetraglycine hydroperiodide
thigh fractures
third-degree burns
thrombophlebitis
thrombosis, venous
thunderstorms
thymus disease
tick fever
tidal volume
tigers
tincture of iodine
tinidazole
tissue plasminogen activator
tongue
tourniquet
tracheitis
traction splints
tragsitz
transient ischemic attack
transportation
fractures and
of ill or injured person
improvised methods of
trauma
account of injury
examining of
eye
“traveler’s” diarrhea
trenchfoot
trichinosis
trimethoprim-sulfamethoxazole
trunk fractures
tuberculosis
tube thoracostomy
tularemia
typhoid fever
U
ulcer
corneal
peptic
ultraviolet light
ultraviolet radiation
understanding
upper extremity fractures
urethral catheterization
urinary retention
urinary tract disorders
urine color
uterine bleeding, abnormal
V
vaccines. See immunizations
vacuum mattress
valvular heart disease
varicose veins
vascular disease
vasovagal syncope
venomous snake bites
venous pressure
venous thrombosis
ventricular fibrillation
vertebral fractures
viral infections
viral pharyngitis
viruses
vital signs
vitamins
vomiting
in brain-injury persons
fluid replacement for
medications for
transporting a person while
treatment of
W
warmth
water disinfection
boiling
chemical systems
chlorine
filtration
flocculation
granular activated charcoal
heat
iodine for
methods of
microfiltration
systems for
ultraviolet light
water replacement
water rescue
wilderness rescues. See rescue
wind chill
wolves
work of breathing
wounds
bandaging of
bite
bleeding from
cleansing of
closing of
foot
hands
infection of
puncture
scalp
wrist fractures
Y
yellow fever
Z
zolpidem
ABOUT THE AUTHORS
James A. Wilkerson, M.D., is a
former associate professor of
pathology at the School of
Medicine, University of Alabama in
Birmingham, and a former member
of the board of directors of the
Wilderness Medical Society. He is
currently chair of the Continuing
Medical Education Committee of
the Wilderness Medical Society and
serves as section editor for review
articles on the editorial board for
Wilderness and Environmental
Medicine.
Dr. Wilkerson is editor of all six
editions of Medicine for
Mountaineering (The Mountaineers
Books) as well as both editions of
Hypothermia, Frostbite, and Other
Cold Injuries (The Mountaineers
Books). He is an active climber
(Denali, Kilimanjaro, Olympic
Mountains, Rocky Mountains,
Sierras), white-water rafter (Grand
Canyon, Middle Fork and Main
Salmon), backpacker (Grand
Canyon, Sierras), scuba diver, and
skier.
Ernest E. Moore, M.D., FACS,
FCCM, has been director of the
Rocky Mountain Regional Trauma
Center at Denver Health Medical
Center since 1976 and is vice-
chairman of surgery at the
University of Colorado Denver
School of Medicine. He also serves
as a medical advisor for the
Steamboat Springs Ski Patrol. Dr.
Moore’s research interests are in
hemorrhagic shock resuscitation
and postinjury multiple organ
failure. He has authored 1100
publications and is currently editor
of the World Journal of Emergency
Surgery and associate editor of the
Journal of Trauma and the
American Journal of Surgery. Dr.
Moore has served as president of a
number of academic societies,
including the International
Association for Trauma Surgery and
Intensive Care, the Panamerican
Trauma Society, and the American
Association for the Surgery of
Trauma.
Ken Zafren, M.D., FAAEM,
FACEP, FAWM, is an emergency
physician in Anchorage, Alaska,
and a member of the clinical faculty
in the Division of Emergency
Medicine at Stanford University
Medical Center in California. He
has many years of experience in
mountaineering and mountain
rescue, is the medical director of
the Alaska Mountain Rescue Group,
and has served as medical director
for the Denali National Park
Mountaineering Rangers. He is the
Emergency Medical Services
(EMS) Director for Lake Clark
National Park. Dr. Zafren has
served as chairman of the Medical
Committee of the Mountain Rescue
Association and as a member of the
board of directors of the
Wilderness Medical Society. He
represents the United States on the
International Commission for
Mountain Emergency Medicine and
is the associate medical director for
the Himalayan Rescue Association
of Nepal.
THE MOUNTAINEERS, founded in
1906, is a nonprofit outdoor activity
and conservation club, whose mission
is “to explore, study, preserve, and
enjoy the natural beauty of the
outdoors{4ell}” Based in Seattle,
Washington, the club is now one of the
largest such organizations in the United
States, with seven branches throughout
Washington State.
The Mountaineers sponsors both
classes and year-round outdoor
activities in the Pacific Northwest,
which include hiking, mountain
climbing, ski-touring, snowshoeing,
bicycling, camping, canoeing and
kayaking, nature study, sailing, and
adventure travel. The club’s
conservation division supports
environmental causes through
educational activities, sponsoring
legislation, and presenting informational
programs.
All club activities are led by skilled,
experienced volunteers, who are
dedicated to promoting safe and
responsible enjoyment and preservation
of the outdoors.
If you would like to participate in
these organized outdoor activities or
the club’s programs, consider a
membership in The Mountaineers. For
information and an application, write or
call The Mountaineers, Club
Headquarters, 7700
Sand Point Way NE, Seattle, WA
98115; 206-521-6001. You can also
visit the club’s website at
www.mountaineers.org or contact The
Mountaineers via email at clubmail
@mountaineers.org.
The Mountaineers Books, an active,
nonprofit publishing program of the
club, produces guidebooks,
instructional texts, historical works,
natural history guides, and works on
environmental conservation. All books
produced by The Mountaineers Books
fulfill the club’s mission. Visit
www.mountaineersbooks.org to find
details about all our titles and the latest
author events, as well as videos, web
clips, links, and more!
The Mountaineers Books

1001 SW Klickitat Way, Suite
201
Seattle, WA 98134
800-553-4453
[email protected]
The Mountaineers Books

is proud to be a corporate
sponsor of The Leave No
Trace Center for Outdoor Ethics,
whose mission is to promote and
inspire responsible outdoor
recreation through education,
research, and partnerships. The
Leave No Trace program is focused
specifically on human-powered
(nonmotorized) recreation.
Leave No Trace strives to
educate visitors about the nature of
their recreational impacts, as well as
offer techniques to prevent and
minimize such impacts. Leave No
Trace is best understood as an
educational and ethical program, not
as a set of rules and regulations.
For more information, visit
www.lnt.org, or call 800-332-4100.

Medicine For Mountaineering and Other Wilderness Activities (6th Edition) (2010) (James A. Wilkerson)

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Medicine For Mountaineering and Other Wilderness Activities (6th Edition) (2010) (James A. Wilkerson)

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MEDICINE

Edited by James A.Wilkerson, M.D.

1001 SW Klickitat Way, Suite 201,

© 1967, 1975, 1985, 1992, 2001, 2010

All rights reserved

First edition 1967. Second edition

No part of this book may be

Distributed in the United Kingdom by

Manufactured in the United States of

Copy Editor: Heath Lynn Silberfeld /

Front cover photograph: Panoramic

Library of Congress Cataloging-in-

Medicine for mountaineering & other

Printed on recycled paper

SECTION I: GENERAL PRINCIPLES

SECTION II: TRAUMATIC

SECTION III: NONTRAUMATIC

SECTION IV: ENVIRONMENTAL

At a convention in Salt Lake City,

“Disease manifests itself by

Most individuals injured in

Comfort and Understanding

CARE FOR TRAUMA VICTIMS

FEVER AND CHILLS

Some medical conditions are

SAFETY AND LEADERSHIP

THE ABC’S: AIRWAY,

The steps in an emergency

5. Ideally, a cuffed endotracheal

Starting and Stopping

Attempts to dislodge the food by

Several initial management

Emotional reactions to traumatic

Case Study: Rescuer’s Responses

Sources of Rescue Stress

Normal Reactions to Stress

Preventing Adverse Stress

Stress Sources for Vietnam

Normally the cycle of protest,

Stress Imposed by an Accident

Responses of Accident Victims

Abnormal Responses to Accidents

Severe Derangement (confused

Trauma or Disease Simulating

Psychological Aid for Accident

In developing countries, infections

TRAVELING WITH CHILDREN

For travel to developing countries,

Efforts to develop a more

The older vaccine licensed in

Infants less than six months old

Yellow fever vaccines must be

Sanitation and water disinfection

Insects can be avoided by wearing

Removing Particulate Material

Granular Activated Charcoal

Boiling is inconvenient and time

Filters are relatively bulky (for